Advanced Cardiovascular Life Support Provider Manual

Ad v a c e d C a r d io v a s c la r Life S p p o r t P R O V I D E R

M A n u A L

Ed itors

ACLS Su b c om m itte e 2010-2011

Elizabeth Sinz, MD, Associate Science Editor Kenneth Navarro, Content Consultant

Clifton W. Callaway, MD, PhD, Chair Robert W. Neumar, MD, PhD, Immediate Past Chair, 2008-2010 Steven Brooks , MD Daniel P. Davis , MD Michael Donnino, MD Andrea Gabrielli, MD Romergryko Geocadin, MD Erik Hes s , MD, MSc Mark S. Link, MD Bryan McNally, MD, MPH Venu Menon, MD Graham Nichol, MD, MPH Brian O’Neil, MD J os eph P. Ornato, MD Charles W. Otto, MD Michael Shus ter, MD Scott M. Silvers , MD Mintu Turakhia, MD, MS Terry L. Vanden Hoek, MD J anice L. Zimmerman, MD

Se n ior Ma n a g in g Ed itor Erik S. Soderberg, MS

Sp e c ia l Con trib u tors Clifton W. Callaway, MD, PhD Diana M. Cave, RN, MSN Heba Cos tandy, MD, MS Mary Fran Hazins ki, RN, MSN Theres a Hoadley, RN, PhD, TNS Robert W. Neumar, MD, PhD Peter D. Panagos , MD Sallie Young, PharmD, BCPS

© 2011 American Heart As s ociation ISBN 978-1-61669-010-6 Printed in the United States of America Firs t American Heart As s ociation Printing May 2011 eBook edition © 2013 American Heart As s ociation. ISBN 978-1-61669-350-3

i

ACLS Subc om m itte e 2009-2010 Robert W. Neumar, MD, PhD, Chair Laurie J . Morris on, MD, MSc, Immediate Past Chair, 2006-2008 Steven Brooks , MD Cli ton W. Callaway, MD, PhD Daniel P. Davis , MD Andrea Gabrielli, MD Romergryko Geocadin, MD Richard Kerber, MD Mark S. Link, MD Bryan McNally, MD, MPH Graham Nichol, MD, MPH Brian O’Neil, MD J os eph P. Ornato, MD Charles Otto, MD, PhD Michael Shus ter, MD Scott M. Silvers , MD Terry L. Vanden Hoek, MD

Ac knowle dgm e nts Peter Olu Anders on, MD Ulrik Chris tens en, MD

To f nd out about any updates or corrections to this text, vis it www.he a rt.o rg /c p r, navigate to the page or this cours e, and click on “Updates .” To acces s the Student Webs ite or this cours e, go to www.he a rt.o rg /e c c s tud e nt and enter this code: algorithm ii

Conte nts P a rt 1 Co u r s e Ove r vie w

1 Cours e De s c ription a nd Goa l

1

Cours e Obje c tive s

1

Cours e De s ign

2

Cours e Pre re q uis ite s a nd P re p a ra tion

2

BLS Skills

2

ECG Rhythm Interpretation for Core ACLS Rhythms

3

Bas ic ACLS Drug and Pharmacology Knowledge

3

Practical Application of ACLS Rhythms and Drugs

3

Effective Res us citation Team Concepts

3

Cours e Ma te ria ls

3

ACLS Provider Manual

4

Student Webs ite

5

Pocket Reference Cards

6

Precours e Preparation Checklis t

6

Re quire m e nts for Suc c e s s fu l Cours e Com ple tion

7

ACLS Upda te Cours e

7

ACLS P rovide r Ma nua l Abb re via tions

7

P a rt 2 Th e S ys t e m a t ic Ap p ro a c h : Th e BLS a n d ACLS S u r ve ys

11

Introduction

11

Learning Objectives

11

The Sys te m a tic Ap p roa c h : The BLS a nd ACLS Su rve ys Overview of the Sys tematic Approach

The BLS Surve y Overview of the BLS Survey

The ACLS Surve y Overview of the ACLS Survey

11 11

12 12

14 14

iii

C o n t e n t s

P a rt 3 Effe c t ive Re s u s c it a t io n Te a m Dyn a m ic s

17

Introduction

17

Learning Objectives

17

Role s of th e Te a m Le a d e r a n d Te a m Me m b e rs

18

Role of the Team Leader

18

Role of the Team Member

18

Ele m e n ts of Effe c tive Re s u s c ita tion Te a m Dyn a m ic s

19

Clos ed-Loop Communications

19

Clear Mes s ages

19

Clear Roles and Res pons ibilities

20

Knowing One’s Limitations

21

Knowledge Sharing

22

Cons tructive Intervention

22

Reevaluation and Summarizing

23

Mutual Res pect

23

P a rt 4 S ys t e m s o f Ca re

25 Introduction

25

Learning Objectives

25

Ca rd iop u lm on a ry Re s u s c ita tion

25

Quality Improvement in Res us citation Sys tems , Proces s es , and Outcomes A Sys tems Approach

26

Meas urement

27

Benchmarking and Feedback

27

Change

27

Summary

27

Pos t–Ca rd ia c Arre s t Ca re

28

Therapeutic Hypothermia

28

Hemodynamic and Ventilation Optimization

28

Immediate Coronary Reperfus ion With PCI

28

Glycemic Control

28

Neurologic Care and Prognos tication

29

Ac ute Coron a ry Syndrom e s

iv

25

29

Starts “On the Phone” With Activation of EMS

29

EMS Components

29

Hos pital-Bas ed Components

29

Con te n ts

Ac ute Stroke

30

Regionalization of Stroke Care

30

Community and Profes s ional Education

30

EMS

30

Ed u c a tion , Im p le m e n ta tion , a n d Te a m s

30

The Need for Teams

30

Cardiac Arres t Teams (In-Hos pital)

31

Rapid Res pons e Sys tem

31

Medical Emergency Teams and Rapid Res pons e Teams

31

Regional Sys tems of Emergency Cardiovas cular Care

32

Publis hed Studies

32

Implementation of a Rapid Res pons e Sys tem

32

P a rt 5 Th e ACLS Ca s e s

33 Overview of the Cas es

Re s pira tory Arre s t Ca s e

33

34

The BLS Survey

34

The ACLS Survey

36

Management of Res piratory Arres t

38

Giving Supplementary Oxygen

38

Opening the Airway

38

Providing Bas ic Ventilation

40

Bas ic Airway Adjuncts : Oropharyngeal Airway

42

Bas ic Airway Adjuncts : Nas opharyngeal Airway

43

Suctioning

45

Providing Ventilation With an Advanced Airway

47

Precautions for Trauma Patients

49

VF Tre a te d With CP R a n d AED Ca s e

49

The BLS Survey

50

AED Us e in Special Situations

57

VF/P u ls e le s s VT Ca s e

59

Managing VF/Puls eles s VT: The Cardiac Arres t Algorithm

60

Application of the Cardiac Arres t Algorithm: VF/VT Pathway

62

Routes of Acces s for Drugs

69

Vas opres s ors

70

Antiarrhythmic Agents

71

Immediate Pos t–Cardiac Arres t Care

72

Application of the Immediate Pos t–Cardiac Arres t Care Algorithm

73

P u ls e le s s Ele c tric a l Ac tivity Ca s e Des cription of PEA

78 78 v

C o n t e n t s Managing PEA: The Cardiac Arres t Algorithm

79

Managing PEA: Diagnos ing and Treating Underlying Caus es

82

As ys tole Ca s e

86

Approach to As ys tole

86

Managing As ys tole

87

Application of the Cardiac Arres t Algorithm: As ys tole Pathway

88

Terminating Res us citative Efforts

89

Ac ute Coron a ry Syndrom e s Ca s e

91

Goals for ACS Patients

92

Managing ACS: The Acute Coronary Syndromes Algorithm

95

Identification of Ches t Dis comfort Sugges tive of Is chemia (Box 1)

96

EMS As s es s ment, Care, and Hos pital Preparation (Box 2)

96

Immediate ED As s es s ment and Treatment (Box 3)

99

STEMI (Boxes 5 Through 8)

100

Clas s ify Patients According to ST-Segment Deviation (Boxes 5, 9, and 13)

Bra d yc a rd ia Ca s e

104

Des cription of Bradycardia

107

Managing Bradycardia: The Bradycardia Algorithm

108

Application of the Bradycardia Algorithm

109

Trans cutaneous Pacing

112

Un s ta b le Ta c h yc a rd ia Ca s e

114

The Approach to Uns table Tachycardia

114

Managing Uns table Tachycardia: The Tachycardia Algorithm

116

Application of the Tachycardia Algorithm to the Uns table Patient

118

Cardiovers ion

120

Synchronized Cardiovers ion Technique

122

Sta b le Ta c h yc a rd ia Ca s e

124

Approach to Stable Tachycardia

125

Managing Stable Tachycardia: The Tachycardia Algorithm

126

Application of the Tachycardia Algorithm to the Stable Patient

127

Ac ute Stroke Ca s e

vi

101

130

Approach to Stroke Care

132

Identification of Signs of Pos s ible Stroke (Box 1)

135

Critical EMS As s es s ments and Actions (Box 2)

138

In-Hos pital, Immediate General As s es s ment and Stabilization (Box 3)

139

Immediate Neurologic As s es s ment by Stroke Team or Des ignee (Box 4)

140

CT Scan: Hemorrhage or No Hemorrhage (Box 5)

141

Fibrinolytic Therapy

143

General Stroke Care (Boxes 11 and 12)

146

Con te n ts

Ap p e n d ix

149 Te s tin g Ch e c klis ts a n d Le a rn in g Sta tion Ch e c klis ts

151

2010 AHA Guid e line s fo r CPR a nd ECC Su m m a ry Ta b le

163

ACLS Ph a rm a c ology Sum m a ry Ta ble

165

Glos s a ry

168

Founda tion Inde x

171

In d e x

173

No t e o n Me d ic a t io n Do s e s Emergency cardiovas cular care is a dynamic s cience. Advances in treatment and drug therapies occur rapidly. Readers s hould us e the following s ources to check for changes in recommended dos es , indications , and contraindications : the ECC Handbook, available as optional s upplementary material, and the package ins ert product information s heet for each drug and medical device. vii

C o n t e n t s

Part

1

Cours e Ove rvie w Co u r s e De s c r ip t io n a n d Go a l The Advanced Cardiovas cular Life Support (ACLS) Provider Cours e is des igned for healthcare providers who either direct or participate in the management of cardiopulmonary arres t or other cardiovas cular emergencies . Through didactic ins truction and active participation in s imulated cas es , s tudents will enhance their s kills in the diagnos is and treatment of cardiopulmonary arres t, acute arrhythmia, s troke, and acute coronary s yndromes (ACS). After s ucces s ful completion of this cours e, s tudents will be able to apply important concepts , including • The Bas ic Life Support (BLS) Survey • High-quality cardiopulmonary res us citation (CPR) • The ACLS Survey • The ACLS algorithms • Effective res us citation team dynamics • Immediate pos t–cardiac arres t care The goal of the ACLS Provider Cours e is to improve outcomes for adult patients with cardiac arres t or other cardiopulmonary emergencies through provider training.

Co u r s e Ob je c t ive s Upon s ucces s ful completion of this cours e s tudents s hould be able to • Recognize and initiate early management of periarres t conditions that may res ult in cardiac arres t or complicate res us citation outcome • Demons trate proficiency in providing BLS care, including prioritizing ches t compres s ions and integrating automated external defibrillator (AED) us e • Recognize and manage res piratory arres t • Recognize and manage cardiac arres t until termination of res us citation or trans fer of care, including immediate pos t–cardiac arres t care • Recognize and initiate early management of ACS, including appropriate dis pos ition • Recognize and initiate early management of s troke, including appropriate dis pos ition • Demons trate effective communication as a member or leader of a res us citation team and recognize the impact of team dynamics on overall team performance

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1

Co u r s e De s ig n To help you achieve thes e objectives , the ACLS Provider Cours e includes practice learning s tations and a Megacode evaluation s tation. The practice learning stations give you an opportunity to actively participate in a variety of learning activities , including • Simulated clinical s cenarios • Demons trations by ins tructors or video • Dis cus s ion and role playing • Practice in effective res us citation team behaviors In thes e learning s tations you will practice es s ential s kills both individually and as part of a team. This cours e emphas izes effective team s kills as a vital part of the res us citative effort. You will have the opportunity to practice as a team member and a team leader. At the end of the cours e, you will participate in a Megacode evaluation station to validate your achievement of the cours e objectives . A s imulated cardiac arres t s cenario will evaluate the following: • Knowledge of core cas e material and s kills • Knowledge of algorithms • Unders tanding of arrhythmia interpretation • Us e of appropriate bas ic ACLS drug therapy • Performance as an effective team leader

Co u r s e P re re q u is it e s a n d P re p a r a t io n The American Heart As s ociation (AHA) limits enrollment in the ACLS Provider Cours e to healthcare providers who direct or participate in the res us citation of a patient either in or out of hos pital. Participants who enter the cours e mus t have the bas ic knowledge and s kills to participate actively with the ins tructor and other s tudents . Before the cours e, pleas e read the ACLS Provider Manual, complete the s elf-as s es s ment modules on the Student Webs ite (www.he a rt.o rg /e c c s tud e nt), identify any gaps in your knowledge, and remediate thos e gaps by s tudying the applicable content in the ACLS Provider Manual or other s upplementary res ources . The following knowledge and s kills are required for s ucces s ful cours e completion: • BLS s kills • Electrocardiogram (ECG) rhythm interpretation for core ACLS rhythms • Knowledge of airway management and adjuncts • Bas ic ACLS drug and pharmacology knowledge • Practical application of ACLS rhythms and drugs • Effective res us citation team concepts

BLS S k ills

The foundation of advanced life s upport is s trong BLS s kills . You mus t pas s the 1-Res cuer CPR and AED Tes ting Station to s ucces s fully complete the ACLS cours e. Make sure that you are proficient in BLS skills before attending the course. Watch the CPR and AED Skills video found on the Student Webs ite (www.he a rt.o rg /e c c s tud e nt). Review the CPR and AED Tes ting Checklis t located in the Appendix.

2

Cou rs e Ove rvie w

ECG Rh yt h m In t e r p r e t a t io n fo r Co r e ACLS Rh yt h m s

The bas ic cardiac arres t and periarres t algorithms require s tudents to recognize thes e ECG rhythms : • Sinus rhythm • Atrial fibrillation and flutter • Bradycardia • Tachycardia • Atrioventricular (AV) block • As ys tole • Puls eles s electrical activity (PEA) • Ventricular tachycardia (VT) • Ventricular fibrillation (VF) The AHA recommends that you complete the ECG rhythm identification s elfas s es s ment on the Student Webs ite (www.he a rt.o rg /e c c s tud e nt). At the end of the as s es s ment you will receive your s core and feedback to help you identify areas of s trength and weaknes s . Remediate any gaps in your knowledge before entering the cours e. During the cours e you mus t be able to identify and interpret rhythms during practice as well as during the final Megacode evaluation s tation.

Ba s ic ACLS Dr u g a n d P h a r m a c o lo g y Kn o w le d g e

You mus t know the drugs and dos es us ed in the ACLS algorithms . You will als o need to know when to us e which drug bas ed on the clinical s ituation.

P r a c t ic a l Ap p lic a t io n o f ACLS Rh yt h m s a n d Dr u g s

Take the ACLS practical application s elf-as s es s ment on the Student Webs ite (www.he a rt.o rg /e c c s tud e nt) to evaluate your ability to integrate both rhythm interpretation and the us e of pharmacologic agents . This as s es s ment pres ents a clinical s cenario and an ECG rhythm. You will need to take an action, give a s pecific drug, or direct your team to intervene. Us e this s elf-as s es s ment to confirm that you have the knowledge you need to be an active participant in the cours e and pas s the final Megacode tes t.

Effe c t ive Re s u s c it a t io n Te a m Co n c e p t s

Ins tructors throughout the cours e will evaluate your effectivenes s as a team leader and a team member. A clear unders tanding of thes e concepts is integral to s ucces s ful performance in the learning activities and the Megacode tes t. Review Part 3 in the ACLS Provider Manual before the cours e. During the Megacode the ins tructor will evaluate your team leader s kills with a major emphas is on your ability to direct the integration of BLS and ACLS activities by your team members .

The AHA recommends that you complete the ACLS pharmacology review s elfas s es s ment on the Student Webs ite (www.he a rt.o rg /e c c s tud e nt). At the end of the as s es s ment you will receive your s core and feedback to help you identify areas of s trength and weaknes s . Remediate any gaps in your knowledge before entering the cours e.

Co u r s e Ma t e r ia ls Cours e materials cons is t of the ACLS Provider Manual, Student Webs ite (www.he a rt.o rg /e c c s tud e nt), 2 pocket reference cards , and Precours e Preparation Checklis t. The icon on the left directs you to additional s upplemental information on the Student Webs ite.

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1

ACLS P r o vid e r Ma n u a l

The ACLS Provider Manual contains the bas ic information you need for effective participation in the cours e. This important material includes the s ys tematic approach to a cardiopulmonary emergency, effective res us citation team communication, and the ACLS cas es and algorithms . Please review this manual before attending the course. Bring it with you for use and reference during the course. The manual is organized into the following parts :

Co n t e n t s P a rt 1

Cours e Overview

P a rt 2

The Sys tematic Approach

P a rt 3

Effective Res us citation Team Dynamics

P a rt 4

Sys tems of Care

P a rt 5

The ACLS Cas es

Ap p e nd ix • Te s ting Che c klis ts a nd Le a rning Sta tio n Che c klis ts • 2010 AHA Gu id e lin e s for CP R a n d ECC Sum m a ry Ta b le

Summary of the new 2010 AHA Guidelines for CPR and ECC

• ACLS P ha rm a c o lo g y Sum m a ry Ta b le

Bas ic ACLS drugs , dos es , indications /contraindications , and s ide effects

• Glo s s a ry

Alphabetical lis t of terms

• Fo und a tio n Ind e x

Pages where key s ubjects can be found (eg, epinephrine, cardiovers ion, pacing)

Ind e x The AHA s trongly recommends that s tudents complete the Precours e Self-As s es s ment found on the Student Webs ite and print their s cores for s ubmis s ion to their ACLS Ins tructor. Supplemental topics located on the Student Webs ite are us eful but not es s ential for s ucces s ful completion of the cours e.

Ca ll-ou t Boxe s The ACLS Provider Manual contains important information pres ented in call-out boxes that require the reader’s attention. Pleas e pay particular attention to the call-out boxes , lis ted below: • Critical Concepts • Caution • FYI 2010 Guidelines • Foundational Facts

Cr it ic a l Co n c e p t s Im p o rta nt Info rm a tio n to Re vie w a nd Stud y

4

• Pay particular attention to the Critic a l Co nc e p ts boxes that appear in the ACLS Provider Manual. Thes e boxes contain the mos t important information that you mus t know.

Cou rs e Ove rvie w

Ca u t io n

• Ca utio n boxes emphas ize s pecific ris ks as s ociated with interventions .

FYI 2 0 1 0 Gu id e lin e s

• FYI 2010 Guid e line s boxes contain the new 2010 AHA Guidelines for CPR and ECC information.

Fo u n d a t io n a l Fa c t s

• You will s ee Fo und a tio na l Fa c ts boxes throughout the ACLS Provider Manual. Thes e boxes contain bas ic information that will help you unders tand the topics c overed in the cours e.

S t u d e n t We b s it e

The ACLS Student Webs ite (www.he a rt.o rg /e c c s tud e nt) contains the following s elf-as s es s ment and s upplementary res ources :

Re s o u rc e

De s c r ip t io n

Ho w t o Us e

ACLS Rhythm Id e ntific a tio n

Web-bas ed s elf-as s es s ment: recognition of bas ic ECG rhythms

ACLS P ha rm a c o lo g y

Web-bas ed s elf-as s es s ment: drugs us ed in algorithms

P ra c tic a l Ap p lic a tio n o f ACLS Alg o rithm s

Web-bas ed s elf-as s es s ment: evaluates the practical application of rhythm recognition and pharmacology in the ACLS algorithms

ACLS Sup p le m e nta ry Info rm a tio n

• Bas ic Airway Management • Advanced Airway Management • ACLS Core Rhythms • Defibrillation • Acces s for Medications • Acute Coronary Syndromes • Human, Ethical, and Legal Dimens ions of ECC and ACLS

Additional information to s upplement bas ic concepts pres ented in ACLS cours e

Supplementary res ources : review current BLS s equence and s kills

Review BLS s kills to p repare for the 1-Res cuer CPR and AED Tes ting Station

CP R a nd AED Skills vid e o

Complete before the cours e to help evaluate your proficiency and determine the need for additional review and practice

Some information is s upplementary; other areas are for the interes ted s tudent or advanced p rovider

(continued)

5

P a r t

1 (continued)

Re s o u rc e

P o c k e t Re fe r e n c e Ca r d s

6

Ho w t o Us e

ACS vid e o

Supplementary res ources : ACS as s es s ment and treatment

Review for ACS Learning Station

Stro ke vid e o

Supplementary res ources : s troke as s es s ment and treatment

Review for Stroke Learning Station

ACLS Sc ie nc e Ove rvie w vid e o

Supplementary res ources : core emphas is of the ACLS cours e from a s cience pers pective

Update ACLS knowledge and learn about changes in application of ACLS s cience

IO a nim a tio n

Supplementary res ources : information and demons tration of intraos s eous (IO) ins ertion

Expanded information on IOs

The Pocket Reference Cards are 2 s tand-alone cards packaged with the ACLS Provider Manual. Thes e cards can be carried in your pocket for quick reference on the following topics :

To p ic

Pre c ours e P r e p a r a t io n Ch e c k lis t

De s c r ip t io n

Re fe re n c e Ca rd s

Ca rd ia c a rre s t, a rrhythm ia s , a nd tre a tm e nt

• Cardiac Arres t Algorithms • Gray box with drugs and dos age reminders • Immediate Pos t–Cardiac Arres t Care Algorithm • Bradycardia Algorithm • Tachycardia Algorithm

ACS a nd s tro ke

• ACS Algorithm • Fibrinolytic Checklis t for STEMI • Fibrinolytic Contraindications for STEMI • Sus pected Stroke Algorithm • Stroke As s es s ment–CPSS • Us e of IV rtPA for Acute Is chemic Stroke • Hypertens ion Management in Acute Is chemic Stroke

The Precours e Preparation Checklis t is packaged with the ACLS Provider Manual. Pleas e review and check the boxes after you have completed preparation for each s ection.

Cou rs e Ove rvie w

Re q u ire m e n t s fo r S u c c e s s fu l Co u r s e Co m p le t io n To s ucces s fully complete the ACLS Provider Cours e and obtain your cours e completion card, you mus t • Pas s the 1-Res cuer Adult CPR and AED Tes t • Pas s the Bag-Mas k Ventilation Tes t • Demons trate competency in learning s tation s kills • Pas s the Megacode Tes t • Pas s the clos ed-book written exam with a minimum s core of 84%

ACLS Up d a t e Co u r s e The ACLS Update Cours e is for s tudents who have a current ACLS Provider card and need to update and refres h their ACLS s kills . This cours e is primarily focus ed on s kills competency tes ting. • Maximum renewal period: 2 years • Update requirements : Previous ACLS cours e completion card (not expired)

ACLS P r o vid e r Ma n u a l Ab b re via t io n s A ABCD

ACLS Survey: Airway, Breathing, Circulation, Differential Diagnos is

ACE

Angiotens in-converting enzyme

ACLS

Advanced cardiovas cular life s upport

ACS

Acute coronary s yndromes

AED

Automated external defibrillator

AHF

Acute heart failure

AIVR

Accelerated idioventricular rhythm

AMI

Acute myocardial infarction

a P TT

Activated partial thromboplas tin time

B BLS

Bas ic life s upport: Check res pons ivenes s , activate emergency res pons e s ys tem, check carotid puls e, provide defibrillation

C CARES

Cardiac Arres t Regis try to Enhance Survival

CP R

Cardiopulmonary res us citation

CP SS

Cincinnati Prehos pital Stroke Scale

CT

Computed tomography (continued) 7

P a r t

1 (continued)

D DNAR

Do not attempt res us citation

E ECG

Electrocardiogram

ED

Emergency department

EMS

Emergency medical s ervices

ET

Endotracheal

F FDA

Food and Drug Adminis tration

F io 2

Fraction of ins pired oxygen

G GI

Gas trointes tinal

I ICU

Intens ive care unit

INR

International normalized ratio

IO

Intraos s eous

IV

Intravenous

L LMWH

Low-molecular-weight heparin

LV

Left ventricle or left ventricular

M mA

Milliamperes

MACE

Major advers e cardiac events

MET

Medical emergency team

MI

Myocardial infarction

m m Hg

Millimeters of mercury

N NIH

National Ins titutes of Health

NIHSS

National Ins titutes of Health Stroke Scale

NINDS

National Ins titute of Neurological Dis orders and Stroke

NPA

Nas opharyngeal airway

NSAIDs

Nons teroidal anti-inflammatory drugs

NSTEMI

Non–ST-s egment elevation myocardial infarction (continued)

8

Cou rs e Ove rvie w

(continued)

O OPA

Oropharyngeal airway

P Paco2

Partial pres s ure of carbon dioxide in arterial blood

P CI

Percutaneous coronary intervention

PE

Pulmonary embolis m

P EA

Puls eles s electrical activity

PT

Prothrombin time

R ROSC

Return of s pontaneous circulation

RRT

Rapid res pons e team

rtPA

Recombinant tis s ue plas minogen activator

RV

Right ventricle or right ventricular

S SBP

Sys tolic blood pres s ure

STEMI

ST-s egment elevation myocardial infarction

SVT

Supraventricular tachycardia

T TCP

Trans cutaneous pacing

U UA

Uns table angina

UFH

Unfractionated heparin

V VF

Ventricular fibrillation

VT

Ventricular tachycardia

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1

Part

2

The Sys te m a tic Approa c h: The BLS a nd ACLS Surve ys In t r o d u c t io n

Healthcare providers us e a s ys tematic approach to as s es s and treat arres t and acutely ill or injured patients for optimum care. The goal of the res us citation team’s interventions for a patient in res piratory or cardiac arres t is to s upport and res tore effective oxygenation, ventilation, and circulation with return of intact neurologic function. An intermediate goal of res us citation is the return of s pontaneous circulation (ROSC). The actions us ed are guided by the following s ys tematic approaches : • BLS Survey (s teps des ignated by the numbers 1, 2, 3, 4) • ACLS Survey (s teps des ignated by the letters A, B, C, D)

Le a r n in g Ob je c t ive s

By the end of this part you s hould be able to 1. Des cribe the critical actions of the BLS Survey and ACLS Survey 2. Des cribe as s es s ment and management that occur with each s tep of the s ys tematic approach 3. Des cribe how the as s es s ment/management approach is applicable to mos t cardiopulmonary emergencies

Th e S ys t e m a t ic Ap p ro a c h : Th e BLS a n d ACLS S u r ve ys Ove r vie w o f t h e S ys t e m a t ic Ap p r o a c h

The s ys tematic approach firs t requires ACLS providers to determine the patient’s level of cons cious nes s . As you approach the patient: • If the patient appears uncons cious – Us e the BLS Survey for the initial as s es s ment. – After completing all of the appropriate s teps of the BLS Survey, us e the ACLS Survey for more advanced as s es s ment and treatment. • If the patient appears cons cious – Us e the ACLS Survey for your initial as s es s ment. The details of the BLS and ACLS Surveys are des cribed below.

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2

Th e BLS S u r ve y Ove r vie w o f t h e BLS S u r ve y

The BLS Survey is a s ys tematic approach to bas ic life s upport that any trained healthcare provider can perform. This approach s tres s es early CPR and early defibrillation. It does not include advanced interventions , s uch as advanced airway techniques or drug adminis tra tion. By us ing the BLS Survey, healthcare providers may achieve their goal of s upporting or res toring effective oxygenation, ventilation, and circulation until ROSC or initiation of ACLS interventions . Performing the actions in the BLS Survey s ubs tantially improves the patient’s chance of s urvival and a good neurologic outcome. Be fore c on d u c tin g th e BLS or ACLS Su rve y, look to m a ke s u re th e s c e n e is s a fe . • The BLS Survey us es a s eries of 4 s equential as s es s ment s teps des ignated by the numbers 1, 2, 3, and 4. Simultaneous ly with each as s es s ment s tep, you s hould perform appropriate corrective action(s ) before proceeding to the next s tep. As s es s ment is a key component in this approach (eg, check the puls e before s tarting ches t compres s ions or attaching an AED). Re m e m b e r: As s e s s …th e n p e rform a p p rop ria te a c tion .

FYI 2 0 1 0 Gu id e lin e s

Pleas e note the 2 key changes from the 2005 AHA Guidelines for CPR and ECC:

Cha ng e s in the BLS Surve y

• The 2010 AHA Guidelines for CPR and ECC alters the BLS s equence by eliminating “look, lis ten, and feel” followed by 2 res cue breaths . This change promotes earlier initiation of ches t compres s ions in cardiac arres t patients . • The BLS Survey is no longer repres ented by the letters A, B, C, D but is repres ented by the numbers 1, 2, 3, 4 ins tead.


• Although no publis hed human or animal evidence demons trates that s tarting CPR with 30 compres s ions rather than 2 ventilations leads to improved outcomes , it is clear that blood flow depends on ches t compres s ions . Therefore, providers mus t minimize delays in and interruptions of ches t compres s ions throughout the entire res us citation. Pos itioning the head, achieving a s eal for mouth to mouth res cue breaths , or getting a bag mas k device for res cue breaths takes time. Beginning CPR with 30 compres s ions rather than 2 ventilations leads to a s horter delay to the firs t compres s ion. • Once one provider begins ches t compres s ions , a s econd trained healthcare provider s hould deliver res cue breaths to provide oxygenation and ventilation as follows : – Deliver each res cue breath over 1 s econd – Give a s ufficient tidal volume to produce vis ible ches t ris e

Sta rting With Che s t Co m p re s s io ns vs 2 Bre a ths

Although the BLS Survey requires no advanced equipment, healthcare providers can us e any readily available univers al precaution s upplies or adjuncts , s uch as a bag mas k venti lation device. Whenever pos s ible, place the patient on a firm s urface in a s upine pos ition to maximize the effectivenes s of ches t compres s ions . Table 1 is an overview of the BLS Survey, and Figures 1 through 4 illus trate the s teps needed during the BLS Survey. Before approaching the patient, ens ure s cene s afety. For more details , review the VF Treated With CPR and AED Cas e in Part 5 of this manual and watch the CPR and AED Skills video on the Student Webs ite (www.he a rt.o rg /e c c s tud e nt).

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Th e Sys te m a tic Ap p roa c h

Ta b le 1 . The BLS Surve y

As s e s s 1

Che c k re s p o ns ive ne s s

As s e s s m e n t Te c h n iq u e a n d Ac t io n • Tap and s hout, “Are you a ll rig h t? ” • Check for abs ent or abnormal breathing (no breathing or only gas ping) by looking at or s c a nning the c he s t fo r m o ve m e nt (about 5 to 10 s econds )

Fig u re 1 . Check res pons ivenes s .

2

Ac tiva te the e m e rg e nc y re s p o ns e s ys te m /g e t AED

• Activate the emergency res pons e s ys tem and get an AED if one is available or s end s omeone to activate the emergency res pons e s ys tem and get an AED or defibrillator

Fig u re 2 . Activate the emergency res pons e s ys tem.

3

Circ ula tio n

• Che c k the c a ro tid p uls e for 5 to 10 s econds • If no puls e within 10 s econds , s tart CPR (30:2) beginning with ches t compres s ions – Compres s the center of the ches t (lower half of the s ternum) hard and fas t with at leas t 100 compres s ions per minute at a depth of at leas t 2 inches – Allow complete ches t recoil after each compres s ion – Minimize interruptions in compres s ions (10 s econds or les s ) – Switch providers about every 2 minutes to avoid fatigue – Avoid exces s ive ventilation • If there is a puls e, s tart res cue breathing at 1 breath every 5 to 6 s econds (10 to 12 breaths per minute). Check puls e about every 2 minutes

4

De fib rilla tio n

Fig u re 3 . Check the carotid puls e.

• If no puls e, check for a s hockable rhythm with an AED/ defibrillator as s oon as it arrives • Provide s hocks as indicated • Follow each s hock immediately with CPR, beginning with compres s ions

Fig u re 4 . Defibrillation.

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Cr it ic a l Co n c e p t s Minim izing Inte rrup tio ns

ACLS p ro vid e rs m us t m a ke e ve ry e ffo rt to m inim ize a ny inte rrup tio ns in c he s t c o m p re s s io ns . Try to limit interruptions in ches t compres s ions (eg, defibrillation and advanced airway) to no longer than 10 s econds , except in extreme circums tances , s uch as removing the patient from a dangerous environment. When you s top ches t compres s ions , blood flow to the brain and heart s tops . Avo id : • Prolonged rhythm analys is • Frequent or inappropriate puls e checks • Taking too long to give breaths to the patient • Unneces s arily moving the patient

Fo u n d a t io n a l Fa c t s Lo ne He a lthc a re P ro vid e r Ma y Ta ilo r Re s p o ns e

Cr it ic a l Co n c e p t s Hig h-Qua lity CP R

• Lone healthcare providers may tailor the s equence of res cue actions to the mos t likely caus e of arres t. For example, if a lone healthcare provider s ees an adoles cent s uddenly collaps e, it is reas onable to as s ume that the patient has s uffered a s udden cardiac arres t. • The lone res cuer s hould call for help (activate the emergency res pons e s ys tem), get an AED (if nearby), return to the patient to attach the AED, and then provide CPR. • On the other hand, if hypoxia is the pres umed caus e of the cardiac arres t (s uch as in a drowning patient), the healthcare provider may give about 5 cycles (approximately 2 minutes ) of CPR before activating the emergency res pons e s ys tem.

• Compres s the ches t hard and fas t. • Allow complete ches t recoil after each compres s ion. • Minimize interruptions in compres s ions (10 s econds or les s ). • Switch providers about every 2 minutes to avoid fatigue. • Avoid exces s ive ventilation.

Th e ACLS S u r ve y Ove r vie w o f t h e ACLS S u r ve y

For uncons cious patients in arres t (cardiac or res piratory): • Healthcare providers s hould conduct the ACLS Survey after completing the BLS s urvey. For cons cious patients who may need more advanced as s es s ment and management techniques : • Healthcare providers s hould conduct the ACLS Survey firs t. An important component of this s urvey is the differential diagnos is , where identification and treatment of the underlying caus es may be critical to patient outcome. In the ACLS Survey you continue to as s es s and perform an action as appropriate until trans fer to the next level of care. Many times , team members perform as s es s ments and actions in ACLS s imultaneous ly. Re m e m b e r: As s e s s …th e n p e rform a p p rop ria te a c tion .

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Th e Sys te m a tic Ap p roa c h

Table 2 provides an overview of the ACLS Survey. The ACLS cas es provide details on thes e components . Ta b le 2 . The ACLS Surve y

As s e s s Airwa y – Is the airway patent? – Is an advanced airway indicated? – Is proper placement of airway device confirmed? – Is tube secured and placement reconfirmed frequently?

Ac t io n a s Ap p ro p r ia t e • Ma inta in a irwa y p a te nc y in unc o ns c io us p a tie nts by us e of the head tilt–chin lift, oropharyngeal airway (OPA), or nas opharyngeal airway (NPA) • Us e a d va nc e d a irwa y m a na g e m e nt if ne e d e d (eg, laryngeal mas k airway, laryngeal tube, es ophageal-tracheal tube, endotracheal tube [ET tube]) Healthcare providers must weigh the benefit of advanced airway placement against the adverse effects of interrupting chest compressions. If bagmask ventilation is adequate, healthcare providers may defer insertion of an advanced airway until the patient fails to respond to initial CPR and defibrillation or until spontaneous circulation returns. Advanced airway devices such as a laryngeal mask airway, laryngeal tube, or esophageal-tracheal tube can be placed while chest compressions continue. If us ing advanced airway devices : • Co nfirm p ro p e r inte g ra tio n o f CP R a nd ve ntila tio n • Co nfirm p ro p e r p la c e m e nt o f a d va nc e d a irwa y d e vic e s by – Phys ical examination – Quantitative waveform capnography ▪ Clas s I recommendation for ET tube ▪ Reas onable for s upraglottic airways • Se c ure the d e vic e to p re ve nt d is lo d g m e nt • Mo nito r a irwa y p la c e m e nt with c o ntinuo us q ua ntita tive wa ve fo rm c a p no g ra p hy

Bre a thing – Are ventilation and oxygenation adequate? – Are quantitative waveform capnography and oxyhemoglobin saturation monitored?

• Give s up p le m e nta ry o xyg e n whe n ind ic a te d – For cardiac arres t patients , adminis ter 100% oxygen – For others , titrate oxygen adminis tration to achieve oxygen s aturation values of ≥94% by puls e oximetry • Mo nito r the a d e q ua c y o f ve ntila tio n a nd o xyg e na tio n by – Clinical criteria (ches t ris e and cyanos is ) – Quantitative waveform capnography – Oxygen s aturation • Avo id e xc e s s ive ve ntila tio n (continued)

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2 (continued)

As s e s s Circ ula tio n – Are chest compressions effective? – What is the cardiac rhythm? – Is defibrillation or cardioversion indicated? – Has IV/IO access been established? – Is ROSC present? – Is the patient with a pulse unstable? – Are medications needed for rhythm or blood pressure? – Does the patient need volume (fluid) for resuscitation? Diffe re ntia l d ia g no s is – Why did this patient develop symptoms or arrest? – Is there a reversible cause that can be treated?

Ac t io n a s Ap p ro p r ia t e • Mo nito r CP R q ua lity – Quantitative waveform capnography (if P e t c o 2 is <10 mm Hg, attempt to improve CPR quality) – Intra-arterial pres s ure (if relaxation phas e [dias tolic] pres s ure is <20 mm Hg, attempt to improve CPR quality) • Atta c h m o nito r/d e fib rilla to r fo r a rrhythm ia s o r c a rd ia c a rre s t rhythm s (eg, VF, puls eles s VT, as ys tole, PEA) • P ro vid e d e fib rilla tio n/c a rd io ve rs io n • Ob ta in IV/IO a c c e s s • Give a p p ro p ria te d rug s to manage rhythm and blood pres s ure • Give IV/IO fluid s if ne e d e d

• Se a rc h fo r, find , a nd tre a t re ve rs ib le c a us e s (ie, definitive care)

P e t c o 2 is the partial pres s ure of CO 2 in exhaled air at the end of the exhalation phas e.

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Part

3

Effe c tive Re s us c ita tion Te a m Dyna m ic s

In t r o d u c t io n

Succes s ful res us citation attempts often require healthcare providers to s imultaneous ly perform a variety of interventions . Although a CPR-trained bys tander working alone can res us citate a patient within the firs t moments after collaps e, mos t attempts require the concerted efforts of multiple healthcare providers . Effective teamwork divides the tas ks while multiplying the chances of a s ucces s ful outcome. Succes s ful teams not only have medical expertis e and mas tery of res us citation s kills , but they als o demons trate effective communication and team dynamics . Part 3 of this manual dis cus s es the importance of team roles , behaviors of effective team leaders and team members , and elements of effective res us citation team dynamics . During the cours e you will have an opportunity to practice performing different roles as a member and a leader of a s imulated res us citation team.


By the end of this part you s hould be able to 1. Des cribe team leader’s and team members ’ roles 2. Explain the importance of the team leader and team members unders tanding their s pecific roles 3. Des cribe how s kills mas tery combined with team dynamics may lead to increas ed s ucces s in res us citation outcomes 4. Des cribe key elements of an effective res us citation 5. Coordinate team functions while ens uring continuous high-quality CPR, defibrillation, and rhythm as s es s ment

Fo u n d a t io n a l Fa c t s Und e rs ta nd ing Te a m Ro le s

Whether you are a team member or team leader during a res us citation attempt, you s hould u n d e rs ta n d n ot on ly you r role b u t a ls o th e role s of oth e r te a m m e m b e rs . This awarenes s will help you anticipate • What actions will be performed next • How to communicate and work as a member or leader of the team

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Ro le s o f t h e Te a m Le a d e r a n d Te a m Me m b e r s Ro le o f t h e Te a m Le a d e r

The role of the team leader is multifaceted. The team leader • Organizes the group • Monitors individual performance of team members • Backs up team members • Models excellent team behavior • Trains and coaches • Facilitates unders tanding • Focus es on comprehens ive patient care Every res us citation team needs a leader to organize the efforts of the group. The team leader is res pons ible for making s ure everything is done at the right time in the right way by monitoring and integrating individual performance of team members . The role of the team leader is s imilar to that of an orches tra conductor directing individual mus icians . Like a conductor, the team leader does not play the ins truments but ins tead knows how each member of the orches tra fits into the overall mus ic. The role of the team leader als o includes modeling excellent team behavior and leaders hip s kills for the team and other people involved or interes ted in the res us citation. The team leader s hould s erve as a teacher or guide to help train future team leaders and improve team effectivenes s . After res us citation the team leader can facilitate analys is , critique, and practice in preparation for the next res us citation attempt. The team leader als o helps team members unders tand why they mus t perform certain tas ks in a s pecific way. The team leader s hould be able to explain why it is es s ential to • Pus h hard and fas t • Ens ure complete ches t recoil • Minimize interruptions in ches t compres s ions • Avoid exces s ive ventilations Whereas team members s hould focus on their individual tas ks , the team leader mus t focus on comprehens ive patient care. Review the ACLS Science Overview video on the Student Webs ite (www.he a rt.o rg /e c c s tud e nt) to help prepare for this role.

Ro le o f t h e Te a m Me m b e r

Team members mus t be proficient in performing the s kills authorized by their s cope of practice. It is es s ential to the s ucces s of the res us citation attempt that team members are • Clear about role as s ignments • Prepared to fulfill their role res pons ibilities • Well practiced in res us citation s kills • Knowledgeable about the algorithms • Committed to s ucces s

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Effe c tive Re s u s c ita tion Te a m Dyn a m ic s

Ele m e n t s o f Effe c t ive Re s u s c it a t io n Te a m Dyn a m ic s Clo s e d -Lo o p Co m m u n ic a t io n s

When communicating with res us citation team members , the team leader s hould us e clos ed-loop communication by taking thes e s teps : 1. The team leader gives a mes s age, order, or as s ignment to a team member. 2. By receiving a clear res pons e and eye contact, the team leader confirms that the team member heard and unders tood the mes s age. 3. The team leader lis tens for confirmation of tas k performance from the team member before as s igning another tas k.

Do Te a m le a d e r

• As s ign another tas k after receiving oral confirmation that a tas k has been completed, s uch as , “Now that the IV is in, give 1 mg of epinephrine”

Te a m m e m b e rs

• Clos e the loop: Inform the team leader when a tas k begins or ends , s uch as , “The IV is in”

Do n ’t

Cle a r Me s s a g e s

Te a m le a d e r

• Give more tas ks to a team member without as king or receiving confirmation of a completed as s ignment

Te a m m e m b e rs

• Give drugs without verbally confirming the order with the team leader • Forget to inform the team leader after giving the drug or performing the procedure

Clear mes s ages cons is t of concis e communication s poken with dis tinctive s peech in a controlled tone of voice. All healthcare providers s hould deliver mes s ages and orders in a calm and direct manner without yelling or s houting. Unclear communication can lead to unneces s ary delays in treatment or to medication errors . For example: “Did the patient get IV propofol s o I can proceed with the cardiovers ion? ” “No, I thought you s aid to give him propranolol.” Yelling or s houting can impair effective team interaction. Only one pers on s hould talk at any time.


• Encourage team members to s peak clearly

Te a m m e m b e rs

• Repeat the medication order • Ques tion an order if the s lightes t doubt exis ts

Do n ’t Te a m le a d e r

• Mumble or s peak in incomplete s entences • Give unclear mes s ages and drug/medication orders • Yell, s cream, or s hout

Te a m m e m b e rs

• Feel patronized by dis tinct and concis e mes s ages

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Cle a r Ro le s a n d Re s p o n s ib ilit ie s

Every member of the team s hould know his or her role and res pons ibilities . J us t as different s haped pieces make up a jigs aw puzzle, each team member’s role is unique and critical to the effective performance of the team. Figure 5 identifies 6 team roles for res us citation. When <6 people are pres ent, all tas ks mus t be as s igned to the healthcare providers pres ent. When roles are unclear, team performance s uffers . Signs of unclear roles include • Performing the s ame tas k more than once • Mis s ing es s ential tas ks • Freelancing of team members To avoid inefficiencies , the team leader mus t clearly delegate tas ks . Team members s hould communicate when and if they can handle additional res pons ibilities . The team leader s hould encourage team members to participate in leaders hip and not s imply follow directions blindly.


• Clearly define all team member roles in the clinical s etting

Te a m m e m b e rs

• Seek out and perform clearly defined tas ks appropriate to your level of competence • As k for a new tas k or role if you are unable to perform your as s igned tas k becaus e it is beyond your level of experience or competence

Do n ’t

20

Te a m le a d e r

• Neglect to as s ign tas ks to all available team members • As s ign tas ks to team members who are uns ure of their res pons ibilities • Dis tribute as s ignments unevenly, leaving s ome with too much to do and others with too little

Te a m m e m b e rs

• Avoid taking as s ignments • Take as s ignments beyond your level of competence or expertis e


Airwa y

Co m p re s s o r

IV/IO/Me d s

Mo nito r/ De b rilla to r Ob s e rve r/ Re c o rd e r

TEAM LEADER Fig u re 5 . Sugges ted locations of team leader and team members during cas e s imulations .

Kn o w in g On e ’s Lim it a t io n s

Not only s hould everyone on the team know his or her own limitations and capabilities , but the team leader s hould als o be aware of them. This allows the team leader to evaluate team res ources and call for backup of team members when as s is tance is needed. Team members s hould anticipate s ituations in which they might require as s is tance and inform the team leader. During the s tres s of an attempted res us citation, do not practice or explore a new s kill. If you need extra help, reques t it early. It is not a s ign of weaknes s or incompetence to as k for help; it is better to have more help than needed rather than not enough help, which might negatively affect patient outcome.

Do Te a m le a d e r a nd te a m m e m b e rs

• Call for as s is tance early rather than waiting until the patient deteriorates to the point that help is critical • Seek advice from more experienced pers onnel when the patient’s condition wors ens des pite primary treatment

Do n ’t Te a m le a d e r a nd te a m m e m b e rs

• Reject offers from others to carry out an as s igned tas k you are unable to complete, es pecially if tas k completion is es s ential to treatment

Te a m m e m b e rs

• Us e or s tart an unfamiliar treatment or therapy without s eeking advice from more experienced pers onnel • Take on too many as s ignments at a time when as s is tance is readily available

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Kn o w le d g e S h a r in g

Sharing information is a critical component of effective team performance. Team leaders may become trapped in a s pecific treatment or diagnos tic approach; this common human error is called a fixation error. Examples of 3 common types of fixation errors are • “Everything is okay.” • “This and only this is the correct path.” • “Anything but this .” When res us citative efforts are ineffective, go back to the bas ics and talk as a team. “Well, we’ve gotten the following on the ACLS Survey…. Have we mis s ed s omething? ” Team members s hould inform the team leader of any changes in the patient’s condition to ens ure that decis ions are made with all available information.


• Encourage an environment of information s haring and as k for s ugges tions if uncertain of the next bes t interventions • As k for good ideas for differential diagnos es • As k if anything has been overlooked (eg, IV acces s s hould have been obtained or drugs s hould have been adminis tered)

Te a m m e m b e rs

• Share information with other team members

Do n ’t

Co n s t r u c t ive In t e r ve n t io n

Te a m le a d e r

• Ignore others ’ s ugges tions for treatment • Overlook or fail to examine clinical s igns that are relevant to the treatment

Te a m m e m b e rs

• Ignore important information to improve your role

During a res us citation attempt the team leader or a team member may need to intervene if an action that is about to occur may be inappropriate at the time. Although cons tructive intervention is neces s ary, it s hould be tactful. Team leaders s hould avoid confrontation with team members . Ins tead, conduct a debriefing afterward if cons tructive criticis m is needed.


• As k that a different intervention be s tarted if it has a higher priority

Te a m m e m b e rs

• Sugges t an alternative drug or dos e in a confident manner • Ques tion a colleague who is about to make a mis take

Do n ’t

22

Te a m le a d e r

• Fail to reas s ign a team member who is trying to function beyond his or her level of s kill

Te a m m e m b e rs

• Ignore a team member who is about to adminis ter a drug incorrectly


Re e va lu a t io n a n d S u m m a r iz in g

An es s ential role of the team leader is monitoring and reevaluating • The patient’s s tatus • Interventions that have been performed • As s es s ment findings A good practice is for the team leader to s ummarize this information out loud in a periodic update to the team. Review the s tatus of the res us citation attempt and announce the plan for the next few s teps . Remember that the patient’s condition can change. Remain flexible to changing treatment plans and revis iting the initial differential diagnos is . As k for information and s ummaries from the code recorder as well.


• Draw continuous attention to decis ions about differential diagnos es • Review or maintain an ongoing record of drugs and treatments adminis tered and the patient’s res pons e

Te a m le a d e r a nd te a m m e m b e rs

• Clearly draw attention to s ignificant changes in the patient’s clinical condition • Increas e monitoring (eg, frequency of res pirations and blood pres s ure) when the patient’s condition deteriorates

Do n ’t Te a m le a d e r

Mu t u a l Re s p e c t

• Fail to change a treatment s trategy when new information s upports s uch a change • Fail to inform arriving pers onnel of the current s tatus and plans for further action

The bes t teams are compos ed of members who s hare a mutual res pect for each other and work together in a collegial, s upportive manner. To have a high-performing team, everyone mus t abandon ego and res pect each other during the res us citation attempt, regardles s of any additional training or experience that the team leader or s pecific team members may have.

Do Te a m le a d e r a nd te a m m e m b e rs

• Speak in a friendly, controlled tone of voice • Avoid s houting or dis playing aggres s ion if you are not unders tood initially

Te a m le a d e r

• Acknowledge correctly completed as s ignments by s aying, “Thanks —good job!”

Do n ’t Te a m le a d e r a nd te a m m e m b e rs

• Shout or yell at team members —when one pers on rais es his voice, others will res pond s imilarly • Behave aggres s ively or confus e directive behavior with aggres s ion • Be uninteres ted in others

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3

Part

4

Sys te m s of Ca re


A s ys tem is a group of regularly interacting and interdependent components . The s ys tem provides the links for the chain and determines the s trength of each link and the chain as a whole. By definition, the s ys tem determines the ultimate outcome and s trength of the chain and provides collective s upport and organization. For patients with pos s ible ACS, the s ys tem rapidly triages patients , determines a pos s ible or provis ional diagnos is , and initiates a s trategy bas ed on initial clinical characteris tics .


By the end of this part you s hould be able to 1. Des cribe how s ys tems of care are coordinated on the bas is of the individual’s health needs 2. Define s ys tems of care that provide early acces s to coronary angiography, pos tarres t therapeutic hypothermia, and admis s ion to units providing s pecialized care 3. Des cribe the components of a rapid res pons e s ys tem 4. Dis cus s how the us e of a rapid res pons e team (RRT) or medical emergency team (MET) may improve patient outcomes

Ca rd io p u lm o n a r y Re s u s c it a t io n Qu a lit y Im p r o ve m e n t in Re s u s c it a t io n S ys t e m s , P r o c e s s e s , a n d Ou t c o m e s

Cardiopulmonary res us citation is a s eries of lifes aving actions that improve the chance of s urvival following cardiac arres t. Although the optimal approach to CPR may vary, depending on the res cuer, the patient, and the available res ources , the fundamental challenge remains how to achieve early and effective CPR.

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4

A S ys t e m s Ap p r o a c h

Succes s ful res us citation following cardiac arres t requires an integrated s et of coordinated actions repres ented by the links in the adult Chain of Survival (Figure 6). The links include the following: • Immediate recognition of cardiac arres t and activation of the emergency res pons e s ys tem • Early CPR with an emphas is on ches t compres s ions • Rapid defibrillation • Effective advanced life s upport • Integrated pos t–cardiac arres t care Effective res us citation requires an integrated res pons e known as a s ys tem of care. Fundamental to a s ucces s ful res us citation s ys tem of care is the collective appreciation of the challenges and opportunities pres ented by the Chain of Survival. Thus , individuals and groups mus t work together, s haring ideas and information, to evaluate and improve their res us citation s ys tem. Leaders hip and accountability are important components of this team approach. To improve care, leaders mus t as s es s the performance of each s ys tem component. Only when performance is evaluated can participants in a s ys tem effectively intervene to improve care. This proces s of quality improvement cons is ts of an iterative and continuous cycle of • Sys tematic evaluation of res us citation care and outcome • Benchmarking with s takeholder feedback • Strategic efforts to addres s identified deficiencies

Fig u re 6 . The adult Chain of Survival.

Fo u n d a t io n a l Fa c t s Me d ic a l Em e rg e nc y Te a m s (METs ) a nd Ra p id Re s p o ns e Te a m s (RRTs )

26

• Many hos pitals have implemented the us e of METs or RRTs . The purpos e of thes e teams is to improve patient outcomes by identifying and treating early clinical deterioration (Figure 7). In-hos pital cardiac arres t is commonly preceded by phys iologic changes . In one s tudy nearly 80% of hos pitalized patients with cardiores piratory arres t had abnormal vital s igns documented for up to 8 hours before the actual arres t. Many of thes e changes can be recognized by monitoring routine vital s igns . Intervention before clinical deterioration or cardiac arres t may be pos s ible. • Cons ider this ques tion: “Would you have done anything differently if you knew 15 minutes before the arres t that…? ”

Sys te m s of Ca re

U n s t a b le l P a t ie n t Ra p id Re s p o n s e Te a m

Cod e Te a m

Cr it ic a l Ca re Te a m

Fig u re 7 . Management of life-threatening emergencies requires integration of multidis ciplinary teams that can involve rapid res pons e teams , cardiac arres t teams , and intens ive care s pecialties to achieve s urvival of the patient. Team leaders have an es s ential role in coordination of care with team members and other s pecialis ts .

Me a s u r e m e n t

Quality improvement relies on valid as s es s ment of res us citation performance and outcome. The Uts tein Guidelines provide guidance for core performance meas ures , including – Rate of bys tander CPR – Time to defibrillation – Survival to hos pital dis charge Importance of information s haring among all links in the s ys tem of care – Dis patch records – Emergency medical s ervices (EMS) patient care report – Hos pital records

Be n c h m a r k in g a n d Fe e d b a c k

Data s hould be s ys tematically reviewed and compared internally to prior performance and externally to s imilar s ys tems . Exis ting regis tries can facilitate this benchmarking effort. Examples include the Cardiac Arres t Regis try to Enhance Survival (CARES) for out-of-hos pital cardiac arres t Get With The Guidelines ®–Res us citation program for in-hos pital cardiac arres t

Ch a n g e

Simply meas uring and benchmarking care can pos itively influence outcome. However, ongoing review and interpretation are neces s ary to identify areas for improvement, s uch as Increas ed bys tander CPR res pons e rates Improved CPR performance Shortened time to defibrillation Citizen awarenes s Citizen and healthcare profes s ional education and training

Su m m a r y

Over the pas t 50 years the modern-era bas ic life s upport fundamentals of early recognition and activation, early CPR, and early defibrillation have s aved hundreds of thous ands of lives around the world. However, we s till have a long road to travel if we are to fulfill the potential offered by the Chain of Survival. Survival dis parities pres ent a generation ago appear to pers is t. Fortunately, we currently pos s es s the knowledge and tools — repres ented by the Chain of Survival—to addres s many of thes e care gaps , and future dis coveries will offer opportunities to improve rates of s urvival.

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P a r t

4

P o s t –Ca rd ia c Ar re s t Ca re The healthcare s ys tem s hould implement a comprehens ive, s tructured, multidis ciplinary s ys tem of care in a cons is tent manner for the treatment of pos t–cardiac arres t patients . Programs s hould addres s therapeutic hypothermia, hemodynamic and ventilation optimization, immediate coronary reperfus ion with percutaneous coronary intervention (PCI), glycemic control, neurologic care and prognos tication, and other s tructured interventions . Individual hos pitals with a high frequency of treating cardiac arres t patients s how an increas ed likelihood of s urvival when thes e interventions are provided.

Th e r a p e u t ic Hyp o t h e r m ia

The 2010 AHA Guidelines for CPR and ECC recommends cooling comatos e (ie, lack of meaningful res pons e to verbal commands ) adult patients with ROSC after out-of-hos pital VF cardiac arres t to 32°C to 34°C (89.6°F to 93.2°F) for 12 to 24 hours . Healthcare providers s hould als o cons ider induced hypothermia for comatos e adult patients with ROSC after in-hos pital cardiac arres t of any initial rhythm or after out-of-hos pital cardiac arres t with an initial rhythm of PEA or as ys tole.

He m o d yn a m ic a n d Ve n t ila t io n Op t im iz a t io n

Although providers often us e 100% oxygen while performing the initial res us citation, providers s hould titrate ins pired oxygen during the pos t–cardiac arres t phas e to the lowes t level required to achieve an arterial oxygen s aturation of ≥94% . This helps to avoid any potential complications as s ociated with oxygen toxicity. Avoid exces s ive ventilation of the patient becaus e of potential advers e hemodynamic effects when intrathoracic pres s ures are increas ed and becaus e of potential decreas es in cerebral blood flow when Pa c o 2 decreas es . Healthcare providers may s tart ventilation rates at 10 to 12 breaths per minute and titrate to achieve a P e t c o 2 of 35 to 40 mm Hg or a Pa c o 2 of 40 to 45 mm Hg. Healthcare providers s hould titrate fluid adminis tration and vas oactive or inotropic agents as needed to optimize blood pres s ure, cardiac output, and s ys temic perfus ion. The optimal pos t–cardiac arres t blood pres s ure remains unknown; however, a mean arterial pres s ure ≥65 mm Hg is a reas onable goal.

Im m e d ia t e Co r o n a r y Re p e r fu s io n Wit h P CI

Following ROSC, res cuers s hould trans port the patient to a facility capable of reliably providing coronary reperfus ion (eg, PCI) and other goal-directed pos tarres t care therapies . The decis ion to perform PCI can be made irres pective of the pres ence of coma or the decis ion to induce hypothermia, becaus e concurrent PCI and hypothermia are reported to be feas ible and s afe and have good outcomes .

Glyc e m ic Co n t r o l

Cons ider s trategies to target moderate glycemic control (144 to 180 mg/dL [8 to 10 mmol/L]) in adult patients with ROSC after cardiac arres t. Healthcare providers s hould not attempt to alter glucos e concentration within a lower range (80 to 110 mg/dL [4.4 to 6.1 mmol/L]) due to the increas ed ris k of hypoglycemia.

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Sys te m s of Ca re

Ne u r o lo g ic Ca r e a n d P r o g n o s t ic a t io n

The goal of pos t–cardiac arres t management is to return patients to their prearres t functional level. Reliable early prognos tication of neurologic outcome is an es s ential component of pos t–cardiac arres t care. Mos t importantly, when cons idering decis ions to limit or withdraw life-s us taining care, tools us ed to prognos ticate poor outcome mus t be accurate and reliable, with a fals e-pos itive rate approaching 0% .

Ac u t e Co ro n a r y S yn d ro m e s The primary goals of therapy for patients with ACS are to 1. Reduce the amount of myocardial necros is that occurs in patients with acute myocardial infarction (AMI), thus pres erving left ventricular (LV) function, preventing heart failure, and limiting other cardiovas cular complications 2. Prevent major advers e cardiac events (MACE): death, nonfatal MI, and the need for urgent revas cularization 3. Treat acute, life-threatening complications of ACS, s uch as VF, puls eles s VT, uns table tachycardias , s ymptomatic bradycardias , pulmonary edema, cardiogenic s hock, and mechanical complications of AMI

S t a r t s “On t h e P h o n e ” Wit h Ac t iva t io n o f EMS

Prompt diagnos is and treatment offers the greates t potential benefit for myocardial s alvage. Thus , it is imperative that healthcare providers recognize patients with potential ACS in order to initiate evaluation, appropriate triage, and management as expeditious ly as pos s ible.

EMS Co m p o n e n t s

• Prehos pital ECGs • Notification of the receiving facility of a patient with pos s ible ST-s egment elevation myocardial infarction (“STEMI alert”) • Activation of the cardiac catheterization team to s horten reperfus ion time • Continuous review and quality improvement

Ho s p it a l-Ba s e d Co m p o n e n t s

• Em e rg e nc y d e p a rtm e nt (ED) p ro to c o ls – Activation of the cardiac catheterization laboratory – Admis s ion to the coronary intens ive care unit (ICU) – Quality as s urance, real-time feedback, and healthcare provider education • Em e rg e nc y p hys ic ia n – Empowered to s elect the mos t appropriate reperfus ion s trategy – Empowered to activate the cardiac catheterization team as indicated • Ho s p ita l le a d e rs hip – Mus t be involved in the proces s and committed to s upport rapid acces s to STEMI reperfus ion therapy

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4

Ac u t e S t ro k e The healthcare s ys tem has achieved s ignificant improvements in s troke care through integration of public education, emergency dis patch, prehos pital detection and triage, hos pital s troke s ys tem development, and s troke unit management. Not only have the rates of appropriate fibrinolytic therapy increas ed over the pas t 5 years , but overall s troke care has als o improved, in part through the creation of s troke centers .

Re g io n a liz a t io n o f S t r o k e Ca r e

With the National Ins titute of Neurological Dis orders and Stroke (NINDS) recombinant tis s ue plas minogen activator (rtPA) trial, the crucial need for local partners hips between academic medical centers and community hos pitals became clear. The time-s ens itive nature of s troke requires s uch an approach, even in dens ely populated metropolitan centers .

Co m m u n it y a n d P r o fe s s io n a l Ed u c a t io n

Community and profes s ional education is es s ential and has s ucces s fully increas ed the proportion of s troke patients treated with fibrinolytic therapy.

EMS

The integration of EMS into regional s troke models is crucial for improvement of patient outcomes :

• Patient education efforts are mos t effective when the mes s age is clear and s uccinct. • Educational efforts need to couple the knowledge of the s igns and s ymptoms of s troke with action—activate the emergency res pons e s ys tem.

• EMS res pons e pers onnel trained in s troke recognition • Stroke-prepared hos pitals –primary s troke centers • Acces s to s troke expertis e via telemedicine from the neares t s troke center

Ed u c a t io n , Im p le m e n t a t io n , a n d Te a m s The Chain of Survival is a metaphor us ed to organize and des cribe the integrated s et of time-s ens itive coordinated actions neces s ary to maximize s urvival from cardiac arres t. The us e of evidence-bas ed education and implementation s trategies can optimize the links in the chain.

Th e Ne e d fo r Te a m s

Mortality from in-hos pital cardiac arres t remains high. The average s urvival rate is approximately 21% des pite s ignificant advances in treatments . Survival rates are particularly poor for arres t as s ociated with rhythms other than VF/VT. Non-VF/VT rhythms are pres ent in >75% of arres ts in the hos pital. Many in-hos pital arres ts are preceded by eas ily recognizable phys iologic changes , many of which are evident with routine monitoring of vital s igns . In recent s tudies nearly 80% of hos pitalized patients with cardiores piratory arres t had abnormal vital s igns documented for up to 8 hours before the actual arres t. This finding s ugges ts that there is a period of increas ing ins tability before the arres t. Of the s mall percentage of in-hos pital cardiac arres t patients who experience ROSC and are admitted to the ICU, 80% ultimately die before dis charge. In comparis on, only 44% of nonarres t patients admitted to intens ive care urgently from the floor (ie, before an arres t occurs ) die before dis charge.

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Sys te m s of Ca re

Ca r d ia c Ar r e s t Te a m s (In -Ho s p it a l)

Cardiac arres t teams are unlikely to prevent arres ts becaus e their focus has traditionally been to res pond only after the arres t has occurred. Unfortunately, the mortality rate is about 80% once the arres t occurs . Over the pas t few years , hos pitals have s hifted the focus away from cardiac arres t teams to patient s afety and prevention of arres t. The bes t way to improve a patient’s chance of s urvival from a cardiores piratory arres t is to prevent it from happening. The majority of cardiores piratory arres ts in the hos pital s hould be clas s ified as a “failure to res cue” rather than as an is olated, unexpected, random occurrence. Doing s o requires a s ignificant cultural s hift within ins titutions . Actions and interventions need to be proactive with the goal of improving rates of morbidity and mortality rather than reacting to a catas trophic event. Rapid as s es s ment and intervention for many abnormal phys iologic variables can decreas e the number of arres ts occurring in the hos pital.

Ra p id Re s p o n s e S ys t e m

Over the pas t decade, hos pitals in s everal countries have des igned s ys tems to identify and treat early clinical deterioration in patients . The purpos e of thes e rapid res pons e s ys tems is to improve patient outcomes by bringing critical care expertis e to patients . The rapid res pons e s ys tem has s everal components : • Event detection and res pons e triggering arm • A planned res pons e arm, s uch as the RRT • Quality monitoring • Adminis trative s upport Many rapid res pons e s ys tems allow activation by a nurs e, phys ician, or family member who is concerned that the patient is deteriorating. Some rapid res pons e s ys tems us e s pecific phys iologic criteria to determine when to call the team. The following lis t gives examples of s uch criteria for adult patients : • Threatened airway • Res piratory rate <6 or >30 breaths per minute • Heart rate <40/min or >140/min • Sys tolic blood pres s ure (SBP) <90 mm Hg • Symptomatic hypertens ion • Unexpected decreas e in level of cons cious nes s • Unexplained agitation • Seizure • Significant fall in urine output • Subjective concern about the patient

Me d ic a l Em e r g e n c y Te a m s a n d Ra p id Re s p o n s e Te a m s

There are s everal names for rapid res pons e s ys tems , including medical emergency team, rapid response team, and rapid assessment team. The rapid res pons e s ys tem is critically dependent on early identification and activation to immediately s ummon the team to the patient’s beds ide. Thes e teams typically cons is t of healthcare providers with both the critical care or emergency care experience and s kills to s upport immediate intervention for life-threatening s ituations . Thes e teams are res pons ible for performing a rapid patient as s es s ment and initiating appropriate treatment to revers e phys iologic deterioration and prevent a poor outcome.

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P a r t

4

Re g io n a l S ys t e m s o f Em e r g e n c y Ca r d io va s c u la r Ca r e

Hos pitals with larger patient volumes have a better s urvival-to–hos pital dis charge rate than low-volume centers for patients treated for either in- or out-of-hos pital cardiac arres t.

P u b lis h e d S t u d ie s

The majority of publis hed “before and after” s tudies of METs or rapid res pons e s ys tems have reported a 17% to 65% drop in the rate of cardiac arres ts after the intervention. Other documented benefits of thes e s ys tems include • A decreas e in unplanned emergency trans fers to the ICU • Decreas ed ICU and total hos pital length of s tay • Reductions in pos toperative morbidity and mortality rates • Improved rates of s urvival from cardiac arres t The recently publis hed MERIT trial is the only randomized controlled trial comparing hos pitals with a MET and thos e without one. The s tudy did not s how a difference in the compos ite primary outcome (cardiac arres t, unexpected death, unplanned ICU admis s ion) between the 12 hos pitals in which a MET s ys tem was introduced and 11 hos pitals that had no MET s ys tem in place. Further res earch is needed about the critical details of implementation and the potential effectivenes s of METs in preventing cardiac arres t or improving other important patient outcomes .

Im p le m e n t a t io n o f a Ra p id Re s p o n s e S ys t e m

Implementing any type of rapid res pons e s ys tem will require a s ignificant cultural change in mos t hos pitals . Thos e who des ign and manage the s ys tem mus t pay particular attention to is s ues that may prevent the s ys tem from being us ed effectively. Examples of s uch is s ues are ins ufficient res ources , poor education, fear of calling the team, fear of los ing control over patient care, and res is tance from team members . Implementation of a rapid res pons e s ys tem requires ongoing education, impeccable data collection and review, and feedback. Development and maintenance of thes e programs requires a long-term cultural and financial commitment from the hos pital adminis tration, which mus t unders tand that the potential benefits from the s ys tem (decreas ed res ource us e and improved s urvival rates ) may have independent pos itive financial ramifications . Hos pital adminis trators and healthcare profes s ionals need to reorient their approach to emergency medical events and develop a culture of patient s afety with a primary goal of decreas ing morbidity and mortality.

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5

Part

The ACLS Ca s e s Ove r vie w o f t h e Ca s e s The ACLS s imulated cas es are des igned to review the knowledge and s kills you need to s ucces s fully participate in cours e events and pas s the Megacode s kills tes t. Each cas e contains the following topics : • Introduction • Learning objectives • Rhythms and drugs • Des criptions or definitions of key concepts • Overview of algorithm • Algorithm figure • Application of the algorithm to the cas e • Other related topics This part contains the following cas es :

Ca s e

Page

Res piratory Arres t

34

VF Treated With CPR and AED

49

VF/Puls eles s VT

59

Puls eles s Electrical Activity

78

As ys tole

86

Acute Coronary Syndromes

91

Bradycardia

104

Uns table Tachycardia

114

Stable Tachycardia

124

Acute Stroke

130

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5

Re s p ir a t o r y Ar re s t Ca s e In t r o d u c t io n

This cas e reviews appropriate as s es s ment, intervention, and management options for an unconscious, unresponsive adult patient in respiratory arrest. Respirations are completely absent or clearly inadequate to maintain effective oxygenation and ventilation. A pulse is present. (Do not confus e agonal gas ps with adequate res pirations .) The BLS Survey and the ACLS Survey are us ed even though the patient is in res piratory arres t and not in cardiac arres t.


By the end of this cas e you s hould be able to 1. Des cribe the us e of the BLS and ACLS Surveys for a patient with res piratory arres t with a puls e 2. Des cribe when airway adjuncts s hould be us ed to manage an airway 3. Demons trate us e of an OPA to manage an airway 4. Demons trate us e of an NPA to manage an airway 5. Demons trate us e of bag-mas k ventilation to manage an airway

Ca s e Dr u g s

This cas e involves the following drugs : • Oxygen Sys tems or facilities us ing rapid s equence intubation may cons ider additional drugs .

Th e BLS S u r ve y BLS S u r ve y As s e s s m e n t

Proceed with the BLS Survey As s es s ment as des cribed on the next page. Note th a t th e BLS Su rve y foc u s e s on e a rly CP R a n d e a rly d e fib rilla tion . IV/IO acces s is not dis cus s ed here even though medications may provide a clinical benefit to s ome patients . Advanced as s es s ments and interventions are part of the ACLS Survey.

As s e s s a n d Re a s s e s s t h e P a t ie n t

The s ys tematic approach of the BLS Survey is assessment, then action, for each s tep in the s equence. Re m e m b e r: As s e s s …th e n p e rform a p p rop ria te a c tion . In this cas e you as s es s and find that the patient has a puls e, s o you do not us e the AED or begin ches t compres s ions . During the cours e your ins tructor will emphas ize the need to reas s es s the patient and be ready to do CPR, attach the AED, and s hock the patient if indicated.

Ve n t ila t io n a n d P u ls e Ch e c k

34

In the cas e of a patient in res piratory arres t with a puls e, give 1 breath every 5 to 6 s econds (10 to 12 breaths per minute) with a bag-mas k or any advanced airway device. Recheck the puls e about every 2 minutes . Take at leas t 5 s econds but no more than 10 s econds for a puls e check.

Th e ACLS Ca s e s : Re s p ira tory Arre s t

As s e s s 1



Check res pons ivenes s .

2



Activate the emergency res pons e s ys tem.

3

Circ ula tio n


4

De fib rilla tio n

Check the carotid puls e.


Defibrillation.

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P a r t

5

Ve n t ila t io n Ra t e s Air w a y De vic e

Ve n t ila t io n s Du r in g Ca rd ia c Ar re s t

Ba g -m a s k

2 ventilations after every 30 compres s ions

Any a d va nc e d a irwa y

1 ve ntila tio n e ve ry 6 to 8 s e c o nd s (8 to 10 breaths per minute)

Ve n t ila t io n s Du r in g Re s p ir a t o r y Ar re s t 1 ve ntila tio n e ve ry 5 to 6 s e c o nd s (10 to 12 breaths per minute)

Th e ACLS S u r ve y Air w a y Ma n a g e m e n t in Re s p ir a t o r y Ar r e s t

If bag-mas k ventilation is adequate, providers may defer ins ertion of an advanced airway. Healthcare providers s hould make the decis ion to place an advanced airway during the ACLS Survey. Advanced airway equipment includes the laryngeal mas k airway, the laryngeal tube, the es ophageal-tracheal tube, and the ET tube. If it is within your s cope of practice, you may us e advanced airway equipment in the cours e when appropriate and available. The following is a s ummary of the ACLS Survey:

As s e s s Airwa y – Is the airway patent? – Is an advanced airway indicated? – Is proper placement of airway device confirmed? – Is tube secured and placement reconfirmed frequently?

Ac t io n a s Ap p ro p r ia t e • Ma inta in a irwa y p a te nc y in unc o ns c io us p a tie nts by us e of head tilt–chin lift, OPA, or NPA • Us e a d va nc e d a irwa y m a na g e m e nt if ne e d e d (eg, laryngeal mas k airway, laryngeal tube, es ophageal-tracheal tube, ET tube) The benefit of advanced airway placement is weighed against the adverse effects of interrupting chest compressions. If bag-mask ventilation is adequate, healthcare providers may defer insertion of an advanced airway until the patient fails to respond to initial CPR and defibrillation or until spontaneous circulation returns. An advanced airway such as a laryngeal mask airway, laryngeal tube, or esophagealtracheal tube can be placed while chest compressions continue. If using advanced airway devices: • Co nfirm p ro p e r inte g ra tio n o f CP R a nd ve ntila tio n • Co nfirm p ro p e r p la c e m e nt o f a d va nc e d a irwa y d e vic e s by – Phys ical examination – Quantitative waveform capnography Clas s I recommendation for ET tube Reas onable for s upraglottic airways • Se c ure the d e vic e to p re ve nt d is lo d g m e nt • Mo nito r a irwa y p la c e m e nt with c o ntinuo us q ua ntita tive wa ve fo rm c a p no g ra p hy (continued)

36


(continued)

As s e s s Bre a thing – Are ventilation and oxygenation adequate? – Are quantitative waveform capnography and oxyhemoglobin saturation monitored?

Circ ula tio n – What is the cardiac rhythm? – Is the patient with a pulse unstable? – Is defibrillation or cardioversion indicated? – Are chest compressions effective? – Is ROSC present? – Has IV/IO access been established? – Are medications needed for rhythm or blood pressure? – Does the patient need volume (fluid) for resuscitation? Diffe re ntia l d ia g no s is – Why did this patient develop symptoms or arrest? – Is there a reversible cause that can be treated?

Ac t io n a s Ap p ro p r ia t e • Give s up p le m e nta ry o xyg e n whe n ind ic a te d – For cardiac arres t patients , adminis ter 100% oxygen – For others , titrate oxygen adminis tration to achieve oxygen s aturation values of ≥94% by puls e oximetry • Mo nito r the a d e q ua c y o f ve ntila tio n a nd o xyg e na tio n b y – Clinical criteria (ches t ris e and cyanos is ) – Quantitative waveform capnography – Oxygen s aturation • Avo id e xc e s s ive ve ntila tio n • Mo nito r CP R q ua lity – Quantitative waveform capnography (if P e t c o 2 is <10 mm Hg, attempt to improve CPR quality) – Intra-arterial pres s ure (if relaxation phas e [dias tolic] pres s ure is <20 mm Hg, attempt to improve CPR quality) • Atta c h m o nito r/d e fib rilla to r fo r a rrhythm ia s o r c a rd ia c a rre s t rhythm s (eg, VF, puls eles s VT, as ys tole, PEA) • De fib rilla tio n/c a rd io ve rs io n • Ob ta in IV/IO a c c e s s • Give a p p ro p ria te d rug s to m a na g e rhythm a nd b lo o d p re s s ure • Give IV/IO fluid s if ne e d e d

• Se a rc h fo r, find , a nd tre a t re ve rs ib le c a us e s (ie, definitive care)

P e t c o 2 is the partial pres s ure of end-tidal CO 2 , a meas ure of the amount of carbon dioxide pres ent in the exhaled air.

Ve n t ila t io n s

FYI 2 0 1 0 Gu id e lin e s Co rre c t P la c e m e nt o f End o tra c he a l Tub e

In this cas e the patient is in res piratory arres t but continues to have a puls e. You s hould ventilate the patient o nc e e ve ry 5 to 6 s e c o nd s (10 to 12 times per minute). Each breath s hould take 1 s econd and achieve vis ible ches t ris e. Be careful to avoid exces s ive ventilation (too many breaths per minute or too large a volume per breath).

• The AHA recommends continuous waveform capnography in addition to clinical as s es s ment as the mos t reliable method of confirming and monitoring correct placement of an ET tube.

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P a r t

5

Ma n a g e m e n t o f Re s p ir a t o r y Ar re s t Ove r vie w

Management of res piratory arres t includes both BLS and ACLS interventions . Thes e interventions may include • Giving s upplementary oxygen • Opening the airway • Providing bas ic ventilation • Us ing bas ic airway adjuncts (OPA and NPA) • Suctioning Ac c ord in g to th e 2010 AHA Guid e line s fo r CP R a nd ECC, for p a tie n ts with a p e rfu s in g rh yth m , d e live r 1 b re a th e ve ry 5 to 6 s e c o nd s (10 to 12 b re a th s p e r m in u te ).

Cr it ic a l Co n c e p t s Avo id ing Exc e s s ive Ve ntila tio n

• When us ing any form of as s is ted ventilation, you mus t avoid delivering exces s ive ventilation (too many breaths per minute or too large a volume per breath). Exces s ive ventilation can be harmful becaus e it increas es intrathoracic pres s ure, decreas es venous return to the heart, and diminis hes cardiac output. It may als o caus e gas tric inflation and predis pos e the patient to vomiting and as piration of gas tric contents .

Givin g S u p p le m e n t a r y Oxyg e n Ma in t a in Oxyg e n S a t u r a t io n

Give oxygen to patients with acute cardiac s ymptoms or res piratory dis tres s . Monitor oxygen s aturation and titrate s upplementary oxygen to maintain a s aturation of ≥94% . See the Student Webs ite (www.he a rt.o rg /e c c s tud e nt) for details on us e of oxygen in patients not in res piratory or cardiac arres t.

Op e n in g t h e Air w a y Co m m o n Ca u s e o f Air w a y Ob s t r u c t io n

38

Figure 8 demons trates the anatomy of the airway. The mos t common caus e of upper airway obs truction in the uncons cious /unres pons ive patient is los s of tone in the throat mus cles . In this cas e the tongue falls back and occludes the airway at the level of the pharynx (Figure 9A).


Nas al Cavity Nas op harynx

Oral Cavity Tongue Vallecula

Orop harynx

Epiglottis Vocal Fold (Cords ) Laryngopharynx

Thyroid Cartilage Cricoid Cartilage Trachea Es ophagus

Fig u re 8 . Airway anatomy.

A

B

C

Fig u re 9 . Obs truction of the airway by the tongue and epiglottis . When a patient is unres pons ive, the tongue can obs truct the airway. The head tilt–chin lift relieves obs truction in the unres pons ive patient. A, The tongue is obs tructing the airway. B, The head tilt–chin lift lifts the tongue, relieving the obs truction. C, If cervical s pine trauma is s us pected, healthcare providers s hould us e the jaw thrus t without head extens ion.

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5

Ba s ic Air w a y Op e n in g Te c h n iq u e s

Bas ic airway opening techniques will effectively relieve airway obs truction caus ed either by the tongue or from relaxation of mus cles in the upper airway. The bas ic airway opening technique is head tilt with anterior dis placement of the mandible, ie, head tilt–chin lift (Figure 9B). In the trauma patient with s us pected neck injury, us e a jaw thrus t without head extens ion (Figure 9C). Becaus e maintaining an open airway and providing ventilation is a priority, us e a head tilt–chin lift maneuver if the jaw thrus t does not open the airway. ACLS providers s hould be aware that current BLS training cours es teach the jaw thrus t technique to healthcare providers but not to lay res cuers .

Air w a y Ma n a g e m e n t

Proper airway pos itioning may be all that is required for patients who can breathe s pontaneous ly. In patients who are uncons cious with no cough or gag reflex, ins ert an OPA or NPA to maintain airway patency. If you find an uncons cious /unres pons ive patient who was known to be choking and is now unres pons ive and in res piratory arres t, open the mouth wide and look for a foreign object. If you s ee one, remove it with your fingers . If you do not s ee a foreign object, begin CPR. Each time you open the airway to give breaths , open the mouth wide and look for a foreign object. Remove it with your fingers if pres ent. If there is no foreign object, res ume CPR.

P ro vid in g Ba s ic Ve n t ila t io n Ba s ic Air w a y S k ills

Bas ic airway s kills us ed to ventilate a patient are • Head tilt–chin lift • J aw thrus t without head extens ion (s us pected cervical s pine trauma) • Mouth-to-mouth ventilation • Mouth-to-nos e ventilation • Mouth-to–barrier device (us ing a pocket mas k) ventilation (Figure 10) • Bag-mas k ventilation (Figures 11 and 12)

Fig u re 1 0 . Mouth-to-mas k ventilation, 1 res cuer. The res cuer performs 1-res cuer CPR from a pos ition at the patient’s s ide. Perform a head tilt–chin lift to open the airway while holding the mas k tightly agains t the face.

40


Fig u re 1 1 . E-C clamp technique for holding the mas k while lifting the jaw. Pos ition yours elf at the patient’s head. Circle the thumb and firs t finger around the top of the mas k (forming a “C”) while us ing the third, fourth, and fifth fingers (forming an “E”) to lift the jaw.

Fig u re 1 2 . Two-res cuer us e of the bag-mas k. The res cuer at the patient’s head tilts the patient’s head and s eals the mas k agains t the patient’s face with the thumb and firs t finger of each hand creating a “C” to provide a complete s eal around the edges of the mas k. The res cuer us es the remaining 3 fingers (the “E”) to lift the jaw (this holds the airway open). The s econd res cuer s lowly s queezes the bag (over 1 s econd) until the ches t ris es . Both providers s hould obs erve ches t ris e.

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Ba g -Ma s k Ve n t ila t io n

5 A bag-mas k ventilation device cons is ts of a ventilation bag attached to a face mas k. Thes e devices have been a mains tay of emergency ventilation for decades . Bag-mas k devices are the mos t common method of providing pos itive-pres s ure ventilation. When us ing a bag-mas k device, deliver approximately 600 mL tidal volume s ufficient to produce ches t ris e over 1 s econd. The univers al connections pres ent on all airway devices allow you to connect any ventilation bag to numerous adjuncts . Valves and ports may include • One-way valves to prevent the patient from rebreathing exhaled air • Oxygen ports for adminis tering s upplementary oxygen • Medication ports for adminis tering aeros olized and other medications • Suction ports for clearing the airway • Ports for quantitative s ampling of end-tidal CO 2 You can attach other adjuncts to the patient end of the valve, including a pocket face mas k, laryngeal mas k airway, laryngeal tube, es ophageal-tracheal tube, and ET tube. See the Student Webs ite (www.he a rt.o rg /e c c s tud e nt) for more information on bag-mas k ventilation.

Ba s ic Air w a y Ad ju n c t s : Oro p h a r yn g e a l Air w a y In t r o d u c t io n

The OPA is us ed in patients who are at ris k for developing airway obs truction from the tongue or from relaxed upper airway mus cles . This J -s haped device (Figure 13A) fits over the tongue to hold it and the s oft hypopharyngeal s tructures away from the pos terior wall of the pharynx. The OPA is us ed in unconscious patients if procedures to open the airway (eg, head tilt– chin lift or jaw thrus t) fail to provide and maintain a clear, unobs tructed airway. An OPA should not be used in a conscious or semiconscious patient becaus e it may s timulate gagging and vomiting. The key as s es s ment is to check whether the patient has an intact cough and gag reflex. If s o, do not us e an OPA. The OPA may be us ed to keep the airway open during bag-mas k ventilation when providers might unknowingly pus h down on the chin, blocking the airway. The OPA is als o us ed during s uctioning of the mouth and throat and in intubated patients to prevent them from biting and occluding the ET tube.

A

B

Fig u re 1 3 . Oropharyngeal airways . A, Oropharyngeal airway devices . B, Oropharyngeal airway device ins erted.

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Te c h n iq u e o f OPA In s e r t io n

Ste p

Ac t io n

1

Cle a r the m o uth a nd p ha rynx of s ecretions , blood, or vomit us ing a rigid pharyngeal s uction tip if pos s ible.

2

Se le c t the p ro p e r s ize OPA. Place the OPA agains t the s ide of the face. When the tip of the OPA is at the corner of the mouth, the flange is at the angle of the mandible. A properly s ized and ins erted OPA res ults in proper alignment with the glottic opening.

3

Ins e rt the OPA s o that it curves upward toward the hard palate as it enters the mouth.

4

As the OPA pas s es through the oral cavity and approaches the pos terior wall of the pharynx, ro ta te it 180° into the proper pos ition (Figure 13B). The OPA can als o be ins erted at a 90° angle to the mouth and then turned down toward the pos terior pharynx as it is advanced. In both methods , the goal is to curve the device around the tongue s o that the tongue is not inadvertently pus hed back into the pharynx rather than being pulled forward by the OPA. An a lte rna tive m e tho d is to ins ert the OPA s traight in while us ing a tongue depres s or or s imilar device to hold the tongue forward as the OPA is advanced.

After ins ertion of an OPA, monitor the patient. Keep the head and jaw pos itioned properly to maintain a patent airway. Suction the airway as needed.

Ca u t io n Be Awa re o f the Fo llo wing Whe n Us ing a n OPA

• OPAs that are too large may obs truct the larynx or caus e trauma to the laryngeal s tructures . • OPAs that are too small or ins erted improperly may pus h the bas e of the tongue pos teriorly and obs truct the airway. • Ins ert the OPA carefully to avoid s oft tis s ue trauma to the lips and tongue. Remember to us e the OPA only in the unres pons ive patient with no cough or gag reflex. If the patient has a cough or gag reflex, the OPA may s timulate vomiting and laryngos pas m.

Ba s ic Air w a y Ad ju n c t s : Na s o p h a r yn g e a l Air w a y In t r o d u c t io n

The NPA is us ed as an alternative to an OPA in patients who need a bas ic airway management adjunct. The NPA is a s oft rubber or plas tic uncuffed tube (Figure 14A) that provides a conduit for airflow between the nares and the pharynx. Unlike oral airways , NPAs may be used in conscious or semiconscious patients (patients with an intact cough and gag reflex). The NPA is indicated when ins ertion of an OPA is technically difficult or dangerous . Examples include patients with a gag reflex, tris mus , mas s ive trauma around the mouth, or wiring of the jaws . The NPA may als o be us ed in patients who are neurologically impaired with poor pharyngeal tone or coordination leading to upper airway obs truction.

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A

B

Fig u re 1 4 . Nas opharyngeal airways . A, Nas opharyngeal airway devices . B, Nas opharyngeal airway device ins erted.

Te c h n iq u e o f NPA In s e r t io n

Ste p 1

Ac t io n Se le c t the p ro p e r s ize NPA. • Compare the outer circumference of the NPA with the inner aperture of the nares . The NPA s hould not be s o large that it caus es s us tained blanching of the nos trils . Some providers us e the diameter of the patient’s s malles t finger as a guide to s electing the proper s ize. • The length of the NPA s hould be the s ame as the dis tance from the tip of the patient’s nos e to the earlobe.

2

Lub ric a te the a irwa y with a wa te r-s o lub le lub ric a nt o r a ne s the tic je lly.

3

Ins e rt the a irwa y through the nos tril in a pos terior direction perpendicular to the plane of the face. Pas s it gently along the floor of the nas opharynx (Figure 14B). If you encounter res is tance: • Slightly rotate the tube to facilitate ins ertion at the angle of the nas al pas s age and nas opharynx. • Attempt placement through the other nos tril becaus e patients have different-s ized nas al pas s ages .

Reevaluate frequently. Maintain head tilt by providing anterior dis placement of the mandible us ing a chin lift or jaw thrus t. Mucus , blood, vomit, or the s oft tis s ues of the pharynx can obs truct the NPA, which has a s mall internal diameter. Frequent evaluation and suctioning of the airway may be necessary to ensure patency.

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Ca u t io n Be Awa re o f the Fo llo wing Whe n Us ing a n NPA

• Take care to ins ert the airway gently to avoid complications . The airway can irritate the mucos a or lacerate adenoidal tis s ue and caus e bleeding, with pos s ible as piration of clots into the trachea. Suction may be neces s ary to remove blood or s ecretions . • An improperly s ized NPA may enter the es ophagus . With active ventilation, s uch as bag-mas k ventilation, the NPA may caus e gas tric inflation and pos s ible hypoventilation. • An NPA may caus e laryngos pas m and vomiting, even though it is commonly tolerated by s emicons cious patients . • Us e caution in patients with facial trauma becaus e of the ris k of mis placement into the cranial cavity through a fractured cribriform plate.


Take the following precautions when us ing an OPA or NPA:

P re c a utio ns fo r OPAs a nd NPAs

• Always check s pontaneous res pirations immediately after ins ertion of either an OPA or an NPA. • If res pirations are abs ent or inadequate, s tart pos itive-pres s ure ventilations at once with an appropriate device. • If adjuncts are unavailable, us e mouth-to-mas k barrier device ventilation.

S u c t io n in g In t r o d u c t io n

Suctioning is an es s ential component of maintaining a patient’s airway. Providers s hould s uction the airway immediately if there are copious s ecretions , blood, or vomit. Suction devices cons is t of both portable and wall-mounted units . • Portable s uction devices are eas y to trans port but may not provide adequate s uction power. A s uction force of −80 to −120 mm Hg is generally neces s ary. • Wall-mounted s uction units s hould be capable of providing an airflow of >40 L/min at the end of the delivery tube and a vacuum of more than −300 mm Hg when the tube is clamped at full s uction. • Adjus t the amount of s uction force for us e in children and intubated patients .

S o ft vs Rig id Ca t h e t e r s

Both s oft flexible and rigid s uctioning catheters are available. Soft flexible catheters may be us ed in the mouth or nos e. Soft flexible catheters are available in s terile wrappers and can als o be us ed for ET tube deep s uctioning. Rigid catheters (eg, Yankauer) are us ed to s uction the oropharynx. Thes e are better for s uctioning thick s ecretions and particulate matter.

Ca t h e t e r Typ e

Us e fo r

So ft

• As piration of thin s ecretions from the oropharynx and nas opharynx • Performing intratracheal s uctioning • Suctioning through an in-place airway (ie, NPA) to acces s the back of the pharynx in a patient with clenched teeth

Rig id

• More effective s uctioning of the oropharynx, particularly if there is thick particulate matter

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Or o p h a r yn g e a l S u c t io n in g P roc e d u re

En d o t r a c h e a l Tu b e S u c t io n in g P roc e d u re

Follow the s teps below to perform oropharyngeal s uctioning.

Ste p

Ac t io n

1

• Meas ure the catheter before s uctioning and do not ins ert it any further than the dis tance from the tip of the nos e to the earlobe. • Gently ins ert the s uction catheter or device into the oropharynx beyond the tongue.

2

• Apply s uction by occluding the s ide opening of the catheter while withdrawing with a rotating or twis ting motion. • If us ing a rigid s uction device (eg, Yankauer s uction) place the tip gently into the oral cavity. Advance by pus hing the tongue down to reach the oropharynx if neces s ary.

Patients with pulmonary s ecretions may require s uctioning even after endotracheal intubation. Follow the s teps below to perform ET tube s uctioning:

Ste p

Ac t io n

1

• Us e s terile technique to reduce the likelihood of airway contamination.

2

• Gently ins ert the catheter into the ET tube. Be s ure the s ide opening is not occluded during ins ertion. Ins ertion of the catheter beyond the tip of the ET tube is not recommended becaus e it may injure the endotracheal mucos a or s timulate coughing or bronchos pas m.

3

• Apply s uction by occluding the s ide opening only while withdrawing the catheter with a rotating or twis ting motion. • Su c tion a tte m p ts s h ou ld n ot e xc e e d 10 s e c on d s . To avoid hypoxemia, precede and follow s uctioning attempts with a s hort period of adminis tration of 100% oxygen.

Mon itor th e p a tie n t’s h e a rt ra te , p u ls e , oxyg e n s a tu ra tion , a n d c lin ic a l a p p e a ra n c e d u rin g s u c tion in g . If b ra d yc a rd ia d e ve lop s , oxyg e n s a tu ra tion d rop s , or c lin ic a l a p p e a ra n c e d e te riora te s , in te rru p t s u c tion in g a t on c e . Ad m in is te r h ig h -flow oxyg e n u n til th e h e a rt ra te re tu rn s to n orm a l a n d th e c lin ic a l c on d ition im p rove s . As s is t ve n tila tion a s n e e d e d .

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P ro vid in g Ve n t ila t io n Wit h a n Ad va n c e d Air w a y In t r o d u c t io n

Selection of an advanced airway device depends on the training, s cope of practice, and equipment of the providers on the res us citation team. Advanced airways include • Laryngeal mas k airway • Laryngeal tube • Es ophageal-tracheal tube • Endotracheal tube Becaus e a s mall proportion of patients cannot be ventilated with a laryngeal mas k airway, providers who us e this device s hould have an alternative airway management s trategy. A bag-mas k can be this alternate s trategy. This cours e will familiarize you with types of advanced airways . Ins truction in the s killed placement of thes e airways is beyond the s cope of the bas ic ACLS Provider Cours e. To be proficient in the us e of advanced airway devices , you mus t have adequate initial training and ongoing experience. Providers who ins ert advanced airways mus t participate in a proces s of continuous quality improvement to document and minimize complications . In this cours e you will practice ventilating with an advanced airway in place and integrating ventilation with ches t compres s ions .

Ve n t ila t io n Ra t e s

Ve n t ila t io n s Du r in g Ca rd ia c Ar re s t

Ve n t ila t io n s Du r in g Re s p ir a t o r y Ar re s t

Ba g -m a s k

2 ventilations after every 30 compres s ions

Any a d va nc e d a irwa y



Air w a y De vic e

La r yn g e a l Ma s k Air w a y

The laryngeal mas k airway is an advanced airway alternative to endotracheal intubation and provides comparable ventilation. It is acceptable to us e the laryngeal mas k airway as an alternative to an ET tube for airway management in cardiac arres t. Only experienced providers s hould perform laryngeal mas k airway ins ertion. See the Student Webs ite (www.he a rt.o rg /e c c s tud e nt) for more information on the laryngeal mas k airway.

La r yn g e a l Tu b e

The advantages of the laryngeal tube are s imilar to thos e of the es ophageal-tracheal tube; however, the laryngeal tube is more compact and les s complicated to ins ert. Healthcare profes s ionals trained in the us e of the laryngeal tube may cons ider it as an alternative to bag-mas k ventilation or endotracheal intubation for airway management in cardiac arres t. Only experienced providers s hould perform laryngeal tube ins ertion. See the Laryngeal Intubation s ection on the Student Webs ite (www.he a rt.o rg /e c c s tud e nt) for more information on this procedure.

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Es o p h a g e a lTr a c h e a l Tu b e

The es ophageal-tracheal tube is an advanced airway alternative to endotracheal intubation. This device provides adequate ventilation comparable to an ET tube. It is acceptable to us e the es ophageal-tracheal tube as an alternative to an ET tube for airway management in cardiac arres t. Fatal complications may occur with us e of this device. Only providers experienced with its us e s hould perform es ophageal-tracheal tube ins ertion. See the Student Webs ite (www.he a rt.o rg /e c c s tud e nt) for more information on the es ophageal-tracheal tube.

En d o t r a c h e a l Tu b e

A brief s ummary of the bas ic s teps for performing endotracheal intubation is given here to familiarize the ACLS provider who may as s is t with the procedure. • Prepare for intubation by as s embling the neces s ary equipment. • Perform endotracheal intubation (s ee the Student Webs ite). • Inflate cuff or cuffs on the tube. • Attach the ventilation bag. • Confirm correct placement by phys ical examination and a confirmation device. Continuous waveform capnography is recommended (in addition to clinical as s es s ment) as the mos t reliable method of confirming and monitoring correct placement of an ET tube. Healthcare providers may us e colorimetric and nonwaveform carbon dioxide detectors when waveform capnography is not available. • Secure the tube in place. • Monitor for dis placement. Only experienced providers s hould perform endotracheal intubation. See the Endotracheal Intubation s ection on the Student Webs ite (www.he a rt.o rg /e c c s tud e nt) for more information on this procedure.

Ca u t io n Us e o f Cric o id P re s s ure

FYI 2 0 1 0 Gu id e lin e s Cric o id P re s s ure

Fo u n d a t io n a l Fa c t s Re s c ue Bre a ths fo r CP R With a n Ad va nc e d Airwa y in P la c e

• Cricoid pres s ure in nonarres t patients may offer s ome meas ure of protection to the airway from as piration and gas tric ins ufflation during bag-mas k ventilation. However, it als o may impede ventilation and interfere with placement of a s upraglottic airway or intubation.

• The role of cricoid pres s ure during out-of-hos pital and in-hos pital cardiac arres t has not been s tudied. If cricoid pres s ure is us ed in a few s pecial circums tances during cardiac arres t, the pres s ure s hould be adjus ted, relaxed, or releas ed if it impedes ventilation or advanced airway placement. The routine us e of cricoid pres s ure in cardiac arres t is not recommended.

• During CPR the compres s ion-to-ventilation ratio is 30:2. But once an advanced airway is in place (ie, laryngeal mas k airway, laryngeal tube, es ophageal-tracheal tube, or ET tube), ches t compres s ions are no longer interrupted for ventilations . • When ventilating through a properly placed advanced airway, give 1 breath every 6 to 8 s econds (approximately 8 to 10 breaths per minute) without trying to s ynchronize breaths to compres s ions . Ideally deliver the breath during ches t recoil between compres s ions . Continuous ly reevaluate compres s ions and ventilations . Be prepared to make modifications if either is ineffective. In this cas e the patient has a puls e, and compres s ions are not indicated. Give 1 breath every 5 to 6 s econds (10 to 12 breaths per minute).

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Th e ACLS Ca s e s : VF Tre a te d With CP R a n d AED

P re c a u t io n s fo r Tr a u m a P a t ie n t s Su m m a r y

When providing as s is ted ventilation for patients with known or s us pected cervical s pine trauma, avoid unneces s ary s pine movement. Exces s ive head and neck movement in patients with an uns table cervical s pinal column can caus e irrevers ible injury to the s pinal cord or wors en a minor s pinal cord injury. Approximately 2% of patients with blunt trauma s erious enough to require s pinal imaging in the ED have a s pinal injury. This ris k is tripled if the patient has a head or facial injury. As s ume that any patient with multiple trauma, head injury, or facial trauma has a s pine injury. Be particularly cautious if a patient has s us pected cervical s pine injury. Examples are patients who have been involved in a highs peed motor vehicle collis ion, have fallen from a height, or were injured while diving. Follow thes e precautions if you s us pect cervical s pine trauma: • Open the airway by us ing a jaw thrus t without head extension. Becaus e maintaining a patent airway and providing adequate ventilation are priorities , us e a head tilt–chin lift maneuver if the jaw thrus t is not effective. • Have another team member s tabilize the head in a neutral pos ition during airway manipulation. Us e m a n u a l s p in a l m otion re s tric tion ra th e r th a n im m ob iliza tion d e vic e s . Manual s pinal immobilization is s afer. Cervical collars may complicate airway management and may even interfere with airway patency. • Spinal immobilization devices are helpful during trans port.

VF Tre a t e d Wit h CP R a n d AED Ca s e In t r o d u c t io n

This cas e will provide the knowledge you need to pas s the CPR and AED Tes ting Station. This cas e dis cus s es how to res pond as a lone res cuer to an out-of-hos pital emergency, equipped with only CPR s kills and an AED. The cas e s cenario pres ents a patient who collapses from either VF or pulseless VT. The only equipment available is an AED s tocked with a pocket face mas k. Becaus e other providers are not pres ent, you mus t care for the patient without help. ACLS interventions , including advanced airway control and IV medications , are not options in this s cenario. Note that during the cours e you will be required to demons trate both your knowledge of this cas e and competency in bas ic s kill performance.


By the end of this cas e you s hould be able to 1. Demons trate the s kills and s equence outlined in the BLS Healthcare Providers Algorithm (Figures 15 and 16), including high-quality CPR and AED us e 2. Implement the BLS Healthcare Provider Algorithm by performing 1-res cuer CPR 3. Implement the BLS Healthcare Provider Algorithm by operating an AED

Rh yt h m s fo r VF Tr e a t e d Wit h CP R a n d AED

With an AED, there are no rhythms to learn. The AED will ans wer the ques tion “Is the rhythm s hockable, ie, VF or puls eles s VT? ”

Dr u g s fo r VF Tr e a t e d Wit h CP R a n d AED

There are no new drugs to learn in this cas e. You will us e only your CPR s kills and an AED.

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Th e BLS S u r ve y In t r o d u c t io n

The BLS Survey is us ed in all cas es of cardiac arres t. In the Res piratory Arres t Cas e you learned the bas ics of airway as s es s ment and management of a patient in res piratory arres t with a puls e. In this cas e you will as s es s and manage a patient without a puls e and us e the AED.

As s e s s m e n t Fo u n d a t io n a l Fa c t s Sta rting CP R Whe n Yo u Are No t Sure Ab o ut a P uls e

50

Perform the BLS Survey s teps on the next page.

• If you are uns ure about the pres ence of a puls e, begin cycles of compres s ions and ventilations . Unneces s ary compres s ions are les s harmful than failing to provide compres s ions when needed. Delaying or failing to s tart CPR in a patient without a puls e reduces the chance of s urvival.


As s e s s 1



Check res pons ivenes s .

2



Activate the emergency res pons e s ys tem.

3

Circ ula tio n


4

De fib rilla tio n

Check the carotid puls e.


Defibrillation.

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5

Ad ult BLS He a lthc a re P ro vid e rs 1

Unre s p o ns ive No b re a thing o r no no rm a l b re a thing (ie, only gas ping)

Hig h-Qua lity CP R • Rate at leas t 100/min • C ompres s ion depth at leas t 2 inches (5 cm)

2

• Allow complete ches t recoil after each compres s ion

Ac tiva te e m e rg e nc y re s p o ns e s ys te m Ge t AED/d e fib rilla to r or s end s econd res cuer (if available) to do this

• Minimize interruptions in ches t compres s ions • Avoid exces s ive ventilation

3

De fin it e P u ls e

Che c k p uls e : DEFINITE p uls e within 10 s e c o nd s ?

3A • G ive 1 b re a th e ve ry 5 to 6 s e c o nd s • R e c he c k p uls e e ve ry 2 m inute s

No P u ls e

4

Begin cycles of 30 COMP RESSIONS and 2 BREATHS

5 AED/d e fib rilla to r ARRIVES

6

Che c k rhythm Sho c ka b le rhythm ? S h o c k a b le 7

No t S h o c k a b le 8

Give 1 s ho c k Re s um e CP R im m e d ia te ly for 2 minutes

Re s um e CP R im m e d ia te ly for 2 minutes Check rhythm every 2 minutes ; continue until ALS providers take over or victim s tarts to move

Note: The boxes bordered with das hed lines are performed by healthcare providers and not by lay res cuers

Fig u re 1 5 . The BLS Healthcare Provider Algorithm.

52

© 2010 American Heart As s ociation


Sim p lifie d Ad ult BLS HCP

Unre s p o ns ive No b re a thing o r no no rm a l b re a thing (o nly g a s p ing )

Ac tiva te e m e rg e nc y re s p o ns e

Ge t d e fib rilla to r

Che c k p uls e

Sta rt CP R

Che c k rhythm / s ho c k if ind ic a te d Re p e a t e ve ry 2 m inute s

s

Ha

s

u

t

P

h

rd • P u s h

a F

© 2010 American Hea rt As s ociation

Fig u re 1 6 . The Simplified Adult BLS Algorithm.

53

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Pu rpos e of De fib r illa t io n

Defibrillation does not res tart the heart. Defibrillation s tuns the heart and briefly terminates all electrical activity, including VF and VT. If the heart is s till viable, its normal pacemakers may eventually res ume electrical activity (return of s pontaneous rhythm) that ultimately res ults in a perfus ing rhythm (ROSC). In the firs t minutes after s ucces s ful defibrillation, however, any s pontaneous rhythm is typically s low and does not create puls es or adequate perfus ion. The patient needs CPR (beginning with ches t compres s ions ) for s everal minutes until adequate heart function res umes . This is the rationale for res uming high-quality CPR, beginning with ches t compres s ions immediately after a s hock.

P r in c ip le o f Ea r ly De fib r illa t io n

The interval from collaps e to defibrillation is one of the mos t important determinants of s urvival from cardiac arres t. Early defibrillation is critical for patients with s udden cardiac arres t for the following reas ons : • A common initial rhythm in out-of-hos pital witnes s ed s udden cardiac arres t is VF. Puls eles s VT rapidly deteriorates to VF. When VF is pres ent, the heart quivers and does not pump blood. • Electrical defibrillation is the mos t effective way to treat VF (delivery of a s hock to s top the VF). • The probability of s ucces s ful defibrillation decreas es quickly over time. • VF deteriorates to as ys tole if not treated. The earlier defibrillation occurs , the higher the s urvival rate. When VF is pres ent, CPR can provide a s mall amount of blood flow to the heart and brain but cannot directly res tore an organized rhythm. The likelihood of res toring a perfus ing rhythm is optimized with immediate CPR and defibrilliation within a few minutes of the initial arres t. Res toration of a perfus ing rhythm requires immediate CPR and defibrillation within a few minutes of the initial arres t (Figure 17). For every minute that pas s es between collaps e and defibrillation, the chance of s urvival from a witnes s ed VF s udden cardiac arres t declines by 7% to 10% per minute if no bys tander CPR is provided. When bys tanders perform CPR, the decline is more gradual and averages 3% to 4% per minute. CPR performed early can double or triple s urvival from witnes s ed s udden cardiac arres t at mos t defibrillation intervals . Lay res cuer AED programs increas e the likelihood of early CPR and attempted defibrillation. This helps s horten the time between collaps e and defibrillation for a greater number of patients with s udden cardiac arres t. Co lla p s e EMS no ti c a tio n Dis p a tc h o f EMS units Tim e to CP R

Tim e to d e b rilla tio n

Sta rt o f CP R Sta rt o f d e b rilla tio n Re turn o f p e rfus ing rhythm

Tim e to d e nitive c a re

Arriva l o f full ACLS s up p o rt

Fig u re 1 7 . Sequence of events and key intervals that occur with cardiac arres t. Modified from Eis enberg MS, Cummins RO, Damon S, Lars en MP, Hearne TR. Survival rates from outof-hos pital cardiac arres t: recommendations for uniform definitions and data to report. Ann Emerg Med. 1990;19:1249-1259. With permis s ion from Els evier.

54


AED Op e r a t io n

Us e AEDs only when patients have the following 3 clinical findings : • No res pons e • Abs ent or abnormal breathing (ie, no breathing or only gas ping) • No puls e In the firs t few minutes after the ons et of s udden cardiac arres t, the patient may demons trate agonal gas ps , which are not adequate breathing. A nonres pons ive patient with agonal gas ping who has no puls e is in cardiac arres t.

Cr it ic a l Co n c e p t s

Ag o na l g a s p s a re no t a d e q ua te b re a thing .

Ag o na l Ga s p s

A patient who gas ps us ually looks like he is drawing air in very quickly. The patient may open his mouth and move his jaw, head, or neck. Gas ps may appear forceful or weak, and s ome time may pas s between gas ps becaus e they us ually happen at a s low rate. The gas p may s ound like a s nort, s nore, or groan. Gas ping is not regular or normal breathing. It is a s ign of cardiac arres t in s omeone who does n’t res pond.

Kn o w Yo u r AED

You mus t be familiar with the AED us ed in your clinical s etting and be ready to us e it at any time. Review the troubles hooting checklis t s upplied by the AED manufacturer. Learn to perform daily maintenance checks . Not only are thes e checks an effective review of the s teps of operation, but they are als o a means of verifying that the AED is ready for us e.

Th e Un ive r s a l AED: Co m m o n S t e p s t o Op e r a t e All AEDs

Once the AED arrives , place it at the patient’s s ide, next to the res cuer who will operate it. This pos ition provides ready acces s to the AED controls and eas y placement of electrode pads . It als o allows a s econd res cuer to perform CPR from the oppos ite s ide of the patient without interfering with AED operation. AEDs are available in different models . Although there are s mall differences from model to model, all AEDs operate in bas ically the s ame way. The following table lis ts the 4 univers al s teps for operating an AED:

Ste p 1

Ac t io n P o we r o n the AED (this activates voice prompts for guidance in all s ubs equent s teps ). • Open the carrying cas e or the top of the AED. • Turn the power on (s ome devices will “power on” automatically when you open the lid or cas e).

2

Atta c h e le c tro d e p a d s to the patient’s bare ches t. • Choos e the correct s ize pads (adult vers us pediatric) for the patient’s s ize/age. Peel the backing away from the electrode pads . • Quickly wipe the patient’s ches t if it is covered with water or s weat (but do not delay attaching the pads or s hock delivery). • Attach the adhes ive electrode pads to the patient’s bare ches t. – Place one electrode pad on the upper-right s ide of the bare ches t to the right of the s ternum directly below the clavicle. – Place the other pad to the left of the nipple, with the top margin of the pad a few inches below the left armpit (Figure 18). – Attach the AED connecting cables to the AED box (s ome are preconnected). (continued) 55

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5 (continued)

Ste p 3

Ac t io n Ana lyze rhythm . • Always clear the patient during analys is . Be s ure no one is touching the patient, not even the pers on in charge of giving breaths . • Some AEDs will ins truct you to pus h a button to allow the AED to begin analyzing the heart rhythm; others will do that automatically. The AED rhythm analys is may take about 5 to 15 s econds . • The AED rhythm analys is will determine if the patient needs a s hock.

4

If the AED advis es a s hock, it will tell you to BE SURE TO CLEAR THE PATIENT (ie , d o no t to uc h the p a tie nt): • Clear the patient before delivering the s hock; be s ure no one is touching the patient. • Loudly and quickly s tate a “clear the patient” mes s age, s uch as “Clear, I am going to s hock on three,” “One, two, three, s hocking,” or s imply “Clear.” • Perform a vis ual check to ens ure that no one is in contact with the patient. • Pres s the SHOCK button. • The s hock will produce a s udden contraction of the patient’s mus cles .

As s oon as the s hock is delivered, res ume CPR, s tarting with ches t compres s ions , and give cycles of 30 compres s ions and 2 breaths . Do not perform a puls e or rhythm check. After 2 minutes of CPR the AED will prompt you to repeat s teps 3 and 4.

Fig u re 1 8 . AED electrode pad placement on the patient.

56



There are 4 acceptable AED electrode pad pos itions :

Alte rna tive AED Ele c tro d e P a d P la c e m e nt P o s itio ns

• Anterolateral • Anteropos terior • Anterior-left infras capular • Anterior-right infras capular All 4 pos itions are equally effective in s hock s ucces s and are reas onable for defibrillation. For eas e of placement, anterolateral is a reas onable default electrode placement. Providers may cons ider alternative pad pos itions bas ed on individual patient characteris tics .

Tr o u b le s h o o t in g t h e AED

Studies of AED “failures ” have s hown that mos t problems are caus ed by operator error rather than by AED defects . Operator error is les s likely if the operator is experienced in us ing the AED, has had recent training or practice with the AED, and is us ing a well-maintained AED. If the AED does not promptly analyze the rhythm, do the following: • Res ume high-quality ches t compres s ions and ventilations . • Check all connections between the AED and the patient to make s ure that they are intact. Ne ve r d e la y c h e s t c om p re s s ion s to trou b le s h oot th e AED.

S h o c k Fir s t vs CP R Fir s t

When you care for an adult patient in cardiac arres t, s hould you attempt to s hock firs t with an AED or provide CPR firs t? • Healthcare providers who treat cardiac arres t in hos pitals and other facilities s hould provide immediate CPR until the AED/defibrillator is ready for us e. Us e the AED as s oon as it is available. • At this time the benefit of delaying defibrillation to perform CPR before defibrillation is unclear. EMS s ys tem medical directors may cons ider implementing a protocol that allows EMS res ponders to provide CPR while preparing for defibrillation of patients found by EMS pers onnel to be in VF.

FYI 2 0 1 0 Gu id e lin e s Co o rd ina ting Sho c k De live ry a nd CP R

• The AHA s trongly recommends performing CPR while a defibrillator or AED is readied for us e and while charging for all patients in cardiac arres t. • Res ponders us ing an AED s hould follow the machine’s voice prompts .

AED Us e in S p e c ia l S it u a t io n s In t r o d u c t io n

The following s pecial s ituations may require the operator to take extra care in placing the electrode pads when us ing an AED.

Ha ir y Ch e s t

If the patient has a hairy ches t, the AED pads may s tick to the hair and not to the s kin on the ches t. If this occurs , the AED will not properly analyze the patient’s heart rhythm. The AED will give a “check electrodes ” or “check electrode pads ” mes s age. If this happens , complete the following s teps and actions while minimizing interruptions in ches t compres s ions .

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5

Ste p

Wa t e r

Ac t io n

1

If the pads s tick to the hair ins tead of the s kin, pres s down firmly on each pad.

2

If the AED continues to prompt you to “check pads ” or “check electrodes ,” quickly pull off the pads . This will remove much of the hair.

3

If too much hair remains where you will put the pads , s have the area with the razor in the AED carrying cas e, if available.

4

Put on a new s et of pads . Follow the AED voice prompts .

Do not us e an AED in the water. If water is pres ent on the patient’s ches t, it may conduct the s hock electricity acros s the s kin of the ches t. This will prevent the delivery of an adequate s hock dos e to the heart.

If...

Im p la n t e d P a c e m a ke r

Th e n ...

The patient is in the water

Pull the patient out of the water

The patient’s ches t is covered with water

Wipe the ches t quickly before attaching the electrodes

The patient is lying on s now or ice or in a s mall puddle

Us e the AED

Patients known to be at high ris k for s udden cardiac arres t may have implanted defibrillators /pacemakers that automatically deliver s hocks directly to the heart mus cle if a lifethreatening arrhythmia is detected. You can immediately identify thes e devices becaus e they create a hard lump beneath the s kin of the upper ches t or abdomen. The lump ranges in s ize from the s ize of a s ilver dollar to half the s ize of a deck of cards , with a s mall overlying s car. The pres ence of an implanted defibrillator or pacemaker is not a contraindication to attaching and us ing an AED. Avoid placing the AED electrode pads directly over the device becaus e the devices may interfere with each other. If you identify an implanted defibrillator/pacemaker: • If pos s ible, place the AED electrode pad to either s ide and not directly on top of the implanted device. • Follow the normal s teps for operating an AED. Occas ionally the analys is and s hock cycles of implanted defibrillators and AEDs will conflict. If the implanted defibrillator is delivering s hocks to the patient (the patient’s mus cles contract in a manner like that obs erved after an AED s hock), allow 30 to 60 s econds for the implanted defibrillator to complete the treatment cycle before delivering a s hock from the AED.

Tr a n s d e r m a l Me d ic a t io n P a t c h e s

58

Do not place AED electrodes directly on top of a medication patch (eg, a patch of nitroglycerin, nicotine, pain medication, hormone replacement therapy, or antihypertens ive medication). The medication patch may block the trans fer of energy from the electrode pad to the heart or caus e s mall burns to the s kin. To prevent thes e complications , remove the patch and wipe the area clean before attaching the AED electrode pad. Try to minimize interruptions in ches t compres s ions and do not delay s hock delivery.

Th e ACLS Ca s e s : VF/ P u ls e le s s VT

VF/ P u ls e le s s VT Ca s e In t r o d u c t io n

This cas e focus es on the as s es s ment and actions us ed for a witnes s ed cardiac arres t due to VF or puls eles s VT that is refractory (unres pons ive) to the firs t s hock. You will us e a manual defibrillator in this cas e. In this cas e and during the cours e you will have an opportunity to demons trate effective res us citation team behaviors while performing the as s es s ment and action s kills . During the BLS Survey, team members will perform continuous high-quality CPR with effective ches t compres s ions and ventilation with a bag-mas k device. The team leader will conduct the ACLS Survey, including rhythm recognition (s hockable vers us nons hockable), defibrillation us ing a manual defibrillator, res us citation drugs , a dis cus s ion of IV/IO acces s , and advanced airways . The success of any resuscitation attempt is built on a strong base of high-quality CPR and defibrillation when required by the patient’s ECG rhythm.


By the end of this cas e you s hould be able to 1. Des cribe s igns that the patient is experiencing VF/puls eles s VT 2. Recognize VF and VT on the ECG 3. Manage VF/puls eles s VT according to the Cardiac Arres t Algorithm 4. Recall indications for drugs recommended for refractory VF/puls eles s VT 5. Recall contraindications for drugs recommended for refractory VF/puls eles s VT 6. Recall dos es for drugs recommended for refractory VF/puls eles s VT 7. Recall routes of adminis tration for drugs recommended for refractory VF/puls eles s VT 8. State appropriate electrical dos es us ed for VF/puls eles s VT arres t 9. Perform defibrillation with minimal (10 s econds or les s ) interruption of ches t compres s ions 10. ROSC: Support blood pres s ure with fluids 11. ROSC: Support blood pres s ure with pres s ors 12. ROSC: Ens ure ventilation by us ing quantitative waveform capnography 13. ROSC: Titrate Fio 2 by us ing puls e oximetry 14. ROSC: As s es s for STEMI: 12-lead and intervention 15. ROSC: As s es s level of cons cious nes s 16. ROSC: Cons ider hypothermia for comatos e patients 17. ROSC: Treat revers ible caus es 18. ROSC: Place patient into appropriate s ys tem of care

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Rh yt h m s fo r VF/ P u ls e le s s VT

This cas e involves thes e ECG rhythms :

Dr u g s fo r VF/ P u ls e le s s VT

This cas e involves thes e drugs :

• VF • VT • ECG artifact that looks like VF • New left bundle branch block

• Epinephrine • Norepinephrine • Vas opres s in • Amiodarone • Lidocaine • Magnes ium s ulfate • Dopamine • Oxygen

Ma n a g in g VF/ P u ls e le s s VT: Th e Ca rd ia c Ar re s t Alg o r it h m Ove r vie w

The Cardiac Arres t Algorithm (Figure 19) is the mos t important algorithm to know for adult res us citation. This algorithm outlines all as s es s ment and management s teps for the puls eles s patient who does not initially res pond to BLS interventions , including a firs t s hock from an AED. The AHA s implified and redes igned the 2005 algorithm to emphas ize the importance of minimally interrupted high-quality CPR. The algorithm cons is ts of the 2 pathways for a cardiac arres t: • A s hockable rhythm (VF/puls eles s VT) dis played on the left s ide of the algorithm • A nons hockable rhythm (as ys tole/PEA) dis played on the right s ide of the algorithm Throughout the cas e dis cus s ion of the Cardiac Arres t Algorithm, we will refer to Boxes 1 through 12. Thes e are the numbers as s igned to the boxes on the algorithm.

VF/ VT (Le ft S id e )

Becaus e many patients with s udden cardiac arres t demons trate VF at s ome point in their arres t, it is likely that ACLS providers will frequently follow the left s ide of the Cardiac Arres t Algorithm (Figure 19). Rapid treatment of VF according to this s equence is the bes t s cientific approach to res toring s pontaneous circulation. Puls eles s VT is included in the algorithm becaus e it is treated as VF. VF and puls eles s VT require CPR until a defibrillator is available. Both are treated with high-energy uns ynchronized s hocks .

60

As ys t o le / P EA (Rig h t S id e )

The right s ide of the algorithm outlines the s equence of actions to perform if the rhythm is nons hockable. You will have an opportunity to practice this s equence in the as ys tole and PEA cas es .

Su m m a r y

The VF/Puls eles s VT Cas e gives you the opportunity to practice performing rapid treatment of VF/VT by following the s teps on the left s ide of the Cardiac Arres t Algorithm (Boxes 1 through 8).


CP R Qua lity

Ad ult Ca rd ia c Arre s t Sho ut fo r He lp /Ac tiva te Em e rg e nc y Re s p o ns e compres s ions

1

Sta rt CP R 30:2 compres s ionYe s

No

Rhythm s ho c ka b le ?

2

capnography ETCO2

9

VF/VT

attempt to improve

As ys to le /P EA

3 Shoc k Re turn o f Sp o nta ne o us Circ ula tio n (ROSC)

4

CP R 2 m in

creas e in P ETCO 2


No

Sho c k Ene rg y

Ye s

5

6

Shoc k -

10

CP R 2 m in

CP R 2 m in

Ep ine p hrine every 3-5 min


capnography

360 J Drug The ra p y

capnography Va s o p re s s in


No


Ye s epinephrine

Ye s

7

Shoc k

No

Ad va nc e d Airwa y

11

8

CP R 2 m in

CP R 2 m in

Am io d a ro ne

compres s ions No


Ye s

12 Go to 5 o r 7 10 or 11


Re ve rs ib le Ca us e s – H – H – H – H – Hypothermia – T – T – T – T – T

Fig u re 1 9 . 61

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FYI 2 0 1 0 Gu id e lin e s ACLS Ca rd ia c Arre s t Alg o rithm s

• The 2010 Cardiac Arres t Algorithms (Figures 19 and 21) are pres ented in the t raditional box-and-line format and a new circular format (Figure 21). The 2 formats facilitate learning and memorization of the treatment recommendations . Overall thes e algorithms reflect an emphas is on the importance of high-quality, minimally interrupted CPR. This action is fundamental to the management of all cardiac arres t rhythms .

Ap p lic a t io n o f t h e Ca rd ia c Ar re s t Alg o r it h m : VF/ VT P a t h w a y In t r o d u c t io n (Bo xe s 1 Th r o u g h 4 )

This cas e dis cus s es the as s es s ment and treatment of a patient with refractory VF or puls eles s VT. This algorithm as s umes that healthcare providers have completed the BLS Survey, including activation of the emergency res pons e s ys tem, performing CPR, attaching the manual defibrillator, and delivering the firs t s hock (Boxes 1 through 4). The ACLS res us citation team now intervenes and conducts the ACLS Survey. In this cas e the team as s es s es the patient and takes actions as needed. The team leader coordinates the efforts of the res us citation team as they perform the s teps lis ted in the VF/VT pathway on the left s ide of the Cardiac Arres t Algorithm.

Min im a l In t e r r u p t io n o f Ch e s t Co m p r e s s io n s

A team member s hould continue to perform high-quality CPR until the defibrillator arrives and is attached to the patient. The team leader as s igns roles and res pons ibilities and organizes interventions to minimize interruptions in ches t compres s ions . This a ccomplis hes the mos t critical interventions for VF or puls eles s VT: CPR with minimal interruptions in ches t compres s ions and defibrillation during the firs t minutes of arres t. The AHA does not recommend continued us e of an AED (or the automatic mode) when a manual defibrillator is available and the provider’s s kills are adequate for rhythm interpretation. Rhythm analys is and s hock adminis tration with an AED may res ult in p rolonged interruptions in ches t compres s ions . Ch e s t c om p re s s ion s s h ou ld id e a lly b e in te rru p te d on ly for ve n tila tion (u n le s s a n a d va n c e d a irwa y is p la c e d ), rh yth m c h e c ks , a n d a c tu a l s h oc k d e live ry. P e rform a p u ls e c h e c k on ly if a n org a n ize d rh yth m is ob s e rve d .

Fig u re 2 0 . Relations hip of quality CPR to coronary perfus ion pres s ure (CPP) demons trating the need to minimize interruptions in compres s ions . Coronary perfus ion pres s ure is aortic relaxation (“dias tolic”) pres s ure minus right atrial relaxation (“dias tolic”) pres s ure. During CPR, CPP correlates with both myocardial blood flow and ROSC. In one human s tudy ROSC did not occur unles s a CPP ≥15 mm Hg was achieved during CPR.

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Fo u n d a t io n a l Fa c t s Re s um e CP R While Ma nua l De fib rilla to r Is Cha rg ing

De live r 1 S h o c k (Bo x 3 )

• Shortening the interval between the las t compres s ion and the s hock by even a few s econds can improve s hock s ucces s (defibrillation and ROSC). Thus , it is reas onable for healthcare providers to practice efficient coordination between CPR and d efibrillation to minimize the hands -off interval between s topping compres s ions and adminis tering the s hock. • For example, after verifying a s hockable rhythm and initiating the charging s equence on the defibrillator, another res cuer s hould res ume ches t compres s ions and continue until the defibrillator is fully charged. The defibrillator operator s hould deliver the s hock as s oon as the compres s or removes his or her hands from the patient’s ches t and all providers are “clear” of contact with the patient. • Us e of a multimodal defibrillator in manual mode may reduce the duration of ches t compres s ion interruption required for rhythm analys is compared with automatic mode but could increas e the frequency of inappropriate s hock. Individuals who are not comfortable interpreting cardiac rhythms can continue to us e an AED. • For an AED, follow the device’s prompts .

Box 3 directs you to deliver 1 s hock. The appropriate energy dos e is determined by the identity of the defibrillator—monophas ic or biphas ic. See the column on the right of the algorithm. If you are us ing a monophasic defibrillator, give a s ingle 360-J s hock. Us e the s ame e nergy dos e for s ubs equent s hocks . Biphasic defibrillators us e a variety of waveforms , each of which is effective for terminating VF over a s pecific dos e range. When us ing biphas ic defibrillators , providers s hould us e the manufacturer’s recommended energy dos e (eg, initial dos e of 120 to 200 J ). Many biphas ic defibrillator manufacturers dis play the effective energy dos e range on the face of the device. If you do not know the effective dos e range, deliver the maximal energy dos e for the firs t and all s ubs equent s hocks . If the initial s hock terminates VF but the arrhythmia recurs later in the res us citation attempt, deliver s ubs equent s hocks at the previous ly s ucces s ful energy level. Im m e d ia te ly a fte r th e s h oc k, re s u m e CP R, b e g in n in g with c h e s t c om p re s s ion s . Give 2 m in u te s (a b ou t 5 c yc le s ) of CP R. A c yc le c on s is ts of 30 c om p re s s ion s followe d b y 2 ve n tila tion s in th e p a tie n t with ou t a n a d va n c e d a irwa y.

Re s u m e CP R (Bo x 4 )

• Immediately res ume CPR, beginning with ches t compres s ions . • Do not perform a rhythm or puls e check at this point. • Es tablis h IV/IO acces s .

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Fo u n d a t io n a l Fa c t s Cle a ring fo r De fib rilla tio n

To ens ure s afety during defibrillation, always announce the s hock warning. State the warning firmly and in a forceful voice before delivering each s hock (this entire s equence s hould take <5 s econds ): • “Cle a r. I a m g o ing to s ho c k o n thre e .” – Check to make s ure you are clear of contact with the patient, the s tretcher, or other equipment. – Make a vis ual check to ens ure that no one is touching the patient or s tretcher. – Be s ure oxygen is not flowing acros s the patient’s ches t. • “One , two , thre e . Sho c king .” When pres s ing the SHOCK button, the defibrillator operator s hould face the patient, not the machine. This helps to ens ure coordination with the ches t compres s or and to verify that no one res umed contact with the patient. You need not us e thes e exact words , but you mus t warn others that you are about to deliver s hocks and that everyone mus t s tand clear of the patient.

Rh yt h m Ch e c k

Conduct a rhythm check after 2 minutes (about 5 cycles ) of CPR. Be careful to minimize interruptions in ches t compres s ions . Th e p a u s e in c h e s t c om p re s s ion s to c h e c k th e rh yth m s h ou ld n ot e xc e e d 10 s e c on d s . • If a nons hockable rhythm is pres ent and the rhythm is organized, a team member s hould try to palpate a puls e. If there is any doubt about the pres ence of a puls e, immediately res ume CPR. • Re m e m b e r: Perform a pulse check—preferably during rhythm analysis—only if an organized rhythm is present. • If the rhythm is organized and there is a palpable puls e, proceed to pos t–cardiac arres t care. • If the rhythm check reveals a nons hockable rhythm and there is no puls e, proceed along the as ys tole/PEA pathway on the right s ide of the Cardiac Arres t Algorithm (Boxes 9 through 11). • If the rhythm check reveals a s hockable rhythm, give 1 s hock and res ume CPR immediately for 2 minutes after the s hock (Box 6).

Fo u n d a t io n a l Fa c t s P a d d le s vs P a d s

• Us ing conductive materials during the defibrillation attempt reduces trans thoracic impedance, or the res is tance that ches t s tructures have on electrical current. • Conductive materials include paddles with electrode pas te, gel pads , or s elfadhes ive pads . • No exis ting data s ugges t that one is better than the others . Self-adhes ive pads , however, reduce the ris k of arcing, allow monitoring of the patient’s underlying rhythm, and permit the rapid delivery of a s hock if neces s ary. For thes e reas ons , the AHA recommends routine us e of s elf-adhes ive pads ins tead of paddles .

64


Sh oc k a n d Va s o p r e s s o r s (Bo x 6 )

For pers is tent VF/puls eles s VT, give 1 s hock and res ume CPR immediately for 2 minutes (about 5 cycles ) after the s hock. Im m e d ia te ly a fte r th e s h oc k, re s u m e CP R, b e g in n in g with c h e s t c om p re s s ion s . Give 2 m in u te s (a b ou t 5 c yc le s ) of CP R. When IV/IO acces s is available, give a vas opres s or during CPR (either before or after the s hock) as follows : • Ep ine p hrine 1 mg IV/IO—repeat every 3 to 5 minutes or • Va s o p re s s in 40 units IV/IO—may s ubs titute for the firs t or s econd dos e of epinephrine Note: If additional team members are available, they s hould anticipate the need for drugs and prepare them in advance. Ep ine p hrine hydrochloride is us ed during res us citation primarily for its α -adrenergic effects , ie, vas ocons triction. Vas ocons triction increas es cerebral and coronary blood flow during CPR by increas ing mean arterial pres s ure and aortic dias tolic pres s ure. In previous s tudies , es calating and high-dos e epinephrine adminis tration did not improve s urvival to dis charge or neurologic outcome after res us citation from cardiac arres t. Va s o p re s s in is a nonadrenergic peripheral vas ocons trictor. A meta-analys is of 5 randomized trials found no difference between vas opres s in and epinephrine for ROSC, 24-hour s urvival, or s urvival to hos pital dis charge.

Rh yt h m Ch e c k

Conduct a rhythm check after 2 minutes (about 5 cycles ) of CPR. Be careful to minimize interruptions in ches t compres s ions . In te rru p tion in CP R to c on d u c t a rh yth m a n a lys is s h ou ld n ot e xc e e d 10 s e c on d s . • If a nons hockable rhythm is pres ent and the rhythm is organized, a team member s hould try to palpate a puls e. If there is any doubt about the pres ence of a puls e, immediately res ume CPR. • If the rhythm check is organized and there is a palpable puls e, proceed to pos t– cardiac arres t care. • If the rhythm check reveals a nons hockable rhythm and there is no puls e, proceed along the as ys tole/PEA pathway on the right s ide of the Cardiac Arres t Algorithm (Boxes 9 through 11). • If the rhythm check reveals a s hockable rhythm, res ume ches t compres s ions if indicated while the defibrillator is charging (Box 8). The team leader is res pons ible for team s afety while compres s ions are being performed and the defibrillator is charging.

Sh oc k a n d An t ia r r h yt h m ic s (Bo x 8 )

Give 1 s hock and res ume CPR beginning with ches t compres s ions for 2 minutes (about 5 cycles ) immediately after the s hock. Healthcare providers may cons ider giving antiarrhythmic drugs , either before or after the s hock; however, there is no evidence that any antiarrhythmic drug given during cardiac arres t increas es s urvival to hos pital dis charge. If adminis tered, amiodarone is the firs t-line antiarrhythmic agent given in cardiac arres t becaus e it has been clinically demons trated that it improves the rate of ROSC and hos pital admis s ion in adults with refractory VF/ puls eles s VT.

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5 • Am io d a ro ne 300 mg IV/IO bolus , then cons ider an additional 150 mg IV/IO once If amiodarone is not available, providers may adminis ter lidocaine. • Lid o c a ine 1 to 1.5 mg/kg IV/IO firs t dos e, then 0.5 to 0.75 mg/kg IV/IO at 5- to 10-minute intervals , to a maximum dos e of 3 mg/kg Providers s hould cons ider magnes ium s ulfate only for tors ades de pointes as s ociated with a long QT interval. • Ma g ne s ium s ulfa te for tors ades de pointes , loading dos e 1 to 2 g IV/IO diluted in 10 mL (eg, D5 W, normal s aline) given as IV/IO bolus , typically over 5 to 20 minutes Routine adminis tration of magnes ium s ulfate in cardiac arres t is not recommended unles s tors ades de pointes is pres ent. Search for and treat any treatable underlying caus e of cardiac arres t. See column on the right of the algorithm.

Ca r d ia c Ar r e s t Tr e a t m e n t Se q u e n c e s

The Cardiac Arres t Circular Algorithm (Figure 21) s ummarizes the recommended s equence of CPR, rhythm checks , s hocks , and delivery of drugs bas ed on expert cons ens us . The optimal number of cycles of CPR and s hocks required before s tarting pharmacologic therapy remains unknown. Note that rhythm checks and s hocks are organized around 5 cycles of compres s ions and ventilations , or 2 minutes if a provider is timing the arres t.

Ad ult Ca rd ia c Arre s t Shout for He lp/Ac tiva te Em e rge nc y Re s pons e Sta rt CP R • Give oxygen • Attach monitor/de brillator Re turn o f Sp o nta ne o us Circ ula tio n (ROSC)

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Drug The ra p y IV/IO acces s Epinephrine every 3-5 minutes Amiodarone for refractory VF/VT

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Co ns id e r Ad va nc e d Airwa y Quantitative waveform capnography o

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Re turn o f Sp o nta ne o us Circ ula tio n (ROSC) • P uls e and blood pres s ure • Abrupt s us tained increas e in P e t c o 2 (typically ≥40 mm Hg) • S pontaneous arterial pres s ure waves with intra-arterial monitoring Sho c k Ene rg y • Bip ha s ic : Manufacturer recommendation (eg, initial dos e of 120-200 J ); if unknown, us e maximum available. Second and s ubs equent dos es s hould be equivalent, and higher dos es may be cons idered. • Mo no p ha s ic : 360 J

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CP R Qua lity • P us h hard (≥2 inches [5 cm]) and fas t (≥100/min) and allow complete ches t recoil • Minimize interruptions in compres s ions • Avoid exces s ive ventilation • Rotate compres s or every 2 minutes • If no advanced airway, 30:2 compres s ion-ventilation ratio • Q uantitative waveform capnography – If P e t c o 2 <10 mm Hg, attempt to improve CPR quality • Intra-arterial pres s ure – If relaxation phas e (dias tolic) pres s ure <20 mm Hg, attempt to improve CPR quality

it y l a u


Drug The ra p y • E p ine p hrine IV/IO Do s e : 1 mg every 3-5 minutes • Va s o p re s s in IV/IO Do s e : 40 units can replace firs t or s econd dos e of epinephrine • Amioda rone IV/IO Dos e : First dose: 300 mg bolus. Second dose: 150 mg. Ad va nc e d Airwa y • S upraglottic advanced airway or endotracheal intubation • Waveform capnography to confirm and monitor ET tube placement • 8 -10 breaths per minute with continuous ches t compres s ions Re ve rs ib le Ca us e s – Hypovolemia – Hypoxia – Hydrogen ion (acidos is ) – Hypo-/hyperkalemia – Hypothermia

– – – – –

Tens ion pneumothorax Tamponade, cardiac Toxins Thrombos is , pulmonary Thrombos is , coronary

Fig u re 2 1 . The Cardiac Arres t Circular Algorithm. Do not delay s hock. Continue CPR while preparing and adminis tering drugs and charging the defibrillator. Interrupt ches t compres s ions only for the minimum amount of time required for ventilation (until advanced airway placed), rhythm check, and actual s hock delivery.

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FYI 2 0 1 0 Gu id e lin e s Ca rd ia c Arre s t Circ ula r Alg o rithm

P h ys io lo g ic Mo n it o r in g Du r in g CP R

• The 2010 AHA Guidelines for CPR and ECC introduced a new circular format for the Cardiac Arres t Algorithm (Figure 21) to facilitate learning and memorization of the treatment recommendations . This new algorithm emphas izes the importance of highquality, minimally interrupted CPR, which is fundamental to the management of all cardiac arres t rhythms .

The 2010 AHA Guidelines for CPR and ECC recommend us ing quantitative waveform capnography in intubated patients to monitor CPR quality (Figure 22A), optimize ches t compres s ions , and detect ROSC during ches t compres s ions (Figure 23) or when rhythm check reveals an organized rhythm. Although placement of invas ive monitors during CPR is not generally warranted, phys iologic parameters s uch as intra-arterial relaxation pres s ures (Figure 22A) and central venous oxygen s aturation (Scvo 2 ), when available, may als o be helpful for optimizing CPR and detecting ROSC. Animal and human s tudies indicate that P e t c o 2 , CPP, and Scvo 2 monitoring provides valuable information on both the patient’s condition and the res pons e to therapy. Mos t important, P e t c o 2 , CPP, and Scvo 2 correlate with cardiac output and myocardial blood flow during CPR. When ches t compres s ions fail to achieve identified thres hold values , ROSC is rarely achieved. Furthermore, an abrupt increas e in any of thes e parameters is a s ens itive indicator of ROSC that can be monitored without interrupting ches t compres s ions . Although no clinical s tudy has examined whether titrating res us citative efforts to phys iologic parameters improves outcome, it is reas onable to us e thes e parameters , if available, to optimize compres s ions and guide vas opres s or therapy during cardiac arres t.

En d -Tid a l CO 2 The main determinant of P e t c o 2 during CPR is blood delivery to the lungs . Pers is tently low P e t c o 2 values <10 mm Hg during CPR in intubated patients (Figure 22B) s ugges t that ROSC is unlikely. If P e t c o 2 abruptly increas es to a normal value of 35 to 40 mm Hg, it is reas onable to cons ider this an indicator of ROSC. • If the P e t c o 2 is <10 mm Hg during CPR, it is reas onable to try to improve ches t compres s ions and vas opres s or therapy.

Coron a ry P e rfu s ion P re s s u re or Arte ria l Re la xa tion P re s s u re Increas ed CPP correlates with both myocardial blood flow and ROSC. A reas onable s urrogate for CPP during CPR is arterial relaxation (“dias tolic”) pres s ure, which can be meas ured by us ing an intra-arterial catheter. • If the arterial relaxation pres s ure is <20 mm Hg (Figure 22B), it is reas onable to try to improve ches t compres s ions and vas opres s or therapy.

Ce n tra l Ve n ou s Oxyg e n Sa tu ra tion If oxygen cons umption, arterial oxygen s aturation, and hemoglobin are cons tant, changes in Scvo 2 reflect changes in oxygen delivery due to changes in cardiac output. Scvo 2 can be meas ured continuous ly by us ing oximetric tipped central venous catheters placed in the s uperior vena cava or pulmonary artery. Normal range is 60% to 80% . • If the Scvo 2 is <30% , it is reas onable to try to improve ches t compres s ions and vas opres s or therapy.

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Fig u re 2 2 . Phys iologic monitoring during CPR. A, High-quality compres s ions are s hown through waveform capnography and intra-arterial relaxation pres s ure. P e t c o 2 values <10 mm Hg in intubated patients or intra-arterial relaxation pres s ures <20 mm Hg indicate that cardiac output is inadequate to achieve ROSC. In either of thos e cas es it is reas onable to cons ider trying to improve quality of CPR by optimizing ches t compres s ion parameters or giving a vas opres s or or both. B, Ineffective CPR compres s ions s hown through waveform capnography and intra-arterial relaxation pres s ure.

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ROSC

Fig u re 2 3 . Waveform capnography during CPR with ROSC. This capnography tracing dis plays P e t c o 2 in millimeters of mercury on the vertical axis over time. This patient is intubated and receiving CPR. Note that the ventilation rate is approximately 8 to 10 breaths per minute. Ches t compres s ions are given continuous ly at a rate s lightly fas ter than 100/min but are not vis ible with this tracing. The initial P e t c o 2 is <12.5 mm Hg during the firs t minute, indicating very low blood flow. P e t c o 2 increas es to between 12.5 and 25 mm Hg during the s econd and third minutes , cons is tent with the increas e in blood flow with ongoing res us citation. ROSC occurs during the fourth minute. ROSC is recognized by the abrupt increas e in P e t c o 2 (vis ible jus t after the fourth vertical line) to >50 mm Hg, which is cons is tent with a s ubs tantial improvement in blood flow.

Tr e a t m e n t o f VF/ VT in Hyp o t h e r m ia

For a cardiac arres t patient in VF/VT who has s evere hypothermia and a body temperature of <30°C (<86°F), a s ingle defibrillation attempt is appropriate. If the patient fails to res pond to the initial s hock, it is reas onable to perform additional defibrillation attempts according to the us ual BLS guidelines while engaging in active rewarming. The hypothermic patient may have a reduced rate of drug metabolis m, rais ing concern that drug levels may accumulate to toxic levels with s tandard dos ing regimens . Although the evidence does not s upport the us e of antiarrhythmic drug therapy in hypothermic patients in cardiac arres t, it is reas onable to cons ider adminis tration of a vas opres s or according to the s tandard ACLS algorithm concurrent with rewarming s trategies . ACLS treatment of the patient with s evere hypothermia in cardiac arres t in the hos pital s hould be aimed at rapid core rewarming. For patients in cardiac arres t with moderate hypothermia (30°C to 34°C [86°F to 93.2°F]), s tart CPR, attempt defibrillation, give medications s paced at longer intervals , and, if in hos pital, provide active core rewarming.

Ro u t e s o f Ac c e s s fo r Dr u g s P r io r it ie s

Priorities during cardiac arres t are high-quality CPR and early defibrillation. Ins ertion of an advanced airway and drug adminis tration are of s econdary importance. No drug given during cardiac arres t has been s hown to improve s urvival to hos pital dis charge or improve neurologic function after cardiac arres t. His torically in ACLS, providers have adminis tered drugs via either the IV or endotracheal route. Endotracheal abs orption of drugs is poor and optimal drug dos ing is not known. For this reas on, the IO route is preferred when IV acces s is not available. Priorities for vas cular acces s are • IV route • IO route • Endotracheal route

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In t r a ve n o u s Ro u t e

A peripheral IV is preferred for drug and fluid adminis tration unles s central line acces s is already available. Central line acces s is not neces s ary during mos t res us citation attempts . Central line acces s may caus e interruptions in CPR and complications during ins ertion, including vas cular laceration, hematomas , and bleeding. Ins ertion of a central line in a noncompres s ible ves s el is a relative (not abs olute) contraindication to fibrinolytic therapy in patients with ACS. Es tablis hing a peripheral line does not require interruption of CPR. Drugs , however, typically require 1 to 2 minutes to reach the central circulation when given by the peripheral IV route. Keep in mind that drugs adminis tered during the CPR s equence will likely not take effect until completion of s everal cycles of CPR. If a drug is given by the peripheral venous route, adminis ter it as follows : • Give the drug by bolus injection unles s otherwis e s pecified. • Follow with a 20-mL bolus of IV fluid. • Elevate the extremity for about 10 to 20 s econds to facilitate delivery of the drug to the central circulation.

In t r a o s s e o u s Ro u t e

Drugs and fluids during res us citation can be delivered s afely and effectively via the IO route if IV acces s is not available. Important points about IO acces s are • IO acces s can be es tablis hed in all age groups . • IO acces s often can be achieved in 30 to 60 s econds . • The IO route of adminis tration is preferred over the endotracheal route. • Any ACLS drug or fluid that is adminis tered IV can be given IO. IO cannulation provides acces s to a noncollaps ible marrow venous plexus , which s erves as a rapid, s afe, and reliable route for adminis tration of drugs , crys talloids , colloids , and blood during res us citation. The technique us es a rigid needle, preferably a s pecially des igned IO or bone marrow needle from an IO acces s kit. For more information on IO acces s , s ee the Acces s for Medications s ection on the Student Webs ite (www.he a rt.o rg /e c c s tud e nt).

En d o t r a c h e a l Ro u t e

IV and IO adminis tration routes are preferred over the endotracheal adminis tration route. When cons idering adminis tration of drugs via the endotracheal route during CPR, keep thes e concepts in mind: • The optimal dos e of mos t drugs given by the endotracheal route is unknown. • The typical dos e of drugs adminis tered via the endotracheal route is 2 to 2½ times the IV route. Studies demons trate that epinephrine, vas opres s in, and lidocaine are abs orbed into the circulatory s ys tem after adminis tration via the endotracheal route. When giving drugs via the endotracheal route, dilute the dos e in 5 to 10 mL of s terile water or normal s aline. Inject the drug directly into the trachea.

Va s o p re s s o r s In t r o d u c t io n

70

There is no evidence to date that routine us e of any vas opres s or at any s tage during management of cardiac arres t increas es rates of s urvival to hos pital dis charge. But there is evidence that the us e of vas opres s ors favors initial res us citation with ROSC.


Va s o p r e s s o r s Us e d Du r in g Ca r d ia c Ar r e s t

Vas opres s ors optimize cardiac output and blood pres s ure. The vas opres s ors us ed during cardiac arres t are • Epinephrine: 1 mg IV/IO (repeat every 3 to 5 minutes ) • Vas opres s in: 1 dos e of 40 units IV/IO may replace either the firs t or s econd dos e of epinephrine If IV/IO acces s cannot be es tablis hed or is delayed, give epinephrine 2 to 2.5 mg diluted in 5 to 10 mL of s terile water or normal s aline and injected directly into the ET tube. Remember, the endotracheal route of drug adminis tration res ults in variable and unpredictable drug abs orption and blood levels .

Ep in e p h r in e

Although healthcare providers have us ed epinephrine for years in res us citation, there are few data to s how that it improves outcome in humans . Epinephrine adminis tration does appear to improve ROSC. No s tudies demons trate improved rates of s urvival to hos pital dis charge or neurologic outcome when comparing s tandard epinephrine dos es with initial high-dos e or es calating dos e epinephrine. Therefore, the AHA cannot recommend the routine us e of high-dos e or es calating dos es of epinephrine. Epinephrine is thought to s timulate adrenergic receptors , producing vas ocons triction, increas ing blood pres s ure and heart rate, and improving perfus ion pres s ure to the brain and heart. Repeat epinephrine 1 mg IV/IO every 3 to 5 minutes during cardiac arres t. Re m e m b e r, follow e a c h d os e g ive n b y p e rip h e ra l in je c tion with a 20-m L flu s h of IV flu id a n d e le va te th e e xtre m ity a b ove th e le ve l of th e h e a rt for 10 to 20 s e c on d s .

Va s o p r e s s in

Fo u n d a t io n a l Fa c t s Va s o p re s s o rs

Vas opres s in is a nonadrenergic peripheral vas ocons trictor that increas es arterial blood pres s ure. Becaus e the efficacy of vas opres s in is no different from that of epinephrine in cardiac arres t, a s ingle dos e of vas opres s in (40 units IV/IO) may replace either the firs t or s econd dos e of epinephrine.

Becaus e the effects of vas opres s in have not been s hown to differ from thos e of epinephrine in cardiac arres t, either vas opres s in or epinephrine can be us ed as the initial vas opres s or during cardiac arres t. • A vas opres s or is given every 3 to 5 minutes during cardiac arres t. • One dos e of vas opres s in 40 units IV/IO may replace either the firs t or s econd dos e of epinephrine in the treatment of cardiac arres t. • Epinephrine is adminis tered 3 to 5 minutes after the dos e of vas opres s in if there is a continuing need for a vas opres s or.

An t ia r r h yt h m ic Ag e n t s In t r o d u c t io n

There is no evidence that any antiarrhythmic drug given routinely during human cardiac arres t increas es s urvival to hos pital dis charge. Amiodarone, however, has been s hown to increas e s hort-term s urvival to hos pital admis s ion when compared with placebo or lidocaine.

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Am io d a r o n e

• Cons ider amiodarone for treatment of VF or puls eles s VT unres pons ive to s hock delivery, CPR, and a vas opres s or. • Amiodarone is a complex drug that affects s odium, potas s ium, and calcium channels . It als o has α -adrenergic and ß-adrenergic blocking properties . • During cardiac arres t, cons ider amiodarone 300 mg IV/IO pus h for the firs t dos e. If VF/puls eles s VT pers is ts , cons ider giving a s econd dos e of 150 mg IV/IO in 3 to 5 minutes .

Lid o c a in e

• Lidocaine is an alternative antiarrhythmic of long-s tanding and wides pread familiarity. However, it has no proven s hort-term or long-term efficacy in cardiac arres t. Providers may cons ider giving lidocaine when amiodarone is not available. • The initial lidocaine dos e is 1 to 1.5 mg/kg IV/IO. Repeat if indicated at 0.5 to 0.75 mg/kg IV/IO over 5- to 10-minute intervals to a maximum of 3 mg/kg. • If no IV/IO acces s is available, the dos e for endotracheal adminis tration is 2 to 4 mg/kg.

Ma g n e s iu m S u lfa t e

• IV magnes ium may terminate or prevent recurrent tors ades de pointes in patients who have a prolonged QT interval during normal s inus rhythm. When VF/puls eles s VT c ardiac arres t is as s ociated with tors ades de pointes , give magnes ium s ulfate at a loading dos e of 1 to 2 g IV/IO diluted in 10 mL (eg, D5 W, normal s aline) over 5 to 20 minutes . If a prearres t 12-lead ECG is available for review, check the QT interval for prolongation. • Remember that puls eles s VT is treated with an immediate high-energy s hock, whereas magnes ium is an adjunctive agent us ed to prevent recurrent or treat pers is tent VT as s ociated with tors ades de pointes . • Magnes ium s ulfate is als o indicated for patients with known or s us pected low s erum magnes ium, s uch as patients with alcoholis m or other conditions as s ociated with malnutrition or hypomagnes emic s tates . For patients in refractory VF/puls eles s VT, check the patient’s his tory, if available, for one of thes e conditions that s ugges ts the pres ence of a revers ible electrolyte abnormality.

Im m e d ia t e P o s t –Ca rd ia c Ar re s t Ca re In t r o d u c t io n

There is increas ing recognition that s ys tematic pos t–cardiac arres t care after ROSC can improve the likelihood of patient s urvival with good quality of life. This cas e focus es on the management of and optimization of cardiopulmonary function and perfus ion of vital organs after ROSC. To ens ure the s ucces s of pos t–cardiac arres t care, healthcare providers mus t • Optimize the patient’s hemodynamic and ventilation s tatus • Initiate therapeutic hypothermia • Provide immediate coronary reperfus ion with PCI • Ins titute glycemic control • Provide neurologic care and prognos tication and other s tructured interventions In this cas e you will have an opportunity to us e the 12-lead ECG while us ing the as s es s ment and action s kills typically performed after ROSC.

Ma n a g in g P o s t – Ca r d ia c Ar r e s t Ca r e : Th e P o s t –Ca r d ia c Ar r e s t Ca r e Alg o r it h m 72

The Immediate Pos t–Cardiac Arres t Care Algorithm (Figure 24) outlines all the s teps for immediate as s es s ment and management of pos t–cardiac arres t patients with ROSC. During this cas e team members will continue to maintain good ventilation and oxygenation with a bag-mas k device or advanced airway. Throughout the cas e dis cus s ion of the Pos t– Cardiac Arres t Care Algorithm, we will refer to Boxes 1 through 8. Thes e are the numbers as s igned to the boxes on the algorithm.


Ad ult Im m e d ia te P o s t–Ca rd ia c Arre s t Ca re 1 Re turn o f Sp o nta ne o us Circ ula tio n (ROSC)

2 Op tim ize ve ntila tio n a nd o xyg e na tio n • Maintain oxygen s aturation ≥94% • Cons ider advanced airway and waveform capnography • Do not hyperventilate

3 Tre a t hyp o te ns io n (SBP <90 m m Hg ) • IV/IO bolus • Vas opres s or infus ion • Cons ider treatable caus es • 12-Lead ECG

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Fo llo w c o m m a nd s ?

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Ad va nc e d c ritic a l c a re

Do s e s /De ta ils Ve ntila tio n/Oxyg e na tio n Avoid exces s ive ventilation. Start at 10-12 breaths /min and titrate to target P e t c o 2 of 35-40 mm Hg. When feas ible, titrate Fio 2 to minimum neces s ary to achieve Sp o 2 ≥94% . IV Bo lus 1-2 L normal s aline or lactated Ringer’s . If inducing hypothermia, may us e 4°C fluid. Ep ine p hrine IV Infus io n: 0.1-0.5 mcg/kg per minute (in 70-kg adult: 7-35 mcg per minute) Do p a m ine IV Infus io n: 5-10 mcg/kg per minute No re p ine p hrine IV Infus io n: 0.1-0.5 mcg/kg per minute (in 70-kg adult: 7-35 mcg per minute) Re ve rs ib le Ca us e s – Hypovolemia – Hypoxia – Hydrogen ion (acidos is ) – Hypo-/hyperkalemia – Hypothermia – Tens ion pneumothorax – Tamponade, cardiac – Toxins – Thrombos is , pulmonary – Thrombos is , coronary


Fig u re 2 4 . The Immediate Pos t–Cardiac Arres t Care Algorithm.

Ap p lic a t io n o f t h e Im m e d ia t e P o s t –Ca rd ia c Ar re s t Ca re Alg o r it h m In t r o d u c t io n (Bo x 1 )

This cas e dis cus s es the as s es s ment and treatment of a patient who had cardiac arres t and was res us citated with the us e of the BLS Survey and ACLS Survey. During rhythm check in the ACLS Survey, the patient’s rhythm was organized and a puls e was detected (Box 12, Cardiac Arres t Algorithm [Figure 19]). The team leader will coordinate the efforts of the pos t–cardiac arres t care team as they perform the s teps of the Pos t–Cardiac Arres t Care Algorithm.

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Op t im iz e Ve n t ila t io n a n d Oxyg e n a t io n (Bo x 2 )

Box 2 directs you to ens ure an adequate airway and s upport breathing immediately after ROSC. An uncons cious /unres pons ive patient will require an advanced airway for mechanical s upport of breathing. • Us e continuous waveform capnography to confirm and monitor correct placement of the ET tube (Figures 25 and 26). • Us e the lowes t ins pired oxygen concentration that will maintain arterial oxyhemoglobin s aturation ≥94% . When titration of ins pired oxygen is not feas ible (eg, in an outof-hos pital s etting), it is reas onable to empirically us e 100% oxygen until the patient arrives at the ED. • Avoid exces s ive ventilation of the patient (do not ventilate too fas t or too much). Providers may begin ventilations at 10 to 12 breaths per minute and titrate to achieve a P e t c o 2 of 35 to 40 mm Hg or a Pa c o 2 of 40 to 45 mm Hg. If appropriate equipment is available, adjus t the Fio 2 after achieving ROSC to the minimum concentration needed to achieve arterial oxyhemoglobin s aturation ≥94% . The goal is to avoid hyperoxia while ens uring adequate oxygen delivery. Becaus e an oxygen s aturation of 100% may corres pond to a Pa o 2 between approximately 80 and 500 mm Hg, in general it is appropriate to wean Fio 2 for a s aturation of 100% , provided the patient can maintain oxyhemoglobin s aturation ≥94% .

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Time

Fig u re 2 6 . Waveform capnography with an ET tube, s howing normal (adequate) ventilation pattern: P e t c o 2 35 to 40 mm Hg

Cr it ic a l Co n c e p t s Wa ve fo rm Ca p no g ra p hy

Ca u t io n Thing s to Avo id During Ve ntila tio n

• In addition to monitoring ET tube pos ition, quantitative waveform capnography allows healthcare pers onnel to monitor CPR quality, optimize ches t compres s ions , and detect ROSC during ches t compres s ions or when a rhythm check reveals an organized rhythm.

• When s ecuring an advanced airway, avoid us ing ties that pas s circumferentially around the patient’s neck, thereby obs tructing venous return from the brain. • Exces s ive ventilation may potentially lead to advers e hemodynamic effects when intrathoracic pres s ures are increas ed and becaus e of potential decreas es in cerebral blood flow when Pa c o 2 decreas es .

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P a r t

5

Fo u n d a t io n a l Fa c t s Wa ve fo rm Ca p no g ra p hy

FYI 2 0 1 0 Gu id e lin e s Wa ve fo rm Ca p no g ra p hy

Tr e a t Hyp o t e n s io n (S BP <9 0 m m Hg ) (Bo x 3 )

• End-tidal CO 2 is the concentration of carbon dioxide in exhaled air at the end of expiration. It is typically expres s ed as a partial pres s ure in millimeters of mercury (P e t c o 2 ). Becaus e CO 2 is a trace gas in atmos pheric air, CO2 detected by capnography in exhaled air is produced in the body and delivered to the lungs by circulating blood. • Cardiac output is the major determinant of CO2 delivery to the lungs . If ventilation is relatively cons tant, P e t c o 2 correlates well with cardiac output during CPR. • Providers s hould obs erve a pers is tent capnographic waveform with ventilation to confirm and monitor ET tube placement in the field, in the trans port vehicle, on arrival at the hos pital, and after any patient trans fer to reduce the ris k of unrecognized tube mis placement or dis placement. • Although capnography to confirm and monitor correct placement of s upraglottic airways (eg, laryngeal mas k airway, laryngeal tube, or es ophageal-tracheal tube) has not been s tudied, effective ventilation through a s upraglottic airway device s hould res ult in a capnography waveform during CPR and after ROSC.

• Continuous waveform capnography is recommended, in addition to clinical as s es s ment, as the mos t reliable method of confirming and monitoring correct placement of an ET tube.

Box 3 directs you to treat hypotens ion when SBP is <90 mm Hg. Providers s hould obtain IV acces s if not already es tablis hed. Verify the patency of any IV lines . IV lines s hould replace IO acces s if IO is us ed during res us citation. ECG monitoring s hould continue after ROSC, during trans port, and throughout ICU care until deemed clinically not neces s ary. At this s tage, cons ider treating any revers ible caus es that might have precipitated the cardiac arres t but pers is t after ROSC. When IV is es tablis hed, treat hypotens ion as follows : • IV b o lus 1-2 L normal s aline or lactated Ringer’s . If therapeutic hypothermia is indicated or will be performed, you may us e 4°C fluids . • Ep ine p hrine 0.1-0.5 mcg/kg per minute (in 70-kg adult: 7-35 mcg per minute) IV infus ion titrated to achieve a minimum SBP of >90 mm Hg or a mean arterial pres s ure of >65 mm Hg • Do p a m ine 5-10 mcg/kg per minute IV infus ion titrated to achieve a minimum SBP of >90 mm Hg or a mean arterial pres s ure of >65 mm Hg • No re p ine p hrine 0.1-0.5 mcg/kg per minute (in 70-kg adult: 7-35 mcg per minute) IV infus ion titrated to achieve a minimum SBP of >90 mm Hg or a mean arterial pres s ure of >65 mm Hg Ep ine p hrine can be us ed in patients who are not in cardiac arres t but who require inotropic or vas opres s or s upport. Do p a m ine hydrochloride is a catecholamine-like agent and a chemical precurs or of norepinephrine that s timulates the heart through both α - and ß-adrenergic receptors . No re p ine p hrine (levarterenol) is a naturally occurring potent vas ocons trictor and inotropic agent. It may be effective for management of patients with s evere hypotens ion (eg, SBP <70 mm Hg) and a low total peripheral res is tance who fail to res pond to les s potent adrenergic drugs s uch as dopamine, phenylephrine, or methoxamine.

Fo llo w in g Co m m a n d s (Bo x 4 )

76

Box 4 directs you to examine the patient’s ability to follow verbal commands . If the patient fails to follow commands , the healthcare team s hould cons ider implementing therapeutic hypothermia (Box 5). If the patient is able to follow verbal commands , move to Box 6.


Th e r a p e u t ic Hyp o t h e r m ia (Bo x 5 )

To protect the brain and other organs , the res us citation team s hould induce therapeutic hypothermia in adult patients who remain comatos e (lack of meaningful res pons e to verbal commands ) with ROSC after out-of-hos pital VF cardiac arres t. When ROSC occurs in the out-of-hos pital s etting, EMS pers onnel may initiate the cooling proces s and s hould trans port the patient to a facility that reliably provides this therapy. Healthcare providers s hould cool patients to a target temperature of 32°C to 34°C for a period of 12 to 24 hours . Although the optimal method of achieving the target temperature is unknown, any combination of rapid infus ion of ice-cold, is otonic, non–glucos e-containing fluid (30 mL/kg), endovas cular catheters , s urface cooling devices , or s imple s urface interventions (eg, ice bags ) appears s afe and effective. Healthcare providers s hould als o cons ider induced hypothermia for comatos e adult patients with ROSC after in-hos pital cardiac arres t of any initial rhythm or after out-ofhos pital cardiac arres t with an initial rhythm of PEA or as ys tole.

Ca u t io n Avo id Ac tive Re wa rm ing Afte r ROSC

Fo u n d a t io n a l Fa c t s Ind uc e d Hyp o the rm ia

• In comatos e patients who s pontaneous ly develop a mild degree of hypothermia (>32°C) after res us citation from cardiac arres t, avoid active rewarming during the firs t 12 to 24 hours after ROSC.

• Therapeutic hypothermia is the only intervention demons trated to improve neurologic recovery after cardiac arres t. • The optimal duration of induced hypothermia is at leas t 12 hours and may be >24 hours . The effect of a longer duration of cooling on outcome has not been s tudied in adults , but hypothermia for up to 72 hours was us ed s afely in newborns . • Healthcare providers s hould monitor the patient’s core temperature during induced hypothermia by us ing an es ophageal thermometer, a bladder catheter in nonanuric patients , or a pulmonary artery catheter if one is placed for other indications . Axillary and oral temperatures are inadequate for meas urement of core temperature changes . • Induced hypothermia s hould not affect the decis ion to perform PCI, becaus e concurrent PCI and hypothermia are reported to be feas ible and s afe.

S TEMI Is P r e s e n t o r Hig h S u s p ic io n o f AMI (Bo x 6 )

Both in- and out-of-hos pital medical pers onnel s hould obtain a 12-lead ECG as s oon as pos s ible after ROSC in order to identify thos e patients with STEMI or a high s us picion of AMI. Once identified, hos pital pers onnel s hould attempt coronary reperfus ion (Box 7). EMS pers onnel s hould trans port thes e patients to a facility that reliably provides this therapy (Box 7).

Co r o n a r y Re p e r fu s io n (Bo x 7 )

Aggres s ive treatment of STEMI or AMI s hould begin if detected after ROSC, regardles s of coma or induced hypothermia, including coronary reperfus ion with PCI. In the cas e of out-of-hos pital STEMI, provide advance notification to receiving facilities for patients diagnos ed with STEMI to reduce reperfus ion delay.

Ad va n c e d Cr it ic a l Ca r e (Bo x 8 )

Following coronary reperfus ion interventions or in cas es where the pos t–cardiac arres t patient has no ECG evidence or s us picion of MI, the healthcare team s hould trans fer the patient to an intens ive care unit.

P o s t –Ca r d ia c Ar r e s t Ma in t e n a n c e Th e r a p y

There is no evidence to s upport continued prophylactic adminis tration of antiarrhythmic medications once the patient achieves ROSC.

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P a r t

5

P u ls e le s s Ele c t r ic a l Ac t ivit y Ca s e In t r o d u c t io n

This cas e focus es on as s es s ment and management of a cardiac arrest patient with PEA. During the BLS Survey, team members will demons trate high-quality CPR with effective ches t compres s ions and ventilation with a bag-mas k. In the ACLS Survey the team leader will recognize PEA and implement the appropriate interventions outlined in the Cardiac Arres t Algorithm. Becaus e correction of an underlying caus e of PEA, if pres ent and identified, is critical to patient outcome, the team leader will verbalize the differential diagnos is while leading the res us citation team in the s earch for and treatment of revers ible caus es .


By the end of this cas e you s hould be able to 1. Des cribe s igns and s ymptoms of PEA 2. Demons trate treatment priorities of individuals experiencing PEA as s pecified by the Cardiac Arres t Algorithm 3. State the correct dos age of epinephrine in PEA 4. Recall the correct method of adminis tering epinephrine in PEA 5. State the correct dos age of vas opres s in in PEA 6. Des cribe the target of PEA (treatment of the caus e, not the rhythm) 7. Des cribe the mos t likely caus es of PEA 8. As s ign team functions , monitor CPR, monitor treatments , and monitor drug adminis tration

Rh yt h m s fo r P EA

You will need to recognize the following rhythms : • Rate—too fas t or too s low • Width of QRS complexes —wide vers us narrow

Dr u g s fo r P EA

This cas e involves thes e drugs : • Epinephrine • Vas opres s in • Other medications , depending on the caus e of the PEA arres t

De s c r ip t io n o f P EA In t r o d u c t io n

PEA encompas s es a heterogeneous group of rhythms that are organized or s emiorganized, but lack a palpable puls e. PEA includes • Idioventricular rhythms • Ventricular es cape rhythms • Pos tdefibrillation idioventricular rhythms • Sinus rhythm Any organized rhythm without a puls e is defined as PEA. Even s inus rhythm without a detectable puls e is called PEA. Puls eles s rhythms that are excluded by definition include VF, VT, and as ys tole.

78

Th e ACLS Ca s e s : P u ls e le s s Ele c tric a l Ac tivity

His t o r ic a l P e r s p e c t ive

Previous ly res us citation teams us ed the term electromechanical dissociation (EMD) to des cribe patients who dis played electrical activity on the cardiac monitor but lacked apparent contractile function becaus e of an undetectable puls e. That is , weak contractile function is pres ent—detectable by invas ive monitoring or echocardiography—but the cardiac function is too weak to produce a puls e or effective cardiac output. This is the mos t common initial condition pres ent following s ucces s ful defibrillation. PEA als o includes other conditions where the heart is empty becaus e of inadequate preload. In this cas e, the contractile function of the heart is adequate, but there is inadequate volume for the ventricle to eject. This may occur as a res ult of s evere hypovolemia, or as a res ult of decreas ed venous return from pulmonary embolis m or pneumothorax.

Ma n a g in g P EA: Th e Ca rd ia c Ar re s t Alg o r it h m Ove r vie w

As des cribed earlier, the Cardiac Arres t Algorithm cons is ts of 2 cardiac arres t pathways (Figures 19 and 27). The left s ide of the algorithm outlines treatment for a s hockable rhythm (VF/VT). The right s ide of the algorithm (Boxes 9 through 11) outlines treatment for a nons hockable rhythm (as ys tole/PEA). Becaus e of the s imilarity in caus es and management, the Cardiac Arres t Algorithm combines the as ys tole and PEA pathways , although we will review thes e rhythms in s eparate cas es . In both pathways , therapies are organized around periods (2 minutes or 5 cycles ) of uninterrupted, high-quality CPR. The ability to achieve a good res us citation outcome with return of a perfus ing rhythm and s pontaneous res pirations depends on the ability of the res us citation team to provide effective CPR and to identify and correct a caus e of PEA if pres ent. Everyone on the res us citation team mus t carry out the s teps outlined in the algorithm and at the s ame time focus on the identification and treatment of revers ible caus es of the arres t.

79

5

P a r t

CP R Qua lity • P us h hard (≥2 inches [5 cm]) and fast (≥100/min) and allow complete ches t recoil • Minimize interruptions in compres s ions • Avoid excessive ventilation • Rotate compres s or every 2 minutes • If no advanced airway, 30:2 compres s ionventilation ratio • Q uantitative waveform capnography – If P e t c o 2 <10 mm Hg, attempt to improve CPR quality • Intra-arterial pres s ure – If relaxation phas e (dias tolic) pres s ure <20 mm Hg, attemp t to improve CPR quality

Ad ult Ca rd ia c Arre s t Shout for He lp/Ac tiva te Em e rge nc y Re s pons e 1

Sta rt CP R

• G ive oxygen • Attach monitor/defibrillator

Ye s

No


2

9

VF/VT

As ys to le /P EA

3 Shoc k

Re turn o f Sp o nta ne o us Circ ula tio n (ROSC) • P ulse and blood pressure • Ab rupt s us tained increas e in P e t c o 2 (typically ≥40 mm Hg) • S pontaneous arterial pres s ure waves with intra-arterial monitoring

4

CP R 2 m in • IV/IO acces s

No

Rhythm s ho c ka b le ? Ye s

5

6

Shoc k

10

CP R 2 m in

• IV/IO acces s • E p ine p hrin e every 3-5 min • C ons ider advanced airway, capnography

• E p in e p hrin e every 3-5 min • C ons ider advanced airway, capnography


CP R 2 m in

No

Ye s


Shoc k

No

Ad va nc e d Airwa y • S up raglottic ad vanced airway or endotracheal intubation • Waveform capnography to confirm and monitor ET tube placement • 8 -10 breaths per minute with continuous ches t compres s ions

11

8

CP R 2 m in

CP R 2 m in

• Am io d a ro ne • Treat revers ible caus es

• Treat revers ib le caus es

No


Ye s

12 • If no s igns of return of s pontaneous circulation (ROSC), go to 10 or 11 • If ROSC, go to Pos t–Cardiac Arres t Care © 2010 American Heart As s ociation

Fig u re 2 7 . The Cardiac Arres t Algorithm. 80

Drug The ra p y • Epine phrine IV/IO Do s e : 1 mg every 3-5 minutes • Va s o p re s s in IV/IO Do s e : 40 units can replace firs t or second dose of epinephrine • Am io d a ro ne IV/IO Do s e : First dose: 300 mg bolus. Second dos e: 150 mg.

Ye s

7

Sho c k Ene rg y • Bipha s ic : Manufacturer recommendation (eg, initial dos e of 120-200 J ); if unknown, us e maximum available. Second and subsequent doses should be equivalent, and higher doses may be considered. • Mo no p ha s ic : 360 J

Go to 5 o r 7

Re ve rs ib le Ca us e s – Hypovolemia – Hypoxia – Hydrogen ion (acidos is ) – Hypo-/hyperkalemia – Hypothermia – Tens ion pneumothorax – Tamponade, cardiac – Toxins – Thrombos is , pulmonary – Thrombos is , coronary


Th e P EA P a t h w a y o f t h e Ca r d ia c Ar r e s t Alg o r it h m

In this cas e the patient is in cardiac arrest. Team members initiate and perform highquality CPR throughout the BLS Survey and the ACLS Survey. The team interrupts CPR for 10 s econds or les s for rhythm and puls e checks . This patient has an organized rhythm on the monitor but no pulse. The condition is PEA (Box 9). Ches t compres s ions res ume immediately. The team leader now directs the team in the s teps outlined in the PEA pathway of the Cardiac Arres t Algorithm (Figure 27), beginning with Box 10. IV/IO access is a priority over advanced airway management unless bag-mask ventilation is ineffective or the arrest is caused by hypoxia. All resuscitation team members must simultaneously conduct a search for an underlying and treatable cause of the PEA in addition to performing their assigned roles.

Rh yt h m Ch e c k : De c is io n P o in t

Conduct a rhythm check and give 2 minutes (about 5 cycles ) of CPR after adminis tration of the drugs . Be careful to minimize interruptions in ches t compres s ions . Th e p a u s e in CP R to c on d u c t a rh yth m c h e c k s h ou ld n ot e xc e e d 10 s e c on d s .

Ad m in is t e r Va s o p r e s s o r s (Bo x 1 0 )

• Give a vas opres s or as s oon as IV/IO acces s becomes available. – Epinephrine 1 mg IV/IO—repeat every 3 to 5 minutes or – Vas opres s in 40 units IV/IO to replace firs t or s econd dos e of epinephrine Ad m in is te r d ru g s d u rin g CP R. Do n ot s top CP R to a d m in is te r d ru g s . No known vas opres s or (epinephrine and vas opres s in) increas es s urvival from PEA. Becaus e thes e medications can improve aortic dias tolic blood pres s ure, coronary artery perfus ion pres s ure, and the rate of ROSC, the AHA continues to recommend their us e. • Cons ider advanced airway and capnography.

FYI 2 0 1 0 Gu id e lin e s No Atro p ine During Ca rd ia c Arre s t

• There is no evidence that atropine has detrimental effects during bradycardic or as ys tolic cardiac arres t. On the other hand, available evidence s ugges ts that routine us e of atropine during PEA or as ys tole is unlikely to have a therapeutic benefit. For this reas on, the AHA has removed atropine from the Cardiac Arres t Algorithm.

No n s h o c k a b le Rh yt h m (Bo x 1 2 )

• If no electrical activity is present (as ys tole), go back to Box 10. • If organized electrical activity is pres ent, try to palpate a puls e. Take at leas t 5 s econds but do not take more than 10 s econds to check for a puls e. • If no pulse is present, or if there is any doubt about the pres ence of a puls e, immediately res ume CPR for 2 minutes , s tarting with ches t compres s ions . Go back to Box 10 and repeat the s equence. • If a palpable puls e is pres ent and the rhythm is organized, begin pos t–cardiac arres t care.

De c is io n P o in t : S h o c k a b le Rh yt h m

• If the rhythm check reveals a s hockable rhythm, res ume CPR with ches t compres s ions while the defibrillator is charging if pos s ible. • Switch to the left s ide of the algorithm and perform s teps according to the VF/VT s equence s tarting with Box 5 or 7.

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P a r t

5

As ys t o le a n d P EA Tr e a t m e n t Se q u e n c e s

Figure 28 s ummarizes the recommended s equence of CPR, rhythm checks , and delivery of drugs for PEA and as ys tole bas ed on expert cons ens us .

Ad ult Ca rd ia c Arre s t Shout for He lp/Ac tiva te Em e rge nc y Re s pons e Sta rt CP R • Give oxygen • Attach monitor/de brillator Re turn o f Sp o nta ne o us Circ ula tio n (ROSC)

2 m inute s

P

If VF/VT Sh oc k

Drug The ra p y IV/IO acces s Epinephrine every 3-5 minutes Amiodarone for refractory VF/VT

n o

o

u

u

n

s

ti

ni

su

u

Co ns id e r Ad va nc e d Airwa y Quantitative waveform capnography

C

Mo

n it o r

CP R Q

R

o

P

C

tn

Tre a t Re ve rs ib le Ca us e s

Re turn o f Spo nta ne o us Circ ula tio n (ROSC) • P uls e and blood pres s ure • Abrupt s us tained increa s e in P e t c o 2 (typically ≥40 mm Hg) • S pontaneous arterial pres s ure waves with intra-arterial monitoring Sho c k Ene rg y • Bipha s ic : Manufacturer recommendation (eg, initial dos e of 120-200 J ); if unknown, us e maximum available. Second and s ubs equent dos es s hould be equivalent, and higher dos es may be cons idered. • Mo no p ha s ic : 360 J

o

C

P o s t–Ca rd ia c Arre s t Ca re

C

R

Che c k Rhythm

CP R Qua lity • P us h hard (≥2 inches [5 cm]) and fas t (≥100/min) and allow complete ches t recoil • Minimize interruptions in compres s ions • Avoid exces s ive ventilation • Rotate compres s or every 2 minutes • If no advanced airway, 30:2 compres s ion-ventilation ratio • Q uantitative waveform capnography – If P e t c o 2 <10 mm Hg, attempt to improve CPR quality • Intra-arterial pres s ure – If relaxation phas e (dias tolic) pres s ure <20 mm Hg, atte mpt to improve CPR quality

y t i l ua


Drug The ra p y • E p ine p hrine IV/IO Do s e : 1 mg every 3-5 minutes • Va s o p re s s in IV/IO Do s e : 40 units can replace firs t or s econd dos e of epinephrine • Amioda rone IV/IO Dos e : First dose: 300 mg bolus. Second dose: 150 mg. Ad va nc e d Airwa y • S upraglottic advanced airway or endotracheal intubation • Waveform capnography to confirm and monitor ET tube placement • 8 -10 breaths per minute with continuous ches t compres s ions Re ve rs ib le Ca us e s – Hypovolemia – Hypoxia – Hydrogen ion (acidos is ) – Hypo-/hyperkalemia – Hypothermia

– – – – –

Tens ion pneumothorax Tamponade, cardiac Toxins Thrombos is , pulmonary Thrombos is , coronary

Fig u re 2 8 . The Cardiac Arres t Circular Algorithm.

Ma n a g in g P EA: Dia g n o s in g a n d Tre a t in g Un d e r lyin g Ca u s e s In t r o d u c t io n

Patients with PEA have poor outcomes . Rapid as s es s ment and aggres s ive management offer the bes t chance of s ucces s . PEA may be caus ed by a revers ible problem. If you can quickly identify a s pecific condition that has caus ed or is contributing to PEA and correct it, you may achieve ROSC. The identification of the underlying caus e is of paramount importance in cas es of PEA and as ys tole. In the s earch for the underlying caus e, do the following: • Cons ider frequent caus es of PEA by recalling the H’s and T’s • Analyze the ECG for clues to the underlying caus e • Recognize hypovolemia • Recognize drug overdos e/pois onings

82


H’s a n d T’s

PEA is as s ociated with many conditions . Healthcare providers s hould memorize the lis t of common caus es to keep from overlooking an obvious caus e of PEA that might be revers ed by appropriate treatment. The mos t common caus es of PEA are pres ented as H’s and T’s in the table below:

H’s

Co n d it io n s a n d Ma n a g e m e n t

T’s

Hypovolemia

Tens ion pneumothorax

Hypoxia

Tamponade (cardiac)

Hydrogen ion (acidos is )

Toxins

Hyper-/hypokalemia

Thrombos is (pulmonary)

Hypothermia

Thrombos is (coronary)

The factors in the patient’s his tory and phys ical exam that may help identify revers ible caus es of PEA have been combined with potentially effective interventions in Table 3.

Ta b le 3 . P o te ntia lly Re ve rs ib le Ca us e s o f P EA a nd As ys to le (H’s a nd T’s )

Co n d it io n Hyp o vo le m ia

Clu e s Fro m ECG a n d Mo n it o r Narrow complex

Clu e s Fro m His t o r y a n d P h ys ic a l Exa m in a t io n

P o t e n t ia l Effe c t ive In t e r ve n t io n s

His tory, flat neck veins

Volume infus ion

Rapid rate Hyp o xia

Slow rate (hypoxia)

Cyanos is , blood gas es , airway problems

Oxygenation, ventilation, advanced airway

Hyd ro g e n io n (a c id o s is )

Smaller-amplitude QRS complexes

His tory of diabetes , bicarbonate-res pons ive preexis ting acidos is , renal failure

Ventilation, s odium bicarbonate

Hyp e rka le m ia

“High- potassium” ECG:

His tory of renal failure, diabetes , recent dialys is , dialys is fis tulas , medications

Hyperkalemia:

Abnormal los s of potas s ium, diuretic us e

Hypokalemia:

His tory of expos ure to cold, central body temperature

Rewarm according to local protocol

or

Hyp o ka le m ia

• T waves taller and peaked • P waves get s maller • QRS widens • Sine-wave PEA “Low-potassium” ECG: • T waves flatten • Prominent U waves • QRS widens • QT prolongs • Wide-complex tachycardia

Hyp o the rm ia

J or Os borne waves

• Calcium chloride • Sodium bicarbonate • Glucos e plus ins ulin • Pos s ibly albuterol

• Add magnes ium if cardiac arres t

(continued)

83

P a r t

5

(continued)

Co n d it io n Te ns io n p ne um o tho ra x

Clu e s Fro m ECG a n d Mo n it o r Narrow complex Slow rate (hypoxia)

Ta m p o na d e , c a rd ia c

Narrow complex Rapid rate

Clu e s Fro m His t o r y a n d P h ys ic a l Exa m in a t io n

P o t e n t ia l Effe c t ive In t e r ve n t io n s

His tory, no puls e felt with CPR, neck vein dis tention, tracheal deviation, unequal breath s ounds , difficult to ventilate patient

Needle decompres s ion

His tory, no puls e felt with CPR, vein dis tention

Pericardiocentes is

Tube thoracos tomy

To xins (d rug o ve rd o s e ): tric yc lic s , d ig o xin, ß-b lo c ke rs , c a lc ium c ha nne l b lo c ke rs

Various effects on ECG, predominately prolongation of QT interval

Bradycardia, empty bottles at the s cene, pupils , neurologic exam

Intubation, s pecific antidotes and agents per toxidrome

Thro m b o s is , lung s : m a s s ive p ulm o na ry e m b o lis m

Narrow complex

His tory, no puls e felt with CPR, dis tended neck veins , prior pos itive tes t for deep vein thrombos is or pulmonary embolis m

Surgical embolectomy, fibrinolytics

Thro m b o s is , he a rt: a c ute , m a s s ive MI

Abnormal 12-lead ECG:

An a lyz e ECG fo r Clu e s t o Un d e r lyin g Ca u s e

Rapid rate

• Q waves • ST-s egment changes • T waves , invers ions

His tory, cardiac markers , good puls e with CPR

The ECG may provide valuable clues to the pos s ible caus es of PEA. Many providers think that the term PEA refers to the broad, s lurred, s low, and dis organized electrical activity that bears no s imilarity to a normal P wave–QRS–T wave complex. The ECG, however, may dis play normal intervals or complexes or both. For example, s inus rhythm due to hypovolemia or s eps is may pres ent as PEA. Other ECG findings in PEA may include widecomplex QRS. Reas s es s the monitored rhythm and note the rate and width of the QRS complexes . PEA with narrow complexes is more likely to have a noncardiac caus e.

Hyp o vo le m ia

Hypovolemia, a common caus e of PEA, initially produces the clas s ic phys iologic res pons e of a rapid, narrow-complex tachycardia (sinus tachycardia) and typically produces increas ed dias tolic and decreas ed s ys tolic pres s ures . As los s of blood volume continues , blood pres s ure drops , eventually becoming undetectable, but the narrow QRS complexes and rapid rate continue (ie, PEA). You s hould cons ider hypovolemia as a caus e of hypotens ion, which can deteriorate to PEA. Providing prompt treatment can revers e the puls eles s s tate by rapidly correcting the hypovolemia. Common nontraumatic caus es of hypovolemia include occult internal hemorrhage and s evere dehydration. Cons ider volume infus ion for PEA as s ociated with a narrow-complex tachycardia.

84


Ca r d ia c a n d P u lm o n a r y Co n d it io n s

ACS involving a large amount of heart mus cle can pres ent as PEA. That is , occlus ion of the left main or proximal left anterior des cending coronary artery can pres ent with cardiogenic s hock rapidly progres s ing to cardiac arres t and PEA. However, in patients with cardiac arres t and without known pulmonary embolis m (PE), routine fibrinolytic treatment given during CPR s hows no benefit and is not recommended. Mas s ive or s addle PE obs tructs flow to the pulmonary vas culature and caus es acute right heart failure. In patients with cardiac arres t due to pres umed or known PE, it is reas onable to adminis ter fibrinolytics . Cardiac tamponade may be a revers ible condition. Volume infus ion in this condition may als o help while definitive therapy is initiated. Tens ion pneumothorax can be effectively treated once recognized. Note that cardiac tamponade, tens ion pneumothorax, and mas s ive PE cannot be treated unles s recognized. Beds ide ultras ound, when performed by a s killed provider, may aid in rapid identification of tamponade and PE. There is growing evidence that pneumothorax can be identified us ing beds ide ultras ound as well. Treatment for cardiac tamponade may require pericardiocentes is . Tens ion pneumothorax requires needle as piration and ches t tube placement. Thes e procedures are beyond the s cope of the ACLS Provider Cours e.

Dr u g Ove r d o s e s o r To xic Exp o s u r e s

Certain drug overdos es and toxic expos ures may lead to peripheral vas cular dilatation and/or myocardial dys function with res ultant hypotens ion. Thes e are another caus e of PEA. The approach to pois oned patients s hould be aggres s ive becaus e the toxic effects may progres s rapidly and may be of limited duration. In thes e s ituations myocardial dys function and arrhythmias may be revers ible. Numerous cas e reports confirm the s ucces s of many s pecific limited interventions with one thing in common—they buy time. Treatments that can provide this level of s upport include • Prolonged bas ic CPR in s pecial res us citation s ituations • Cardiopulmonary bypas s • Intra-aortic balloon pumping • Renal dialys is • Specific drug antidotes (digoxin immune Fab, glucagon, bicarbonate) • Trans cutaneous pacing (TCP) • Correction of s evere electrolyte dis turbances (potas s ium, magnes ium, calcium, acidos is ) • Specific adjunctive agents (eg, naloxone) Re m e m b e r, if the p a tie nt s ho ws s ig ns o f ROSC, p o s t–c a rd ia c a rre s t c a re s ho uld b e initia te d .

Cr it ic a l Co n c e p t s Co m m o n Re ve rs ib le Ca us e s o f P EA

• Hypovolemia and hypoxia are the 2 mos t common and eas ily revers ible caus es of PEA. Be s ure to look for evidence of thes e problems as you as s es s the patient.

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As ys t o le Ca s e In t r o d u c t io n

In this cas e the patient is in cardiac arrest. Team members initiate and perform highquality CPR throughout the BLS Survey and the ACLS Survey. The team interrupts CPR for 10 s econds or les s for a rhythm check. This patient has no pulse and the rhythm on the monitor is asystole. Ches t compres s ions res ume immediately. The team leader now directs the team in the s teps outlined in the as ys tole pathway of the Cardiac Arres t Algorithm (Figure 27, page 80), beginning with Box 10. IV/IO access is a priority over advanced airway management unless bag-mask ventilation is ineffective or the arrest is caused by hypoxia. All resuscitation team members must simultaneously conduct a search for an underlying and treatable cause of the asystole in addition to performing their assigned roles. At the end of this cas e the team will dis cus s the criteria for terminating res us citative efforts ; in s ome cas es we mus t recognize that the patient is dead and that it would be more appropriate to direct efforts to s upporting the family.


By the end of the cas e you s hould be able to 1. Dis cus s when res us citation s hould not be initiated, including do-not-attemptres us citation (DNAR) orders 2. Recall why s urvival from as ys tole is poor 3. Differentiate as ys tole and PEA: caus es , treatments , and early, diligent s earch for correctable caus es 4. Recall revers ible caus es of as ys tole 5. Outline treatments for caus es of as ys tole 6. Des cribe the Cardiac Arres t Algorithm for as ys tole 7. Des cribe correct dos ages and adminis tration of epinephrine and vas opres s in during cardiac arres t 8. As s ign team member roles : monitor performance

Rh yt h m s fo r As ys t o le

You will need to recognize the following rhythms : • As ys tole • Slow PEA terminating in bradyas ys tolic rhythm

Dr u g s fo r As ys t o le

This cas e involves thes e drugs : • Epinephrine • Vas opres s in

Ap p ro a c h t o As ys t o le In t r o d u c t io n

As ys tole is a cardiac arres t rhythm as s ociated with no dis cernible electrical activity on the ECG (als o referred to as flat line). You s hould confirm that the flat line on the monitor is indeed “true as ys tole” by validating that the flat line is • Not another rhythm (eg, fine VF) mas querading as a flat line • Not the res ult of an operator error

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Th e ACLS Ca s e s : As ys tole

Fo u n d a t io n a l Fa c t s As ys to le a nd Te c hnic a l P ro b le m s

As ys tole is a s pecific diagnos is , but flat line is not. The term flat line is nons pecific and can res ult from s everal pos s ible conditions , including abs ence of cardiac electrical activity, lead or other equipment failure, and operator error. Some defibrillators and monitors s ignal the operator when a lead or other equipment failure occurs . Some of thes e problems are not applicable to all defibrillators . For a patient with cardiac arres t and as ys tole, quickly rule out any other caus es of an is oelectric ECG, s uch as • Loos e leads or leads not connected to the patient or defibrillator/monitor • No power • Signal gain (amplitude/s ignal s trength) too low

P a t ie n t s Wit h DNAR Or d e r s

During the BLS Survey and ACLS Survey, you s hould be aware of reas ons to s top or withhold res us citative efforts . Some of thes e are • Rigor mortis • Indicators of DNAR s tatus (eg, bracelet, anklet, written documentation) • Threat to s afety of providers Out-of-hos pital providers need to be aware of EMS-s pecific policies and protocols applicable to thes e s ituations . In-hos pital providers and res us citation teams s hould be aware of advance directives or s pecific limits to res us citation attempts that are in place. That is , s ome patients may cons ent to CPR and defibrillation but not to intubation or invas ive procedures . Many hos pitals will record this in the medical record.

As ys t o le a s a n En d P o in t

The prognos is for cardiac arres t with as ys tole is very poor. A large percentage of as ys tolic patients do not s urvive. Often as ys tole repres ents the final rhythm. Cardiac function has diminis hed until electrical and functional cardiac activity finally s top and the patient dies . As ys tole is als o the final rhythm of a patient initially in VF or VT. Prolonged efforts are unneces s ary and futile unles s s pecial res us citation s ituations exis t, s uch as hypothermia and drug overdos e.

Ma n a g in g As ys t o le Ove r vie w

The management of as ys tole cons is ts of the following components : • Implementing the s teps in the Cardiac Arres t Algorithm • Identifying and correcting underlying caus es • Terminating efforts as appropriate

Ca r d ia c Ar r e s t Alg o r it h m

As des cribed in the VF/Puls eles s VT and PEA Cas es , the Cardiac Arres t Algorithm cons is ts of 2 pathways (Figure 27). The left s ide of the algorithm outlines treatment for a s hockable rhythm (VF/puls eles s VT). The right s ide of the algorithm (Boxes 9 through 11) outlines treatment for a nons hockable rhythm (as ys tole/PEA). In both pathways therapies are des igned around periods (2 minutes or 5 cycles ) of uninterrupted, high-quality CPR. In this cas e we will focus on the as ys tole component of the as ys tole/PEA pathway.

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Id e n t ific a t io n a n d Co r r e c t io n o f Un d e r lyin g Ca u s e

Treatment of as ys tole is not limited to the interventions outlined in the algorithm. Healthcare providers s hould attempt to identify and correct an underlying caus e if pres ent. Res cuers mus t s top, think, and as k “Why did this pers on have this cardiac arres t at this time? ” It is es s ential to s earch for and treat revers ible caus es of as ys tole for res us citative efforts to be potentially s ucces s ful. Us e the H’s and T’s to recall conditions that could have contributed to as ys tole. See column on the right of the algorithm and the PEA cas e for more information on the H’s and T’s , including clinical clues and s ugges ted treatments .

Ap p lic a t io n o f t h e Ca rd ia c Ar re s t Alg o r it h m : As ys t o le P a t h w a y In t r o d u c t io n

In this cas e you have a patient in cardiac arres t. High-quality CPR is performed throughout the BLS Survey and the ACLS Survey. Interrupt CPR for 10 s econds or les s while you perform a rhythm check. You interpret the rhythm on the monitor as as ys tole. CPR beginning with ches t compres s ions for 2 minutes res umes immediately. You now conduct the s teps outlined in the as ys tole pathway of the Cardiac Arres t Algorithm beginning with Box 9. At the s ame time you are s earching for a pos s ible underlying caus e of the as ys tole.

Co n fir m e d As ys t o le

Give priority to IV/IO acces s . Do not routinely ins ert an advanced airway unles s ventilations with a bag-mas k are ineffective. Do not interrupt CPR while es tablis hing IV or IO acces s .

Ad m in is t e r Va s o p r e s s o r s (Bo x 1 0 )

• Continue high-quality CPR, and as s oon as IV/IO acces s is available, give a vas opres s or as follows : – Ep ine p hrine 1 mg IV/IO—repeat every 3 to 5 minutes or – Va s o p re s s in 40 units IV/IO to replace firs t or s econd dos e of epinephrine Ad m in is te r d ru g s d u rin g CP R. Do n ot s top CP R to a d m in is te r d ru g s . You can s ubs titute vas opres s in for either the firs t or s econd dos e of epinephrine. • Cons ider advanced airway and capnography.

FYI 2 0 1 0 Gu id e lin e s No Atro p ine During As ys to le

De c is io n P o in t : Rh yt h m Ch e c k

• Although there is no evidence that atropine has detrimental effects during bradycardic or as ys tolic cardiac arres t, routine us e of atropine during PEA or as ys tole is unlikely to have a therapeutic benefit. The AHA removed atropine from the Cardiac Arres t Algorithm.

Check the rhythm after 2 minutes (about 5 cycles ) of CPR. In te rru p tion of c h e s t c om p re s s ion s to c on d u c t a rh yth m c h e c k s h ou ld n ot e xc e e d 10 s e c on d s .

No n s h o c k a b le Rh yt h m

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• If no electrical activity is present (as ys tole), go back to Box 10 or 11. • If electrical activity is pres ent, try to palpate a puls e. • If no pulse is present or if there is any doubt about the pres ence of a puls e, continue CPR, s tarting with ches t compres s ions for 2 minutes . Go back to Box 10 and repeat the s equence. • If a good pulse is present and the rhythm is organized, begin pos t–cardiac arres t care.

Th e ACLS Ca s e s : As ys tole

S h o c k a b le Rh yt h m

If the rhythm check reveals a s hockable rhythm, prepare to deliver a s hock (res uming ches t compres s ions during charging if appropriate). Refer to the left s ide of the algorithm and perform s teps according to the VF/VT s equence, s tarting with Box 5 or 7.

As ys t o le a n d P EA Tr e a t m e n t S e q u e n c e s

The diagram in Figure 28 (in the previous cas e, PEA) s ummarizes the recommended s equence of CPR, rhythm checks , and delivery of drugs for PEA and as ys tole bas ed on expert cons ens us .

TCP No t Re c o m m e n d e d

Several randomized controlled trials failed to s how benefit from attempted TCP for as ys tole. At this time the AHA does not recommend the us e of TCP for patients with as ys tolic cardiac arres t.

Ro u t in e S h o c k Ad m in is t r a t io n No t Re c o m m e n d e d

There is no evidence that attempting to “defibrillate” as ys tole is beneficial. In one s tudy the group that received s hocks had a trend toward wors e outcome. Given the importance of minimizing interruption of ches t compres s ions , there is no jus tification for interrupting ches t compres s ions to deliver a s hock to patients with as ys tole.

Wh e n in Do u b t

If it is unclear whether the rhythm is fine VF or as ys tole, an initial attempt at defibrillation may be warranted. Fine VF may be the res ult of a prolonged arres t. At this time the benefit of delaying defibrillation to perform CPR before defibrillation is unclear. EMS s ys tem medical directors may cons ider implementing a protocol that allows EMS res ponders to provide CPR while preparing for defibrillation of patients found by EMS pers onnel to be in VF.

Te r m in a t in g Re s u s c it a t ive Effo r t s Te r m in a t in g In -Ho s p it a l Re s u s c it a t ive Effo r t s

If res cuers cannot rapidly identify a revers ible caus e and the patient fails to res pond to the BLS and ACLS Surveys and s ubs equent interventions , termination of all res us citative efforts s hould be cons idered. The decis ion to terminate res us citative efforts res ts with the treating phys ician in the hos pital and is bas ed on cons ideration of many factors , including • Time from collaps e to CPR • Time from collaps e to firs t defibrillation attempt • Comorbid dis eas e • Prearres t s tate • Initial arres t rhythm • Res pons e to res us citative meas ures None of thes e factors alone or in combination is clearly predictive of outcome. However, the duration of res us citative efforts is an important factor as s ociated with poor outcome. The chance that the patient will s urvive to hos pital dis charge and be neurologically intact diminis hes as res us citation time increas es . Stop the res us citation attempt when you determine with a high degree of certainty that the patient will not res pond to further ACLS.

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Te r m in a t in g Ou t -o f-Ho s p it a l Re s u s c it a t ive Effo r t s

Continue out-of-hos pital res us citative efforts until one of the following occurs :

Du r a t io n o f Re s u s c it a t ive Effo r t s

Available s cientific s tudies demons trate that in the abs ence of mitigating factors , prolonged res us citative efforts are unlikely to be s ucces s ful. The final decis ion to s top res us citative efforts can never be as s imple as an is olated time interval. If ROSC of any duration occurs , it may be appropriate to cons ider extending the res us citative effort.

• Res toration of effective, s pontaneous circulation and ventilation • Trans fer of care to a s enior emergency medical profes s ional • The pres ence of reliable criteria indicating irrevers ible death • The healthcare provider is unable to continue becaus e of exhaus tion or dangerous environmental hazards or becaus e continued res us citation places the lives of others in jeopardy • A valid DNAR order is pres ented • Online authorization from the medical control phys ician or by prior medical protocol for termination of res us citation

Experts have developed clinical rules to as s is t in decis ions to terminate res us citative efforts for in-hos pital and out-of-hos pital arres ts . You s hould familiarize yours elf with the es tablis hed policy or protocols for your hos pital or EMS s ys tem. It may als o be appropriate to cons ider other is s ues , s uch as drug overdos e and s evere prearres t hypothermia (eg, s ubmers ion in icy water) when deciding whether to extend res us citative efforts . Special res us citation interventions and prolonged res us citative efforts may be indicated for patients with hypothermia, drug overdos e, or other potentially revers ible caus es of arres t.

As ys t o le : An Ag o n a l Rh yt h m Co n fir m in g De a t h

You will s ee as ys tole mos t frequently in 2 s ituations :

Et h ic a l Co n s id e r a t io n s

The res us citation team mus t make a cons cientious and competent effort to give patients “a trial of CPR and ACLS,” provided the patient had not expres s ed a decis ion to forego res us citative efforts and the victim is not obvious ly dead (eg, rigor mortis , decompos ition, hemis ection, decapitation) (s ee the DNAR dis cus s ion on the Student Webs ite). The final decis ion to s top res us citative efforts can never be as s imple as an is olated time interval.

• As a terminal rhythm in a res us citation attempt that s tarted with another rhythm • As the firs t rhythm identified in a patient with unwitnes s ed or prolonged arres t In either of thes e s cenarios , as ys tole mos t often repres ents an agonal rhythm confirming death rather than a rhythm to be treated or a patient who can be res us citated if the attempt pers is ts long enough. Pers is tent as ys tole repres ents extens ive myocardial is chemia and damage from prolonged periods of inadequate coronary perfus ion. Prognos is is very poor unles s a s pecial res us citation circums tance or immediately revers ible caus e is pres ent. Survival from as ys tole is better for in-hos pital than for out-of-hos pital arres ts according to data from Get With The Guidelines ®–Res us citation, formerly the National Regis try of CPR (www.he a rt.o rg /re s us c ita tio n).

See Human, Ethical, and Legal Dimens ions of CPR on the Student Webs ite (www.he a rt.o rg /e c c s tud e nt).

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Th e ACLS Ca s e s : Ac u te Coron a ry Syn d rom e s

Tr a n s p o r t o f P a t ie n t s in Ca r d ia c Ar r e s t

Emergency medical res pons e s ys tems s hould not require field pers onnel to trans port every patient in cardiac arres t back to a hos pital or to an ED. Trans portation with continuing CPR is jus tified if interventions available in the ED cannot be performed in the outof-hos pital s etting and they are indicated for s pecial circums tances (ie, cardiopulmonary bypas s or extracorporeal circulation for patients with s evere hypothermia). After out-of-hos pital cardiac arres t with ROSC, trans port the patient to an appropriate hos pital with a comprehens ive pos t–cardiac arres t treatment s ys tem of care that includes acute coronary interventions , neurologic care, goal-directed critical care, and hypothermia. Trans port the in-hos pital pos t–cardiac arres t patient to an appropriate critical care unit capable of providing comprehens ive pos t–cardiac arres t care.

Ac u t e Co ro n a r y S yn d ro m e s Ca s e In t r o d u c t io n

The ACLS provider mus t have the bas ic knowledge to as s es s and s tabilize patients with ACS. Patients in this case have signs and symptoms of ACS, including possible AMI. You will us e the ACS Algorithm as the guide to clinical s trategy. The initial 12-lead ECG is us ed in all ACS cas es to clas s ify patients into 1 of 3 ECG categories , each with different s trategies of care and management needs . Thes e 3 ECG categories are ST-s egment elevation s ugges ting current injury, ST-s egment depres s ion s ugges ting is chemia, and nondiagnos tic or normal ECG. Thes e are outlined in the ACS Algorithm, but STEMI with time-s ens itive reperfus ion s trategies is the focus of this cours e (Figure 30). Key components of this cas e are • Identification, as s es s ment, and triage of acute is chemic ches t dis comfort • Initial treatment of pos s ible ACS • Emphas is on early reperfus ion of the patient with ACS/STEMI


By the end of this cas e you s hould be able to 1. Dis cus s the differential diagnos is of life-threatening ches t dis comfort 2. Apply the ACS Algorithm for initial us e of drugs 3. Apply the ACS Algorithm for initial drug dos es 4. Apply the ACS Algorithm for initial res us citation s trategies and triage patients with s udden cardiac death to PCI facilities 5. Explain early identification of patients with ACS 6. Explain ris k s tratification of patients with ACS 7. Explain initial treatment of patients with ACS 8. Explain actions , indications , precautions , contraindications , dos age, and adminis tration for oxygen, as pirin, nitroglycerin, morphine, and heparin (low-molecular-weight heparin [LMWH] or unfractionated heparin [UFH]) 9. Des cribe guidelines for reperfus ion s trategies

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Rh yt h m s fo r ACS

Sudden cardiac death due to VF and hypotens ive bradyarrythmias occurs with acute is chemia. Providers will unders tand to anticipate thes e rhythms and be prepared for immediate attempts at defibrillation and adminis tration of drug or electrical therapy for s ymptomatic bradyarrhythmias . Although 12-lead ECG interpretation is beyond the s cope of the ACLS Provider Cours e, s ome ACLS providers will have 12-lead ECG reading s kills . For them, this cas e s ummarizes the identification and management of patients with STEMI.

Dr u g s fo r ACS

Drug therapy and treatment s trategies continue to evolve rapidly in the field of ACS. ACLS providers and ins tructors will need to monitor important changes . The ACLS Provider Cours e pres ents only bas ic knowledge focus ing on early treatment and the priority of rapid reperfus ion, relief of is chemic pain, and treatment of early life-threatening complications . Reperfus ion may involve the us e of fibrinolytic therapy or coronary angiography with PCI (ie, balloon angioplas ty/s tenting). When us ed as the initial reperfus ion s trategy for STEMI, PCI is called primary percutaneous coronary intervention or PPCI. Treatment of ACS involves the initial us e of drugs to relieve is chemic dis comfort, dis s olve clots , and inhibit thrombin and platelets . Thes e drugs are • Oxygen • As pirin • Nitroglycerin • Morphine • Fibrinolytic therapy (overview) • Heparin (UFH, LWMH) Additional agents that are adjunctive to initial therapy and will not be dis cus s ed in the ACLS Provider Cours e are • ß-Blockers • Adenos ine diphos phate (ADP) antagonis ts (clopidogrel, pras ugrel) • Angiotens in-converting enzyme (ACE) inhibitors • HMG-CoA reductas e inhibitor (s tatin therapy)

Go a ls fo r ACS P a t ie n t s Fo u n d a t io n a l Fa c t s Out-o f-Ho s p ita l Ca rd ia c Arre s t Re s p o ns e

Half of the patients who die of ACS do s o before reaching the hos pital. VF or puls eles s VT is the precipitating rhythm in mos t of thes e deaths . VF is mos t likely to develop during the firs t 4 hours after ons et of s ymptoms . Communities s hould develop programs to res pond to out-of-hos pital cardiac arres t. Such programs s hould focus on • Recognizing s ymptoms of ACS • Activating the EMS s ys tem, with EMS advance notification of the receiving hos pital • Providing early CPR • Providing early defibrillation with AEDs available through public acces s defibrillation programs and firs t res ponders • Providing a coordinated s ys tem of care among the EMS s ys tem, the ED, and Cardiology

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FYI 2 0 1 0 Gu id e lin e s Go a ls o f The ra p y fo r ACS

The 2010 AHA Gu id e lin e s for CP R a n d ECC c o m b ine d the p rim a ry a nd s e c o nd a ry g o a ls a nd c o ns id e re d a ll g o a ls “p rim a ry g o a ls .” The primary goals are • Identification of patients with STEMI and triage for early reperfus ion therapy • Relief of is chemic ches t dis comfort • Prevention of MACE, s uch as death, nonfatal MI, and the need for urgent pos tinfarction revas cularization • Treatment of acute, life-threatening complications of ACS, s uch as VF/puls eles s VT, s ymptomatic bradycardias , and uns table tachycardias Reperfus ion therapy opens an occluded coronary artery with either drugs or mechanical means . “Clot bus ter” drugs are called fibrinolytics, a more accurate term than thrombolytics. PCI, performed in the heart catheterization s uite following coronary angiography, allows balloon dilation and/or s tent placement for an occluded coronary artery. PCI performed as the initial reperfus ion method is called primary PCI.

P a t h o p h ys io lo g y o f ACS

Patients with coronary atheros cleros is may develop a s pectrum of clinical s yndromes repres enting varying degrees of coronary artery occlus ion. Thes s yndromes include Ae Uns tab le plaq ue uns table Ea rly(UA), p la q NSTEMI, ue fo rm aand tio nSTEMI. Sudden cardiac death may occur with each of thes e angina B Plaq ue rupture s yndromes . Figure 29 illus trates the pathophys iology of ACS. C Uns table angina A AUnsUns tabletab plaque le plaq ue D Microemboli Ea rly p la q ue fo rm a tio n B Plaque rupture Plaq ueive rupture EUnsOccus thrombus CB table angina D CMicroemboli Uns table angina Sig ni c a nt p la q ue fo rm a tio n E Occlus ive thrombus A D Microemboli E Occus ive thrombus

Sig ni c a nt p la q ue fo rm a tio n A

B

P la q ue rup ture /thro m b us

C D

B

P la q ue rup ture /thro m b us

STEMI

E

STEMI

E

C

Uns ta b le a ng ina / D NSTEMI

Uns ta b le a ng ina / NSTEMI Re s o lutio n /s ta b le a ng ina

Re s o lutio n /s ta b le a ng ina Fig u re 2 9 . Pathophys iology of ACS.

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Ac ute Co ro na ry Synd ro m e s 1 Sym p to m s s ug g e s tive o f is c he m ia o r infa rc tio n 2 EMS a s s e s s m e nt a nd c a re a n d h o s p ita l p re p a ra tio n : • Monitor, s upport ABCs . Be prepare d to provide CPR and defibrilla tion • Adminis ter a s pirin and cons id er oxyge n, nitroglyc erin, and morphine if nee ded • O btain 12-lea d ECG; if ST elevation: – Notify re ceiving hos p ital with trans mis s ion or interpretation; note time of ons et and firs t med ica l conta ct • Notified hos pital s hould mobilize hos pital res ources to res pond to STEMI • If cons idering prehos pital fibrinolys is , us e fibrinolytic checklis t

3 Co nc urre nt ED a s s e s s m e nt (<10 m inute s ) • C heck vital s igns ; evaluate oxygen s a turation • Es ta blis h IV acce s s • P erform brie f, targeted his tory, phys ic al exa m • Review/c omp lete fibrinolytic chec klis t; che ck contra indications • O btain initial c ardia c marker levels , initial e lectrolyte and coagulation s tudie s • O bta in portable ches t x-ra y (<30 minute s )

Im m e d ia te ED g e ne ra l tre a tm e nt • If O 2 s a t <94% , s tart o xyg e n at 4 L/min, titrate • As p irin 160 to 325 mg (if not give n b y EMS) • Nitro g lyc e rin s ublingua l or s pray • Mo rp hine IV if dis c omfort not relieved by nitroglycerin

4 ECG inte rp re ta tio n

5

9

13

ST d e p re s s io n o r d yna m ic T-wa ve inve rs io n; s tro ng ly s us p ic io us fo r is c he m ia Hig h-ris k uns ta b le a ng ina / n o n–ST-e le va tio n MI (UA/NSTEMI)

No rm a l o r no nd ia g no s tic c ha ng e s in ST s e g m e nt o r T wa ve Lo w-/inte rm e d ia te -ris k ACS

ST e le va tio n o r ne w o r p re s um a b ly ne w LBBB; s tro ng ly s us p ic io us fo r injury ST-e le va tio n MI (STEMI)

14

6

7 Tim e fro m o ns e t of s ym p tom s ≤12 ho urs ?

Co ns id e r a d m is s io n to ED c he s t p a in unit o r to a p p ro p ria te b e d a nd fo llo w: • S e ria l cardiac markers (including trop onin) • Rep eat ECG/continuous ST-s egment monitoring • C ons ider noninvas ive diagnos tic te s t

10

• S ta rt a d ju nc tive the ra p ie s a s indica te d • Do no t d e la y re p e rfus io n >1 2 hours

Tro p o n in e le va te d o r h ig h -ris k p a tie nt Cons ider e arly inva s ive s trategy if: • Re frac tory is c hemic c hes t d is comfort • Re curre nt/pe rs is tent ST devia tion • Ventricula r tachycard ia • Hemod yna mic ins tab ility • Signs of heart failure

11 ≤1 2 h ou rs

8 Re p e rfus io n g o a ls : Therap y de fined b y p atient and center c rite ria • Do o r-to –b a llo o n infla tio n (P CI) g o a l o f 90 m inute s • Do o r-to -n e e d le (fib rin o lys is ) g o a l o f 30 m inute s

Sta rt a d junc tive tre a tm e nts a s ind ic a te d • Nitroglycerin • Heparin (UFH or LMWH) • Cons ider: PO ß-blockers • Cons ider: Clopidogrel • Cons ider: Glycoprotein IIb/IIIa inhibitor

Ye s

12

De ve lo p s 1 o r m o re : • Clinic a l high-ris k fe a ture s • Dyna m ic ECG c ha ng e s c o ns is te nt with is c he m ia • Tro po nin e le va te d

16

Ad m it to m o nito re d b e d As s e s s ris k s ta tus Co ntinue ASA, he p a rin, a nd o the r the ra p ie s a s ind ic a te d • ACE inhibitor/ARB • HMG CoA reduc ta s e inhibitor (s tatin therap y) Not a t high ris k: ca rdiology to ris k s tratify


Fig u re 3 0 . The Acute Coronary Syndromes Algorithm.

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15

No Abno rm a l d ia g nos tic no ninva s ive im a g ing o r p hys io lo g ic te s ting ?

Ye s

17

No

If no e vid e nc e o f is c he m ia o r infa rc tio n b y te s ting , c a n d is c ha rg e with fo llo w-up


Ma n a g in g ACS : Th e Ac u t e Co ro n a r y S yn d ro m e s Alg o r it h m Ove r vie w o f t h e Alg o r it h m

The Acute Coronary Syndromes Algorithm (Figure 30) outlines the as s es s ment and management s teps for a patient pres enting with s ymptoms s ugges tive of ACS. The EMS res ponder in the out-of-hos pital environment can begin immediate as s es s ments and actions . Thes e include giving oxygen, as pirin, nitroglycerin, and morphine if needed, and obtaining an initial 12-lead ECG (Box 2). Bas ed on the ECG findings , the EMS provider may complete a fibrinolytic therapy checklis t and notify the receiving ED of a potential AMI-STEMI when appropriate (Box 3). If out-of-hos pital providers are unable to complete thes e initial s teps before the patient’s arrival at the hos pital, the ED provider s hould implement this component of care. Subs equent treatment occurs on the patient’s arrival at the hos pital. ED pers onnel s hould review the out-of-hos pital 12-lead ECG if available. If not performed, acquis ition of the 12-lead ECG s hould be a priority. The goal is to analyze the 12-lead ECG within 10 minutes of the patient’s arrival in the ED (Box 4). Hos pital pers onnel s hould categorize patients into 1 of 3 groups according to analys is of the ST s egment or the pres ence of left bundle branch block (LBBB) on the 12-lead ECG. Treatment recommendations are s pecific to each group. • STEMI • High-ris k UA/non–ST-elevation MI (NSTEMI) • Intermediate/low-ris k UA The ACS Cas e will focus on the early reperfus ion of the STEMI patient, emphas izing initial care and rapid triage for reperfus ion therapy.

Im p o r t a n t Co n s id e r a t io n s

The ACS Algorithm (Figure 30) provides general guidelines that apply to the initial triage of patients bas ed on s ymptoms and the 12-lead ECG. Healthcare pers onnel often obtain s erial cardiac markers (CK-MB, cardiac troponins ) in mos t patients that allow additional ris k s tratification and treatment recommendations . Two important points for STEMI need emphas is : • The ECG is central to the initial ris k and treatment s tratification proces s . • Healthcare pers onnel do not need evidence of elevated cardiac markers to make a decis ion to adminis ter fibrinolytic therapy or perform diagnos tic coronary angiography with coronary intervention (angioplas ty/s tenting) in STEMI patients .

Ap p lic a t io n o f t h e ACS Alg o r it h m

FYI 2 0 1 0 Gu id e lin e s ACS Alg o rithm

The boxes in the algorithm guide as s es s ment and treatment: • Identification of ches t dis comfort s ugges tive of is chemia (Box 1) • EMS as s es s ment, care, trans port, and hos pital prearrival notification (Box 2) • Immediate ED as s es s ment and treatment (Box 3) • Clas s ification of patients according to ST-s egment analys is (Boxes 5, 9, and 13) • STEMI (Boxes 5 through 8)

• The AHA introduced changes to the ACS Algorithm to ens ure prompt diagnos is and treatment. This offers the greates t potential benefit for myocardial s alvage in the firs t hours of STEMI, and provides early and focus ed management of UA and NSTEMI. Thes e changes s hould reduce advers e events and improve outcome.

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Id e n t if c a t io n o Ch e s t Dis c o m o r t S u g g e s t ive o Is c h e m ia (Bo x 1 ) S ig n s a n d Co n d it io n s

You s hould know how to identify ches t dis comfort s ugges tive of is chemia. Conduct a prompt and targeted evaluation of every patient whos e initial complaints s ugges t pos s ible ACS. The mos t common s ymptom of myocardial is chemia and infarction is retros ternal ches t dis comfort. The patient may perceive this dis comfort more as pres s ure or tightnes s than actual pain. Symptoms s ugges tive of ACS may als o include • Uncomfortable pres s ure, fullnes s , s queezing, or pain in the center of the ches t las ting s everal minutes (us ually more than a few minutes ) • Ches t dis comfort s preading to the s houlders , neck, one or both arms , or jaw • Ches t dis comfort s preading into the back or between the s houlder blades • Ches t dis comfort with light-headednes s , dizzines s , fainting, s weating, naus ea, or vomiting • Unexplained, s udden s hortnes s of breath, which may occur with or without ches t dis comfort Cons ider the likelihood that the pres enting condition is ACS or one of its potentially lethal mimics . Other life-threatening conditions that may caus e acute ches t dis comfort are aortic dis s ection, acute PE, acute pericardial effus ion with tamponade, and tens ion pneumothorax.

Fig u re 3 1 . The STEMI Chain of Survival.

S t a r t in g Wit h Dis p a t c h

All dis patchers and EMS providers mus t receive training in ACS s ymptom recognition along with the potential complications . Dis patchers , when authorized by medical control or protocol, s hould tell patients with no his tory of as pirin allergy or s igns of active or recent gas trointes tinal (GI) bleeding to chew an as pirin (160 to 325 mg) while waiting for EMS providers to arrive.

EMS As s e s s m e n t , Ca re , a n d Ho s p it a l P re p a r a t io n (Bo x 2 ) In t r o d u c t io n

EMS as s es s ment, care, and hos pital preparation are outlined in Box 2. EMS res ponders may perform the following as s es s ments and actions during the s tabilization, triage, and trans port of the patient to an appropriate facility: • Monitor and s upport ABCs • Adminis ter as pirin and cons ider oxygen if O 2 s aturation <94% , nitroglycerin, and morphine if dis comfort unres pons ive to nitrates • Obtain a 12-lead ECG; interpret or trans mit for interpretation • Complete a fibrinolytic checklis t if indicated • Provide prearrival notification to the receiving facility if ST elevation

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Mo n it o r a n d S u p p o r t ABCs

Monitoring and s upport of ABCs includes

Ad m in is t e r Oxyg e n a n d Dr u g s

Providers s hould be familiar with the actions , indications , cautions , and treatment of s ide effects .

• Monitoring vital s igns and cardiac rhythm • Being prepared to provide CPR • Us ing a defibrillator if needed

Oxyg e n EMS providers s hould adminis ter oxyg e n if the patient is dys pneic, is hypoxemic, has obvious s igns of heart failure, has an arterial oxygen s aturation <94% or the oxygen s aturation is unknown. Providers s hould titrate oxygen therapy to a noninvas ively monitored oxyhemoglobin s aturation ≥94% . There is ins ufficient evidence to s upport the routine us e of oxygen in uncomplicated ACS without s igns of hypoxemia or heart failure or both.

As p irin (Ac e tyls a lic ylic Ac id ) If the patient has not taken a s p irin and has no his tory of true as pirin allergy and no evidence of recent GI bleeding, give the patient as pirin (160 to 325 mg) to chew. In the initial hours of an ACS, as pirin is abs orbed better when chewed than when s wallowed, particularly if morphine has been given. Us e rectal as pirin s uppos itories (300 mg) for patients with naus ea, vomiting, active peptic ulcer dis eas e, or other dis orders of the upper GI tract.

Nitrog lyc e rin (Glyc e ryl Trin itra te ) Give the patient 1 s ublingual n itrog lyc e rin tablet (or s pray “dos e”) every 3 to 5 minutes for ongoing s ymptoms if it is permitted by medical control and no contraindications exis t. Healthcare providers may repeat the dos e twice (total of 3 dos es ). Adminis ter nitroglycerin only if the patient remains hemodynamically s table: SBP is >90 mm Hg or no lower than 30 mm Hg below bas eline (if known) and the heart rate is 50 to 100/min. Nitroglycerin is a venodilator and needs to be us ed cautious ly or not at all in patients with inadequate ventricular preload. Thes e s ituations include • Infe rio r wa ll MI a nd rig ht ve ntric ula r (RV) infa rc tio n. RV infarction may complicate an inferior wall MI. Patients with acute RV infarction are very dependent on RV filling pres s ures to maintain cardiac output and blood pres s ure. If RV infarction cannot be confirmed providers mus t us e caution in adminis tering nitrates to patients with inferior STEMI. If RV infarction is confirmed by right-s ided precordial leads or clinical findings by an experienced provider, nitroglycerin and other vas odilators (morphine) or volumedepleting drugs (diuretics ) are contraindicated as well. • Hyp o te ns io n, b ra d yc a rd ia , o r ta c hyc a rd ia . Avoid us e of nitroglycerin in patients with hypotens ion (SBP <90 mm Hg), marked bradycardia (<50/min), or tachycardia. • Re c e nt p ho s p ho d ie s te ra s e inhib ito r us e . Avoid the us e of nitroglycerin if it is s us pected or known that the patient has taken s ildenafil or vardenafil within the previous 24 hours or tadalafil within 48 hours . Nitrates may caus e s evere hypotens ion refractory to vas opres s or agents .

Morp h in e Give m orp h in e for ches t dis comfort unres pons ive to s ublingual or s pray nitroglycerin if authorized by protocol or medical control. Morphine is indicated in STEMI when ches t dis comfort is unres pons ive to nitrates . Us e morphine with caution in UA/NSTEMI becaus e of an as s ociation with increas ed mortality.

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5 Morphine is an important treatment for ACS becaus e it • Produces central nervous s ys tem analges ia, which reduces the advers e effects of neurohumoral activation, catecholamine releas e, and heightened myocardial oxygen demand • Produces venodilation, which reduces left ventricular (LV) preload and oxygen requirements • Decreas es s ys temic vas cular res is tance, thereby reducing LV afterload • Helps redis tribute blood volume in patients with acute pulmonary edema Remember, morphine is a venodilator. Like nitroglycerin, us e morphine with caution in patients who may be preload dependent. If hypotens ion develops , adminis ter fluids as a firs t line of therapy.

Cr it ic a l Co n c e p t s P a in Re lie f With Nitro g lyc e rin

Ca u t io n Us e o f No ns te ro id a l Anti-infla m m a to ry Drug s

Ob t a in a 1 2 -Le a d ECG

• Relief of pain with nitroglycerin is neither s pecific nor a us eful diagnos tic tool to determine the etiology of s ymptoms in ED patients with ches t pain or dis comfort. GI etiologies as well as other caus es of ches t dis comfort can “res pond” to nitroglycerin adminis tration. Therefore, the res pons e to nitrate therapy is not diagnos tic of ACS.

• Us e of nons teroidal anti-inflammatory drugs (NSAIDs ) is contraindicated (except for as pirin) and s hould be dis continued. Both nons elective as well as COX-2 s elective drugs s hould not be adminis tered during hos pitalization for STEMI becaus e of the increas ed ris k of mortality, reinfarction, hypertens ion, heart failure, and myocardial rupture as s ociated with their us e.

EMS providers s hould obtain a 12-lead ECG. The 2010 AHA Guidelines for CPR and ECC recommends out-of-hos pital 12-lead ECG diagnos tic programs in urban and s uburban EMS s ys tems .

EMS Ac t io n

Re c o m m e n d a t io n

12-Le a d ECG if a va ila b le

The AHA recommends routine us e of 12-lead out-of-hos pital ECGs for patients with s igns and s ymptoms of pos s ible ACS.

P re a rriva l ho s p ita l no tific a tio n fo r STEMI

Prearrival notification of the ED s hortens the time to treatment (10 to 60 minutes has been achieved in clinical s tudies ) and s peeds reperfus ion therapy with fibrinolytics or PCI or both, which may reduce mortality and minimize myocardial injury.

Fib rino lytic c he c klis t if a p p ro p ria te

If STEMI is identified on the 12-lead ECG, complete a fibrinolytic checklis t if appropriate.

See the Student Webs ite (www.he a rt.o rg /e c c s tud e nt) for a s ample fibrinolytic checklis t.

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Im m e d ia t e ED As s e s s m e n t a n d Tre a t m e n t (Bo x 3 ) In t r o d u c t io n

The healthcare team s hould quickly evaluate the patient with potential ACS on the patient’s arrival in the ED. Within the firs t 10 minutes , obtain a 12-lead ECG (if not already performed before arrival) and as s es s the patient. Th e 12-le a d ECG is a t th e c e n te r of th e d e c is ion p a th wa y in th e m a n a g e m e n t of is c h e m ic c h e s t d is c om fort a n d is th e on ly m e a n s of id e n tifyin g STEMI. A targeted evaluation s hould be performed and focus on ches t dis comfort, s igns and s ymptoms of heart failure, cardiac his tory, ris k factors for ACS, and his torical features that may preclude the us e of fibrinolytics . For the patient with STEMI, the goals of reperfus ion are to give fibrinolytics within 30 minutes of arrival or perform PCI within 90 minutes of arrival. Figure 32 s hows how to meas ure ST-s egment deviation. J point plus 0.04 second

II

ST-segment baseline

ST-segment deviation = 5.0 mm

TP s egment (baseline)

A

V2

V5

J point plus 0.04 s econd

ST-s egment baseline

ST-segment deviation = 4.5 mm

B

TP s egment (baseline)

Fig u re 3 2 . How to meas ure ST-s egment deviation. A, Inferior MI. The ST s egment has no low point (it is covered or concave). B, Anterior MI.

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P a t ie n t As s e s s m e n t In <1 0 Min u t e s (Bo x 3 )

As s es s ment of the patient in the firs t 10 minutes s hould include the following: • Check vital s igns and evaluate oxygen s aturation. • Es tablis h IV acces s . • Take a brief focus ed his tory and perform a phys ical examination. • Complete the fibrinolytic checklis t and check for contraindications , if indicated. • Obtain a blood s ample to evaluate initial cardiac marker levels , electrolytes , and coagulation. • Obtain and review portable ches t x-ray (<30 minutes after the patient’s arrival in the ED). This s hould not delay fibrinolytic therapy for STEMI or activation of the PCI team for STEMI. Note: The res ults of cardiac markers , ches t x-ray, and laboratory s tudies s hould not delay reperfus ion therapy unles s clinically neces s ary, eg, s us pected aortic dis s ection or coagulopathy.

P a t ie n t Ge n e r a l Tr e a t m e n t (Bo x 3 )

Unles s allergies or contraindications exis t, 4 agents are routinely recommended for cons ideration in patients with is chemic-type ches t dis comfort: • Oxygen if hypoxemic (O 2 % <94% ) or s igns of heart failure • As pirin • Nitroglycerin • Morphine (if ongoing dis comfort or no res pons e to nitrates ) Becaus e thes e agents may have been given out of hos pital, adminis ter initial or s upplemental dos es as indicated. (See the dis cus s ion of thes e drugs in the previous s ection, “EMS As s es s ment, Care, and Hos pital Preparation.”)

Cr it ic a l Co n c e p t s Oxyg e n, As p irin, Nitra te s , Mo rp hine

• Unles s contraindicated, initial therapy with oxygen if needed, as pirin, nitrates , and, if indicated, morphine is recommended for all patients s us pected of having is chemic ches t dis comfort. • The major contraindication to nitroglycerin and morphine is hypotens ion, including hypotens ion from an RV infarction. The major contraindications to as pirin are true as pirin allergy and active or recent GI bleeding.

S TEMI (Bo xe s 5 Th ro u g h 8 ) In t r o d u c t io n

Patients with STEMI us ually have complete occlus ion of an epicardial coronary artery. Th e m a in s ta y of tre a tm e n t for STEMI is e a rly re p e rfu s ion th e ra p y a c h ie ve d with fib rin olytic s or p rim a ry P CI. Reperfus ion therapy for STEMI is perhaps the mos t important advancement in treatment of cardiovas cular dis eas e in recent years . Early fibrinolytic therapy or direct catheterbas ed reperfus ion has been es tablis hed as a s tandard of care for patients with STEMI who pres ent within 12 hours of ons et of s ymptoms with no contraindications . Reperfus ion therapy reduces mortality and s aves heart mus cle; the s horter the time to reperfus ion, the greater the benefit. A 47% reduction in mortality was noted when fibrinolytic therapy was provided in the firs t hour after ons et of s ymptoms .

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Cr it ic a l Co n c e p t s De la y o f The ra p y

Ea r ly Re p e r fu s io n Th e r a p y

• Routine cons ultation with a cardiologis t or another phys ician s hould not delay diagnos is and treatment except in equivocal or uncertain cas es . Cons ultation delays therapy and is as s ociated with increas ed hos pital mortality rates . • Potential delay during the in-hos pital evaluation period may occur from d o o r to data (ECG), from d a ta to decis ion, and from d e c is io n to d rug (or PCI). Thes e 4 major points of in-hos pital therapy are commonly referred to as the “4 D’s .” • All providers mus t focus on minimizing delays at each of thes e points . Out-ofhos pital trans port time cons titutes only 5% of delay to treatment time; ED evaluation cons titutes 25% to 33% of this delay.

Rapidly identify patients with STEMI and quickly s creen them for indications and contraindications to fibrinolytic therapy by us ing a fibrinolytic checklis t if appropriate. The firs t qualified phys ician who encounters a patient with STEMI s hould interpret or confirm the 12-lead ECG, determine the ris k/benefit of reperfus ion therapy, and direct adminis tration of fibrinolytic therapy or activation of the PCI team. Early activation of PCI may occur with es tablis hed protocols . The following time frames are recommended: • If the patient meets the criteria for fib rin olytic th e ra p y, an ED door-to-needle time (needle time is the beginning of infus ion of a fibrinolytic agent) of 30 minutes is the medical s ys tem goal that is cons idered the longes t time acceptable. Sys tems s hould s trive to achieve the s hortes t time pos s ible. • For P CI, this goal for ED door–to–balloon inflation time is 90 minutes . • Patients who are ineligible for fibrinolytic therapy s hould be cons idered for trans fer to a PCI facility regardles s of delay. The s ys tem s hould prepare for a door-to-departure time of 30 minutes when a trans fer decis ion is made. Adjunctive treatments may als o be indicated.

Cla s s ify P a t ie n t s Ac c o rd in g t o ST-S e g m e n t De via t io n (Bo xe s 5 , 9 , a n d 1 3 ) Cla s s ify In t o 3 Gr o u p s Ba s e d o n S T-S e g m e n t De via t io n

Review the initial 12-lead ECG (Box 4) and clas s ify patients into 1 of the 3 following clinical groups (Boxes 5, 9, and 13):

Ge n e r a l Gro u p

De s c r ip t io n

STEMI

ST elevation

Hig h-ris k UA/NSTEMI

ST depres s ion or dynamic T-wave invers ion

Inte rm e d ia te /lo w-ris k UA

Normal or nondiagnos tic ECG

• STEMI is characterized by ST-s egment elevation in 2 or more contiguous leads or new LBBB. Thres hold values for ST-s egment elevation cons is tent with STEMI are J -point elevation greater than 2 mm (0.2 mV) in leads V2 and V3* and 1 mm or more in all other leads or by new or pres umed new LBBB. *2.5 mm in men <40 years ; 1.5 mm in all women. • Hig h -ris k UA/ NSTEMI is characterized by is chemic ST-s egment depres s ion ≥0.5 mm (0.05 mV) or dynamic T-wave invers ion with pain or dis comfort. Nonpers is tent or trans ient ST elevation ≥0.5 mm for <20 minutes is als o included in this category. • In te rm e d ia te or low-ris k UA is characterized by normal or nondiagnos tic changes in the ST s egment or T wave that are inconclus ive and require further ris k s tratification. This clas s ification includes patients with normal ECGs and thos e with ST-s egment deviation in either direction of <0.5 mm (0.05 mV) or T-wave invers ion ≤2 mm or 0.2 mV. Serial cardiac s tudies and functional tes ting are appropriate. Note that additional information (troponin) may place the patient into a higher ris k clas s ification after initial clas s ification. 101

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5 The ECG clas s ification of is chemic s yndromes is not meant to be exclus ive. A s mall percentage of patients with normal ECGs may be found to have MI, for example. If the initial ECG is nondiagnos tic and clinical circums tances indicate (eg, ongoing ches t dis comfort), repeat the ECG.

Us e o f Fib r in o lyt ic Th e r a p y

A fibrinolytic agent or “clot bus ter” is adminis tered to patients with J -point ST-s egment elevation greater than 2 mm (0.2 mV) in leads V2 and V3 and 1 mm or more in all other leads or by new or pres umed new LBBB (eg, leads III, aVF; leads V3 , V4 ; leads I and aVL) without contraindications . Fibrin-s pecific agents are effective in achieving normal flow in about 50% of patients given thes e drugs . Examples of fibrin-s pecific drugs are rtPA, reteplas e, and tenecteplas e. Streptokinas e was the firs t fibrinolytic us ed widely, but it is not fibrin s pecific. It is s till the mos t common agent us ed worldwide for acute STEMI reperfus ion therapy. Cons iderations for the us e of fibrinolytic therapy are as follows : • In the abs ence of contraindications and in the pres ence of a favorable ris k-benefit ratio, fibrinolytic therapy is one option for reperfus ion in patients with STEMI and onset of symptoms within 12 hours of presentation with qualifying ECG findings and if PCI is not available within 90 minutes of firs t medical contact. • In the abs ence of contraindications , it is als o reas onable to give fibrinolytics to patients with onset of symptoms within the prior 12 hours and ECG findings cons is tent with true pos terior MI. Experienced providers will recognize this as a condition where ST-s egment depres s ion in the early precordial leads is equivalent to ST-s egment elevation in others . When thes e changes are as s ociated with other ECG findings , it is s ugges tive of a “STEMI” on the pos terior wall of the heart. • Fibrinolytics are generally not recommended for patients pres enting >12 hours after onset of symptoms. But they may be cons idered if is chemic ches t dis comfort continues with pers is tent ST-s egment elevation. • Do not give fibrinolytics to patients who pres ent >24 hours after the onset of symptoms or patients with ST-s egment depres s ion unles s a true pos terior MI is s us pected.

Us e o f P CI

The mos t commonly us ed form of PCI is coronary intervention with s tent placement. Primary PCI is us ed as an alternative to fibrinolytics . Rescue PCI is us ed early after fibrinolytics in patients who may have pers is tent occlus ion of the infarct artery (failure to reperfus e with fibrinolytics ), although this term has been recently replaced and included by the term pharmacoinvasive strategy. PCI has been s hown to be s uperior to fibrinolys is in the combined end points of death, s troke, and reinfarction in many s tudies for patients pres enting between 3 and 12 hours after ons et. However, thes e res ults have been achieved in experienced medical s ettings with s killed providers (performing >75 PCIs per year) at a s killed PCI facility (performing >200 PCIs for STEMI with cardiac s urgery capabilities ). Cons iderations for the us e of PCI include the following: • At the time of publication of the 2010 AHA Guidelines for CPR and ECC, percutaneous coronary intervention is the treatment of choice for the management of STEMI when it can be performed effectively with a door-to-balloon time of <90 minutes from firs t medical contact by a s killed provider at a s killed PCI facility. • Primary PCI may als o be offered to patients pres enting to non-PCI centers if PCI can be initiated promptly within 90 minutes from EMS arrival–to-balloon time at the PCIcapable hos pital. The TRANSFER AMI (Trial of Routine Angioplas ty and Stenting After Fibrinolys is to Enhance Reperfus ion in Acute Myocardial Infarction) trial s upports the trans fer of high-ris k patients who receive fibrinolys is in a non-PCI center witihin 12 hours of s ymptom ons et to a PCI center within 6 hours of fibrinolytic adminis tration to receive routine early PCI.

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• For patients admitted to a hos pital without PCI capabilities , there may be s ome benefit as s ociated with trans fer for PCI vers us adminis tration of on-s ite fibrinolytics in terms of reinfarction, s troke, and a trend to lower mortality when PCI can be performed within 90 minutes of ons et of STEMI. • PCI is als o preferred in patients with contraindications to fibrinolytics and is indicated in patients with cardiogenic s hock or heart failure complicating MI. • In patients with STEMI who pres ent 3 hours or less from onset of symptoms, treatment is more time s ens itive, and PCI is s uperior to fibrinolys is .

Ad ju n c t ive Tr e a t m e n t s

Other drugs are us eful when indicated in addition to oxygen, s ublingual or s pray nitroglycerin, as pirin, morphine, and fibrinolytic therapy. Thes e include • IV nitroglycerin • Heparin • Clopidogrel • ß-Blockers • ACE inhibitors • HMG–CoA reductas e inhibitor therapy (s tatin) IV nitroglycerin and heparin are commonly us ed early in the management of patients with STEMI. Thes e agents are briefly dis cus s ed below. We will not review the us e of ß-blockers , ACE inhibitors , and s tatin therapy in STEMI. Us e of thes e agents requires additional ris k s tratification s kills and a detailed knowledge of the s pectrum of ACS and, in s ome ins tances , continuing knowledge of the res ults of clinical trials .

IV Nitrog lyc e rin Routine us e of IV nitroglycerin is not indicated and has not been s hown to s ignificantly reduce mortality in STEMI. IV nitroglycerin is indicated and us ed widely in is chemic s yndromes . It is preferred over topical or long-acting forms becaus e it can be titrated in a patient with potentially uns table hemodynamics and clinical condition. Indications for initiation of IV nitroglycerin in STEMI are • Recurrent or continuing ches t dis comfort unres pons ive to s ublingual or s pray nitroglycerin • Pulmonary edema complicating STEMI • Hypertens ion complicating STEMI Treatment goals us ing IV nitroglycerin are as follows :

Tre a t m e n t Go a l

Ma n a g e m e n t

Re lie f o f is c he m ic c he s t d is c o m fo rt

• Titrate to effect • Keep SBP >90 mm Hg • Limit drop in SBP to 30 mm Hg below bas eline in hypertens ive patients

Im p ro ve m e nt in p ulm o na ry e d e m a a nd hyp e rte ns io n

• Titrate to effect • Limit drop in SBP to 10% of bas eline in normotens ive patients • Limit drop in SBP to 30 mm Hg below bas eline in hypertens ive patients

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He p a rin Heparin is routinely given as an adjunct for PCI and fibrinolytic therapy with fibrin-s pecific agents (rtPA, reteplas e, tenecteplas e). It is als o indicated in other s pecific high-ris k s ituations , s uch as LV mural thrombus , atrial fibrillation, and prophylaxis for pulmonary thromboembolis m in patients with prolonged bed res t and heart failure complicating MI. If you us e thes e drugs you mus t be familiar with dos ing s chedules for s pecific clinical s trategies . Th e in a p p rop ria te d os in g a n d m on itorin g of h e p a rin th e ra p y h a s c a u s e d e xc e s s in tra c e re b ra l b le e d in g a n d m a jor h e m orrh a g e in STEMI p a tie n ts . P rovid e rs u s in g h e p a rin n e e d to kn ow th e in d ic a tion s , d os in g , a n d u s e in th e s p e c ific ACS c a te g orie s . Th e d os in g , u s e , a n d d u ra tion h a ve b e e n d e rive d from u s e in c lin ic a l tria ls . Sp e c ific p a tie n ts m a y re q u ire d os e m od ific a tion . Se e th e ECC Ha n d b ook for we ig h t-b a s e d d os in g g u id e lin e s , in te rva ls of a d m in is tra tion , a n d a d ju s tm e n t (if n e e d e d ) in re n a l fu n c tion . Se e th e ACC/ AHA Gu id e lin e s for d e ta ile d d is c u s s ion in s p e c ific c a te g orie s .

Br a d yc a rd ia Ca s e In t r o d u c t io n

This cas e dis cus s es as s es s ment and management of a patient with symptomatic bradycardia (heart rate <50/min). The corners tones of managing bradycardia are to • Differentiate between s igns and s ymptoms that are caus ed by the s low rate vers us thos e that are unrelated • Correctly diagnos e the pres ence and type of AV block • Us e atropine as the drug intervention of firs t choice • Decide when to s tart TCP • Decide when to s tart epinephrine or dopamine to maintain heart rate and blood pres s ure • Know when to call for expert cons ultation regarding complicated rhythm interpretation, drugs , or management decis ions In addition, you mus t know the techniques and cautions for us ing TCP.


By the end of this cas e you s hould be able to 1. Recognize s igns and s ymptoms of s ymptomatic bradycardia 2. Recognize caus es of s ymptomatic bradycardia 3. State treatments for s ymptomatic bradycardia 4. Determine whether s igns and s ymptoms are caus ed by bradycardia or another condition 5. Identify s econd- and third-degree AV blocks 6. Des cribe indications for TCP and dos es of drugs us ed to treat bradycardia: atropine, dopamine, and epinephrine

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Th e ACLS Ca s e s : Bra d yc a rd ia

Rh yt h m s fo r Br a d yc a r d ia

This cas e involves thes e ECG rhythms : • Sinus bradycardia • Firs t-degree AV block • Second-degree AV block – Type I (Wenckebach/Mobitz I) – Type II (Mobitz II) • Third-degree AV block You s hould know the major AV blocks becaus e important treatment decis ions are bas ed on the type of block pres ent (Figure 33). Complete AV block is generally the mos t important and clinically s ignificant degree of block. Als o, complete or third-degree AV block is the degree of block mos t likely to caus e cardiovas cular collaps e and require immediate pacing. Recognition of a symptomatic bradycardia due to AV block is a primary goal. Recognition of the type of AV block is a s econdary goal.

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A

B

C

D

E Fig u re 3 3 . Examples of AV block. A, Sinus bradycardia with borderline firs t-degree AV block. B, Second-degree AV block type I. C, Seconddegree AV block type II. D, Complete AV block with a ventricular es cape pacemaker (wide QRS: 0.12 to 0.14 s econd). E, Third-degree AV block with a junctional es cape pacemaker (narrow QRS: <0.12 s econd).

Dr u g s fo r Br a d yc a r d ia

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This cas e involves thes e drugs : • Atropine • Dopamine (infus ion) • Epinephrine (infus ion)


De s c r ip t io n o f Br a d yc a rd ia De fin it io n s

Definitions us ed in this cas e are as follows :

Te r m

De fin it io n

Bra d ya rrhythm ia o r b ra d yc a rd ia *

Any rhythm dis order with a heart rate <60/min—eg, third-degree AV block—or s inus bradycardia. When bradycardia is the caus e of s ymptoms , the rate is generally <50/min.

Sym p to m a tic b ra d ya rrhythm ia

Signs and s ymptoms due to the s low heart rate

*For the purpos es of this cas e we will us e the term bradycardia interchangeably with bradyarrhythmia unles s s pecifically defined.

S ym p t o m a t ic Br a d yc a r d ia

Sinus bradycardia may have multiple caus es . Some are phys iologic and require no as s es s ment or therapy. For example, a well-trained athlete may have a heart rate in the range of 40 to 50/min or occas ionally lower. In contras t, s ome patients have heart rates in the normal s inus range, but thes e heart rates are inappropriate or ins ufficient for them. This is called a functional or relative bradycardia. For example, a heart rate of 70/min is too s low for a patient in cardiogenic or s eptic s hock. This cas e will focus on the patient with a bradycardia and heart rate <50/min. Key to the cas e management is the determination of s ymptoms or s igns due to the decreas ed heart rate. A s ymptomatic bradycardia exis ts clinically when 3 criteria are pres ent: 1. The heart rate is s low. 2. The patient has s ymptoms . 3. The s ymptoms are due to the s low heart rate.

S ig n s a n d S ym p t o m s

You mus t perform a focus ed his tory and phys ical examination to identify the s igns and s ymptoms of a bradycardia. Symptoms include ches t dis comfort or pain, s hortnes s of breath, decreas ed level of cons cious nes s , weaknes s , fatigue, light-headednes s , dizzines s , and pres yncope or s yncope. Signs include hypotens ion, drop in blood pres s ure on s tanding (orthos tatic hypotens ion), diaphores is , pulmonary conges tion on phys ical examination or ches t x-ray, frank conges tive heart failure or pulmonary edema, and bradycardia-related (es cape) frequent premature ventricular complexes or VT.

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Ma n a g in g Br a d yc a rd ia : Th e Br a d yc a rd ia Alg o r it h m Ove r vie w o f t h e Alg o r it h m

The Bradycardia Algorithm (Figure 34) outlines the s teps for as s es s ment and manage ment of a patient pres enting with s ymptomatic bradycardia with puls e. Implementation of this algorithm begins with the identification of bradycardia (Box 1); the heart rate is <50/min. Firs t s teps include the components of the BLS Survey and the ACLS Survey, s uch as s upporting circulation and airway management, giving oxygen, monitoring the rhythm and vital s igns , es tablis hing IV acces s , and obtaining a 12-lead ECG if available (Box 2). In the differential diagnos is you determine if the patient has s igns or s ymptoms of poor perfus ion and if thes e are caus ed by the bradycardia (Box 3). The primary decis ion point in the algorithm is the determination of adequate perfus ion. If the patient has adequate perfus ion, you obs erve and monitor (Box 4). If the patient has poor perfus ion, you adminis ter atropine (Box 5). If atropine is ineffective, prepare for TCP or cons ider dopamine or epinephrine infus ion (Box 5). If indicated, you prepare for trans venous pacing, s earch for and treat contributing caus es , and s eek expert cons ultation (Box 6). The treatment s equence in the algorithm is determined by the s everity of the patient’s condition. You may need to implement multiple interventions s imultaneous ly. If cardiac arres t develops , go to the Cardiac Arres t Algorithm.

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Ad ult Bra d yc a rd ia (With Puls e)

1

As s es s appropriatenes s for clinical condition. Heart rate typically <50/min if bradyarrhythmia.

2 Id e ntify a nd tre a t und e rlying c a us e • Maintain patent airway; as s is t breathing as neces s ary • Oxygen (if hypoxemic) • Cardiac monitor to identify rhythm; monitor blood pres s ure and oximetry • IV acces s • 12-Lead ECG if available; don’t delay therapy

3 P e rs is te nt b ra d ya rrhythm ia c a us ing :

4 Mo nito r a nd o b s e rve

No

• Hypotens ion? • Acutely altered mental s tatus ? • Signs of s hock? • Is chemic ches t dis comfort? • Acute heart failure? Ye s

5

Atro p ine If atropine ineffective: • Trans cutaneous pacing OR • Do p a m ine infus ion OR • Ep ine p hrine infus ion

Do s e s /De ta ils Atro p ine IV Do s e : Firs t dos e: 0.5 mg bolus Repeat every 3-5 minutes Maximum: 3 mg Do p a m ine IV Infus io n: 2-10 mcg/kg per minute Ep ine p hrine IV Infus io n: 2-10 mcg per minute

6 Co ns id e r: • Expert cons ultation • Trans venous pacing © 2010 American Heart As s ociation

Fig u re 3 4 . The Bradycardia Algorithm.

FYI 2 0 1 0 Gu id e lin e s The Bra d yc a rd ia Alg o rithm

• The Bradycardia Algorithm has been modified to reflect the changes in treatment pres ented in the 2010 AHA Guidelines for CPR and ECC. • The initial treatment of bradycardia is atropine. If bradycardia is unres pons ive to atropine, IV infus ion of ß-adrenergic agonis ts with rate-accelerating effects (dopamine, epinephrine) or TCP can be effective while the patient is being prepared for emergent trans venous temporary pacing if required.

Ap p lic a t io n o f t h e Br a d yc a rd ia Alg o r it h m In t r o d u c t io n

In this cas e you have a patient pres enting with s ymptoms of bradycardia. You conduct appropriate as s es s ment and interventions as outlined in the Bradycardia Algorithm. At the s ame time you are s earching for and treating pos s ible contributing factors . 109

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Id e n t ific a t io n o f Br a d yc a r d ia (Bo x 1 )

Identify whether the bradycardia is

BLS a n d ACLS S u r ve ys (Bo x 2 )

Next, perform the ACLS Survey, including the following:

Ar e S ig n s o r S ym p t o m s Ca u s e d b y Br a d yc a r d ia ? (Bo x 3 )

• Pres ent by definition, ie, heart rate <50/min • Inadequate for the patient’s condition (functional or relative)

A

Maintain patent airway.

B

As s is t breathing as needed; give oxygen in cas e of hypoxemia; monitor oxygen s aturation.

C

Monitor blood pres s ure and heart rate; obtain and review a 12-lead ECG; es tablis h IV acces s .

D

Conduct a problem-focus ed his tory and phys ical examination; s earch for and treat pos s ible contributing factors .

Box 3 prompts you to cons ider if the s igns or s ymptoms of poor perfus ion are caus ed by the bradycardia. The key clinical ques tions are • Are there “s erious ” s igns or s ymptoms ? • Are the s igns and s ymptoms related to the s low heart rate? Look for advers e s igns and s ymptoms of the bradycardia: • Symptoms (eg, ches t dis comfort, s hortnes s of breath, decreas ed level of cons cious nes s , weaknes s , fatigue, light-headednes s , dizzines s , pres yncope or s yncope) • Signs (eg, hypotens ion, conges tive heart failure, ventricular arrhythmias related to the bradycardia) Sometimes the “s ymptom” is not due to the bradycardia. For example, hypotens ion as s ociated with bradycardia may be due to myocardial dys function rather than the bradycardia. Keep this in mind when you reas s es s the patient’s res pons e to treatment.

Cr it ic a l Co n c e p t s Bra d yc a rd ia

• The key clinical ques tion is whether the bradycardia is caus ing the patient’s s ymptoms or s ome other illnes s is caus ing the bradycardia.

De c is io n P o in t : Ad e q u a t e P e r fu s io n ?

You mus t now decide if the patient has adequate or poor perfus ion.

Tr e a t m e n t S e q u e n c e S u m m a r y (Bo x 5 )

If the patient has poor perfus ion s econdary to bradycardia, the treatment s equence is as follows :

• If the patient has a d e q u a te p e rfu s ion , obs erve and monitor (Box 4). • If the patient has p oor p e rfu s ion , proceed to Box 5.

Atropine 0.5 mg IV—may repeat to a total dos e of 3 mg

Give atropine as firs t-line treatment

If a t ro p in e is in e ffe c t ive Trans cutaneous pacing or

110

• Dopamine 2 to 10 mcg/kg per minute (chronotropic or heart rate dos e) • Epinephrine 2 to 10 mcg/min


The treatment s equence is determined by the s everity of the patient’s clinical pres entation. For patients with s ymptomatic bradycardia, move quickly through this s equence. Thes e patients may be “pre–cardiac arres t” and may need multiple interventions s imultaneous ly.

Tr e a t m e n t S e q u e n c e : At r o p in e

In the abs ence of immediately revers ible caus es , atropine remains the firs t-line drug for acute s ymptomatic bradycardia. Atropine adminis tration s hould not delay implementation of external pacing for patients with poor perfus ion. Dopamine and epinephrine may be s ucces s ful as an alternative to TCP. For bradycardia, give atropine 0.5 mg IV every 3 to 5 minutes to a total dos e of 0.04 mg/kg (maximum total dos e of 3 mg). Atropine dos es of <0.5 mg may paradoxically res ult in further s lowing of the heart rate. Us e atropine cautious ly in the pres ence of acute coronary is chemia or MI. An atropinemediated increas e in heart rate may wors en is chemia or increas e infarct s ize. Do not rely on atropine in Mobitz type II s econd- or third-degree AV block or in patients with third-degree AV block with a new wide QRS complex.

Tr e a t m e n t S e q u e n c e : P a c in g

TCP may be us eful for treatment of s ymptomatic bradycardia. TCP is noninvas ive and can be performed by ACLS providers . Healthcare providers s hould cons ider immediate pacing in uns table patients with highdegree heart block when IV acces s is not available. It is reas onable for healthcare providers to initiate TCP in uns table patients who do not res pond to atropine. Following initiation of pacing, confirm electrical and mechanical capture. Reas s es s the patient for s ymptom improvement and hemodynamic s tability. Give analges ics and s edatives for pain control. Note that many of thes e drugs may further decreas e blood pres s ure and affect the patient’s mental s tatus . Try to identify and correct the caus e of the bradycardia. Some limitations apply. TCP can be painful and may fail to produce effective electrical and mechanical capture. If s ymptoms are not caus ed by the bradycardia, pacing may be ineffective des pite capture. If you chos e TCP as the s econd–line treatment and it is als o ineffective (eg, incons is tent capture), begin an infus ion of dopamine or epinephrine and prepare for pos s ible trans venous pacing by obtaining expert cons ultation.

Fo u n d a t io n a l Fa c t s Se d a tio n a nd P a c ing

Mos t cons cious patients s hould be given s edation before pacing. If the patient is in cardiovas cular collaps e or rapidly deteriorating, it may be neces s ary to s tart pacing without prior s edation, particularly if drugs for s edation are not immediately available. The clinician mus t evaluate the need for s edation in light of the patient’s condition and need for immediate pacing. A review of the drugs us ed is beyond the s cope of the ACLS Provider Cours e. The general approach could include the following: • Give parenteral benzodiazepine for anxiety and mus cle contractions . • Give a parenteral narcotic for analges ia. • Us e a chronotropic infus ion once available. • Obtain expert cons ultation for trans venous pacing.

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Tr e a t m e n t S e q u e n c e : Ep in e p h r in e , Do p a m in e

Although ß-adrenergic agonis ts with rate-accelerating effects are not firs t-line agents for treatment of s ymptomatic bradycardia, they are alternatives to TCP or in s pecial circums tances s uch as overdos e with a ß-blocker or calcium channel blocker. Becaus e epinephrine and dopamine are vas ocons trictors , as well as chronotropes , healthcare providers mus t as s es s the patient’s intravas cular volume s tatus and avoid hypovolemia when us ing thes e drugs . Both epinephrine and dopamine infus ions may be us ed for patients with s ymptomatic bradycardia, particularly if as s ociated with hypotens ion, for whom atropine may be inappropriate or after atropine fails . Begin epinephrine infus ion at a dos e of 2 to 10 mcg/min and titrate to patient res pons e. Begin dopamine infus ion at 2 to 10 mcg/kg per minute and titrate to patient res pons e. At lower dos es dopamine has a more s elective effect on inotropy and heart rate; at higher dos es (>10 mcg/kg per minute) it als o has vas ocons trictive effects .

Ne xt Ac t io n s (Bo x 6 )

After cons ideration of the treatment s equence in Box 5, you may need to • Prepare the patient for trans venous pacing • Treat the contributing caus es of the bradycardia • Cons ider expert cons ultation—but do not delay treatment if the patient is uns table or potentially uns table

Tr a n s c u t a n e o u s P a c in g In t r o d u c t io n

A variety of devices can pace the heart by delivering an electrical s timulus , caus ing electrical depolarization and s ubs equent cardiac contraction. TCP delivers pacing impuls es to the heart through the s kin by us e of cutaneous electrodes . Mos t manufacturers have added a pacing mode to manual defibrillators . The ability to perform TCP is now often as clos e as the neares t defibrillator. Providers need to know the indications , techniques , and hazards for us ing TCP.

In d ic a t io n s

Indications for TCP are as follows : • Hemodynamically uns table bradycardia (eg, hypotens ion, acutely altered mental s tatus , s igns of s hock, is chemic ches t dis comfort, acute heart failure hypotens ion) • Uns table clinical condition likely due to the bradycardia • For pacing readines s in the s etting of AMI as follows : – Symptomatic s inus bradycardia – Mobitz type II s econd-degree AV block – Third-degree AV block – New left, right, or alternating bundle branch block or bifas cicular block • Bradycardia with s ymptomatic ventricular es cape rhythms

P r e c a u t io n s

Precautions for TCP are as follows : • TCP is contraindicated in s evere hypothermia and is not recommended for as ys tole. • Cons cious patients require analges ia for dis comfort unles s delay for s edation will caus e/contribute to deterioration. • Do not as s es s the carotid puls e to confirm mechanical capture; electrical s timulation caus es mus cular jerking that may mimic the carotid puls e.

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Te c h n iq u e

Perform TCP by following thes e s teps :

Ste p

Ac t io n

1

Place pacing electrodes on the ches t according to package ins tructions .

2

Turn the pacer ON.

3

Set the demand rate to approximately 60/min. This rate can be adjus ted up or down (bas ed on patient clinical res pons e) once pacing is es tablis hed.

4

Set the current milliamperes output 2 mA above the dos e at which cons is tent capture is obs erved (s afety margin).

External pacemakers have either fixed rates (as ynchronous mode) or demand rates .

As s e s s Re s p o n s e t o Tr e a t m e n t

Rather than target a precis e heart rate, the goal of therapy is to ens ure improvement in clinical s tatus (ie, s igns and s ymptoms related to the bradycardia). Signs of hemodynamic impairment include hypotens ion, acutely altered mental s tatus , s igns of s hock, is chemic ches t dis comfort, acute heart failure, or other s igns of s hock related to the bradycardia. Start pacing at a rate of about 60/min. Once pacing is initiated, adjus t the rate bas ed on the patient’s clinical res pons e. Mos t patients will improve with a rate of 60 to 70/min if the s ymptoms are primarily due to the bradycardia. Cons ider giving atropine before pacing in mildly s ymptomatic patients . Do not delay pacing for uns table patients , particularly thos e with high-degree AV block. Atropine may increas e heart rate, improve hemodynamics , and eliminate the need for pacing. If atropine is ineffective or likely to be ineffective or if es tablis hment of IV acces s or atropine adminis tration is delayed, begin pacing as s oon as it is available. Patients with ACS s hould be paced at the lowes t heart rate that allows clinical s tability. Higher heart rates can wors en is chemia becaus e heart rate is a major determinate of myocardial oxygen demand. Is chemia, in turn, can precipitate arrhythmias . An alternative to pacing if s ymptomatic bradycardia is unres pons ive to atropine is a chronotropic drug infus ion to s timulate heart rate: • Epinephrine: Initiate at 2 to 10 mcg/min and titrate to patient res pons e • Dopamine: Initiate at 2 to 10 mcg/kg per minute and titrate to patient res pons e

Br a d yc a r d ia Wit h Es c a p e Rh yt h m s

A bradycardia may lead to bradycardia-dependent ventricular rhythms . When the heart rate falls , an electrically uns table ventricular area may “es cape” s uppres s ion by higher and fas ter pacemakers (eg, s inus node), es pecially in the s etting of acute is chemia. Thes e ventricular rhythms often fail to res pond to drugs . With s evere bradycardia s ome patients will develop wide-complex ventricular beats that can precipitate VT or VF. Pacing may increas e the heart rate and eliminate bradycardia-dependent ventricular rhythms . However, an accelerated idioventricular rhythm (s ometimes called AIVR) may occur in the s etting of inferior wall MI. This rhythm is us ually s table and does not require pacing. Patients with ventricular es cape rhythms may have normal myocardium with dis turbed conduction. After correction of electrolyte abnormalities or acidos is , rapid pacing can s timulate effective myocardial contractions until the conduction s ys tem recovers .

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S t a n d b y P a c in g

Several bradycardic rhythms in ACS are caus ed by acute is chemia of conduction tis s ue and pacing centers . Patients who are clinically s table may decompens ate s uddenly or become uns table over minutes to hours from wors ening conduction abnormalities . Thes e bradycardias may deteriorate to complete AV block and cardiovas cular collaps e. Place TCP electrodes in anticipation of clinical deterioration in patients with acute myocardial is chemia or infarction as s ociated with the following rhythms : • Symptomatic s inus node dys function with s evere and s ymptomatic s inus bradycardia • As ymptomatic Mobitz type II s econd-degree AV block • As ymptomatic third-degree AV block • Newly acquired left, right, or alternating bundle branch block or bifas cicular block in the s etting of AMI

Un s t a b le Ta c h yc a rd ia Ca s e In t r o d u c t io n

If you are the team leader in this cas e, you will conduct the as s es s ment and management of a patient with a rapid, unstable heart rate. You mus t be able to clas s ify the tachycardia and implement appropriate interventions as outlined in the Tachycardia Algorithm. You will be evaluated on your knowledge of the factors involved in s afe and effective s ynchronized cardiovers ion as well as your performance of the procedure.


By the end of this cas e you s hould be able to 1. Differentiate characteris tics of s table and uns table tachycardias 2. Des cribe the ACLS priorities of care in the Tachycardia Algorithm 3. Identify uns table patients and follow this arm of the Tachycardia Algorithm 4. Des cribe energy levels required for electrical cardiovers ion of tachycardia varieties 5. Demons trate s afety procedures when performing cardiovers ion

Rh yt h m s fo r Un s t a b le Ta c h yc a r d ia

This cas e involves thes e ECG rhythms :

Dr u g s fo r Un s t a b le Ta c h yc a r d ia

Drugs are generally not us ed to manage patients with uns table tachycardia. Immediate cardiovers ion is recommended. Cons ider adminis tering s edative drugs in the cons cious patient. But do not delay immediate cardiovers ion in the uns table patient.

• Atrial fibrillation • Atrial flutter • Reentry s upraventricular tachycardia (SVT) • Monomorphic VT • Polymorphic VT • Wide-complex tachycardia of uncertain type

Th e Ap p ro a c h t o Un s t a b le Ta c h yc a rd ia In t r o d u c t io n

114

A tachyarrhythmia (rhythm with heart rate >100/min) has many potential caus es and may be s ymptomatic or as ymptomatic. The key to management of a patient with any tachycardia is to determine whether puls es are pres ent. If puls es are pres ent, determine whether the patient is s table or uns table and then provide treatment bas ed on patient condition and rhythm.

Th e ACLS Ca s e s : Un s ta b le Ta c h yc a rd ia

If the tachyarrhythmia is s inus tachycardia, conduct a diligent s earch for the caus e of the tachycardia. Treatment and correction of this caus e will improve the s igns and s ymptoms .

De fin it io n s

Definitions us ed in this cas e are as follows :

Te r m

De fin it io n

Ta c hya rrhythm ia , ta c hyc a rd ia *

Heart rate >100/min

Sym p to m a tic ta c hya rrhythm ia

Signs and s ymptoms due to the rapid heart rate

*For the purpos es of this cas e we will us e the term tachycardia interchangeably with tachyarrhythmia. Sinus tachycardia will be s pecifically indicated.

P a t h o p h ys io lo g y o f Un s t a b le Ta c h yc a r d ia

Uns table tachycardia exis ts when the heart rate is too fas t for the patient’s clinical condition and the exces s ive heart rate caus es s ymptoms or an uns table condition becaus e the heart is • Beating so fast that cardiac output is reduced; this can caus e pulmonary edema, coronary is chemia, and reduced blood flow to vital organs (eg, brain, kidneys ) • Beating ineffectively s o that coordination between the atrium and ventricles or the ventricles thems elves reduces cardiac output

S ym p t o m s a n d S ig n s

Uns table tachycardia leads to s erious s igns and s ymptoms that include • Hypotens ion • Acutely altered mental s tatus • Signs of s hock • Is chemic ches t dis comfort • Acute heart failure (AHF)

Ra p id Re c o g n it io n Is t h e Ke y t o Ma n a g e m e n t

The 2 keys to management of patients with uns table tachycardia are 1. Rapid recognition that the patient is significantly symptomatic or even unstable 2. Rapid recognition that the signs and symptoms are caused by the tachycardia You m u s t q u ic kly d e te rm in e wh e th e r th e p a tie n t’s ta c h yc a rd ia is p rod u c in g h e m od yn a m ic in s ta b ility a n d s e riou s s ig n s a n d s ym p tom s or wh e th e r th e s ig n s a n d s ym p tom s (e g , th e p a in a n d d is tre s s of a n AMI) a re p rod u c in g th e ta c h yc a rd ia . This determination can be difficult. Many experts s ugges t that when a heart rate is <150/min, it is unlikely that s ymptoms of ins tability are caus ed primarily by the tachycardia unles s there is impaired ventricular function. A heart rate >150/min is an inappropriate res pons e to phys iologic s tres s (eg, fever, dehydration) or other underlying conditions .

S e ve r it y

As s es s for the pres ence or abs ence of s igns and s ymptoms and for their s everity. Frequent patient as s es s ment is indicated.

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In d ic a t io n s fo r Ca r d io ve r s io n

Rapid identification of s ymptomatic tachycardia will help you determine whether you s hould prepare for immediate cardiovers ion. For example: • Sinus tachycardia is a phys iologic res pons e to extrins ic factors , s uch as fever, anemia, or hypotens ion/s hock, which create the need for increas ed cardiac output. There is us ually a high degree of s ympathetic tone and neurohormonal factors . Sinus tachycardia will not res pond to cardiovers ion. In fact, if a s hock is delivered, the heart rate often increas es . • If the patient with tachycardia is s table (ie, no s erious s igns related to the tachycardia), patients may await expert cons ultation becaus e treatment has the potential for harm. • Atrial flutter typically produces a heart rate of approximately 150/min (lower rates may be pres ent in patients who have received antiarrhythmic therapy). Atrial flutter at this rate is often s table in the patient without heart or s erious s ys temic dis eas e. • At rates >150/min, s ymptoms are often pres ent and cardiovers ion is often required if the patient is uns table. • If the patient is s erious ly ill or has underlying cardiovas cular dis eas e, s ymptoms may be pres ent at lower rates . You mus t know when cardiovers ion is indicated, how to prepare the patient for it (including appropriate medication), and how to s witch the defibrillator/monitor to operate as a cardioverter.

Ma n a g in g Un s t a b le Ta c h yc a rd ia : Th e Ta c h yc a rd ia Alg o r it h m In t r o d u c t io n

The Tachycardia Algorithm s implifies initial management of tachycardia. The pres ence or abs ence of puls es is cons idered key to management of a patient with any tachycardia. If puls es are pres ent, determine whether the patient is s table or uns table and then provide treatment bas ed on the patient’s condition and rhythm. If a puls eles s tachycardia is pres ent, then manage the patient according to the Cardiac Arres t Algorithm (Figure 19, page 61). The ACLS provider s hould either be an expert or be able to obtain expert cons ultation. Actions in the boxes require advanced knowledge of ECG rhythm interpretation and antiarrhythmic therapy and are intended to be accomplis hed in the in-hos pital s etting with expert cons ultation available.

Ove r vie w

The Tachycardia Algorithm (Figure 35) outlines the s teps for as s es s ment and management of a patient pres enting with s ymptomatic tachycardia with puls es . Implementation of this algorithm begins with the identification of tachycardia with puls es (Box 1). If a tachycardia and a puls e are pres ent, perform as s es s ment and management s teps guided by the BLS Survey and the ACLS Survey (Box 2). The key in this as s es s ment is to decide if the tachycardia is s table or uns table. If s igns and s ymptoms pers is t des pite provis ion of s upplementary oxygen and s upport of airway and circulation and if s ignificant s igns or s ymptoms are due to the tachycardia (Box 3), then the tachycardia is uns table and immediate s ynchronized cardiovers ion is indicated (Box 4).

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If the patient is s table, you will evaluate the ECG, and determine if the QRS complex is wide or narrow and regular or irregular (Box 5). The treatment of s table tachycardia is pres ented in the next cas e (Box 6). A precis e diagnos is of the rhythm (eg, reentry SVT, atrial flutter) may not be pos s ible at this time.

Fo u n d a t io n a l Fa c t s Se rio us o r Sig nific a nt Sym p to m s Uns ta b le Co nd itio n

Intervention is determined by the pres ence of s ignificant s ymptoms or by an uns table condition res ulting from the tachycardia.* Serious s ymptoms and s igns include • Hypotens ion • Acutely altered mental s tatus • Signs of s hock • Is chemic ches t dis comfort • Acute heart failure (AHF) Ventricular rates <150/min us ually do not caus e s erious s igns or s ymptoms .

FYI 2 0 1 0 Gu id e lin e s Ta c hyc a rd ia With a P uls e Alg o rithm

Su m m a r y

• The 2010 Tachycardia With a Puls e Algorithm (Figure 35) is pres ented in the traditional box-and-line format. Overall, the algorithm has been s implified and redes igned to facilitate learning and memorization of the treatment recommendations and to emphas ize the importance of identifying whether the tachycardia is a caus e or a s ymptom of an underlying condition, which is fundamental to the management of all tachyarrhythmias .

Your as s es s ment and management of this patient will be guided by the following key ques tions pres ented in the Tachycardia Algorithm: • Are s ymptoms pres ent or abs ent? • Is the patient s table or uns table? • Is the QRS narrow or wide? • Is the rhythm regular or irregular? • Is the QRS monomorphic or polymorphic? Your ans wers to thes e ques tions will determine the next appropriate s teps .

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Ad ult Ta c hyc a rd ia (With Puls e)

1 As s es s appropriatenes s for clinical condition. Heart rate typically ≥150/min if tachyarrhythmia.

2 Id e ntify a nd tre a t und e rlying c a us e

Do s e s /De ta ils

• Maintain patent airway; as s is t breathing as neces s ary • Oxygen (if hypoxemic) • C ardiac monitor to identify rhythm; monitor blood pres s ure and oximetry

Sync hro nize d Ca rd io ve rs io n Initial recommended dos es : • Narrow regular: 50-100 J • Narrow irregular: 120-200 J biphas ic or 200 J monophas ic • Wide regular: 100 J • Wide irregular: defibrillation dos e (NOT s ynchronized)

3 4

P e rs is te nt ta c hya rrhythm ia c a us ing : • Hypotens ion? • Acutely altered mental s tatus ? • Signs of s hock? • Is chemic ches t dis comfort? • Acute heart failure?

Ye s

6

No

5

Wid e QRS? ≥0.12 s e c o nd

Sync hro nize d c a rd io ve rs io n • Cons ider s edation • If regular narrow complex, cons ider adenos ine

Ye s

• IV acces s and 12-lead ECG if available • C ons ider adenos ine only if regular and monomorphic • Cons ider antiarrhythmic infus ion • Cons ider expert cons ultation

No

7

• IV acces s and 12-lead ECG if available • Vagal maneuvers • Adenos ine (if regular) • ß-Blocker or calcium channel blocker • Cons ider expert cons ultation

Ad e no s ine IV Do s e : Firs t dos e: 6 mg rapid IV pus h; follow with NS flus h. Second dos e: 12 mg if required. An tia rrh yth m ic In fu s ion s for Sta b le Wid e -QRS Ta c h yc a rd ia P ro c a ina m id e IV Do s e : 20-50 mg/min until arrhythmia s uppres s ed, hypotens ion ens ues , QRS duration increas es >50% , or maximum dos e 17 mg/kg given. Maintenance infus ion: 1-4 mg/min. Avoid if prolonged QT or CHF. Am io d a ro ne IV Do s e : Firs t dos e: 150 mg over 10 minutes . Repeat as needed if VT recurs . Follow by maintenance infus ion of 1 mg/min for firs t 6 hours . So ta lo l IV Do s e : 100 mg (1.5 mg/kg) over 5 minutes . Avoid if prolonged QT.


Fig u re 3 5 . The Tachycardia With a Puls e Algorithm.

Ap p lic a t io n o f t h e Ta c h yc a rd ia Alg o r it h m t o t h e Un s t a b le P a t ie n t

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In this cas e you have a patient with tachycardia and a puls e. You conduct the s teps outlined in the Tachycardia Algorithm to evaluate and manage the patient.

As s e s s Ap p r o p r ia t e n e s s fo r Clin ic a l Co n d it io n (Bo x 1 )

• Tachycardia is defined as an arrhythmia with a rate >100/min. • The rate takes on clinical s ignificance at its greater extremes and is more likely attributable to an arrhythmia rate of ≥150/min. • It is unlikely that s ymptoms of ins tability are caus ed primarily by the tachycardia when the heart rate is <150/min unles s there is impaired ventricular function.


Id e n t ify a n d Tr e a t t h e Un d e r lyin g Ca u s e : BLS a n d ACLS S u r ve ys (Bo x 2 )

Us e the BLS Survey and the ACLS Survey to guide your approach. • Look for s igns of increas ed work of breathing (tachypnea, intercos tal retractions , s upras ternal retractions , paradoxical abdominal breathing) and hypoxemia as determined by puls e oximetry. • Give oxygen, if indicated and monitor oxygen s aturation. • Obtain an ECG to identify the rhythm. • Evaluate blood pres s ure. • Es tablis h IV acces s . • Identify and treat revers ible caus es . If s ymptoms pers is t des pite s upport of adequate oxygenation and ventilation, proceed to Box 3.

Cr it ic a l Co n c e p t s Uns ta b le P a tie nts

De c is io n P o in t : Is t h e P e r s is t e n t Ta c h ya r r h yt h m ia Ca u s in g S ig n ific a n t S ig n s o r S ym p t o m s ? (Bo x 3 )

• Healthcare providers s hould obtain a 12-lead ECG early in the as s es s ment to better define the rhythm. • However, uns table patients require immediate cardiovers ion. • Do not delay immediate cardiovers ion for acquis ition of the 12-lead ECG if the patient is uns table.

As s es s the patient’s degree of ins tability and determine if the ins tability is related to the tachycardia.

Un s ta b le If the patient demons trates rate-related cardiovas cular compromis e with s igns and s ymptoms s uch as hypotens ion, acutely altered mental s tatus , s igns of s hock, is chemic ches t dis comfort, acute heart failure, or other s igns of s hock s us pected to be due to a tachyarrhythmia, proceed to immediate s ynchronized cardiovers ion (Box 4). Serious s igns and s ymptoms are unlikely if the ventricular rate is <150/min in patients with a healthy heart. However, if the patient is s erious ly ill or has s ignificant underlying heart dis eas e or other conditions , s ymptoms may be pres ent at a lower heart rate.

Sta b le If the patient does not have rate-related cardiovas cular compromis e, proceed to Box 5. The healthcare provider has time to obtain a 12-lead ECG, evaluate the rhythm, determine if the width of the QRS, and determine treatment options . Stable patients may await expert cons ultation becaus e treatment has the potential for harm.

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Fo u n d a t io n a l Fa c t s Tre a tm e nt Ba s e d o n Typ e o f Ta c hyc a rd ia

You may not always be able to dis tinguis h between s upraventricular and ventricular rhythms . Mos t wide-complex (broad-complex) tachycardias are ventricular in origin (es pecially if the patient has underlying heart dis eas e or is older). If the patient is puls eles s , treat the rhythm as VF and follow the Cardiac Arres t Algorithm. If the patient has a wide-complex tachycardia and is uns table, as s ume it is VT until proven otherwis e. The amount of energy required for cardiovers ion of VT is determined by the morphologic characteris tics . • If the patient is uns table but has a puls e with regular uniform wide-complex VT (monomorphic VT). – Treat with s ynchronized cardiovers ion and an initial s hock of 100 J (monophas ic waveform). – If there is no res pons e to the firs t s hock, increas ing the dos e in a s tepwis e fas hion is reas onable.* • Arrhythmias with a polymorphic QRS appearance (polymorphic VT), s uch as tors ades de pointes will us ually not permit s ynchronization. If the patient has polymorphic VT: – Treat as VF with high-energy uns ynchronized s hocks (eg, defibrillation dos es ). If there is any doubt about whether an uns table patient has monomorphic or polymorphic VT, do not delay treatment for further rhythm analys is . Provide high-energy, uns ynchronized s hocks . *No s tudies that addres s ed this is s ue had been identified at the time that the manus cript for the 2010 AHA Guidelines for CPR and ECC was in preparation. Thus , this recommendation repres ents expert opinion.

P e r fo r m Im m e d ia t e S yn c h r o n iz e d Ca r d io ve r s io n (Bo x 4 )

• If pos s ible es tablis h IV acces s before cardiovers ion and adminis ter s edation if the patient is cons cious . • Do not delay cardiovers ion if the patient is extremely uns table. Further information about cardiovers ion appears below. If the patient with a regular narrow-complex SVT or a monomorphic wide-complex tachycardia is not hypotens ive, healthcare providers may adminis ter adenos ine while preparing for s ynchronized cardiovers ion. If cardiac arres t develops , s ee the Cardiac Arres t Algorithm.

De t e r m in e t h e Wid t h o f t h e QRS Co m p le x (Bo x 5 )

• If the width of the QRS complex is ≥0.12 s econd, go to Box 6. • If the width of the QRS complex is <0.12 s econd, go to Box 7.

Ca rd io ve r s io n In t r o d u c t io n

You mus t know when cardiovers ion is indicated and what type of s hock to adminis ter. Before cardiovers ion, es tablis h IV acces s and s edate the res pons ive patient if pos s ible, but do not delay cardiovers ion in the uns table or deteriorating patient. This s ection dis cus s es the following important concepts about cardiovers ion: • The difference between uns ynchronized and s ynchronized s hocks • Potential challenges to delivery of s ynchronized s hocks • Energy dos es for s pecific rhythms

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Un s yn c h r o n iz e d vs S yn c h r o n iz e d S h o c k s

Modern defibrillator/cardioverters are capable of delivering 2 types of s hocks : • Uns ynchronized s hocks • Synchronized s hocks An unsynchronized s hock s imply means that the electrical s hock will be delivered as s oon as the operator pus hes the SHOCK button to dis charge the device. Thus , the s hock may fall randomly anywhere within the cardiac cycle. These shocks should use higher energy levels than synchronized cardioversion. Synchronized cardioversion us es a s ens or to deliver a s hock that is s ynchronized with a peak of the QRS complex (eg, the highes t point of the R wave). When this option (the “s ync” option) is engaged, the operator pres s es the SHOCK button to deliver a s hock. There will likely be a delay before the defibrillator/cardioverter delivers a s hock becaus e the device will s ynchronize s hock delivery with the peak of the R wave in the patient’s QRS complex. This s ynchronization may require analys is of s everal complexes . Synchronization avoids the delivery of a s hock during cardiac repolarization (repres ented on the s urface ECG as the T wave), a period of vulnerability in which a s hock can precipitate VF. Synchronized cardiovers ion us es a lower energy level than attempted defibrillation. Low-energy s hocks s hould always be delivered as s ynchronized s hocks to avoid precipitating VF.

P o t e n t ia l P r o b le m s Wit h S yn c h r o n iz a t io n

In theory, s ynchronization is s imple. The operator pus hes the SYNC control on the face of the defibrillator/cardioverter. In practice, however, there are potential problems . For example: • If the R-wave peaks of a tachycardia are undifferentiated or of low amplitude, the monitor s ens ors may be unable to identify an R-wave peak and therefore will not deliver the s hock. • Many cardioverters will not s ynchronize through the handheld quick-look paddles . An unwary practitioner may try to s ynchronize—uns ucces s fully in that the machine will not dis charge—and may not recognize the problem. • Synchronization can take extra time (eg, if it is neces s ary to attach electrodes or if the operator is unfamiliar with the equipment).

Re c o m m e n d a t io n s

Wh e n to Us e Syn c h ron ize d Sh oc ks Synchronized s hocks are recommended for patients with • Uns table • Uns table • Uns table • Uns table

SVT atrial fibrillation atrial flutter regular monomorphic tachycardia with puls es

Wh e n to Us e Un s yn c h ron ize d Sh oc ks Uns ynchronized high-energy s hocks are recommended • For a patient who is puls eles s • For a patient demons trating clinical deterioration (in prearres t), s uch as thos e with s evere s hock or polymorphic VT, when you think a delay in converting the rhythm will res ult in cardiac arres t • When you are uns ure whether monomorphic or polymorphic VT is pres ent in the uns table patient Should the uns ynchronized s hock caus e VF (occurring in only a very s mall minority of patients des pite the theoretical ris k), immediately attempt defibrillation.

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En e r g y Do s e s fo r Ca r d io ve r s io n

Select the energy dos e for the s pecific type of rhythm. For uns table atrial fibrillation: • Monophas ic cardiovers ion: Deliver an initial 200-J s ynchronized s hock. • Biphas ic cardiovers ion: Deliver an initial 120- to 200-J s ynchronized s hock. • In either cas e, increas e the energy dos e in a s tepwis e fas hion for any s ubs equent cardiovers ion attempts . A dos e of 120 J to 200 J is reas onable with a biphas ic waveform. Es calate the s econd and s ubs equent s hock dos e as needed. Cardiovers ion of atrial flutter and SVT generally require les s energy. An initial energy dos e of 50 J to 100 J with a monophas ic or biphas ic waveform is often s ufficient. If the initial 50-J dos e fails , increas e the dos e in a s tepwis e fas hion. Monomorphic VT (regular form and rate) with a puls e res ponds well to monophas ic or biphas ic waveform cardiovers ion (s ynchronized) s hocks at an initial dos e of 100 J . If there is no res pons e to the firs t s hock, increas e the dos e in a s tepwis e fas hion. No s tudies were identified that addres s ed this is s ue. Thus , this recommendation repres ents expert opinion.

S yn c h ro n iz e d Ca rd io ve r s io n Te c h n iq u e In t r o d u c t io n

Synchronized cardiovers ion is the treatment of choice when a patient has a s ymptomatic (uns table) reentry SVT or VT with puls es . It is als o recommended to treat uns table atrial fibrillation and uns table atrial flutter. Cardiovers ion is unlikely to be effective for treatment of junctional tachycardia or ectopic or multifocal atrial tachycardia becaus e thes e rhythms have an automatic focus aris ing from cells that are s pontaneous ly depolarizing at a rapid rate. Delivery of a s hock generally cannot s top thes e rhythms and may actually increas e the rate of the tachyarrhythmia. In s ynchronized cardiovers ion, s hocks are adminis tered through adhes ive electrodes or handheld paddles . You will need to place the defibrillator/monitor in synchronized (sync) mode. The s ync mode is des igned to deliver energy jus t after the R wave of the QRS complex.

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Te c h n iq u e

Follow thes e s teps to perform s ynchronized cardiovers ion. Modify the s teps for your s pecific device.

Ste p

Ac t io n

1

Sedate all cons cious patients unles s uns table or deteriorating rapidly.

2

Turn on the defibrillator (monophas ic or biphas ic).

3

Attach monitor leads to the patient (“white to right, red to ribs , what’s left over to the left s houlder”) and ens ure proper dis play of the patient’s rhythm. Pos ition adhes ive electrode (conductor) pads on the patient.

4

Pres s the SYNC control button to engage the s ynchronization mode.

5

Look for markers on the R wave indicating s ync mode.

6

Adjus t monitor gain if neces s ary until s ync markers occur with each R wave.

7

Select the appropriate energy level. Deliver monophas ic s ynchronized s hocks in the following s equence:

If

In it ia l Do s e *

Uns ta b le a tria l fib rilla tio n

200 J

Uns ta b le m o no m o rp hic VT

100 J

Othe r uns ta b le SVT/Atria l flutte r

50 to 100 J

P o lym o rp hic VT (irre g ula r fo rm a nd ra te ) a nd uns ta b le

Treat as VF with high-energy s hock (defibrillation dos es )

*Biphas ic waveforms us ing lower energy are acceptable if documented to be clinically equivalent or s uperior to reports of monophas ic s hock s ucces s . Extrapolation from elective cardiovers ion of atrial fibrillation s upports an initial biphas ic dos e of 120 J to 200 J with es calation as needed. Cons ult the device manufacturer for s pecific recommendations . 8

Announce to team members : “Charging defibrillator—s tand clear!”

9

Pres s the CHARGE button.

10

Clear the patient when the defibrillator is charged. (See “Foundational Facts : Clearing for Defibrillation” in the VF/Puls eles s VT Cas e.)

11

Pres s the SHOCK button(s ).

12

Check the monitor. If tachycardia pers is ts , increas e the energy level (joules ) according to the Electrical Cardiovers ion Algorithm.

13

Activate the s ync mode after delivery of each s ynchronized s hock. Most defibrillators default back to the unsynchronized mode after delivery of a synchronized shock. This default allows an immediate s hock if cardiovers ion produces VF.

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S t a b le Ta c h yc a rd ia Ca s e In t r o d u c t io n

This cas e reviews as s es s ment and management of a stable patient (ie, no serious signs related to the tachycardia) with a rapid heart rate. Patients with heart rates >100/min have a tachyarrhythmia or tachycardia. In this cas e we will us e the terms tachycardia and tachyarrhythmia interchangeably. Note that s inus tachycardia is excluded from the treatment algorithm. Sinus tachycardia is almos t always phys iologic, developing in res pons e to a compromis e in s troke volume or a condition that requires an increas e in cardiac output (eg, fever, hypovolemia). Treatment involves identification and correction of that underlying problem. You mus t be able to clas s ify the type of tachycardia (wide or narrow; regular or irregular) and implement appropriate interventions as outlined in the Tachycardia Algorithm. During this cas e you will • Perform initial as s es s ment and management • Treat regular narrow-complex rhythms (except s inus tachycardia) with vagal maneuvers and adenos ine If the rhythm does not convert, you will monitor the patient and trans port or obtain expert cons ultation. If the patient becomes clinically uns table, you will prepare for immediate uns ynchronized s hock or s ynchronized cardiovers ion as dis cus s ed in the Uns table Tachycardia Cas e.


By the end of this cas e you s hould be able to 1. Perform an initial patient as s es s ment to identify s ymptoms of a s table tachycardia 2. Identify s inus tachycardia 3. State that treatment of s inus tachycardia involves identification of an underlying caus e 4. Differentiate between tachycardias with narrow or wide QRS complexes 5. Treat s table tachycardias by us ing the Tachycardia Algorithm 6. Verbalize when to cons ider expert cons ultation

Rh yt h m s fo r S t a b le Ta c h yc a r d ia

Tachycardias can be clas s ified in s everal ways bas ed on the appearance of the QRS complex, heart rate, and whether they are regular or irregular: • Narrow–QRS complex (SVT) tachycardias (QRS <0.12 s econd) in order of frequency – Sinus tachycardia – Atrial fibrillation – Atrial flutter – AV nodal reentry • Wide–QRS complex tachycardias (QRS ≥0.12 s econd) – Monomorphic VT – Polymorphic VT • Regular or irregular tachycardias – Irregular narrow-complex tachycardias are probably atrial fibrillation

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Th e ACLS Ca s e s : Sta b le Ta c h yc a rd ia

Dr u g s fo r S t a b le Ta c h yc a r d ia

This cas e involves the following drug: • Adenos ine Several agents are als o us ed to provide analges ia and s edation during electrical cardiovers ion. Thes e agents are not covered in the ACLS Provider Cours e.

Ap p ro a c h t o S t a b le Ta c h yc a rd ia In t r o d u c t io n

In this cas e a s table tachycardia refers to a condition in which the patient has • A heart rate >100/min • No s ignificant s igns or s ymptoms caus ed by the increas ed rate • An underlying cardiac electrical abnormality that generates the rhythm

Qu e s t io n s t o De t e r m in e Cla s s ific a t io n

Clas s ification of the tachycardia depends on the careful clinical evaluation of thes e ques tions : • Are s ymptoms pres ent or abs ent? • Are s ymptoms due to the tachycardia? • Is the patient s table or uns table? • Is the QRS complex narrow or wide? • Is the rhythm regular or irregular? • Is the QRS monomorphic or polymorphic? • Is the rhythm s inus tachycardia? The ans wers guide s ubs equent diagnos is and treatment.

Fo u n d a t io n a l Fa c t s Und e rs ta nd ing Sinus Ta c hyc a rd ia

• Sinus tachycardia is a heart rate that is >100/min and is generated by s inus node dis charge. The heart rate in s inus tachycardia does not exceed 220/min and is agerelated. Sinus tachycardia us ually does not exceed 120 to 130/min, and it has a gradual ons et and gradual termination. Reentry SVT has an abrupt ons et and termination. • Sinus tachycardia is caus ed by external influences on the heart, s uch as fever, anemia, hypotens ion, blood los s , or exercis e. Thes e are s ys temic conditions , not cardiac conditions . Sinus tachycardia is a regular rhythm, although the rate may be s lowed by vagal maneuvers . Cardiovers ion is contraindicated. • ß-Blockers may caus e clinical deterioration if the cardiac output falls when a compensatory tachycardia is blocked. This is becaus e cardiac output is determined by the volume of blood ejected by the ventricles with each contraction (s troke volume) and the heart rate. Cardiac output (CO) = Stroke volume (SV) × Heart rate • If a condition s uch as a large AMI limits ventricular function (s evere heart failure or cardiogenic s hock), the heart compens ates by increas ing the heart rate. If you attempt to reduce the heart rate in patients with a compens atory tachycardia, cardiac output will fall and the patient’s condition will likely deteriorate. In s in u s ta c h yc a rd ia th e g oa l is to id e n tify a n d tre a t th e u n d e rlyin g s ys te m ic cause.

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Ma n a g in g S t a b le Ta c h yc a rd ia : Th e Ta c h yc a rd ia Alg o r it h m In t r o d u c t io n

As noted in the Uns table Tachycardia Cas e, the key to management of a patient with any tachycardia is to determine whether puls es are pres ent, and if puls es are pres ent, to determine whether the patient is s table or uns table and then to provide treatment bas ed on patient condition and rhythm. If the patient is puls eles s , manage the patient according to the Cardiac Arres t Algorithm (Figure 19, page 61). If the patient has puls es , manage the patient according to the Tachycardia Algorithm (Figure 36, page 127).

Ove r vie w

If a tachycardia and a puls e are pres ent, perform as s es s ment and management s teps guided by the BLS Survey and the ACLS Survey. Determine if s ignificant s ymptoms or s igns are pres ent and if thes e s ymptoms and s igns are due to the tachycardia. This will direct you to either the stable (Boxes 5 through 7) or unstable (Box 4) s ection of the algorithm. • If s ignificant s igns or s ymptoms are due to the tachycardia, then the tachycardia is unstable and immediate cardiovers ion is indicated (s ee the Uns table Tachycardia Cas e). • If the patient develops pulseless VT, deliver uns ynchronized high-energy s hocks (defibrillation energy) and follow the Cardiac Arres t Algorithm. • If the patient has polymorphic VT, treat the rhythm as VF and deliver high-energy uns ynchronized s hocks (ie, defibrillation energy). In this cas e the patient is s table, and you will manage according to the s table s ection of the Tachycardia Algorithm (Figure 36). A precis e identification of the rhythm (eg, reentry SVT, atrial flutter) may not be pos s ible at this time.

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1 As s es s appropriatenes s for clinical condition. Heart rate typically ≥150/min if tachyarrhythmia.

2 Id e ntify a nd tre a t und e rlying c a us e

Do s e s /De ta ils

• Maintain patent airway; as s is t breathing as neces s ary • Oxygen (if hypoxemic) • C ardiac monitor to identify rhythm; monitor blood pres s ure and oximetry

Sync hro nize d Ca rd io ve rs io n Initial recommended dos es : • Narrow regular: 50-100 J • Narrow irregular: 120-200 J biphas ic or 200 J monophas ic • Wide regular: 100 J • Wide irregular: defibrillation dos e (NOT s ynchronized)

3 4


5

Ye s

6

No Wid e QRS? ≥0.12 s e c o nd


Ye s

• IV acces s and 12-lead ECG if available • C ons ider adenos ine only if regular and monomorphic • Cons ider antiarrhythmic infus ion • Cons ider expert cons ultation

No

7

• IV acces s and 12-lead ECG if available • Vagal maneuvers • Adenos ine (if regular) • ß-Blocker or calcium channel blocker • Cons ider expert cons ultation

Ad e no s ine IV Do s e : Firs t dos e: 6 mg rapid IV pus h; follow with NS flus h. Second dos e: 12 mg if required. An tia rrh yth m ic In fu s ion s for Sta b le Wid e -QRS Ta c h yc a rd ia P ro c a ina m id e IV Do s e : 20-50 mg/min until arrhythmia s uppres s ed, hypotens ion ens ues , QRS duration increas es >50% , or maximum dos e 17 mg/kg given. Maintenance infus ion: 1-4 mg/min. Avoid if prolonged QT or CHF. Am io d a ro ne IV Do s e : Firs t dos e: 150 mg over 10 minutes . Repeat as needed if VT recurs . Follow by maintenance infus ion of 1 mg/min for firs t 6 hours . So ta lo l IV Do s e : 100 mg (1.5 mg/kg) over 5 minutes . Avoid if prolonged QT.


Fig u re 3 6 . The Tachycardia With a Puls e Algorithm.

Ap p lic a t io n o f t h e Ta c h yc a rd ia Alg o r it h m t o t h e S t a b le P a t ie n t In t r o d u c t io n

In this cas e a patient has stable tachycardia with a pulse. Conduct the s teps outlined in the Tachycardia Algorithm to evaluate and manage the patient.

P a t ie n t As s e s s m e n t (Bo x 1 )

Box 1 directs you to as s es s the patient’s condition. Typically, a heart rate >150/min at res t is due to tachyarrhythmias other than s inus tachycardia.

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BLS a n d ACLS S u r ve ys (Bo x 2 )

Us ing the BLS Survey and the ACLS Survey to guide your approach, evaluate the patient and do the following as neces s ary: • Look for s igns of increas ed work of breathing and hypoxia as determined by puls e oximetry. • Give oxygen; monitor oxygen s aturation. • Support the airway, breathing, and circulation. • Obtain an ECG to identify the rhythm; check blood pres s ure. • Identify and treat revers ible caus es . If s ymptoms pers is t, proceed to Box 3.

De c is io n P o in t : S t a b le o r Un s t a b le (Bo x 3 )

Un s ta b le If the patient is unstable with s igns or s ymptoms as a res ult of the tachycardia (eg, hypotens ion, acutely altered mental s tatus , s igns of s hock, is chemic ches t dis comfort, or AHF), go to Box 4 (perform immediate s ynchronized cardiovers ion). See the Uns table Tachycardia Cas e.

Sta b le If the patient is s table, go to Box 5.

IV Ac c e s s a n d 1 2 -Le a d ECG (Bo x 5 )

If the patient with tachycardia is stable (ie, no s erious s igns or s ymptoms related to the tachycardia), you have time to evaluate the rhythm and decide on treatment options . Es tablis h IV acces s if not already obtained. Obtain a 12-lead ECG (when available) or rhythm s trip to determine if the QRS is narrow (<0.12 s econd) or wide (≥0.12 s econd).

De c is io n P o in t : Na r r o w o r Wid e (Bo x 6 , Bo x 7 )

The path of treatment is now determined by whether the QRS is wide (Box 6) or narrow (Box 7), and whether the rhythm is regular or irregular. If a monomorphic wide-complex rhythm is pres ent and the patient is s table, expert cons ultation is advis ed. Polymorphic wide-complex tachycardia s hould be treated with immediate uns ynchronized cardiovers ion.

Fo u n d a t io n a l Fa c t s Tre a ting Ta c hyc a rd ia

Wid e (Br o a d )Co m p le x Ta c h yc a r d ia s (Bo x 6 )

• You may not always be able to dis tinguis h between s upraventricular (aberrant) and ventricular wide-complex rhythms . If you are uns ure, be aware that mos t widecomplex (broad-complex) tachycardias are ventricular in origin. • If a patient is pulseless, follow the Cardiac Arres t Algorithm. • If a patient becomes unstable, do not delay treatment for further rhythm analys is . For stable patients with wide-complex tachycardias , trans port and monitor or cons ult an expert, becaus e treatment has the potential for harm.

Wide-complex tachycardias are defined as a QRS of ≥0.12 s econd. Consider expert consultation. The mos t common forms of life-threatening wide-complex tachycardias likely to deteriorate to VF are: • Monomorphic VT • Polymorphic VT Determine if the rhythm is regular or irregular. • A regular wide-complex tachycardia is pres umed to be VT or SVT with aberrancy. • An irregular wide-complex tachycardia may be atrial fibrillation with aberrancy, preexcited atrial fibrillation (atrial fibrillation us ing an acces s ory pathway for antegrade conduction), or polymorphic VT/tors ades de pointes . Thes e are advanced rhythms requiring additional expertis e or expert cons ultation.

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If the rhythm is likely VT or SVT in a s table patient, treat bas ed on the algorithm for that rhythm. If the rhythm etiology cannot be determined and is regular in its rate and monomorphic, recent evidence s ugges ts that IV adenos ine is relatively s afe for both treatment and diagnos is . IV antiarrhythmic drugs may be effective. We recommend procainamide, amiodarone, or s otalol. See the right column on the algorithm (Figure 36, page 127) for recommended dos es . In the cas e of irregular wide-complex tachycardia, management focus es on control of the rapid ventricular rate (rate control), convers ion of hemodynamically uns table atrial fibrillation to s inus rhythm (rhythm control), or both. Expert cons ultation is advis ed.

Ca u t io n Drug s to Avo id in P a tie nts With Irre g ula r Wid e -Co m p le x Ta c hyc a rd ia

Na r r o w QRS , Re g u la r Rh yt h m (Bo x 7 )

• Avoid AV nodal blocking agents s uch as adenos ine, calcium channel blockers , digoxin, and pos s ibly ß-blockers in patients with pre-excitation atrial fibrillation, becaus e thes e drugs may caus e a paradoxical increas e in the ventricular res pons e.

The therapy for narrow QRS with regular rhythm is : • Attempt vagal maneuvers • Give adenos ine Vagal maneuvers and adenos ine are the preferred initial interventions for terminating narrow-complex tachycardias that are s ymptomatic and s upraventricular in origin (SVT). Vagal maneuvers alone (Vals alva maneuver or carotid s inus mas s age) will terminate about 25% of SVTs . Adenos ine is required for the remainder. If SVT does not res pond to vagal maneuvers : • Give a d e no s ine 6 mg as a rapid IV pus h in a large (eg, antecubital) vein over 1 s econd. Follow with a 20 mL s aline flus h and elevate the arm immediately. • If SVT does not convert within 1 to 2 minutes , give a s econd dos e of adenos ine 12 mg rapid IV pus h following the s ame procedure above. Adenos ine increas es AV block and will terminate approximately 90% of reentry arrhythmias within 2 minutes . Adenos ine will not terminate atrial flutter or atrial fibrillation but will s low AV conduction, allowing for identification of flutter or fibrillation waves . Adenos ine is s afe and effective in pregnancy. Adenos ine does , however, have s everal important drug interactions . Larger dos es may be required for patients with s ignificant blood levels of theophylline, caffeine, or theobromine. The initial dos e s hould be reduced to 3 mg in patients taking dipyridamole or carbamazepine. There have been recent cas e reports of prolonged as ys tole following adenos ine adminis tration to patients with trans planted hearts or following central venous adminis tration, s o lower dos es s uch as 3 mg may be cons idered in thes e s ituations . Adenos ine may caus e bronchos pas m; therefore, adenos ine s hould not be given to patients with as thma.

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5 If the rhythm converts with adenos ine, it is probable reentry SVT. Obs erve for recurrence. Treat recurrence with adenos ine or longer-acting AV nodal blocking agents s uch as the non-dihydropyridine calcium channel blockers (verapamil and diltiazem) or ß-blockers . Typically you s hould obtain expert cons ultation if the tachycardia recurs . If the rhythm does not convert with adenos ine, it is pos s ible atrial flutter, ectopic atrial tachycardia, or junctional tachycardia. Obtain expert cons ultation about diagnos is and treatment.

Ca u t io n : Wha t to Avo id With AV No d a l Blo c king Ag e nts

Ta c h yc a r d ia Alg o r it h m : Ad va n c e d Ma n a g e m e n t S t e p s

• AV nodal blocking drugs s hould not be us ed for pre-excited atrial fibrillation or flutter. Treatment with an AV nodal blocking agent is unlikely to s low the ventricular rate and in s ome ins tances may accelerate the ventricular res pons e. Caution is advis ed when combining AV nodal blocking agents that have a longer duration of action, s uch as calcium channel blockers or ß-blockers , becaus e their actions may overlap if given s erially, which can provoke profound bradycardia.

Some ACLS providers may be familiar with the differential diagnos is and therapy of s table tachycardias that do not res pond to initial treatment. The bas ic ACLS provider is expected to recognize a s table narrow-complex or wide-complex tachycardia and clas s ify the rhythm as regular or irregular. Regular narrow-complex tachycardias may be treated initially with vagal maneuvers and adenos ine. If thes e are uns ucces s ful, the ACLS provider s hould trans port or seek expert consultation. If ACLS providers have experience with the differential diagnos is and therapy of s table tachycardias beyond initial management, the Tachycardia Algorithm lis ts additional s teps and pharmacologic agents us ed in the treatment of thes e arrhythmias , both for rate control and for termination of the arrhythmia. If a t a n y p oin t you b e c om e u n c e rta in or u n c om forta b le d u rin g th e tre a tm e n t of a s ta b le p a tie n t, s e e k e xp e rt c on s u lta tion . Th e tre a tm e n t of s ta b le p a tie n ts m a y a wa it e xp e rt c on s u lta tion b e c a u s e tre a tm e n t h a s th e p ote n tia l for h a rm .

Ac u t e S t ro k e Ca s e In t r o d u c t io n

The identification and initial management of patients with acute s troke is within the s cope of an ACLS provider. This cas e covers principles of out-of-hospital care and fundamental aspects of initial in-hospital acute stroke care. Out-of-hos pital acute s troke care focus es on • Rapid identification and as s es s ment of patients with s troke • Rapid trans port (with prearrival notification) to a facility capable of providing acute s troke care In-hos pital acute s troke care includes the • Ability to rapidly determine patient eligibility for fibrinolytic therapy • Adminis tration of fibrinolytic therapy to appropriate candidates , with availability of neurologic medical s upervis ion within target times • Initiation of the s troke pathway and patient admis s ion to a s troke unit if available The target times and goals are recommended by the National Ins titute of Neurological Dis orders and Stroke (NINDS), which has recommended meas urable goals for the evaluation of s troke patients . Thes e targets or goals s hould be achieved for at leas t 80% of patients with acute s troke.

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Th e ACLS Ca s e s : Ac u te Stroke


By the end of this cas e you s hould be able to 1. Des cribe the major s igns and s ymptoms of s troke 2. Clas s ify s trokes to explain s troke type–s pecific treatments 3. Demons trate the us e of one of the out-of-hos pital s troke s cales (s creening tools ) to identify patients with s us pected s troke 4. Apply the 8 D’s of Stroke Care 5. Explain why timely action is crucial when s omeone experiences a s troke 6. Follow the Sus pected Stroke Algorithm: NINDS time goals 7. Des cribe why rapid trans port to a healthcare facility capable of providing acute s troke care is recommended 8. Recall general eligibility criteria for fibrinolytic therapy 9. Activate the s troke team

P o t e n t ia l Ar r h yt h m ia s Wit h S t r o k e

The ECG does not take priority over obtaining a computed tomography (CT) s can. No arrhythmias are s pecific for s troke, but the ECG may identify evidence of a recent AMI or arrhythmias s uch as atrial fibrillation as a caus e of an embolic s troke. Many patients with s troke may demons trate arrhythmias , but if the patient is hemodynamically s table, mos t arrhythmias will not require treatment. There is general agreement to recommend cardiac monitoring during the firs t 24 hours of evaluation in patients with acute is chemic s troke to detect atrial fibrillation and potentially life-threatening arrhythmias .

Dr u g s fo r S t r o k e

This cas e involves thes e drugs : • Approved fibrinolytic agent (rtPA) • Glucos e (D50 ) • Labetalol • Nicardipine • Enalaprilat • As pirin • Nitroprus s ide

Fo u n d a t io n a l Fa c t s Ma jo r Typ e s o f Stro ke

Stroke is a general term. It refers to acute neurologic impairment that follows interruption in blood s upply to a s pecific area of the brain. Although expeditious s troke care is important for all patients , this cas e emphas izes reperfus ion therapy for acute is chemic s troke. The major types of s troke are • Is chemic s troke: accounts for 87% of all s trokes and is us ually caus ed by an occlus ion of an artery to a region of the brain (Figure 37). • Hemorrhagic s troke: accounts for 13% of all s trokes and occurs when a blood ves s el in the brain s uddenly ruptures into the s urrounding tis s ue. Fibrinolytic therapy is contraindicated in this type of s troke. Avoid anticoagulants .

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10% 87%

Is c he m ic

3%

Intra c e re b ra l Sub a ra c hno id

Fig u re 3 7 . Types of s troke. Eighty-s even percent of s trokes are is chemic and potentially eligible for fibrinolytic therapy if patients otherwis e qualify. Thirteen percent of s trokes are hemorrhagic, and the majority of thes e are intracerebral. The male-to-female incidence ratio is 1.25 in pers ons 55 to 64 years of age, 1.50 in thos e 65 to 74, 1.07 in thos e 75 to 84, and 0.76 in thos e 85 and older. Blacks have almos t twice the ris k of firs tever s troke compared with whites .

Ap p ro a c h t o S t ro k e Ca re In t r o d u c t io n

Each year in the United States about 795 000 people s uffer a new or recurrent s troke. Stroke remains a leading caus e of death in the United States . Early recognition of acute is chemic s troke is important becaus e IV fibrinolytic treatment s hould be provided as early as pos s ible, generally within 3 hours of ons et of s ymptoms , or within 4.5 hours of ons et of s ymptoms for s elected patients . Mos t s trokes occur at home, and only half of acute s troke patients us e EMS for trans port to the hos pital. Stroke patients often deny or try to rationalize their s ymptoms . Even high-ris k patients , s uch as thos e with atrial fibrillation or hypertens ion, fail to recognize the s igns of s troke. This delays activation of EMS and treatment, res ulting in increas ed morbidity and mortality. Community and profes s ional education is es s ential, and it has been s ucces s ful in increas ing the proportion of eligible s troke patients treated with fibrinolytic therapy. Healthcare providers , hos pitals , and communities mus t continue to develop s ys tems to improve the efficiency and effectivenes s of s troke care.

Fo u n d a t io n a l Fa c t s Stro ke Cha in o f Surviva l

The goal of s troke care is to minimize brain injury and maximize the patient’s recovery. The Stroke Chain of Survival (Figure 38) des cribed by the AHA and the American Stroke As s ociation is s imilar to the Chain of Survival for s udden cardiac arres t. It links actions to be taken by patients , family members , and healthcare providers to maximize s troke recovery. Thes e links are • Rapid • Rapid • Rapid • Rapid

recognition and reaction to s troke warning s igns EMS dis patch EMS s ys tem trans port and prearrival notification to the receiving hos pital diagnos is and treatment in the hos pital

Fig u re 3 8 . The Stroke Chain of Survival. 132


FYI 2 0 1 0 Gu id e lin e s Stro ke Cha in o f Surviva l

Fo u n d a t io n a l Fa c t s The 8 D’s o f Stro ke Ca re

• The background and icons in the figure depicting the s troke Chain of Survival (Figure 38) differ s lightly from thos e in the figure publis hed in the 2006 edition of the ACLS Provider Manual. The figure was revis ed to enhance memorization and avoid confus ion with the adult Chain of Survival (Figure 6, page 26), which is new to the 2011 edition of the Provider Manual.

The 8 D’s of Stroke Care highlight the major s teps in diagnos is and treatment of s troke and key points at which delays can occur: • De te c tio n: Rapid recognition of s troke s ymptoms • Dis p a tc h: Early activation and dis patch of EMS by 911 • De live ry: Rapid EMS identification, management, and trans port • Do o r: Appropriate triage to s troke center • Da ta : Rapid triage, evaluation, and management within the ED • De c is io n: Stroke expertis e and therapy s election • Drug : Fibrinolytic therapy, intra-arterial s trategies • Dis p o s itio n: Rapid admis s ion to the s troke unit or critical care unit For more information on thes e critical elements , s ee the Sus pected Stroke Algorithm (Figure 39).

Go a ls o f S t r o k e Ca r e

The Sus pected Stroke Algorithm (Figure 39) emphas izes important elements of out-ofhos pital care for pos s ible s troke patients . Thes e actions include a s troke s cale or s creen and rapid trans port to the hos pital. As with ACS, prior notification of the receiving hos pital s peeds the care of the s troke patient upon arrival. The NINDS has es tablis hed critical in-hos pital time goals for as s es s ment and management of patients with s us pected s troke. This algorithm reviews the critical in-hos pital time periods for patient as s es s ment and treatment: 1. Immediate general as s es s ment by the s troke team, emergency phys ician, or another expert within 10 minutes of arrival; order urgent noncontras t CT s can 2. Neurologic as s es s ment by the s troke team or des ignee and CT s can performed within 25 minutes of hos pital arrival 3. Interpretation of the CT s can within 45 minutes of ED arrival 4. Initiation of fibrinolytic therapy in appropriate patients (thos e without contraindications ) within 1 hour of hos pital arrival and 3 hours from s ymptom ons et 5. Door-to-admis s ion time of 3 hours

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ACLS_Suspected_StrokeAlgo_NoTables.pdf 1 12/16/10 6:14 PM

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Ad ult Sus p e c te d Stro ke 1

Id e ntify s ig ns a nd s ym p to m s o f p o s s ib le s tro ke Ac tiva te Em e rg e nc y Re s p o ns e 2

Critic a l EMS a s s e s s m e nts a nd a c tio ns • Support ABCs ; give o xyg e n if needed • Perform prehos pital s troke as s es s ment • Es tablis h time of s ymptom ons et (las t normal) • Triage to s troke center • Alert hos pital • Check glucos e if pos s ible

NINDS TIME GOALS

ED Arriva l

3

Im m e d ia te g e ne ra l a s s e s s m e nt a nd s ta b iliza tio n • As s es s ABCs , vital s igns • Provide o xyg e n if hypoxemic • Obtain IV acces s and perform lab oratory as s es s ments • Check glucos e; treat if indicated • Perform neurologic s creening as s es s ment • Activate s troke team • Order emergent CT s can or MRI of brain • Obtain 12-lead ECG

10 m in

ED Arriva l

4

Im m e d ia te ne uro lo g ic a s s e s s m e nt b y s tro ke te a m o r d e s ig ne e • Review patient his tory • Es tablis h time of s ymptom ons et or las t known normal • Perform neurologic examination (NIH Stroke Scale or Canadian Neurological Scale)

25 m in ED Arriva l

5

Doe s CT s ca n s how he m orrha ge ?

45 m in

No He m o r r h a g e

He m o r r h a g e

6

7

Cons ult neurologis t or neuros urgeon; cons ider trans fer if not a vailable

P ro b a b le a c ute is c he m ic s tro ke ; c o ns id e r b rino lytic the ra p y • Check for brinolytic exclus ions • Repeat neurologic exam: are de cits rapidly improving to normal? 8 ED Arriva l 60 m in

9

P a tie n t re m a ins c a nd id a te for b rin olytic th e ra p y? 10

No t a Ca n d id a t e

Ca n d id a t e

Re vie w ris ks /b e ne ts with p a tie n t a n d fa m ily. If a c c e p ta b le : • Give rtPA • No anticoagulants or antiplatelet treatment for 24 hours Stro ke Ad m is s io n 3 ho urs

Adminis te r a s p irin 11

• Begin s troke or he morrhage pa thway • Admit to s troke unit or intens ive ca re unit

12

• Begin pos t-rtPA s troke pathway • Aggres s ively monitor: – BP per protocol – For neurologic d eterioration • Emergent admis s ion to s troke unit or intens ive care unit © 2010 America n Heart As s ociation

Fig u re 3 9 . The Sus pected Stroke Algorithm. 134


Fo u n d a t io n a l Fa c t s : The Na tio na l Ins titute o f Ne uro lo g ic a l Dis o rd e rs a nd Stro ke

Cr it ic a l Tim e P e r io d s

• The NINDS is a branch of the National Ins titutes of Health (NIH). Its mis s ion is to reduce the burden of neurologic dis eas e by s upporting and conducting res earch. NINDS res earchers have s tudied s troke and reviewed data leading to recommendations for acute s troke care. The NINDS has s et critical time goals for as s es s ment and management of s troke patients bas ed on experience obtained in large s tudies of s troke patients .

Patients with acute is chemic s troke have a time-dependent benefit for fibrinolytic therapy s imilar to that of patients with ST-s egment elevation MI, but this time-dependent benefit is much s horter. The critical time period for adminis tration of IV fibrinolytic therapy begins with the ons et of s ymptoms . Critical time periods from hos pital arrival are s ummarized below:

Ap p lic a t io n o f t h e Su s p e c te d Stroke Alg o r it h m

Im m e d ia te g e ne ra l a s s e s s m e nt

10 minutes

Im m e d ia te ne uro lo g ic a s s e s s m e nt

25 minutes

Ac q uis itio n o f CT o f the he a d

25 minutes

Inte rp re ta tio n o f the CT s c a n

45 minutes

Ad m inis tra tio n o f fib rino lytic the ra p y, tim e d fro m ED a rriva l

60 minutes

Ad m inis tra tio n o f fib rino lytic the ra p y, tim e d fro m o ns e t o f s ym p to m s

3 hours , or 4.5 hours in s elected patients

Ad m is s io n to a m o nito re d b e d

3 hours

We will now dis cus s the s teps in the algorithm, as well as other related topics : • Identification of s igns and s ymptoms of pos s ible s troke and activation of emergency res pons e (Box 1) • Critical EMS as s es s ments and actions (Box 2) • Immediate general as s es s ment and s tabilization (Box 3) • Immediate neurologic as s es s ment by the s troke team or des ignee (Box 4) • CT s can: hemorrhage or no hemorrhage (Box 5) • Fibrinolytic therapy ris k s tratification if candidate (Boxes 6, 8, and 10) • General s troke care (Boxes 11 and 12)

Id e n t if c a t io n o S ig n s o P o s s ib le S t ro k e (Bo x 1 ) Wa r n in g S ig n s a n d S ym p t o m s

The s igns and s ymptoms of a s troke may be s ubtle. They include • Sudden weaknes s or numbnes s of the face, arm, or leg, es pecially on one s ide of the body • Sudden confus ion • Trouble s peaking or unders tanding • Sudden trouble s eeing in one or both eyes • Sudden trouble walking • Dizzines s or los s of balance or coordination • Sudden s evere headache with no known caus e 135

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Ac t iva t e EMS S ys t e m Im m e d ia t e ly

Stroke patients and their families mus t be educated to activate EMS as s oon as they detect potential s igns or s ymptoms of s troke. Currently half of all s troke patients are driven to the ED by family or friends . EMS provides the s afes t and mos t efficient method of emergency trans port to the hos pital. The advantages of EMS trans port include the following: • EMS pers onnel can identify and trans port a s troke patient to a hos pital capable of providing acute s troke care and notify the hos pital of the patient’s impending arrival. • Prearrival notification allows the hos pital to prepare to evaluate and manage the patient efficiently. Emergency medical dis patchers als o play a critical role in timely treatment of potential s troke by • Identifying pos s ible s troke patients • Providing high-priority dis patch • Ins tructing bys tanders in lifes aving CPR s kills or other s upportive care if needed while EMS providers are on the way

S t r o k e As s e s s m e n t To o ls

The 2010 AHA Guidelines for CPR and ECC recommends that all EMS pers onnel be trained to recognize s troke us ing a validated, abbreviated out-of-hos pital neurologic evaluation tool s uch as the Cincinnati Prehos pital Stroke Scale (CPSS) (Table 4).

Cin c in n a ti P re h os p ita l Stroke Sc a le The CPSS identifies s troke on the bas is of 3 phys ical findings : • Facial droop (have the patient s mile or try to s how teeth) • Arm drift (have the patient clos e eyes and hold both arms out, with palms up) • Abnormal s peech (have the patient s ay “You can’t teach an old dog new tricks ” By us ing the CPSS, medical pers onnel can evaluate the patient in <1 minute. The pres ence of 1 finding on the CPSS has a s ens itivity of 59% and a s pecificity of 89% when s cored by prehos pital providers . With s tandard training in s troke recognition, paramedics demons trated a s ens itivity of 61% to 66% for identifying patients with s troke. After receiving training in us e of a s troke as s es s ment tool, paramedic s ens itivity for identifying patients with s troke increas ed to 86% to 97% .

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Ta b le 4 . The Cinc inna ti P re ho s p ita l Stro ke Sc a le

Te s t

Fin d in g s

Fa c ia l d ro o p : Have patient s how teeth or s mile (Figure 40)

• No rm a l—both s ides of face move equally • Ab no rm a l—one s ide of face does not move as well as the other s ide

Arm d rift: Patient clos es eyes and extends both arms s traight out, with palms up, for 10 s econds (Figure 41)

• No rm a l—both arms move the s ame or both arms do not move at all (other findings , s uch as pronator drift, may be helpful) • Ab no rm a l—one arm does not move or one arm drifts down compared with the other

Ab no rm a l s p e e c h: Have patient s ay “you can’t teach an old dog new tricks ”

• No rm a l—patient us es correct words with no s lurring • Ab no rm a l—patient s lurs words , us es the wrong words , or is unable to s peak

Interpretation: If any 1 of thes e 3 s igns is abnormal, the probability of a s troke is 72% . The pres ence of all 3 findings indicates that the probability of s troke is >85% . Modified from Kothari RU, Pancioli A, Liu T, Brott T, Broderick J . Cincinnati Prehospital Stroke Scale: reproducibility and validity. Ann Emergency Med. 1999;33:373-378. With permis sion from Elsevier.

Fig u re 4 0 . Facial droop.

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Fig u re 4 1 . One-s ided motor weaknes s (right arm).

Cr it ic a l EMS As s e s s m e n t s a n d Ac t io n s (Bo x 2 ) In t r o d u c t io n

Prehos pital EMS providers mus t minimize the interval between the ons et of s ymptoms and patient arrival in the ED. Specific s troke therapy can be provided only in the appropriate receiving hos pital ED, s o time in the field only delays (and may prevent) definitive therapy. More extens ive as s es s ments and initiation of s upportive therapies can continue en route to the hos pital or in the ED.

Cr it ic a l EMS As s e s s m e n t s a n d Ac t io n s (Bo x 2 )

To provide the bes t outcome for the patient with potential s troke:

Id e n t ify S ig n s

De fin e a n d Re c o g n iz e t h e S ig n s o f S t ro k e (Bo x 1 )

Sup p o rt ABCs

Support the ABCs and provide s upplemental oxygen to hypoxemic (eg, oxygen s aturation <94% ) s troke patients or thos e patients with unknown oxygen s aturation.

P e rfo rm s tro ke a s s e s s m e nt

Perform a rapid out-of-hos pital s troke as s es s ment (CPSS, Table 4).

Es ta b lis h tim e

Determine when the patient was las t known to be normal or at neurologic bas eline. This repres ents time zero. If the patient wakes from s leep with s ymptoms of s troke, time zero is the las t time the patient was s een to be normal.

Tria g e to s tro ke c e nte r

Trans port the patient rapidly and cons ider triage to a s troke center. Support cardiopulmonary function during trans port. If pos s ible, bring a witnes s , family member, or caregiver with the patient to confirm time of ons et of s troke s ymptoms . (continued)

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(continued)

Id e n t ify S ig n s

De fin e a n d Re c o g n iz e t h e S ig n s o f S t ro k e (Bo x 1 )

Ale rt ho s p ita l

Provide prearrival notification to the receiving hos pital.

Che c k g luc o s e

During trans port, check blood glucos e if protocols or medical control allows .

The patient with acute s troke is at ris k for res piratory compromis e from as piration, upper airway obs truction, hypoventilation, and (rarely) neurogenic pulmonary edema. The combination of poor perfus ion and hypoxemia will exacerbate and extend is chemic brain injury, and it has been as s ociated with wors e outcome from s troke. Both out-of-hos pital and in-hos pital medical pers onnel s hould provide s upplementary oxygen to hypoxemic (ie, oxygen s aturation <94% ) s troke patients or patients for whom oxygen s aturation is unknown.

Fo u n d a t io n a l Fa c t s Stro ke Ce nte rs a nd Stro ke Units

Initial evidence indicates a favorable benefit from triage of s troke patients directly to des ignated s troke centers , but the concept of routine out-of-hos pital triage of s troke patients requires continued evaluation. Each receiving hos pital s hould define its capability for treating patients with acute s troke and s hould communicate this information to the EMS s ys tem and the community. Although not every hos pital has the res ources to s afely adminis ter fibrinolytics , every hos pital with an ED s hould have a written plan that des cribes how patients with acute s troke will be managed in that ins titution. The plan s hould • Detail the roles of healthcare providers in the care of patients with acute s troke, including identifying s ources of neurologic expertis e • Define which patients to treat with fibrinolytics at that facility • Des cribe when patient trans fer to another hos pital with a dedicated s troke unit is appropriate Patients with stroke who require hospitalization should be admitted to a stroke unit when a stroke unit with a multidisciplinary team experienced in managing stroke is available within a reasonable transport interval. Studies have documented improvement in 1-year s urvival rate, functional outcomes , and quality of life when patients hos pitalized for acute s troke receive care in a dedicated unit with a s pecialized team.

In -Ho s p it a l, Im m e d ia t e Ge n e r a l As s e s s m e n t a n d S t a b iliz a t io n (Bo x 3 ) In t r o d u c t io n

Once the patient arrives in the ED, a number of as s es s ments and management activities mus t occur quickly. Protocols s hould be us ed to minimize delay in definitive diagnos is and therapy. Th e g oa l of th e s troke te a m , e m e rg e n c y p h ys ic ia n , or oth e r e xp e rts s h ou ld b e to a s s e s s th e p a tie n t with s u s p e c te d s troke with in 10 m inute s o f a rriva l in th e ED: “Tim e Is Bra in ” (Box 3).

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Im m e d ia t e Ge n e r a l As s e s s m e n t a n d S t a b iliz a t io n

ED providers s hould do the following:

Ste p

Ac t io n s

As s e s s ABCs

As s es s the ABCs and evaluate bas eline vital s igns .

P ro vid e o xyg e n

Provide s upplemental oxygen to hypoxemic (eg, oxyhemoglobin s aturation <94% ) s troke patients or thos e patients with unknown oxygen s aturation.

Es ta b lis h IV a c c e s s a nd o b ta in b lo o d s a m p le s

Es tablis h IV acces s and obtain blood s amples for bas eline blood count, coagulation s tudies , and blood glucos e. Do not let this delay obtaining a CT s can of the brain.

Che c k g luc o s e

Promptly treat hypoglycemia.

P e rfo rm ne uro lo g ic a s s e s s m e nt

Perform a neurologic s creening as s es s ment. Us e the NIH Stroke Scale (NIHSS) or a s imilar tool.

Ac tiva te the s tro ke te a m

Activate the s troke team or arrange cons ultation with a s troke expert bas ed on predetermined protocols .

Ord e r CT b ra in scan

Order an emergent CT s can of the brain. Have it read promptly by a qualified phys ician.

Ob ta in 12-le a d ECG

Obtain a 12-lead ECG, which may identify a recent or ongoing AMI or arrhythmias (eg, atrial fibrillation) as a caus e of embolic s troke. A s mall percentage of patients with acute s troke or trans ient is chemic attack have coexis ting myocardial is chemia or other abnormalities . There is general agreement to recommend cardiac monitoring during the firs t 24 hours of evaluation in patients with acute is chemic s troke to detect atrial fibrillation and potentially lifethreatening arrhythmias . Life-threatening arrhythmias can follow or accompany s troke, particularly intracerebral hemorrhage. If the patient is hemodynamically s table, treatment of non–life-threatening arrhythmias (bradycardia, VT, and AV conduction blocks ) may not be neces s ary. Do n ot d e la y th e CT s c a n to ob ta in th e ECG.

Im m e d ia t e Ne u ro lo g ic As s e s s m e n t b y S t ro k e Te a m o r De s ig n e e (Bo x 4 ) Ove r vie w

The s troke team, neurovas cular cons ultant, or emergency phys ician does the following: • Reviews the patient’s his tory, performs a general phys ical examination, and es tablis hes time of s ymptom ons et • Performs a neurologic examination (eg, NIHSS) Th e g oa l for n e u rolog ic a s s e s s m e n t is with in 25 m inute s o f the p a tie nt’s a rriva l in th e ED: “Tim e Is Bra in ” (Box 4).

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Es t a b lis h S ym p t o m On s e t

Es tablis hing the time of s ymptom ons et may require interviewing out-of-hos pital providers , witnes s es , and family members to determine the time the patient was las t known to be normal.

Ne u r o lo g ic Exa m in a t io n

As s es s the patient’s neurologic s tatus us ing one of the more advanced s troke s cales . Following is an example: Na tio na l Ins titute s o f He a lth Stro ke Sc a le The NIHSS us es 15 items to as s es s the res pons ive s troke patient. This is a validated meas ure of s troke s everity bas ed on a detailed neurologic examination. A detailed dis cus s ion is beyond the s cope of the ACLS Provider Cours e.

CT S c a n : He m o r r h a g e o r No He m o r r h a g e (Bo x 5 ) In t r o d u c t io n

A critical decis ion point in the as s es s ment of the patient with acute s troke is the performance and interpretation of a noncontras t CT s can to differentiate is chemic from hemorrhagic s troke. As s es s ment als o includes identifying other s tructural abnormalities that may be res pons ible for the patient’s s ymptoms or that repres ent contraindication to fibrinolytic therapy. The initial noncontras t CT s can is the mos t important tes t for a patient with acute s troke. • If a CT s can is not readily available, s tabilize and promptly trans fer the patient to a facility with this capability. • Do not give as pirin, heparin, or rtPA until the CT s can has ruled out intracranial hemorrhage. The CT s ca n s hould be c om ple te d within 25 m inute s of the pa tie nt’s a rriva l in the ED a nd s hould be re a d within 45 m inute s from ED a rriva l: “Tim e Is Bra in” (Box 5).

De c is io n P o in t : He m o r r h a g e o r No He m o r r h a g e

Additional imaging techniques s uch as CT perfus ion, CT angiography, or magnetic res onance imaging s cans of patients with s us pected s troke s hould be promptly interpreted by a phys ician s killed in neuroimaging interpretation. Obtaining thes e s tudies s hould not delay initiation of IV rtPA in eligible patients . The pres ence of hemorrhage vers us no hemorrhage determines the next s teps in treatment (Figures 42A and B).

Ye s , He m orrh a g e Is P re s e n t If hemorrhage is noted on the CT s can, the patient is not a candidate for fibrinolytics . Cons ult a neurologis t or neuros urgeon. Cons ider trans fer for appropriate care (Box 7).

No, He m orrh a g e Is Not P re s e n t If the CT s can s hows no evidence of hemorrhage and no s ign of other abnormality (eg, tumor, recent s troke), the patient may be a candidate for fibrinolytic therapy (Boxes 6 and 8). If hemorrhage is not pres ent on the initial CT s can and the patient is not a candidate for fibrinolytics for other reas ons , cons ider giving as pirin (Box 9) either rectally or orally after performing a s wallowing s creen (s ee below). Although as pirin is not a time-critical intervention, it is appropriate to adminis ter as pirin in the ED if the patient is not a candidate for fibrinolys is . The patient mus t be able to s afely s wallow before as pirin is given orally. Otherwis e us e the s uppos itory form.

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A

Is chemic Penumbra

Infarcted Brain Tis s ue

B

Fig u re 4 2 . Occlus ion in a cerebral artery by a thrombus . A, Area of infarction s urrounding immediate s ite and dis tal portion of brain tis s ue after occlus ion. B, Area of is chemic penumbra (is chemic, but not yet infarcted [dead] brain tis s ue) s urrounding areas of infarction. This is chemic penumbra is alive but dys functional becaus e of altered membrane potentials . The dys function is potentially revers ible. Current s troke treatment tries to keep the area of permanent brain infarction as s mall as pos s ible by preventing the areas of revers ible brain is chemia in the penumbra from trans forming into larger areas of irrevers ible brain infarction.

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Fib r in o lyt ic Th e r a p y In t r o d u c t io n

Several s tudies have s hown a higher likelihood of good to excellent functional outcome when rtPA is given to adults with acute is chemic s troke within 3 hours of ons et of s ymptoms , or within 4.5 hours of ons et of s ymptoms for s elected patients . But thes e res ults are obtained when rtPA is given by phys icians in hos pitals with a s troke protocol that rigorous ly adheres to the eligibility criteria and therapeutic regimen of the NINDS protocol. Evidence from pros pective randomized s tudies in adults als o documents a greater likelihood of benefit the earlier treatment begins . The AHA and s troke guidelines recommend giving IV rtPA to patients with acute is chemic s troke who meet the NINDS eligibility criteria if it is given by • Phys icians us ing a clearly defined ins titutional protocol • A knowledgeable interdis ciplinary team familiar with s troke care • An ins titution with a commitment to comprehens ive s troke care and rehabilitation The s uperior outcomes reported in both community and tertiary care hos pitals in the NINDS trials can be difficult to replicate in hos pitals with les s experience in, and ins titutional commitment to, acute s troke care. There is s trong evidence to avoid all delays and treat patients as s oon as pos s ible. Failure to adhere to protocol is as s ociated with an increas ed rate of complications , particularly ris k of intracranial hemorrhage.

Eva lu a t e fo r Fib r in o lyt ic Th e r a p y (Bo x 6 )

If the CT s can is negative for hemorrhage, the patient may be a candidate for fibrinolytic therapy. Immediately perform further eligibility and ris k s tratification: • If the CT s can s hows no hemorrhage, the probability of acute is chemic s troke remains . Review inclusion and exclusion criteria for IV fibrinolytic therapy (Table 5) and repeat the neurologic exam (NIHSS or Canadian Neurological Scale). • If the patient’s neurologic function is rapidly improving toward normal, fibrinolytics may be unneces s ary. Ta b le 5 . Inc lus io n a nd Exc lus io n Cha ra c te ris tic s o f P a tie nts With Is c he m ic Stro ke Who Co uld Be Tre a te d With rtPA Within 3 Hou rs Fro m Sym p to m Ons e t*

In c lu s io n Cr it e r ia • Diagnos is of is chemic s troke caus ing meas urable neurologic deficit • Ons et of s ymptoms <3 hours before beginning treatment • Age ≥18 years

Exc lu s io n Cr it e r ia • Head trauma or prior s troke in previous 3 months • Symptoms s ugges t s ubarachnoid hemorrhage • Arterial puncture at noncompres s ible s ite in previous 7 days • His tory of previous intracranial hemorrhage • Elevated blood pres s ure (s ys tolic >185 mm Hg or dias tolic >110 mm Hg) • Evidence of active bleeding on examination • Acute bleeding diathes is , including but not limited to – Platelet count <100 000/mm 3 – Heparin received within 48 hours , res ulting in an aPTT greater than the upper limit of normal – Current us e of anticoagulant with INR >1.7 or PT >15 s econds • Blood glucos e concentration <50 mg/dL (2.7 mmol/L) • CT demons trates multilobar infarction (hypodens ity >¹⁄³ cerebral hemis phere) (continued) 143

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Re la t ive Exc lu s io n Cr it e r ia Recent experience s ugges ts that under s ome circums tances —with careful cons ideration and weighing of ris k to benefit—patients may receive fibrinolytic therapy des pite 1 or more relative contraindications . Cons ider ris k to benefit of rtPA adminis tration carefully if any one of thes e relative contraindications is pres ent: • Only minor or rapidly improving s troke s ymptoms (clearing s pontaneous ly) • Seizure at ons et with pos tictal res idual neurologic impairments • Major s urgery or s erious trauma within previous 14 days • Recent gas trointes tinal or urinary tract hemorrhage (within previous 21 days ) • Recent acute myocardial infarction (within previous 3 months ) Abbreviations : aPTT, activated partial thromboplas tin time; INR, international normalized ratio; PT, prothrombin time; rtPA, recombinant tis s ue plas minogen activator. *Adams HP J r, del Zoppo G, Alberts MJ , Bhatt DL, Bras s L, Furlan A, Grubb RL, Higas hida RT, J auch EC, Kidwell C, Lyden PD, Morgenstern LB, Qureshi AI, Ros enwas ser RH, Scott PA, Wijdicks EFM. Guidelines for the early management of adults with is chemic s troke: a guideline from the American Heart Ass ociation/ American Stroke Ass ociation Stroke Council, Clinical Cardiology Council, Cardiovascular Radiology and Intervention Council, and the Atheros clerotic Peripheral Vascular Disease and Quality of Care Outcomes in Research Interdisciplinary Working Groups . Stroke. 2007;38:1655-1711.

P o t e n t ia l Ad ve r s e Effe c t s

As with all drugs , fibrinolytics have potential advers e effects . At this point weigh the patient’s ris k for advers e events agains t the potential benefit and dis cus s with the patient and family. • Confirm that no exclus ion criteria are pres ent (Table 5). • Cons ider ris ks and benefits . • Be prepared to monitor and treat any potential complications . The major complication of IV rtPA for s troke is intracranial hemorrhage. Other bleeding complications may occur and may range from minor to major. Angioedema and trans ient hypotens ion may occur.

P a t ie n t Is a Ca n d id a t e fo r Fib r in o lyt ic Th e r a p y (Bo xe s 8 a n d 1 0 )

If the patient remains a candidate for fibrinolytic therapy (Box 8), dis cus s the ris ks and potential benefits with the patient or family if available (Box 10). After this dis cus s ion, if the patient or family members decide to proceed with fibrinolytic therapy, give the patient rtPA. Begin your ins titution’s s troke rtPA protocol, often called a “pathway of care.” Do n ot a d m in is te r a n tic oa g u la n ts or a n tip la te le t tre a tm e n t for 24 h ou rs a fte r a d m in is tra tion of rtPA, typ ic a lly u n til a follow-u p CT s c a n a t 24 h ou rs s h ows n o in tra c ra n ia l h e m orrh a g e .

Ext e n d e d IV r t PA Win d o w 3 t o 4 .5 Ho u r s

144

Treatment of carefully s elected patients with acute is chemic s troke with IV rtPA between 3 and 4.5 hours after ons et of s ymptoms has als o been s hown to improve clinical outcome, although the degree of clinical benefit is s maller than that achieved with treatment within 3 hours . Data s upporting treatment in this time window come from a large, randomized trial (ECASS-3 [European Cooperative Acute Stroke Study]) that s pecifically enrolled patients between 3 and 4.5 hours after s ymptom ons et, as well as a meta-analys is of prior trials .


At pres ent, us e of IV rtPA within the 3- to 4.5-hour window has not yet been approved by the US Food and Drug Adminis tration (FDA), although it is recommended by an AHA/ American Stroke As s ociation s cience advis ory. Adminis tration of IV rtPA to patients with acute is chemic s troke who meet the NINDS or ECASS-3 eligibility criteria (Table 6) is recommended if rtPA is adminis tered by phys icians in the s etting of a clearly defined protocol, a knowledgeable team, and ins titutional commitment. Ta b le 6 . Inc lus io n a nd Exc lus io n Cha ra c te ris tic s o f P a tie nts With Is c he m ic Stro ke Who Co uld Be Tre a te d With rtPA Fro m 3 to 4.5 Ho urs Fro m Sym p to m Ons e t*

In c lu s io n Cr it e r ia • Diagnos is of is chemic s troke caus ing meas urable neurologic deficit • Ons et of s ymptoms 3 to 4.5 hours before beginning treatment

Exc lu s io n Cr it e r ia • Age >80 years • Severe s troke (NIHSS >25) • Taking an oral anticoagulant regardles s of INR • His tory of both diabetes and prior is chemic s troke No te s • The checklis t includes s ome US FDA–approved indications and contraindications for adminis tration of rtPA for acute is chemic s troke. Recent AHA/ASA guideline revis ions may differ s lightly from FDA criteria. A phys ician with expertis e in acute s troke care may modify this lis t. • Ons et time is either witnes s ed or las t known normal. • In patients without recent us e of oral anticoagulants or heparin, treatment with rtPA can be initiated before availability of coagulation s tudy res ults but s hould be dis continued if INR is >1.7 or PT is elevated by local laboratory s tandards . • In patients without a his tory of thrombocytopenia, treatment with rtPA can be initiated before availability of platelet count but s hould be dis continued if platelet count is <100 000/mm 3 . Abbreviations : FDA, Food and Drug Adminis tration; INR, international normalized ratio; NIHSS, National Ins titutes of Health Stroke Scale; PT, prothrombin time; rtPA, recombinant tis s ue plas minogen activator.

*del Zoppo

GJ , Saver J L, J auch EC, Adams HP J r; on behalf of the American Heart As s ociation Stroke Council. Expans ion of the time window for treatment of acute is chemic s troke with intravenous tis s ue plas minogen activator: a s cience advis ory from the American Heart As s ociation/American Stroke As s ociation. Stroke. 2009;40:2945-2948.

In t r a -a r t e r ia l r t PA

Improved outcome from us e of cerebral intra-arterial rtPA has been documented. For patients with acute is chemic s troke who are not candidates for s tandard IV fibrinolys is , cons ider intra-arterial fibrinolys is in centers with the res ources and expertis e to provide it within the firs t 6 hours after ons et of s ymptoms . Intra-arterial adminis tration of rtPA is not yet approved by the FDA.

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Ge n e r a l S t ro k e Ca re (Bo xe s 1 1 a n d 1 2 ) In t r o d u c t io n

The general care of all patients with s troke includes the following: • Begin s troke pathway. • Support airway, breathing, and circulation. • Monitor blood glucos e. • Monitor blood pres s ure. • Monitor temperature. • Perform dys phagia s creening. • Monitor for complications of s troke and fibrinolytic therapy. • Trans fer to general intens ive care if indicated.

Be g in S t r o k e P a t h w a y (Bo xe s 1 1 and 12)

Admit patients to a s troke unit (if available) for careful obs ervation (Box 11), including monitoring of blood pres s ure and neurologic s tatus . If neurologic s tatus wors ens , order an emergent CT s can. Determine if cerebral edema or hemorrhage is the caus e; cons ult neuros urgery as appropriate. Additional s troke care includes s upport of the airway, oxygenation, ventilation, and nutrition. Provide normal s aline to maintain intravas cular volume (eg, approximately 75 to 100 mL/h) if needed.

Mo n it o r Blo o d Glu c o s e

Hyperglycemia is as s ociated with wors e clinical outcome in patients with acute is chemic s troke. But there is no direct evidence that active glucos e control improves clinical outcome. There is evidence that ins ulin treatment of hyperglycemia in other critically ill patients improves s urvival rates . For this reas on, cons ider giving IV or s ubcutaneous ins ulin to lower blood glucos e in patients with acute is chemic s troke when the s erum glucos e level is >185 mg/dL.

Mo n it o r fo r Co m p lic a t io n s of Stroke a n d Fib r in o lyt ic Th e r a p y

Prophylaxis for s eizures is not recommended. But treatment of acute s eizures followed by adminis tration of anticonvuls ants to prevent further s eizures is recommended. Monitor the patient for s igns of increas ed intracranial pres s ure. Continue to control blood pres s ure to reduce the potential ris k of bleeding.

Hyp e r t e n s io n Ma n a g e m e n t in r t PA Ca n d id a t e s

Although management of hypertens ion in the s troke patient is controvers ial, patients who are candidates for fibrinolytic therapy s hould have their blood pres s ure controlled to lower the ris k of intracerebral hemorrhage following adminis tration of rtPA. General guidelines for the management of hypertens ion are outlined in Tables 7 and 8. If patient is eligible for fibrinolytic therapy, blood pres s ure mus t be ≤185 mm Hg s ys tolic and ≤110 mm Hg dias tolic to limit the ris k of bleeding complications . Becaus e the maximum interval from ons et of s troke until effective treatment of s troke with rtPA is limited, mos t patients with s us tained hypertens ion above thes e levels will not be eligible for IV rtPA.

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Ta b le 7 . P o te ntia l Ap p ro a c he s to Arte ria l Hyp e rte ns io n in P a tie nts With Ac ute Is c he m ic Stro ke Who Are P ote ntia l Ca nd id a te s fo r Ac ute Re p e rfus io n The ra p y*

Patient otherwis e eligible for acute reperfus ion therapy except that blood pres s ure is >185/110 mm Hg: • Labetalol 10-20 mg IV over 1-2 minutes , may repeat × 1, or • Nicardipine IV 5 mg per hour, titrate up by 2.5 mg per hour every 5-15 minutes , maximum 15 mg per hour; when des ired blood pres s ure is reached, lower to 3 mg per hour, or • Other agents (hydralazine, enalaprilat, etc) may be cons idered when appropriate If blood pres s ure is not maintained at or below 185/110 mm Hg, do not adminis ter rtPA. Management of blood pres s ure during and after rtPA or other acute reperfus ion therapy: Monitor blood pres s ure every 15 minutes for 2 hours from the s tart of rtPA therapy, then every 30 minutes for 6 hours , and then every hour for 16 hours . If s ys tolic blood pres s ure 180-230 mm Hg or dias tolic blood pres s ure 105-120 mm Hg: • Labetalol 10 mg IV followed by continuous IV infus ion 2-8 mg per minute, or • Nicardipine IV 5 mg per hour, titrate up to des ired effect by 2.5 mg per hour every 5-15 minutes , maximum 15 mg per hour If blood pres s ure not controlled or dias tolic blood pres s ure >140 mm Hg, cons ider s odium nitroprus s ide. *Adams HP J r, del Zoppo G, Alberts MJ , Bhatt DL, Bras s L, Furlan A, Grubb RL, Higas hida RT, J auch EC, Kidwell C, Lyden PD, Morgens tern LB, Qures hi AI, Ros enwas s er RH, Scott PA, Wijdicks EFM. Guidelines for the early management of adults with is chemic s troke: a guideline from the American Heart As s ociation/ American Stroke As s ociation Stroke Council, Clinical Cardiology Council, Cardiovas cular Radiology and Intervention Council, and the Atheros clerotic Peripheral Vas cular Dis eas e and Quality of Care Outcomes in Res earch Interdis ciplinary Working Groups . Stroke. 2007;38:1655-1711.

Ta b le 8 . Ap p ro a c h to Arte ria l Hyp e rte ns io n in P a tie nts With Ac ute Is c he m ic Stro ke Who Are Not P o te ntia l Ca nd id a te s fo r Ac ute Re p e rfus io n The ra p y*

Cons ider lowering blood pres s ure in patients with acute is chemic s troke if s ys tolic blood pres s ure >220 mm Hg or dias tolic blood pres s ure >120 mm Hg. Cons ider blood pres s ure reduction as indicated for other concomitant organ s ys tem injury: • Acute myocardial infarction • Conges tive heart failure • Acute aortic dis s ection A reas onable target is to lower blood pres s ure by 15% to 25% within the firs t day. *Adams HP J r, del Zoppo G, Alberts MJ , Bhatt DL, Bras s L, Furlan A, Grubb RL, Higas hida RT, J auch EC, Kidwell C, Lyden PD, Morgens tern LB, Qures hi AI, Ros enwas s er RH, Scott PA, Wijdicks EFM. Guidelines for the early management of adults with is chemic s troke: a guideline from the American Heart As s ociation/ American Stroke As s ociation Stroke Council, Clinical Cardiology Council, Cardiovas cular Radiology and Intervention Council, and the Atheros clerotic Peripheral Vas cular Dis eas e and Quality of Care Outcomes in Res earch Interdis ciplinary Working Groups . Stroke. 2007;38:1655-1711.

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Ap p e n d ix

149

Ma n a g e m e n t o f Re s p ir a t o r y Ar re s t Ba g -Ma s k Ve n t ila t io n Te s t in g Ch e c k lis t Student Name: ______________________________________________________________ Tes t Date: _______________________ if d o n e c o r re c t ly

P e r fo r m a n c e Gu id e lin e s a n d Cr it ic a l Ac t io n s BLS S u r ve y a n d In t e r ve n t io n s Checks for res pons ivenes s • Taps and s houts , “Are you all right? ” and • Scans ches t for movement (5-10 s econds ) Activates the emergency res pons e s ys tem • Activates the emergency res pons e s ys tem and gets the AED or • Directs s econd res cuer to activate the emergency res pons e s ys tem and get the AED Checks carotid puls e (5-10 s econds ). Notes that puls e is pres ent Does not initiate ches t compres s ions or attach AED Performs ventilations at the correct rate of 1 breath every 5-6 s econds (10-12 breaths per minute)

ACLS S u r ve y Ca s e S k ills Ins erts oropharyngeal or nas opharyngeal airway Adminis ters oxygen Performs correct bag-mas k ventilation for 1 minute

Cr it ic a l Ac t io n s Effectively ventilates with a bag-mas k device for 1 minute Gives proper ventilation—rate and volume STOP TEST Te s t Re s ults

Circ le P o r NR to Ind ic a te P a s s o r Ne e d s Re m e d ia tio n:

Ins tructor s ignature affirms that s kills tes ts were done according to AHA Guidelines . Save this sheet with course record.

P

NR

Ins tructor Signature: ________________________________________________ Print Ins tructor Name: _____________________________________________ Date: ________________

151

CP R a n d AED S k ills Te s t 1 -Re s c u e r Ad u lt CP R a n d AED Ch e c k lis t Student Name: ______________________________________________________________ Tes t Date: _______________________

S k ill Ste p

if d o n e c o r re c t ly

Cr it ic a l P e r fo r m a n c e S t e p s

BLS S u r ve y a n d In t e r ve n t io n s 1

Checks for res pons ivenes s : Taps and shouts, “Are you all right? ” and scans the chest for movement (5-10 seconds)

2

Tells s omeone to activate the emergency res pons e s ys tem and get an AED

3

Checks carotid puls e (minimum 5 seconds; maximum 10 seconds)

4

Bares patient’s ches t and locates CPR hand pos ition

5

Delivers firs t cycle of compres s ions at correct rate (acceptable: 18 seconds or less for 30 compressions)

6

Gives 2 breaths (1 s econd each)

AED Ar r ive s AED 1

Turns AED on, s elects proper pads , and places pads correctly

AED 2

Clears patient to analyze (must be visible and verbal check)

AED 3

Clears patient to s hock/pres s es s hock button (must be visible and verbal check; maximum time from AED arrival less than 45 seconds)

S t u d e n t Co n t in u e s CP R 7

Delivers s econd cycle of compres s ions at correct hand pos ition (acceptable: greater than 23 of 30 compressions)

8

Gives 2 breaths (1 s econd each) with vis ible ches t ris e

The next step is performed only if the manikin is equipped with a feedback device, such as a clicker or light. If there is no feedback device, STOP THE TEST. 9

Delivers third cycle of compres s ions of adequate depth with complete ches t recoil (acceptable: greater than 23 compressions) STOP TEST

Te s t Re s ults



NR


152

P

Me g a c o d e Te s t in g Ch e c k lis t 1 / 2 Br a d yc a rd ia VF/ P u ls e le s s VT

As ys t o le

ROS C

Student Name: ______________________________________________________________ Tes t Date: _______________________ if d o n e c o r re c t ly

Cr it ic a l P e r fo r m a n c e S t e p s Te a m Le a d e r Ens ures high-quality CPR at all times As s igns team member roles Ens ures that team members perform well

Br a d yc a rd ia Ma n a g e m e n t Starts oxygen if needed, places monitor, s tarts IV Places monitor leads in proper pos ition Recognizes s ymptomatic bradycardia Adminis ters correct dos e of atropine Prepares for s econd-line treatment

VF/ P u ls e le s s VT Ma n a g e m e n t Recognizes VF Clears before ANALYZE and SHOCK Immediately res umes CPR after s hocks Appropriate airway management Appropriate cycles of drug–rhythm check/s hock–CPR Adminis ters appropriate drug(s ) and dos es

As ys t o le Ma n a g e m e n t Recognizes as ys tole Verbalizes potential revers ible caus es of as ys tole/PEA (H’s and T’s ) Adminis ters appropriate drug(s ) and dos es Immediately res umes CPR after rhythm checks

P o s t –Ca rd ia c Ar re s t Ca re Identifies ROSC Ens ures BP and 12-lead ECG are performed, O 2 s aturation is monitored, verbalizes need for endotracheal intubation and waveform capnography, and orders laboratory tes ts Cons iders therapeutic hypothermia STOP TEST Te s t Re s ults



P

NR


153

Me g a c o d e Te s t in g Ch e c k lis t 3 Ta c h yc a rd ia VF/ P u ls e le s s VT

P EA

ROS C



Ta c h yc a rd ia Ma n a g e m e n t Starts oxygen if needed, places monitor, s tarts IV Places monitor leads in proper pos ition Recognizes uns table tachycardia Recognizes s ymptoms due to tachycardia Performs immediate s ynchronized cardiovers ion


P EA Ma n a g e m e n t Recognizes PEA Verbalizes potential revers ible caus es of PEA/as ys tole (H’s and T’s ) Adminis ters appropriate drug(s ) and dos es Immediately res umes CPR after rhythm and puls e checks




NR


154

P


P EA

ROS C



Ta c h yc a rd ia Ma n a g e m e n t Starts oxygen if needed, places monitor, s tarts IV Places monitor leads in proper pos ition Recognizes tachycardia (s pecific diagnos is ) Recognizes no s ymptoms due to tachycardia Attempts vagal maneuvers Gives appropriate initial drug therapy






P

NR

Ins tructor Signature: ________________________________________________ Print Ins tructor Name: _____________________________________________ Date: ________________ 155


P EA

ROS C



Ta c h yc a rd ia Ma n a g e m e n t Starts oxygen if needed, places monitor, s tarts IV Places monitor leads in proper pos ition Recognizes uns table tachycardia Recognizes s ymptoms due to tachycardia Performs immediate s ynchronized cardiovers ion






NR


156

P


P EA

ROS C



Ta c h yc a rd ia Ma n a g e m e n t Starts oxygen if needed, places monitor, s tarts IV Places monitor leads in proper pos ition Recognizes tachycardia (s pecific diagnos is ) Recognizes no s ymptoms due to tachycardia Gives appropriate initial drug therapy






P

NR


157

Ca rd ia c Ar re s t VF/ P u ls e le s s VT Le a r n in g S t a t io n Ch e c k lis t CP R Qua lity

1

Sta rt CP R

No

Ye s

2

ETCO

9

3 Sh oc k Re turn o f Sp o nta ne o us Circ ula tio n (ROSC)

4

ETCO

No

Sho c k Ene rg y

Ye s

5

Sh oc k

10

6 Ep ine p hrine

Ep ine p hrine Drug The ra p y

No

Ye s

Ye s

7

Sh oc k

No

11

8

No

Ye s

12 Go to 5 o r 7 10

158

11

H H H H H T T T T T

Ca rd ia c Ar re s t P EA/ As ys t o le Le a r n in g S t a t io n Ch e c k lis t CP R Qua lity

Ad ult Ca rd ia c Arre s t Shout for He lp/Ac tiva te Em e rge nc y Re s po ns e compres s ions

1

Sta rt CP R 30:2 compres s ionYe s

No


2

ETCO2

9

VF/VT

capnography attempt to improve

As ys to le /P EA

3 Shoc k Re turn o f Sp o nta ne o us Circ ula tio n (ROSC)

4

CP R 2 m in increas e in P ETCO 2


No

Sho c k Ene rg y

Ye s

5

6

Shoc k

10

CP R 2 m in


-

CP R 2 m in

capnography

Drug The ra p y

capnography


360 J


Va s o p re s s in

No


Ye s epinephrine

Ye s

7

Shoc k

No Ad va nc e d Airwa y

11

8

CP R 2 m in

CP R 2 m in

Am io d a ro ne

compres s ions No


Ye s

12 Go to 5 o r 7 10 or 11


Re ve rs ib le Ca us e s – H – H – H – H – Hypothermia – T – T – T – T – T

159

Im m e d ia t e P o s t –Ca rd ia c Ar re s t Ca re Le a r n in g S t a t io n Ch e c k lis t

Ad ult Im m e d ia te P o s t–Ca rd ia c Arre s t Ca re 1 Re turn o f Sp o nta ne o us Circ ula tio n (ROSC)

2 Op tim ize ve ntila tio n a nd o xyg e na tio n • Maintain oxygen s aturation ≥94% • Cons ider advanced airway and waveform capnography • Do not hyperventilate

3 Tre a t hyp o te ns io n (SBP <90 m m Hg ) • IV/IO bolus • Vas opres s or infus ion • Cons ider treatable caus es • 12-Lead ECG

4

5 No

Co ns id e r ind uc e d hyp o the rm ia

Fo llo w c o m m a nd s ?

6

7 Ye s

Co ro na ry re p e rfus io n

8

Ye s STEMI OR high s us picion of AMI No Ad va nc e d c ritic a l c a re


160

Do s e s /De ta ils Ve ntila tio n/Oxyg e na tio n Avoid exces s ive ventilation. Start at 10-12 breaths /min and titrate to target P e t c o 2 of 35-40 mm Hg. When feas ible, titrate Fio 2 to minimum neces s ary to achieve Sp o 2 ≥94% . IV Bo lus 1-2 L normal s aline or lactated Ringer’s . If inducing hypothermia, may us e 4°C fluid. Ep ine p hrine IV Infus io n: 0.1-0.5 mcg/kg per minute (in 70-kg adult: 7-35 mcg per minute) Do p a m ine IV Infus io n: 5-10 mcg/kg per minute No re p ine p hrine IV Infus io n: 0.1-0.5 mcg/kg per minute (in 70-kg adult: 7-35 mcg per minute) Re ve rs ib le Ca us e s – Hypovolemia – Hypoxia – Hydrogen ion (acidos is ) – Hypo-/hyperkalemia – Hypothermia – Tens ion pneumothorax – Tamponade, cardiac – Toxins – Thrombos is , pulmonary – Thrombos is , coronary

Br a d yc a rd ia Le a r n in g S t a t io n Ch e c k lis t

Ad ult Bra d yc a rd ia (With Puls e)

1

As s es s appropriatenes s for clinical condition. Heart rate typically <50/min if bradyarrhythmia.

2 Id e ntify a nd tre a t und e rlying c a us e • Maintain patent airway; as s is t breathing as neces s ary • Oxygen (if hypoxemic) • Cardiac monitor to identify rhythm; monitor blood pres s ure and oximetry • IV acces s • 12-Lead ECG if available; don’t delay therapy

3 P e rs is te nt b ra d ya rrhythm ia c a us ing :

4 Mo nito r a nd o b s e rve

No

• Hypotens ion? • Acutely altered mental s tatus ? • Signs of s hock? • Is chemic ches t dis comfort? • Acute heart failure? Ye s

5

Atro p ine If atropine ineffective: • Trans cutaneous pacing OR • Do p a m ine infus ion OR • Ep ine p hrine infus ion

Do s e s /De ta ils Atro p ine IV Do s e : Firs t dos e: 0.5 mg bolus Repeat every 3-5 minutes Maximum: 3 mg Do p a m ine IV Infus io n: 2-10 mcg/kg per minute Ep ine p hrine IV Infus io n: 2-10 mcg per minute

6 Co ns id e r: • Expert cons ultation • Trans venous pacing © 2010 American Heart As s ociation

161

Ta c h yc a rd ia Le a r n in g S t a t io n Ch e c k lis t


1 As s es s appropriatenes s for clinical cond ition. Heart rate typically ≥150/min if tachyarrhythmia.

2 Id e ntify a nd tre a t und e rlying c a u s e

Do s e s /De ta ils

• Maintain patent airway; as s is t breathing as neces s ary • Oxygen (if hypoxemic) • C ard iac monitor to identify rhythm; monitor b lood pres s ure and oximetry

Sync hro nize d Ca rd io ve rs io n Initial recommend ed dos es : • Narrow regular: 50-100 J • Narrow irregular: 120-200 J b iphas ic or 200 J monophas ic • Wide regular: 100 J • Wide irregular: defibrillation dos e (NOT s ynchronized)

3 4


5

7

Ye s

6

No Wid e QRS? ≥0.12 s e c o nd


Ye s

• IV acces s and 12-lead ECG if availab le • C ons ider adenos ine only if regular and monomorp hic • Cons ider antiarrhythmic infus ion • Cons ider exp ert cons ultation

No • IV acces s and 12-lead ECG if available • Vagal maneuvers • Adenos ine (if regular) • ß-Blocker or calcium channel blocker • Cons id er expert cons ultation

An tia rrh yth m ic In fu s ion s for Sta b le Wid e -QRS Ta c h yc a rd ia P ro c a ina m id e IV Do s e : 20-50 mg/min until arrhythmia s up pres s ed, hypotens ion ens ues , QRS duration increas es >50% , or maximum d os e 17 mg/kg given. Maintenance infus ion: 1-4 mg/min. Avoid if prolonged QT or CHF. Am io d a ro ne IV Do s e : Firs t dos e: 150 mg over 10 minutes . Repeat as needed if VT recurs . Follow by maintenanc e infus ion of 1 mg/min for firs t 6 hours . So ta lo l IV Do s e : 100 mg (1.5 mg/kg) over 5 minutes . Avoid if prolonged QT.


162

Ad e no s ine IV Do s e : Firs t dos e: 6 mg rapid IV pus h; follow with NS flus h. Second dos e: 12 mg if required .

2 0 1 0 AHA Gu id e lin e s fo r CP R a n d ECC S u m m a r y Ta b le To p ic Sys te m a tic Ap p ro a c h: BLS Surve y

2 0 0 5 Gu id e lin e s

2 0 1 0 Gu id e lin e s

• A-B-C-D: Airway, Breathing, Circulation, Defibrillation • “Look, lis ten, and feel” for breathing and give 2 res cue breaths

• 1-2-3-4 1. Che c k re s p o ns ive ne s s . 2. Ac tiva te the e m e rg e nc y re s p o ns e s ys te m a nd g e t a n AED. 3. Circ ula tio n: Check the carotid puls e. If you cannot detect a puls e within 10 s econds , s tart CPR, beginning with ches t compres s ions , immediately. 4. De fib rilla tio n: If indicated, deliver a s hock with an AED or defibrillator.

To p ic BLS: Hig h-Qua lity CP R

2 0 1 0 Gu id e lin e s • A rate of a t le a s t 100 ches t compres s ions per minute • A compres s ion depth of a t le a s t 2 inc he s in adults • Allowing complete ches t recoil after each compres s ion • Minimizing interruptions in compres s ions (10 s econds or les s ) • Switching providers about every 2 minutes to avoid fatigue • Avoiding exces s ive ventilation

ACLS: Ca rd ia c Arre s t a nd Bra d yc a rd ia Alg o rithm s

• The 2010 AHA Guidelines for CPR and ECC s implifies the Cardiac Arres t Alogorithm and includes a circular algorithm. • The priority is the 2-minute continuous period of high-quality CPR and defibrillation. • All advanced interventions —including IV acces s , drug delivery, and advanced airways —s hould not interrupt ches t compres s ions and s hocks . Rather, they s hould be performed or adminis tered s trategically a fte r the brief paus e for defibrillation. • Thes e actions continue until ROSC, when healthcare providers initiate pos t–cardiac arres t care protocols . • During cardiac arres t, providers s hould adminis ter a vas opres s or every 3 to 5 minutes . Epinephrine is commonly us ed, although vas opres s in can replace the firs t or s econd dos e of epinephrine. Regardles s of the vas opres s or given, one s hould be adminis tered every 3 to 5 minutes . ACLS providers s hould adminis ter amiodarone for refractory VF and VT. • The American Heart As s ociation no longer recommends atropine for routine us e in managing PEA or as ys tole. • For treatment of undifferentiated wide-complex tachycardia with regular rhythm, ACLS providers can cons ider adenos ine in the initial treatment. • Atropine remains the firs t-line treatment for all s ymptomatic bradycardias , regardles s of type. • For s ymptomatic bradycardia, the American Heart As s ociation now recommends IV infus ion of chronotropic agents as an equally effective alternative to external trans cutaneous pacing when atropine is ineffective. (continued)

163

(continued)

To p ic ACLS: Ta c hyc a rd ia – Sync hro nize d Ca rd io ve rs io n

2 0 1 0 Gu id e lin e s • The 2010 AHA Guidelines for CPR and ECC s implifies the Tachycardia Algorithm. • For cardiovers ion of uns table atrial fibrillation, the 2010 AHA Guidelines for CPR and ECC recommends that the initial biphas ic energy dos e be between 120 and 200 J . Cardiovers ion with monophas ic waveforms s hould begin at 200 J and increas e in a s tepwis e fas hion if not s ucces s ful. • For cardiovers ion of uns table SVT or uns table atrial flutter, the 2010 AHA Guidelines for CPR and ECC recommends that the initial monophas ic or biphas ic energy dos e be between 50 to 100 J . • The 2010 AHA Guidelines for CPR and ECC als o recommends cardiovers ion for uns table monomorphic VT, with an initial energy dos e of 100 J . • If the initial s hock fails , providers s hould increas e the dos e in a s tepwis e fas hion.

ACLS: P o s t–Ca rd ia c Arre s t Ca re

A new s ection focus ing on pos t–cardiac arres t care was introduced in the 2010 AHA Guidelines for CPR and ECC. Recommendations aimed at improving s urvival after ROSC include • Optimizing cardiopulmonary function and vital organ perfus ion, es pecially to the brain and heart • Trans porting out-of-hos pital cardiac arres t patients to an appropriate facility with pos t–cardiac arres t care that includes acute coronary interventions , neurologic care, goal-directed critical care, and hypothermia • Trans porting in-hos pital cardiac arres t patients to a critical care unit capable of providing comprehens ive pos t–cardiac arres t care • Identifying and treating the caus es of the arres t and preventing recurrence • Cons idering therapeutic hypothermia to optimize s urvival and neurologic recovery in comatos e patients • Identifying and treating acute coronary s yndromes • Optimizing mechanical ventilation to minimize lung injury • Gathering data for prognos is • As s is ting patients and families with rehabilitation s ervices if needed Critic a l a c tio ns fo r p o s t–c a rd ia c a rre s t c a re : • Hemodynamic optimization, including a focus on treating hypotens ion • Acquis ition of a 12-lead ECG • Induction of therapeutic hypothermia • Monitoring advanced airway placement and ventilation s tatus with quantitative waveform capnography in intubated patients • Optimizing arterial oxygen s aturation

ACLS: Ma na g ing the Airwa y

• The 2010 AHA Guidelines for CPR and ECC recommends us ing waveform capnography to monitor the amount of carbon dioxide exhaled by the patient and to verify placement of an endotracheal tube. • Cricoid pres s ure s hould not be us ed routinely during cardiac arres t. This technique is difficult to mas ter and may not be effective for preventing as piration. It may als o delay or prevent placement of an advanced airway. • Agonal gas ps are not effective breaths and s hould not be confus ed with normal breathing.

Hig h-Qua lity P a tie nt Ca re : Sys te m s o f Ca re 164

• Integrated s ys tems of care s hould include community members , EMS, phys icians , and hos pitals .

ACLS P h a r m a c o lo g y S u m m a r y Ta b le Dr u g Ad e no s ine

Am io d a ro ne

In d ic a t io n s

P re c a u t io n s / Co n t r a in d ic a t io n s

Ad u lt Do s a g e

• Firs t drug for mos t forms of s table narrow-complex SVT. Effective in terminating thos e due to reentry involving AV node or s inus node • May cons ider for uns table narrow-complex reentry tachycardia while preparations are made for cardiovers ion • Regular and monomorphic wide-complex tachycardia, thought to be or previous ly defined to be reentry SVT • Does not convert atrial fibrillation, atrial flutter, or VT • Diagnos tic maneuver: s table narrow-complex SVT

• Contraindicated in pois on/ drug-induced tachycardia or s econd- or third-degree heart block • Trans ient s ide effects include flus hing, ches t pain or tightnes s , brief periods of as ys tole or bradycardia, ventricular ectopy • Les s effective (larger dos es may be required) in patients taking theophylline or caffeine • Reduce initial dos e to 3 mg in patients receiving dipyridamole or carbamazepine, in heart trans plant patients , or if given by central venous acces s • If adminis tered for irregular, polymorphic wide-complex tachycardia/VT, may caus e deterioration (including hypotens ion) • Trans ient periods of s inus bradycardia and ventricular ectopy are common after t ermination of SVT • Safe and effective in pregnancy

IV Ra p id P us h • Place patient in mild revers e Trendelenburg pos ition before adminis tration of drug • Initial bolus of 6 mg given rapidly over 1 to 3 s econds followed by NS bolus of 20 mL; then elevate the extremity • A s econd dos e (12 mg) can be given in 1 to 2 minutes if needed

Becaus e its us e is as s ociated with toxicity, amiodarone is indicated for us e in patients with life-threatening arrhythmias when adminis tered with appropriate monitoring:

Ca u tion : Multip le c o m p le x d rug inte ra c tio ns

VF/VT Ca rd ia c Arre s t Unre s p o ns ive to CP R, Sho c k, a nd Va s o p re s s o r

• Rapid infus ion may lead to hypotens ion • With multiple dos ing, cumulative dos es >2.2 g over 24 hours are as s ociated with s ig• VF/puls eles s VT unres pons ive nificant hypotens ion in clinical to s hock delivery, CPR, and a trials vas opres s or • Do not adminis ter with other • Recurrent, hemodynamically drugs that prolong QT interval uns table VT (eg, procainamide) With expert consultation amiod• Terminal elimination is arone may be us ed for treatment extremely long (half-life las ts of s ome atrial and ventricular up to 40 days ) arrhythmias

Inje c tio n Te c hniq ue • Record rhythm s trip during adminis tration • Draw up adenos ine dos e and flus h in 2 s eparate s yringes • Attach both s yringes to the IV injection port clos es t to patient • Clamp IV tubing above injection port • Pus h IV adenos ine as quickly as possible (1 to 3 s econds ) • While maintaining pres s ure on adenos ine plunger, pus h NS flus h as rapidly as possible after adenos ine • Unclamp IV tubing

• Firs t d o s e : 300 mg IV/IO pus h • Se c o nd d o s e (if ne e d e d ): 150 mg IV/IO pus h Life -Thre a te ning Arrhythm ia s Ma xim um c um ula tive d o s e : 2.2 g IV over 24 hours . May be adminis tered as follows : • Ra p id infus io n: 150 mg IV over firs t 10 minutes (15 mg per minute). May repeat rapid infus ion (150 mg IV) every 10 minutes as needed • Slo w infus io n: 360 mg IV over 6 hours (1 mg per minute) • Ma inte na nc e infus io n: 540 mg IV over 18 hours (0.5 mg per minute) (continued)

165

(continued)

Dr u g Atro p ine Sulfa te Can be given via endotracheal tube

In d ic a t io n s • Firs t drug for s ymptomatic s inus bradycardia • May be beneficial in pres ence of AV nodal block. No t like ly to b e e ffe c tive fo r typ e II s e c o nd -d e g re e o r third d e g re e AV b lo c k o r a b lo c k in no n-no d a l tis s ue • Routine us e during PEA or as ys tole is unlikely to have a therapeutic benefit • Organophos phate (eg, nerve agent) pois oning: extremely large dos es may be needed

P re c a u t io n s / Co n t r a in d ic a t io n s • Us e with caution in pres ence of myocardial is chemia and hypoxia. Increas es myocardial oxygen demand • Avoid in hypothermic bradycardia • May not be effective for infranodal (type II) AV block and new third-degree block with wide QRS complexes . (In thes e patients may caus e paradoxical s lowing. Be prepared to pace or give catecholamines ) • Dos es of atropine <0.5 mg may res ult in paradoxical s lowing of heart rate

Ad u lt Do s a g e Bra d yc a rd ia (With o r Witho ut ACS) • 0.5 mg IV every 3 to 5 minutes as needed, not to exceed total dos e of 0.04 mg/kg (total 3 mg) • Us e s horter dos ing interval (3 minutes ) and higher dos es in s evere clinical conditions Org a no p ho s p ha te P o is o ning Extremely large dos es (2 to 4 mg or higher) may be needed

Do p a m ine IV infusion

• Second-line drug for s ymp• Correct hypovolemia with tomatic bradycardia (after volume replacement before atropine) initiating dopamine • Us e for hypotens ion (SBP ≤70 • Us e with caution in cardioto 100 mm Hg) with s igns and genic s hock with accompanys ymptoms of s hock ing CHF • May caus e tachyarrhythmias , exces s ive vas ocons triction • Do not mix with s odium bicarbonate

Ep ine p hrine Can be given via endotracheal tube

• Ca rd ia c a rre s t: VF, puls eles s • Rais ing blood pres s ure and Ca rd ia c Arre s t VT, as ys tole, PEA increas ing heart rate may • IV/IO d o s e : 1 mg (10 mL of caus e myocardial is chemia, 1:10 000 s olution) adminis • Sym p to m a tic b ra d yc a rd ia : angina, and increas ed myotered every 3 to 5 minutes Can be cons idered after atrocardial oxygen demand during res us citation. Follow pine as an alternative infus ion each dos e with 20 mL flus h, to dopamine • High dos es do not improve elevate arm for 10 to 20 s ecs urvival or neurologic out• Se ve re hyp o te ns io n: Can be onds after dos e come and may contribute to us ed when pacing and atropos tres us citation myocardial • Hig he r d o s e : Higher dos es pine fail, when hypotens ion dys function (up to 0.2 mg/kg) may be accompanies bradycardia, us ed for s pecific indications or with phos phodies teras e • Higher dos es may be required (ß-blocker or calcium channel enzyme inhibitor to treat pois on/drug-induced blocker overdos e) s hock • Ana p hyla xis , s e ve re a lle rg ic • Co ntinuo us infus io n: Initial re a c tio ns : Combine with large rate: 0.1 to 0.5 mcg/kg per fluid volume, corticos teroids , minute (for 70-kg patient: 7 to antihis tamines 35 mcg per minute); titrate to res pons e • End o tra c he a l ro ute : 2 to 2.5 mg diluted in 10 mL NS

Available in 1:10 000 and 1:1000 concentrations

IV Ad m inis tra tio n • Us ual infus ion rate is 2 to 20 mcg/kg per minute • Titrate to patient res pons e; taper s lowly

P ro fo und Bra d yc a rd ia o r Hyp o te ns io n 2 to 10 mcg per minute infus ion; titrate to patient res pons e (continued)

166

(continued)

Dr u g Lid o c a ine Can be given via endotracheal tube

In d ic a t io n s • Alternative to amiodarone in cardiac arres t from VF/VT • Stable monomorphic VT with pres erved ventricular function • Stable polymorphic VT with normal bas eline QT interval and pres erved LV function when is chemia is treated and electrolyte balance is corrected • Can be us ed for s table polymorphic VT with bas eline QT-interval prolongation if tors ades s us pected

P re c a u t io n s / Co n t r a in d ic a t io n s • Co ntra ind ic a tio n: Prophylactic us e in AMI is contraindicated • Reduce maintenance dos e (not loading dos e) in pres ence of impaired liver function or LV dys function • Dis continue infus ion immediately if s igns of toxicity develop

Ad u lt Do s a g e Ca rd ia c Arre s t Fro m VF/VT • Initial dos e: 1 to 1.5 mg/kg IV/IO • For refractory VF may give additional 0.5 to 0.75 mg/kg IV pus h, repeat in 5 to 10 minutes ; maximum 3 dos es or total of 3 mg/kg P e rfus ing Arrhythm ia For s table VT, wide-complex tachycardia of uncertain type, s ignificant ectopy: • Dos es ranging from 0.5 to 0.75 mg/kg and up to 1 to 1.5 mg/kg may be us ed • Repeat 0.5 to 0.75 mg/kg every 5 to 10 minutes ; maximum total dos e: 3 mg/kg Ma inte na nc e Infus io n 1 to 4 mg per minute (30 to 50 mcg/kg per minute)

Ma g ne s ium Sulfa te

Va s o p re s s in Can be given via endotracheal tube

• Recommended for us e in cardiac arres t only if tors ades de pointes or s us pected hypomagnes emia is pres ent • Life-threatening ventricular arrhythmias due to digitalis toxicity • Routine adminis tration in hos pitalized patients with AMI is no t recommended

• Occas ional fall in blood pres s ure with rapid adminis tration • Us e with caution if renal failure is pres ent

• May be us ed as alternative pres s or to epinephrine in treatment of adult s hockrefractory VF • May be us eful alternative to epinephrine in as ys tole, PEA • May be us eful for hemodynamic s upport in vas odilatory s hock (eg, s eptic s hock)

• Potent peripheral vas ocons trictor. Increas ed peripheral vas cular res is tance may provoke cardiac is chemia and angina • Not recommended for res pons ive patients with coronary artery dis eas e

Ca rd ia c Arre s t (Due to Hyp o m a g ne s e m ia o r To rs a d e s d e P o inte s ) 1 to 2 g (2 to 4 mL of a 50% s olution diluted in 10 mL [eg, D5 W, normal s aline] given IV/IO) To rs a d e s d e P o inte s With a P uls e o r AMI With Hyp o m a g ne s e m ia • Loading dose of 1 to 2 g mixed in 50 to 100 mL of diluent (eg, D5 W, normal s aline) over 5 to 60 minutes IV • Follow with 0.5 to 1 g per hour IV (titrate to control tors ades ) IV Ad m inis tra tio n Ca rd ia c a rre s t: One dos e of 40 units IV/IO pus h may replace either firs t or s econd dos e of epinephrine. Epinephrine can be adminis tered every 3 to 5 minutes during cardiac arres t Va s o d ila to ry s ho c k: Continuous infus ion of 0.02 to 0.04 units per minute

167

Glo s s a r y A Ac ute

Having a s udden ons et and s hort cours e

Ac ute m yo c a rd ia l infa rc tio n (AMI)

The early critical s tage of necros is of heart mus cle tis s ue caus ed by blockage of a coronary artery

Ad va nc e d c a rd io va s c ula r life s up p o rt (ACLS)

Emergency medical procedures in which bas ic life s upport efforts of CPR are s upplemented with drug adminis tration, IV fluids , etc

As ys to le

Abs ence of electrical and mechanical activity in the heart

Atria l fib rilla tio n

In atrial fibrillation the atria “quiver” chaotically and the ventricles beat irregularly

Atria l flutte r

Rapid, irregular atrial contractions due to an abnormality of atrial excitation

Atrio ve ntric ula r b lo c k

A delay in the normal flow of electrical impuls es that caus e the heart to beat

Auto m a te d e xte rna l d e fib rilla to r (AED)

A portable device us ed to res tart a heart that has s topped

B Ba s ic life s up p o rt (BLS)

Emergency treatment of a victim of cardiac or res piratory arres t through cardiopulmonary res us citation and emergency cardiovas cular care

Bra d yc a rd ia

Slow heartbeat, whether phys iologically or pathologically

C Ca p no g ra p hy

The meas urement and graphic dis play of CO 2 levels in the airways , which can be performed by infrared s pectros copy

Ca rd ia c a rre s t

Temporary or permanent ces s ation of the heartbeat

Ca rd io p ulm o na ry re s us c ita tio n (CP R)

A bas ic emergency procedure for life s upport, cons is ting of mainly manual external cardiac mas s age and s ome artificial res piration

Co ro na ry s ynd ro m e

A group of clinical s ymptoms compatible with acute myocardial is chemia (als o called coronary heart disease)

Co ro na ry thro m b o s is

The blocking of the coronary artery of the heart by a thrombus

E

168

Ele c tro c a rd io g ra m (ECG)

A tes t that provides a typical record of normal heart action

Enc e p ha lo p a thy

Degeneration of brain function. Als o called cephalopathy, cerebropathy.

End o tra c he a l intub a tio n

The pas s age of a tube through the nos e or mouth into the trachea for maintenance of the airway

Es o p ha g e a l d e te c to r d e vic e

A dis pos able tool us ed to verify proper endotracheal tube placement by us ing the anatomical differences between the trachea and es ophagus

Es o p ha g e a l-tra c he a l tub e

A double-lumen tube with inflatable balloon cuffs that s eal off the hypopharynx from the oropharynx and es ophagus ; us ed for airway management

H Hyd ro g e n io n (a c id o s is )

The accumulation of acid and hydrogen ions or depletion of the alkaline res erve (bicarbonate content) in the blood and body tis s ues , decreas ing the pH

Hyp e rka le m ia

An abnormally high concentration of potas s ium ions in the blood. Als o called hyperpotassemia.

Hyp o g lyc e m ia

An abnormally low concentration of glucos e in the blood

Hyp o ka le m ia

An abnormally low concentration of potas s ium ions in the blood. Als o called hypopotassemia.

Hyp o the rm ia

A potentially fatal condition that occurs when body temperature falls below 95°F (35°C)

Hyp o vo le m ia

A decreas e in the volume of circulating blood

Hyp o xia

A deficiency of oxygen reaching the tis s ues of the body

I Intra o s s e o us (IO)

Within a bone

Intra ve no us (IV)

Within a vein

M Mild hyp o the rm ia

When the patient’s body temperature is between 90 and 95°F

Mo d e ra te hyp o the rm ia

When the patient’s body temperature is between 86 and 90°F

N Na s o p ha ryng e a l

Pertaining to the nos e and pharynx

O Oro p ha ryng e a l a irwa y

A tube us ed to provide free pas s age of air between the mouth and pharynx

P P e rfus io n

The pas s age of fluid (s uch as blood) through a s pecific organ or area of the body (s uch as the heart)

P ro p hyla xis

Prevention of or protection agains t dis eas e

P ulm o na ry e d e m a

A condition in which fluid accumulates in the lungs

P uls e le s s e le c tric a l a c tivity (P EA)

Continued electrical rhythmicity of the heart in the abs ence of effective mechanical function

R Re c o m b ina nt tis s ue p la s m ino g e n a c tiva to r (rtPA)

A clot-dis s olving s ubs tance produced naturally by cells in the walls of blood ves s els

S Se ve re hyp o the rm ia

When the patient’s body temperature is <86°F

Sinus rhythm

The rhythm of the heart produced by impuls es from the s inoatrial node

Sup ra g lo ttic

Situated or occurring above the glottis

Sync hro nize d c a rd io ve rs io n

Us es a s ens or to deliver a s hock that is s ynchronized with a peak in the QRS complex 169

Sync o p e

A los s of cons cious nes s over a s hort period of time, caus ed by a temporary lack of oxygen in the brain

T Ta c hyc a rd ia

Increas ed heartbeat, us ually ≥100/min

Ta m p o na d e (c a rd ia c )

A condition caus ed by accumulation of fluid between the heart and the pericardium, res ulting in exces s pres s ure on the heart. This impairs the heart’s ability to pump s ufficient blood.

Te ns io n p ne um o tho ra x

Pneumothorax res ulting from a wound in the ches t wall which acts as a valve that permits air to enter the pleural cavity but prevents its es cape

Thro m b us

A blood clot formed within a blood ves s el

U Uns ync hro nize d s ho c k

An electrical s hock that will be delivered as s oon as the operator pus hes the SHOCK button to dis charge the defibrillator. Thus , the s hock can fall anywhere within the cardiac cycle.

V

170

Ve ntric ula r fib rilla tio n (VF)

Very rapid uncoordinated fluttering contractions of the ventricles

Ve ntric ula r ta c hyc a rd ia (VT)

A rapid heartbeat that originates in one of the lower chambers (ventricles ) of the heart

Fo u n d a t io n In d e x A Acute coronary s yndromes

91

Amiodarone

72

Antiarrhythmic drugs

71

As pirin

97

As ys tole

86

Atrioventricular (AV) block

105

Atropine

110

B Bag-mas k

42

Bradycardia

104

D Defibrillation

54

Dopamine

76, 112

E Endotracheal tube s uctioning procedure

46

Epinephrine

65

Es ophageal-tracheal tube

48

F Fibrinolytic therapy

102

Firs t-degree AV block

105

H Head tilt–chin lift

40

Heparin

104

I IV/IO acces s

69

L Laryngeal mas k airway

47

Lidocaine

72

Lone healthcare provider

14

M Magnes ium s ulfate

72

Morphine

97

N Nitroglycerin

97

O Oropharyngeal s uctioning procedure

46

Oxygen

38 171

P Paddles vers us pads

64

Puls eles s electrical activity (PEA)

78

Puls eles s VT

59

R Recombinant tis s ue plas minogen activator (rtPA)

144

Refractory VF

59

Reteplas e

102

S Second-degree AV block

105

Streptokinas e

102

ST-s egment elevation myocardial infarction (STEMI)

101

T Tachycardia

114

Tenecteplas e

102

Third-degree AV block

105

Trans cutaneous pacing (TCP)

111

V Vas opres s in

65

Vas opres s or agents

65

Ventricular fibrillation (VF)

59

Ventricular tachycardia (VT)

128

Y Yankauer

172

45

In d e x Abbreviations us ed, 7-9 ABCD approach, 7, 163 Accelerated idioventricular rhythm (AIVR), 7, 113 ACE inhibitors in acute coronary s yndromes , 94, 103 Acetyls alicylic acid

emergency department as s es s ment and treatment in, 29, 94, 99-100 emergency medical s ervices in, 29, 92, 95, 96-98; algorithm on, 94 goals o therapy in, 29, 92-93

in acute coronary s yndromes , 96, 100

pathophys iology o , 93

in s troke, 131, 134, 141

percutaneous coronary interventions in, 93, 102-103;

Acidos is , 169 as ys tole/PEA in, 83

primary, 92, 93, 102; res cue, 102; in ST-s egment elevation, 100, 101, 102-103

Cardiac Arres t Algorithm on, 61, 66, 80, 82, 158, 159

puls eles s electrical activity in, 85

Pos t–Cardiac Arres t Care Algorithm on, 73, 160

s igns and s ymptoms in, 96

ACLS. See Advanced cardiovas cular li e s upport ACLS cas es , 33-147 on acute coronary s yndromes , 91-104

time to treatment in, 94, 95, 99, 100, 101; in f brinolytic therapy, 102; in percutaneous coronary interventions , 102-103

on acute s troke, 130-147

Acute Coronary Syndromes Algorithm, 94, 95-104

on as ys tole, 86-91

Acute s troke, 30, 130-147. See also Stroke

on bradycardia, 104-114

Adenos ine in tachycardia, 125, 129-130, 165

on lone res cuer CPR and AED us e in VF/puls eles s VT, 49-58 overview o , 33

algorithm on, 118, 127, 162 ß-Adrenergic blockers

on puls eles s electrical activity, 78-85


on re ractory VF/puls eles s VT, 59-77

in tachycardia, 125, 129, 130; algorithm on, 118, 127, 162

on res piratory arres t, 34-49

Advanced cardiovas cular li e s upport, 7

on s table tachycardia, 124-130

def nition o , 168

on uns table tachycardia, 114-123

provider cours e on (see Provider Cours e)

ACLS Provider Manual, 4-5, 6 abbreviations us ed in, 7-9 ACLS Survey, 11, 14-16

s urvey in (see ACLS Survey) s ys temic approach in, 11 AED. See Automated external def brillator

in as ys tole, 81, 88, 89

Agonal gas ps , 55

in bradycardia, 108, 110

Airway as s es s ment and management, 15

in puls eles s electrical activity, 78, 81

in as ys tole, 82, 86, 88, 159

in res piratory arres t, 36-37, 151

in bradycardia, 109, 110, 161

in s table tachycardia, 126, 128

Cardiac Arres t Algorithm on, 61, 80, 82, 158, 159

in uns table tachycardia, 116, 119

in cervical s pine trauma, 39, 40, 49

in ventricular f brillation/puls eles s VT, 62

changes in 2010 Guidelines , 164

Acute coronary s yndromes , 7, 29, 91-104

in pos t–cardiac arres t care, 73, 74, 75, 160

algorithm on, 94, 95-104

in puls eles s electrical activity, 81, 82, 159

bradycardia in, 113, 114

in res piratory arres t, 36, 38-49

drug therapy in, 92, 93, 96, 102; adjunctive, 103-104;

in s troke, 146

algorithm on, 94; in emergency department, 100; in prehos pital care, 97-98; in ST-s egment elevation, 100, 101

in tachycardia with puls e, 119, 128; algorithm on, 118, 127, 162 in ventricular f brillation/puls eles s VT, 61, 66, 158 173

I n d e x AIVR (accelerated idioventricular rhythm), 7, 113 Algorithms

drug therapy in, 111 rs t-degree, 105, 106

on acute coronary s yndromes , 94, 95-104

s econd-degree, 105, 106, 111, 112, 114

on as ys tole, 60, 61, 79, 86, 88-89, 159

third-degree, 105, 106, 111, 112, 114

on bas ic li e s upport, 52-53

trans cutawneous pacing in, 112, 113, 114

on bradycardia, 108-112, 161 on pos t–cardiac arres t care, 72-77, 160

Atrioventricular nodal blocking drugs , precautions in us e o , 129, 130

on puls eles s electrical activity, 60, 61, 78, 79-82, 159

Atrioventricular nodal reentry tachycardia, 124

on s troke, 133-147

Atropine s ul ate, 166

on tachycardia with puls e, 118, 127, 162; s table, 126-130; uns table, 116-120 on ventricular brillation/puls eles s VT, 60-69, 158 Amiodarone, 165

in as ys tole/puls eles s electrical activity, 81, 88 in bradycardia, 106, 108, 166; algorithm on, 109, 161; in treatment s equence, 110, 111, 113 Automated external de brillator, 7, 13

Cardiac Arres t Algorithm on, 61, 80, 82, 158, 159

ches t hair a ecting, 57-58

in tachycardia with puls e, 129; algorithm on, 118, 127, 162

de nition o , 168

in ventricular brillation/puls eles s VT, 66, 72, 158, 165

electrode pad placement, 55, 56, 57

Angina, uns table, 9, 93, 95 electrocardiography and ris k clas s i cation in, 101 Angiotens in-converting enzyme inhibitors , in acute coronary s yndromes , 94, 103 Antiarrhythmic drugs

implanted pacemaker a ecting, 58 lay res cuer us ing, 54 in lone res cuer, 49-58, 152 in res piratory arres t, 34, 35 trans dermal medication patches a ecting, 58

in tachycardia with puls e, 129; algorithm on, 118, 127, 162

univers al s teps in operation o , 55-56

in ventricular brillation/puls eles s VT, 65-66, 71-72

in ventricular brillation/puls eles s VT: and CPR, 52, 53, 54,

Anti-inf ammatory drugs , nons teroidal, 8 contraindications in ACS, 98 Arm dri t in s troke, 136, 137

57; and lone res cuer, 49-58; s teps in us e o , 55-57; troubles hooting problems with, 57 water a ecting, 58

As pirin in acute coronary s yndromes , 96, 100 in s troke, 131, 134, 141 As ys tole, 86-91 as agonal rhythm con rming death, 90 Cardiac Arres t Algorithm on, 60, 61, 79, 86, 88-89, 159

in cardiac arres t, 36, 47 E-C clamp technique, 41 in 2 res cuers , 41 Bas ic li e s upport, 7

common caus es o , 86, 88

de nition o , 168

de nition o , 168

prerequis ite s kills required, 2

drug therapy in, 86, 88; algorithm on, 61, 80, 82, 159

s ummary o 2010 Guidelines on, 163

duration o res us citation e orts in, 87, 90

s urvey in (see BLS Survey)

ethical is s ues in, 90

s ys temic approach in, 11

Megacode evaluation o s kills in, 153

Benchmarks on CPR per ormance and outcome, 27

termination o res us citation e orts in, 86, 87, 89-90

ß-Blockers

trans port o patients in, 91


treatment s equence in, 82, 86, 89


Atheros cleros is , acute coronary s yndromes in, 93 Atrial brillation and f utter, 114, 124, 128 cardiovers ion in, 116, 121, 122, 123

Biphas ic de brillators , 63, 66 Cardiac Arres t Algorithm on, 61, 80, 82, 158, 159 Blood pres s ure, 9

de nitions o , 168

in hypotens ion (see Hypotens ion)

drug therapy in, 129


s troke in, 131, 140

in res piratory arres t, 37

Atrioventricular block

174

Bag-mas k ventilation, 36, 41, 42, 151

in s troke, 146-147

bradycardia in, 105, 106, 111, 112, 113

BLS. See Bas ic li e s upport

de nition o , 168

BLS Survey, 11, 12-14

In d e x

in as ys tole, 81, 88, 89 in bradycardia, 108, 110 changes in 2010 Guidelines on, 12, 163

arterial partial pres s ure (Paco 2 ), 9; in pos t–cardiac arres t care, 28, 74 end-tidal partial pres s ure (P e t c o 2 ), 16, 76; Cardiac Arres t


Algorithm on, 61, 80, 82, 158, 159; during CPR, 67-69;

in res piratory arres t, 34-36, 151

in pos t–cardiac arres t care, 28, 73, 74, 75, 160; in

in s table tachycardia, 126, 128

res piratory arres t, 37

in uns table tachycardia, 116, 119 in ventricular f brillation/puls eles s VT, 50-57, 62 Bradycardia, 104-114

Cardiac arres t, 28-29 in acute coronary s yndromes , 92 as ys tole in, 86-91

in airway s uctioning procedure, 46

cricoid pres s ure in, 48

algorithm on, 108-112, 161; changes in 2010 Guidelines ,

def nition o , 168

109, 163

hypothermia induced in, 28, 73, 77, 160

contributing actors in, 110

in-hos pital, 30-32

def nition o , 107, 168

lone res cuer in, 14, 49-58

drug therapy in, 106, 108; algorithm on, 109, 161;

and pos t–cardiac arres t care, 28-29, 72-77 (see also Pos t–

nitroglycerin precautions in, 97; and trans cutaneous pacing, 113; in treatment s equence, 110, 111, 112

cardiac arres t care) with puls eles s electrical activity, 78-85

es cape rhythms in, 112, 113

in re ractory VF/VT, 59-77

unctional or relative, 107

revers ible caus es o , 61, 66, 73, 80, 82; learning s tation

learning s tation checklis t on, 161

checklis ts on, 158-160

Megacode evaluation o s kills in, 153

team approach to, 26-27, 30-32, 73

per us ion as s es s ment in, 110

trans port o patients in, 91

rhythms included in, 105, 106

treatment s equence in, 57, 66

s igns and s ymptoms in, 107, 110

ventilation rate in, 36, 47

s inus , 105, 106, 107 trans cutaneous pacing in, 108, 110, 111, 112-114; algorithm on, 109, 161

Cardiac Arres t Algorithm, 163 in as ys tole, 60, 61, 79, 86, 88-89, 159 circular ormat, 66, 67, 82

trans venous pacing in, 108, 109, 112, 161

learning s tation checklis ts on, 158-159

treatment s equence in, 108, 110-111

in puls eles s electrical activity, 60, 61, 78, 79-82, 159

Bradycardia Algorithm, 108-112, 161 changes in 2010 Guidelines , 109, 163 Breathing as s es s ment, 15 agonal gas ps in, 55

in ventricular f brillation/puls eles s VT, 60-69, 158 Cardiac Arres t Regis try to Enhance Survival (CARES), 7, 27 Cardiac output, 76, 125 Cardiopulmonary res us citation, 25-27

in res piratory arres t, 35, 37

in ACLS Survey, 15, 16, 36, 37

in ventricular f brillation/puls eles s VT, 51, 52, 53, 55

in acute coronary s yndromes , 92

Bundle branch block

in as ys tole, 86, 88, 89-90; algorithm on, 61, 80, 82, 159

acute coronary s yndromes in, 95

in BLS Survey, 12, 13, 34, 35

trans cutaneous pacing in, 112, 114

ches t compres s ions in (see Ches t compres s ions )

ventricular f brillation/puls eles s VT in, 60

coronary per us ion pres s ure in, 62, 67 def nition o , 168

Calcium channel blockers in tachycardia, 129, 130 algorithm on, 118, 127, 162

high-quality, 14, 52, 62, 163 in lone res cuer, 15, 49-58, 152

Canadian Neurological Scale, 134, 143

meas urements on per ormance and outcome o , 27

Capnography

in puls eles s electrical activity, 79, 81; algorithm on, 61, 80,

def nition o , 168

82, 159

in endotracheal tube as s es s ment, 37, 48, 76

quality improvement in, 25, 27


res cue breathing in (see Res cue breathing)


in res piratory arres t, 34, 35, 36, 37, 40; and advanced

in ventricular f brillation/puls eles s VT and CPR, 67-69 Carbon dioxide

airway, 48 in s troke, 136 175

I n d e x s ummary o 2010 Guidelines on, 163

Ches t pain and dis com ort

s ys tems approach to, 26

in acute coronary s yndromes , 96; nitroglycerin in, 98

team approach to, 3, 17-23

in bradycardia, 107, 110, 113, 161; algorithm on, 109, 161

in ventricular f brillation/puls eles s VT: AED us e with, 52,

in tachycardia, 115, 117, 119; algorithm on, 118, 127

53, 54, 57; Cardiac Arres t Algorithm on, 61, 62-63, 66,

Cincinnati Prehos pital Stroke Scale (CPSS), 7, 136-138

158; drug therapy with, 65-66; and lone res cuer, 49-58;

Circulation

manual def brillator us e with, 59, 61, 62-63, 64, 65,

in ACLS Survey, 16, 37

66; phys iologic monitoring during, 67-69; in treatment

in BLS Survey, 13, 35

s equence, 66

in bradycardia, 110

Cardiovers ion in s table tachycardia, 116 s ynchronized: changes in 2010 Guidelines , 164; compared

in res piratory arres t, 35, 37 return o s pontaneous circulation (see Return o s pontaneous circulation)

to uns ynchronized, 121; def nition o , 169; potential

Clarity o communication in res us citation team, 19

problems in, 121; Tachycardia With Puls e Algorithm on,

Clopidogrel in acute coronary s yndromes , 94, 103

118, 127, 162; in uns table tachycardia, 118, 120, 121,

Clos ed-loop communication in res us citation team, 19

122-123

Communication in res us citation team, 19

in uns table tachycardia, 114, 119, 120-123; algorithm on,

clarity o mes s ages in, 19

118; indications or, 116, 121; s ynchronized s hocks

cons tructive interventions in, 22

in, 118, 120, 121, 122-123; uns ynchronized s hocks in,

delegation o roles and res pons ibilities in, 20-21

120, 121

knowledge s haring in, 22

CARES (Cardiac Arres t Regis try to Enhance Survival), 7, 27

mutual res pect in, 23

Carotid puls e, 13

on patient s tatus , 22, 23

in res piratory arres t, 35 in trans cutaneous pacing, 112 in ventricular f brillation/puls eles s VT, 51 Catheterization

reques ts or as s is tance in, 21 Computed tomography, 7 in s troke, 131, 134, 135, 140; criteria or f brinolytic therapy in, 143; hemorrhagic, 134, 141; time to, 135, 141

or airway s uctioning, 45

Cons tructive interventions in res us citation team, 22

intraos s eous (see Intraos s eous acces s )

Cons ultation with expert

intravenous (see Intravenous acces s ) Cerebral artery thrombos is , is chemic s troke in, 142 Cervical s pine trauma airway as s es s ment and management in, 39, 40, 49 immobilization in, 49 Chain o Survival, 26, 27, 30 in acute coronary s yndromes , 96 in acute s troke, 132-133 Ches t compres s ions , 12, 13, 36, 47 in as ys tole, 86, 88, 89, 159

in bradycardia, algorithm on, 109, 161 in tachycardia, 128, 129, 130; algorithm on, 118, 127, 162 Coronary per us ion pres s ure in CPR, 62, 67 Coronary s yndromes acute, 91-104 (see also Acute coronary s yndromes ) def nition o , 168 Coronary thrombos is , 168 as ys tole/PEA in, 83, 84 Cardiac Arres t Algorithm on, 61, 66, 80, 82, 158, 159 Pos t–Cardiac Arres t Care Algorithm on, 73, 160

coronary per us ion pres s ure in, 62

CPR, 7, 168. See also Cardiopulmonary res us citation

in high-quality CPR, 14, 163

CPSS (Cincinnati Prehos pital Stroke Scale), 7, 136-138

minimizing interruptions in, 12, 13, 14, 81

Cricoid pres s ure, 48

in puls eles s electrical activity, 81, 159 ratio to ventilation, 48, 61, 80, 82, 158, 159 in res piratory arres t, 35, 36, 37, 48

in as ys tole/puls eles s electrical activity, 80, 89, 159

in ventricular f brillation/puls eles s VT, 50, 51, 158; and

with automated external def brillator (see Automated

AED us e, 52, 53, 56, 57; in cycles o CPR, 56, 64, 65;

external def brillator)

and manual def brillator us e, 59, 62-63; minimizing

with implanted device, a ecting AED us e, 58

interruptions in, 62, 65; phys iologic monitoring during,

in res piratory arres t, 34, 35, 37

67-69

in ventricular f brillation/puls eles s VT: algorithm on, 61,

Ches t hair a ecting AED us e, 57-58 176

Def brillation, 13

158; with automated external def brillator, 49-58; in

In d e x

BLS Survey, 51; clearing warning in, 56, 64; and drug

Electrode pad placement in AED us e, 55, 56, 57

therapy, 65-66; early, importance o , 54; and lone

Electromechanical dis s ociation, 79

res cuer, 49-58; with manual de brillator, 59, 61, 62-63,

Embolis m, pulmonary, 9, 84, 85. See also Pulmonary

64, 66, 158; purpos e o , 54; treatment s equence in, 57 Di erential diagnos is in ACLS Survey, 16

thromboembolis m Emergency department as s es s ment and treatment

in bradycardia, 108

in acute coronary s yndromes , 29, 94, 99-100


in s troke, 134, 139-140

Digoxin in tachycardia, 129 Do not attempt res us citation (DNAR), 8 in as ys tole, 87, 90 Dopamine, 166 in bradycardia, 106, 108, 113, 166; algorithm on, 109, 161; in treatment s equence, 110, 112 in pos t–cardiac arres t care, 73, 76, 160

Emergency medical s ervices , 8, 13, 29 in acute coronary s yndromes , 29, 92, 95, 96-98; algorithm on, 94 in res piratory arres t, 35 in s troke, 30, 130, 132, 134, 135; activation o , 136; critical actions in, 138-139 in ventricular brillation/puls eles s VT, 51, 52, 53

Drug overdos e, 84, 85, 90

Enalaprilat in s troke, 131

Drug therapy, 165-167

Encephalopathy, 168

in acute coronary s yndromes (see Acute coronary s yndromes , drug therapy in) in as ys tole, 86, 88; algorithm on, 61, 80, 82, 159

End-tidal carbon dioxide. See Carbon dioxide, end-tidal partial pres s ure Endotracheal intubation

in bradycardia (see Bradycardia, drug therapy in)

as s es s ment o tube placement in, 37, 48, 76

in pos t–cardiac arres t care, 73, 76, 160

de nition o , 168

prerequis ite knowledge required, 3

in pos t–cardiac arres t care, 74, 75

in puls eles s electrical activity, 78, 81; algorithm on, 61, 80,

in res piratory arres t, 36, 47, 48; s uctioning procedure in, 46

82, 159

in ventricular brillation/puls eles s VT, 69, 70

in s table tachycardia, 125, 129-130; algorithm on, 118, 127

Epiglottis , airway obs truction rom, 39

in s troke (see Stroke, drug therapy in)

Epinephrine, 166

s ummary table on, 165-167 with trans dermal medication patches , AED us e in, 58 in uns table tachycardia, 114, 118 in ventricular brillation and tachycardia (see Ventricular brillation and tachycardia, drug therapy in)

in as ys tole/puls eles s electrical activity, 80, 81, 82, 88, 159, 166 in bradycardia, 106, 108, 113, 166; algorithm on, 109, 161; in treatment s equence, 110, 112 Cardiac Arres t Algorithm on, 61, 80, 82, 158, 159 in pos t–cardiac arres t care, 73, 76, 160

ECASS (European Cooperative Acute Stroke Study), 144, 145

in ventricular brillation/puls eles s VT, 61, 65, 66, 70, 71, 158

Edema, pulmonary, de nition o , 169

Es cape rhythms in bradycardia, 112, 113

Education, community and pro es s ional, on s troke, 30, 132

Es ophageal detector device, 168

Electrocardiography, 8, 168

Es ophageal-tracheal tube, 168

in acute coronary s yndromes , 91, 92, 95; algorithm on, 94;

in res piratory arres t, 36, 47, 48

in emergency department, 99; in prehos pital care, 98;

Ethical is s ues in as ys tole, 90

ris k clas s i cation bas ed on, 101-102

European Cooperative Acute Stroke Study, 144, 145

in as ys tole, 86, 87 in bradycardia, 105, 106, 110; algorithm on, 109, 161 de nition o , 168

Exhaled air, carbon dioxide concentration in, 76. See also Carbon dioxide, end-tidal partial pres s ure Expert cons ultation. See Cons ultation with expert

prerequis ite interpretation s kills required, 3 in puls eles s electrical activity, 83-84

Facial droop in s troke, 136, 137

in s table tachycardia, 128

Fibrillation

in s troke, 131, 134, 140

atrial (see Atrial brillation and f utter)

technical problems in, 87

ventricular (see Ventricular brillation and tachycardia)

in uns table tachycardia, 114, 117, 118, 119; and s ynchronized cardiovers ion, 121 in ventricular brillation/puls eles s VT, 60

Fibrinolytic therapy in acute coronary s yndromes , 92, 93, 102; in prehos pital care, 98; in ST-s egment elevation, 100, 101, 102 177

I n d e x in acute s troke, 130, 131, 141, 143-145; advers e e ects

in hypovolemia, 84

o , 144; algorithm on, 134; complications o , 146;

nitroglycerin precautions in, 97

exclus ion criteria on, 141, 143-144, 145; inclus ion

pos t–cardiac arres t, 73, 76, 160

criteria on, 143, 145; intra-arterial adminis tration o ,


145; time to treatment in, 135, 143, 144-145 Fixation errors in res us citation team, 22 Fluid adminis tration

Hypothermia, 169 bradycardia and trans cutaneous pacing contraindication in, 112




de brillation in, 69

routes o , 70

drug metabolis m in, 69

in s troke, 146

duration o res us citation e orts in, 90

Flutter, atrial. See Atrial brillation and f utter

electrocardiography in, 83

Foreign body airway obs truction, 40

his tory and phys ical examination in, 83 Pos t–Cardiac Arres t Care Algorithm on, 73, 160

Gas ps , agonal, 55

rewarming in, 69, 77

Get With The Guidelines –Res us citation, 27, 90

therapeutic, in cardiac arres t, 28, 73, 77, 160

Glucos e blood levels

Hypovolemia, 169

in hypoglycemia, 28, 169

as ys tole/PEA in, 83, 84, 85

in pos t–cardiac arres t care, 28


in s troke, 134, 139, 140, 146

Pos t–Cardiac Arres t Care Algorithm on, 73, 160 Hypoxia, 169

Hairy ches t a ecting AED us e, 57-58

as ys tole/PEA in, 83, 85

Head tilt–chin li t maneuver, 36, 39, 40, 49


Heart ailure, acute, 7


bradycardia algorithm on, 109, 161 in tachycardia, 115, 117, 119; algorithm on, 118, 127, 162 Heparin, 8, 9

Idioventricular rhythm, accelerated, 7, 113 Immobilization in cervical s pine trauma, 49

in acute coronary s yndromes , 94, 103, 104

Implanted de brillator/pacemaker, AED us e in, 58

in s troke, 141

In ormation s haring in res us citation team, 22

HMG-CoA reductas e inhibitors in acute coronary s yndromes , 94, 103 Hos pital s etting

Intens ive care unit, 8 trans er to, pos t–cardiac arres t, 77 Intraos s eous acces s , 8, 169

acute coronary s yndrome therapy in, 29

in as ys tole, 81, 88, 159

cardiac arres t in, 30-32


s troke care in, 130, 139-140

in ventricular brillation/puls eles s VT, 69, 70, 158

Hydrogen ion accumulation in acidos is , 169. See also Acidos is

Intravenous acces s , 8, 169

Hyperglycemia in s troke, 146

in as ys tole, 81, 88, 159

Hyperkalemia, 169


as ys tole/PEA in, 83

in pos t–cardiac arres t care, 73, 76, 160




in s troke, 140

Hypertens ion, s troke and brinolytic therapy in, 146-147

in tachycardia with puls e, 118, 127, 162

Hypoglycemia, 28, 169

in ventricular brillation/puls eles s VT, 69, 70, 158

Hypokalemia, 169 as ys tole/PEA in, 83

J aw thrus t maneuver, in trauma and res piratory arres t, 40, 49

Cardiac Arres t Algorithm on, 61, 66, 80, 82, 158, 159 Pos t–Cardiac Arres t Care Algorithm on, 73, 160 Hypomagnes emia, 72, 167

Laryngeal mas k airway, 36, 47, 48

Hypotens ion

Laryngeal tube, 36, 47, 48

in bradycardia, 107, 110, 113; algorithm on, 109, 161 178

Labetalol in s troke, 131, 147

Lay res cuer AED programs , 54

In d e x

Leaders hip s kills in res us citation team, 3, 17-23

precautions in, 45

Lidocaine, 167

s ize s election, 44

in ventricular f brillation/puls eles s VT, 66, 72, 167 Lone res cuer, 15 in res piratory arres t, 40 s kill checklis t on, 152 in ventricular f brillation/puls eles s VT, 49-58

National Ins titute o Neurological Dis orders and Stroke (NINDS), 8, 30, 130, 133, 135, 143, 145 National Ins titutes o Health Stroke Scale (NIHSS), 8, 140, 141, 143 Neurologic as s es s ment in cardiac arres t, 29, 77

Magnes ium s ul ate, 167 in tors ades de pointes , 66, 72, 167 Meas urements on CPR per ormance and outcomes , 27

in s troke, 134, 135, 136-138, 140-141, 143 Nicardipine in s troke, 131, 147 NIHSS (National Ins titutes o Health Stroke Scale), 8, 140,

Medical emergency teams , 8, 26 in cardiac arres t, 31, 32

141, 143 NINDS (National Ins titute o Neurological Dis orders and

Megacode evaluation, 2, 153-157 Mental s tatus alteration

Stroke), 8, 30, 130, 133, 135, 143, 145 Nitroglycerin in acute coronary s yndromes , 98, 103

bradycardia algorithm on, 109, 161

algorithm on, 94


in emergency department, 100

MERIT trial, 32

precautions in, 97

Mobitz types o atrioventricular block, 105

in prehos pital care, 97

drug therapy in, 111

Nitroprus s ide in s troke, 131, 147


Non–ST-s egment elevation myocardial in arction (NSTEMI), 8,

Monophas ic def brillators , 63, 66 Cardiac Arres t Algorithm on, 61, 80, 82, 158, 159 Morphine in acute coronary s yndromes , 94, 97-98, 100 Mouth-to-mas k ventilation, 40

93, 95, 101 Norepinephrine in pos t–cardiac arres t care, 73, 76, 160 NSTEMI (non–ST-s egment elevation myocardial in arction), 8, 93, 95, 101

Myocardial is chemia and in arction, 8, 91-104 accelerated idioventricular rhythm in, 113

Organophos phate pois oning, atropine s ul ate in, 166

acute, 7, 29, 168; Pos t–Cardiac Arres t Care Algorithm on,

Oropharyngeal airway, 9, 36, 40, 42-43

73, 77

def nition o , 169

drug therapy in, 92

indications or, 42

electrocardiography in, 91, 92; ris k clas s if cation bas ed on,

ins ertion technique, 43

101-102 in erior wall, 97

precautions in, 43, 45 s ize s election, 43

non–ST-s egment elevation, 8, 93, 95, 101

Oropharyngeal s uctioning procedure, 46

pathophys iology in, 93

Oxygen

right ventricular, 97

central venous s aturation in CPR, 67

s igns and s ymptoms in, 96

raction o ins pired, 8; in pos t–cardiac arres t care, 73, 74,

ST-s egment depres s ion in, 91, 94, 101, 102 ST-s egment elevation in (see ST-s egment elevation myocardial in arction)

160 Oxygen therapy, 15 in acute coronary s yndromes , 94, 96, 97, 100

tachycardia in, 125


time to treatment in, 94, 95, 99, 100, 101; and f brinolytic


therapy, 102; and percutaneous coronary interventions ,


102-103

in s troke, 134, 139, 140


in tachycardia with puls e, 119, 128; algorithm on, 118, 127,

uns table tachycardia in, 115

162 toxicity o , 28

Nas opharyngeal airway, 8, 36, 40 indications or, 43 ins ertion technique, 44

Pacing with implanted pacemaker, AED us e in, 58 179

I n d e x trans cutaneous , 9; in as ys tole, 89; in bradycardia, 108, 109, 110, 111, 112-114, 161 trans venous , in bradycardia, 108, 109, 112, 161 Paddles and pads o def brillators , 64 o automated external def brillators , 55, 56, 57

Webs ite) or updating and re res hing s kills , 7 Pulmonary edema, def nition o , 169 Pulmonary thromboembolis m, 9 as ys tole/PEA in, 83, 84, 85

Patch or trans dermal medications , AED us e in, 58


PEA. See Puls eles s electrical activity


Percutaneous coronary interventions , 9 in acute coronary s yndromes , 93, 102-103; as primary

Puls e checks , 13 in as ys tole, 86, 88

therapy, 92, 93, 102; as res cue therapy, 102; in ST-

in puls eles s electrical activity, 81

s egment elevation, 100, 101, 102-103


in pos t–cardiac arres t care, 28

in s table tachycardia, 126

Per us ion, def nition o , 169

in uns table tachycardia, 114, 116, 117

Pharmacology. See Drug therapy

in ventricular f brillation/tachycardia, 50, 51; BLS algorithms

Phos phodies teras e inhibitor us e, nitroglycerin precautions in, 97 Plaque in atheros cleros is , ormation and rupture o , 93 Plas minogen activator, recombinant tis s ue. See Tis s ue plas minogen activator, recombinant Pneumothorax, tens ion, 170

on, 52, 53; ches t compres s ion interruption or, 62, 64, 65 Puls eles s electrical activity, 9, 78-85 Cardiac Arres t Algorithm on, 60, 61, 78, 79-82 common caus es o , 82-85 def nition o , 169


drug therapy in, 78, 80, 81


his torical des cription o , 79


Megacode evaluation o s kills in, 154-157

Pocket Re erence Cards , 6

rhythms included in, 78

Pos t–cardiac arres t care, 28-29, 72-77

treatment s equence in, 81, 82, 89

changes in 2010 Guidelines , 164

Puls eles s ventricular tachycardia, 49-77

critical actions in, 164

lone res cuer CPR and AED us e in, 49-58


re ractory, 59-77

Megacode evaluation o s kills in, 153-157 trans port o patients or, 91

QRS complex, in tachycardia, 117, 118, 120, 124, 128-129

Pos t–Cardiac Arres t Care Algorithm, 72-77, 160

algorithm on, 118, 127, 162

Practice learning s tations , 2

and s ynchronized cardiovers ion, 121, 122

Precours e Preparation Checklis t, 6

Quality improvement in CPR, 25, 27

Prerequis ite knowledge and s kills required or Provider Cours e, 2-3

Rapid res pons e teams , 9, 26-27

s el -as s es s ment o , 2-3, 5 Procainamide in tachycardia with puls e, 129 algorithm on, 118, 127, 162

Recombinant tis s ue plas minogen activator. See Tis s ue plas minogen activator, recombinant

Prophylaxis , def nition o , 169

Re ractory VF/puls eles s VT, 59-77

Provider Cours e, 1-9

Regional care s ys tems

abbreviations us ed in, 7-9

in cardiac arres t, 32

ACLS cas es in, 33-147 (see also ACLS cas es )

in s troke, 30

completion requirements in, 7 components o , 2

Reper us ion therapy in acute coronary s yndromes , 92, 93, 100-101; f brinolytics

critical concepts in, 4

in, 92, 93, 98, 100, 101, 102; percutaneous coronary

des cription o , 1

interventions in, 92, 93, 100, 101, 102-103

materials us ed in, 3-6 objectives o , 1 prerequis ite knowledge and s kills required or, 2-3; s el as s es s ment o , 2-3, 5 Student Webs ite res ources or, 2, 3, 5-6 (see also Student 180

in cardiac arres t, 31, 32

in acute s troke, 147; f brinolytics in, 130, 131, 134, 135, 141, 143-145, 146 in pos t–cardiac arres t care, 28, 73, 77, 160 Res cue breathing, 12, 13 in cardiac arres t, 36, 47

In d e x

in res piratory arres t, 34, 35, 36; and advanced airway, 36, 47, 48; exces s ive ventilation in, 38; rate o , 35, 36, 37, 38, 47, 48; ratio to ches t compres s ions , 48; without ches t compres s ions , 48 in ventricular f brillation/puls eles s VT: and AED us e, 56; rate o , 51 Res cuer, lone. See Lone res cuer

in hypovolemia, 84 Sotalol in tachycardia with puls e, 129 algorithm on, 118, 127, 162 Speech dis orders in s troke, 136, 137 Spinal injuries , cervical airway as s es s ment and management in, 39, 40, 49 immobilization in, 49

Res pect in res us citation team, 23

ST-s egment depres s ion myocardial in arction, 91, 94, 101, 102

Res piratory arres t, 34-49

ST-s egment elevation myocardial in arction, 9, 29, 91-104

ACLS Survey in, 36-37, 151

adjunctive therapy in, 103-104

airway as s es s ment and management in, 36, 38-49

algorithm on, 94

BLS Survey in, 34-36, 151

electrocardiography and ris k clas s if cation in, 101

critical concepts in, 38

emergency department as s es s ment and treatment in,

lone res cuer in, 40

99-100

oxygen therapy in, 37, 38

emergency medical s ervices in, 96-98

in trauma, 39, 49

goals o therapy in, 93

Res pons ivenes s as s es s ment, 13

percutaneous coronary interventions in, 92

in pos t–cardiac arres t care, 73, 76


in res piratory arres t, 35; and nas opharyngeal airway, 43;

reper us ion therapy in, 100-101, 102-103

and oropharyngeal airway, 42, 43 in ventricular f brillation/puls eles s VT, 51, 52, 53

Stable tachycardia, 124-130 algorithm on, 118, 127

Reteplas e in acute coronary s yndromes , 102

Statin therapy in acute coronary s yndromes , 94, 103

Return o s pontaneous circulation, 9

STEMI. See ST-s egment elevation myocardial in arction

in as ys tole/puls eles s electrical activity, 61, 80, 82, 90, 159

Streptokinas e in acute coronary s yndromes , 102

in in-hos pital cardiac arres t, 30

Stroke, 30, 130-147


algorithm on, 133-147

in out-o -hos pital cardiac arres t, 91

arrhythmias in, 131, 140

pos t–cardiac arres t care in, 28, 72-77, 160

as s es s ment tools in, 136-138

in ventricular f brillation/puls eles s VT, 61, 63, 66, 67-69, 158

Chain o Survival in, 132-133

Rewarming techniques in hypothermia, 69 precautions a ter ROSC, 77 Roles and res pons ibilities in res us citation team, 17, 18, 20-21 ROSC. See Return o s pontaneous circulation

community and pro es s ional education on, 30, 132 critical elements in, 133 drug therapy in, 30, 130, 131, 132, 135, 143-145; algorithm on, 134; complications o , 146; exclus ion criteria on, 141, 143-144, 145; hypertens ion management in,

Sa ety concerns in BLS Survey, 12

146-147; inclus ion criteria on, 143, 145; intra-arterial

Sedation

adminis tration o , 145; time to treatment in, 135, 143,

in bradycardia and trans cutaneous pacing, 111 in tachycardia and cardiovers ion, 118, 120, 125, 127 Seizures in s troke, 146 Sel -as s es s ment

144-145 emergency medical s ervices in, 30, 130, 132, 134, 135; activation o , 136; critical actions in, 138-139 general care in, 134, 146-147

on cours e prerequis ite s kills , 2-3, 5

goals o care in, 132, 133

on res us citation team s kills , 21

hemorrhagic, 131, 132, 134, 140; computed tomography in,

Shock in bradycardia, 113, 161 in tachycardia, 115, 117, 119; algorithm on, 118, 127, 162 Sinus bradycardia, 105, 106, 107 Sinus rhythm, def nition o , 169 Sinus tachycardia, 115, 124 cardiovers ion in, 116 caus es o , 125

134, 141; drug therapy contraindications in, 141, 143, 144 in-hos pital care in, 130, 139-140 is chemic, 131, 132, 134, 140, 142; f brinolytic therapy in, 143-145 neurologic as s es s ment in, 134, 136-138, 140-141, 143; time to, 135, 140 NINDS res earch on, 30, 130, 133, 135, 143, 145 181

I n d e x regionalization o care in, 30

o , 124, 125; di erentiated rom uns table tachycardia,

s igns and s ymptoms in, 132, 135

116, 119, 126, 128; drug therapy in, 118, 125,

team approach in, 134, 139, 140

127, 129-130; rhythms in, 124, 128-130; s igns and

time to treatment in, 132, 133, 134, 135, 138, 139, 143,

s ymptoms in, 126; vagal maneuvers in, 118, 127, 129

144-145 trans port o patients in, 136; to s troke centers and s troke units , 138, 139 Student Webs ite, 2, 3, 5-6

s upraventricular (see Supraventricular tachycardia) uns table, 114-123; algorithm on, 116-120; cardiovers ion in, 114, 116, 119, 120-123; di erentiated rom s table tachycardia, 116, 119, 126, 128; drug therapy in, 114,

on bag-mas k ventilation, 42

118; pathophys iology o , 115; rapid recognition o , 115;

on BLS Survey, 12

rhythms in, 114, 117; s everity o , 115, 117; s igns and

on endotracheal intubation, 48

s ymptoms in, 115, 117, 118, 119; underlying caus e o ,

on es ophageal-tracheal tube, 48

118, 119

on ethical is s ues in CPR, 90 on f brinolytic therapy, 98 on heparin therapy, 104 on intraos s eous acces s , 70

ventricular, 9, 170 (see also Ventricular f brillation and tachycardia) wide-complex, 114, 118, 120, 124, 128-129, 130 Tachycardia With Puls e Algorithm, 118, 127, 164

on laryngeal intubation, 47


on laryngeal mas k airway, 47

in s table patient, 126-130

on oxygen therapy, 38

in uns table patient, 116-120

on team approach, 18

Tamponade, cardiac, 170

Suctioning o airways in res piratory arres t, 45-46


Supraventricular tachycardia, 9, 128, 129


cardiovers ion in, 120, 121, 122, 123 di erentiated rom VT, 120, 128

Pos t–Cardiac Arres t Care Algorithm on, 73, 160 Team approach, 3, 17-23

drug therapy in, 129-130

in as ys tole, 86

reentry, 114, 122, 125

in cardiac arres t, 26-27, 73; in-hos pital, 30-32

vagal maneuvers in, 129

communication in, 19, 20-21, 22, 23

Sus pected Stroke Algorithm, 133-147

cons tructive interventions in, 22

Synchronized cardiovers ion. See Cardiovers ion, s ynchronized

knowledge s haring in, 22

Syncope, def nition o , 170

medical emergency teams in, 8, 26, 31, 32

Sys tems o care, 25-32, 164

Megacode evaluation o s kills in, 3, 153-157

in acute coronary s yndromes , 29

monitoring, reevaluating, and s ummarizing in, 23

in cardiac arres t, 28-29

mutual res pect in, 23

cardiopulmonary res us citation in, 25-27


Chain o Survival in, 26

rapid res pons e teams in, 9, 26-27, 31, 32

publis hed s tudies on, 32

reques ts or as s is tance in, 21

rapid res pons e in, 32

roles and res pons ibilities in, 17, 18, 20-21

regional, 32

s el -awarenes s o abilities and limitations in, 21

in s troke, 30

in s troke, 134, 139, 140

team approach in, 30-31

in uns table tachycardia, 114 in ventricular f brillation/puls eles s VT, 59

Tachycardia, 114-130 def nition o , 115, 118, 170

Tens ion pneumothorax. See Pneumothorax, tens ion


Thrombos is

narrow-complex, 124, 128, 129-130

cerebral, is chemic s troke in, 142

nitroglycerin precautions in, 97

coronary (see Coronary thrombos is )

s inus , 115, 124; cardiovers ion in, 116; caus es o , 125; in

def nition o , 170

hypovolemia, 84 s table, 124-130; advanced management in, 130; algorithm on, 118, 126-130; cardiovers ion in, 116; clas s if cation 182

Tenecteplas e in acute coronary s yndromes , 102

pulmonary (see Pulmonary thromboembolis m) Tis s ue plas minogen activator, recombinant, 9 in acute coronary s yndromes , 102

In d e x

def nition o , 169 in s troke, 30, 134, 141, 143-145; algorithm on, 134;

manual def brillator us e, 59; rate o breaths in, 51 Ventricular f brillation and tachycardia, 49-77

hypertens ion management in, 146-147; intra-arterial

abbreviations or, 9, 170

adminis tration o , 145

ACLS Survey in, 62

Tongue, airway obs truction rom, 38, 39, 40, 42

BLS Survey in, 50-57, 62

Tors ades de pointes , 128

in bradycardia with es cape rhythms , 113

magnes ium s ul ate in, 66, 72, 167 Toxic conditions

Cardiac Arres t Algorithm in, 60-69, 158 cycles o CPR in, 64, 65


def nitions o , 170


drug therapy in, 60, 65-66, 69-72; algorithm on, 61, 65-66,


158; antiarrhythmics in, 65-66, 71-72; hypothermia

Tracheal intubation. See Endotracheal intubation

a ecting, 69; routes o acces s or, 69-70; in treatment

Trans dermal medication patches , AED us e in, 58

s equence, 66, 69; vas opres s ors in, 65, 70-71

Trans port o patients

in hypothermia, 69

in cardiac arres t, 91

lone res cuer CPR and AED us e in, 49-58

s pinal immobilization in, 49

manual def brillators in, 59, 61, 62-63; biphas ic, 61, 63,

in s troke, 136; to s troke centers and s troke units , 138, 139 Trauma, res piratory arres t and airway management in, 39, 40, 49

66; Cardiac Arres t Algorithm on, 61, 62-63, 66, 158; clearing warning in, 64; and drug therapy, 65-66; monophas ic, 61, 63, 66; paddles and pads o , 64;

Uns table angina, 9, 93, 95 electrocardiography and ris k clas s if cation in, 101 Uns table tachycardia, 114-123 Uns ynchronized s hocks , 170 in uns table tachycardia, 120, 121 Uts tein Guidelines , 27

s hock delivery in, 61, 63 Megacode evaluation o s kills in, 153-157 monomorphic VT, 114, 120, 124, 128, 129; cardiovers ion in, 121, 122, 123 phys iologic monitoring in, 67-69 polymorphic VT, 114, 120, 124, 126, 128; cardiovers ion in, 121, 123

Vagal maneuvers in tachycardia, 129 algorithm on, 118, 127, 162 Vas opres s in, 167 in as ys tole, 88, 159

re ractory, 59-77 team res pons e to, 59 time to def brillation and CPR in, 54 treatment s equence in, 57, 66, 69

Cardiac Arres t Algorithm on, 61, 80, 82, 158, 159 in puls eles s electrical activity, 81, 82, 159 in ventricular f brillation/puls eles s VT, 65, 66, 71, 158; routes o adminis tration, 70, 71 Vas opres s or drugs

Warming techniques in hypothermia, 69 precautions a ter ROSC, 77 Water a ecting AED us e, 58 Webs ite res ources or Provider Cours e. See Student Webs ite

in as ys tole, 88

Wenckebach atrioventricular block, 105

in puls eles s electrical activity, 81

Withdrawal o li e-s us taining care

in ventricular f brillation/puls eles s VT, 65, 70-71 Ventilation techniques

in as ys tole, 87 pos t–cardiac arres t, 29

bag-mas k ventilation in (see Bag-mas k ventilation) compres s ion-ventilation ratio in, 48, 61, 80, 82, 158, 159

Yankauer catheters , 45, 46

coronary per us ion pres s ure in, 62 in pos t–cardiac arres t care, 28, 73, 74, 160; exces s ive ventilation in, 28, 73, 74, 75 in res piratory arres t, 34, 35, 36; and advanced airway, 36, 47, 48; bag-mas k ventilation in, 36, 41, 42, 151; compres s ion-to-ventilation ratio in, 48; exces s ive ventilation in, 38; rate o breaths in, 35, 36, 37, 38, 47, 48 in ventricular f brillation/puls eles s VT: and AED us e, 56; and 183

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