Clinicall Revie Clinica Review w & Educa Education tion
Challenges Challe nges in Clinica Clinicall Electro Electrocardio cardiograph graphy y
Alternating Ventricular Complex Alternating Complexes es After Overdos Overdose e From Fr om an He Herb rbal al Me Medi dica cati tion on KathyT.Vo,MD; Ka thyT.Vo,MD; Je Jeffr ffreyA. eyA. Taba abas, s, MD;Crai MD;Craig g G. Smo Smolli llin, n, MD
A woman in her 50s with no medical problems presented to the emergency department with complaints of chest burning, shortness of breath, diffuse paresthesias, and dizziness. She was in her norma no rmall st stateof ateof hea healthuntil lthuntil an hou hourr aft after er dri drinki nking ng a hom home-b e-brew rewed ed tea containing leaves and roots prescribed by a Chinese herbalist. She had normal mental status and vital signs. Seventeen minutes after arrival, the patient complained of feeling worse. An ECG was obtained obta ined (Fig Figure ure 1). Question: What Question: What are the pertinent electrocardiogram (ECG) findin fin dings, gs, an and d wha whatt is th the e lik likelycause elycause??
Interpretation The ECGshows bidirectio bidirectional nal ventric ventricular ular tachyca tachycardia rdia at a regularrate of 158 bpm. There are 2 distinct QRS complexes that are alternatingbeattobeat.TheQRS com comple plex x lab labele eled d 1 dis displa playsRBBBwithleft ysRBBBwithleft anter an teriorfasc iorfascicu icularbloc larblock k (LA (LAFB) FB).. The There re is an RR RR’’ in lea lead d V1, a sl slur urre red d S wave in lead V6, and left axis deviation, as evidenced by a negative QRS in aVF and a positive QRS in lead 1. The QRS complex labeled bel ed 2 dis displa plays ys rig right ht bun bundle dle bra branchblock nchblock (R (RBBB BBB)) wit with h lef leftt pos posteteriorfascicularblock(LPFB).ThereisanRR’inleadV1,aslurredSwave inleadV6, an and d ext extrem reme e rig right ht axi axiss dev deviat iatio ion n asevide asevidence nced d by a pos posiitive QRS in aVL and a negative QRS in lead I. P waves are present afte af terr ea eachQRS.TheR-Pint chQRS.TheR-Pinterv erval(st al(star artt ofQRS tosta tostart rt ofP wa wave ve)) is 0.16 0. 16 milliseconds. Clinical Cours Clinical Course e Laborato Labo ratory ry stud studies ies cond conducted10 ucted10 minut minutes es afterpatien afterpatientt arriv arrival al were only notable for a white blood cell count of 11 300/μL (reference
range,4000-11 range,400011 000 000/μL /μL;; toconver toconvertt to×109/L,multipl /L,multiply y by .0 .001)and 01)and a pota potassiumlevel ssiumlevel of 3.3mEq/L (refe (referencerange, rencerange, 3.53.5-5. 5.0 0 mEq/L mEq/L;; to convert con vert to mmol mmol/L, /L, mult multiply iply by 1). Tr Tropon oponin in wasundetecta wasundetectable.The ble.The patient’s condition rapidly deteriorated and she developed multiple different rhythms with widened QRS morphology and intermittentt pulselessnes mitten pulselessnesss requiringcardiopulmonaryresuscitation.She wasintubatedandcardioversionwasattempted.Inconsultationwith the cardiology and electrophysiology services, multiple interventionss were atte tion attemptedwithoutsuccess,includin mptedwithoutsuccess,including g adeno adenosine,amiosine,amiodarone, lidocaine, lidocaine, diltiazem, and verapamil. After 3 hours of attempted resuscitation, venoarterial extracorporeal membrane oxygena oxy genationwas tionwas inst institute ituted. d. After12 hours hours,, hercardiacrhythm converted vert ed backto norm normal al sinus sinus.. Her clin clinicalcoursewas icalcoursewas compl complicat icated ed by multiorgan multiorg an failureresulting from the prolongedresuscitation.Laboratoryanalyse rat oryanalysess of herinitia herinitiall seru serum m andurine,and samp samplesof lesof thetea she sh e dra drank nk on theday of pre presen sentat tation ion,, wer were e pos positi itive ve foraconi foraconitin tine. e.
Discussion Aconitine and other related alkaloids are highly potent cardiovascularr andneurolo cula andneurologica gicall tox toxinsand insand belon belong g tothe Aconitum plan plantt species. In Europe and the United States, toxic effects typically occur after inadvertent ingestion of the wild, unprocessed plant. 1 In traditiona diti onall Chi Chinesemedici nesemedicine,aconi ne,aconiterootsare terootsare typi typicall cally y usedafterprocessing, and are prescribed for the treatment of arthritis, general pains, and other conditions. 2 The plant processing involves soaking in g andboil andboilingto ingto hy hydro drolyz lyze e th the e aco aconit nite e alk alkalo aloidsintoless idsintoless to toxicdexicderivatives. However, However, faulty processing after harvest or medicinal preparationmay result in higher-than-int higher-than-intended ended toxinconcentration.3
Figure Figu re 1. Elect Electroca rocardio rdiogramat gramat Pres Presenta entation tion
I
aVR
V1
V4
II
aVL
V2
V5
III
aVF
V3
V6
VI
II
V5
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Clinical Review & Education Challenges in Clinical Electrocardiography
Figure 2. EnlargedView of Electrocardiogram A
Enlarged view of V 1
1
2 P
P
P
V1
B
QRS
P
QRS
QRS
QRS
Enlarged view of aVR, aVL, aVF, and rhythm strip
P
aVR
aVL
P
aVF
P
P wavesare present after each QRScomplex(arrowheads).
Thispatient presented with multiple rhythms, includinga patternof bidirectionalventriculartachycardia, a formof fascicular left ventricular tachycardia whichalternates conduction down the left anteriorand left posterior fascicle. With fascicular VT, the QRScan be as narrow as 100milliseconds, possiblyowingto a junctional origin with spread of activation over the His-Purkinje system, although typically it is wider.4 In addition, there was ventriculoatrial (VA) retrograde conduction,illustrated in leadV 1 (Figure2A).Toconfirm the presence of a retrograde P wave rather than misinterpretation ofa portion oftheQRS complex,examinetheP wavein other simultaneouslyrecordedleads(Figure2B). Whilea retrograde Pwave canalsooccurwithAVjunctionaltachycardias,itmaybepresentwith E2
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ventricular tachycardia, and the longer R-P interval (0.16 milliseconds) is more suggestive of VA conduction. An R-P interval duration less than 0.10 milliseconds favors junctional tachycardia. Other diagnosesto consider include bigeminy, whichwill have a sinus P wave and conducted QRS, followed by a premature ventricular complex (PVC).Therewillbe a compensatorypauseafterthe PVCand beforethe next sinus P wave. Therefore, it is important to look for “paired beats”witha P wavepreceding1 ofthe complexes. Interpolated PVCsmay be another mimic, an uncommonfindingin which PVCs are not followed by a compensatory pause but rather occurearly andcan appear sandwichedbetween2 normal beats. In addition, the presence of electrical alternans may suggest pericardialeffusion, whichtypicallypresentswith a low-voltage ECGin additionto varyingamplitudesof theQRS. Alternatingpatternsof normalconductionwith bundle branchblock mayalsoappear similarly. Controversy existsin themedical literature with regard to the siteof origin ofbidirectionalVT.Electrophysiologic studies have demonstratedthat a ventricular originis themostcommon, with many bidirectional tachycardias showing a classic RBBB and alternating fasicular block morphology. Tai et al5 favored automaticity or triggered activity vsisolatedreentryor reentryas themechanismin aconite poisoning. Aconite alkaloids exert their toxic effect on the sodium channelsin cardiac,nerve,and muscle tissue.The affinityfor cardiacfast sodium channelsresultsin increasedinotropy while delayingthe finalrepolarization phaseof theactionpotential, thereby promoting premature excitation.6 Refractory ventriculartachycardiaand asystole arethe leading causes of death after aconite ingestion. 3 Aconitecanproduceavarietyofarrhythmias,includingventricular ectopy, ventricular tachycardia, ventricular fibrillation, and torsadesde pointes.7 BidirectionalVT,an unusual tachyarrhythmia that typicallyoccursinthesettingofseverestructuralheartdisease,isalso causedby aconite toxicity. However,in toxicology, bidirectionalVT is more frequentlyassociated with digitalispoisoning.In a reviewof 72 casesof bidirectional VT by Cohen et al,8 44% of cases had atrial fibrillationanddigitaliswasusedin82%.BidirectionalVThasalsobeen observedin otherclinical settings in whichpatients havestructurally normal hearts, such as catecholaminergic polymorphic VT and hyperkalemic or hypokalemic periodic paralysis.9 Treatmentof aconitepoisoningis largelysupportive.In oneretrospectivereview of the literature, Coulsonet al10 found flecainide oramiodaroneto beassociated with a greater returnto sinusrhythm thanlidocaine or cardioversion. Prolongedcardiopulmonary resuscitation and extracorporeal therapies may help support hemodynamic status as thetoxin is excreted.
Take-Home Points • Bidirectional ventriculartachycardia isa form offascicularleft ventriculartachycardia, whichalternatesconduction downthe left anterior and left posterior fascicle. • Fascicular ventricular tachycardia can present with narrow QRS complexes. • Retrograde P waves may be present in ventricular tachycardias. • Bidirectional ventricular tachycardia suggests a toxic effect from aconite or digoxin. • Aconitealkaloids havea highaffinity forcardiacfast sodium channels, causing premature excitation of myocytes.
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REFERENCES
Author Affiliations: Departmentof Emergency Medicine,Universityof California, San Francisco, San Francisco(Vo, Tabas, Smollin); California Poison Control System, San FranciscoDivision, San Francisco(Vo, Smollin).
1. Pullela R, Young L, GallagherB, Avis SP, Randell EW. A case of fatal aconitinepoisoning by Monkshood ingestion. J Forensic Sci . 2008;53(2): 491-494.
Corresponding Author: Kathy Vo,MD, University of California, San Francisco, California Poison Control System, San FranciscoDivision, 278925th St,Suite2202,San Francisco, CA 94110 (
[email protected]).
2. ChanTY. Aconite poisoning. Clin Toxicol (Phila). 2009;47(4):279-285. 3. Chan TY, Tomlinson B, Tse LK,ChanJC, Chan WW, CritchleyJA. Aconitinepoisoning dueto Chinese herbal medicines:a review. VetHum Toxicol . 1994;36(5):452-455.
Section Editors: Zachary D.Goldberger, MD,MS; NoraGoldschlager,MD; Elsayed Z. Soliman, MD, MSc,MS.
4. Rothfeld EL. Bidirectionaltachycardia with normalQRS duration. Am Heart J . 1976;92(2): 231-233.
Published Online: June5, 2017. doi:10.1001/jamainternmed.2017.1839
5. Tai YT, LauCP, ButPP, Fong PC,Li JP. Bidirectionaltachycardia induced by herbalaconite poisoning. Pacing ClinElectrophysiol . 1992;15(5): 831-839.
Conflict of Interest Disclosures: Nonereported.
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6. HonerjägerP, Meissner A. Thepositive inotropic effect of aconitine. Naunyn Schmiedebergs Arch Pharmacol . 1983;322(1):49-58. 7. LuHR,De ClerckF.R 56865, a Na+/Ca(2+)-overload inhibitor, protects against aconitine-inducedcardiac arrhythmiasin vivo. J CardiovascPharmacol . 1993;22(1):120-125. 8. CohenSI, Deisseroth A, HechtHS. Infra-His bundleorigin of bidirectionaltachycardia.Circulation. 1973;47(6):1260-1266. 9. Al-Khafaji A, Corwin HL,AdharGC, Greenberg ML. Bidirectionaltachycardia: two cases anda review. Anesth Analg. 2002;95(2):310-315. 10. CoulsonJM, Caparrotta TM, Thompson JP. Themanagement of ventriculardysrhythmia in aconite poisoning. ClinToxicol (Phila). 2017;55(5): 313-321.
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