Curr Hypertens Rep (2015) 17:5 DOI 10.1007/s11906-014-0515-z
HYPERTENSIVE EMERGENCIES (BM BAUMANN, SECTION EDITOR)
Cardiovascular Hypertensive Emergencies D. P. Papadopoulos E. A. Sanidas N. A. Viniou V. Gennimata V. Chantziara I. Barbetseas T. K. Makris &
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# Springer Science+Business Science+Business Media New York 2015
Abstract Inevit Inevitabl ably y, a sma small ll pro propor portio tion n of pat patien ients ts wit with h systematic system atic hyper hypertensio tension n will develo develop p hypert hypertensive ensive crisis at so some me po poin int. t. Hy Hype perte rtens nsiv ivee cr crise isess ca can n be di divi vide ded d in into to hypertensive emergency or hypertensive urgency according to th thee pr prese esenc ncee or lac lack k of acu acute te tar target get organ organ da damag mage. e. In this review r eview,, we discuss cardiovascular cardiovascular hyperten hypertensive sive emergencies, including acute coronary syndrome, aortic dissection, congestive heart failure, and sympathomimetic hypertensive crises cri ses,, inc inclu ludin ding g th those ose cau cause sed d by coc cocain ainee us use. e. Ea Each ch pre prese sents nts in a unique fashion, although some hypertensive emergency patients report nonspecific symptoms. Treatment includes several seve ral effe effectiv ctivee and rapi rapid-ac d-acting ting medi medicati cations ons to safe safely ly redu reduce ce the blood pressure, protect remaining end-organ function, relieve symptoms, minimize the risk of complications, and thereby improve patient outcomes.
Hypertensive emergenc emergencies ies . Myocardial Keywords Hypertensive infarction . Acut Acutee coro coronary nary synd syndrome rome . Congestiv Congestivee heart . . failure Aortic dissection Sympathom Sympathomimetic imetic activity
Introduction
Recent data suggest that systematic hypertension is the responsible cause for nearly 7.1 million deaths per year This Th is art articl iclee is pa part rt of theTop theTopica icall Col Colle lecti ction on on Hypertensi Hypertensive ve Emerge Emergencies ncies D. P. Papadopoulos (*) : E. A. Sanidas : N. A. Vinio Viniou u: : : V. Gennimata V. Chantziara I. Barbetse Barbetseas as ESH Excellent Center of Hypertension, Department of Cardiolog Cardiology, y, “Laiko” General Hospital, Athens, Greece e-mail:
[email protected] T. K. Makris ESH Exc Excellen ellentt Cent Center er of Hype Hyperten rtension sion,, “Elena Venizelou” Maternity Hospital, Athens, Greece
worldwide. Approximately 1 – 2 % of patients with hypertension will develop a hypertensive crisis which can be further categorized as either hypertensive emergency or urgency de pending on either the presence or absence of acute end-org end-organ an dysfunction, respectively. Hypertensive crises can develop in patients with or without preexisti preexisting ng chronic hypertens hypertension ion [1 – 3] and the prevalence mirrors the distribution of essential hypertension in the general population, with men, AfricanAmericans, and the elderly being most commonly affected [4]. The most common cardiac emergencies associated with severely elevated blood pressure are acute left ventricular (LV) dysfunction with pulmonary edema (22 %), acute coronary syndromes (including acute myocardial infarction — MI) MI) (18 %), and aortic dissection (8 %). In the context of sympathomimetic drug abuse that can cause or mimic the above clinical conditions, cocaine accounts for almost one third of all visits to emergency departments [5 [5]. Classical cardiac and pulmonary symptoms (dyspnea, chest pain, arrhythmias, and syncope) seem to be less common in patients presenting with hypertensive crises (28.3 %). The majority present with nonspecific symptoms [6 [6•]. The risk of a future cardiovascular event attributable to hypertension is greater in individuals with established cardiovascular disease, diabetes mellitus, or chronic kidney disease compared to those without these comorbid conditions. This increased risk led the 2003 Seventh Joint National Committee (JNC 7) report on high blood pr es su re to li st he ar t di se as e, he ar t fa il ur e, di ab et es , chronic kidney disease, and cerebrovascular disease as “ compelling indications” for the treatment of hypertension. Other risk factors include peripheral artery disease and traditional coronary risk factors such as cigarette smoking and family history of cardiac disease [7 [7]. Mortality rates of patients with hypertensive emergencies has decreased significantly over the years (from 80 % in 1928
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to 10 % in 1989) [8], mainly due to the availability of antihy pertensive medications. The therapeutic goal is to protect remaining end-organ function, reduce the risk of complications, and thereby improve patient outcomes [9, 10]. The aim of this review is to summarize the current evaluation and treatment recommendations for the most common cardiovascular clinical presentations encountered in patients with hypertensive crisis.
Myocardial Infarction
Epidemiology Published results indicate acute MI as the leading cause of death and hospital admission in patients with severely elevated blood pressure. Moreover, nearly 50 % of all patients originally admitted with a hypertensive emergency died as a result of an acute MI during long-term follow-up. Of note, no differences were found in regard to the presence of other cardiovascular risk factors like smoking or prevalence of diabetes mellitus [11, 12]. Pathophysiology Hypertension is linked to MI as a risk factor, an atherogenic factor, and a hemodynamic factor with profound effects on morbidity and mortality. During a hypertensive emergency, the increase in blood pressure generates mechanical stress and endothelial injury leading to increased permeability, activation of the coagulation cascade and platelets, and deposition of fibrin. This process results in ischemia and release of additional vasoactive mediators generating a vicious cycle of ongoing injury. The renin-angiotensin system is often activated leading to further vasoconstriction and production of proinflammatory cytokines such as IL-6. Furthermore, NADPH oxidase activity is increased and generates reactive oxygen species. These collective mechanisms can culminate in end-organ hypoperfusion, ischemia, and dysfunction manifested as a hypertensive emergency [13]. Clinical Presentation and Evaluation Hypertensive crisis may lead to ischemia and MI causing angina-like chest pain. Evaluation of cardiovascular risk factors and other comorbidities is essential. An electrocardiogram (ECG) is the gold standard exam to reveal myocardial ischemia or infarction. Also, vital signs should be checked carefully during the physical examination of a patient with hypertensive crisis, namely, blood pressure, oxygen saturation, and heart rate. Baseline laboratory analyses should be performed rapidly after the initial evaluation of the patient. These laboratory analyses include cardiac enzymes and a cardiac troponin-I. In a retrospective study, patients with hypertensive crises and elevated cardiac c-troponin-I (cTnI) had 2.7 times higher risk for the occurrence of major adverse cardiovascular and
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cerebrovascular events (MACCE) at 2 years follow-up com pared to those with normal cTnI values. In patient s with hypertensive crisis, elevated cTnI confers a significantly greater risk of long-term MACCE and is a strong predictor of obstructive coronary artery disease [14]. Management Severe hypertension associated with an acute MI is appropriately treated with intravenous nitroglycerin, clevidipine, nicardipine, labetalol, or esmolol to reduce the underlying coronary ischemia and/or increased myocardial oxygen consumption and to improve prognosis. In addition, reducing blood pressure improves hemodynamics, ameliorates the risk of pulmonary edema, and decreases the size of the infarct area. If available, especially in ST-elevation MI, primary angioplasty is the best option for reperfusion therapy in patients with high blood pressure since thrombolysis might increase the risk of cerebral bleeding [15 – 18]. Nitroglycerin is a venodilator that mainly reduces the preload and decreases the cardiac oxygen demands. This agent is primarily used in acute MI and acute pulmonary edema along with other antihypertensive regimens [15 – 17]. Labetalol is an alpha1 adrenergic receptor blocker and nonselective beta-blocker. It reduces the systemic vascular resistance, but it maintains the cerebral, renal, and coronary blood flow. Of note, despite the beta-blocking effect, cardiac output is maintained [1]. Esmolol is an intravenous beta1 cardioselective receptor blocker with rapid onset and very short duration of action that can be safely used in most patients treated for acute MI with relative contraindications to beta-blockers. Tolerance to higher maintenance doses of esmolol is a good predictor of subsequent outcome with oral beta-blocker therapy [19]. Other agents that can be used in hypertensive emergencies include nicardipine (dihydropyridine calcium channel blocker), which is a useful agent for patients with coronary artery disease due to its beneficial effect on coronary blood flow or clevidipine, which is a relatively new short-acting, intravenous dihydropyridine calcium channel blocker with non-weight-based dosing regimen, allowing prolonged infusion and successful transition to oral therapy [20 – 22]. The optimal blood pressure after an acute coronary syndrome remains controversial. Numerous large studies have shown an inverse relationship between diastolic pressure and adverse cardiac ischemic events (i.e., the lower the diastolic pressure, the greater the risk of coronary heart disease and adverse outcomes). This effect is defined as the J-curve phenomenon which describes the shape of the relationship between blood pressure and the risk of cardiovascular morbidity and/or mortality. The aforementioned observation appears to be even more pronounced in patients with underlying coronary artery disease. Since coronary blood flow mainly occurs during diastolic phase in patients with coronary heart disease, a fall in diastolic pressure might lower perfusion pressure
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distal to a stenosis below the critical level at which autoregulation is effective. Hence, reducing systolic blood pressure to values close or below 120 – 125 mmHg and diastolic pressure below 70 – 75 mmHg in patients at high cardiovascular risk might be accompanied by an increase in the incidence of coronary events [23 – 25].
Congestive Heart Failure
Epidemiology The most common clinical manifestations of hypertensive crises include pulmonary edema (22.5 %) and congestive heart failure (12 %) [26]. Pathophysiology Acute congestive heart failure is most commonly related to systolic or diastolic dysfunction, with or without additional cardiac pathology, such as coronary artery disease or valve abnormalities. Nonetheless, a variety of conditions or events can cause cardiogenic pulmonary edema in the absence of heart disease including severe hypertension. Patients presenting with cardiogenic pulmonary edema frequently suffer from uncontrolled severe hypertension. Many of these patients have a preserved (normal or near normal) LV ejection fraction. Increased afterload, instead of or in addition to fluid overload, may precipitate decompensation in these patients [27]. Clinical Presentation and Evaluation Cardiac decompensation may lead to symptoms like dyspnea, orthopnea, cough, fatigue, or pulmonary edema. In a recent study of 189 patients, normal heart rate was associated with hypertensive urgency, whereas tachycardia denoted a hypertensive complication in the setting of LV failure [28]. Imaging may include radiogra phy or echocardiography. A plain chest radiograph is extremely helpful for documentation of cardiomegaly or pulmonary edema. Although newer echocardiography techniques are not extensively used in daily clinical practice, speckle tracking echocardiography may detect depression of global longitudinal LV systolic strain and global systolic strain rate during hypertensive crisis and improvement after medical therapy [29•]. Management It has been reported that most patients with elevated blood pressure, particularly the elderly, experience acute pulmonary edema with normal LV systolic function, presumably due to diastolic dysfunction. However, it has also been reported that uncontrolled hypertension may be responsible for the development of LV systolic dysfunction and heart failure with consequent functional mitral regurgitation and subendocardial myocardial ischemia [30]. For patients with heart failure due to systolic dysfunction, the goal of therapy is the lowest blood pressure not associated with symptoms of
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hypotension or evidence of hypoperfusion (i.e., worsening prerenal azotemia). In some patients with severe heart failure, this may be a systolic pressure as low as 90 mmHg [7, 27]. Although related data are not convincing, there may be a threshold diastolic pressure below which adverse cardiovascular outcomes might increase in elderly patients with isolated systolic hypertension. When treating such patients, a minimum posttreatment diastolic pressure of 60 mmHg overall or perhaps 65 mmHg in those with known coronary artery disease is suggested unless there are symptoms attributable to hypoperfusion that occur at higher pressures [7, 27]. Most patients with systolic heart failure are treated with inhibition of the renin-angiotensin system (i.e., angiotensin converting enzyme inhibitors or angiotensin II receptor blockers), beta-blockers, and, in selected patients, an aldosterone antagonist. These agents have favorable effects on survival in heart failure that are independent of their effects on blood pressure [31]. Patients with acute LV dysfunction and pulmonary edema should usually receive loop diuretics. Diuretics are not generally recommended agents for the treatment of hypertensive emergencies with the exception of acute pulmonary edema. However, in a recent small controlled trial, 59 patients with acute pulmonary edema due to hypertensive crisis were randomized to either furosemide or placebo. The investigators concluded that the subjective perception of dyspnea in patients with hypertensive pulmonary edema was not influenced by the administration of a loop diuretic. This is probably related to the fact that patients with hypertensive heart failure are often euvolemic or only mildly hypervolemic [32•]. An easily titratable vasodilator (i.e., sodium nitroprusside, nitroglycerin) is often added to reduce afterload. However, drugs that increase cardiac work (i.e., hydralazine) or acutely decrease cardiac contractility (i.e., labetalol) should be avoided [33]. Treatment of hypertension in patients with heart failure must take into account the type of heart failure that is present: systolic dysfunction, in which impaired cardiac contractility is the primary abnormality, or diastolic dysfunction, in which there is a limitation to diastolic filling and therefore in forward output due to increased ventricular stiffness. All the above therapies aim to ameliorate heart failure which can often be achieved with a 10 – 15 % reduction in blood pressure [31].
Aortic Dissection
Epidemiology Aortic dissection has an estimated incidence of 3/100,000 per year. Seventy percent of these patients are hypertensive and most of them are over 50 years of age, as there is reduced resistance of arterial walls with age [34, 35].
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Pathophysiology In aortic dissection, target organ damage occurs in the form of retrograde dissection into the heart with involvement of aortic branches accompanied by endothelial injury. Of note, the propagation of the dissection is dependent not only on the elevation in blood pressure itself but also on the velocity of LV ejection [34, 35].
arterial pressure <80 mmHg is crucial for the patient). Blood pressure should be maintained as low in this range as can be achieved without compromising mentation or urine output [20, 39].
Clinical Presentation and Evaluation Patients frequently present with sudden onset of chest pain radiating to the back and elevated blood pressure. Pulse deficit occurs in 20 % of patients with type A dissection, while hypertension at initial presentation is more common in patients with type B dissection [36]. Clinical presentation, however, sometimes varies and diagnosis may be elusive if not initially considered in the differential. Physical examination should include auscultation of the abdomen for murmur and blood pressure measurements in both arms to determine if they are symmetric. Confirmation of aortic dissection is usually obtained by using contrast-enhanced computed tomography or transesophageal echocardiogram. Timely recognition of this disease entity coupled with urgent and appropriate management is the key to a successful outcome in a majority of patients [35, 37].
Increased Sympathomimetic Activity
Management Antihypertensive therapy in acute aortic dissection aims specifically to lessen pulsatile load or aortic stress (dp/dt) by lowering the blood pressure in order to retard the propagation of the dissection and prevent aortic rupture. Pharmacological treatment aims to prevent myocardial ischemia and decrease LV afterload and myocardial oxygen consumption. Still, only few comparative studies or randomized controlled trials provide definitive conclusions and recommendations regarding the efficacy and safety of comparative agents [30, 38]. Hypertensive emergencies mainly require rapid blood pressure control with a parenteral antihypertensive medication while the patient is usually admitted to the intensive care unit. Typically, blood pressure should be reduced within minutes to an hour approximately 20 – 25 % and then gradually to 160/100 or 160/110 mmHg within the next 2 to 6 h. An abrupt fall in blood pressure in patients with preexisting hypertension may induce severe ischemic injury in major organs as a result of the chronic adaptation of autoregulation mechanisms [20]. Unlike other hypertensive emergencies, aortic dissection is an exception, where the rapid and immediate reduction of blood pressure within 5 to 10 min is required. Management includes primarily a parenteral beta-blocker. Esmolol is the drug of choice, but labetalol, propranolol, and metoprolol can also be used to reduce the heart rate below 60 beats per minute and decrease the shear stress on the aortic wall. If the blood pressure remains elevated after beta blockade administration, a vasodilator such as nitroglycerin can be added to achieve a systolic blood pressure of 100 to 120 mmHg (blood pressure target: systolic blood pressure <120 mmHg and a mean
Epidemiology Hyperadrenergic states can be produced by the use of drugs such as cocaine, amphetamines, phencyclidine, or monoamine oxidase inhibitors or recent discontinuation of clonidine or other sympatholytic agents. Pheochromocytoma and severe autonomic dysfunction (i.e., Guillain-Barré and Shy-Drager syndromes or acute spinal cord injury) are associated with hypertensive emergencies as well. Recent data showed that the number of individuals with cocaine dependence or abuse visiting an emergency department is growing [5]. Pathophysiology Sympathomimetic agents can cause severe hypertension and end-organ damage. In particular, cocaine and other sympathomimetic drugs have various physiological actions in peripheral circulation including stimulation of heart rate and vasoconstriction. Although the majority of cocainedependent individuals are normotensive, cocaine may precipitate hypertensive emergency due to central nervous system stimulation and peripheral alpha-agonist effects. The influence of cocaine on heart rate and blood pressure is dosedependent and is mediated through a-adrenergic stimulation [5]. Clinical Presentation and Evaluation Such conditions may cause chest pain either due to increased oxygen demand or decreased oxygen delivery. Symptoms involve the presence of chest pain, tachycardia, dilated pupils, combativeness, altered mental status, and seizures. The differential diagnosis of chest pain in patients that have used cocaine is similar to the general population; however, the likelihood of the patient having a serious event is increased. In a consecutive series of 233 emergency visits by cocaine-using patients, 56 % presented with cardiovascular complaints, including 40 % with chest pain. The minority of these patients suffered from an acute MI (6 %) but the overall mortality was low (<1 %). Other known complications of cocaine intoxication include arrhythmias, myocarditis, pneumothorax, pulmonary hypertension, acute pulmonary edema, aortic dissection, and bronchospasm [40, 41]. Methamphetamine intoxication may mimic cocaine intoxication and cause similar cardiac complications. In one study of patients presenting to the emergency de partment with chest pain after meth amphetamine use,
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25 % of patients suffered acute coronary syndromes, and 8 % had other cardiac complications such as tachyarrhythmias [42]. Management Stress testing and myocardial imaging have been suggested to facilitate safe, rapid discharge of patients with cocaine-associated chest pain. Toxicity may be superimposed on preexisting hypertension in patients that have become dependent on elevated blood pressure to maintain cerebral perfusion. Hypertension secondary to cocaine is mainly responsive to intravenous benzodiazepines because benzodiazepines minimize the stimulant effects of cocaine on the central nervous system. A vasodilator, such as nitroglycerin or nitroprusside, may be titrated to effect if further therapy is indicated. Nitroglycerin is the drug of choice in patients with chest pain. The use of nitroprusside to control hypertension has the additional advantage of aiding heat loss by peripheral vasodilatation. However, frequent monitoring is required since this drug can produce a sudden and drastic drop in blood pressure [43, 44]. No ns el ec ti ve be ta -b loc ke rs su ch as pr op ra no lo l should generally be avoided because of the risk of an abrupt rise in blood pressure as well as coronary vasoconstriction due to the exaggerated effect of catecholamines on unblocked alpha-receptors [5].
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Conclusions
Cardiovascular events related to hypertensive emergencies are life-threatening situations requiring immediate evaluation and management to prevent end-organ damage. Several regimens have proven to be effective enough but the choice of treatment depends on the clinical presentation of the patient. A very important aspect of care for these patients is to assure highquality outpatient follow-up since a large proportion of them will return to the hospital with a recurrent hypertensive emergency. Adequate control of blood pressure should be pursued as a way to avoid this severe com plication of hypertension. Compliance with Ethics Guidelines Conflict of Interest D.P. Papadopoulos, E.A. Sanidas, N.A. Viniou, V. Chantziara, I. Barbetseas, and T.K. Makris declare that they have no conflicts of interest. Human and Animal Rights and Informed Consent This article does not contain any studies with human or animal subjects performed by any of the authors.
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