Open Journal Systems

REVIEW ARTICLES

Received: 15/10/2015

Accepted: 23/11/2015

Cardiovascular complications of hypertensive crisis

Martín Rosas-Peralta,^a Gabriela Borrayo-Sánchez,^b Alejandra Madrid-Miller,^c Erick Ramírez-Arias,^d Gilberto Pérez-Rodríguez^e

^aDivisión de Investigación en Salud

^bDirección Médica

^cServicio de Terapia Posquirúrgica

^dServicio de Urgencias

^eDirección General

Hospital de Cardiología, Centro Médico Nacional Siglo XXI, Instituto Mexicano del Seguro Social, Ciudad de México, México

Communication with: Martín Rosas-Peralta

Email: mrosas_peralta@hotmail.com

It is inexorable that a proportion of patients with systemic arterial hypertension will develop a hypertensive crisis at some point in their lives. The hypertensive crises can be divided in hypertensive patients with emergency or hypertensive emergency, according to the presence or absence of acute end-organ damage. In this review, we discuss the cardiovascular hypertensive emergencies, including acute coronary syndrome, congestive heart failure, aortic dissection and sympathomimetic hypertensive crises (those caused by cocaine use included). Each is presented in a unique way, although some patients with hypertensive emergency report non-specific symptoms. Treatment includes multiple medications for quick and effective action with security to reduce blood pressure, protect the function of organs remaining, relieve symptoms, minimize the risk of complications and improve patient outcomes.

Key words: Emergencies; Hypertension; Myocardial infarction; Acute coronary syndrome; Heart failure

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Recent data suggest that hypertension (HT) is the cause of nearly 7.1 million deaths per year worldwide. About 1 to 2% of patients with hypertension develop a hypertensive crisis that can be classified as emergency or hypertensive emergency, depending on the presence or absence of acute dysfunction of a target organ, respectively. Hypertensive crisis can develop in patients with or without preexisting chronic hypertension,^1-3 and the prevalence reflects the distribution of essential hypertension in the general population, with African American men and the elderly as the groups most commonly affected.⁴

The cardiac emergencies most commonly associated with severely elevated blood pressure are: acute left ventricular dysfunction (LV) with pulmonary edema (22%), acute coronary syndromes (including acute myocardial infarction -MI) (18%), and aortic dissection (8%). In the context of misuse of sympathomimetic drugs, which can cause or mimic clinical conditions, cocaine accounts for almost a third of all emergency room visits.⁵ Classic symptoms, both cardiac and pulmonary (dyspnea, chest pain, arrhythmia and syncope), appear to be less common in patients with hypertensive crisis (28.3%). Most present with non-specific symptoms.⁶

The risk of a future cardiovascular event attributable to hypertension is higher in patients with established cardiovascular disease, diabetes mellitus, or chronic kidney disease, compared to those without these comorbid conditions. This increased risk was addressed in the Seventh report of the Joint National Committee (JNC-7) in 2003 on high blood pressure. It states in that heart disease, heart failure, diabetes, chronic kidney disease, and cerebrovascular disease are "compelling evidence" for the treatment of hypertension. Other risk factors include peripheral arterial disease and traditional coronary risk factors, such as cigarette smoking and family history of heart disease.⁷

Mortality rates of patients with hypertensive emergencies have decreased significantly over the years (80% in 1928 to 10% in 1989),⁸ mainly due to the availability of antihypertensive medications. The therapeutic goal is to protect the function of other organs, reduce the risk of complications, and improve patient outcomes.^9,10

The objective of this review is to summarize current recommendations for the evaluation and treatment of the most common cardiovascular clinical presentations found in patients with hypertensive crisis.

Myocardial infarction

Epidemiological data indicate that MI is the leading cause of death and hospitalization in patients with severely elevated blood pressure. Moreover, almost 50% of all hypertension patients originally admitted to the emergency room died of acute MI during long-term follow-up. Notably, no differences were found in the presence of other risk factors such as smoking or the prevalence of diabetes mellitus.^11,12

The pathophysiology of 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, increased blood pressure generates mechanical stress and endothelial damage, leading to increased permeability, activation of the coagulation and platelet cascade, and fibrin deposition. This process results in ischemia and the release of additional vasoactive mediators, which creates a vicious cycle of permanent damage. The renin-angiotensin system is frequently activated, leading to more vasoconstriction and to the production of proinflammatory cytokines such as IL-6. 

Furthermore, NADPH oxidase activity increases and generates reactive oxygen species. These collective mechanisms may culminate in the hypoperfusion of an organ, ischemia, and dysfunction, which manifests as hypertensive emergency.¹³

The evaluation of hypertensive crisis can lead us to detect manifestations of ischemia and even find acute coronary syndrome as responsible for chest discomfort.

Cardiovascular risk assessment and the study of comorbidities are essential. An electrocardiogram is the gold standard for detection of ischemia or MI. In addition, vital signs, blood pressure, oxygen saturation, and heart rate should be measured carefully during the physical examination of a patient with hypertensive crisis.

The reference laboratory analysis must be done quickly after the initial patient assessment. These laboratory tests include cardiac enzymes and troponin-I analysis. In a retrospective study, patients with hypertensive crisis and elevated c-troponin-I (cTnI) heart had 2.7 times higher risk of major adverse cardiovascular events and stroke (MACCE) at two years of follow-up, compared to those with normal cTnI values.

In patients with hypertensive crisis, elevation of cTnI confers a significantly increased risk of long-term MACCE and is a strong predictor of coronary obstructive heart disease.¹⁴

The management of severe hypertension associated with acute MI should be treated appropriately with intravenous nitroglycerin, amlodipine, clevidipine, nicardipine, labetalol, or esmolol to reduce underlying coronary ischemia or to not increase myocardial oxygen consumption and to improve prognosis. In addition, lowering blood pressure improves hemodynamics, improves the risk of pulmonary edema, and decreases the size of the infarct zone. If available, especially in MI with ST segment elevation, primary angioplasty is the best choice for reperfusion therapy in patients with high blood pressure, as thrombolysis may increase the risk of cerebral bleeding.^15-18

Nitroglycerin is a venodilator that mainly reduces the preload and decreases cardiac oxygen demand. This agent is mainly used in MI and acute pulmonary edema, along with other antihypertensive regimens.^15-17

Labetalol is an Alpha-1 adrenergic receptor blocker and a nonselective beta-blocker. It reduces systemic vascular resistance, but maintains the cerebral, renal, and coronary blood flow. It is important to note that despite the beta-blocker effect, cardiac output is maintained.¹

Esmolol is an intravenous beta-receptor blocker 1; it is a cardioselective with rapid onset and short duration of action that can be used safely in most patients treated for acute MI with contraindications to beta-blockers. Tolerance of greater maintenance doses of esmolol is a good predictor of results with beta-blocker oral therapy.¹⁹

Other agents that can be used in hypertensive emergencies include amlodipine, nicardipine (dihydropyridine calcium antagonists), which are useful agents for patients with coronary artery disease because of their beneficial effect on coronary blood flow, and clevidipine, which is a relatively new short-acting dihydropyridine calcium channel blocker, which is given intravenously and has a dosing regimen not based on weight, which allows prolonged infusion and a successful transition to oral therapy.^20-22

Optimal blood pressure after acute coronary syndrome remains controversial. Numerous studies have shown an inverse relationship between diastolic pressure and adverse cardiac ischemic events (that is, 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, describing the shape of the relationship between blood pressure and the risk of cardiovascular morbidity and mortality. The observation mentioned appears to be more pronounced in patients with underlying coronary artery disease.

Since coronary blood flow occurs primarily during diastole in patients with coronary heart disease, a drop in diastolic blood pressure could reduce perfusion pressure distal to a stenosis below the critical level at which self-regulation is effective. Therefore, lowering systolic blood pressure values ​​to near or below 120-125 mmHg and diastolic pressure below 70-75 mm Hg in patients at high cardiovascular risk may be accompanied by an increase in the incidence of coronary events.^23-26

Heart failure

The most common clinical manifestations of hypertensive crisis include pulmonary edema (22.5%) and congestive heart failure (12%).

The pathophysiology of acute congestive heart failure is commonly associated with systolic or diastolic dysfunction, with or without additional cardiac pathology, as with valvular abnormalities or coronary artery disease. However, a variety of conditions or events can cause cardiogenic pulmonary edema in the absence of heart disease, including severe hypertension itself. Patients presenting with cardiogenic pulmonary edema often suffer from uncontrolled severe hypertension. Many of these patients have preserved left ventricle ejection fraction (normal or nearly normal). The increasing afterload, instead of or in addition to fluid overload, can precipitate decompensation in these patients.²⁷

The clinical decompensation of cardiac evaluation and presentation can cause symptoms such as dyspnea, orthopnea, cough, fatigue, or pulmonary edema. In a recent study of 189 patients, normal heart rate was associated more with hypertensive emergency, while tachycardia was associated more with heart failure.²⁸ Imaging may include radiography or echocardiography. A simple chest X-ray is extremely useful for documenting cardiomegaly or pulmonary edema. Echocardiography gives more information about the real situation of heart function.²⁹

Management of hypertensive crisis

It has been reported that most patients with high blood pressure, particularly older adults, may experience acute pulmonary edema with normal systolic left ventricular function, presumably due to diastolic dysfunction. However, it has been observed that uncontrolled hypertension may be responsible for the development of ventricular systolic dysfunction and heart failure with consequent functional mitral regurgitation or subendocardial 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 hypotension or evidence of hypoperfusion (i.e., worsening prerenal azotemia). In some patients with severe heart failure, this can be established with a systolic pressure of just 90 mm Hg.^7,27

Although some related data are not convincing, there may be a diastolic pressure with a threshold below which adverse cardiovascular outcomes may increase in older patients with isolated systolic hypertension. When treating these patients, a post-treatment diastolic pressure of 60 mm Hg or perhaps 65 mm Hg is suggested in those with known coronary artery disease, unless there are symptoms attributable to hypoperfusion, which occur at higher pressures.^7,27-31

Most patients with systolic heart failure are treated with renin-angiotensin system inhibitors (i.e., angiotensin-converting enzyme inhibitors or angiotensin II receptor blockers), beta-blockers and, in selected patients, aldosterone antagonists. These agents have favorable effects on survival in heart failure, which are independent of their effects on blood pressure.³¹

Patients with acute pulmonary edema and ventricular dysfunction should generally receive loop diuretics. Diuretics are generally not recommended as agents for the treatment of hypertensive emergencies, with the exception of acute pulmonary edema. However, a small recent controlled trial in 59 patients with acute pulmonary edema due to hypertensive crisis assigned patients randomly to furosemide or placebo. The researchers concluded that the subjective perception of dyspnea in patients with hypertensive pulmonary edema was not influenced by the administration of a diuretic. This probably relates to the fact that patients with hypertensive heart failure are often euvolemic or only slightly hypovolemic.³²  

A vasodilator that is easy to titrate (i.e., sodium nitroprusside, nitroglycerin) is often added to reduce afterload. However, avoid drugs that increase cardiac output (for example, hydralazine) or decrease cardiac contractility (e.g. labetalol).³³

Treatment of hypertension in patients with heart failure should take into account the type of heart failure: systolic dysfunction, in which impaired cardiac contractility is the primary abnormality, or diastolic dysfunction, in which there is a limitation of diastolic filling and, therefore, in the forward exit, due to increased ventricular stiffness. All the above treatments aim to improve heart failure, which often can be achieved with a 10-15% reduction in blood pressure.31

Aortic dissection

Regarding epidemiology, aortic dissection has an estimated incidence of three cases per 100,000 per year. Of these patients, 70% are hypertensive and most are over 50 years old because with age there is less resistance in the arterial walls.34,35 As for its pathophysiology, in aortic dissection, the target organ damage occurs in the form of retrograde dissection towards the heart, with the involvement of aortic branches accompanied by endothelial injury. It is noteworthy that the propagation of the dissection depends not only on the elevation of blood pressure per se, but also on the left ventricular ejection fraction.^34,35

Patients often present with sudden onset of chest pain that radiates to the back, in addition to high blood pressure. The pulse deficit occurs in 20% of patients with type A dissection, whereas hypertension on initial presentation is more common in patients with type B dissection.³⁶

The clinical presentation, however, sometimes varies and diagnosis can be difficult if not initially considered in the differential diagnosis. Physical examination should include abdominal auscultation to record murmurs, and blood pressure in both arms to determine if they are symmetrical. Confirmation of aortic dissection is generally obtained by using contrasted CT scan or transesophageal echocardiogram.

The timely recognition of this entity in conjunction with appropriate and urgent management is the key to optimal results in most patients.^35,37

Antihypertensive treatment in the management of acute aortic dissection specifically aims to reduce pulsatile load or aortic stress (dp/dt) by reducing blood pressure in order to retard the spread of dissection and prevent aortic rupture. Medication treatment aims to prevent myocardial ischemia and decrease left ventricular afterload and myocardial oxygen consumption. Still, a few comparative studies or randomized controlled trials provide definitive conclusions and recommendations regarding the comparative efficacy and safety of agents.^30,38

Hypertensive emergencies mainly require rapid control of blood pressure with a parenteral antihypertensive medication while the patient is usually admitted to the intensive care unit. Usually blood pressure should be reduced 20 to 25% over a period ranging from a few minutes to an hour or so, and then gradually to 160/100 or 160/110 mm Hg within two to six hours.

A sudden drop in blood pressure in patients with preexisting hypertension can 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, which necessitates rapid and immediate reduction in blood pressure in a period ranging from five to 10 minutes.

Treatment primarily includes a parenteral beta-blocker. Esmolol is the drug of choice, but labetalol, propranolol, and metoprolol also be used to reduce heart rate below 60 beats per minute and thus reduce shear stress on the aortic wall.

If blood pressure remains high after the administration of beta-blockers, a vasodilator may be added such as nitroglycerin to achieve a systolic blood pressure of 100-120 mm Hg (the blood pressure sought is a systolic blood pressure < 120 mm Hg; also, an average blood pressure < 80 mmHg is crucial for the patient).

Blood pressure should be kept as low in this range as can be achieved without compromising urinary output.^20,39

Increased sympathomimetic activity

In connection with its epidemiology, hyperadrenergic states can be caused by the use of drugs such as cocaine, amphetamines, phencyclidine, monoamine oxidase inhibitors, or recent withdrawal from clonidine or other sympatholytic agents. Pheochromocytoma or severe autonomic dysfunction (i.e. Guillain-Barré syndrome and Shy-Drager syndrome, or acute spinal cord injury) are associated with hypertensive emergencies. Recent data showed that the number of cocaine-dependent people attending an emergency department is increasing.⁵

In terms of pathophysiology, sympathomimetic agents can cause severe hypertension and visceral involvement. Cocaine and other sympathomimetic drugs have various physiological actions in the peripheral circulation, including stimulation of heart rhythm and vasoconstriction. While most cocaine-dependent people are normotensive, this drug can precipitate a hypertensive emergency due to the stimulation of the central nervous system and its peripheral alfa-agonist effects. The influence of cocaine on heart rate and blood pressure is dose-dependent and is mediated through adrenergic stimulation.⁵

About the clinical presentation and evaluation of increased sympathomimetic activity, these conditions can cause chest pain or, due to increased oxygen demand, decreased oxygen. Symptoms include the presence of chest pain, tachycardia, dilated pupils, altered mental state, and seizures.

The differential diagnosis of chest pain in patients who have used cocaine is similar to the general population. However, the probability that the patient has a serious event increases.

In a consecutive series of emergencies in which there were 233 visits to an emergency department due to cocaine use by patients, 56% had cardiovascular complaints and 40% had chest pain. A minority of these patients suffered acute MI (6%) and 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 is similar to cocaine intoxication and can cause similar cardiac complications. In a study of patients presenting to the emergency department with chest pain after using methamphetamine, 25% suffered acute coronary syndrome and 8% had other cardiac complications, such as tachyarrhythmia.⁴²

Stress tests and myocardial imaging have been suggested to facilitate the safe and rapid discharge of patients with chest pain associated with cocaine.

Toxicity can be superimposed on preexisting hypertension in patients who have become dependent on high blood pressure to maintain cerebral perfusion. Hypertension secondary to cocaine mainly responds to intravenous benzodiazepines because these minimize the stimulating effects of cocaine on the central nervous system.

A vasodilator, such as nitroglycerin or nitroprusside, can be titrated to effect if therapy is indicated. Nitroglycerin is the drug of choice in patients with chest pain. The use of nitroprusside to control hypertension has the additional benefit of helping heat loss from peripheral vasodilatation. However, frequent monitoring is required, as this drug can cause a drastic and sudden drop in blood pressure.^43,44

Nonselective beta-blockers, such as propranolol, should generally be avoided because of the risk of a sudden rise in blood pressure and a coronary vasoconstriction caused by the exaggerated effect of catecholamine on unblocked alpha receptors.⁵

Conclusions

Cardiovascular events associated with hypertensive emergencies are life-threatening situations that require immediate evaluation to avoid visceral involvement. Several regimens have proven effective, but the choice of treatment depends on the patient's clinical presentation. A crucial aspect of care for these patients is to ensure high quality ambulatory monitoring, since a large proportion of them return to the hospital with a recurring emergency. Adequate blood pressure control should be sought as a way to avoid these serious complications of hypertension.

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