Hypertensive Crises

Anand Swaminathan and Michael P. Jones

BACKGROUND

Hypertension affects an estimated 50 million individuals in the United States.¹ Management of this largely preventable disease focuses on chronic reduction of blood pressure through dietary and lifestyle modifications and, when necessary, pharmacologic management. Patients with hypertension frequently seek emergency care, and hypertension is one of the most common primary diagnoses of patients admitted with critical illness.

Hypertensive emergency refers to the presence of end-organ damage directly attributable to uncontrolled elevations in blood pressure and requires immediate administration of antihypertensive medications to prevent irreversible injury. Hypertensive urgency, a more benign diagnosis, is defined as symptomatic (e.g., headache, shortness of breath, anxiety) hypertension without evidence of end-organ damage. The most common presentations of hypertensive emergency include cerebral infarction or hemorrhage (24.5%), acute pulmonary edema (APE) (22.5%), and hypertensive encephalopathy (16.3%). Other complications include acute coronary syndrome (ACS), aortic dissection (AD), preeclampsia and eclampsia, acute renal failure, microangiopathic hemolytic anemia, and hypertensive retinopathy.

This chapter presents an approach to the management of severe hypertension in the setting of four important emergency department (ED) diagnostic concerns: APE, hypertensive encephalopathy, ACS, and AD. Stroke—the most common of all hypertensive emergencies—is addressed in detail in Chapter 20. A review of antihypertensive agents used in the management of these four conditions is provided in Tables 16.1 and 16.2.

ACUTE PULMONARY EDEMA

History and Physical Exam

Cardiogenic APE is a relatively common clinical entity in the ED and carries a mortality rate of 15% to 20%. The most common presenting complaints are dyspnea, tachypnea, and, in severe cases, cough productive of frothy sputum.

The history and physical exam in patients with APE should focus on determining the etiology of the heart failure causing the edema. Potential etiologies include myocardial infarction (MI), exacerbation of chronic CHF, mitral/aortic valve dysfunction, and infection. Eliciting a history of chronic renal failure is also important, as these patients, if volume overloaded, will often require hemodialysis to remove excess fluid. Physical exam will reveal findings—such as tachypnea and abnormal lung sounds—common to other disease processes such as pneumonia. Findings more specific to APE include elevated jugular venous pressure and an S₃ gallop.^2,3 New murmurs are also important to note as these may suggest rupture of a valve leaflet—a critical finding that can require surgical management.

Diagnostic Evaluation

There is no single test that confirms the diagnosis of APE. Diagnostic evaluation commonly employs laboratory testing, electrocardiogram (ECG), chest radiography (CXR), and bedside ultrasound (US). Serum B-type natriuretic peptide is a relatively sensitive marker for APE (90%), but lacks specificity (76%).⁴ Cardiac-specific troponin (cTnT) assays can be helpful in establishing myocardial ischemia or infarction as the underlying cause of APE, but troponin levels may also be elevated secondary to increased right ventricular wall stress, rate-related or stress ischemia, or underlying end-stage renal disease (ESRD).⁵ As a result, many patients with CHF will have chronically mild troponin elevations. A number of trials have found a correlation between an elevated cTnT and increased mortality in acute heart failure patients.^6,7

The ECG is an essential diagnostic test in APE, as it can reveal precipitating ischemia or dysrhythmias that require additional interventions (cardiac catheterization or rate/rhythm control, respectively). The CXR is equally important; in diagnosing APE, its findings of cephalization, interstitial edema, and alveolar edema are highly specific (96%, 98%, and 99%, respectively) but have low sensitivity (41%, 27%, and 6%, respectively). Up to 18% of CXRs in patients with APE will demonstrate no vascular congestion.^8,9 Finally, bedside ultrasonography is a relatively new but valuable tool for evaluation of patients with suspected APE. Bedside transthoracic echocardiography (TTE) can be used to estimate left ventricular (LV) function and diagnose valvular rupture; it can also reveal B-lines, a highly sensitive and specific finding (97% and 95%, respectively) for interstitial edema. In trained hands, lung ultrasonography is more accurate than plain radiography for the diagnosis of APE.^10,11

Management Guidelines

In patients with APE, treatment focuses on reducing the work of breathing (and thus the risk of respiratory failure) and shifting fluid out of the interstitial and alveolar spaces through reduction of preload and afterload. Respiratory support for patients with APE traditionally necessitated intubation and mechanical ventilation. In the last 10 years, the use of noninvasive positive pressure ventilation (NIPPV) using continuous positive airway pressure (CPAP) and bilevel positive airway pressure (BiPAP) has become increasingly common. NIPPV, by increasing intrathoracic pressure, effects a reduction in preload, thereby decreasing blood flow into the pulmonary vasculature and reducing pulmonary capillary pressures. Although not shown to reduce mortality, NIPPV has been associated with decreased need for intubation, fewer critical care unit admissions, and fewer overall treatment failures.^12–16

Pharmacologic treatment of increased preload emphasizes use of nitrates (specifically nitroglycerin), morphine sulfate, and loop diuretics (furosemide). Nitroglycerin (sublingual, topical, or intravenous) is a potent vasodilator, and small studies have shown it to be capable of producing rapid, significant decreases in LV pressure.¹⁷ Sublingual nitroglycerin (SLNTG) should be started immediately upon recognition of APE and followed by a continuous IV infusion. A 400-mcg tab of SLNTG provides a dose equivalent to an intravenous infusion of 80 mcg/min for 5 minutes, so the IV infusion should be started at this or a similar infusion rate and rapidly titrated to effect. Morphine and loop diuretics have been used for decades in the treatment of APE, but the physiologic rationale for their efficacy is flawed, and there is little evidence to support their use. The ADHERE study group found that APE patients receiving morphine had increased rates of mechanical ventilation (15.4% vs. 2.8%), ICU admissions (38.7% vs. 14.4%), and mortality (13.0% vs. 2.4%).⁶ These results have also been reproduced in ED-based studies.¹⁷ Loop diuretics for the treatment of APE historically were recommended based on the cardiorenal pathogenesis model, which hypothesized that edema and decreased cardiac function result from decreased kidney function and subsequent volume overload. However, more recent studies have shown that less than half of patients with APE have total body increased volume.^18,19 Furosemide was shown to initially increase PCWP in patients in the ICU with APE and did not lead to significant drops in preload until 20 minutes after administration.²⁰ Additionally, loop diuretics activate the renin–angiotensin–aldosterone system (RAAS) and the sympathetic nervous system, leading to increased vasoconstriction and impaired cardiac function.²¹ Finally, many patients with APE also have ESRD and will not benefit from loop diuretics regardless of volume status.

Correction of elevated afterload—the result of activation of the RAAS and an increase in sympathetic drive—is equally important in the management of APE; afterload reduction improves LV function and helps restore adequate circulation. Bilevel positive airway pressure (BPAP), in addition to its ability to reduce preload and support respiratory function, produces afterload reduction; however, the mechanism of this response is not fully understood.^12–16 High-dose IV nitroglycerin (>100 mcg/min) also results in arterial vasodilation and afterload reduction. The use of angiotensin-converting enzyme inhibitors (ACEI) for afterload reduction in the treatment of cardiogenic APE is supported by a number of small studies. One of these demonstrated a reduced need for mechanical ventilation in patients receiving ACEI, while a second demonstrated a lower ICU admission rate (OR = 0.29) and lower intubation rates (OR = 0.16) with its use.^22,23 Nicardipine is another alternative for achieving afterload reduction; it can be rapidly titrated and effects a coronary blood flow increase, which may be beneficial in systolic heart failure.^24,25

Finally, emphasis should be placed on identifying reversible causes of APE and involving subspecialty consultation—cardiac catheterization for AMI, cardiac surgery for valvular rupture, and hemodialysis for ESRD—as appropriate.

HYPERTENSIVE ENCEPHALOPATHY

History and Physical Exam

Hypertensive encephalopathy is one of the more insidious consequences of uncontrolled hypertension. It is classically defined as the triad of hypertension, altered mental status, and papilledema.²⁶ Hypertensive encephalopathy must be treated immediately to prevent further end-organ damage. First described in 1928, hypertensive encephalopathy is a rare disease that leads to death if untreated.²⁷

A patient history may be difficult to obtain, as these patients may in fact be obtunded; in this case, evaluation for other life-threatening causes of altered mental status—such as hypoglycemia, hypoxia, and intracranial injury—should take precedence. Once these causes have been ruled out, hypertensive encephalopathy should be considered. Symptoms will commonly include headache, irritability and nausea. Seizures may also be reported. Physical exam should center on accurate measurement of blood pressure (using an appropriately sized cuff or arterial blood pressure monitoring) and a detailed neurologic examination looking for focal deficits. Papilledema and retinal hemorrhages may be observed. There is no set value of measured blood pressure required for hypertensive encephalopathy; a patient with long-standing hypertension may tolerate blood pressures greater than 200 mm Hg systolic and 150 mm Hg diastolic, while a pregnant woman or child can develop symptoms at diastolic blood pressures greater than 100 mm Hg.²⁸

Diagnostic Evaluation

Hypertensive encephalopathy is a diagnosis of exclusion. Its workup includes a noncontrast CT head to rule out mass lesion or hemorrhagic or ischemic stroke as well as laboratory examinations to exclude metabolic causes of altered mental status. Suggestive findings on CT include signs of edema, particularly in the posterior regions. Brain MRI will show edema of a vasogenic origin, but obtaining this degree of imaging is often neither feasible nor necessary in the ED, unless there is concern for a more subtle focal insult not visualized on CT.

Electroencephalographic (EEG) examination will show evidence of generalized slowing and epileptiform discharges as well as loss of alpha-wave rhythms, signifying an impaired consciousness. The utility of continuous EEG monitoring in the ED, however, is not well established; this is in part due to the typically rapid improvement in symptoms following initiation of aggressive therapy, and in part to the practical challenges of obtaining an EEG in the ED.

Management Guidelines

Hypertensive encephalopathy is a fully reversible condition if appropriate treatment is instituted in a timely manner. The mainstay of treatment is a rapid, but controlled, decline in blood pressure, with adequate maintenance of cerebral perfusion pressure. Most experts recommend a reduction in mean arterial pressure of no more than 20% to 25% in the first hour of therapy guided by an arterial blood pressure monitor for more timely and accurate monitoring. In a busy emergency department, at a minimum, the blood pressure should be noninvasively monitored every 3 to 5 minutes until more invasive monitoring can be made available. Preferred antihypertensive agents include sodium nitroprusside, labetalol, and nicardipine.

Literature suggests that labetalol, in particular, has minimal impact on cerebral perfusion pressure—making it optimal for treating hypertensive encephalopathy. Unlike pure beta-blocking agents (e.g., esmolol) that reduce cardiac output, labetalol reduces systemic vascular resistance (SVR) without reducing total peripheral blood flow, which is essential in maintaining cerebral, renal, and cardiac perfusion.^29–32

ACUTE CORONARY SYNDROME

History and Physical Exam

Hypertension is a known risk factor for the development of coronary artery disease.^1,33 Acute elevations in blood pressure can lead to increased LV demand without a proportionate increase in myocardial perfusion, resulting in ischemia. In all patients with elevated blood pressure who complain of chest pain or chest pain equivalents (e.g., shortness of breath), ACS should be considered.

The physical exam in the patient with ACS is nonspecific but plays an important role in ruling out the alternative diagnoses of AD and APE. The presence, in particular, of pulse deficits, aortic insufficiency murmurs, and neurologic deficits points to AD.²⁶ The presence of jugular venous distension, lower extremity edema, severe dyspnea, and crackles on pulmonary exam points to APE.

Diagnostic Evaluation

ECG, CXR, bedside echocardiography, and serum cardiac enzyme testing are essential to the evaluation of ACS in the setting of hypertensive emergency. An ECG should be performed immediately and evaluated for the presence of an ST-segment elevation myocardial infarction (STEMI) necessitating emergent cardiac catheterization. While CXR rarely establishes a diagnosis of ACS on its own, it is helpful in identifying alternative hypertensive emergencies (e.g., AD or APE). Similarly, echocardiography may reveal LV wall motion abnormalities consistent with MI, but may also show findings consistent with AD (pericardial effusion, proximal dissection flap) or APE (B-lines, flail leaflet). An elevated serum cardiac troponin (cTn) supports a diagnosis of ACS; however, it is important to note that cTn may be elevated in a number of disease processes including pericarditis/myocarditis, pulmonary embolism, tachydysrhythmias, takotsubo cardiomyopathy, ESRD, sepsis, stroke, and rhabdomyolysis.⁵

Management Guidelines

The treatment of ACS in the setting of hypertensive emergency requires the use of pharmacologic agents directed both at blood pressure control—to reduce shear forces, LV strain, and ischemia and platelet activation—and platelet inhibition. Antiplatelet agent recommendations can be found in the American College of Cardiology/American Heart Association (ACC/AHA) guidelines.^34,35 For rapid reduction in blood pressure, nitroglycerin and beta-blockers are the most commonly recommended agents.^34,35 Nitroglycerin (sublingual or intravenous) reduces both LV filling pressure and SVR, thereby decreasing both myocardial oxygen demand and the likelihood of further ischemia.³⁶ At higher doses, nitroglycerin produces coronary artery vasodilation.³⁶ These factors, along with its short half-life and ease in titration, make it an ideal therapeutic agent in hypertension-associated ACS.

Beta-blockers are beneficial both for blood pressure reduction and for prevention of ventricular dysrhythmias in ACS. The ACC/AHA recommends beta-blockers be given within 24 hours of presentation, with a goal of 20% to 30% blood pressure reduction.^35,37–39 Although both labetalol and esmolol are commonly recommended, esmolol has a more favorable profile with rapid onset, short half-life, and ease of titration.²⁸ Beta-blocking agents should, however, be used with caution in the setting of ACS, as these agents can exacerbate LV failure. The COMMIT trial found that patients with acute MI given beta-blockers early in their clinical course had higher rates of cardiogenic shock and recommended beta-blocker therapy be considered only after a patient’s hemodynamic condition had stabilized.⁴⁰ In patients at risk for cardiogenic shock, it is advisable to obtain an echocardiogram to further assess cardiac function prior to the administration of intravenous beta-blockers.

AORTIC DISSECTION

History and Physical Exam

AD represents one of the most challenging diagnoses to make in the emergency department. The disease carries a high mortality rate (Stanford type A, 34.9%, and Stanford type B, 14.9%) and should be considered in any patient with hypertension and a complaint of chest or back pain. The majority of patients with AD complain of chest pain (72.7%), abrupt onset of pain (84.8%), and severe pain at onset (90.6%).⁴¹ The classic presentation—sudden onset of sharp or tearing chest pain radiating to the back—is, however, rarely observed.⁴¹ Patients with Stanford type B dissections (descending aorta only) can present with isolated back pain.

Commonly described physical exam findings are equally unreliable in ruling out AD. While the majority of patients (72.1%) have a history of hypertension, only 50% will be hypertensive on presentation (in the patient in whom an ascending dissection has resulted in a pericardial effusion, hypotension may actually be observed).⁴¹ Other exam findings, including a murmur of aortic insufficiency (31.6%) and pulse deficit (15.1%), are equally unlikely to be found. However, in a patient with chest pain that has one of these findings, the diagnosis of AD should be more seriously considered.

Diagnostic Evaluation

The most important diagnostic modalities in AD are the ECG, CXR, and chest CT with IV contrast. An ECG will frequently demonstrate either no abnormal findings or nonspecific findings (31.3% and 41.4%, respectively); about 3.2%, however, will show findings consistent with an STEMI. An STEMI can be observed in the setting of an ascending AD when the dissection extends into either the right or left coronary ostium, leading to occlusion of any of the major coronary arteries. The most common coronary artery involvement occurs via extension into the right coronary artery leading to an inferior wall infarction. In patients with evidence of STEMI on ECG, a diagnosis of AD should be considered if the patient’s symptoms or presentation are atypical for ACS.

Chest radiography may reveal a widened mediastinum (61.6%) or abnormal aortic contour (49.6%), but is normal in up to 15% of patients. Chest CT with IV contrast, which has a high sensitivity (95%) and specificity (87% to 100%) and can be performed rapidly, is the primary diagnostic modality for AD in the ED.⁴² Transesophageal echocardiography is an effective alternative imaging modality (sensitivity of 98%, specificity of 95%) for patients that cannot tolerate CT, but may not be available in the ED and/or may delay diagnosis. Although TTE is rarely adequate to make a definitive diagnosis of AD, it can help identify pericardial effusions or tamponade that provide indirect evidence of AD.

Management Guidelines

Once AD is diagnosed, all efforts should be made to obtain emergent cardiothoracic surgery consultation for operative repair. Mortality increases by 1% to 2% for every hour from symptom onset to definitive treatment.⁸ ED management should focus on “anti-impulse therapy,” that is, control of blood pressure and heart rate in order to reduce the shear forces of LV ejection (dP/dT). Elevated shear forces result in a forceful flow of blood against the dissection flap that can cause the flap to extend.⁴² AD is the only hypertensive emergency in which rapid lowering of blood pressure (ideally within 5 to 10 minutes) is indicated. The recommended target systolic blood pressure is 100 to 110 mm Hg, with some experts advocating lowering to subnormal numbers (SBP = 90 to 100).^28,42 Heart rate should be lowered to less than 60 bpm.^28,42

First-line agents for anti-impulse therapy are beta-blockers, as they have the ability to lower heart rate and blood pressure simultaneously. Although there is no consensus on a preferred beta blocker, esmolol’s rapid onset and ease of titration make it an ideal agent.^28,39,42,43 Labetalol can be used, but has a slower onset of action and a longer half-life and is more difficult to titrate. If beta-blockers are contraindicated, calcium channel blockers (CCBs) (e.g., diltiazem) are acceptable alternatives.

Once goal heart rate is achieved, an arterial vasodilator should be added to achieve an SBP <110 mm Hg. Historically, sodium nitroprusside was the vasodilator of choice, but this agent has multiple limitations, including labile blood pressure and reflex tachycardia.^28,39,42,43 Clevidipine and nicardipine offer more reliable effects on blood pressure. Both agents are dihydropyridine CCBs and pure afterload reducers that have a rapid onset and a short half-life, are easily titratable, and have been demonstrated safe to use concurrently with intravenous beta-1–selective agents.⁴⁴ An ED-based study found that 89% of patients with hypertensive emergencies who received clevidipine reached goal BP targets within 30 minutes.⁴⁴ If neither of these agents is available, intravenous nitroglycerin at higher doses may provide adequate blood pressure control, however use as a solo agent can produce a reflex tachycardia.

Finally, bedside US should be performed in all patients with AD to determine whether the patient has cardiac tamponade and requires immediate pericardiocentesis.

CONCLUSION

Hypertensive crisis requires prompt intervention. Recognition of the common complications of severe hypertension and appreciation of optimal antihypertensive agents enable the emergency physician to respond to these emergencies in a timely and effective manner.

Related posts:

Extracorporeal Membrane Oxygenation Sickle Cell Disease Tissue Oxygenation and Cardiac Output Heart Failure and Cardiogenic Shock ED Evaluation of the Critically Ill Patient Seizure and Status Epilepticus