Hypertensive Emergencies: Are You Prepared?

The untreated hypertensive emergency carries a one-year mortality of more than 90%. This review provides keys to the management of critical states of cardiopulmonary, neurologic, and renal dysfunction due to hypertension.
Hypertension is a disorder that virtually all physicians encounter routinely, regardless of their practice setting. About 25% of all patients seen in emergency departments, for example, have elevated blood pressure. Hypertension is well known for being a “silent killer” because of its long asymptomatic phase and chronic adverse effects on a person’s cardiovascular health. Under certain circumstances, however, an elevated blood pressure can represent an immediately life-threatening condition in the form of a hypertensive emergency. With a one-year mortality of more than 90% if left untreated, a hypertensive emergency is an ominous syndrome associated with impending morbidity or even death if not properly recognized and treated.

In this article, three patients were presented with symptoms and signs of a hypertensive emergency and then discussed the condition in terms of its pathophysiology and its effects on the cardiopulmonary, neurologic, and renal systems. Lastly, reviewed appropriate diagnostic testing and management strategies.


The following three cases represent scenarios that physicians may encounter in patients presenting with elevated blood pressure.

Patient #1.

A 70-year-old woman presents with tearing chest pain that started suddenly 30 minutes earlier and radiates to her back. She has no other complaints. Her medical history is significant for hyperlipidemia and hypertension, for which she was taking a statin and two blood pressure pills. However, she says she stopped taking all three pills a week ago because she “felt fine.”
Physical examination

Physical examination reveals a thin woman clutching her chest in moderate distress. Her vital signs are: pulse, 100; blood pressure, 210/120 mm Hg; respiratory rate, 22; temperature, 98.6oF. The cardiac exam reveals a II/IV blowing diastolic rumble heard at the base but no gallops or rubs. She has a decreased right radial pulse compared with her other three extremities and bibasilar inspiratory crackles.
The rest of her exam is normal. An ECG shows left ventricular hypertrophy, and a chest x-ray shows a widened mediastinum.

Patient #2.

A 45-year-old woman presents with sudden onset of headache and confusion. The rest of her history, unfortunately, is limited by her altered mental status. Physical examination reveals a confused woman in mild distress from the headache. Her vital signs are: pulse, 100; blood pressure, 210/110 mm Hg; respiratory rate, 22; temperature, 98.6ºF. The neurologic exam is significant for left-sided sensory neglect and agnosia. The remainder of the exam is normal.

A stat unenhanced computed tomography (CT) scan is obtained (see image). It shows an intraparenchymal hemorrhage from an arteriovenous malformation.
Patient #3.

A 55-year-old man presents with progressive chest pain and dyspnea that started an hour ago. Twelve months earlier, he was diagnosed with diffuse scleroderma; he has no other medical or surgical history. Physical examination reveals a fully oriented man in severe respiratory distress. His vital signs are: pulse, 100; blood pressure, 210/110 mm Hg; respiratory rate, 40; temperature, 98.6oF. Auscultation detects extensive rales. He has the classic cutaneous findings of scleroderma—taut skin, sclerodactyly, and Raynaud’s phenomenon. An ECG shows left ventricular strain, and a chest x-ray reveals severe pulmonary edema.

His laboratory values are: blood urea nitrogen, 40 mg/dl; creatinine, 2.5 mg/dl; and serum renin plasma activity, 24.5 ng/ml/hr (normal = 0.77 to 4.6 ng/ml/hr). Cardiac enzymes are normal.



Hypertensive encephalopathy is a diagnosis of exclusion that results from progressively worsening cerebral edema. It is characterized by the insidious onset of headache, nausea, and vomiting, followed by nonlocalized symptoms such as irritability and confusion. If left untreated, it progresses to seizures, coma, and ultimately death. Papilledema is usually present, along with significant retinopathy (cotton wool spots). Focal deficits can occur but usually do not localize to a single anatomic lesion.

These neurologic symptoms differ from the abrupt onset of focal neurologic symptoms typically seen with a stroke, such as the hemorrhagic stroke suffered by patient #2 presented above. Both hemorrhagic and ischemic strokes present with focal neurologic deficits that localize to a single lesion, corroborated by an unenhanced CT or MRI scan (or magnetic resonance angiography). Subarachnoid hemorrhage is a type of hemorrhagic stroke that presents with the sudden onset of a severe headache, typically described by the patient as “the worst headache of my life” or “like a thunderclap.” It is diagnosed by classic findings on head CT or lumbar puncture and confirmed by cerebral angiography.

Distinguishing between the various neurologic hypertensive emergencies is important because appropriate management of these conditions is somewhat different. Sodium nitroprusside is still the drug of choice for encephalopathy and can be used in the other conditions. Labetalol is a good alternative. Nimodipine, a calcium channel blocker, is a useful treatment adjunct for subarachnoid hemorrhage. It is thought to decrease the incidence and severity of reflex cerebral vasospasm, thus preventing conversion of the hemorrhagic stroke to an ischemic one.

Target blood pressure also depends on the presumptive diagnosis. It is lower for encephalopathy than for an acute stroke in progress.

Eclampsia is an obstetric hypertensive emergency marked by seizure activity or coma in the absence of an alternative disease process. It can occur at any time from the second trimester to the first 48 hours after delivery. Treatment includes reduction of blood pressure, prevention or control of seizures, and early obstetric consultation since definitive treatment requires delivery of the fetus.

The antihypertensive agent of choice for eclampsia is hydralazine, a direct vasodilator that is a class B drug and therefore safe during pregnancy. Nicardipine and fenoldopam are alternatives. Labetolol can be used but some sources label it as pregnancy category D during the second and third trimesters. Nitroprusside should be avoided because of the potential for cyanide toxicity. It should be considered only after all other agents have failed.


Renal function and blood pressure directly affect one another. A severely elevated blood pressure may lead to acute renal failure or may exacerbate chronic renal failure, which can lead to hypertension. Elevated blood pressure impairs the kidneys’ autoregulatory properties, resulting in decreased renal perfusion. The renin-angiotensin-aldosterone cascade is triggered, leading to even further vasoconstriction, sodium retention, and increased blood pressure and further impairment of autoregulation. This vicious cycle continues until arteriolar necrosis occurs and renal failure results.

Patients present clinically with decreased urine output, increased blood urea nitrogen and creatinine levels, proteinuria, or the finding of red blood cells or red blood cell casts in the urine. Worsening renal function in the setting of hypertension is a hypertensive emergency requiring an immediate reduction in blood pressure. Fenoldapam, a dopamine agonist is a reasonable treatment option, as are nicardipine and labetalol. Diuretics are a useful adjunct to help manage fluid balance.

Scleroderma renal crisis is a rare condition that deserves special mention because of its unique treatment. Initial blood pressure control can be achieved with traditional medications targeted at presenting symptoms, such as the pulmonary edema seen in patient #3 above. However, definitive treatment is intravenous (IV) enalaprilat.


An alphabet-based mnemonic can assist in the assessment of any patient with severely elevated blood pressure and the determination as to whether a hypertensive emergency is present (see algorithm). The recommended evaluation process centers on obtaining accurate bilateral blood pressures, a focused history, a careful physical examination emphasizing neurologic, pulmonary, and cardiovascular findings, and objective studies such as a chest x-ray, ECG, urinalysis, renal function testing, and CT of the head. If possible, test results should be compared with the patient’s medical records to determine which, if any, of the abnormalities are acute.

Patients with a true hypertensive emergency are best treated in an intensive care unit (ICU) with IV drug therapy and close observation. Immediate transport should be arranged for patients diagnosed in a clinic or community setting. The treatment goal is to restore blood pressure to a range in which autoregulatory forces can be re-established. This can be accomplished by a reduction in blood pressure of no more than 25% within the first hour. Further acute reductions can cause end organ ischemia. If the reduced blood pressure is well tolerated and the patient remains clinically stable, gradual reductions toward a normal blood pressure can be implemented over the next 24 to 48 hours by an intensivist in an ICU setting.

There are exceptions to this approach. No clear evidence exists from clinical trials to support immediate antihypertensive treatment in evolving strokes. Furthermore, it is theorized that the hypertensive state is necessary to maintain perfusion and salvage the edematous area adjacent to the infarcted brain, the so-called ischemic penumbra. If the patient’s blood pressure is extremely high (mean arterial pressure above 130 mm Hg or systolic blood pressure above 220 mm Hg), a reasonable approach would be to gradually lower the blood pressure while doing serial neurologic exams. Clinical improvement warrants continued reductions toward the aforementioned goal of 25%. However, any deterioration in the patient’s condition mandates immediate discontinuation of antihypertensive treatment.

Conversely, however, patients with aortic dissection require a rapid decrease in blood pressure. The target systolic blood pressure for this emergent condition of less than 120 mm Hg, if tolerated, will likely violate the 25% rule.

The drug regimen used to treat a hypertensive emergency often depends on physician preference, the specific emergency that is present, and patient comorbidities. The table below provides an overview of the commonly used medications.

An intra-arterial catheter is useful when treating a true hypertensive emergency. By calculating the area under the blood pressure curve, it can provide the most accurate determination of mean arterial pressure. It also provides real-time fluctuations in mean arterial pressure with medical interventions and infusion adjustments and can be helpful with fast-acting medications such as nitroprusside. However, treatment should not be delayed to place an intra-arterial catheter. Initial management can safely proceed in the emergency department using traditional noninvasive blood pressure monitoring.

A final note: The term “urgency” can lead to overly aggressive management of patients with severe, uncomplicated hypertension. There is no evidence to suggest that aggressively lowering blood pressure in the emergency department is associated with improved outcomes. Such patients are best managed in consultation with their outpatient provider. They may benefit from adjustments in their antihypertensive therapy or resumption of medications if noncompliance was the problem, or they may not need any changes at all in their treatment plan. The most important part of the discharge plan is to ensure a follow-up visit within the next few days.


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