Hypertensive Emergency

Etiology

Various inciting events can cause hypertensive emergencies. The majority of hypertensive emergencies occur in patients already diagnosed with chronic hypertension. Noncompliance with antihypertensive medications and the use of sympathomimetics are two of the more common causes. These lead to a rapid rise in blood pressure beyond the body's innate autoregulation capacity.

The levels of hypertension that constitute a hypertensive emergency, while often quoted, are not universally established and are arbitrary. The rate of rise above baseline is likely a more important contributor and explains why patients without chronic hypertension may show signs of hypertensive emergency at much lower levels. In contrast, patients with longstanding hypertension may tolerate exceedingly high blood pressure without developing acute organ dysfunction.[4][5]

Epidemiology

An estimated 30% of adults in the US have hypertension. Of these, 1% to 2% will have a hypertensive crisis, a term inclusive of hypertensive emergency and hypertensive urgency. Acute pulmonary edema, cardiac ischemia, and neurologic emergencies are the most common types of acute target organ dysfunction.[6] In North America, the ready availability of antihypertensive medications has lowered hypertensive emergencies and improved survival. Nonetheless, untreated hypertensive emergencies can also be fatal.

Pathophysiology

The pathophysiology resulting in end-organ dysfunction in hypertensive emergencies is not fully understood. However, the mechanical stress on vascular walls likely leads to endothelial damage and a proinflammatory response. This results in increased vascular permeability, platelet activation, and activation of the coagulation cascade, and fibrin clot deposition, leading to hypoperfusion of the target organ tissue.

Histopathology

Fibrinoid necrosis may be seen in the renal arterioles, a classic feature of malignant hypertension. The majority of patients with this feature are dead within 24 months if the hypertension is left untreated.

History and Physical

In patients who present with markedly elevated blood pressure, a careful history and exam are necessary to determine which of these patients is having a true hypertensive emergency. Symptoms such as headache, dizziness, altered mental status, shortness of breath, chest pain, decreased urine output, vomiting, or changes in vision warrant further evaluation. The source of the abrupt onset of hypertension should also be investigated to direct treatment.

The expected examination findings vary depending on the specific target organ most affected. With cardiac dysfunction, rales may be heard on lung auscultation, jugular venous distention or peripheral edema may be noted, and extra heart sounds may be apparent. In the event of a very rapid onset of hypertension, often seen with sympathomimetic abuse, marked dyspnea in the absence of peripheral edema due to flash pulmonary edema may be encountered. Neurologic dysfunction may result in altered mental status, blurry vision, ataxia or other cerebellar dysfunction, aphasia, or unilateral numbness or weakness. A careful neurologic examination, including a cranial nerve examination, strength and sensation testing, and cerebellar and gait testing, should be performed. The eye exam may reveal papilledema as well as exudates and flame-shaped hemorrhages. Acute renal failure may also result in signs of pulmonary edema or peripheral edema.

Evaluation

The evaluation of hypertensive emergencies also depends on the presenting symptoms and signs. Once it is determined that a true hypertensive emergency is present or likely, labs such as metabolic panels, urinalysis, B-natriuretic peptide, and cardiac enzymes may be useful. An electrocardiogram is recommended in any patient suspected of having cardiac ischemia. Head CT is recommended in patients with acute neurologic complaints or signs on an exam. A chest x-ray may prove to be useful in patients with shortness of breath. A chest x-ray may also show widening of the mediastinum in the setting of aortic dissection, but this is a relatively insensitive marker, and CT angiography of the chest and abdomen should be obtained to rule out or confirm a dissection and to determine the extent of the intimal tear.[7]

Treatment / Management

While the specific target organ affected may dictate certain aspects of treatment, rapid lowering of blood pressure is the mainstay of therapy for hypertensive emergencies. The goal would be to lower the mean arterial pressure by 20% to 25% within the first 1 to 2 hours. Several agents can be used, but the unifying characteristics are that they act rapidly and are easily titratable. For this reason, oral medications, such as clonidine and nifedipine, play no role in the immediate management of a hypertensive emergency. Intravenous vasoactive drips such as labetalol, esmolol, nicardipine, and nitroglycerin are typically effective options.[5][8]

The key feature of management is that if there is no evidence of organ damage, then the blood pressure reduction should be gradual over a few days. On the other hand, severe hypertension in pregnancy demands immediate treatment. Women who become pregnant should be prescribed nifedipine, methyldopa, or labetalol during pregnancy; these women should not be treated with angiotensin converting enzyme inhibitors or angiotensin receptor blockers. During the acute event, intravenous hydralazine or oral nifedipine can be used to lower blood pressure.

Current Guidelines

1. Patients with a hypertensive emergency need admission with continuous blood pressure monitoring.
2. Assess for target organ injury and start parenteral medications as needed.
3. If the patient has an acute emergency such as aortic dissection, lower the blood pressure to below 140 mm Hg within the first hour.
4. For adults with no organ damage, lower blood pressure by 25% in the first hour, then to 160/100 over the next 2 to 6 hours, and gradually to normal over 2 days.

Differential Diagnosis

The differential diagnosis includes:

• Acute kidney injury
• Aortic coarctation
• Aortic dissection
• Chronic kidney disease
• Eclampsia
• Hypocalcemia
• Hyperthyroidism
• Pheochromocytoma
• Renal artery stenosis
• Subarachnoid hemorrhage

Prognosis

In the past, hypertensive emergencies were frequently associated with kidney impairment, myocardial infarction, stroke, or death. With more awareness and better control of blood pressure, mortality has decreased significantly in the past 3 decades. However, after acute treatment, tighter control of blood pressure is vital to reduce morbidity and mortality.[9] Unfortunately, the overall long-term prognosis of patients with hypertensive emergencies is guarded. A significant number of these patients may develop adverse cardiac events or a stroke within 12 months.

Complications

Failure to make a diagnosis or to treat a hypertensive emergency can lead to the following:

• Renal failure
• Vision loss
• Myocardial infraction
• Stroke