Hypertension is a very common finding in emergency department patients. Evidence of acute end-organ dysfunction in the setting of hypertension is rare but requires emergent diagnosis and treatment.
Depend on the history and physical to guide the clinical evaluation of patients with severe hypertension.
Emergent blood pressure control is contraindicated in asymptomatically hypertensive patients without evidence of end-organ dysfunction.
Hypertension affects up to 30% of the total adult population and is one of the most common medical conditions in the United States. Of these individuals, nearly 75% have inadequately controlled blood pressure (BP) (beyond normotensive limits of 140/90 mmHg), and only half are taking their medications correctly as prescribed. That said, fewer than 1% of all patients with hypertension will ever develop a hypertensive emergency.
Patients presenting with a systolic BP ≥180 mmHg or a diastolic BP ≥110 mmHg are classified as having severe hypertension. Evaluating a patient with severe hypertension should focus on the rapid distinction between hypertensive emergency or hypertensive urgency, as the treatment and disposition differ dramatically. Hypertensive emergency is defined as an acute elevation in BP (≥180/110 mmHg) associated with active end-organ damage, specifically ongoing injury to the brain, heart, aorta, kidneys, and/or eyes. Hypertensive urgency is less clearly defined, but can be thought of as a severe elevation in blood pressure without evidence of acute end-organ dysfunction.
The suggested mechanism behind hypertensive emergency requires a sudden increase in systemic vascular resistance due to an unregulated surge in circulating vasoconstrictors. This spike in BP causes undo stress on the vascular wall with consequent endothelial injury. The injured endothelium produces pathologic increases in vascular permeability, activation of the platelets and coagulation cascade, and the localized deposition of intraluminal fibrin. Secondary fibrinoid necrosis of the arteriolar end-organ circulation results in significant tissue hypoperfusion and consequent organ system dysfunction.
Most individuals presenting with hypertensive emergency will carry a previous diagnosis of hypertension. When determining the goals for BP treatment, it is important to understand the effects of longstanding hypertension on the cerebral circulation. Chronic hypertension forces a shift in cerebral autoregulation, allowing patients to tolerate significant elevations in blood pressure without any signs of cerebral end-organ damage. Consequently, the overaggressive reduction of systemic BP in this setting, even if only decreased to normotensive limits, may lead to secondary hypoperfusion and ischemia of the central nervous system (CNS). Always remember that treating blood pressure based on numbers alone, without considering the clinical context, can be altogether quite harmful for the patient.
Patients with severe hypertension require a rapid evaluation for evidence of end-organ damage. Start with a focused history and comprehensive review of systems, inquiring about the presence of chest pain, back pain, shortness of breath, hematuria or decreased urine output, and neurologic complaints including numbness, weakness, headache, confusion, and visual disturbances. A more detailed history related to specific diagnoses follows.
Hypertensive encephalopathy. Patients with hypertensive encephalopathy present with neurologic complaints including altered mental status, severe headache, seizures, vomiting, and visual disturbances. The mental status changes range from drowsiness to confusion to outright coma.
Intracranial hemorrhage. Patients with intracranial hemorrhage present with severe headache (often sudden onset), focal neurologic deficits, and/or altered mental status.
Acute pulmonary edema. Patients with flash pulmonary edema present with acute shortness of breath. Variable associated symptoms include orthopnea, hemoptysis, and chest pain or pressure.
Acute coronary syndrome. Patients with acute coronary syndrome usually present with chest pain, although subtle signs of congestive heart failure may be the only presenting complaint.
Aortic dissection. Patients with aortic dissection present with severe chest and/or back pain, often of a tearing quality. Associated symptoms include neurologic deficits, syncope, and abdominal pain, as well as constitutional symptoms such as nausea, vomiting, or diaphoresis.
Acute renal failure. Patients with acute renal failure often present with relatively subtle symptoms. A carful history will often elicit hematuria, oliguria, or anuria. Patients may also present with swelling of the lower extremities or shortness of breath due to significant fluid retention.
Begin by verifying that the elevated BP reading was obtained with a cuff appropriately sized for the patient. Cuffs that are too small will lead to spuriously high BP readings. The width of the cuff bladder (inflatable portion of the cuff) should equal approximately 40% of the arm circumference. The length of the cuff bladder should equal ~80% of the arm circumference. Perform a detailed physical exam, focusing on the neurologic, cardiac, pulmonary, and abdominal examinations. A more detailed description of expected findings related to specific diagnoses follows.
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