Hypertensive crises are thought to be initiated by humoral vasoconstrictors causing an abrupt increase in systemic vascular resistance, ultimately overwhelming the body’s autoregulatory mechanisms.2 Failure of these mechanisms begins a physiologic cascade: Elevated pressures in proximal capillary beds accompany arteriolar dilation, and ultimately smaller arterioles may rupture or leak, resulting in fibrin deposition into their walls. This fibrinoid necrosis is responsible for end organ damage, resulting in ischemia and further release of vasoactive mediators, effectively activating a cycle of progressively worsening blood pressure elevation and subsequent organ injury.8
The most common presentations of hypertensive emergencies in the ED are cerebral infarction (24.5%), pulmonary edema (22.5%), hypertensive encephalopathy (16.3%), and congestive heart failure (12%). Other important presentations include aortic dissection, intracranial hemorrhage, sympathetic crises (cocaine toxicity/pheochromocytoma), eclampsia, and MI9 (Table 1.)
According to the JNC 7 report, “the initial goal of therapy in hypertensive emergencies is to reduce the mean arterial blood pressure by no more than 25% (within minutes to 1 hour), then, if stable, to 160/100-110 mm Hg within the next 2-6 hours.”5 This general approach is often applicable, but there are also specific guidelines or recommendations that apply to many of the presentations/diagnoses listed in Table 1. Generally, relatively rapid but controlled reduction in blood pressure is indeed warranted. The emergency practitioner must be aware that the elevated blood pressure in many of these patients is often a physiologic response to their acute condition, and aggressive treatment of the hypertension may actually increase morbidity and mortality. This is especially true for patients with acute intracranial events.10
Detailed review of the treatment guidelines and recommendations for each of the hypertensive emergencies listed in Table 1 is beyond the scope of this article, but a brief review of some of the treatment recommendations in this context, particularly those that differ from the aforementioned general recommendations for blood pressure reduction, will serve to further the discussion of when and how elevated blood pressure should be treated in the ED setting.
In most patients with stroke, elevated blood pressure is the physiologic response to the stroke, as opposed to the cause. Approximately 85% of strokes are nonhemorrhagic. Patients with nonhemorrhagic strokes often have moderate hypertension that actually portends a better prognosis. Rapid reduction of blood pressure can compromise cerebral blood flow and cause increased ischemia.11 The Intravenous Nimodipine West European Trial for acute stroke was stopped because of increased negative neurologic outcomes in the treatment group, which were attributed to effects of blood pressure reduction.2,12