Cocaine-induced hypertension results predominantly from a- and b-adrenergic-induced tachycardia, inotropy, and afterload. It has been implicated in aortic dissection and cerebrovascular accidents, as well as in myocardial ischemia and infarction, because of increased myocardial oxygen demand and concomitant vasoconstriction. These life-threatening complications must be considered in those who use cocaine.

Benzodiazepines are the first line of treatment to decrease sympathetic outflow. If adequate sedation alone does not control blood pressure, the persistence of the a-adrenergic effects of cocaine may be responsible. An a-adrenergic antagonist such as phentolamine may decrease the vasoconstriction, or direct vasodilators such as nitroprusside or nitroglycerin (glyceryl trinitrate) may be employed.

Beta-adrenergic antagonists are contraindicated. Even b -,-specific agents have some activity at b2-receptors that can counteract existing vasodilation. Peripheral a-adrenergic effects would then be unopposed, with a resultant worsening of vasoconstriction and afterload. Even agents with both a- and b-adrenergic antagonism (such as labetalol) have relatively greater b effects (a b/a potency ratio of at least 7:1). In addition, b-adrenergic antagonists such as propanolol have been shown to worsen coronary vasoconstriction and to increase coronary vascular resistance and myocardial oxygen demand in patients during coronary catheterization ( Lange et.. al 1990). Calcium-channel blockers should also be avoided since animal studies have shown morbidity with decreased time to seizure and ventricular fibrillation.

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