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Appropriate Agents for Cocaine-Induced Hypertensive Emergencies

Appropriate Agents for Cocaine-Induced Hypertensive Emergencies

In their article, "Hypertensive Emergencies and Urgencies: Update on Management" (CONSULTANT, March 2004, page 341), Drs Iris Reyes and Rex Mathew write that labetalol is specifically indicated for most hypertensive emergencies, "especially stroke and acute cocaine intoxication." In fact, labetalol is potentially deadly and is contraindicated in acute hypertension and/or concomitant chest pain related to cocaine intoxication. Labetalol and other -blockers should be avoided in this setting. Cocaine is a powerful sympathomimetic agent that stimulates both 1- and 1- and 2-receptors. 1-Stimulation causes marked vasoconstriction of peripheral arteries, which results in hypertension; more importantly, it causes vasoconstriction of the epicardial coronary arteries, which can lead to ischemic myocardial injury. Fortunately, the potent 1-mediated vasoconstriction associated with cocaine is limited by the coexisting vasodilatory effect mediated by the 2-receptors. If a patient with hypertension caused by acute cocaine intoxication were given labetalol (or any other -blocker), the result would be complete -blockade, which would lead to relatively unopposed vasoconstriction mediated solely by 1-receptors. Labetalol, which has both - and -adrenergic blocking activity, reverses the cocaine-induced increase in systemic arterial pressure but exerts no demonstrable effect on cocaine-induced vasoconstriction of the coronary arteries. It is prudent to assume that there may likely be coronary vasoconstriction along with hypertension even in young, otherwise healthy patients with no comorbid evidence of other atherosclerotic risk factors. Cocaine-related hypertension can be reversed safely and effectively with nitroglycerin and calcium channel blockers, such as verapamil. Cocaine-induced vasoconstriction of the coronary arteries can be reversed with phentolamine, an 1-receptor antagonist. The revised guidelines of the American Heart Association (AHA) for emergency cardiovascular care recommend nitroglycerin, calcium channel blockers, and benzodiazepines as first-line agents for patients with cocaine-related myocardial ischemia and hypertension. Phentolamine is a second-line agent, and -blockers are contraindicated in this setting. ---- Matthew Zaccheo, DO
St Luke's Hospital
Bethlehem, Pa

Much debate surrounds the treatment of hypertension associated with cocaine toxicity. The advantage of labetalol over pure -blockers is the additional -adrenergic blockade that labetalol provides. Treatment with pure -adrenergic blockers, such as propranolol, has been shown to enhance some of the cardiovascular effects of cocaine. A controlled study by Sofuoglu and colleagues1 demonstrated that labetalol reduces the increases in systolic blood pressure and heart rate induced by repeated doses of smoked cocaine. In another study, labetalol failed to reverse the coronary vasoconstriction induced by intranasal cocaine in subjects who underwent cardiac catheterization, but it exerted no demonstrable adverse effect on cocaine-induced vasoconstriction of the coronary arteries.2 Numerous authors therefore recommend the selective use of labetalol in patients with cocaine toxicity--first intravenously in the acute setting and then orally for long-term therapy. Intravenous nitroglycerin or verapamil can also be used because they reverse both the vasoconstriction and hypertension caused by acute cocaine exposure. Still, the use of -blockers as a class in the setting of cocaine toxicity remains controversial. The American College of Cardiology/AHA guidelines recommend - blockers for select conditions caused by cocaine toxicity.3 However, it should be noted that this recommendation is based only on expert consensus. The Advanced Cardiovascular Life Support guideline revision of 2000 recommends that nitrates be used as first-line therapy in patients with a history of cocaine abuse and ventricular arrhythmias or acute coronary syndromes.4 It also suggests that separate review of the literature surrounding this issue, Knuepfer5 justifiably concludes that there are insufficient experimental and clinical data at this time to determine whether labetalol may be beneficial in treating cocaine toxicity. ---- Rex Mathew, MD
Hospital of the University of Pennsylvania


Sofuoglu M, Brown S, Babb DA, et al. Effects of labetalol treatment on the physiological and subjective response to smoked cocaine. Pharmacol Biochem Behav. 2000;65:255-259.
2. Boehrer JD, Moliterno DJ, Willard JE, et al. Influence of labetalol on cocaine-induced coronary vasoconstriction in humans. Am J Med. 1993;94:608-610.
3. Braunwald E, Antman EM, Beasley JW, et al. ACC/AHA 2002 guideline update for the management of patients with unstable angina and non-ST–segment elevation myocardial infarction—summary article: a report of the American College of Cardiology/American Heart Association task force on practice guidelines (Committee on the Management of Patients With Unstable Angina). J Am Coll Cardiol. 2002;40:1366-1374.
4. Guidelines 2000 for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care. Part 6: advanced cardiovascular life support: section 1: Introduction to ACLS 2000: overview of recommended changes in ACLS from the guidelines 2000 conference. The American Heart Association in collaboration with the International Liaison Committee on Resuscitation. Circulation. 2000;102(8 suppl):I86-I89.
5. Knuepfer MM. Cardiovascular disorders associated with cocaine use: myths and truths. <Pharmacol Ther. 2003;97:181-222.

  • Eagle KA, Isselbacher EM, DeSanctis RW, and the International Registry for Aortic Dissection (IRAD) Investigators. Cocaine-related aortic dissection in perspective. Circulation. 2002;105:1529-1530.
  • Lange RA, Hillis LD. Cardiovascular complications of cocaine use. N Engl J Med. 2001;345:351-358.
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