http://www.emedicine.com/emerg/topic102.htm
"Strong evidence supports avoidance of nonselective beta-blockers for cocaine-induced ischemia. Echocardiographic studies suggest that the antihypertensive effect of propranolol results from depression of cardiac output, rather than relief of systemic vascular resistance. Propranolol exacerbates the depression of coronary blood flow induced by cocaine because of unopposed alpha stimulation following beta-blockade. Finally, just before fatality, cocaine toxicity usually results in hypotension, a condition that would be compounded further by use of a beta-blocker.
Malbrain et al note that esmolol has been recommended for "save use" in managing life-threatening hypertension and tachycardia. Esmolol is a selective beta1-adrenergic blocker with rapid onset and short duration of action (elimination half-life is 9 min). They advise that the coadministration of esmolol and sodium nitroprusside should be reserved for severe hypertension that is unresponsive to other treatment and/or is complicated by aortic dissection.
Guidelines 2000 discusses use of carefully titrated doses of labetalol as a third-line agent in treating drug-induced hypertensive emergencies. Labetalol, a combined alpha- and beta-blocking agent, is, however, predominantly a beta-blocker and has an alpha-to-beta blockade ratio of 1:7. It may not, therefore, provide enough protection for cocaine-toxic patients from (relatively) unopposed alpha stimulation. Thus, its risk of exacerbating myocardial ischemia parallels the risk of beta-blockers. In addition, labetalol has been found to increase seizures and mortality in animal models; therefore its use cannot, at present, be promoted."
Sounds like beta blockers would do more harm than good regardless of whether or not you are experiencing toxic effects from the cocaine.
"Drugs that increase intrasynaptic dopamine produce changes in the density and sensitivity of dopamine receptors; they have different effects on different receptor subtypes in different areas of the brain (Ruttenber et al, 1997). Excited delirium (ED), cocaine-associated rhabdomyolysis (CAR), and neuroleptic malignant syndrome (NMS) share many common features that can be explained by aberrant dopaminergic function (discussed below).
Long-term cocaine use, rather than short-term use, is responsible for persistent changes in dopaminergic function that place users at risk for ED [excited delirium] and CAR [cocaine associated rhabdomyolysis]. Elevations in muscle enzyme levels are observed in asymptomatic chronic cocaine users and in untreated persons with schizophrenia; this evidence lends support to the hypothesis that chronic alterations in dopaminergic function can affect skeletal muscle physiology.
Temperature dysregulation is also a problem, which is demonstrated by Calloway and Clark who report patients presenting with rectal temperatures as high as 45.6C. Because dopamine plays a role in the regulation of core body temperature, increased dopaminergic neurotransmission may contribute to psychostimulant-induced hyperthermia in people, including those with ED.
D2 receptors are involved with processes that decrease core temperature. The number of D2 receptors in the temperature regulatory centers of the hypothalamus is substantially reduced in persons with ED. These decreases in D2 receptors lead to unopposed increases in temperature mediated through D1 receptors, which are not affected in individuals who die of ED.
In animal studies, hyperthermia has been found to be the most significant parameter in the lethality of continuous cocaine infusion.
Agitated delirium, also known as excited delirium (ED), is a common presentation in patients dying of cocaine toxicity. Of cocaine-associated deaths investigated by the Metropolitan Dade County (FL) Medical Examiner Department between 1979 and 1990, ED was the terminal event in approximately 1 out of every 6 fatalities. Patients with ED exhibited immediate onset of bizarre and violent behavior, which included aggression, combativeness, hyperactivity, hyperthermia, extreme paranoia, unexpected strength, and/or incoherent shouting. All of these were followed by cardiorespiratory arrest.
Although heart weight, ventricular hypertrophy, and past MI are not risk factors, repeated binges of cocaine use are associated with fatal ED. The frequency of use that increases risk, however, has not been determined. Individuals with ED may be more sensitive to the life-threatening effects of catecholamine surges than other cocaine users. ED appears to be generated by increased intrasynaptic dopamine concentrations resulting from a defect in the regulation of the dopamine transporter. When compared to drug-free controls, cocaine recognition sites on the striatal dopamine transporter are increased in cocaine users without ED. Persons dying of ED have no such increase; thus, they may have problems clearing dopamine from the synapses, a condition that easily could result in agitation and delirium.
Hyperthermia, which also may be caused by dopamine receptor down-regulation, increases the incidence of fatal ED."
I agree that dopamine doesn't have the same magnitude of cardiovascular effects as epinephrine (although it has some pressor effects independent of its metabolism into norepinephrine). But its possible that many of the fatalities from cocaine aren't caused solely by its cardiovascular effects. Also, the author from above mentions an association between frequency of use and severity of toxic effects. I would think that people like Chris Farley probably didn't die the first time they took a speedball. It was probably at the end of a long binge and there is no telling how long he had been using coke/heroin in the months before he died.
