Cocaine and it’s effect on the cardiovascular physiology

 The direct effect of cocaine on the vagal centre in the brain can cause bradycardia, but the bradycardia is seldom seen clinically. At the usual doses taken by people who abuse cocaine, the peripheral adrenergic actions of the drug dominates over its central vagal response. The phenomenon is explained by the pharmacokinetics of the drug. Cocaine is a low molecular weight tropane alkaloid (Pka=8.6), which is easily transported across the nasal, gut and alveolar membranes. However, it transport into the brain depends upon a proton driven antiporter. The stimulatory action of cocaine is rapid and provides the abuser with the sought for “kick”. At any time point after the intake of the drug, the peripheral cardiovascular effects of the drug dominates over the central vagal action. The peripheral adrenergic action is due to over accumulation of catecholamines in the synaptic cleft of the adrenergic neurones leading to vasoconstriction (blood vessels) and tachycardia (heart). Any reflex bradycardia mediated by central mechanism is overwhelmed by the peripheral adrenergic action. No doubt, subjects abusing cocaine present with accelerated hypertension, tachycardia and agitation in the emergency department. The severe vasoconstriction effect of cocaine may also precipitate coronary vasospasm and myocardial infarction in some drug abusers.