We assessed the effects of i.v.
cocaine on parasympathetic and sympathetic nervous system activity, and on the complexity vs. regularity of changes in heart rate over time. Fourteen otherwise healthy men with histories of i.v.
cocaine abuse received bolus
injections of
cocaine (20 mg or 40 mg) and placebo (saline) on different days. Cardiovascular measures derived from the electrocardiogram, including heart rate, Porges' vagal tone (respiratory sinus arrhythmia), the 0.10 Hz rhythm, Toichi's vagal index, Toichi's sympathetic index, and approximate entropy (ApEn), were measured continuously. As predicted,
cocaine produced
tachycardia, accompanied by pronounced decreases in response to 40 mg
cocaine in two different vagal tone indexes that precisely mirrored the increases in heart rate. The measure of sympathetic (and vagal) neural influences on the heart (0.10 Hz wave) also decreased in response to
cocaine. Converging evidence from Toichi's vagal index supported the conclusion that the
tachycardia from
cocaine was due to withdrawal of cardiac vagal tone. These findings, and evidence that
cocaine decreased cardiovascular complexity, contradict the prevailing assumption that the mechanism by which
cocaine produces
tachycardia is sympathetic (beta-
adrenergic). We discuss implications for
cardiac arrhythmias associated with
cocaine abuse and death due to overdose.