Cocaine and cardiovascular function in dogs: Effects on heart and peripheral circulation

The effects of cocaine on the heart and peripheral circulation were examined in seven mongrel dogs. Hemodynamic variables, in addition to data on ventricular relaxation, mean circulatory filling pressure and arterial compliance, were measured during an intravenous infusion (0.5 mg/kg per min) of cocaine. Holter monitor recordings (6 h) and coronary arteriograms were also obtained. Cocaine increased (p < 0.01) mean aortic pressure from 72 ± 5 to 92 ± 5, left ventricular systolic pressure from 102 ± 3 to 121 ± 5, left ventricular end-diastolic pressure from 4.9 ± 1.3 to 8.2 ± 1.4 and mean circulatory filling pressure from 7.9 ± 0.4 to 10.9 ± 0.5 mm Hg. Cardiac index and stroke volume decreased (p < 0.01) from 166 ± 17 to 125 ± 8 ml/min per kg and from 44 ± 4 to 29 ± 3 ml, respectively. Ejection fraction decreased (p < 0.01) from 61 ± 1 to 49 ± 3%. Heart rate, first derivative of left ventricular pressure ( dP dt) and right atrial, mean pulmonary artery and pulmonary artery wedge pressures did not change. The result was a 58% increase in systemic vascular resistance and a 32% decrease in arterial compliance. The pressure gradient for venous return did not change, but resistance to venous return increased 42%. Cocaine prolonged (p < 0.05) the half-time of left ventricular isovolumic relaxation from 13.4 ± 0.8 to 16.4 ± 0.8 ms and the time constant of left ventricular isovolumic relaxation from 19.3 ± 1.2 to 23.6 ± 1.1 ms. There were occasional premature ventricular beats on Hoiter monitoring, bat no ventricular tachycardia or ventricular fibrillation. Coronary artery diameters did not change with cocaine administration and there was no evidence of coronary artery spasm. In conclusion, intravenous cocaine in dogs causes arterial and venous constriction without evidence of coronary artery spasm or lifethreatening ventricular arrhythmias.