Kleerup E C, Wong M, Marques-Magallanes J A, Goldman M D, Tashkin D P
Division of Pulmonary and Critical Care Medicine, UCLA School of Medicine 90095-1690, USA.
Chest. 1997 Jan;111(1):30-5. doi: 10.1378/chest.111.1.30.
Some habitual crack cocaine smokers who deny IV drug abuse show decreased pulmonary transfer of carbon monoxide (DCO). We speculated that repeated elevations in pulmonary artery pressure (PAP) might cause pulmonary capillary damage and result in a lowered DCO, or that the reduction could be due to anoxic lung injury secondary to repeated episodes of cocaine-induced pulmonary vascular constriction.
Compare the acute effects of i.v. cocaine HCl and placebo on PAP, cardiac stroke volume, and cardiac output estimated indirectly by continuous Doppler echocardiography.
A single-blind crossover study in which placebo always preceded the active drug.
Ten current crack-smoking subjects, 32 to 47 years of age, with a history of limited previous i.v. cocaine use.
PAP, cardiac stroke volume, heart rate, and BP were measured continuously after injection of placebo followed by cocaine HCl (0.5 mg/kg).
i.v. cocaine resulted in no significant change in PAP (-0.14 +/- 3.3[SD] mm Hg, 95% confidence interval [CI] for difference -2.48, +2.21). Stroke volume index showed no significant change after cocaine (-0.1 +/- 2.0 mL; 95% CI, -1.5, +1.3). Heart rate showed a significant increase (10.0 +/- 7.2 min-1; p = 0.0017, 95% CI, +4.9, +15.1). Cardiac index showed a significant increase (0.48 +/- 0.32 L/min; p = 0.0012, 95% CI, +0.25, +0.71). Pulmonary vascular resistance showed no significant change (-44 +/- 101 dyne.s.cm-5/m2, 95% CI, -116, +29).
i.v. cocaine HCl does not cause short-term increases in PAP or stroke volume index, but causes an increase in cardiac index due to its chronotropic effect.
