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• W2063742148 abstract "Background 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. Study Objective Compare the acute effects of IV cocaine HCl and placebo on PAP, cardiac stroke volume, and cardiac output estimated indirectly by continuous Doppler echocardiography. Design: A single-blind crossover study in which placebo always preceded the active drug. Subjects Ten current crack-smoking subjects, 32 to 47 years of age, with a history of limited previous IV cocaine use. Methods PAP, cardiac stroke volume, heart rate, and BP were measured continuously after injection of placebo followed by cocaine HCl (0.5 mg/kg). Results IV 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/m 2 Weiss R.D. Tilles D.S. Goldenheim P.D. et al. Decreased single breath carbon monoxide diffusing capacity in cocaine freebase smokers. Drug Alcohol Depend. 1987; 19: 271-276 Abstract Full Text PDF PubMed Scopus (16) Google Scholar , 95% CI, −116, +29). Conclusions IV 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. 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 IV cocaine HCl and placebo on PAP, cardiac stroke volume, and cardiac output estimated indirectly by continuous Doppler echocardiography. Design: 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 IV 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). IV 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/m 2 Weiss R.D. Tilles D.S. Goldenheim P.D. et al. Decreased single breath carbon monoxide diffusing capacity in cocaine freebase smokers. Drug Alcohol Depend. 1987; 19: 271-276 Abstract Full Text PDF PubMed Scopus (16) Google Scholar , 95% CI, −116, +29). IV 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." @default.
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• W2063742148 date "1997-01-01" @default.
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• W2063742148 title "Acute Effects of Intravenous Cocaine on Pulmonary Artery Pressure and Cardiac Index in Habitual Crack Smokers" @default.
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• W2063742148 doi "https://doi.org/10.1378/chest.111.1.30" @default.
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