Author + information
- Received October 28, 1991
- Revision received January 2, 1992
- Accepted January 18, 1992
- Published online July 1, 1992.
- James D. Boehrer, MD,
- David J. Moliterno, MD,
- John E. Willard, MD,
- Richard W. Snyder II, MD,
- Rodney P. Horton, MD,
- D.Brent Glamann, MD,
- Richard A. Lange, MD, FACC and
- L.David Hillis, MD, FACC∗
- ↵∗Address for correspondence: L. David Hillis, MD, Room CS 7.102, University of Texas Southwestern Medical Center, 5323 Harry Hines Boulevard, Dallas, Texas 75235.
Intranasal cocaine, 2 to 3 mg/kg body weight, is a commonly used local anesthetic for rhinolaryngologic procedures, and many persons who abuse it ingest a similar amount. Previous studies in humans showed that this dose of cocaine causes coronary vasoconstriction, and studies in animals showed that larger amounts given intravenously diminish myocardial performance. This study assessed the hemodynamic effects of intranasal cocaine, 2 mg/kg, in humans.
In 15 patients (8 men and 7 women, aged 30 to 70 years) referred for cardiac catheterization, heart rate, systemic arterial pressure, cardiac index, pulmonary capillary wedge and pulmonary artery pressures and left ventricular pressure and its first derivative (dP/dt) were measured before and 15, 30 and 45 min after intranasal administration of saline solution (n = 5) or cocaine, 2 mg/kg (n = 10). No variable changed with saline solution. In those given cocaine, there was an increase in heart rate (17 ± 16%, mean ± SD), mean systemic arterial pressure (8 ± 7%), cardiac index (18 ± 18%) and positive and negative dP/dt (18 ± 20% and 15 ± 22%, respectively) (p < 0.05 for all).
Thus, intranasal cocaine in a dose similar to that used medicinally or “recreationally” does not exert a deleterious influence on intracardiac pressures and left ventricular performance.
- Received October 28, 1991.
- Revision received January 2, 1992.
- Accepted January 18, 1992.