| ||||||||||||||
|
|
|||||||||||||



*Associate Professor Anesthesiology/Surgery.
Instructor in Anesthesiology.
Fellow in Anesthesiology.
Technical Research Supervisor.
Department of Anesthesiology, University of Utah College of Medicine, 50 North Medical Drive, Salt Lake City, Utah 84132.
Abstract
The cardiovascular effects of a large dose of meperidine (8 mg/kg IV) followed by continued slower infusion of the drug (4 mg/kg/hr) and then addition of increasing concentrations (10 to 70 percent) of N2O or nitrogen during continued meperidine infusion were determined in 18 dogs. Meperidine (8 mg/kg) produced a marked (p<0.01) decrease in stroke volume (SV), cardiac output (
T), systemic vascular resistance (SVR), mean arterial blood pressure
|
|
mean pulmonary artery pressure
|
|
and also reduced (p<0.05) mean right atrial pressure
|
|
but did not significantly change heart rate (HR). During continued meperidine infusion, SV,
T, and
|
|
increased until they became similar to premeperidine controls, while HR increased so that it was higher (p<0.05) than controls.
|
|
|
|
and SVR also increased during continued meperidine infusion; however, they remained less than control values. Addition of N2O did not significantly change SV or
|
|
but produced reductions in HR and
T and increases in
|
|
|
|
and SVR when compared to similar concentrations of nitrogen.
These data demonstrate that rapid infusions of large doses of meperidine produce marked depression in cardiovascular dynamics which recover when the meperidine infusion is slowed. Addition of Na2O during meperidine infusion results in significant reductions in HR and
T and increases in
|
|
|
|
and SVR. Our findings indicate that N2O-meperidine anesthesia tends to preserve systemic blood pressure but at the expense of a reduced
T and increased SVR.
Key Words: ANESTHETICS, gases, nitrous oxide ANALGESICS, narcotic, meperidine HEART, myocardial function
|