COCAINE TOXICITY AND ISOFLURANE ANESTHESIA - HEMODYNAMIC, MYOCARDIAL METABOLIC, AND REGIONAL BLOOD-FLOW EFFECTS IN SWINE

Citation
Jf. Boylan et al., COCAINE TOXICITY AND ISOFLURANE ANESTHESIA - HEMODYNAMIC, MYOCARDIAL METABOLIC, AND REGIONAL BLOOD-FLOW EFFECTS IN SWINE, Journal of cardiothoracic and vascular anesthesia, 10(6), 1996, pp. 772-777
Citations number
23
Categorie Soggetti
Anesthesiology,"Peripheal Vascular Diseas","Cardiac & Cardiovascular System
ISSN journal
10530770
Volume
10
Issue
6
Year of publication
1996
Pages
772 - 777
Database
ISI
SICI code
1053-0770(1996)10:6<772:CTAIA->2.0.ZU;2-H
Abstract
Objectives: Increasing numbers of people use cocaine recreationally an d may require anesthesia care, having recently abused the drug. Howeve r, no data currently exist concerning potential interactions between t oxic levels of cocaine and volatile anesthetic agents. This study inve stigated the effects of cocaine infusion on systemic hemodynamics, myo cardial metabolism, and regional organ blood flow in relation to depth of isoflurane anesthesia. Design: Prospective, randomized, controlled trial. Setting: A laboratory at a university medical center. Particip ants: Twelve miniature pigs. Interventions: An open-chest swine model was used. Isoflurance (ISO) was the sole anesthetic, administered at 0 .75 and 1.5 minimum alveolar concentration (MAC), and cocaine was infu sed (n = 6) at a rate of 0.5 mg/kg/min. Control animals (n = 6) receiv ed an equivalent amount of normal saline. Measurements and Main Result s: Systemic and pulmonary arterial pressures and thermodilution cardia c output data were collected at 0.75 MAC and 1.5 MAC ISO. Regional myo cardial and blood flows to other organs were measured using radiolabel ed microspheres. Arrhythmias and altered ventricular conduction were n oted only in the cocaine group, along with significant elevations in d iastolic arterial pressure, coronary perfusion pressure, and systemic vascular resistance. Increased subendocardial blood flow occurred duri ng cocaine infusion (p = 0.03); subepicardial perfusion was unchanged. Cerebral (p < 0.01) and spinal cord (p < 0.05) blood flows were reduc ed in animals receiving cocaine. Other organ blood flows were unchange d with depth of anesthesia or cocaine administration, with the excepti on of splenic blood flow (p < 0.04). Conclusions: Moderately toxic coc aine levels occurring during isoflurane at 0.75 MAC and 1.5 MAC are as sociated with hemodynamic abnormalities, a marked increase in systemic vascular resistance, and a tendency to produce cardiac arrhythmias. A reversal of endo/epicardial myocardial perfusion ratio occurs associa ted with cocaine infusion during ISO anesthesia. This is probably not related to a primary redistribution of subendocardial blood flow and m ay be related to a combination of increased myocardial oxygen demand a nd epicardial coronary vasoconstriction. The reductions in cerebral an d spinal cord perfusion observed may explain, in part, the neurologic sequelae of cocaine toxicity. Copyright (C) 1996 by W.B. Saunders Comp any