Adverse effects of halothane in a canine model of acute right ventricular hypertension.

Abstract

The effects of acute right ventricular (RV) hypertension (RVH) induced by pulmonary artery (PA) constriction, and of two concentrations (mean inspired 0.8 and 1.5%) of halothane (HAL) during RVH on global and regional RV performance (ultrasonic dimension technique), and on coronary hemodynamics (electromagnetic flow probes) were studied in 12 open-chest dogs anesthetized and paralyzed by continuous infusions of fentanyl and pancuronium. Following PA constriction, RV systolic pressure more than doubled, RV end-diastolic and systolic dimensions increased, and stroke volume (SV) and segment shortening fell (P all less than 0.05). There was no evidence of regional myocardial dysfunction (i.e., akinesis, systolic lengthening, postsystolic shortening), and reactive hyperemia in response to right coronary artery occlusion was present. Subsequent addition of HAL (0.8%) resulted in further increases in end-diastolic and systolic dimensions, and in marked decreases in right coronary blood flow, segment shortening, SV, and aortic pressure. During HAL 1.5% (range: 1.2-1.6%), regional myocardial dysfunction developed in three animals, reactive hyperemia was abolished in five out of six animals tested, and metabolic acidosis developed. Release of PA constriction during 1.5% HAL in seven animals resulted in improved global and regional RV performance, disappearance of regional myocardial dysfunction, and restoration of reactive hyperemia. In this canine model of acute RVH, increasing concentrations of HAL led to increasing deterioration in global and regional RV performance most likely due to inadequate coronary perfusion.