Extended evaluation of effects of anoxia on ventricular performance and compliance.
Eight dogs were prepared by implanting a left ventricular pressure transducer, aortic flow probe, and endocardial ultrasound crystals across the maximum transverse left ventricular diameter. In an unanesthetized state, the dogs were evaluated at rest and with acute volume loading, both before ischemic cardiac arrest and sequentially (2, 4, 6, 12, 24, and 48 hours) after 20 minutes of arrest during normothermic cardiopulmonary bypass. At a left ventricular end-diastolic diameter comparable to preoperative levels, left ventricular systolic pressure, heart rate, and rate of rise of left ventricular pressure were not changed, but at 2 to 6 hours there was a significant decrease in cardiac output (p less than 0.01), left ventricular stroke work (p less than 0.01), ejection fraction (p less than 0.05), maximum rate of systolic diameter shortening (p less than 0.05), and circumferential fiber shortening (p less than 0.05). They gradually returned to control levels by 24 hours postoperatively. Left ventricular compliance, as measured by left ventricular end-diastolic pressure at a set end-diastolic diameter and by left ventricular diastolic pressure/diameter, was reduced at 2 hours (p less than 0.01) and gradually returned to control values at 48 hours. Thus, reversible myocardial injury due to anoxia is associated with both decreased contractility and compliance, with resultant depressed left ventricular performance for 24 to 48 hours after injury.
D000818:Animals; D001794:Blood Pressure; D001810:Blood Volume; D002302:Cardiac Output; D002306:Cardiac Volume; D003971:Diastole; D004285:Dogs; D006323:Heart Arrest / Q000209:etiology / Q000503:physiopathology*; D006339:Heart Rate; D006352:Heart Ventricles / Q000503:physiopathology*; D006439:Hemodynamics; D000860:Hypoxia / Q000503:physiopathology*; D009200:Myocardial Contraction; D013318:Stroke Volume