Changes in myocardial oxygen consumption, efficiency and haemodynamics when systemic pressure is increased during morphine and added halothane anaesthesia in dogs.

Abstract

Depression of left ventricular function by the combination of halothane anaesthesia and increased ventricular afterload may undesirably reduce stroke volume and increase myocardial oxygen consumption by increasing ventricular wall stress. To investigate this possibility we studied six dogs instrumented to measure systemic and left ventricular pressures, ascending aortic and left anterior descending coronary artery flows and external left ventricular diameters. We sampled arterial and coronary sinus blood gases and oxygen contents. During morphine anaesthesia (4mg·kg-1 intravenously with hourly supplements of 0.1 mg·kg-1) and during added halothane anaesthesia (1.5 per cent end tidal) we measured systemic pressure, heart rate, stroke volume, stroke work, cardiac output, left ventricular end diastolic pressure and diameter and myocardial oxygen consumption. After infusing phenylephrine (0.02 mg/ml) to increase systolic pressure to 23.28 kPa (175 torr) we repeated measurements in both groups. We found that added halothane depressed systemic pressures (52 per cent), stroke volume (30 per cent), and myocardial oxygen consumption (46 per cent) compared to morphine alone. When afterload was increased with phenylephrine, stroke volume (20 per cent), cardiac output (25 per cent) and myocardial efficiency (47 per cent) were further depressed during added halothane anaesthesia compared to control halothane anaesthesia. Left ventricular end diastolic diameter (5 per cent) and pressure (320 per cent) were significantly increased by added afterload, compared to the control added halothane state. Conversely, increased afterload produced few changes during morphine anaesthesia alone. However, at comparable systemic pressures, myocardial oxygen consumption was similar during both anaesthetic states. We conclude that during added halothane anaesthesia increased afterload decreases stroke volume and myocardial efficiency. Cardiac output is reduced without increased myocardial oxygen consumption compared to morphine anaesthesia at comparable afterload states. In patients with already compromised cardiac output, further depression of stroke volume by increased ventricular afterload during halothane anaesthesia may be deleterious.