Haemodynamic changes during sodium nitroprusside induced hypotension and halothane/nitrous oxide anaesthesia.

The haemodynamic effects of nitroprusside (SNP) were studied in six patients undergoing surgery for intracranial aneurysm under controlled hypotension in endotracheal anaesthesia with halothane-nitrous oxide during hypocapnia. Mean arterial pressure was reduced with SNP from mean 12.25 kPa to mean 8.29 kPa (32%). There were concomitant statistically significant decreases in systemic vascular resistance (-21%), cardiac index (-17%), stroke index (-23%), pulmonary arterial mean pressure (-27%) and pulmonary capillary wedge pressure (-27%). Heart rate, central venous pressure and pulmonary vascular resistance did not change significantly. After the infusion of SNP was discontinued all parameters, except cardiac index and heart rate, returned to values not significantly different from the control values. The hypotension induced by SNP resulted from reductions in cardiac index and systemic vascular resistance. The reduction in cardiac index did not reach a critical level in any of the patients.

The haemodynamic effects of sodium nitroprusside-induced hypotension during beta-adrenergic blockade and anaesthesia. A case report.

We present the central haemodynamic data obtained during halothane/nitrous oxide anaesthesia in a patient under antihypertensive treatment with propranolol who underwent surgery for intracranial aneurysms in sodium nitroprusside-induced hypotension. Cardiac output remained unchanged when hypotension was induced. Pulmonary capillary wedge pressure decreased. There was a slight increase in heart rate, as well as a minor decrease in stroke volume. Systemic vascular resistance decreased, but pulmonary vascular resistance remained unchanged. The response observed is discussed.

Effects of acid-base changes, hypoxia, and catecholamines on ventricular performance.

Extracellular pH changes were produced in dogs with tris (hydroxy-methyl)-aminomethane (Tris) or NaHCO3 in the presence or absence of hypoxemia and before and after beta-adrenergic blockade with propranolol. Ventricular performance (VP) was evaluated by measurement of maximum rate of rise of left ventricular pressure (dp/dt max) and left ventricular end-diastolic pressure in the canine right heart bypass preparation with aortic pressure, heart rate, and cardiac output held constant. Low pH diminished VP. Hypoxemia did not alter VP within the pH, suggesting that decreased V observed with acidosis before propranolol was due primarily to decreased myocardial response to catecholamines. Increase of pH with Tris increased VP significantly more than with NaHCO3. Beta blockade diminished the response of VP to Tris at a high pH;prior administration of reserpine abolished the inotropic effect of Tris. The data suggest that Tris can influence VP independent of its effect on pH. This effect is probably mediated by the interaction between endogenous catecholamines and myocardial beta receptors.

The echocardiogram of the anterior leaflet of the mitral valve. Correlation with hemodynamic and cineroentgenographic studies in dogs.

The echocardiogram of the anterior leaflet of the mitral valve (ECHO) was compared to hemodynamic and cineroentgenographic data to evaluate its accuracy in timing mitral valve (MV) opening and closure, and to validate it as an indicator of MV motion. The ECHO, high speed cineroentgenography at 250 frames/sec, and/or measurement of intracardiac pressures allowed accurate timing of the events of MV motion in dogs on right heart bypass. The intersection of left ventricular and left atrial pressures in early diastole preceded the onset of rapid anterior motion of ECHO (D' point) by 17 to 33 plus or minus 7.6 msec; r equals 0.98. The onset of left ventricular systole occurred before the termination of final rapid posterior motion of the ECHO in end diastole (Co point) by 25 plus or minus 10 msec; r equals 0.96. Radiopaque clips were attached to the free edges of both leaflets of the MV. Cineroentgenographically determined plots of clip distance from the ultrasound transducer were morphologically similar to the simultaneously recorded ECHO. A delay of 23 plus or minus 3 (0 to 40) msec was observed in the ECHO peaks of diastolic anterior excursion compared to clip motion. Contrast medium advances beyond the free edges of MV leaflets mixing with left ventricular blood 43 plus or minus 3 msec after initial separation. These cineroentgenographic studies elucidate nonuniformity of leaflet motion responsible for ECHO delays. Thus, ECHO D' and Co correlate well with hemodynamic indicators of MV opening and closure. However, ECHO motion, although qualitatively similar, is unpredictably delayed compared to cineroentgenography of clips on the MV free edge. Since the ECHO correlates well with hemodynamic indices of MV opening and closure, this noninvasive technique can be used as a reference in the timing of intracardiac events and in the determination of systolic and diastolic time intervals.