Left ventricular performance during propofol or methohexital anesthesia: isotopic and invasive cardiac monitoring.

Using gated radionuclide ventriculography and invasive cardiac monitoring, the effects of propofol and methohexital on left ventricular volumes and function were investigated in 22 unpremedicated patients (ASA physical status III, 50-78 yr) with chronic coronary artery disease (NYHA class II-III). Anesthesia was induced with either propofol or methohexital (2 mg/kg), followed by a maintenance infusion of 100 micrograms.kg-1.min-1. Vecuronium (0.05 mg/kg) was administered and ventilation (FIO2, 1.0) was manually controlled (FECO2, 0.04-0.05). Data acquisitions were serially obtained over 15 min. Propofol and methohexital anesthesia caused an average 15% decrease in mean arterial pressure, associated with a 20% decrease in cardiac index without a decrease in systemic vascular resistance index. It is interesting that the determinants of these hemodynamic effects were different. Heart rate did not change during propofol infusion despite the decrease in mean arterial pressure, whereas heart rate increased during methohexital infusion. In the propofol group, the decrease in cardiac index was associated with decreases in indicators of preload (end-diastolic volume and pulmonary capillary wedge pressure), whereas end-systolic volume and global ejection fraction did not change statistically. In the methohexital group, the decrease in cardiac index was associated with a decrease in global ejection fraction and an increase in end-systolic volume, whereas indicators of preload remained unchanged. It is concluded that methohexital reduces left ventricular performance. In contrast, propofol preserves left ventricular performance despite a likely negative inotropic effect.

Left ventricular function during propofol and fentanyl anesthesia in patients with coronary artery disease: assessment with a radionuclide approach.

Using gated radionuclide ventriculography and invasive cardiac monitoring, the effects of propofol alone and in combination with fentanyl on left ventricular (LV) volumes and function were investigated in 10 ASA III, unpremedicated patients (51-75 years) with coronary artery disease (NYHA II-III). Anesthesia was induced with propofol (2 mg/kg) followed by an infusion (100 micrograms.kg-1.min-1). Vecuronium (0.05 mg/kg) was administered and ventilation (FIO2, 1.0) was manually controlled via a face mask (FECO2, 4-5%). Data acquisitions were serially obtained over 15 minutes after the bolus IV injection of propofol and 5 minutes after the injection of fentanyl (5 micrograms/kg). Propofol induced a rapid decrease (15%) in mean arterial pressure (MAP) exclusively related to a decrease in cardiac index (CI), without reduction in indexed systemic vascular resistances (SVRI). Despite the decrease in MAP, heart rate did not change. The decrease in CI was associated with a lower preload. After the addition of fentanyl, MAP decreased significantly (35%) below the last set of propofol measurements. The decrease in MAP was associated with a reduction in CI and SVRI. Fentanyl was also associated with a significant decrease in heart rate (16%) resulting in a decrease in CI, whereas stroke index and end diastolic volume did not change. Neither global ejection fraction (EF) nor end systolic volume changed significantly at any time, nor were there changes in the ECG or in regional ejection fractions (REF). The absence of changes in REF was consistent with lack of wall motion abnormalities of the left ventricle. Propofol alone and in combination with fentanyl does not alter LV performance in patients with good LV function.(ABSTRACT TRUNCATED AT 250 WORDS)

Sustained ventricular unloading action of the alpha-adrenergic antagonist nicergoline in the dog.

Preliminary studies indicate that nicergoline, a new alpha-antagonist, can lower HR at doses which decrease arterial BP. The present animal study was designed to quantitate the systemic and carotid (pulsed Doppler) hemodynamic and renin release consequences of nicergoline ventricular unloading, and to investigate the hemodynamic mechanisms of hypotension. In 11 anesthetized dogs, nicergoline infusion induced progressive, moderate, and prolonged hypotension associated with reduced vascular resistance and capacitance. Hypotension resulted from decreased HR and cardiac output, without an increase in plasma renin activity. The effects on carotid hemodynamics were less marked than those on the systemic circulation. Hypotension was caused primarily by vasoplegia, and was magnified subsequently by inhibition of the reflex rapid pressor control mechanisms. This suggests that repeated iv doses of nicergoline are preferable to prolonged infusion.

Common carotid haemodynamic and metabolic effects of acutely administered nifedipine in human subarachnoid haemorrhage.

Although the drugs known as "calcium antagonists" exert inhibitory actions on vascular smooth muscle, there are no quantitative data concerning the clinical use of these vasodilator agents in human subarachnoid haemorrhage. In the present clinical study, we have measured the effects of nifedipine (20 mg tablet) on common carotid artery diameter (D) blood flow velocity (V) common carotid blood flow (CCBF) as an index of cerebral blood flow, systolic (Qs) and diastolic (Qd) blood flow fractions using a pulsed Doppler apparatus and on carotid arterial pressure (CAP), heart rate (HR) and oxygen consumption (VO2). Eight patients with subarachnoid haemorrhage were studied during anaesthesia for cerebral angiography. Thirty minutes after sublingual nifedipine, diameter (P less than 0.05), blood flow velocity (P less than 0.001), CCBF (P less than 0.001), Qs (P less than 0.05), and Qd (P less than 0.05) increased with a decrease in Qs/Qd ratio (P less than 0.05). carotid vascular resistance (CVR) fell (P less than 0.02) and oxygen consumption of the brain increased (P less than 0.01). Systolic, diastolic, and mean carotid blood pressure, heart rate, and arteriovenous difference in oxygen were unchanged. The increase in CCBF was closely correlated with the vascular resistance in the control state (r = 0.928, P less than 0.001) and with oxygen consumption (r = 0.869, P less than 0.001). We conclude that in vivo, nifedipine exerts a preferential action on cerebral vessels, vasodilating large arteries and arterioles. This action is more powerful if the vessels are already vasoconstricted. Thus, the use of nifedipine could be fruitful in cerebral ischaemia that is secondary to subarachnoid haemorrhage.

Systemic and carotid haemodynamics and plasma renin activity during deliberate hypotension in dogs: a comparison of sodium nitroprusside with nicergoline.

This study was designed to compare at the same level of hypotension (-30%) nitroprusside (SNP) and nicergoline (NIC) effects on systemic haemodynamics and carotid haemodynamics (pulsed Doppler) and on plasma renin activity (PRA) in 20 anaesthetized dogs before and at the 20th minute of hypotension. In SNP group (n = 9) cardiac output (CO) and heart rate (HR) increased. Stroke volume (SV), pulmonary wedge pressure (PWP), central venous pressure (CVP) and systemic vascular resistance (SVR) decreased. Common carotid diameter (D) increased and blood flow velocity (V) decreased with constant common carotid blood flow (CCBF). CCBF/CO ratio was unchanged. PRA levels increased. In NIC group (n = II), HR, CO, SV were unchanged and PWP, CVP, SVR decreased. D, V and CCBF were unchanged. CCBF/CO ratio increased and PRA was unchanged. NIC provoked mild hypotension without reflex sympathetic activation unlike SNP. Only SNP dilated large arteries. The autoregulation of CCBF is maintained with both drugs but CCBF/CO ratio is increased only with NIC.