Esmolol infusion during nitroprusside-induced hypotension: Impact on hemodynamics, ventricular performance, and venous admixture

The impact of esmolol infusion on hemodynamics, ventricular performance, venous admixture, sympathoadrenal, and renin-angiotensin system responses during sodium nitroprusside (SNP)-induced hypotension was studied in 11 patients undergoing lymph node dissection during general anesthesia with 60% nitrous oxide and fentanyl. Radial arterial and thermistor-tipped pulmonary catheters were employed for hemodynamic monitoring. Arterial and mixed venous blood gas tensions, arterial plasma renin activity (PRA), and plasma catecholamine levels were measured. Derived hemodynamic parameters and venous admixture (Qs/Qt) data were obtained from standard equations. Transesophageal echocardiography (6 patients) was used to assess left ventricular performance using the relationship between end-systolic wall stress (ESWS) and velocity of circumferential shortening (VCFC). After surgical incision, arterial hypotension was induced with SNP alone. Esmolol was infused at each of the following rates in sequence: 200, 300, and 400 μg/kg/min. Each esmolol infusion lasted 20 minutes and the SNP dose was adjusted to maintain MAP at 55 to 60 mm Hg. The mean dose of SNP required to induce hypotension was 5.5 μg/kg/min ± 0.5 SE. Compared to prehypotension values, SNP induced significant increases in Qs/Qt and reductions in PaO 2, systemic vascular resistance (SVR), and stroke volume index (SVI). Esmolol infusion caused dose-dependent (highest with 400 μg/kg/min) reductions in the SNP requirement, heart rate (HR), SVI, Qs/Qt, and PRA, and also led to significant increases in SVR and left ventricular (LV) internal diameter in diastole as well as systole. Furthermore, esmolol infusion was associated with a dose-dependent downward and leftward shift of the ESWS versus VCFC relationship, implying diminished contractility. These findings indicate that β-blockade with esmolol during SNP-induced hypotension is effective in reducing SNP dose requirement and PRA, while improving arterial oxygenation. However, in this setting, esmolol causes reductions in cardiac inotropic and chronotropic responses, resulting in diminished ventricular performance.