Mechanisms contributing to hypotension after anesthetic induction with sufentanil, propofol, and rocuronium: a prospective observational study

Abstract

It remains unclear whether reduced myocardial contractility, venous dilation with decreased venous return, or arterial dilation with reduced systemic vascular resistance contribute most to hypotension after induction of general anesthesia. We sought to assess the relative contribution of various hemodynamic mechanisms to hypotension after induction of general anesthesia with sufentanil, propofol, and rocuronium. In this prospective observational study, we continuously recorded hemodynamic variables during anesthetic induction using a finger-cuff method in 92 non-cardiac surgery patients. After sufentanil administration, there was no clinically important change in arterial pressure, but heart rate increased from baseline by 11 (99.89% confidence interval: 7 to 16) bpm (P < 0.001). After administration of propofol, mean arterial pressure decreased by 23 (17 to 28) mmHg and systemic vascular resistance index decreased by 565 (419 to 712) dyn*s*cm^-5*m² (P values < 0.001). Mean arterial pressure was < 65 mmHg in 27 patients (29%). After propofol administration, heart rate returned to baseline, and stroke volume index and cardiac index remained stable. After tracheal intubation, there were no clinically important differences compared to baseline in heart rate, stroke volume index, and cardiac index, but arterial pressure and systemic vascular resistance index remained markedly decreased. Anesthetic induction with sufentanil, propofol, and rocuronium reduced arterial pressure and systemic vascular resistance index. Heart rate, stroke volume index, and cardiac index remained stable. Post-induction hypotension therefore appears to result from arterial dilation with reduced systemic vascular resistance rather than venous dilation or reduced myocardial contractility.

Keywords: Blood pressure; Cardiac output; Cardiovascular dynamics; Hemodynamic monitoring; Intraoperative hypotension.

Fig. 1

Measurement time points. We recorded hemodynamic variables before induction of general anesthesia, during preoxygenation, 45 s after administration of sufentanil, 45 s after administration of propofol, 90 s after administration of rocuronium, 60 s after tracheal intubation, and 180 s after tracheal intubation

Fig. 2

Hemodynamic variables during the induction of general anesthesia. Boxplots showing mean (triangle) and median (horizontal bar) with 25th–75th percentile (box) of hemodynamic variables during the induction of general anesthesia. Whiskers extend to the most extreme observations within 1.5 times the interquartile range of the first and third quartiles, respectively. Circles represent outliers. MAP mean arterial pressure, SAP systolic arterial pressure, DAP diastolic arterial pressure, SVRI systemic vascular resistance index, HR heart rate, SVI stroke volume index, CI cardiac index