Arterial dP/dtmax Response to Fluids and Norepinephrine During Intraoperative Hypotension: A Prospective Physiological Study
TL;DR
Radial arterial dP/dtmax increased after both fluid administration and norepinephrine, confirming its sensitivity to haemodynamic loading conditions and should be interpreted as an integrated haemodynamic variable influenced by ventricular performance, preload, and arterial properties rather than as a direct measure of intrinsic myocardial contractility.
Abstract
Background: Intraoperative hypotension during major abdominal surgery is common and can result from changes in preload, afterload, or myocardial contractility. Recognising the underlying cause is essential for targeted haemodynamic management. Arterial dP/dtmax has been proposed as a surrogate marker for ventricular systolic function, but its behaviour during fluid and vasopressor administration under general anaesthesia remains not fully understood. This study evaluated changes in radial arterial dP/dtmax following protocol-guided fluid administration and norepinephrine boluses during intraoperative hypotension. Methods: This prospective observational study involved 88 adult patients undergoing elective major abdominal surgery with continuous radial arterial waveform monitoring. Hypotensive episodes were defined as a mean arterial pressure <65 mmHg persisting for at least 60 s and were managed according to a predefined algorithm based on stroke volume variation and dynamic arterial elastance. The primary outcome was the change in arterial dP/dtmax from baseline to 5 min after fluid administration. Linear mixed-effects models were used to account for repeated intervention episodes within patients. Results: A total of 502 protocol-guided intervention episodes contributed by 76 patients were included in the primary analysis: 228 fluid-treated episodes and 274 norepinephrine-treated episodes. Estimated mean arterial dP/dtmax increased from 517 mmHg·s−1 (95% CI 477–557) at baseline to 631 mmHg·s−1 (95% CI 591–671) at 5 min during fluid-treated episodes and from 575 mmHg·s−1 (95% CI 536–615) to 647 mmHg·s−1 (95% CI 608–686) during norepinephrine-treated episodes (both p < 0.001). A significant intervention-condition-by-time interaction was observed (F = 5.55, p = 0.019), indicating that temporal evolution of arterial dP/dtmax differed between the two algorithm-defined haemodynamic conditions. Conclusions: Radial arterial dP/dtmax increased after both fluid administration and norepinephrine, confirming its sensitivity to haemodynamic loading conditions. It should therefore be interpreted as an integrated haemodynamic variable influenced by ventricular performance, preload, and arterial properties rather than as a direct measure of intrinsic myocardial contractility.