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Intra-operative hypotension is a known predictor of adverse events and poor outcomes following major surgery. Hypotension often occurs on induction of anaesthesia, typically attributed to hypovolaemia and the haemodynamic effects of anaesthetic agents. We assessed the efficacy of fluid optimisation for reducing the incidence of hypotension on induction of anaesthesia. This prospective trial enrolled 283 patients undergoing radical cystectomy and randomly allocated them to goal-directed fluid therapy (n = 142) or standard fluid therapy (n = 141). Goal-directed fluid therapy patients received fluid optimisation based on stroke volume response to passive leg raise before induction; those with positive passive leg raise received intravenous crystalloid fluid boluses until stroke volume was optimised. Baseline mean arterial pressure was measured on the morning of surgery and on arriving in the operating theatre. This post-hoc analysis defined haemodynamic instability as either a > 30% relative drop in mean arterial pressure compared with baseline or absolute mean arterial pressure < 55 mmHg, within 15 min of induction. Forty-two (30%) goal-directed fluid therapy patients underwent fluid optimisation after finding an intravascular fluid deficit via passive leg raise testing; 106 (75%) goal-directed fluid therapy and 112 (79%) standard fluid therapy patients met criteria for haemodynamic instability. There was no significant difference in the incidence of haemodynamic instability between the goal-directed fluid therapy and standard fluid therapy groups using absolute mean arterial pressure drop below 55 mmHg (p = 0.58) or using pre-surgical testing or pre-surgical mean arterial pressure values as baseline (p = 0.21, p = 0.89, respectively); however, the difference in the incidence of haemodynamic instability was significant using the operating theatre baseline mean arterial pressure (p = 0.004). We conclude that fluid optimisation before induction of general anaesthesia did not significantly impact haemodynamic instability.

Objectives The aim of this study was to investigate the value of bedside echocardiography with a passive leg raise as a noninvasive marker of volume responsiveness. Methods This work was a prospective observational study of patients with end-stage renal disease presenting to the emergency department. The left ventricular outflow tract (LVOT) velocity time integral (VTI) was obtained. Measurements before and after dialysis as well as before and after the passive leg raise were recorded. Results Fifty-four patients were enrolled, in whom the mean volume of fluid removed ± SD was 3.89 ± 0.91 L. In the predialysis cohort, the mean LVOT VTI was 28.05 cm (95% confidence interval [CI], 26.55-29.55 cm). After the passive leg raise, the mean VTI was 28.52 cm (95% CI, 26.98-30.07 cm). In the postdialysis cohort, the mean VTI was 30.31 cm (95% CI, 28.92-31.69 cm), and it increased to 34.91 cm (95% CI, 33.11-36.72 cm) after the passive leg raise. The Δ VTI values were 1.83% (95% CI, 0.12%-3.55%) in the predialysis group and 15.05% (95% CI, 12.76%-17.34%) in the postdialysis cohort. When stratified by fluid removal, the mean Δ VTI values after hemodialysis were 12.64% (95% CI, 9.79%-15.49%) and 16.84% (95% CI, 13.47%-20.22%) for patients who had less than 4 L and 4 L or greater removed, respectively. In patients without congestive heart failure, the Δ VTI was 15.28% (95% CI, 12.25%-18.32%), whereas for those with congestive heart failure, the mean change was 14.63% (95% CI, 10.91%-18.35%). Conclusions The LVOT VTI in conjunction with a passive leg raise seems to correlate with the volume status and volume responsiveness.

Current guidelines for intra-operative fluid management recommend the use of increments in stroke volume following intravenous fluid bolus administration as a guide to subsequent fluid therapy. To study the physiological premise of this paradigm, we tested the hypothesis that healthy, non-starved volunteers would develop an increment in their stroke volume following a passive leg raise manoeuvre. Subjects were positioned supine and stroke volume was measured by transthoracic echocardiography at baseline, 30 s, 1 min, 3 min and 5 min after passive leg raise manoeuvre to 45°. Stroke volume was measured at end-expiration during quiet breathing, as the mean of three sequential measurements. Seventeen healthy volunteers were recruited; one volunteer in whom it was not possible to obtain Doppler measurements and a further five for reasons of poor Doppler image quality were not included in the study. Mean (SD) percentage difference from baseline to the largest change in stroke volume was 5.7 (9.6)% (p = 0.16). Of the 11 volunteers evaluated, five (45%) had stroke volume increases of greater than 10%. Mean (SD) maximum percentage change in cardiac index was 14.8 (9.7)% (p = 0.004). A wide variation in baseline stroke volume and response to the passive leg raise manoeuvre was seen, suggesting greater heterogeneity in the normal population than current clinical guidelines recognise.