Intraoperative tachycardia burden, diastolic hypotension, and in-hospital mortality after noncardiac surgery: a retrospective cohort study

Intraoperative hypotension is an established perioperative risk marker, but the relevance of intraoperative tachycardia remains uncertain. We examined tachycardia, diastolic blood pressure (DBP), mean arterial pressure (MAP), and temporal co-occurrence in noncardiac surgery. We conducted a retrospective cohort study using INSPIRE version 1.4.2. Adults undergoing first eligible noncardiac surgery under general anaesthesia were included. The primary cohort required ≥ 70% paired heart-rate (HR) and invasive DBP coverage. Tachycardia burden was the proportion of monitored time with HR ≥ 90 beats min − 1. The primary outcome was in-hospital mortality. Modified Poisson regression with robust standard errors was used. Sensitivity analyses assessed common-denominator epochs, severity-sensitive HR metrics, and available pre-anaesthesia HR. The primary arterial-monitoring cohort included 33,478 operations with 543 deaths (1.62%); the broader HR cohort included 79,001 operations with 708 deaths (0.90%). Each 5-percentage-point increase in tachycardia burden remained associated with higher in-hospital mortality after multivariable adjustment including DBP and MAP burden (RR 1.045, 95% CI 1.031–1.060; P < 0.001). Adjusted standardized risk was 1.31% (95% CI 1.13–1.48%) at 0% burden and 2.79% (95% CI 2.27–3.30%) at > 20% burden, an adjusted risk difference of 1.48% points (95% CI 0.91–2.05; P < 0.001). Profound DBP < 45 mm Hg burden was not associated after mutual adjustment, and the incremental concurrent-overlap term provided little additional information after adjustment for tachycardia, DBP, and MAP burdens. Results were robust to alternative HR metrics, a common time denominator, the broader cohort, and pre-anaesthesia HR adjustment. Greater cumulative intraoperative tachycardia burden remained associated with in-hospital mortality after multivariable adjustment. The burden metric reflects duration above the HR threshold rather than tachycardia intensity. These observational findings identify tachycardia burden as a risk marker but do not establish causality, a therapeutic HR threshold, or benefit from pharmacological HR reduction.