The MAP was fine. The flow was not.

Design

Retrospective cohort study with entropy balancing and a mechanistic substudy

Population

30,039 adults undergoing non-cardiac surgery at one South Korean academic centre, 2011-2020; median age 60

Primary outcome

Postoperative acute kidney injury (incidence 6.7%)

Effect

Narrow pulse pressure OR 1.66 (95% CI 1.42-1.94); normotension with narrow PP OR 1.56 (1.27-1.89); hypotension with reference PP OR 1.09 (0.86-1.38); both OR 1.85 (1.21-2.81). Stroke volume index 27 vs 47 ml/m²

Intraoperative haemodynamic targets are almost entirely mean arterial pressure targets, and the working assumption is that a MAP above 65 mmHg means adequate organ perfusion. This retrospective cohort of 30,039 adults having non-cardiac surgery at a single academic centre in South Korea between 2011 and 2020 tests that assumption against acute kidney injury, which occurred in 6.7%.

Patients were stratified by median intraoperative pulse pressure: narrow (under 40 mmHg), reference (40-70), wide (over 70). Entropy balancing adjusted for covariates including cumulative vasopressor load and duration of hypotension — which matters, because the obvious confounder is that narrow pulse pressure marks patients who were also hypotensive and heavily pressed.

Narrow pulse pressure was independently associated with AKI (OR 1.66, 95% CI 1.42-1.94, P<0.001). The two-by-two matrix is where it becomes interesting. Hypotension with a reference pulse pressure did not significantly raise risk (OR 1.09, 95% CI 0.86-1.38, P=0.475). Normotension with a narrow pulse pressure did (OR 1.56, 95% CI 1.27-1.89, P<0.001). Both together gave the highest risk (OR 1.85, 95% CI 1.21-2.81).

The mechanistic substudy explains it: stroke volume index was 27 ml/m² in the normotensive narrow-pulse-pressure group against 47 in the hypotensive reference group. A vasoconstricted patient on phenylephrine can have a reassuring MAP and a stroke volume that is half what it should be. Risk became significant after 40 minutes of that state.

• Read pulse pressure off the arterial trace alongside the MAP, not instead of it
• A narrowing pulse pressure on a rising vasopressor dose is the pattern to notice
• Forty minutes is roughly where the signal appeared — that is a whole case, not a moment
• Consider whether the answer is volume or inotropy rather than more vasoconstrictor
• Where you have cardiac output monitoring, this is an argument for using it in the at-risk patient

Why it matters

It challenges the assumption that a MAP above 65 means the kidney is being perfused.

Don't overread it

Retrospective and single-centre; no trial has yet shown that treating narrow pulse pressure prevents AKI.

The statistics, in plain English

This is observational, so narrow pulse pressure is associated with AKI rather than shown to cause it. The important internal comparison is that hypotension alone was not significant here (interval 0.86 to 1.38, crossing 1.0) while normotension with narrow pulse pressure was — which argues the signal is not simply mislabelled hypotension. Entropy balancing adjusts for measured confounders only; sicker hearts produce narrow pulse pressures, and some of this may be that.

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