Hypotension and pulmonary atelectasis during general anaesthesia: a randomised crossover laboratory study.
rct · Level II
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- Record sourced from PubMed, PMID 42342494.
- Also identified by DOI 10.1016/j.bja.2026.05.008.
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Abstract
Atelectasis is common during general anaesthesia and contributes to postoperative pulmonary complications. Despite preventive strategies targeting established underlying mechanisms, extensive atelectasis still often occurs, suggesting that additional factors may be involved. We tested the hypothesis that hypotension contributes to atelectasis formation during anaesthesia. We conducted a randomised, evaluator-blinded crossover study in 12 anaesthetised, mechanically ventilated pigs under conditions simulating anaesthesia induction, in which preoxygenation was followed by either normotension or profound hypotension induced with nitroprusside. The primary outcome was total atelectasis volume, measured by computed tomography. Pulmonary blood flow distribution was assessed using [<sup>15</sup>O]-water positron emission tomography. Atelectasis volume was greater during induced hypotension (median MAP 46 mmHg [interquartile range: 43-49]), compared with normotension (median MAP 85 mmHg [81-93]) in 11 of 12 pigs (median difference 20 ml [95% CI 9-38]; P<0.001). During hypotension, pulmonary blood flow was redistributed towards the dorsal lung regions, with hypotension resulting in a ratio of dorsal to total pulmonary blood flow of 182% (170-186), compared with 129% (104-150) with normotension. Mixed venous oxygen saturation was lower during hypotension (43% [27-53]) compared with normotension (48% [44-56]). In this experimental model of anaesthesia induction, profound hypotension increased atelectasis compared with normotension. The findings are consistent with redistribution of pulmonary blood flow with low oxygen saturation towards dorsal lung regions that are prone to develop absorption atelectasis. Hypotension during induction of general anaesthesia might therefore be a hitherto unrecognised contributor to pulmonary atelectasis. www.animalstudyregistry.org (https://doi.org/10.17590/asr.0000369).