Anesthesia induction and mechanical ventilation during CABG significantly reduced arterial pressure, decreasing cardiac index by 16.7% and stroke volume by 16.5% in patients with reduced LVEF.
What are the hemodynamic alterations underlying arterial hypotension following anesthesia induction in patients with preserved or impaired myocardial contractility undergoing CABG?
Arterial hypotension after anesthesia induction in CABG patients is driven by pharmacologic vasodilation and impaired cardiac performance under positive pressure ventilation, with pressure-derived parameters often being artifacts of increased intrathoracic pressure.
Background. Arterial hypotension following anesthesia induction and initiation of mechanical ventilation is a common phenomenon with potentially harmful consequences. Effective hemodynamic management requires identification of predominant underlying mechanism. Objective. To examine hemodynamic alterations underlying arterial hypotension following anesthesia induction in patients with preserved or impaired myocardial contractility undergoing coronary artery bypass grafting. Material and methods. A prospective clinical study enrolled 100 patients with chronic heart failure scheduled for CABG: group 1 (n=50) — patients with preserved left ventricular ejection fraction (LVEF ≥50%), group 2 (n=50) — patients with reduced LVEF (41—49%). Hemodynamic assessment included pressure-derived parameters (pulmonary artery catheter) and volumetric measurements (transesophageal echocardiography) at four time points: (1) prior to anesthesia induction; (2) after induction but before neuromuscular blockade (“spontaneous breathing phase”); (3) 10 min after initiation of MV; (4) 3 min after Trendelenburg positioning. Results. Induction of anesthesia resulted significant reduction of mean arterial pressure (MAP) and perfusion pressure in both groups. Pressure further declined after MV initiation (p<0.05). In group 2, this was accompanied by decrease in indexed stroke volume by 16.5% and cardiac index by 16.7% (p<0.05). Central venous pressure significantly increased after MV initiation only in patients with reduced LVEF. Despite Trendelenburg position augmenting venous return, no increase in left ventricular end-diastolic volume or cardiac output was recorded in both groups. Conclusion. Arterial hypotension following anesthesia induction is primarily driven by pharmacologic vasodilation and impaired cardiac performance under positive pressure ventilation. Pressure-derived parameters are often artifacts of increased intrathoracic pressure that limits their clinical value.
Kolotukhin et al. (2026) studied this question. Anesthesia induction and mechanical ventilation during CABG significantly reduced arterial pressure, decreasing cardiac index by 16.7% and stroke volume by 16.5% in patients with reduced LVEF.