2026 FSA Podium and Poster Abstracts

Introduction/Background: Perioperative hypotension is a well-established contributor to myocardial injury and adverse cardiac outcomes. While maintaining adequate mean arterial pressure, or MAP, remains a primary intraoperative goal, emerging evidence suggests that vasopressor choice independent of achieved MAP may influence coronary perfusion, myocardial oxygen supply and demand balance, and arrhythmic risk. Commonly used vasopressors differ in their effects on heart rate, afterload, ventricular arterial coupling, cardiac output, and microvascular perfusion. Agents such as phenylephrine, norepinephrine, vasopressin, and angiotensin II therefore have distinct hemodynamic profiles that may carry different implications for perioperative cardiac risk. This review examines whether vasopressor selection may represent a clinically relevant factor in myocardial injury during surgery.

Methods: A systematic literature review was conducted using PubMed, Embase, and the Cochrane Library from 1990 to 2024. Search terms included combinations of “vasopressor,” “myocardial injury,” “phenylephrine,” “norepinephrine,” “vasopressin,” “angiotensin II,” “coronary perfusion,” and “perioperative hypotension.” Randomized controlled trials, observational studies, physiologic investigations, and systematic reviews involving adult patients undergoing cardiac or high-risk noncardiac surgery were included. Outcomes of interest included troponin-defined myocardial injury, ischemic ECG changes, arrhythmias, markers of coronary perfusion, microcirculatory indices, and associated hemodynamic patterns. Because study methods and endpoints differed, findings were synthesized qualitatively.

Results: Twenty seven studies met inclusion criteria. Phenylephrine was frequently associated with reflex bradycardia and reductions in cardiac output, with several studies reporting impaired markers of coronary perfusion and increased ischemic ECG changes, particularly in patients with coronary artery disease or left ventricular hypertrophy. Norepinephrine generally maintained MAP with more favorable cardiac output and ventricular arterial coupling, although higher doses were associated with increased myocardial oxygen demand. Vasopressin maintained blood pressure with minimal chronotropic effect and, in vasodilatory states, was associated with improved microcirculatory markers and fewer ischemic findings in select cohorts. Limited data on angiotensin II suggested preservation of cardiac output without clear evidence of increased myocardial injury. Across studies, heart rate trends, cardiac output changes, and microcirculatory parameters appeared more closely associated with myocardial injury than MAP targets alone.

Discussion/Conclusion: The available literature suggests that vasopressor choice may influence perioperative cardiac physiology beyond achieving blood pressure targets. Although evidence remains largely associative, consistent physiologic observations support consideration of vasopressor selection when managing patients at elevated cardiac risk. In addition to maintaining MAP, attention to heart rate control, cardiac output, and microcirculatory effects may be important in minimizing myocardial oxygen imbalance. Prospective studies with myocardial injury as a primary endpoint are needed to determine whether tailored vasopressor strategies translate into improved perioperative outcomes.