Key result
In a theoretical circulatory model, V-A ECMO support augmented coronary blood flow, which via the Gregg effect prevented left ventricular distension by reducing end-diastolic pressure and volume.
Why the study?
Previous theoretical studies predicted left ventricular distension during V-A ECMO, but this occurs uncommonly in clinical practice, creating an unexplained discrepancy.
Does V-A ECMO support prevent left ventricular distension by augmenting coronary blood flow and contractility in a theoretical circulatory model?
Does V-A ECMO support prevent left ventricular distension by augmenting coronary blood flow and contractility in a theoretical circulatory model?
Theoretical modeling suggests that V-A ECMO augments coronary blood flow, which may increase LV contractility via the Gregg effect and prevent LV distension.
Objectives Using a lumped parameter-based theoretical circulatory model, we sought to examine the potential effects of veno-arterial (V-A) extracorporeal membrane oxygenation (ECMO) support on coronary blood flow and resultant left ventricular (LV) contractility. Background Previous theoretical studies have suggested that V-A ECMO support results in markedly increased left ventricular intracavity pressures and volumes, i.e., not only inadequate unloading, but exacerbated loading. However, this phenomenon of LV distension occurs only uncommonly in clinical scenarios. This discrepancy between previous theoretical work and clinical experience requires explanation. Methods We defined a piecewise linear relation between the end-systolic pressure and volume of the ventricles to simulate ascending and descending limbs of the Frank-Starling relationship. A linear relationship between coronary blood flow rate and left ventricular contractility was added, defining the so-called “Gregg effect”. Results LV systolic dysfunction resulted in reduced coronary blood flow; V-A ECMO support augmented coronary blood flow, proportionally to the circuit flow rate. On V-A ECMO support, a weak or absent Gregg effect resulted in increased LV end-diastolic pressures and volumes, and increased end-systolic volume with decreased LV ejection fraction (LVEF), consistent with LV distension. In contrast, a more robust Gregg effect resulted in unaffected and/or even reduced LV end-diastolic pressure and volume, end-systolic volume, and unaffected or even increased LVEF. Conclusions In this lumped parameter model-based theoretical study, V-A ECMO support was found to augment coronary arterial blood flow. A resultant proportional augmentation of LV contractility may be an important contributory mechanism underlying why LV distension is uncommon in the setting of V-A ECMO support.
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Myneni et al. (2022) studied Systolic left ventricular failure (simulated). V-A ECMO support with Gregg effect vs. V-A ECMO support without Gregg effect was evaluated on Left ventricular end-diastolic pressure and volume, end-systolic volume, and ejection fraction. In a theoretical circulatory model, V-A ECMO support augmented coronary blood flow, which via the Gregg effect prevented left ventricular distension by reducing end-diastolic pressure and volume.
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