Left Ventricular Unloading During Veno-Arterial ECMO: A Simulation Study

Abstract

Veno-arterial extracorporeal membrane oxygenation (VA ECMO) is widely used in cardiogenic shock. It provides systemic perfusion, but left ventricular (LV) unloading is suboptimal. Using a closed-loop, real-time computer model of the human cardiovascular system, cardiogenic shock supported by peripheral VA ECMO was simulated, and effects of various adjunct LV unloading interventions were quantified. After VA ECMO initiation (4 L/min) in cardiogenic shock (baseline), hemodynamics improved (increased to 85 mm Hg), while LV overload occurred (10% increase in end-diastolic volume [EDV], and 5 mm Hg increase in pulmonary capillary wedge pressure [PCWP]). Decreasing afterload (65 mm Hg mean arterial pressure) and circulating volume (-800 mL) reduced LV overload (12% decrease in EDV and 37% decrease in PCWP) compared with baseline. Additional intra-aortic balloon pumping only marginally decreased cardiac loading. Instead, adjunct Impella™ enhanced LV unloading (23% decrease in EDV and 41% decrease in PCWP). Alternative interventions, for example, left atrial/ventricular venting, yielded substantial unloading. We conclude that real-time simulations may provide quantitative clinical measures of LV overload, depending on the degree of VA ECMO support and adjunct management. Simulations offer insights into individualized LV unloading interventions in cardiogenic shock supported by VA ECMO as a proof of concept for potential future applications in clinical decision support, which may help to improve individualized patient management in complex cardiovascular disease.

Figure 1.

Pressure–volume loop simulation of left ventricular (LV) failure. Normal physiology shown in gray loop for comparison. Red loop shows an LV with reduced systolic contractility, increase in passive LV diastolic stiffness and blood volume (see text) to mimic a clinical case of cardiogenic shock. Red thin lines indicate end-systolic and end-diastolic pressure–volume relations. The black arrow shows an increasing VA extracorporeal membrane oxygenation (ECMO) support 0–4 L/min with resulting decrease in stroke volume and dilatation of the LV.

Figure 2.

Pressure–volume loop analysis representing the effects of afterload reduction in left ventricular systolic failure supported by veno-arterial extracorporeal membrane oxygenation (VA ECMO) 4 L/min. Afterload (systemic vascular resistance) is reduced until systemic mean arterial blood pressure (MAP) reaches 65 mm Hg, an accepted target in clinical care for patients with cardiogenic shock providing a reasonable compromise between low afterload, systemic and coronary perfusion pressure.

Figure 3.

Pressure–volume loop analysis of both afterload and blood volume reduction in left ventricular (LV) systolic failure supported by veno-arterial extracorporeal membrane oxygenation (VA ECMO) 4 L/min. Blood volume is reduced by 800 mL reaching a normal blood volume. Afterload (systemic vascular resistance) is then reduced until mean arterial blood pressure (MAP) reaches 65 mm Hg, as shown in Figure 2. Stroke volume and end-diastolic volume is reduced as compared with afterload reduction alone, thereby illustrating the importance of blood volume reduction in LV unloading.

Figure 4.

Pressure–volume loop analysis of inotropic drug effects in left ventricular failure and veno-arterial extracorporeal membrane oxygenation (VA ECMO) 4 L/min. Inotropy only (gray loop) reduces end-diastolic volume and increases stroke volume as well as systemic mean arterial blood pressure (MAP) as compared with no inotropy (red loop). Systemic vascular resistance is finally readjusted down to an MAP of 65 mm Hg, providing further unloading (green loop).

Figure 5.

Pressure–volume loop analysis of intra-aortic balloon pumping (IABP) effects in left ventricular failure and veno-arterial extracorporeal membrane oxygenation (VA ECMO) 4 L/min. End-diastolic volume decreases only minimally and stroke volume increases as a result of decreasing afterload. In addition, diastolic systemic blood pressure increases providing improved coronary blood flow (Table 1, not shown in pressure–volume loop).

Figure 6.

Pressure–volume loop analysis of Impella effects in left ventricular systolic failure and veno-arterial extracorporeal membrane oxygenation (VA ECMO) 4 L/min. Device flows of 1–5 L/min are shown in gray loops. Systemic vascular resistance is finally readjusted down to systemic mean arterial blood pressure (MAP) 65 mm Hg, resulting in further unloading as indicated in the green loop.

Figure 7.

Pressure–volume loop analysis of atrial septostomy in left ventricular (LV) systolic failure and veno-arterial extracorporeal membrane oxygenation (VA ECMO) 4 L/min. The LV is efficiently unloaded with atrial septal defect (ASD) sizes of 0.5, 1, and 1.5 cm². A nonejecting LV is created with the largest defect.

Figure 8.

Pressure–volume loop analysis of adjunct venting interventions in left ventricular (LV) systolic failure supported by VA ECMO 4 L/min. Left atrial (LA) and pulmonary artery (PUA) venting show similar hemodynamic effects on the LV pressure–volume loop. LV venting provides more efficient unloading. Flows are determined by actual pressure gradients and resistance of a 3/8″ tubing of 2-m length. Venting flows are 1.3 L/min (LA), 1.5 L/min (PUA) and 1.9 L/min (LV).

Figure 9.

Pressure–volume loop analysis of intra-aortic balloon pump (IABP), left ventricular (LV) venting, and Impella in LV systolic failure and VA ECMO 4 L/min. In this simulation, LV systolic function has further deteriorated (contractility 0.3 mm Hg/mL) to create a clinical state with a nonejecting LV, adjunct therapies all facilitate emptying of the LV.