Impact of Venoarterial Extracorporeal Membrane Oxygenation on Hemodynamics and Cardiac Mechanics: Insights From Pressure-Volume Loop Analysis

Abstract

Venoarterial extracorporeal membrane oxygenation (VA-ECMO) serves as a critical mechanical circulatory support modality, sustaining systemic circulation in cases of severe cardiac failure or cardiac arrest. While VA-ECMO improves hemodynamics, it markedly increases left ventricular (LV) afterload, contributing to pulmonary congestion and thrombus formation. This review highlights the hemodynamic and mechanical effects of VA-ECMO, employing the pressure-volume (PV) loop and the generalized circulatory equilibrium model. The PV loop framework clarifies how VA-ECMO elevates afterload, potentially reducing stroke volume and the cardiac output curve when LV contractility is severely impaired. Similarly, the generalized circulatory equilibrium concept illustrates how VA-ECMO shifts the circulatory equilibrium point in both ventricles. These models establish a mechanistic foundation for strategies combining VA-ECMO with other devices, such as an intra-aortic balloon pump, Impella, or central VA-ECMO equipped with LV venting. Based on these frameworks, appropriate patient selection, effective device management, and integration with LV unloading devices may enhance survival in patients requiring VA-ECMO.

Keywords: Heart failure; Hemodynamics; In silico modeling; Physiology; Venoarterial extracorporeal membrane oxygenation.

Figure 1. Schematic diagrams of VA-ECMO.

(A) Peripheral VA-ECMO: Blood is drained from the IVC or RA, and gas-exchanged blood is returned to the aorta. (B) Central VA-ECMO: The pump drains blood from the RA and returns it to the ascending aorta in open-heart surgery. VA-ECMO = venoarterial extracorporeal membrane oxygenation; IVC = inferior vena cava; RA = right atrium.

Figure 2. Pulmonary edema induced by VA-ECMO: ECMO lung.

(A) VA-ECMO leads to an increased LVEDP and (B) resulting in ECMO lung. Chest X-ray image was obtained at the author’s institution. LVEDP = left ventricular end-diastolic pressure; ECMO = extracorporeal membrane oxygenation; VA-ECMO = venoarterial extracorporeal membrane oxygenation.

Figure 3. The concept of the PV loop.

The trajectory of the end-systolic points of the PV loop under varying preloads is referred to as ESPVR. The slope of the ESPVR, denoted as E_es, represents ventricular contractility independent of the preload. The trajectory of the end-diastolic points is termed EDPVR, which indicates ventricular compliance. The slope of the line connecting the end-diastolic volume point on the volume axis to the end-systolic pressure-volume point located at the upper left of the PV loop is called the E_a, representing ventricular afterload. By elucidating the relationships between E_es, E_a, and SV, it becomes clear that SV is determined by the balance between ventricular contractility and afterload, in addition to preload and diastolic function. PV = pressure-volume; ESPVR = end-systolic pressure-volume relationship; EDPVR = end-diastolic pressure-volume relationship; E_a = effective arterial elastance; V₀ = the volume (x-axis) intercept of ESPVR; EDV = end-diastolic volume; EDP = end-diastolic pressure; ESV = end-systolic volume; ESP = end-systolic pressure; SV = stroke volume; LVP = left ventricular pressure; LVV = left ventricular volume; EF = ejection fraction.

Figure 4. PVA.

The area enclosed by the ESPVR, EDPVR, and systolic pressure-volume trajectory (the systolic phase of the PV loop) is defined as the PVA. PVA is the sum of 2 energy components: SW, which represents the external work performed by ventricular contraction as the area within the PV loop, and PE, which denotes the position energy. PVA is proportional to ventricular oxygen consumption. PV = pressure-volume; ESPVR = end-systolic pressure-volume relationship; V₀ = the volume (x-axis) intercept of ESPVR; EDPVR = end-diastolic pressure-volume relationship; PVA = pressure-volume area; SW = stroke work; PE = potential energy; LVP = left ventricular pressure; LVV = left ventricular volume.

Figure 5. The element of CO curve.

A reciprocal exponential function was observed when the SV was plotted against the LVEDP under varying preload conditions. By multiplying the SV by HR and plotting this product on the vertical axis, the resulting plot represents the CO curve. CO = cardiac output; SV = stroke volume; V₀ = the volume (x-axis) intercept of ESPVR; EDPVR = end-diastolic pressure–volume relationship; LVEDP = left ventricular end-diastolic pressure; EDP = end-diastolic pressure; HR = heart rate; E_es = end-systolic elastance; E_a = effective arterial elastance; SV = stroke volume.

Figure 6. The concept of circulatory equilibrium.

(A) Guyton’s circulatory equilibrium. The intersection of the CO and VR curves indicates the operating point where CO and VR are balanced. This concept allows the characterization of CO and venous pressure under various pathological conditions. The circulatory equilibrium point determines the preload. For example, in heart failure, a reduction in the slope of the CO curve (dashed line) causes the operating point to shift downward to the right, resulting in an increased preload. (B) Generalized circulatory equilibrium. The generalized circulatory equilibrium divides the circulation into four components: the right ventricle, pulmonary circulation, left ventricle, and systemic circulation. It models each component individually and then integrates them. By separately determining the CO curve equations for the left and right heart ventricles and combining them into the “integrated CO curve”, the operating point can be derived from the intersection between the integrated CO curve and the VR surface. S_R, H_R, F_R, S_L, H_L, and F_L are constant parameters of the right and left ventricles. W is a parameter that defines the maximum circulatory VR volume against a given SBV. G_p and G_s are constant parameters of VR surface. RAP = right atrial pressure; LAP = left atrial pressure; CO = cardiac output; VR = venous return; LVP = left ventricular pressure; LVV = left ventricular volume; SBV = stressed blood volume.

Figure 7. VA-ECMO impact on PV loop.

(A) In patients with reduced LV function, the increased total blood flow from VA-ECMO (F_ECMO) adds to the pressure, effectively shifting the E_a line upward to the right. Additionally, LVEDP and volume are elevated. (B) VA-ECMO shifts the CO curve of native LV downward. (C) Consequently, the PV loop shifts upward to the right, increasing the PVA. PV = pressure-volume loop; VA-ECMO = venoarterial extracorporeal membrane oxygenation; LVP = left ventricular pressure; LVV = left ventricular volume; CO = cardiac output; F_ECMO = flow of VA-ECMO; LVEDP = left ventricular end-diastolic pressure; PVA = pressure-volume area.

Figure 8. VA-ECMO impact on generalized circulatory equilibrium.

VA-ECMO shifts the integrated CO curve downward as afterload increases. Furthermore, the preload reduction by VA-ECMO shifts the VR surface downward. S_R, H_R, F_R, S_L, H_L, and F_L are constant parameters of the right and left ventricles. W is a parameter that defines the maximum circulatory VR volume against a given SBV. G_p and G_s are constant parameters of VR surface. CO = cardiac output; RAP = right atrial pressure; LAP = left atrial pressure; VR = venous return; ECMO = extracorporeal membrane oxygenation; CO_NTV = CO of the native heart; VA-ECMO = venoarterial extracorporeal membrane oxygenation; F_ECMO = flow of VA-ECMO; SBV = stressed blood volume.

Figure 9. Validation study of the concept of generalized circulatory equilibrium under VA-ECMO.

Relationship between predicted (solid line) and measured CO_NTV + F_ECMO, right atrial pressure (P_RA in this figure), and left atrial pressure (P_LA in this figure) in 6 dogs. The scatter plot (upper panels) shows that the predicted total systemic flow, P_RA, and P_LA matched the measured values well. The Bland-Altman plots show acceptable agreement (bottom panels). Upper panels: Solid lines indicate regression lines. Dashed lines indicate identity lines. Bottom panels: Solid lines indicate the line of bias. Dashed lines indicate the limits of agreement (mean ± 2 standard deviations). RAP and LAP are represented as P_RA and P_LA, respectively, following the original work. Figures are referenced from the author’s previous work. CO = cardiac output; CO_NTV = CO of the native heart; VA-ECMO = venoarterial extracorporeal membrane oxygenation; F_ECMO = flow of VA-ECMO; r² = coefficient of determination; SEE = standard error of estimation; LOA = limits of agreement; RAP = right atrial pressure; LAP = left atrial pressure.

Figure 10. Simulation study of VA-ECMO with several ventricular functions.

Upper panels demonstrate the impact of EF_L on VA-ECMO induced P_LA elevation in normal right heart condition (EF_R=0.5). Lower panels demonstrate the impact of EF_L on VA-ECMO induced P_LA elevation in right heart failure condition (EF_R=0.3). Figures are referenced from the author’s previous work. LAP, F_ECMO, and EF are represented as P_LA, CO_ECM and EF_L respectively, following the original work. LVEF = left ventricular ejection fraction; VA-ECMO = venoatrial extracorporeal membrane oxygenation; LAP = left atrial pressure; EF_L = left ventricular ejection fraction; CO_ECM = flow of VA-ECMO; P_LA = left atrial pressure; EF_R = effective right ventricular ejection fraction.

Figure 11. PV loop simulation.

(A) PV loop in VA-ECMO and IABP. The combination of VA-ECMO and IABP slightly reduced the LVESP and the PVA compared with VA-ECMO alone. (B) PV loop in VA-ECMO and Impella. The combination of VA-ECMO and Impella, so called ECPELLA, exerts a significant LV unloading effect. Impella unloads VA-ECMO increased PVA (left panel). By adjusting VA-ECMO and Impella flow rates, ECPELLA can reduce LVP and PVA to near zero (right panel). PV = pressure-volume; LVP = left ventricular pressure; LVV = left ventricular volume; VA-ECMO = venoarterial extracorporeal membrane oxygenation; IABP = intra-aortic balloon pump; LVESP = left ventricular end-systolic pressure; PVA = pressure-volume area.