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Review
. 2023 Apr 18;147(16):1237-1250.
doi: 10.1161/CIRCULATIONAHA.122.062371. Epub 2023 Apr 17.

Unloading the Left Ventricle in Venoarterial ECMO: In Whom, When, and How?

Affiliations
Review

Unloading the Left Ventricle in Venoarterial ECMO: In Whom, When, and How?

Saad M Ezad et al. Circulation. .

Abstract

Venoarterial extracorporeal membrane oxygenation provides cardiorespiratory support to patients in cardiogenic shock. This comes at the cost of increased left ventricle (LV) afterload that can be partly ascribed to retrograde aortic flow, causing LV distension, and leads to complications including cardiac thrombi, arrhythmias, and pulmonary edema. LV unloading can be achieved by using an additional circulatory support device to mitigate the adverse effects of mechanical overload that may increase the likelihood of myocardial recovery. Observational data suggest that these strategies may improve outcomes, but in whom, when, and how LV unloading should be employed is unclear; all techniques require balancing presumed benefits against known risks of device-related complications. This review summarizes the current evidence related to LV unloading with venoarterial extracorporeal membrane oxygenation.

Keywords: extracorporeal membrane oxygenation; heart failure; heart-assist devices; hemodynamics; myocardial infarction; shock; shock, cardiogenic.

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Figures

Figure 1:
Figure 1:. A comparison of Central vs Peripheral cannulation of VA-ECMO
VA-ECMO maybe cannulated centrally via surgery or peripherally percutaneously. In central VA-ECMO the arterial outflow cannula is placed in the ascending aorta resulting in antegrade flow in the aorta in contrast to peripheral VA-ECMO where the outflow cannula is usually sited in the iliac artery resulting in retrograde flow. Different configurations of the venous inflow cannula can be used in both central and peripheral circuits for example femoral vein inflow cannula use in a central VA-ECMO circuit.
Figure 2:
Figure 2:. Hemodynamic effects of VA-ECMO
VA-ECMO reduces right atrial pressure, decongesting the liver and kidneys. Mean aortic pressure rises increasing afterload, if the left ventricle (LV) is unable to overcome the increased afterload, stroke volume falls resulting in loss of aortic pulsatility and stagnation of blood potentiating thrombus formation. Rising LV end diastolic pressure transmitted to the left atrium leads to pulmonary congestion. Backwards failure eventually increases pulmonary capillary wedge pressure (PCWP) and pulmonary artery diastolic pressure with loss of pulmonary artery pulsatility and worsening lung injury.
Figure 3:
Figure 3:. Pressure volume (PV) loop basics
(a) Normal PV loop, boundaries are created by the end systolic pressure volume relationship (ESPVR) and the non-linear end diastolic pressure volume relationship (EDPVR). Effective arterial elastance (Ea) reflects afterload and is the slope of the line between the end diastolic volume (LV EDV) and the ESPVR. (b) Stroke work (SW) is the work required to eject blood, Potential energy (PE) is energy generated during contraction but not converted to SW. Pressure volume area (PVA) correlates linearly with myocardial oxygen consumption (MVO2) and is the sum of the SW and PE. Ventricular unloading is defined by a reduction in the PVA. (c) Increased afterload whilst maintaining the same level of contractility and preload reduces stroke volume (SV) (d) SV can be increased by either increasing preload, however in a dilated ventricle this will cause a significant rise in end diastolic pressure due to the non-linear EDPVR or by increasing contractility but this also increases MVO2. (e) Cardiogenic shock results in loss of contractility and increases end diastolic pressure (EDP) and volume (EDV). (b) VA-ECMO raises systolic pressure, EDP and afterload thereby increasing pressure volume area (PVA), whilst further reducing SV (f) IABP reduces afterload, increasing SV without significantly reducing EDP, EDV or PVA. In contrast pLVAD actively unloads the ventricle reducing afterload, EDV and EDP thereby significantly reducing PVA. Inotropes increase contractility improving SV; however, this increases PVA.
Figure 4:
Figure 4:. Left ventricular unloading criteria and methods
LVOT VTi: Left ventricular outflow tract velocity time integral, PCWP: Pulmonary capillary wedge pressure.
Figure 5:
Figure 5:. Left ventricular unloading Algorithm
CXR: Chest radiograph, LVOT VTi: Left ventricular outflow tract velocity time integral, PCWP: Pulmonary capillary wedge pressure, SVO2: Mixed venous oxygen saturation

References

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