**1.3 Hemodynamic aspects of VA-ECMO support**

Among all the available AMCS devices, VA-ECMO has the highest capability to reduce myocardial pressure-volume area (sum of myocardial potential energy and

**Figure 1.**

*Various cannulation sites for venoarterial extracorporeal membrane oxygenator.*

myocardial stroke work) in patients with CS reducing left ventricular end-diastolic volume (LVEDV) and left ventricular end-diastolic pressure (LVEDP) while providing complete hemodynamic and respiratory support. Myocardial pressure-volume area is further reduced by the weaning of inotropes and vasopressors. All these prevent the vicious cycle of maladaptive neurohormonal and vascular mechanisms. Also, native RV function is not critical to provide systemic perfusion due to its reduced reliance on transpulmonary flow.

VA-ECMO improves systemic perfusion by increasing the MAP, reducing CVP, and increasing the systemic arteriovenous pressure gradient. This maintains the organ function and reduces the generation and accumulation of toxic metabolites. This may be particularly relevant to improving blood flow in organs with portal circulation, such as the liver and kidney. Fluid removal and reducing the venous congestion can be further enhanced by splicing a continuous veno-venous hemodialysis machine (CVVHD) into the VA-ECMO circuit [15–19].

### **1.4 LV distension**

The Achilles heel of VA-ECMO is LV distension. The LV distension occurs when LV is unable to eject the blood returning to it. Sources for blood return to the LV are aortic regurgitation, Thebesian and bronchial veins draining in the left atrium, and systemic venous return that is not captured by the ECMO venous cannula. Uncaptured systemic venous return is the most significant source of LV blood flow, and it is directly proportional to RV function. Due to the lack of reservoir and longer and thinner peripheral venous cannulas with higher impedance, a significant amount of blood escapes drainage. To eject the blood, LV must have enough contractile function to overcome afterload due to retrograde flow of blood toward aortic valve at a higher pressure. If LV is severely dysfunctional, it may be unable to generate enough pressure and aortic valve may remain closed throughout cardiac cycle. This leads to increased LV wall stress, and myocardial oxygen demands as well as the stasis of blood in the aortic root with a potential risk of thrombus formation. Also, elevated LVEDP may result in pulmonary edema, pulmonary hemorrhage, systemic, cerebral, and myocardial hypoxia. The risk of LV and aortic thrombus formation is higher with peripheral cannulation due to a larger column of aortic root blood stasis and carries the risk of embolization down the coronary arteries, head vessels, or body. Therefore, it is important to vent the LV during VA-ECMO in patients with noncompliant LV and a competent mitral valve [20].

*Overview of Venoarterial Extracorporeal Membrane Oxygenation (VA-ECMO) Support… DOI: http://dx.doi.org/10.5772/intechopen.105838*

### **1.5 Diagnosis**

In a patient on VA-ECMO, a dilated and hypocontractile LV with or without severe MR, stagnation of blood on echocardiography, pulmonary artery diastolic pressure >25 mmHg, and an elevated PCWP on Swan-Ganz catheter monitoring are sufficient to diagnose LV distension [19].
