Veno-Arterial ECMO Physiology

Let’s now move our discussion to the physiology of veno-arterial extracorporeal membrane oxygenation (VA ECMO). As you will come to appreciate, VA ECMO is a very different type of support than veno-venous extracorporeal membrane oxygenation (VV ECMO). These next few chapters will equip you with a much better sense of some of the subtleties related to this mode.

Similar to VV ECMO, VA ECMO involves a drainage cannula in the venous system. The blood is run through the same blood pump, membrane oxygenator, and circuit. However, the return cannula is implanted into the arterial system. As opposed to VV ECMO, which was dependent on the native cardiac output, the blood flow for VA ECMO translates to some of the overall cardiac output ( Fig. 13.1 ).

There are limitations and rationale to the use of VA ECMO support. Let’s start to contextualize these by introducing the vicious cycle of cardiogenic shock.

Vicious cycle of cardiogenic shock

Cardiogenic shock can be one of the most devastating forms of shock, with mortality that can be as high as 85%. Worse yet, it is rapid, with a large proportion of patients dying within hours. You can see why we spent so much time talking about recognition, diagnosis, and identification of shock in the Physiology section. You will see that the reason for the rapid and devastating manifestation is the vicious cycle that is triggered.

The usual way of thinking is that decreased cardiac output leads to decreased perfusion, which leads to decompensation ( Fig. 13.2 )

While this is true, there is much more at play here, with multiple mechanisms of decompensation that re-inforce and compound each other. Let’s explore some of these effects.

Decreased Cardiac Output

Cardiac output is the driver of perfusion pressure, which is ultimately required for the forward flow of blood and delivery of oxygen. An insult to the cardiac function, whether ischemic due to myocardial ischemia, inflammatory as in myocarditis, obstructive as in pulmonary embolism or tamponade, or structural as in valvular/septal rupture, ultimately leads to a drop in cardiac output. As this output drops, the pressure head required to drive the forward flow of blood becomes progressively difficult to maintain, leading to a compensation in systemic vascular resistance (SVR) to maintain the forward flow of blood.

Decreased Coronary Perfusion

A drop in blood pressure affects the perfusion of all organs, but a decrease to the coronary blood vessels can be especially devastating because it serves to further worsen myocardial ischemia and further drop cardiac output.

Increased Left Ventricular End Diastolic Pressures (LVEDP)

Elevated SVR maintains the pressure needed to drive the forward flow of blood, much like putting your thumb over a hose may allow water to reach further if the flow of water decreases. However, this comes at a price – worsening afterload. As afterload increases, the left ventricular output starts to fall, which leads to less blood ejected with each heartbeat, and increasing the blood that remains in the ventricular cavity at the end of diastole ( Fig. 13.3 ).

This elevated pressure has several adverse effects, especially in a failing and potentially ischemic left ventricle:

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Higher pressures can compress cardiac muscle causing wall stress leading to worsening ischemia
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Higher left ventricular pressures can exert higher pressures on blood returning from the lungs which can lead to pulmonary edema
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Pulmonary edema can lead to further hypoxia worsening overall oxygen delivery to the heart tissue which can further drop the cardiac output

You can see how this contributes to a downward spiral, with one adverse effect compounding on another.

Acidosis

As oxygen delivery worsens in the setting of hypoxia and decreased cardiac output, the cells throughout the body have less available oxygen to carry out aerobic metabolism. This causes them to shift to anaerobic metabolism, with worsening acidosis ensuing. While this process temporarily allows for the generation of energy at the cellular level, acidosis can precipitate vasodilation, worsening both venous return and shock.

Acute Kidney Injury

Amongst the first organs affected by worsening shock and oxygen delivery are the kidneys. The response can be adaptive initially, causing fluid retention and improvement in preload, but injury can ensue, leading to further fluid retention and decreased clearance. This can worsen acidosis and lead to volume overload with a host of adverse effect to include worsening pulmonary edema.

Right Ventricular Distension

The other adverse effect of volume overload is right ventricular distension. Remember that preload only helps the right ventricle to a point, after which there is little more stretch that can be accommodated by the less muscular ventricle. Further increase in right ventricular filling pressures can cause a precipitous decline in the output of the failing right ventricle and can decrease left ventricular output as the distended right ventricle begins to compress on the left ventricle ( Fig. 13.4 ).