There is nothing intuitive about retrograde flow.
You are pumping blood in one direction into the arterial system, which is the opposite direction that blood is supposed to flow. At first glance, this seems that it wouldn’t make sense. Doesn’t the aorta just become engorged? Does blood continue flowing backwards through the heart/lungs into the venous system? What happens to the tissues that are distal to the cannula ( Fig. 14.1 )?
Overall, retrograde flow involves understanding the overall directions of blood flow from the heart, the extracorporeal membrane oxygenation (ECMO) circuit, and throughout the vascular system. In this chapter, we will explore these as well as the potential effects that these can have on the body.
The directional flow of the vascular system
If the network of blood vessels in the body was just a static system, then many of the above questions would hold true. However, as we have alluded to, the arterial/capillary/venous network functions as a very dynamic system that functions to drive blood flow forward, facilitating the forward/antegrade flow of blood.
How is this accomplished? The muscular arteries/arterioles contract along with the heart to drive blood forward, and the valved system of the veins accommodates this forward flow to eliminate pooling of blood, which may cause back pressure.
The overall effect is a high-pressure system that exists in the arterial circulation and a lower pressure system that exists in the venous system. This pressure differential drives blood forward and is responsible for filling pressure to the right side of the heart.
This vascular phenomenon is essential to answering our initial questions on blood flow during VA ECMO. What prevents blood from just engorging the aorta or continuing to flow backwards? How does any blood make it to the venous system where it can get drained by the venous cannula? The answer lies in this antegrade flow of the vascular system ( Fig. 14.2 ).
Even if the heart is not beating at all (a phenomenon not uncommon in veno-arterial [VA] ECMO) there will still be antegrade flow from the arterial system through the capillary system into the venous system that allows for venous return. This antegrade flow of the vascular system can feasibly be driven by the ECMO flow, as the flow of blood from the ECMO circuit into the arterial circulation can serve to increase arterial pressure, increasing this pressure differential between arterial and venous systems.
The necessity of retrograde flow
Retrograde flow is a necessary consequence of peripherally inserted veno-arterial [VA] ECMO in adults. The intuitive manner of providing arterial blood flow would be antegrade, in order to pump blood in the direction of the heart and vascular system. However, there are both anatomic and functional limitations to doing so.
Accessing the heart/aorta directly requires surgical exposure. The carotid artery is used in children but is prohibitively risky in adults. The axillary artery can accommodate antegrade flow but is small enough that access requires grafting rather than percutaneous cannulation. This leaves us with the femoral artery, which is large enough to accommodate a cannula in most cases and can be accessed percutaneously, but requires flow to be directed retrograde through the aorta.
Let’s now consider the physiologic effects of this retrograde flow.
The Effect of Retrograde Flow on the Left Ventricle
One of the most important implications of this retrograde flow is the effect on the left ventricle. The effect can be summarized in one word: afterload.
Remember afterload is the pressure that the heart must push against. You will remember from our initial introduction to afterload that the left heart is fairly tolerant of afterload, especially compared to the right heart ( Fig. 14.3 ).
The primary reason for this tolerance is the function and anatomy of the left heart, which is more muscular and able to tolerate a higher pressure to work against. However, there is another phenomenon to consider, namely that as afterload increases, cardiac output drops. This in turn decreases mean arterial pressure (MAP), which decreases afterload.
In VA ECMO, this phenomenon is not necessarily the case, where the ECMO blood flow/afterload remains constant if the native cardiac output drops. This may mean that the effect of afterload due to retrograde flow will be more profound than would be normally observed if ECMO was not in place. The impact on the heart might be minimal or could lead to complete left ventricular dysfunction.
Left ventricular afterload sensitivity
Up until this point, we have generally described the afterload sensitivity of the left ventricle compared to the right ventricle, but there can also be a range of afterload sensitivity of the left ventricle depending on the clinical scenario. Let’s consider the afterload effect of retrograde flow due to VA ECMO in two cases of cardiogenic shock.
Patient 1: Pulmonary embolism with preserved left ventricular function
Patient 2: Left anterior descending lesion with ischemic left ventricle
If both patients were placed on VA ECMO for cardiogenic shock, the responsiveness of their left ventricles may be very different. Patient 1 would be more tolerant to retrograde flow, with minimal impact on left ventricular output, while Patient 2 will experience a significant drop-off in left ventricular function/output ( Fig. 14.4 ).
The degree of afterload sensitivity of the left ventricle will ultimately determine how it will be impacted by retrograde flow. In a case like Patient 1, there may be little to no effect of retrograde flow on the left ventricle, as the cardiogenic shock is only due to the failing right ventricle. In contrast, Patient 2 may experience a host of adverse effects to include worsening of the ischemia that caused the shock in the first place.
Let’s further review these adverse effects of retrograde flow.
Adverse Effects of Retrograde Flow on the Left Ventricle
Imagine the case of Patient 2, our patient with ischemic cardiomyopathy and cardiogenic shock placed on VA ECMO. We gradually begin increasing the blood flow and notice a consequent increase in the MAP. But as MAP increases, you look at the arterial line tracing and notice a gradual narrowing, with a smaller and smaller difference in the pulse pressure. Continuing to increase the blood flow, the arterial line becomes flat. What is happening here?
As we have established to this point, the afterload has increased to the point that it has overwhelmed the ability of the left ventricle to eject blood. It may be still contracting (barely) but these movements may be insufficient to overcome the afterload from the ECMO circuit and the aortic valve may not actually open.
Thrombosis
If the aortic valve is not opening or is barely opening, this increases the static blood that exists around the valve and in the left ventricle. Even if anticoagulation is administered, the risk of clot formation is increased, a dangerous possibility in the arterial circulation due to the risk of valvular damage, stroke, or embolization.
Increased Left Ventricular Distension
As pulse pressure decreases and less blood is ejected out of the left ventricle, the ventricle can continue filling and become dilated.
How Do You Get Left Ventricular Distension If You Are on Complete Ecmo Support?
If ECMO is draining all of the blood from the right ventricle and returning it to the arterial circulation, shouldn’t there be no blood that is returning to the left ventricle? Unfortunately, this is not the case, even if the ECMO circuit is completely bypassing the heart. This is because there are blood vessels that drain directly into the left side of the heart as part of a normal, anatomic shunt. The cardiac veins drain into the Thebesian veins, some of which drain into the left side of the heart. Additionally, the bronchial circulation arises from the aorta, giving rise to the bronchial veins which drain directly into the left atrium. This means that even if your ECMO flow is greater than the cardiac output, the left ventricle will start to distend.
Increased Wall Stress on the Myocardium
Now you have a distended heart and increased afterload, both of which increase the amount of tension on the muscular ventricular wall. This increased wall tension decreases blood supply by compressing on the blood vessels supplying the myocardial cells of the heart. This can lead to worsening ischemia and myocardial damage, which can further any ischemia that precipitated the initial injury.
Elevated Pulmonary Pressures and Pulmonary Edema
As left ventricular pressures increase, it leads to increasing pressure in the left atrium, which eventually translates to increasing pressure in the pulmonary venous circulation. The result is higher hydrostatic pressure and accumulation of edema into the lungs. Pulmonary edema increases pulmonary shunt and will result in worsening oxygenation of any blood that is coming from the right side of the heart through the lungs. The effects of this hypoxic blood can be profound as we will discuss later ( Fig. 14.5 ).
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