Blood Flow Dynamics





We are now going to continue our journey by exploring the physiology of extracorporeal membrane oxygenation (ECMO) support. You may find the chapters to follow to be the cornerstone of the understanding of ECMO. It is a common adage to hear the following:


“ECMO is easy to initiate, the challenge is in the management.”


I fully agree with this sentiment, but the challenge in management is rarely what we think. The stalwarts of good critical care support remain consistent – medications, antibiotics, nutrition, and rehabilitation. However, the true challenge in managing patients on ECMO involves developing an appreciation, understanding, and familiarity with the physiology of extracorporeal support – the following chapters will be aimed to equip you with the tools needed to do just that.


Let’s start by developing our understanding of the limits of blood flow and the ECMO circuit.


Why is blood flow so essential in ECMO support?


You will recall that there are two primary parameters that can be manipulated in ECMO support: sweep gas flow , which contributes to ventilation/CO 2 removal, and blood flow , which primarily contributes to oxygenation.


Why is this the case? Shouldn’t support just be support? Shouldn’t a higher oxygenated gas flow just increase oxygenation?


To answer this, we will have to return to our first chapter on the physiology of oxygen delivery.


Remember when it really comes to oxygen delivery , the ultimate determinant is hemoglobin, because hemoglobin is just so much better at delivering oxygen due to its ability to bind oxygen with increasing affinity in the heart lungs as well as the ability to change forms to and dump ­oxygen in the periphery ( Fig. 10.1 ).




FIG. 10.1


Hemoglobin as a means of delivering oxygen.



We covered in great detail what this means for the body in terms of delivering oxygen – that the better we can leverage the efficiency of hemoglobin, through optimizing saturation/hemoglobin/cardiac output, the better we can deliver oxygen.


Now let’s apply this concept in the context of the ECMO circuit. You will recall for delivery of oxygen in the body we have the following equation:


<SPAN role=presentation tabIndex=0 id=MathJax-Element-1-Frame class=MathJax style="POSITION: relative" data-mathml='DO2=1.34×SaO2×Hb×CO+PaO2×0.003′>DO2=1.34×SaO2×Hb×CO+PaO2×0.003DO2=1.34×SaO2×Hb×CO+PaO2×0.003
DO2=1.34×SaO2×Hb×CO+PaO2×0.003


which can be simplified to the following relationship:


<SPAN role=presentation tabIndex=0 id=MathJax-Element-2-Frame class=MathJax style="POSITION: relative" data-mathml='DO2→SaO2×Hb×CO’>DO2SaO2×Hb×CODO2→SaO2×Hb×CO
DO2→SaO2×Hb×CO


For the delivery of oxygen by the ECMO circuit, the determinants become oxygen saturation, hemoglobin, and instead of cardiac output, the blood flow through the ECMO circuit ( Fig. 10.2 ).




FIG. 10.2


Oxygen delivery capability of the oxygenator


What about FiO 2 ?


Doesn’t increasing FiO 2 improve the delivery of oxygen to the ECMO circuit much the same way that increasing FiO 2 administered to the lungs can increase oxygen delivery? Yes and no. The FiO 2 dial on the blender alters the amount of oxygen running through the oxygenator and drives the gradient at the membrane level, but ultimately, it does not matter how much oxygen diffuses across (otherwise known as your PaO 2 ); what ultimately matters to the delivery of oxygen is the saturation of hemoglobin by that oxygen.


At a certain point, it does not matter how high the PaO 2 of the blood coming out of the oxygenator is, there is a maximum saturation after which hemoglobin does not get much more saturated and the hemoglobin saturation curve flattens out ( Fig. 10.3 ).




FIG. 10.3


Oxygen hemoglobin dissociation curve


The oxygenator is very good at saturating blood, and there is rarely a problem with maintaining adequate saturation of blood coming out of the oxygenator. Rather at this point, we can start to appreciate that the determinants of oxygen delivery of the oxygenator are saturation of the blood coming out of the oxygenator (largely expected to be 100%), hemoglobin concentration, and, ultimately, the blood flow coming out of the oxygenator to the extent that we are able to provide this flow.


So more blood flow, better oxygen delivery – sounds easy enough. If you need more oxygen delivery, you provide more blood flow, right? As we will see, the ability to provide flow has been limited both by the pump/circuit and by the body.


What are the determinants of blood flow on ECMO support?


Said another way, what limits our ECMO blood flow? We will discuss how we can titrate ECMO blood flow in Chapter 17 , but for now, let’s focus only on the limits to blood flow. As we will discover, there are a host of limits to blood flow ranging from patient factors to factors associated with the circuit.


Limits of the membrane oxygenator


Seems like with all of this technology and capability, the membrane oxygenator will be much better at oxygenation than our lungs, right? Actually, the oxygenator doesn’t even come close to the potential capability of the lungs. Ultimately, it all comes down to the blood/gas interface. With the lungs, that interface comes in the form of the blood/alveolar interface. That means that the surface area of the 600 million alveoli in the lungs comes out to around 150 m 2 , roughly the size of a tennis court. Compare this to the 4 m 2 surface area of the plastic fibers of most oxygenators, barely half of one of the service boxes. Additionally this interface is approximately 10–20 times thicker for the oxygenator than for the lungs, further hindering the diffusion of oxygen ( Fig. 10.4 ).




FIG. 10.4


Oxygenation capability of native lungs versus membrane oxygenator


Additionally, blood does not flow smoothly through the oxygenator, rather, it experiences a decrease in laminar flow both on the macro and micro levels as illustrated in Fig. 10.5 .




FIG. 10.5


Disruptions to laminar flow in membrane oxygenator


As seen on the left, there will be areas throughout the oxygenator, such as right angles, corners, and any place where the flow of blood changes direction, where the flow of blood will slow down, giving rise to turbulence and ultimately decreasing the efficiency of the blood flow. The right illustrates how this can happen at the level of the plastic fibers, with blood changing direction to flow past the individual fibers.


Effect of membrane limits: The rated flow of the membrane


With these inefficiencies and limits, we should be able to imagine how these add up to a maximum amount of flow that the membrane can tolerate, past which there would be no further increase in the content of blood (CaO 2 ) provided by the oxygenator (where CaO 2 = 1.34 × SaO 2 × Hb + PaO 2 × 0.003) ( Fig. 10.6 ).




FIG. 10.6


Higher blood flow increases the proportion of shunted blood across the oxygenator


Any further increase in blood flow past this maximum flow would just represent shunt, much in the same way that shunted blood in the lungs represents blood that shunts across without participating in gas exchange.


Let’s now try to conceptualize what this looks like when it comes to how blood flows through an oxygenator. Imagine that you have an oxygenator with blood flowing through it with no limit on the amount of blood that can flow. If we were to plot the relationship between this blood flow and the oxygen content of the blood leaving the oxygenator, we would conceptualize something like what is shown in Fig. 10.7 .


Aug 5, 2023 | Posted by in CRITICAL CARE | Comments Off on Blood Flow Dynamics

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