Updated: 3 days ago
Thanks for joining me in part 2 of the Mechanical Circulatory Support Series! Today we're discussing flow in MCS devices, so stick with me; it’s a bit of a rollercoaster. As I mentioned in the first blog, one of my primary interests in writing these blogs is to discuss the unique considerations of MCS in transport. So, I've added some bullet points specific to the transport environment. Look out for these "CITs" or "Considerations-in-Transport."
Imagine yourself on a simple, short rollercoaster. You're nearly at the top of the first hill. The "clickity clank" noise soon begins to fade, and you notice you're picking up momentum. Screams fill the air as you rush downward toward the ground, picking up speed; in a matter of seconds, you reach terminal velocity and stop accelerating. The bottom of the first hill is quickly approaching, and as you begin to level out and ascend back skyward, your velocity begins to slowly move over the second peak and begin a gentle descent with a few small hills, which you roll gently over. You arrive back to the station looking like Tyler and Brian during their last trip to Disney World and can't help but think of how similar this rollercoaster is to the way flow works in your MCS patients.
What is Flow?
In the context of Mechanical Circulatory Support (MCS): Flow is the general term used to describe the movement of a fluid through a conduit. More specifically, we are talking about blood moving through the circulatory system. The principles we discuss today can be applied to any MCS device that generates or assists in the forward blood flow through the body. This includes ECMO, VADs, Percutaneous VADs (i.e., Impella), and Total Artificial Hearts.
How is flow generated?
Rollercoasters have to spend kinetic energy to get the train to the top of the first hill. Just as the rollercoaster must spend kinetic energy by means of a chain lift to build potential energy within the cars, MCS devices must spend kinetic energy in order to build potential energy within the blood. In modern MCS devices, this is almost always done by way of a centrifugal pump.
Kinetic energy is spent to spin an impeller at a controllable speed; this rotational energy is transferred to the blood, forcing it outward along the vanes to the point where it meets resistance, i.e., the wall of the pump head. This resistance between the outward-moving blood and the wall of the pump head pushing inward creates potential energy, also known as PRESSURE. Because the size of the pump head does not change, we can impart more pressure by increasing the pump speed.
CIT: External centrifugal pumps (such as in ECMO) have an area of negative pressure at the center of the impeller. This is also where the tubing that delivers blood into the pump connects. Be especially careful not to kink the tubing on the negative pressure side while moving the patient, as this can cause "cavitation" and may lead to the formation of gaseous emboli.
Transition from potential energy to Kinetic Energy:
Back to our rollercoaster: As we crest the top of the first hill and begin moving downward, we understand that the potential energy built by the height of the first hill has now transitioned into kinetic energy and forward movement. In other words, we've given the rollercoaster an outlet to spend that potential energy.
Within the MCS circuit, as blood works its way to the outside wall of the pump head, it eventually finds the pump outlet, transitioning from potential energy (building pressure) to kinetic energy (forward flow).
CIT: The area directly at the pump outlet will have the highest pressure in the system. It's important to ensure any external connections in this area are completely secure and tight. With internal pumps such as permanent VADs and impellas, the area directly adjacent to the pump outflow is especially vulnerable to aneurysms or dissections. This differential diagnosis should be considered in acute pain.
Resistance Part 1:
So, you may see where I'm going with this now. And you might think I will compare the second hill to our patient's vascular resistance. You are correct, but I want to discuss another form of resistance first. Something that is often overlooked and is more difficult to change than "the size of our second hill." Can you guess what it is?
I mentioned in the opening paragraph that we had reached terminal velocity and stopped accelerating before reaching the bottom of the first hill. This is, of course, due to Frictional Forces. As frictional forces increase, velocity decreases.
Blood Viscosity is a significant determinant of frictional force within the bloodstream. It must be accounted for when determining flow. Consider that blood viscosity acts upon the walls of the vessel in a phenomenon known as sheer stress. As blood viscosity increases, sheer stress also increases, decreasing forward flow. Of course, the opposite is true as well.
Resistance Part 2:
As we alluded to earlier, vascular resistance is our biggest resistor to flow. This is easily represented in our example by the second hill. It's intuitive to understand that the bigger the second hill is, the more the rollercoaster will slow down. If the second hill is bigger than the first hill, the rollercoaster won't make it up without some assistance (An analogy for ECPELLA, anyone??). Just as with our rollercoaster's hills, as vascular resistance increases, flow decreases.
The combination of the frictional forces and vascular resistance is known as AFTERLOAD. In centrifugal pumps, afterload is important to monitor because it directly affects the flow rate.
At a constant pump speed (RPM), a centrifugal pump will generate a constant pressure. The resulting flow rate is determined by the pressure pushing back against that pump, i.e. afterload. If the afterload pressure is higher, but the RPM remains the same, the overall flow rate will decrease. If there were to be a drop in afterload without a change in RPM, the overall flow rate would increase.
CIT: This concept is important to understand because any changes you make to the patient's hemodynamics will affect the flow rate of the MCS device, and any changes made to the MCS device will subsequently affect your hemodynamics. If you are transporting with an MCS specialist such as a perfusionist or ECMO specialist then Open, concise communication must be established between the transport team and the MCS specialist when making changes to patient hemodynamics.
Putting it all together:
If I had told you at the beginning of this blog that we would be learning about Poiseuille's Law, I don’t even think I would have read it. However, we can see that Poiseuille's Law demonstrates the relationship between flow, pressure, radius, length, and viscosity.
The only thing we didn't touch on is length. We obviously can't control the length of the blood vessels within our patient nor the length of the outflow tracks in VADs, artificial hearts or Impellas. But we do have an opportunity to find the optimal length of our ECMO circuits. ECMO circuits should be kept at the minimum necessary length to safely operate the pump in order to reduce resistance within the circuit.
Wrapping Things Up
Flow is the movement of blood through the body.
Flow is generated by converting potential to kinetic energy via a centrifugal pump.
AFTERLOAD combines frictional forces and vascular resistance, pushing back against the forward-moving flow.
Flow is affected by the speed of the centrifugal pump, afterload, and the length of the conduit in which blood is transported through.
Thank you for making it to the end of the blog and I hope you were able to take something away from this reading. As always, I welcome any feedback, questions, comments, or suggestions for future blog posts. You can reach me at firstname.lastname@example.org
Brian Cress CCP, LP, FP-C, NRP
Brogan, T. V., Lequier, L., Lorusso, R., MacLaren, G.; Peek, G. J. (2022). Extracorporeal life support: The elso red book. ELSO.
Tagusari O, Yamazaki K, Litwak P, Antaki JF, Watach M, Gordon LM, Kono K, Mori T, Koyanagi H, Griffith BP, Kormos RL. Effect of pressure-flow relationship of centrifugal pump on in vivo hemodynamics: a consideration for design. Artif Organs. 1998 May;22(5):399-404. doi: 10.1046/j.1525-1594.1998.06157.x. PMID: 9609348.
Wrisinger WC, Thompson SL. Basics of Extracorporeal Membrane Oxygenation. Surg Clin North Am. 2022 Feb;102(1):23-35. doi: 10.1016/j.suc.2021.09.001. PMID: 34800387; PMCID: PMC8598290.