The Science of Compressions

One sure thing, throughout the changes in advanced cardiac life support (ACLS), is that chest compressions have remained relatively consistent in their AHA recommendation and level of evidence. Besides some clarification in 2015 on the maximum frequency of compressions per minute,¹ the science behind high-quality and continuous chest compressions has remained salient. 

Although chest compressions are one of the key links in the cardiac chain of survival, we seem to see a trend of pawning this skill off to the person on scene with the least clinical training. This is usually to allow the more experienced providers to perform skills such as IV/IO access, intubation, and pushing medications. However, the BLS skill of performing chest compressions and rapid defibrillation is without doubt the highest-priority intervention. So why do we see chest compressions pushed down the line of delegation?

I believe that as healthcare providers, we have a desire to perform skills that challenge us. Simply performing chest compressions doesn’t seem to be a challenging task. Let’s see if by breaking down the science of chest compressions, we can change our outlook. 

Coronary Perfusion Pressure

When teaching chest compressions I commonly ask students, “What is a normal blood pressure?” They usually respond with “120/80.” I then ask them to match each of those numbers to a cycle in the process of performing chest compressions (systole vs. diastole). They immediately put systole and compression together, which leaves diastole and recoil remaining. This is a key point when teaching the importance of coronary perfusion pressure. 

What exactly is coronary perfusion pressure, and why is it pertinent to this discussion? Just like every other tissue in the body, the heart requires its own blood supply. It receives this through the coronary arteries, mostly during diastole. Let’s trace the flow of blood through the heart and watch the path it takes to enter the coronary arteries.

As blood returns to the heart from the inferior and superior vena cava, it enters the right atrium. The right atrium serves as a conduit and dumps the blood through the tricuspid valve and into the right ventricle. Before the ventricle contracts, the atria contract and “top off” the right ventricle. This sequence is known as the atrial kick. The blood is then pushed from the right ventricle (RV) into the pulmonary arteries to offload carbon dioxide and onboard oxygen. The freshly oxygenated blood makes its way via the pulmonary veins through the left atrium, through the mitral valve, and into the left ventricle (LV). This process mimics the right side’s and will duplicate the much-needed atrial kick to augment cardiac output. 

Here is where coronary perfusion comes into play: As the blood is ejected from the left ventricle and through the semilunar aortic valve, it has to overcome the afterload of the systemic vascular resistance. In other words, to keep forward flow with a diastolic pressure of 80, we would have to generate a LV pressure large enough to overcome the 80 mmHg of pressure exerted on the outside walls of the aortic valve.

Once the pressure within the LV is high enough to open the aortic valve, the oxygenated blood from the LV will be pumped to the systemic vasculature. Soon after the initial ejection, the pressure will be once again higher on the systemic side of the aortic valve and cause it to close. 

The closure of the aortic valve is a very important moment in the cardiac sequence. When the aortic valve is open, it covers small holes in the aortic wall called the coronary ostia. These are the entrance into the coronary arteries. Once the aortic valve is closed, these ostia are now open to receive blood from the aorta. 

Now, when we refer to the coronary perfusion pressure, we are not just looking at the pressure available in the aorta during diastole—that would be too easy! There is a pressure the blood within the heart exerts on the walls of the coronary arteries.

Think of it like wearing a pair of jeans: The larger the person in the jeans, the harder it is for them to put their hands in their pockets! In our case the pockets are the coronary arteries, and the large person wearing the jeans is the pressure inside the chambers of the heart. We usually refer to this pressure as the end diastolic pressure, and it changes from RV to LV. 

What kinds of things increase the pressure the coronary arteries must overcome to maintain forward flow? Anything that increases pressure inside the heart’s chambers (fluid overload) or procedures that increase intrathoracic pressure, such as positive pressure ventilation (PPV). This is why the AHA recommends we don’t excessively ventilate patients, especially during cardiac arrest.¹

Research shows there is a direct correlation between coronary perfusion pressure and obtaining return of spontaneous circulation. A 1990 JAMA study showed that at a CPP less than 15 mmHg, patients had a zero chance of obtaining ROSC.³ So this number is pretty important!

Restoring the Gradient

Now let’s look at some of the changes that occur once the heart stops. A 20th-century American physician and physiologist named Arthur Guyton conducted some interesting studies on mean systemic filling pressure and venous return,² but one of the points I found fascinating in his canine experiment was the change in pressure gradients that occurs once the heart stops. When cardiac output drops, venous pressure increases.⁴ This will happen until the vessels come to a certain moment of equipoise. This systemic balance of the vasculature is known as the mean systemic filling pressure (MSFP). The loss of gradient and aortic pressure immediately drops the diastolic pressure and thus the coronary perfusion pressure. How do we restore that gradient?

When we begin chest compressions, we’re essentially shuttling blood from the venous side to the arterial side of the system. As we eject blood into the aorta, we eventually build up a pressure head from the peripheral resistance of systemic vascular beds. This will begin to rebuild the gradient of the arteries having a higher pressure than the veins.

The restoration of the gradient needs to build up enough pressure to create something I call the “aortic reserve.” This is the pressure the coronary arteries will be able to pull from during the recoil phase of chest compressions.

If this reserve is not maintained through continuous chest compressions, the coronary arteries will not have adequate perfusion. The act of recoil acts as a bellows to pull flow from the aortic reserve and into the coronary circulation. Knowing this, allowing full recoil becomes even more important.

Remember, the leaflets of the aortic valve cover the entrance to the coronary arteries when they’re open. This is important because if we deliver chest compressions with too high a frequency, we will essentially be spending more time with the aortic valve open and thus the entrance to the coronary arteries blocked. This is why in 2015 the AHA recommended chest compressions remain between 100 and 120 per minute.¹ This also explains one of the reasons why we can see signs of rate-induced ischemia in tachycardic patients.

The intervention of chest compressions is to hopefully build a very sturdy bridge to defibrillation. To provide enough coronary perfusion to successfully shock someone out of pulseless ventricular tachycardia or ventricular fibrillation, it is vital we completely understand that when we stop performing chest compressions, the vascular gradient begins to equalize. Restoration of the gradient seems to be the key to improving coronary perfusion pressure.

The science behind compressions helped me realize all the mistakes one can make without knowing exactly what they’re doing. With each push and release, we can drastically change the clinical course of our patient. Resuscitation needs to be performed with enough precision to know what to do and enough knowledge to recognize why we’re doing it. 

References

1. American Heart Association. 2015 Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care, www.ahajournals.org/toc/circ/132/18_suppl_2. 

2. Guyton AC, Abernathy B, Langston JB, Kaufmann BN, Fairchild HM. Relative importance of venous and arterial resistances in controlling venous return and cardiac output. Am J Physiol, 1959 May; 196(5): 1,008–14.

3. Paradis NA, Martin GB, Rivers EP, et al. Coronary perfusion pressure and the return of spontaneous circulation in human cardiopulmonary resuscitation. JAMA, 1990 Feb 23; 263(8): 1,106–13.

4. Levy MN. The cardiac and vascular factors that determine systemic blood flow. Circ Research, 1979; 44: 739–47.

Tyler Christifulli, CCP, FP-C, NRP, is a flight paramedic for Life Link III in St. Paul, Minn. He is the cocreator of FOAMfrat blog and podcast and an active educator for FlightBridgeED.