What would you say if I were to ask you to describe how the heart gets its oxygenated blood? Would you describe the major coronary arteries and the areas of the heart they feed? Would you describe the aortic valve’s role in the matter? Can you picture yourself describing WHY the coronaries fill mostly during diastole?
Like the rest of the body, the heart requires a constant supply of freshly oxygenated blood. So, let’s first explore how the heart typically achieves this.
Coronary Arteries traverse the heart. These blood vessels transport blood from the two Coronary Ostia located at the base of the aortic root, just above the aortic valve, throughout the different regions of the heart. The Right Coronary Artery (RCA) originates from the Right Coronary Ostia. This feeds oxygen-rich blood to the right side of the heart and sometimes feeds the posterior area of the left ventricle.
The Left Main Artery (LMA) originates from the Left Coronary Ostia and branches into the Left Circumflex Artery (LCX) and the Left Anterior Descending Artery (LAD), feeding oxygen-rich blood to the anterior and lateral sections of the left heart. Each of these main arteries branches further and further until it implants into the myocardium to deliver blood. Much like a highway branching into side roads or a tree trunk branching out to leaves
Traditionally, we are taught that the coronary arteries fill during diastole. This is true, but there is also a filling component during ventricular systole. To understand this, let’s look at the aortic root.
Normal Diastolic Phase
When closed during diastole, we can see that the aortic valve resembles three cups side-by-side. Blood encounters these “cups” called the coronary sinus and is forced outward along the outer walls of each leaflet. Two of these cups have holes along the outer walls which are… You guessed it… the coronary Ostia. From here, blood takes the path of least resistance, either back up into the aorta or into the coronary arteries. In a normal heart, the path of least resistance is the coronary arteries until the heart enters systole.
Normal Systolic Phase
During systole, the Left Ventricle contracts and pushes the valve open, ejecting blood into the aorta. The path of least resistance during this phase is through the ascending aorta and the aortic arch. This blood flow is mostly laminar, meaning it travels smoothly in one direction, however whenever laminar flow meets a point of constriction (the aortic valve leaflets) a phenomenon called “Eddie Currents” occur. This causes blood to swirl around the tip of the aortic valve and enter the coronary Ostia. For this reason, we can say coronary filling occurs during both systole and diastole, with most filling occurring during diastole and minimal filling occurring during systole.
An equally important factor to the direction of blood flow that influences coronary flow during systole is the physical contraction and tightening of the myocardium itself. The ends of the coronary branches extend into the myocardium muscle. As the ventricle contracts, the muscle squeezes down on the arterioles within the myocardium, creating significantly more resistance in the systolic phase.
Flow and pressure are equally important when discussing the perfusion of distal tissues. Calculating the coronary perfusion pressure, or CPP, is one method for determining adequate coronary perfusion.
Coronary Perfusion Pressure is the pressure within the coronary arteries during the primary filling phase (Diastole). We can find pressure at any point along a closed circuit with the following general formula: (P1 - Pressure of Resistance =. Pressure at that given point)
Put into context, the coronary arteries fill primarily during diastole, so the diastolic blood pressure is used as the starting point (P1).
In this case, the Resistance is the pressure exerted on the myocardial muscle at the distal end of those coronary arteries. This is because the distal arterioles within the myocardium are subject to the pressure put on them by the myocardium. This pressure can be taken from the left ventricular end-diastolic pressure, or LVEDP. This measurement can be taken ultrasonically and by pressure catheter; however, the most common and closest surrogate is the PCWP or Pulmonary-Capillary Wedge Pressure.
Put together, the equation looks like this: (CPP Equation Graphic [DBP-LVEDP=CPP] put PCWP in parentheses under LVEDP)
Let's run some examples:
BP: 118/74 — PCWP: 9
CPP = 74-9 = 65
BP: 157/93 — PCWP: 20
CPP = 93-20 = 73
BP: 84/53 — PCWP: 4
CPP = 49
From these examples, we can quickly see that coronary perfusion pressure is heavily dependent on the starting diastolic pressure. A typical CPP is between 60 and 80mmHg.
In a compromised and failing heart, focusing on increasing the diastolic pressure might initially be intuitive. However, many interventions that achieve a rise in diastolic pressure also increase the pressure within the LV during diastole. Fluids, most mainline Pumps, and Prayers all have detrimental side effects that increase LVEDP. Okay, maybe I was reaching a bit with the prayers.
Therefore, the goal now shifts from increasing DBP to maintaining it and decreasing the LVEDP. This can be achieved with primarily inotropic agents such as dobutamine or milrinone. Additionally, it’s been reported that Glyceryl Trinitrate achieves a decrease in LVEDP without a significant reduction in DBP… What is Glyceryl Trinitrate? It’s our old friend, Nitroglycerin. This may be slightly counterintuitive because by increasing the force of contraction, you increase the force of the squeeze on the coronary arteries during systole, but remember, we are primarily focused on the diastolic phase. By assisting the ventricle in ejecting as much blood as possible, we decrease the ventricular filling pressure required during diastole, achieving our goal of a lower LVEDP.
Here is an excerpt from a blog written by Tyler Christifully on analgesia and nitroglycerin in the context of acute MI, and I echo his sentiments when deciding on analgesic and nitro support:
“…it appears there is more risk in dropping the diastolic pressure than in allowing it to elevate. With the paucity of literature supporting a mortality benefit for patients in ACS who receive nitroglycerin, I have utilized the following mental pathway of deciding on whether to use nitro AND analgesia or strictly analgesia for the sole purpose of pain reduction.
Some will ask: "Why even give nitroglycerin?" While a valid question, I believe there may be some benefit in reducing pre-load, smoother muscle relaxation, and thus ventricular workload. Nitroglycerin requires an enzyme reaction to release nitric oxide from the endothelium. This enzyme is now known to be catalyzed within the mitochondria, which, as you can imagine, is very happy and welcoming during ischemia (EHHHHHHH). This may be why nitrate mortality benefit is higher with agents that do not need an enzymatic reaction to release nitric oxide (nitroprusside).”
So there you have it: Coronary Perfusion Pressure in a nutshell. Maintaining an adequate CPP, especially in a myocardial-compromised state, can be a tricky thing to accomplish. As always, you can reach me at bcress@foamfrat.com with any questions, suggestions, or comments. -Brian Cress
References:
Heward SJ, Widrich J. Coronary Perfusion Pressure. [Updated 2023 Mar 16]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2024 Jan-. Available from: https://www.ncbi.nlm.nih.gov/books/NBK551531/
Zheng, Y., Ley, S. H., & Hu, F. B. (2020). Global aetiology and epidemiology of type 2 diabetes mellitus and its complications. Nature Reviews Endocrinology, 16(2), 69-83. DOI: 10.1161/ATVBAHA.119.313579
