Time to talk about coronary physiology. We spend a ton of time in the cath lab talking about, observing and fixing coronary anatomy, I don’t think we talk about physiology enough.

It is best to think of coronary vascular resistance as a set of three resistances in series. You will remember that resistance in series is additive so that total resistance in this case is R1 + R2 + R3.

 

The LAD or RCA that you see getting a stent is probably the least interesting part of the coronary vasculature (until it get’s clogged up with cheeseburgers and cigarettes). These large caliber arteries simply serve as a mostly passive conduit from the aortic root to the distal coronary bed (where all the action is). Therefore the resistance of the large arteries or “R1” is close to zero. When this resistance goes up, given a constant pressure gradient in the coronary artery bed, coronary blood flow decreases. (If this doesn’t make sense to you, refer to my prior post on Q = deltaP / R).

The coronaries regulate their own pressure in small arteriolar beds (just like in the systemic vasculature). These arterioles are about 100 to 200 micrometers in diameter. There are multiple endocrine, paracrine and neural mechanisms that allow the arterioles to constantly change resistance in order regional coronary blood flow stable over a wide rage of pressures. This is known as “autoregulation.” We will call this resistance, which is regionally variable and constantly changing, “R2“. (If the difference between resistance, flow and pressure doesn’t make sense to you, refer to my prior post on Q = deltaP / R, hint, hint...).

In the vasodilated state, autoregulation is shut off (R2 drops precipitously) and coronary blood flow increases linearly with coronary blood pressure. The difference between coronary blood flow in the autoregulated state and the vasodilated state is known as “coronary flow reserve.” This concept is critical to the understanding of myocardial ischemia and cardiac stress testing.

 

Finally, unlike many other organs, there is a significant and constantly changing interstitial pressure in the coronary vascular bed because all of it except for the large epicardial arteries lies within a mass of contracting muscle. The compressive resistance that the myocardium exerts on the coronary arteries is called “R3.”

Think about when you wake up after lying with your head on your arm for a long period of time. Your arm is numb. There is nothing wrong with your brachial artery or the arterioles regulating blood flow to the arm. Instead

you have caused arm ischemia by the compressive resistance of your head. Luckily the arm tolerates ischemia a lot better than the heart does.

R3 resistance is clinically important in scenarios such as acute hypertension or acute CHF which dramatically increase intracavitary pressures. Ever see a troponin elevation just because of severe hypertension or CHF when coronaries were normal? Well, now you know why.

Because of its proximity to the ventricular chamber, the subendocardium is most vulnerable to ischemia because of the greatest R3 load. The endocardium itself is always well perfused by the blood in the cavity itself). The epicardium is least vulnerable to ischemia because it is the furthest away from the compressive resistance of the ventricle. Ever hear the term “subendocardial ischemia” to mean mild ischemia? Now you know why. The heart compensates for this by allowing the subendocardial R2 arterioles to be almost maximally dilated in a resting state.

A quiz question: which part of the heart (from epicardium to endocardium) has the least about of coronary flow reserve and why?