Oct 19, 2026 · 28 min · 14 segments
Welcome to the Atomic Anesthesia podcast hosted by CRNA professor Dr. Rhea Temmermand and Co-Founder Sachi Lord. On this show, you'll hear clear, clinically grounded discussions designed for nurse…
Rhea TemmermandHost
Okay, cabbage can feel really overwhelming because there are a lot of moving parts.

You have the pump, you have the cannulas, you have cardioplegia, and then you have all these drips that you have set up.

Every decision that you have to make in the case comes down to one main central big idea, and that's the balance between myocardial oxygen supply and demand.

Seems really simple, but a lot of the decisions that we make during the case are going to really come back down to this one concept.

We're talking about coronary artery disease, so that's what it's all about, supply and demand.

Once you really, truly understand that balance, the rest of the case does start to make a little bit more sense.

So your coronary perfusion pressure is the aortic diastolic pressure minus the left ventricular end diastolic pressure or LVEDP.

That's the one equation that I really want you to memorize because it tells you the two ways that you can hurt your patient.

You can either let your diastolic pressure fall or you can let your left ventricular end diastolic pressure climb.

So about 80% of the left ventricular blood flow happens during diastole because during systole, the contracting muscle is actually squeezing its own vessels.

When the heart rate goes up, the diastole gets shorter, and then the coronaries, they lose that time to perfuse.

So the area that is at the most risk is the subendocardium, which is that very inner layer of the ventricle.

It sees the highest wall pressure because it's up against the blood, and especially in coronary artery disease, its autoregulation runs out once that distal pressure falls below about 70 millimeters of mercury.

The biggest determinant of myocardial oxygen demand are the heart rate, the contractility, and the wall stress.

And here is a key board point is that Heart rate shows up on both sides of this equation.

So tachycardia is going to increase the demand and it's going to decrease the supply at the exact same time.

That's why tachycardia is the enemy in a patient with coronary artery disease.

There's one more concept that you need to know is that the heart already extracts almost all of the oxygen that it can, even at rest.

So when the demand goes up, the only way to deliver more oxygen is with more flow.

Okay, cabbage can feel really overwhelming because there are a lot of moving parts.

You have the pump, you have the cannulas, you have cardioplegia, and then you have all these drips that you have set up.

Every decision that you have to make in the case comes down to one main central big idea, and that's the balance between myocardial oxygen supply and demand.

Seems really simple, but a lot of the decisions that we make during the case are going to really come back down to this one concept.

We're talking about coronary artery disease, so that's what it's all about, supply and demand.

Once you really, truly understand that balance, the rest of the case does start to make a little bit more sense.

So your coronary perfusion pressure is the aortic diastolic pressure minus the left ventricular end diastolic pressure or LVEDP.

That's the one equation that I really want you to memorize because it tells you the two ways that you can hurt your patient.

You can either let your diastolic pressure fall or you can let your left ventricular end diastolic pressure climb.

So about 80% of the left ventricular blood flow happens during diastole because during systole, the contracting muscle is actually squeezing its own vessels.

When the heart rate goes up, the diastole gets shorter, and then the coronaries, they lose that time to perfuse.

So the area that is at the most risk is the subendocardium, which is that very inner layer of the ventricle.

It sees the highest wall pressure because it's up against the blood, and especially in coronary artery disease, its autoregulation runs out once that distal pressure falls below about 70 millimeters of mercury.

The biggest determinant of myocardial oxygen demand are the heart rate, the contractility, and the wall stress.

And here is a key board point is that Heart rate shows up on both sides of this equation.

So tachycardia is going to increase the demand and it's going to decrease the supply at the exact same time.

That's why tachycardia is the enemy in a patient with coronary artery disease.

There's one more concept that you need to know is that the heart already extracts almost all of the oxygen that it can, even at rest.

So when the demand goes up, the only way to deliver more oxygen is with more flow.
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