myocardial oxygen 2007

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Myocardial Oxygen Supply and Demand Jason Waechter

2007

Objectives:

• To understand the determinants of myocardial oxygen supply and demand. • To understand that ischemia occurs when supply < demand.

This lecture is usually delivered by Dr. John Cairns. Please also see his lecture handout. Both handouts (90% content overlap) will be examinable. This handout is organised into 2 sections. The first is myocardial supply. The second is myocardial demand.

MYOCARDIAL SUPPLY Myocardial oxygen supply is dependant on the following factors:

• coronary anatomy (covered elsewhere … self directed learning) o left main, left anterior descending (LAD), circumflex o right coronary, posterior descending o coronary dominance (right vs. left) o supply to: RV, LV anterior, LV lateral, LV posterior, LV inferior o supply to: AV node, SA node

• the coronary perfusion gradient • the heart rate (this factor is often overlooked) • oxygen carrying capacity of blood (in other words, the hemoglobin level)

Coronary perfusion gradient The coronary perfusion gradient is the pressure gradient with which the myocardium is perfused. In order to achieve forward blood flow, you need to set up a pressure gradient so that a high pressure chamber drains into a low pressure chamber. The difference between the high pressure chamber and the low pressure chamber is the pressure gradient. When we consider the perfusion gradient of the myocardium, the “chambers” are the aorta (high pressure) and the myocardium (low pressure). Therefore, the perfusion gradient will be: Aortic pressure – Myocardium pressure. Although we are perfusing the myocardium and not the LV chamber, we cannot easily measure the pressure inside the myocardium. However, the myocardium pressure is very close to the LV chamber pressure, so we can measure the LV chamber pressure with a catheter and use it as an estimate for the myocardial pressure.


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Consider the coronary perfusion pressure during systole: in order to have forward flow, you must have a high pressure chamber draining into a low pressure chamber. We have:

LV → Aorta → Epicardial coronary → Perforating coronary branches → Myocardium Can you see a problem with this diagram? Answer: remember that the myocardium and the LV pressures are essentially the same. Therefore, the starting “high” pressure is the same as the receiving “low” pressure. Oops. In this situation, there should be zero flow, and in fact this is true. In fact, the myocardium squeezes down so hard on the perforating branches that they get totally squashed down and occluded shut!

During systole, the coronary perfusion gradient is zero and there is no flow.

By logic we know that there must be myocardial flow and by further logic, we can state that myocardial perfusion must occur during diastole. So … what is the coronary perfusion gradient during diastole? Answer: the same pathway is taken by blood, so we still have:

LV → Aorta → Epicardial coronary → Perforating coronary branches → Myocardium

The difference this time is that when the LV is relaxed during diastole, it has a pressure of about 10. However, the aortic valve closes and the aorta maintains a pressure of about 80 (remember that a normal “textbook blood pressure” is 120/80). We can revise our pathway to show:

Aorta → Epicardial coronary → Perforating coronary branches → Myocardium If the aortic diastolic pressure is 80 and the LVDP (left ventricular diastolic pressure) is 10, then the gradient is 70, and we have flow! Miracle.

The myocardium is only perfused during diastole.

What could you do if the LVDP was really high, making the perfusion gradient small? Hint: read about nitrates in the pharmacology handout. Heart Rate It is easy to understand how heart rate influences myocardial oxygen demand: more heartbeats = more energy and oxygen required. However, we are talking about oxygen supply here. As an extension to the thoughts you were just having while reading the above section, you now understand that diastole is where the money is. The more


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diastolic time you have, the more perfusion you will get. When you have a nice slow heart rate, there are big gaps of time in between heartbeats and the diastolic time is very long. Low heart rates increase myocardial perfusion by increasing diastolic time. Oxygen carrying capacity of blood If you perfused the coronaries with water, the heart would be totally ischemic because the oxygen carrying capacity of water is very very low. Even if you could perfuse the heart with ridiculously high flow rates, you will still have an ischemic heart. Obviously, this is a stupid idea and I only bring it up to prove a point: you can have good flow rates of blood to the myocardium, but if the fluid doesn’t have much oxygen, you will still be in trouble. Now consider that your blood only has 50% of its normal hemoglobin: you would have to perfuse the myocardium with twice the flow rate to get a “normal” amount of oxygen delivered. If you have a stenosis in one of your coronary vessels, you might not be able to increase flow enough through that vessel to compensate for the low hemoglobin. A drop in your hemoglobin level might be significant enough to cause the oxygen supply to be less than the myocardial oxygen demand, and ischemia could result.

Anemia results in a decrease in oxygen supply to the myocardium.

MYOCARDIAL DEMAND Myocardial oxygen demand is dependant on the following factors:

• the heart rate • ventricular wall tension

Heart Rate Each ventricular contraction consumes oxygen. Therefore, high heart rates result in a higher oxygen consumption and therefore increased oxygen demand. Note the double whammy of tachycardia on myocardial ischemia: you get both increased oxygen demand and decreased oxygen supply. Tachycardia + myocardial ischemia is really bad. Can you think of drugs that would be good to slow down the heart rate? Hint: check out beta blockers and calcium channel blockers in the pharmacology handout.


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Ready for another double whammy? How does your cardiac output change in order to compensate for anemia? Answer: it increases, so that enough oxygen can be delivered to the body. How does it increase? Through an increase in both heart rate and contractility. Oops. What did we say about tachycardia and coronary artery disease? What will increasing contractility do to the myocardial oxygen consumption? You can see where this is going … maybe it’s a triple whammy.

Anemia and coronary artery disease just don’t mix well.

Ventricular Wall Tension The concept of wall tension in the ventricle is important but sometimes difficult to conceptualize. Basic principles that you must know:

• Wall tension determines myocardial work. • Increased work results in increased oxygen consumption.

Wall tension is defined by the Law of Laplace as: Tension = P x R h

• P = pressure • R = radius • h = wall thickness

According to the equation, increased pressure, increased radius and decreased wall thickness will all increase wall tension. To (maybe) help you to visualize wall tension, imagine the ventricle is a circle. Make a cut into the circle and straighten it out into a line: ↑ wall tension ↓ In order to eject blood, the circle (ventricle) would need to get smaller. This is the same as saying the straight line will get shorter. The more difficult it is for the line to shorten, the greater the wall tension will be. Let’s look at the 3 factors determining wall tension:


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Pressure: this is probably the easiest to understand. If there is high pressure inside the circle, it will be more difficult for the circle to contract. Therefore, more force will be required to develop within the wall of the circle. Increasing the contractility will increase ventricular pressure. Therefore, increased contractility will increase myocardial O2 demand. High blood pressure will also increase systolic ventricular pressure. Aortic stenosis will also increase the systolic ventricular pressure. Both these factors will increase the afterload which increases the pressure and thus increases wall tension. ↑Ventricular Pressure → ↑Wall tension → ↑Increased myocardial O2 demand

Wall Thickness: the total force generated by the contracting line will be distributed across the width of the line. The thinner the line is, the greater the force is per unit of thickness. The thinner line will experience more force and thus have higher tension. Hypertrophy therefore decreases wall tension. However, a thick walled ventricle will also have more muscle mass and therefore consume more oxygen, so this factor “neutralizes” wall thickness as a factor for myocardial oxygen consumption. Radius: perhaps the most elusive to understand. As a sphere increases in size, the volume increases by the radius cubed (R3), but the circumference increases linearly with the radius (R). Therefore, the volume grows much faster than the circumference (length of the straight line). The bigger the circle is, the more work will be required to shrink it. Increasing the preload increases the volume, and therefore increases wall tension.

Increased preload → ↑Wall tension → ↑Increased myocardial O2 demand Would it be wise to give a fluid bolus to someone with myocardial ischemia (assuming they already have a normal blood volume)? To Summarize Myocardial O2 Demand:

• Heart rate and ventricular wall tension are the main determinants of myocardial oxygen demand.

• Ventricular wall stress is influenced by all of the following: o increased pressure

via increased contractility via increased afterload (hypertension or aortic stenosis)

o increased radius via increased preload (ventricular filling)

o wall thickness – maybe a neutral factor decreased wall tension (lowers O2 consumption) increased myocardial mass (increases O2 consumption)

myocardial oxygen 2007

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