Heart Failure Question

Question

Describe the compensatory mechanisms that are recruited in early heart failure to help maintain cardiac output. Explain how these compensations may be maladaptive.

Answer 1

First of all make sure you understand what heart failure refers to - reduced cardiac output. Cardiac output is a product of heart rate and stroke volume (the amount of blood ejected by the ventricle).

One reason for the stroke volume to be lower is high blood pressure - this means the the left ventricle is constantly pumping against high aortic pressure meaning it has to work harder to create a pressure gradient that forces blood through the aortic valve and into the systemic circulation.

There are a few compensatory mechanisms to counteract reduced stroke volume. One is for the ventricular muscle to get bigger, which sounds good, but this ultimately reduces the compliance of the ventricle which reduces the amount of blood it can hold (i.e. lower end diastolic volume or EDV) when it's being filled from the atrium. Lower EDV will ultimately result in lower CO - there's less blood in the chamber to be pumped out.

What's tricky is that the body "interprets" the reduced cardiac output associated with heart failure as falling blood pressure. This can be confusing because the condition is caused by high blood pressure, but reduced CO means less blood flow in the system which causes the body's blood pressure monitors (baroreceptors) to think BP is falling due to something like a hemmorhage.

Because of this they trigger the normal compensatory mechanisms:

1) increasing total peripheral resistance and

2) retaining fluid in the blood to increase blood volume (meaning that the kidneys will take water back from the filtrate instead of allowing it to be excreted as urine).

Both of these are normal ways to restore homeostasis and raise blood pressure. Remember that increasing the amount of fluid in the tube will increase the pressure of the fluid pushing against the walls, and that narrowing the tube also means the fluid will push against it more (higher pressure).

Regarding the maladaptive consequences of fluid retention - at first this leads to increased EDV because the volume of venous return increases which seems to be good, but ultimately the additional fluid builds up in the interstitial tissue fluid leading to swelling (edema).

The increase in total peripheral resistance occurs through vasoconstriction mediated by the sympathetic nervous system (i.e. the sympathetic nervous system tells the vessels to constrict, reducing their radius and increasing blood pressure) and through hormonal action. Angiotensin II and vasopressin are released when blood pressure needs to be raised and both of these cause vessels to constrict. All of this together increases arterial blood pressure which compounds the problem we started with (pumping against increased pressure), forcing the heart which is already under too much strain, to work even harder.

Answer 2

First, remember what heart failure is. The heart pump doesn’t pump as well as it should. So the body is not receiving enough blood carrying oxygen to the organs. The body will think “hey, there’s not enough blood inside my arteries and veins” so it will increase blood pressure, hold onto sodium and water in the body, and increase the heart rate.

Remember:  cardiac output = heart rate x stroke volume

Heart failure is low stroke volume. The heart will compensate to try to maintain cardiac output by increasing heart rate and increasing stroke volume. 

The adrenal glands release more norepinephrine and signal the heart to beat faster.

The sympathetic nervous system releases catecholamines into blood system which causes blood vessels to constrict (become smaller in diameter) and increase heart rate

The body releases hormones (renin, angiotensin and aldosterone) that also cause the blood vessels to constrict AND causes the body to hold on to more water and sodium to add more fluid in the circulatory system.

How do we increase stroke volume? The heart will allow more blood to fill the ventricle before pumping it out and pump more forcefully. Over time, these mechanisms will weaken the heart muscle. 

Answer 3

Your heart's goal in compensating for heart failure is to maintain your cardiac output. Cardiac output is the amount of blood your heart is able to pump in 1 minute. The problem with heart failure is that the heart isn't pumping out enough blood each time it beats (low stroke volume). To maintain your cardiac output, your heart can try to:

1. Beat faster (increase your heart rate).
2. Pump more blood with each beat (increase your stroke volume).

A faster heart rate allows less time for the ventricle to fill with blood after each heartbeat. Also, a very fast heart rate can itself weaken the heart muscle over time

Your left ventricle compensates by allowing more blood to fill the ventricle before it pumps by expanding its size (dilating) to increase its volume. But, as the heart gets bigger, there is more and more tension on the walls of the heart in order to continue pumping out the blood. This can cause the cardiac muscle to fail. The result is low cardiac output or congestive heart failure