Back To CoursePathophysiology Textbook
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If you are obsessed with being healthy, something not necessarily all that bad, then you probably love to hang out at the gym. You have certainly seen the guys standing in front of the mirror fixated at the sight of their own biceps. Many of those guys are truly huge. In fact, their muscles are so large and thick (technically called hypertrophied) that they actually restrict the man's movement. As a result, you may have watched in amazement as someone had to help them in or out of a shirt they couldn't get over their head because their muscles were so big.
This large muscle size can occur in a very important organ of your body: the heart. Of course, the consequences of this increase in size are far worse than walking around bare-chested and have more to do with life and death.
Hypertrophic Cardiomyopathy (HCM) is a genetic heart condition that results in increased ventricular wall thickness, diastolic dysfunction, heart failure, and sudden death.
Hypertrophy of the heart muscle doesn't have to occur only as a result of genetic changes. Many times, the heart enlarges as a result of lots of different factors. For example, anything that increases the resistance to outflow of blood from either of the two ventricles of the heart increases the ventricular workload. If resistance is increased at the gym by adding on more weight, then muscles get big and thick in order to increase their strength.
If resistance to outflow increases in the heart, then the muscular ventricular walls get big and thick in order to help push blood out of the ventricles with more force in order to overpower the resistance to outflow.
So, let's examine what can cause an increase in resistance to outflow of blood from a ventricle and into its respective blood vessel. The left ventricle normally contracts to pump blood out through the aortic valve and into the aorta. From there, the blood flows to the organs and tissues of the body.
If a person suffers from hypertension, or increased blood pressure, then the afterload increases. Afterload is the force and pressure against which the heart must act in order to eject blood during systole. Systole refers to the time at which the heart contracts to eject blood out into the blood vessels.
If the left ventricle has to work hard against increased blood pressure, then the left ventricular wall thickens in order to become stronger and better able to work against this increased 'weight,' so to speak.
Similarly, if the blood pressure is normal but resistance to outflow increases as a result of aortic stenosis, the same end result will occur. Aortic stenosis refers to the narrowing of the aortic valve. If it's narrow, it's very hard to squeeze blood out into the aorta.
Just go ahead and try it for yourself. Get a mouthful of water and spit it out. It should be easy. Now, take a mouthful of water and put a straw in your lips. Try and squeeze that water out just as quickly as before. It's not possible because the resistance to outflow is so much greater when the outflow tract, the straw, is so thin. That's aortic stenosis for ya!
You'd think based on everything you just learned that this shouldn't be a problem because the heart muscle got big, and its new strength overpowered the afterload, and everything is now hunky dory. Wrong. Nothing significant occurs in physiology without an equal and opposite reaction, so to speak. Isaac Newton was a great physiologist, unbeknownst to him.
Go back to my introduction. Recall how I said that really big guys at the gym have a hard time moving about and doing stuff because their muscles are so large. This observation applies to a hypertrophied ventricle. As the ventricular wall thickens, it cannot move and relax very well. It becomes stiffer and less compliant. Since the ventricle can't move, relax, or open up very well, then the open space in the ventricle, its lumen, doesn't fill with as much blood as usual. The open space in the ventricle may also decrease in size directly as a result of the thick muscle growth. We term this process more technically as 'concentric hypertrophy.'
All of this means less blood can enter and fill the ventricle during diastole, the filling phase of the cardiac cycle that occurs when heart chambers relax. Therefore, hypertrophy results in diastolic dysfunction.
If abnormally low amounts of blood enter the left ventricle in this instance, then the blood begins to back up. First it backs up in the left atrium and then it begins to back up in the pulmonary vasculature. The increased amount of blood in the pulmonary vasculature results in pulmonary hypertension.
Which ventricle has to work harder against this specific hypertension (pulmonary hypertension)? It's the right ventricle that pumps blood into the lungs. Since the right ventricle has to work harder, it thickens as well, resulting in right heart failure if the person lives long enough.
All of these problems can lead to chest pain, fatigue, shortness of breath, and palpitation. Diagnosis of cardiac hypertrophy, HCM or otherwise, is made by way of an echocardiogram. This is a test that helps to visualize the heart using ultrasound. After the diagnosis is made, it's important to move on to a treatment plan ASAP.
This means that we must reduce the heart rate in cases of HCM or any case of cardiac hypertrophy. This allows more time for the ventricles to fill with blood in between beats.
Just go take a mug out of the cupboard and turn the faucet on in the sink. Now hold the mug there for a few seconds as it fills to the max. That's what happens during a slow heart rate. But if you move the mug quickly in and out, as a result of a fast movement, the mug is virtually empty.
Besides slowing down the heart, we must also get the stiff heart to relax in order to allow the ventricles to fill with more blood. Combinations of beta blockers and calcium channel blockers are used to accomplish these two feats.
This lesson went over cardiac hypertrophy, one specific form of which is known as hypertrophic cardiomyopathy (HCM), which is a genetic heart condition that results in increased ventricular wall thickness, diastolic dysfunction, heart failure, and sudden death.
Non-genetic causes of concentric hypertrophy include hypertension, or increased blood pressure, which increases the afterload on the heart. Afterload is the force and pressure against which the heart must act in order to eject blood during systole. Systole refers to the time at which the heart contracts to eject blood out into blood vessels.
Another cause for cardiac hypertrophy is aortic stenosis. In the end, either can result in improper amounts of blood entering the ventricles during diastole, the filling phase of the cardiac cycle that occurs when heart chambers relax. Therefore, hypertrophy results in diastolic dysfunction.
Treatment for this dysfunction includes slowing down the heart and relaxing the heart. Therefore, combinations of beta blockers and calcium channel blockers are used to treat these issues.
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Back To CoursePathophysiology Textbook
20 chapters | 274 lessons