We’re going to talk about cardiomyopathy. It’s a relatively simple topic and isn’t tested often, but if you’ve got a basic understanding of cardiac anatomy and hemodynamics, it’s really easy to understand. We can even break down the terminology here – so we know that “pathy” means disease, “myo” means muscle, and “cardio” means heart – so this is a disease of the heart muscle.

So, by definition cardiomyopathy is an abnormality of heart muscle that leads to functional changes in the heart. You can see here in this image that the muscle of the ventricles is super thick. This makes it really hard for it to contract and relax like it should. The most common causes are Hypertension and Heart Failure – the heart is working overtime and the ventricular muscle starts to change in response to that. There are three types, dilated, hypertrophic – which is what’s pictured here – and restrictive.

In dilated cardiomyopathy, you can see the muscles of the ventricles have enlarged and ballooned out. This muscle gets stretched out and really thin, like an overused rubberband. It’s so stretched that it can’t fully contract like it should. So you get decreased contractility – which leads to a decreased cardiac output.

In hypertrophic cardiomyopathy, you can see the ventricular muscle has gotten super thick. When it’s that thick it’s really stiff and doesn’t have much give. But also, you can see that the space in the ventricle where the blood would fill up is decreased. So you get a decreased preload, which of course leads to a decreased cardiac output.

Then, finally we have restrictive cardiomyopathy. In this type, the walls are normal size and it can contract okay, but the muscle is actually super rigid. Because it’s so rigid, it has NO stretch. If it can’t stretch, it struggles to fill and get a good amount of blood out to the body. So you get a decreased stroke volume and therefore a decreased cardiac output.

So dilated is a contractility problem, hypertrophic is a thick wall preload problem, and restrictive is a filling issue.

When we assess a patient with cardiomyopathy, we’re going to see those signs of heart failure – it almost mimics it. Decreased cardiac output means poor peripheral perfusion – so you’ll see the fatigue, shortness of breath, and dysrhythmias. It can also lead to volume overload because the blood is backing up so you may see JVD or pulmonary edema, or hear extra heart sounds (S3, and S4). Jump back to the heart failure lessons if you need a refresher on those symptoms. You’ll also see an enlarged heart on imaging – either in an echocardiogram or on an X-ray like this one showing how large the heart is, it’s taking up all this space here where the left lung should be. So you can imagine how they may also struggle to breathe because of this.

So when it comes to therapeutic management, one thing to note is that in most cases there’s no cure. Once the damage is done, it’s difficult to reverse. So our primary focus is on supportive care. That involves similar things we would do for a heart failure patient like encouraging rest and minimizing stress. We also want to treat their hypertension. this could be a DASH diet, ACE Inhibitors, or ARB’s, but the one that makes the most difference in this case is Beta Blockers. They will decrease the workload on the heart by decreasing force of contraction. This helps decrease the oxygen demand in the heart so it doesn’t have to keep working so hard – which could cause more damage. Then, in the late stages of cardiomyopathy, it’s possible that the patient could get a ventricular assist device like the one pictured here. The purpose is to help pull the blood out of the left ventricle and push it into the aorta since the ventricle itself is unable to do that. Usually these are used as a bridge to heart transplant.

So to sum up, cardiomyopathy is an abnormality of the heart muscle which leads to functional changes. There are three types – dilated, hypertrophic, and restrictive. Because it causes decreased cardiac output, the symptoms will mimic heart failure – poor peripheral perfusion and possibly volume overload. And finally remember there’s no real cure, we just need to provide supportive care, treat their hypertension, and manage their symptoms.

So, like we said, it’s pretty straight forward. If you understand basic cardiac physiology and hemodynamics, you can understand how this cardiac muscle disease will affect the patient. We hope you learned something! Now, go out and be your best selves today and, as always, happy nursing!