Health and medicine
- Heart disease and heart attacks
- Stenosis, ischemia and heart failure
- Thromboemboli and thromboembolisms
- What is coronary artery disease?
- Risk factors for coronary artery disease
- Heart attack (myocardial infarction) pathophysiology
- Heart attack (myocardial infarct) diagnosis
- Heart attack (myocardial infarct) medications
- Heart attack (myocardial infarction) interventions and treatment
- Healing after a heart attack (myocardial infarction)
- Complications after a heart attack (myocardial infarction)
Complications after a heart attack (myocardial infarction)
Created by Vishal Punwani.
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- Hello, I want to know how does an MI lead to arrhythmias?(2 votes)
- MI can cause death to the heart tissues and the development of scar tissue which results in the heart being able to beat less effectively and efficiently, which results in arrhythmias.(5 votes)
- At7:53, is it the atrium or atria? If you put on the subtitles, it says atria, but I think it's atrium.(1 vote)
- I think he said atria. Atria is the plural form of atrium.(8 votes)
- How do we prevent repurfusion injury during management of acute STEMI?(2 votes)
- Tissue necrosis of a ventricular wall causes the blood to burst through the weakened ventricular wall, and build up within the pericardium. What if, as well as this, the heart suffers from pericarditis (whereby an inflammation damages the pericardium). Wouldn't this cause the blood to also burst through the pericardium and therefore burst through the heart?(0 votes)
- In the case that a free wall rupture occurs to allow blood to escape into the pericardium, the question of whether blood buildup to cause pericarditis to result in rupture of the pericardial sac becomes a bit of a moot point.
By the time blood is able to enter the pericardium, the most immediate problem becomes cardiac tamponade/hemopericardium that may rupture into the thoracic cavity. To relate back to your question, it's seems highly unlikely that someone survives long enough to allow the steps of inflammation to unfold before a more significant problem would occur.(3 votes)
- which level of MI will it lead to death or what is the most sign I should be fear about it?(1 vote)
- MI main sympthon is strong pain from umbilical scar to under your chin, the big majority of cases irradiates the pain to the left arm.(1 vote)
- what will be the effect of increasing preload in anterior wall MI??(1 vote)
- Increased preload will increase the ventricle diameter (think more fluid in the heart stretches it out like filling a water balloon), and that will lead to increased wall stress as seen in the Law of LaPlace. Since the heart now has to pump to a greater pressure to expel more blood, it uses up more oxygen because more energy is required. This will put more stress on the heart when it already is in a state where it's struggling to meet bodily demands.(1 vote)
- [Voiceover] After you've had a myocardial infarct, a heart attack, you are prone to developing complications. A complication in this sort of context is essentially another disease or condition that crops up as a result of your myocardial infarct. Most complications tend to occur within the first few weeks after having a heart attack, so let's look at some of the major complications that can occur after myocardial infarct, and let's sort of do this in a step wise fashion to make everything sort of flow logically in our heads. We can say that myocardial infarcts cause three major problems with our hearts, right? So, one of the things is they cause our heart to have decreased contractility, because after a heart attack, you've sustained some damage to your heart muscle, so it can't always contract very well. You also get this electrical instability in your heart because all of the ions that sort of move back and forth across your heart muscle cell membranes to maintain your electrical gradients, or your heartbeats, properly, they all get really disrupted so you have this electrical instability. You also get tissue necrosis, right? You get death of some of your heart muscle cells. These three sort of effects of having a myocardial infarct, they really underly all of the downstream complications that are possibly going to crop up. So how does reduced contractility do that? Well, if your heart's not contracting properly, then you're not going to effectively be able to push blood out of your left ventricle to the rest of your body, right? So you end up in a state called hypotension and hypotension just means that you have pathologically low blood pressure. When you have pathologically low blood pressure, you're not going to be able to fill your coronary arteries with enough blood, all the blood that they need. Remember, besides the coronary artery that's been blocked to result in your myocardial infarct, there are still other coronary vessels that needs to have a healthy supply of blood coming to them so that they can in turn supply blood to the rest of your heart muscle, right? The heart muscle that isn't infarcted. So if they're not getting enough blood, then you'll start to get ischemia in the muscle and other parts of your heart. If you get ischemia in other parts of your heart, then that will cause more of your heart muscle all over to not contract properly and eventually, you might not be able to maintain your cardiac output at all and end up in a condition called cardiogenic shock and because this wall here, and we're assuming that it's this wall that's been sort of injured in the heart attack, because this wall isn't contracting very well, you'd be predisposed to forming a thrombus, a clot, on the inside of that left ventricle there, because when blood isn't constantly moved around as it might not be in that little area there, it tends to clot and why is that bad? Well, sometimes they can kind of flick off, become separated off of the left ventricle wall there and travel through the aorta and into other vessels of the body where they might get stuck and cause an infarction in another part of the body. For example, if one went up into your brain, it might get stuck in one of your cerebral vessels and cause a stroke, so embolism is a potential problem. Embolism is the mobilization of a thrombus, a clot. Alright, what about this electrical instability over here? Well, the electrical instability can cause arrhythmias, which is when your heart doesn't beat with a normal, regular rhythm like it's supposed to. Again, that's due to a combination of things. That's due to sort of disorganized ion movement within the cardiomyocytes, and it could also be due to a disrupted electrical conduction system within the heart. I should mention, as part of this conduction system compromization here the two major pace maker centers in your heart are located in your right atrium, so you've got your sinoatrial node about there and you have your atrioventricular node around here and these two nodes are really responsible for regulating the normal rhythm of your heart and so if you happen to have a myocardial infarct that affected the right atrium, where both these nodes live, you would probably end up developing an arythmia because you'd potentially knock out the two biggest regulators of your heart beat, your heart rate and rhythm. Alright, what about this tissue necrosis thing? Well, remember, necrosis just refers to death of something so in this case, death of the heart tissue. Well, remember after a myocardial infarct, you get a whole bunch of immune cells that come into your heart and try to sort of tidy things up after your heart attack, and when you're immune cells are involved with sort of tidying something up, that's called an inflammatory reaction, and you might start to get this inflammation around the outside of your heart. I'm drawing this inflammation in a pink here. Pink is supposed to represent all those white blood cells as part of your immune system, mediating this inflammatory response here on the outside of your heart. Now, remember your heart sort of sits inside this fibrous sack. It's encased by this fibrous sort of cover called your pericardium. Your pericardium, peri meaning around and cardium referring to your heart. When you get all this inflammatory sort of stuff happening on just beneath the pericardium on the outside of the heart, you could irritate your pericardium and you could end up with a condition called pericarditis. Now, that's not all that tissue necrosis can do. It can do some pretty nasty stuff here. So, let's say that you start to get necrosis of your septum here, there wall that separates your left ventricle and your right ventricle. Well, you could probably imagine that that wouldn't be very good at all. Your oxygenated blood in your left side of your heart and your deoxygenated blood in your right side of your heart they would mix, and you would probably end up with a pretty significant hypoxemia, or low oxygen level in your blood. A ventricular septal defect would also cause some damage to the arteries in your lungs, because if you can imagine, blood from this high pressure system on the left side of your heart would sort of cross through this defect over to the right side of your heart and be pushed up through to your pulmonary circulation. That's not good for your pulmonary circulation. It can actually cause some pretty big damage there. What else will tissue necrosis do? Well, what if you get that necrosis over on this side? Or, really, any other muscle that forms the outer wall of the heart? Well, where do you think blood in the heart would go if all of a sudden there was no wall anymore? It would just burst out of the heart. So, tissue necrosis can also cause a rupture of the ventricle. But remember this pericardium we talked about? This really tough, fibrous sack that encases the heart? The blood would then just get trapped inside the pericardium and it would start to sort of build up in the pericardium and track along the outer heart muscle and the inside the pericardium so that, obviously, would put a stress on the heart and prevent it from beating as well, and you'd end up with a complication called cardiac tamponade. Tissue necrosis is not done yet though. One of the more common issues that happens as a result of tissue necrosis is this here. You've got these muscles in the bottoms of your ventricles called your papillary muscles and what your papillary muscles do is they sort of hold on to the cusps of your valves, the flaps of your valves, using these structures called chordae tendineae. They're these sort of tough, durable, string-like things. So the papillary muscles and the chordae tendineae work together to make sure that during a heart beat, when your ventricles contract, your mitral valve and your tricuspid valve over on the right side, you have a set of papillary muscles and chordae tendineae over there as well, they make sure that the cusps of your valves don't invert up into the atria, and so sometimes after a heart attack, one or more of these papillary muscles will become necrosed, it will die off. When it dies off, all of a sudden now, the valve flap that it was holding on to can invert. It can go up into the left atrium. This means that when the ventricle contracts to push blood out into the aorta, to get around the body, blood can now get back up into the left atrium. This is called having a leaky valve or a regurgitant valve. In this case, since it's the mitral valve, we call this mitral regurgitation. So, just before we finish up, let me just draw your attention to this. If your heart has decreased contractility then it's going to have to work harder to maintain proper profusion of your body with blood. If you have a mitral regurgitation, then again, your heart's going to have to work a lot harder to maintain proper profusion of your body with blood. If you have a ventricular septal defect, again, your heart is going to have to start working a lot harder. So these three conditions in particular, if you develop any of these after a heart attack or not, you run the risk of developing congestive heart failure, which is when your heart just can't pump out enough blood to meet the oxygen needs of your body.