Myocardial infarction – Osmosis Video Library

According to the world health organization, cardiovascular disease is the leading cause of death worldwide, as well as in the US. Of those, a large proportion are caused by heart attacks, also known as acute myocardial infarctions, or just myocardial infarctions, sometimes just called MI.

The word infarction means that some area of tissue has died due to a lack of blood flow, and therefore a lack of oxygen. Myo refers to the muscle, and cardial refers to the heart tissue. So with a heart attack, or MI, you have death of heart muscle cells because of a lack in blood flow, a process called necrosis. Now the hearts main job is to pump blood to your bodys tissues right? Well, the heart also needs blood, and so it also pumps blood to itself, using the coronary circulation. The coronary circulation is this system of small arteries and veins that help keep the heart cells supplied with fresh oxygen. Heart attacks happen when these small arteries become blocked and stop supplying blood to the heart tissue, and if this happens for long enough, heart tissue dies.

Almost all heart attacks are ultimately a result of endothelial cell dysfunction, which relates to anything that irritates or inflames the slippery inner lining of the arterythe tunica intima. One classic irritant are the toxins found in tobacco which float around in the blood and damage these cells. That damage then becomes a site for atherosclerosis, a type of coronary artery disease where deposits of fat, cholesterol, proteins, calcium, and white blood cells build up and start to block blood flow to the heart tissue. This mound of stuff has two parts to it, the soft cheesy-textured interior and the hard outer shell which is called the fibrous cap. Collectively this whole things ominously called plaque. Usually, though, it takes years for plaque to build up, and this slow blockage only partially blocks the coronary arteries, and so even though less blood makes it to heart tissue, theres still blood. Heart attacks happen when theres a sudden complete blockage or occlusion of a coronary arteryso lets see how that can happen. Since these plaques sit right in the lumen of the blood vessel, theyre constantly being stressed by mechanical forces from blood flow, and interestingly its often the smaller plaques with softer caps rather than the larger ones with harder caps that are especially prone to break or get ripped off. Once that happens the inner cheesy filling which remember is this mix of fat, cholesterol, proteins, calcium, and white blood cells, is thrombogenic, and this means that it tends to form clots very quickly. So platelets, or blood-clotting components in the blood, flow by and get excited; and they adhere to the exposed cheesy material. In addition to piling up, the platelets also release chemicals that enhance the clotting process. Now this happens super fast, think about how quickly a small cut stops bleeding, thats a very similar processit happens in a matter of minutes, right? And now that coronary artery is fully occluded.

So now lets change views a bit, If we take a slice of the heart like this, this side being posterior, or back, and this being anterior, or the front, with the left and right ventricles here, and then we have the three most commonly blocked arteriesthe left anterior descending, or LAD which supplies blood to the anterior wall and septum of the left ventricle which accounts for 40-50% of cases, the right coronary artery, or the RCA which covers the posterior wall, septum and papillary muscles of the left ventricleaccounts for about 30-40% of cases, and finally, the left circumflex artery, or LCX which supplies to the lateral wall of the left ventricle about 15-20% of cases. Notice that the majority of these areas supply the left ventriclemost heart attacks therefore involve the left ventricle, where the right ventricle and both atriathe upper chamberarent as often affected.

Each of these areas is called the arterys zone of perfusion. And, if we take a closer look at one of these zones, well see that basically youve got the endocardium, which is the smooth membrane on the inside of the heart, and then the myocardium, all the heart muscle, and then, the epicardium, the outer surface of the heart, which is where the coronary arteries live. Lets say the LAD gets blocked, the area of perfusion is now at serious risk, and within about a minute, the muscle cells in this zone dont see enough oxygen and become ischemic, and the muscle layers ability to contract is severely reduced. This initial stage is extremely sensitive, since the ischemic damage to cells in the perfusion zone is potentially reversible. After about 20-40 minutes, though, damage starts to become irreversible and the cells start to die, and this zone changes to a zone of necrosis, or dead tissue. Once lost, these cells will never return or regrowthats why quickly identifying and treating an MI quickly is super important.

The first area affected is the inner third of the myocardium, since its farthest from the coronary artery and the last area to receive blood, and its subject to higher pressures from inside the heart. If the blockage suddenly lyses or breaks down and blood flow returns, sometimes patients damage will be limited to the inner third, and this would be called a subendocardial infarct. An ECG, or electrocardiogram, done at this point typically shows an ST-segment depression, or in other words, it doesnt show ST segment elevation, so sometimes we call this an NSTEMI which stands for non-ST elevation myocardial infarction.Other causes of this sort of subendocardial infarcts would be severe atherosclerosis and hypotensionanything that ultimately leads to poor perfusion of the heart tissue. After about 3 to 6 hours, though, the zone of necrosis extends through the entire wall thickness, called a transmural infarct, which this time shows up as ST-segment elevation on ECG, which is why theyre sometimes called STEMIs, or ST elevation myocardial infarctions. So the difference between NSTEMIs and STEMIs is that NSTEMIs dont have ST-segment elevation, and these are caused by partial infarct of the wall, whereas STEMIs have ST-segment elevation and involve the whole wall thickness.

Patients that have an MI will most commonly have severe and crushing chest pain or pressure, that might radiate up to the left arm or jaw, they might have diaphoresis or sweating, nausea, fatigue, and dyspnea. All of these are either a direct result of an end-organ like the heart or the brain not getting enough perfusionso think chest pain and dizziness. Or from the sympathetic response from the body to help the heart work harder and preserve blood pressureso think sweating and clammy skin. Many people also have referred pain where the nerves in the heart are irritated, but that pain can be felt in the jaw, shoulder, arm, or back instead.

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Myocardial infarction - Osmosis Video Library