Welcome to our 11th lecture ischemic heart disease. In this lecture we're going to discuss the manifestations of Lv ischemia, mainly regional Lv dysfunction or the fancy name for it. Regional wall motion abnormalities are w m, and you're gonna hear this acronym a lot, as well as the complications that can result from myocardial infarction. As you know, the Lv CIP, divided by three coronary arteries, this is the heart. This is the aorta. From the aorta arises the left main coronary artery, which bifurcates into the left anterior descending coronary or the LED and the left circumflex coronary artery or the lcsw.
The lady supplies the anterior part of the Lv and the septum model that circumflex wraps around the left side of the heart to supply the lateral Lv wall. This is the right coronary artery which supplies the RV and wraps around to supply The inferior quality Lv in most people, whenever one of these arteries or their branches is occluded ischemia, the supplied segment ensues. With the result these scheming segments become hyperkinetic means that their contractility and motion are reduced, or a kinetic meaning that contractility and motion stopped completely. For descriptive purposes the Lv is divided into 17 segments, each group of segments being supplied by one of the main coronaries or its branches. This is the heart seen from behind. These are the atria and these are the ventricles.
The tie the atria, let's also hide the right ventricle. Now we have just the Lv. The Lv is divided transversely and longitudinally transversely it's divided into basal Lv, mid Lv, atypical Lv and Apex proper. The basal portion of the Lv is at the mitral valve level. And the partner the apex is called the atypical part where no papillary muscles are visible in cross section, while the portion in between is called the mid Lv longitudinally, the Lv is divided into the anterior wall, the inferior wall, the entero settle wall, behind the anterior insertion of the RV. The intro septal wall, between the interceptor and the fear wall, the ventral lateral wall and the inflow lateral wall adjacent to the inferior wall.
These six divisions are present at all the levels of the Lv except at the apex level, where there are only four of them. septal anterior lateral interfere This is the basal level we have basal entero, septal, basal, anterior, basal anthro, lateral, basal infra lateral, basal inferior and basal info septal This is the mid level we have the same segments Amid intro Seto made anterior mid intro lateral mid info lateral medium fear and mid info sceptile vehicle segment we only have four of these segments at the typical level, the septum, the anterior, lateral, and the inferior. So we have six plays or segments six minute segments for a vertical segments that makes 16 and then we add the apex proper and that makes 17 segments. The corner supply for these segments is as follows. The LED usually supplies the intro, septal anterior, as well as the apex proper and the atypical inferior walls.
The LC x usually supplies the impro lateral and intra lateral walls short of the apex and the RCA usually supplies the infor septal and inferior walls at the bezel and Mid levels. In some people, the lcsw can supply the basal and mid inferior inferior lateral walls instead of the RCA. In these cases, it's called a dominant sex. Why are we discussing all this? Because if you have a patient with say an inferior myocardial infarction, you will expect to see a kinesia or hyper kinesia at the segment's supplied by the RCA mentioned above. This can come in particularly handy in situations where you have some of the ECG abnormalities that mimic acute EMI such as pericarditis or early repolarization.
Echocardiography can in these cases differentiate between true Am I in which you'll see obvious or w ma or one of those mimickers in which we'll find normal Lv regional function it's easier to look for rW Ma and the pair sternal short axis but you should know which segments are visible in the rest of the views to let's go over them quickly. And the pair of Sterling long axis view this is the intro Seto Lv wall. And this is the intro lateral or the posterior wall, the bezel and Amid segments are visible in this view. In the even before chamber view, this is the basal antral lateral wall, the mid entry lateral wall and the apical lateral. This is the apex proper. This is the typical septal, mid entry offset tool and bezel interceptor.
In the typical two chamber view, we can see all segments of the anterior and the inferior walls. In the typical three chamber, we have the intro lateral, or the posterior wall and the intro set the law similar to the pair of sternal long axis view, but in this view, all the segments are visible all the way up to the apex. Now let's look at some examples of regional wall motion abnormalities. This is a pair sternal short axis view mid level. I'll let you look at it for a few moments. And then all comments.
Try to find out which segments aren't moving as well. They should be. Okay. So, if you look carefully, you'll notice that the upper half of the image, which is the anterior half of the Lv, isn't moving as well as the lower half of the image. These are the segments I'm talking about. You'll notice how their movement is much less pronounced than the movement of the rest of the Lv.
A trick I was taught, which you might might find useful as well, is to use my hand to cover up one half of the Lv. Look at the contractility in the visible half. Then move my hand and compare. It's now obvious that the upper half is moving much more sluggishly than the lower half. So the affected segments are the mid enter septal mid anterior and the mid antral lateral. This is the same patient and Pair sternal long axis view.
And as we saw in the previous image, the interceptor segment bezel and mid segments of the interceptor wall here are visible. And you can see that they're almost not moving at all. They're a kinetic, this is the same patient in the APR 14 review. And we can see that the mid an APR segments, the interest level as well as the apex proper are a kinetic. When I say a kinetic, it means that the wall isn't contracting because don't expect to see the wall completely frozen in place because it's attached to the rest of the heart. So the other segments are going to pull on it and and you'll get the illusion of it being moving.
But when I when we say a kinetic, it means that the wall is not the segment is not contracting, it's not thickening. And you can see that here. Okay, let's move on to the second example. Again, I'll let you look for a few moments. And then I'll comment, try using that trick we talked about. Okay, if you figured out which segment isn't moving, let's use the trick behind this half.
What do you think about the movement of this half? Let's move our hand now. Okay, this half seems to be moving pretty well. Okay, so I'll reveal the answer. The inferior segment. This is again a pair of sternal short axis mid level.
So the mid inferior segment is a kinetic, it's not moving. The intro lateral segment is is also hyperkinetic? It's not completely a kinetic. It's it's moving a little bit but it's sluggish. So, we have made inferior a can easier and in for lateral hypo kinesia This is the same patient in the atypical two chamber. The anterior wall is moving pretty well.
But the inferior wall, as we see is a kinetic, it's not beginning at all. Remember, that's always important to look at rW MS and more than one view before giving your final opinion. Now that we've been through identifying rW Ma, it's time to look at some of the mechanical complications of EMI. Perhaps the most common among them is systolic dysfunction due to loss of a large portion of myocardial contractility. This is an example. The first thing you'll notice is that the Lv is markedly dilated.
This is also a persona short axis mid level view, the papillary muscles are there but because of the V l because the Lv is so dilated, they're not they're not that prominent. If you look at the segments, you'll find that almost all the segments of this level are a kinetic. Maybe the only segment moving little is the info lateral segment and even that's not normally it's hyperkinetic. ejection fraction by eyeballing would be about 15%. Another complication we see a lot is an lv thrombus. You'll usually see in patients with a large anterior wall myocardial infarction and then a kinetic Apex where the pouch like nature of the economic apex, encourages blood stagnation and consequently, thrombosis.
Always check for thrombus when you've seen a kinetic Apex and don't forget to tilt the probe up and down, what we call sweeping to check our planes. Never forget that echo is 2d, and that not seeing something in the plane you're cutting doesn't mean it's not there lurking in a different plane. Another This is another still image of a larger lB thrombus. Another relatively common complication is acute mitral regurgitation. This is this happens due to papillary muscle dysfunction and rarely due to papillary muscle rupture. In which case we get a flat leaflet with severe Mr. And rapid hemodynamic deterioration this The patient patient is sterilization with vasodilators and emergency valve surgery.
Now to less common, but usually fatal complication, which results from ischemia new structure through the wall of the Lv, this rupture can happen either through the Lv free wall or through the intra ventricular septum. This is the case of rupture through the inter ventricular septum, what we call a VSR ventricular septal rupture, and this results in an acute ventricular septal defect and acute VSD. Also with rapid hemodynamic collapse in shock and also needing emergency surgery, you can see the jet mic flow across the upper part of the Lv septum and purestone on long axis view. This is another example of VSR in the typical portion of the septum. This is an apical for chamber view. And we're zooming in on the apex and you can see the jet light flow across the ethical portion of the septum.
This is a case of rupture through the free wall of the Lv. But in this case the rupture is what we call sub acute ruptured because the rupture happens slowly and the pericardium had time to adhere to the rupture site and seal it. If this rupture had been acute rupture, rapid bleeding into the pericardial cavity would have happened hemorrhagic pericardial effusion with tempo an ad, and the patient probably wouldn't have survived. This concludes our lecture, see you in the next lecture pulmonary embolus