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Hello everyone,
Which of these is the last to appear following coronal artery obstruction?
a) angina pectoris
b) increase of lactate
c) problem in segmentary contractility of the left ventricle
d) subendocardial lesion in ECG
e) reflex tachycardia

I am not able to link these events in the correct chronological order :confused:, so any help you can provide would be appreciated.
 

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Hello everyone,
Which of these is the last to appear following coronal artery obstruction?
a) angina pectoris
b) increase of lactate
c) problem in segmentary contractility of the left ventricle
d) subendocardial lesion in ECG
e) reflex tachycardia

I am not able to link these events in the correct chronological order :confused:, so any help you can provide would be appreciated.
Hello,
first there is increase of lactate which causes angina pectoris leading to subendocardial lesion on the ECG. Segmentary abnormality may be already present depending on the degree of obstruction previously where myocardium may have been hibernating or appear after the onset of total obstruction. Reflex tachycardia in my opinion occurs last, if there is an acute drop in blood pressure due to acute inability of the heart to pump efficiently. This drop in BP causes reflex tachycardia. I am not completely sure of this information so feel free to correct me if I'm wrong
 

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Hello,
first there is increase of lactate which causes angina pectoris leading to subendocardial lesion on the ECG. Segmentary abnormality may be already present depending on the degree of obstruction previously where myocardium may have been hibernating or appear after the onset of total obstruction. Reflex tachycardia in my opinion occurs last, if there is an acute drop in blood pressure due to acute inability of the heart to pump efficiently. This drop in BP causes reflex tachycardia. I am not completely sure of this information so feel free to correct me if I'm wrong
Thank you for your reply. I would be glad if you could explain what exactly are "subendocardial lesion on ECG" and "segmentary abnormality", and what is the mechanism behind each.
I know that after the coronary artery is blocked, the blood supply is cut. Therefore the heart cells start producing energy using anaerobic glycolysis which produces a lot of lactate that can't be eliminated and leads to pain.
I also understand that after the heart starts to fail, the drop in BP will elicit reflex tachycardia. But I can't see where the other two fit in.
 

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Thank you for your reply. I would be glad if you could explain what exactly are "subendocardial lesion on ECG" and "segmentary abnormality", and what is the mechanism behind each.
I know that after the coronary artery is blocked, the blood supply is cut. Therefore the heart cells start producing energy using anaerobic glycolysis which produces a lot of lactate that can't be eliminated and leads to pain.
I also understand that after the heart starts to fail, the drop in BP will elicit reflex tachycardia. But I can't see where the other two fit in.
Hey,
I will first address your question on "segmental abnormality":
Don't think of the heart as being one clump of muscle that pumps well and when one of its blood vessels gets occluded, all of it stops working well. The point I want to make is that if there is an occlusion of one coronary artery, that part of the muscle which is supplied by that artery will be affected, but other parts, as long as they are receiving enough blood from other arteries which are not occluded will function just fine. This is the reason why people don't die following an acute MI even though part of their heart just died. Each coronary artery supplies some parts of the myocardium, and these parts in cardiology are artificially divided into segments for descriptive purposes. When a cardiologist does an echo, he will be able to see that some parts of the myocardium may not be functioning well while others may be functioning just fine (he does so by subjectively comparing movement of the diseased parts with the normal parts. If one part is not moving at all, or moving less there is a "SEGMENTAL" abnormality of that particular segment (or part of the heart) in question. To give you an example: LAD roughly supplies blood to the anterior portion of the heart and 2/3 of the septum while Left circumflex artery supplies blood to the lateral portion of the heart. If for instance left circumflex artery gets occluded, only the lateral portion of the heart will experience ischemia and go on to develop abnormalities. In this case only lateral segments would have abnormalities while anteroseptal segments would function just fine. This is what is meant by segmental abnormalities.

With regard to segmental abnormalities, there are two phenomena which are very important. One is myocardial hibernation and the other one is myocardial stunning.
When the part of the left ventricle is subject to repetitive ischemia due to any reason, the heart may go into some kind of a defense mode on molecular level and decrease its metabolic functions and therefore contractile function as well. On macroscale level it would look like a dead myocardium which would not be moving at all and may look like a scar on echocardiography but still be alive! It would therefore experience segmental abnormalities because of this repetitive ischemia. This may occur before the patient develops a total occlusion and is thought to be a protective mechanism against dying (so in this case the segmental abnormalities would develop BEFORE complete occlusion). Segmental abnormality may also occur acutely when for example the occlusion was not big enough to cause any type of ischemia but all of a sudden a huge thrombus formed, which led to total occlusion and therefore loss of function of that particular part of the heart supplied by the artery. But notice that for your question it does not really matter, and chronology of the "Segmental abnormalities" in this acute case may be before or after developing this particular occlusion in question. The most important part in this question is that reflex tachycardia will occur acutely when some portion of the heart stops functioning well SUDDENLY leading to acute decrease in blood pressure. Keep in mind that not all coronary arteries are equally important. For example if there is an occluson of left circumflex artery, the part of the heart affected may not be big enough to cause any drop in blood pressure, thefefore a patient may experience hypertension instead of drop in BP. Usually drop in blood pressure occurs when large part of the myocardium is affected, and if this happens acutely in the period of minutes one will go on to develop reflex tachycardia. The key word here is "acute" because if the heart started failing a long time ago because of recurrent bouts of ischemia, the drop in blood pressure might initially have led to reflex tachycardia, but it would be compensated by retension of fluid as well as other regulatory mechanisms which would eventually lead to "congestive heart failure". but because of those regulatory mechanisms the heart rate would most probably normalize. Therefore in my mind reflex tachycardia after an occlusion would always occur last.

Regarding your question about "subendocardial lesion on ECG":
I'm sure you know that when the heart undegoes ischemia or infarction, the first part of the muscle affected is the innermost part (subendocardial). Subendocardial part of the myocardium is particularly susceptible to ischemia because the coronary vessels course from the epicardium, through myocardium into endocardium. Hence the last place or place below it is more prone to ischemia.
There are two types of myocardial infarction: STEMI (ST segment elevation on ECG) and NSTEMI (without any ST segment elevation). ST elevation occurs when there is a transmural death of the muscle (whole thickness of the part is affected) while NSTEMI occurs when only subendocardial portion of the affected part is dead: in which case you would not see ST elevation on the ECG. In fact, a simple ischemia may cause typical subendocardial ECG signs, those are: ST depressions as well as T wave flattening and T wave inversions. So most common conditions which may produce "subendocardial ECG signs" are stable angina, unstable angina and NSTEMI (but there may be other conditions which may cause those findings as well like pericarditis so I suggest you going over some ECG book).

Regarding the mechanism of such "subendocardial ECG signs (which literally almost equalst to ST depressions and T wave flattening and inversions):
At cellular level the most important thing that happens in regard to ECG recordings is that the Na/K pump stops working in ischemic cells! A good rule of thumb to remember is that Na/K pump always produces hyperpolarizing current (moves 3 sodium ions out and moves 2 potassium ions in, thus, in total, removing one positive charge carrier from the intracellular space), so if it stops working, the cell would undergo depolarization. There is however something else that is occuring in the background that may complicate matters a little bit: When ATP decreases ATP dependent K channels will open and will cause K to leave the cell and therefore cause hyperpolarization (this is a protective mechanism against ischemia). But if it continues, this mechanism will eventually get overloaded because extracellular concentration of K will keep on rising which will eventually contribute to depolarization. Keep in mind thay because of the occlusion of the blood supply in the vicinity of the ischemia, K will have no chance to be flushed away with the circulation that's why it will keep on accumulating.
This overall depolarization in the area of ischemia is called "Injury current". And this "injury current" may be seen on the ECG! So you may ask now, how come we have ST depressions sometimes while when whole myocardium is involved we see ST elevations? Well because if the endocardium is involved this same injury current will be interpreted by the ECG as ST depressions while ECG will pick up an "injury current" from the epicardium as ST elevations! So it all depends on the region where ischemia is taking place (if it is endocardium or epicardium). And because of this phenomenon that endocardium always gets injured first, we may predict if only endocardium is affected or if the whole thickness of the muscle is affected.
Now the mechanism of those ST depressions relative to the machine:
ischemic myocardium is always depolarized compared to resting myocardium. Therefore the machine is interpreting it as a constant current because it is picked up by an overlying electrode. When this depolarizing current is traveling towards this electrode, it will be interpreted as positive. This occurs when the ventricle is still resting (not depolarized), so it occurs during the PQ interval just before the QRS. So in reality, it is not the ST segment that is depressed, but rather PQ segment is elevated relative to ST!

Now mechanism of ST elevation on the ECG:
When the whole thickness of the myocardium during the resting period is generating the "injury current" (is depolarized during resting state), the current is flowing away from the ECG electrodes. Therefore the isoelectric segment will now appear depressed compared to ST segment and there will be ST segment elevation!

Regarding the mechanism for T wave inversions:
For this we must understand why T wave is concordant with QRS complex in the first place (usually positive but may be negative if QRS is mainly pointing downwards in which case it is normal, therefore it is more appropriate to speak of concordant T waves and not positive or negative). Now the reason why T waves are normally upright is because of the electrophysiological kinetic properties of subendocardial cell's action potential compared to subepicardial cells. Subendocardial action potentials are longer in duration compared to subepicardial cells. Therefore current of repolarization is normally traveling away from the ECG electrodes (remember that current of repolarization traveling towards the electrode is negative and away from the electrode it becomes positive on the ECG. Reverse is true for depolarizing current). Now subendocardial ischemia causes overall depolarization of those subendocardial cells and therefore shorter action potential duration, therefore in this case the current of repolarization would be traveling TOWARDS the ECG electrodes because now the epicardial cells would be the slow "repolarizers"

I apologize for a long post, but I wanted to have it as concise as I possibly could
 
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