AssessmentsECG cardiac infarction and ischemia
ECG cardiac infarction and ischemia
The of the left ventricle is supplied by a terminal branch of the right or left coronary artery.
Content Reviewers:Rishi Desai, MD, MPH
An electrocardiogram - an ECG - or the dutch and german version of the word - elektrokardiogram or EKG, is a tool used to visualize “gram” the electricity “electro” that flows through the heart “cardio”.
An ECG tracing specifically shows how the depolarization wave moves during each heartbeat - which is a wave of positive charge - looks from the perspective of different sets of electrodes.
This particular set of electrodes is called lead II, with one electrode on the right arm and the other on the left leg, so essentially when the wave’s moving toward the left leg electrode, you get a positive deflection, like this big positive deflection correspond to the wave moving down the septum.
To read an ECG there are a few key elements to keep in mind, one of them includes figuring out if part of the heart has is suffering from ischemia or has undergone an infarction.
The term ischemia means that blood flow to a tissue has decreased, which results in hypoxia, or insufficient oxygen in that tissue, whereas infarction goes one step further and means that blood flow has been completely cut off, resulting in necrosis, or cellular death. That typically happens if blood flow has been cut off for about 20 minutes.
In the heart, ischemia and infarction can be transmural, affecting the entire thickness of the myocardium, or subendocardial, affecting just the innermost part of the myocardium - the part just beneath the endocardium.
Out of all four chambers of the heart, the ECG is most sensitive to transmural or subendocardial ischemia or infarction in the left ventricle because that’s the chamber with the thickest walls and therefore has the most cardiac tissue.
Alright, let’s start with subendocardial ischemia, which might happen when there’s incomplete blockage - let’s say 70% - in a coronary artery.
In that situation, at rest there’s enough blood flowing through to meet the demand of the myocardium, but during exercise there’s not enough to meet the increased demand of the myocardium.
In that situation, the subendocardial tissue get ischemic because it’s the last bit of tissue to get blood from the tiny branches of the coronary arteries as they make their way through the ventricular wall from outside to inside.
This condition is called stable angina, because there’s ischemia which causes chest pain with exercise and it disappears with rest.
And there’s also unstable angina, which can occur with incomplete blockage of a coronary artery, but in this case, chest pain appears at rest.
When there’s subendocardial ischemia in a region, it causes ST depressions in the corresponding lead on the ECG.
An ST depression is when the J-point, which is where the QRS complex meets the ST segment, goes down by at least 0.5mm or ½ of a small box.
The ST depression can be upward sloping, downward sloping, or horizontal. In subendocardial ischemia, ST depressions are usually widespread, often affecting leads I, II, and V4-6.
With such widespread involvement, it’s difficult to determine which coronary artery caused the ST-depression. As a side note, if the ST segment is depressed and curved, it may be due to the “digitalis effect” which is when the patient takes the medication digoxin, rather than being due to subendocardial ischemia.
On the other hand, subendocardial infarction occurs if the coronary artery remains blocked for around 20 minutes, and the subendocardial cells begin to die, resulting in necrosis.
And with necrosis, the subendocardial cells leak cardiac enzymes, like troponins and CK-MB, into the blood.
With a subendocardial infarction, there is no ST elevation on the ECG, so this is called a non-ST elevation myocardial infarction, or an NSTEMI for short. Instead, the ECG can show ST depression and T-wave inversion.
Now let’s put these concepts into ECG perspective! On ECG, both unstable angina and NSTEMI’s may show ST-depression as well as T wave inversions.
The difference is that with an NSTEMI, cardiac enzyme levels in the blood are elevated, whereas with unstable angina, the damage resolves in a short time window, so there is no cardiomyocyte death - and therefore no elevated cardiac enzymes.
With an NSTEMI, the ST-depression looks similar to the ones in subendocardial ischemia, and the T wave inversions are usually symmetric and at least 1 mm or 1 little box deep and are most noticeable in the chest leads, but can also appear in the limb leads.
They also have to occur in at least two contiguous leads, For example, lead V2 and V3 are contiguous, but leads V3 and V5 are not contiguous.
There can also be a dominant R wave, meaning that the R wave has a higher amplitude than the S wave. Now, it turns out that a little bit of T wave inversion can be normal in leads III, aVR, and V1, but any sign of T wave inversion in leads V2-V6 is abnormal.
Alright next there’s transmural ischemia. When a coronary artery is narrowed from an atherosclerotic plaque buildup over time, there are two parts to that plaque - a hard fibrous cap and the soft cheese-like interior.