EKG - Ischemia
I suspect most physicians do not truly understand EKGs. And for the purposes of taking care of patients, you don’t need to understand them. But I find not knowing why ST segments are elevated vs depressed to be intolerable and confines me to rote memorization.
The first thing to know about the normal heart is that the myocyte action potential is opposite from what is happening to the extracellular fluid, which is picked up by the EKG. When a myocyte depolarizes, the intracellular membrane is + and the extracellular space is – . If a wave of depolarization travels towards a lead, it is essentially a wave of extracellular negative charges moving toward a positive electrode, manifesting as a positive deflection.
Normally, myocytes depolarizes from endocardium to epicardium but repolarizes in reverse, from epicardium to endocardium. The EKG shows the net charge difference between different regions of the heart. Using V3 as an example, most of the difference results from endocardium vs epicardium.
Ischemia impairs the ability for myocytes to generate ATP. Repolarization phase is the most sensitive to this effect because it is dependent on NA-K ATPase to restore the membrane’s electrochemical gradient. The heart has multiple layers which display patterns of injury depending on the site of pathology.
The endocardium is less dependent on the epicardial vessels because of it has multiple anastomoses and feeds through diffusion of oxygen and nutrients from the ventricular lumen. However, the endocardium is very sensitive to demand mismatches, especially in the context of existing stenosis, because the inner most portion of the heart also squeezes the tightest. When intramural wall pressure increases, it is akin to squeezing your hand until it turns white – there is no nutrient delivery. The first phase of injury is delayed repolarization of the endocardium, which causes a large, fat Tw. This is the pathophysiology of the hyperacute Tw or pseudonormalization. The second phase of injury is incomplete return to resting membrane potential, which causes TP elevation and the illusion of ST depression. This is also why ST depressions are very inaccurate at localizing or predicting critical coronary occlusion – the endocardium is less dependent on the epicardial vessels.
The epicardium is very dependent on the epicardial vessel. With coronary vessel occlusion, the epicardial repolarization phase is prolonged resulting in prolonged QTc but also biphasic Tw or TWI. Prolonged occlusion causes incomplete return to resting membrane potential with TP segment depression and the illusion of ST elevation. It is important to appreciate how fickle these EKG changes can be. Spontaneous reperfusion or decreasing demand on the heart can reverse the process, changing ST elevation to biphasic Tw or TWI. This is the pathophysiology of Wellen’s Tw which frequently occur in the absence of chest pain.
The final phase of epicardial occlusion is the inability for the myocyte in the the epicardium and most of the subendocardium to depolarize at all. When this happens, that aspect of the heart becomes electrically silent. The adjacent EKG lead then peeks past this region to the opposite side of the heart where everything happens in reverse. The morphology during ischemia is constantly evolving and can assume a wide range of intermediary shapes depending on duration of occlusion and reperfusion.