Distance from the Major Coronary Arteries

The ventricles consist of multiple myocardial layers that depend on the coronary arteries for their blood supply. These arteries arise from the aorta and course along the epicardial surfaces before penetrating the thickness of the myocardium. They then pass sequentially through the epicardial, middle, and subendocardial layers (Fig. 9.2). The subendocardial layer is the most distant, innermost layer of the myocardium and is subjected to the highest myocardial wall tension, resulting in greater oxygen needs.⁷ Thus, it is the most susceptible to ischemia.⁸ The thicker walled left ventricle is much more susceptible to insufficient perfusion than is the thinner walled right ventricle because of both the wall thickness itself and the greater workload of the left ventricle.

Workload as Determined by the Pressure Required to Pump Blood

The greater the pressure required by a cardiac chamber to pump blood, the greater its workload and the greater its metabolic demand for oxygen. The myocardial workload is smallest in the atria, intermediate in the right ventricle, and greatest in the left ventricle. Therefore, the susceptibility to ischemia is also lowest in the atria, intermediate in the right ventricle, and greatest in the left ventricle.

Ischemia is a relative condition that depends on the balance among the coronary blood supply, the level of oxygenation of the blood, and the myocardial workload. Theoretically, an individual with normal coronary arteries and fully oxygenated blood could develop myocardial ischemia if the workload were increased either by an extremely elevated arterial blood pressure or an extremely high heart rate. Alternatively, an individual with normal coronary arteries and a normal myocardial workload could develop ischemia if the oxygenation of the blood became extremely diminished. Conversely, the myocardium of someone with severe narrowing (stenoses) in all coronary arteries might never become ischemic if the cardiac workload remained low and the blood was well oxygenated.

When ischemia is produced by an increased workload, it is normally reversed by returning to the resting state before the myocardial cells’ reserve supply of glycogen is entirely depleted. However, a condition that produces myocardial ischemia by decreasing the coronary blood supply may not be reversed so easily.

Coronary arteries may gradually become partly obstructed by plaques in the chronic process of atherosclerosis (Fig. 9.3). This condition produces ischemia when, even though the myocardial blood supply is sufficient at a resting workload, it becomes insufficient when the workload is increased by either emotional or physical stress. The gradual progression of the atherosclerotic process is accompanied by growth of collateral arteries, which supply blood to the myocardium beyond the level of obstruction. Indeed, these collateral arteries may be sufficient to entirely replace the blood-supplying capacity of the native artery if it becomes completely obstructed by the atherosclerotic plaque.⁹

Partially obstructed atherosclerotic coronary arteries may suddenly become completely obstructed by the acute processes of spasm of their smooth-muscle layer or thrombosis within the remaining arterial lumen.^10,11 In either of these conditions, ischemia develops immediately unless the resting metabolic demands of the affected myocardial cells can be satisfied by the collateral blood flow. If the spasm is relaxed or the thrombus is resolved (thrombolysis) before the glycogen reserve of the affected cells is severely depleted, the cells promptly resume their contraction. However, if the acute, complete obstruction continues until the myocardial cells’ glycogen is severely depleted, they become stunned.¹² Even after blood flow is restored, these cells are unable to resume contraction until they have repleted their glycogen reserves. If the complete obstruction further persists until the myocardial cells’ glycogen is entirely depleted, the cells are unable to sustain themselves, are irreversibly damaged, and become necrotic. This clinical process is termed a heart attack or myocardial infarction (MI).

ELECTROCARDIOGRAPHIC CHANGES

Electrophysiologic Changes during Ischemia

Knowledge of the action potential changes that occur during ischemia and the location of ischemia allows one to understand what ECG changes will occur during ischemia. This will be illustrated with the use of the interactive ECG simulation program, ECGSIM.¹³ With the onset of ischemia, there are three principle changes that occur to the action potential:

Experimental and simulation studies have shown that changes in extracellular potassium and pH, along with opening of ATP-dependent potassium channels (K_ATP), can account for the AP changes that occur in acute ischemia.

Electrocardiographic Changes during Supply Ischemia (Insufficient Blood Supply)

Figure 9.4 and its accompanying Video 9.1

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