The ECG is a key tool for diagnosing myocar-dial ischemia and infarction. When the heart becomes ischemic (i.e., when oxygen delivery is inadequate relative to oxygen demand), electrophysiological changes occur that can alter both rhythm and conduction. The ECG can identify the extent, location, and progress of damage to the heart following ischemic injury. This assessment is made by evaluating changes in the electrical activity of the heart by using the 12-lead ECG recording. For example, altered conduction can result in exaggerated Q waves in specific leads following some types of myocardial infarction. Ischemia can also damage conduction pathways, leading to arrhythmias or changes in the shape of the QRS complex. Furthermore, ischemia can produce injury currents flowing from the depolarized ischemic regions to normal regions that can shift the isoelectric portions of the ECG, resulting in upward or downward shifts in the ST segment. The mechanisms by which ischemia and infarction alter the ECG are complex and not fully understood. We do know, however, that tissue hypoxia caused by ischemia results in membrane depolarization. As ATP levels decline during hypoxia, there is a net loss of K+ as it leaks out of cells through Katp channels (normally inhibited by ATP) and as a result of decreased activity of the Na+/K+-ATPase pump. Increased extracellular K+, coupled with decreased intracellular K+, causes membrane depolarization. This depolarization inactivates fast sodium channels as previously described, thereby decreasing action potential upstroke velocity. One result is decreased conduction velocity. Changes in refractory period and conduction velocity can lead to reentry currents and tachycardia. Membrane depolarization also alters pacemaker activity and can cause latent pacemak
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