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Ventricular Repolarization in Myocardial Ischemia and Myocardial Infarction:Theory and Practice

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Comprehensive Electrocardiology

1 18.1 Physiologic and Biochemical Processes Responsible for the ElectrocardiographicAlterations During Myocardial Ischemia and Myocardial Infarction

The dominant effects of ischemia during the first few minutes are cellular K+ loss, extracellular K+ accumulation, and acidosis, resulting in rapid depolarization, inexcitability, and loss of active tension development. After a latency period of several minutes, there is a second phase of K+ loss, increase in free cytosolic Ca2 +, electrical cell-to-cell uncoupling, and development of ischemic contracture [1].

Normally, the cell maintains a balance between influx and efflux of K+. The influx occurs mainly through the Na+ ∕ K+ pump that has been assumed to function normally within the first 10–15 min of ischemia [2, 3]. Thus, the increase in extracellular K+ must be attributed to an increased K+ efflux taking place passively as a consequence of the K concentration gradient and through gated K+ channels. One of the suggested causes of K+...

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Notes

  1. 1.

    Current nomenclature; non-ST elevation myocardial infarction (NSTEMI)

  2. 2.

    ∗ ∗Previously known as acute Q-wave MI

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Surawicz, B. (2010). Ventricular Repolarization in Myocardial Ischemia and Myocardial Infarction:Theory and Practice. In: Macfarlane, P.W., van Oosterom, A., Pahlm, O., Kligfield, P., Janse, M., Camm, J. (eds) Comprehensive Electrocardiology. Springer, London. https://doi.org/10.1007/978-1-84882-046-3_18

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