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Tex Heart Inst J. 1994;21(1):30-41.

Anatomy of the action potential in the heart.

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Department of Medicine, University of Texas Health Science Center at Houston 77030.


The surface electrocardiogram can be simply described as the P, QRS, and T (and U) waves, together with PR and ST segments. However, it is actually the summation of the action potential from the sinoatrial node, the atria, the atrioventricular node, the His-Purkinje system, and the ventricles. Although the action potential can be divided grossly into 5 phases, its characteristics vary in different cardiac tissue. This is because the action potential is the end-result of multiple ion channels, pumps, and exchangers opening and closing in concert, and the properties and distribution of these components can be different from one tissue to another. The ion channels can be activated by changes in the membrane voltage and specific ligands, and can be modulated by factors such as neurotransmitters (e.g., through the G-protein system), the G-proteins directly, or other ions. Only in the last 10 years have investigators been able to use molecular biology techniques to peek into the primary structure of ion channels and to develop more workable models of the channel functions. The primary structure and the putative secondary structure of the ion channels show resemblance among the groups, suggesting that, except for IsK, the development of ion channels started with IK1 and IK(ACh), followed by Ito and IK, and then by INa and ICa. However, limitations still exist in our knowledge of the ion channels and hence of the action potential. This is demonstrated by the lack of effective pharmacologic treatment of cardiac arrhythmias to this date. It is to be hoped that advances in cell electrophysiology, genetic engineering, and molecular imaging techniques will soon end the dark days of antiarrhythmic therapy.

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