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• W1565666890 abstract "There are numerous toxins and drugs that can cause, in overdose, electrocardiogram (ECG) changes, even in patients without history of cardiac pathology. The diagnosis and management of patients with an abnormal ECG encountered in a specific toxicity can challenge experienced physicians. One must have serious knowledge of basic cardiac physiology, in order to understand the ECG changes associated with various drugs and toxins. The main mechanisms involved include membrane – depressant action (sodium channel blockers, slow calcium channel blockers, outward potassium (K+) channel blockers, and sodium-potassium adenosine-triphosphatase blockers), and action on autonomic nervous system and its sites of cardiovascular action (beta-adrenergic blockers and other sympathetic-inhibitors, sympathomimetic, anticholinergic and cholinomimetic substances). Many toxins and medications have actions that involve more than one of these mechanisms, including hypoxia, electrolyte and metabolic imbalances, and thus may result in a combination of electrocardiographic changes. In resting state, the myocardial cell membrane is impermeable to positively charged sodium ions (Na+). The Na+/K+ ATPase maintains a negative electric potential of approximately 90 mV in the myocyte. The rapid opening of Na+ channels and massive Na+ influx (phase 0 of action potential) explains depolarization of the cardiac cell membrane (fig.1), causing the rapid upstroke of the cardiac action potential, which is conducted through the ventricles and is expressed as the QRS complex of the ECG. The closure of Na+ channels and the transient opening of Ito K+ efflux channels (phase 1) mark the peak of the action potential. Then, phase 2 of the action potential occurs when the opening of slow calcium (Ca2+) channels produces an influx of positive ions with a steady maintenance of the membrane potential and myocardial contraction continues. The end of the cardiac cycle is marked by the closure of the Ca2+ channels and the activation of the K+ efflux channels, which allow the action potential to return to its resting potential of – 90 mV (phase 3). This K+ efflux from the myocardial cell is directly responsible for the QT interval on the ECG (Holstege et al., 2006). During phase 4 of the cardiac cell action potential, some cardiac fibers allow sodium ions to enter the cell, increasing the resting membrane potential, known as spontaneous diastolic depolarization. When the threshold in membrane potential is reached, the Na+ channels open and another action potential is generated." @default.
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• W1565666890 date "2012-01-25" @default.
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• W1565666890 title "Toxic and Drug-Induced Changes of the Electrocardiogram" @default.
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• W1565666890 doi "https://doi.org/10.5772/22891" @default.
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