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Potassium during myocardial ischemia

Dofetilide blocks IKr in all myocardial tissues. It blocks open channels, and its binding and release from the channels is voltage dependent. The effects of dofetilide are exaggerated when the extracellular potassium concentration is reduced, which is important, as many patients may be receiving diuretics concurrently. Conversely, hyperkalemia decreases the effects of dofetilide, which may limit its efficacy when local hyperkalemia occurs, such as during myocardial ischemia. Dofetilide demonstrates reverse use dependence, that is, less influence on the action potential at faster heart... [Pg.189]

Coronel R Distribution of Extracellular Potassium during Acute Myocardial Ischemia thesis, Amsterdam,... [Pg.124]

There are a variety of conditions that can increase the myocardial capture threshold. These include metabolic derangements, medications, and traumatic events such as inadvertent conduction of current down the lead during direct current cardioversion or defibrillation that results in tissue injury at the lead-tissue interface. Metabolic disturbances that increase the myocardial capture threshold include myocardial ischemia and infarction, hyperkalemia, hypoxemia, hypercarbia, acidemia, alkalemia, hyperglycemia, and hypothyroidism (59-62). Hyperkalemia is the most common electrolyte abnormality that can leads to failure to capture (Fig. 16.7), and the threshold typically increases when the serum potassium concentration exceeds 7.0mEq/L (63-65). Increasing the stimulus output is only variably successful and should not be relied on. Inunediate reversal of hyperkalemia should be the first priority. [Pg.578]


See other pages where Potassium during myocardial ischemia is mentioned: [Pg.166]    [Pg.487]    [Pg.1807]    [Pg.16]    [Pg.24]    [Pg.85]    [Pg.178]   
See also in sourсe #XX -- [ Pg.3 , Pg.162 ]




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Myocardial ischemia

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