Dynamics of potassium flux in cardiac arrhythmias

Lang, Tzu-Wang; Corday, Eliot; Lozano, J; Carrasco, Hugo; Meerbaum, Samuel

doi:10.1016/0002-9149(72)90630-3

Cited by 6 publications

(1 citation statement)

References 42 publications

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“…Ischemic myocardium extrudes potassium, causing hypopolarization and reducing the arrhythmic threshold (29 -31). Ventricular arrhythmia aggravates the hypopolarization and further lowers the arrhythmic threshold (32).…”

Section: Atherosclerosismentioning

confidence: 99%

What is the optimal serum potassium level in cardiovascular patients?

MacDonald

Struthers

2004

Journal of the American College of Cardiology

285

224

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Humans are prone to sodium overload and potassium depletion. This electrolyte imbalance is important in the pathogenesis of cardiovascular disease and sudden cardiac death. Avoiding hypokalemia is beneficial in several cardiovascular disease states including acute myocardial infarction, heart failure, and hypertension. The evidence highlighting the importance of potassium homeostasis in cardiovascular disease and possible mechanisms explaining potassium's benefits are reviewed. Targets for serum potassium concentration are suggested.

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Section: Atherosclerosismentioning

confidence: 99%

What is the optimal serum potassium level in cardiovascular patients?

MacDonald

Struthers

2004

Journal of the American College of Cardiology

285

224

View full text Add to dashboard Cite

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Tierexperimentelle Untersuchungen zur Frage einer kaliumabhängigen Modifikation der Lidocainwirkung

1976

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Lidocaine was supplied to 10 cats by 2 comparative infusions of 7.5 mg/kg respectively. Once the drug was dissolved in a physiological and the other time in a K-Mg-concentrated electrolyte solution. The sequence of both infusions alternated. Serum potassium remained constant during infusion of the physiological electrolyte solution, but increased by about 1 mEqu/1 under K-concentrated solution. Lidocaine caused an enhancement of ventricular fibrillation threshold to an absolutely identical degree in both groups. Increase in cardiac output and stroke volume and decrease of sinus rate was significant in both groups, but more pronounced under K-Mg concentrated solution. Mean arterial pressure, peripheral vascular resistance, PQ, QRS, and QT interval remained constant on the whole. We deduce from these results for antiarrhythmic therapy on normokalemic patients, that the addition of potassium and magnesium to lidocaine solution does not enhance its antifibrillatory effect. This statement is valid for doses up to 20 mEqu/h of magnesium and 40 mEqu/h of potassium.

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