Hyperkalemia, cardiac conduction, and the electrocardiogram: A review
| Autor: | Philip O. Ettinger, Henry A. Oldewurtel, Timothy J. Regan |
|---|---|
| Rok vydání: | 1974 |
| Předmět: |
Pacemaker
Artificial medicine.medical_specialty Hyperkalemia medicine.medical_treatment Action Potentials Blood Pressure Antiarrhythmic agent Electrocardiography QRS complex Dogs Heart Conduction System Heart Rate Coronary Circulation T wave Internal medicine Cardiac conduction medicine Animals Humans cardiovascular diseases Asystole Fibrillation medicine.diagnostic_test business.industry Arrhythmias Cardiac medicine.disease Heart Block Anesthesia Potassium cardiovascular system Cardiology Polystyrenes medicine.symptom Cardiology and Cardiovascular Medicine business |
| Zdroj: | American Heart Journal. 88:360-371 |
| ISSN: | 0002-8703 |
| Popis: | Increased plasma potassium may occur spontaneously or iatrogenically. At modest hyperkalemia (K + ∼5 to 7 mEq. per liter) a transient and minor acceleration of cardiac conduction can be demonstrated, but profound and rapid depression of conduction occurs progressively at K > 8 to 9 mEq. per liter. Examination of the peripheral ECG reveals inconstant "peaking" of T waves during modest elevation. As K + rises, however, PR prolongs and P ultimately disappears; QRS widens and R-R intervals become irregular. "Sinoventricular" conduction may be observed at this stage. Later sequential changes include atrioventricular junctional delay, followed by acceleration of junctional pacemakers, conduction delays in the His-Purkinje system, and delays in ventricular muscle. As K + rises in animals, asystole is the predominant mechanism of cardiac arrest. His bundle and bundle branch recordings indicate that asystole typically arises from block within the distal conducting system. The resultant peripheral ECG shows regular or irregular rhythm with widened QRS; although the morphology of the QRS may suggest that the arrhythmias are of ventricular origin, animal experiments almost invariably identify the rhythms as junctional or sinus. In man, the effects of K + upon the ECG are greatly modified by other electrolyte disturbances, especially hyponatremia and hypocalcemia. A-V block is not often observed (? recognized) in man. Ventricular pacing threshold may initially decrease (increased excitability) but profound subsequent increases occur as K + rises further. In the experimental animal, potassium and sodium ion concentrations increase uniformly across the myocardial wall. Ventricular pressure and dpdt max tend to fall only after marked QRS prolongation causes the ventricle to contract asynchronously. While K + has been administered as an antiarrhythmic agent, its use involves potential hazards, especially during the simultaneous use of digitalis. It should probably not be used for this purpose except, perhaps, in digitalis-induced paroxysmal atrial tachycardia with block. Although slow systemic increase of K + induces asystole in animals, administration to a region of myocardium produces ventricular ectopic beats and fibrillation. The latter effect may be due to re-entry and may be mechanistically similar to the arrhythmias of early ischemia. |
| Databáze: | OpenAIRE |
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