Potassium homoeostasis in the heart was studied during atrial pacing in 20 patients undergoing diagnostic coronary angiography. The potassium concentrations in the coronary sinus and a systemic artery were recorded continuously by means of catheter tip potassium electrodes. Ten patients with coronary artery disease and a positive exercise test developed chest pain and ST segment depression on the electrocardiogram during atrial pacing. Potassium concentrations in the coronary sinus rose initially and increased further when myocardial ischaemia developed. Ten patients including five with normal coronary arteries remained symptom free during atrial pacing with no electrocardiographic changes. In these patients coronary sinus potassium concentration increased at the onset of pacing, but returned to near control values despite continued pacing. In both groups arterial potassium concentration remained constant. Immediately after the end of pacing there was an abrupt transient fall in potassium concentrations in the coronary sinus to below control values. These results indicate that in man, as in other species, an increase in heart rate causes the transient movement of potassium out of the cell into the extracellular space. The onset of myocardial ischaemia is associated with a further loss of potassium from the cell. The end of pacing or ischaemia is accompanied by a re-uptake of potassium by heart muscle.
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