Dialyzable Currents of Injury in Potassium Intoxication Resembling Acute Myocardial Infarction or Pericarditis

Abstract

A byproduct of experience with the artificial kidney was the detection of reversible electrocardiographic "currents of injury" in patients with electrolyte imbalance. These changes occurred irrespective of anatomic alterations and resembled the changes of acute pericarditis or myocardial infarction. The electrolyte basis for the "current of injury" was established by the prompt abolition of the RS-T segment elevations, when the electrolyte imbalance was corrected by means of artificial hemodialysis.AREGULAR electrocardiographic feature of moderately advanced potassium intoxication is depression of the RS-T segments. The erroneous inference of myocardial infarction is generally avoided because of the direction of the RS-T shifts, the clinical setting in which this phenomenon is recorded and its association with other electrocardiographic abnormalities distinctive of potassium intoxication. In a few exceptional instances of potassium intoxication, however, elevation rather than depression of the RS-T segments may be produced. toxication. He gave no history of chest pain or compression. On examination the heart rate was 150, the cervical veins were distended, coarse bubbling rales were heard throughout the lung fields, a gallop rhythm was heard at the cardiac apex and the liver edge was felt two fingerbreadths below the right costal margin. Tracings recorded on the afternoon of admission showed sinus tachycardia ( fig. 1 B), with left bundle branch block. The RS-T segments in leads V,, V2 and lead aVR showed rather pronounced elevation, probably more than could be accounted for purely on the basis of left bundle branch block. Later in the afternoon the heart rate was 108 and the cardiac rhythm irregular and disturbed by runs of probable paroxysmal ventricular tachycardia. Over the right precordium the RS-T segment elevation was now more pronounced and associated with deep broad Q waves ( fig. 1 C). The persistence of these changes was regarded as strong evidence for a "current of injury" and, it was believed, could not be attributed to left bundle branch block. At 6:40 p.m. hemodialysis was begun. At this time the serum potassium level was 7.8 mEq. per liter, sodium 127 mEq. per liter and the carbon dioxide content 9 mM per liter. Because the patient had marked pulmonary edema, the concentration of sodium in the bath fluid of the artificial kidney was maintained at 127 in order to avoid sodium loading in the presence of heart failure. The bath potassium concentration was initially set at 2 mEq. per liter but following the development of arrhythmia, was raised to 5. Two hours after the beginning of dialysis when the serum potassium level had fallen to 2.6 mEq. per liter and the sodium level had remained at 128 mEq. per liter, the electrocardiogram showed striking improvement. A supraventricular tachycardia (ventricular rate 210) had developed, the QRS complex had sharpened and shortened and the RS-T segment shifts over the right ventricle had almost disappeared ( fig. 1 D). Though the patient improved temporarily af...

Heat Stroke

“…Hyperkalemia has been implicated as a cause of ST-segment elevation and may precipitate these symptoms in classic heat stroke patients (217). Hypokalemia may be a consequence of overproduction of aldosterone, excessive sweating, or respiratory alkalosis resulting in polyuria and increased urinary potassium loss (360,393).…”

Severe Hypercalcemia Mimicking ST-Segment Elevation Myocardial Infarction

“…2,3 Additionally, approximately 3% of patients with suspected STEMI are found to have angiographically normal coronary arteries. 4 Electrolyte abnormalities including hyperkalemia [5][6][7] and hypercalcemia [7][8][9][10][11] may present with STsegment elevation and a pseudo-infarction pattern on the electrocardiogram (ECG). In patients presenting with suspected STEMI, the decision to proceed with invasive angiography must often be made before laboratory results are available.…”

Adrenergic-mediated exposure of hyperkalemia in the electrocardiogram

“…According to the former, the transmural APD differences mostly reflect the heterogeneity in I Ks expression: epicardial and endocardial cells have a larger I Ks density than M cells; in fact, removing intrinsic I Ks disparity alters the repolarization sequence, such that it follows the activation sequence; when, as in the case under discussion, EPI is given, I Ks is activated in such a way that its expression is increased and redistributed in the myocardial layers allowing a ''concordant'' repolarization, irrespective of the hypertrophy present. This redistribution in the I Ks expression also explain the ST-segment elevation observed (and reported almost fifty years ago as a ''dialyzable''current of injury) [10]; in fact, the AP plateau is maintained by a delicate balance between inward/outward ionic currents; diverse combination involving these ionic currents may shift the ST-segment (as in acute injury lesions, manifest or drugaccentuated Brugada syndrome. .…”