A Clinical Correlative Study of the Electrocardiogram in Electrolyte Imbalance

Abstract

There is no general agreement concerning the action of specific electrolyte disorders and acid-base balance upon concentrations by determining their intracellular/extracellular relationships. Crismon and associates8 could not relate the intracellular potassium concentration to typical electrocardiographic events in hyperkalemia. Bellet, too, could not establish a definite relationship of the electrocardiographic changes to skeletal muscle potassium content.9 He considered, among other possibilities, that differences in the metabolic activity of heart and skeletal muscle were the cause of this lack of correlation. His comparison of intracellular to extracellular potassium concentrations with the electrocardiogram gave no better results than serum potassium concentration alone. Ktihns,10 on the other hand, noted such a relationship in animal experiments. In relating intracellular/extracellular potassium concentrations he used a value termed "cardiac potassium quotient" with a normal range of 25 to 32. Reduction of this quotient was associated with typical hyperkalemic changes, and elevation with typical hypokalemic changes in the electrocardiogram. There was, however, no consistency between the electrocardiographic alterations and absolute potassium or sodium concentrations, intracellular or extracellular. Changes in the autonomic nerve tone and pharmacologic actions of epinephrine, insulin, veratrine, and in particular quinidine, have been noted to simulate electrocardiographic patterns of hypokalemia.9 [11][12][13] It is also well known that pre-existent or concomitant alterations of the ST-T segment caused by heart Circulation, Volume XIV, November 1956 by guest on May 9, 2018 http://circ.ahajournals.org/ Downloaded from

Prediction of Hyperkalemia in Dogs from Electrocardiographic Parameters Using an Artificial Neural Network

“…The Heart rate P width P-R segment (end P to beginning QRS) T-syst (interval from R peak to end T) Diaz (interval from beginning P to end T) S-T interval specificity was 85% for potassium > 5 mmol/L. These results are similar to those reported in the mid-1950s by Dreifus and Pick, 3 who found a 54% sensitivity for one clinician in recognition of hyperkalemia from the ECG. Clearly, even the highest reported sensitivity among those studies (58.5%) is unacceptable for detecting a potentially lethal condition.…”

Effects of Presentation and Electrocardiogram on Time to Treatment of Hyperkalemia

“…11 It is now known that at the tissue level, hyperkalemia reduces myocardial conduction velocity and accelerates the repolarization phase, producing well-described changes on the surface electrocardiogram (ECG), including a narrow, symmetrical T wave, prolonged PR interval, diminished P-wave amplitude, QRS widening, and ultimately a sinusoidal ''QRST'' that terminates in asystole or ventricular fibrillation. [12][13][14][15][16][17] Other ECG changes that have been associated with hyperkalemia include conduction blocks (fascicular block, bundle branch block, seconddegree heart block, and complete heart block) and block of bypass tracts with loss of the delta wave in patients with Wolff-Parkinson-White syndrome. [18][19][20] Although few maneuvers are necessary for the initial management of hyperkalemia, prior studies in hospitalized patients have shown an average delay of 2.1 hours after laboratory notification before initiation of treatment for severe hyperkalemia.…”

Predicting hyperkalemia by a two-staged artificial neural network

“…For examples, peaked T waves and widen T waves could be observed in some chest leads during mild hyperkalemia, and flatten P waves in some limb and chest leads. Other vulnerable variable such as increased PR interval, QRS interval, and RR interval could be seen during mild to severe hyperkalemia [2,3]. However, the choice of exact features in response to hyperkalemia is difficult because of the variability of features.…”