The Electrocardiographic Pattern of Hypopotassemia with and without Hypocalcemia

Surawicz, Borys; Lepeschkin, E.

doi:10.1161/01.cir.8.6.801

Cited by 109 publications

(17 citation statements)

References 6 publications

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“…All these factors may have played a role in the development of hypokalemia in our patients. Arrhythmias, including ventricular extrasystoles and ventricular bigeminy, have been consistently observed by Surawicz and Lepeschkin [16] when the potassium values are below 2.6 meq./l, and disappear after administration of potassium. Weaver and liurcheU found extrasystoles with a potassium below 3.6 meq./l in 24% of normotensive and in 30% of hypertensive pa tients [18].…”

Section: Discussionmentioning

confidence: 59%

Ectopic Ventricular Tachycardia, Hypokalemia and Convulsions in Alcoholics

Scherf¹,

Cohen²,

Shafiiha³

1967

Cardiology

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Section: Discussionmentioning

confidence: 59%

Ectopic Ventricular Tachycardia, Hypokalemia and Convulsions in Alcoholics

Scherf¹,

Cohen²,

Shafiiha³

1967

Cardiology

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“…14 In 1953, Surawicz and Lepeschkin described a series of patients with hypokalemia and frequent junctional and ventricular premature beats; in all cases the arrhythmias disappeared with administration of potassium. 15 Gettes et al used a microelectrode technique to show that perfusion of low potassium solutions resulted in ventricular ectopic beats, ventricular tachycardia, and ventricular fibrillation. 16 Several clinical studies have demonstrated that an increased incidence of ventricular arrhythmias is associated with the hypokalemia induced by diuretic therapy.…”

Section: Discussionmentioning

confidence: 99%

Torsade de Pointes With a Normal QT Interval Associated With Hypokalemia

et al. 2001

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olymorphic ventricular tachycardia (PVT) and ventricular fibrillation (VF) are rare but malignant arrhythmias, which are usually associated with long QT syndrome, cardiomyopathy and ischemic heart disease. However, PVT/VF without clinical evidence of heart disease has been reported.We report a case of PVT initiated by short-coupled premature ventricular complex (PVC) that was related to hypokalemia. Case ReportA 46-year-old man had experienced syncope attack after diarrhea, and when he was admitted to a local hospital, nonsustained polymorphic ventricular tachycardia (PVT) initiated by short-coupled PVC was detected (Fig 1). Subsequently, the nonsustained PVT was detected 97 times (max 11 beats) during the day by Holter monitoring, and the patient experienced several episodes of faintness. The QT interval preceding the PVT was normal, and the coupling interval of the preceding PVC was short (300 ms). According to the Holter monitoring, the QRS morphology of the initiating PVC was the same and always a left bundle branch block pattern with a superior axis. The patient was treated with oral disopyramide at the local hospital and was referred to us. On admission, the results of physical examination, blood chemistry and chest X-ray were normal, and the serum potassium concentration was 4.0 mmol/L. There Japanese Circulation Journal Vol.65, August 2001 was no family history of syncope attack or sudden death. A 12-lead ECG during sinus rhythm showed no ST segment change and a normal QT interval (Fig 1). The results of 2-dimensional echocardiography, coronary angiography, left and right ventriculograms, and endomyocardial biopsy were all normal. Electrophysiologic FindingsAfter obtaining informed consent, electrophysiologic studies were performed in a fasting state according to a protocol approved by the institutional human research committee. All antiarrhythmic drugs were discontinued for a period of 48 h. Considering the circumstances of the syncope attack, we suspected that PVT was related to hypokalemia and therefore performed the electrophysiologic studies under 3 different conditions: artificial hypokalemia, after potassium loading, and after oral amiodarone therapy.Three quadripolar electrode catheters (7Fr), with a distance of 2-5 mm between electrodes, were each inserted percutaneously and positioned in the right atrial appendage, in the region of the His bundle, and in the right ventricular (RV) apex. A decapolar 6Fr catheter was placed in the coronary sinus through the right jugular vein. We also recorded the monophasic action potential (MAP) using a 7Fr Franz catheter at filter bandpass settings between 0.5 and 400 Hz, and we calculated the MAP duration at 90% repolarization (MAPD90). Programmed electrical stimulation was performed up to double ventricular extrastimuli at 2 basic cycle lengths (500 and 400 ms) at 3 ventricular sites (RV apex, RV outflow tract and left ventricular posterior) under the condition of artificial hypokalemia and after potassium loading. All stimulation was performed with a con...

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“…The same sequence was observed recently in rabbit hearts perfused with a low potassium solution.25 On the other hand, potassium decreases the U waves and the afterpotentials, and suppresses all coupled extrasystoles. 23 In acidosis, which is known to elevate the U waves, a supernormal phase was found to appear in the mammalian heart, and this was accompanied by the appearance of ventricular extrasystoles with coupling intervals corresponding to the duration of this phase. 19 Slowing of the heart rate, which tends to elevate the U waves, also favors the appearance of coupled rhythms; we have seen this event in many cases of atrial fibrillation treated with digitalis, where coupled extrasystoles were precipitated only by ventricular complexes appearing after long pauses.…”

Section: Discussionmentioning

confidence: 99%