Thiazide-Induced Hypokalemia With Associated Major Ventricular Arrhythmias

Redleaf, Paul D.

doi:10.1001/jama.1968.03150060076022

Cited by 38 publications

(7 citation statements)

References 7 publications

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“…Hypokalemia (serum levels below 3.2 mEq/l) may have profound effects on cardiac impulse formation and conduction, and enhance spontaneous ectopic activity in pacemaker cells (Curry, Fitchett, Stubbs & Krikler, 1976). It has long been known that thiazide diuretics produce hypokalemia (Redleaf & Lerner, 1968), and that this can lead to arrhythmias (Duke, 1978). In the present study, HCT consistently caused significant decreases (P < 0.01) in serum K+, but such alterations were smaller and less frequent with .…”

Section: Discussionmentioning

confidence: 42%

A double‐blind comparison of a novel indanone diuretic (MK‐196) with hydrochlorothiazide in the treatment of essential hypertension.

Ce¹,

Ja²,

Moerlin³

et al. 1979

Brit J Clinical Pharma

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1 The antihypertensive effect and tolerability of MK‐196 (10 mg and 15 mg daily) was compared to hydrochlorothiazide (HCT; 50 mg daily) in a 4‐ week multiclinic, double‐blind study involving 42 patients with mild to moderate, essential hypertension. 2 Both doses of MK‐196 were as effective and sometimes more effective than HCT in lowering standing and supine systolic and diastolic blood pressures. 3 HCT consistently brought about significant increases in serum uric acid and significant decreases in serum potassium; both doses of MK‐196 produced similar but less frequent and smaller changes in both of these parameters. 4 Both doses of MK‐196 brought about significant decreases in body weight at Weeks 3 and 4 of drug treatment. 5 Patients taking MK‐196 reported fewer adverse clinical reactions (10 mg = 15%; 15 mg = 13% than those taking HCT (21%). 6 MK‐196 may offer a therapeutic advantage over HCT as an antihypertensive agent for use in the treatment of mild to moderate, essential hypertension.

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Section: Discussionmentioning

confidence: 42%

A double‐blind comparison of a novel indanone diuretic (MK‐196) with hydrochlorothiazide in the treatment of essential hypertension.

Ce¹,

Ja²,

Moerlin³

et al. 1979

Brit J Clinical Pharma

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“…Redleaf and Lerner (22) stated that half the patients whose serum potassium levels were below 3.6 mEq/L had cardiac ectopic beats or rhythms, the common arrhythmias being atrial premature beats, atrial tachycardia with AV block and occasionally ventricular premature beats. They reported a patient taking 50 mg of hydrochlorothiazide daily, whose serum potassium concentration was 3.4 mEq/L.…”

Section: Thiazidesmentioning

confidence: 69%

“…Control of the situation was obtained with large doses of potassium chloride intravenously (380 mEq in the first thirty‐six hours). Figure 6 [reproduced from Redleaf and Lerner (22)] summarizes the findings in this case.…”

Section: Thiazidesmentioning

confidence: 93%

Management of Hypertension—further Sodium and Potassium Studies

Priddle¹,

Liu²,

Breithaupt³

1970

J American Geriatrics Society

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Since the senior author's first publication forty years ago on the relationship of sodium and potassium to hypertension, these clinical investigations have continued, and in 1958 were established at the Geriatric Study Centre in Toronto. Here, studies were started on the urinary excretion (as an index of intake) of sodium and potassium in subjects with normal blood pressure and in patients with hypertension. Some of the findings are reported in this article, including evidence for the accuracy of the laboratory values, and determination of the normal ranges for serum sodium, serum potassium, serum chloride and blood urea nitrogen in a small group of elderly persons. These studies demonstrated: 1) in persons with normal blood pressure, the urinary excretion (and presumably the intake) of sodium averaged 3.75 gm (9.375 gm NaCl) per day; 2) sodium‐restricted diets, as applied before the study, had been grossly inadequate (excretion 2 gm sodium per day); 3) the study regimen (sodium‐restricted, potassium‐rich intake plus chlorothiazide) had a beneficial effect on hypertension; 4) the potassium supplements induced a sharp rise in the urinary excretion of potassium; and 5) the lack of serious abnormalities in the levels of serum sodium, serum potassium and blood urea nitrogen indicated the safety of this regimen within the limits of this study. The authors have continued to treat hypertension with a sodium‐restricted (400 mg daily) diet, a small dosage (250 mg daily) of chlorothiazide, and potassium (4 gm daily) supplements. The findings on groups of patients treated as long as twelve years are recorded. Hypokalemia as a complication of thiazide therapy is discussed and its potential dangers emphasized. A case of recurrent hypokalemia during a three‐year period is presented to demonstrate certain clinical manifestations and the influence of hypokalemia on the electrocardiogram. The effect of the described therapeutic regimen is also detailed in a case of renovascular hypertension engrafted on essential hypertension, and in a case of hypertension treated by the Smithwick operation. The effect of therapy on morbidity and mortality from hypertension is discussed.

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“…This is consistent with other reports of bretylium's salvage of virtually moribund patients with drug and countershock refractory VF. [142][143][144]170,177,184,185,188,190,192,194,195,[197][198][199][200][201][202] It should be noted that the crossover patients who received bretylium later than 24 hours after admission all developed confirmed infarctions.…”

Section: Crossover Patientsmentioning

confidence: 99%

Prevention of Ventricular Fibrillation, Acute Myocardial Infarction (Myocardial Necrosis), Heart Failure, and Mortality by Bretylium

Bacaner

Brietenbucher²,

LaBree³

2004

American Journal of Therapeutics

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It is widely, but mistakenly, believed that ischemic heart disease (IsHD) and its complications are the sole and direct result of reduced coronary blood flow by obstructive coronary artery disease (CAD). However, cardiac angina, acute myocardial infarction (AMI), and sudden cardiac death (SCD) occur in 15%-20% of patients with anatomically unobstructed and grossly normal coronaries. Moreover, severe obstructive coronary disease often occurs without associated pathologic myocardiopathy or prior symptoms, ie, unexpected sudden death, silent myocardial infarction, or the insidious appearance of congestive heart failure (CHF). The fact that catecholamines explosively augment oxidative metabolism much more than cardiac work is generally underappreciated. Thus, adrenergic actions alone are likely to be more prone to cause cardiac ischemia than reduced coronary blood flow per se. The autonomic etiology of IsHD raises contradictions to the traditional concept of anatomically obstructive CAD as the lone cause of cardiac ischemia and AMI. Actually, all the signs and symptoms of IsHD reflect autonomic nervous system imbalance, particularly adrenergic hyperactivity, which may by itself cause ischemia as in rest angina. Adrenergic activity causing ischemia signals cardiac pain to pain centers via sympathetic efferent pathways and tend to induce arrhythmogenic and necrotizing ischemic actions on the cardiovascular system. This may result in ischemia induced metabolic myocardiopathy not unlike that caused by anatomic or spasmogenic coronary obstruction. The clinical study and review presented herein suggest that adrenergic hyperactivity alone without CAD can be a primary cause of IsHD. Thus, adrenergic heart disease (AdHD), or actually adrenergic cardiovascular heart disease (ACVHD), appears to be a distinct entity, most commonly but not necessarily occurring in parallel with CAD. CAD certainly contributes to vulnerability as well as the progression of IsHD. This vicious cycle, which explains the frequent parallel occurrence of arteriosclerosis and IHD, an association that appears to be linked by the same cause, comprises a common vulnerability to deleterious adrenergic actions on the myocardium, lipid metabolism, and vascular system alike, rather than viewing CAD and IsHD as having a putative cause and effect relationship as commonly thought. Adrenergic actions can also cause the abnormal lipid metabolism that is associated with CAD and IsHD by catecholamine-induced metabolic actions on lipid mobilization by activation of phospholipases. This may also be part of toxic catecholamine hypermetabolic actions by enhancing deleterious cholesterol and lipid actions in damaging coronary vessels by plaque formation as well as inducing obstructive coronary spasm and platelet aggregation. This may also cause direct toxic necrosis on the myocardium as well as atherosclerosis in blood vessels. In fact, drugs that inhibit adrenergic actions like propranolol, reserpine, and guanethidine all inhibit arteriosclerosis induced by hypercholestero...

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Thiazide-Induced Hypokalemia With Associated Major Ventricular Arrhythmias

Cited by 38 publications

References 7 publications

A double‐blind comparison of a novel indanone diuretic (MK‐196) with hydrochlorothiazide in the treatment of essential hypertension.

A double‐blind comparison of a novel indanone diuretic (MK‐196) with hydrochlorothiazide in the treatment of essential hypertension.

Management of Hypertension—further Sodium and Potassium Studies

Prevention of Ventricular Fibrillation, Acute Myocardial Infarction (Myocardial Necrosis), Heart Failure, and Mortality by Bretylium

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