Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “Hyperkalemia”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 19 recordsLinked to original sources
PubMed1976

Electrocardiogram in Hyperkalemia: electrocardiographic pattern of anteroseptal myocardial infarction mimicked by hyperkalemia-induced disturbance of impulse conduction.

In a patient with renal failure and shortness of breath, Q waves transiently appeared in the right precordial leads of the electrocardiogram (ECG) during episodes of hyperkalemia, without a substantial change in mean electrical axis. With restoration of the plasma potassium level to normal, R waves reappeared in these leads. It is concluded that the transient development of Q waves in the right precordial leads during hyperkalemia resulted from a hyperkalemia-induced conduction disturbance. Hyperkalemia, by affecting conduction in Purkinje fibers of ventricular muscle, or both, disturbed the normal sequence of septal and anterior wall depolarization and resulted in an ECG pattern that mimicked that of anteroseptal myocardial infarction. Clinically, hyperkalemia-induced conduction disturbances of this type must be included in the differential diagnosis of the ECG that suggests an anteroseptal myocardial infarction.

Adult↗
PubMed1976

Role of hyperkalemia in the metabolic acidosis of isolated hypoaldosteronism.

We studied the relative importance of hyperkalemia and mineralocorticoid deficiency in the metabolic acidosis of a patient with proved isolated hyporeninemic hypoaldosteronism and moderate kidney failure. The hyperkalemia and acidosis were severe in relation to the slight azotemia. Despite the systemic acidosis and urinary pH of 4.9, urinary ammonium excretion was distinctly blunted. Correction of the hyperkalemia by potassium-sodium exchange resin alone resolved the acidosis and restored the previously diminished urinary ammonium excretion to normal. Administration of mineralocorticoids only partially corrected the hyperkalemia and the acidosis. Hyperkalemia by itself, rather than hypoaldosteronism per se, caused the acidosis in this patient. Hyperkalemia apparently suppresses urinary ammonium excretion and thus interferes with urinary acidification.

Acidosis↗
PubMed1975

Disorders of impulse conduction and impulse formation caused by hyperkalemia in man.

In eight patients we have demonstrated manifold types of impairment of impulse conduction produced by hyperkalemia. These abnormalities of impulse conduction occurred either simultaneously or in sequence, and were located in the atria, in the A-V junction, in the fascicular distribution of the ventricular conduction system, or in the free ventricular walls. In association with the abnormalities of conduction, abnormal impulse formation was also frequently observed as manifested by acceleration of normal pacemakers or the emergence of ectopic pacemakers. In one patient hyperkalemia produced alteration in sinus and A-V junctional impulse formation which overshadowed conduction disorders. In all of the eight cases the hyperkalemia was considered to be noniatrogenic. Hyperkalemia appears to potentiate subclinical conduction abnormalities, especially in the His-Purkinje system. However, the presence of pre-existent intraventricular conduction defects such as a bifascicular block does not exclude the possibility that the site of an A-V conduction delay during hyperkalemia can be in the A-V node, as demonstrated by His bundle recording in one instance after development of second-degree (type I) A-V block.

Adolescent↗
PubMed1979

"Outpatient hyperkalemia" syndrome in renal and hypertensive patients with suppressed aldosterone production.

"Outpatient hyperkalemia" is a new clinical syndrome in which high serum potassium levels (SK) are found in the outpatient condition returning toward normal without any specific treatment after admission to the hospital. We report here of six patients with high blood pressure of various origin (chronic glomerulonephritis, interstitial nephritis, diabetic nephropathy, Gordon syndrome) in whom dietary and postural factors were found to be responsible for the outpatient hyperkalemia. The Na content of the "ad libitum" outpatient diet was definitely higher than that of the regular hospital diet. Increasing the Na intake from 120 mEq to 300 mEq induced a marked elevation of SK (from 5.21 +/- 0.16 to 6.34 +/- 0.40 mEq/l; p less than 0.001) in two hospitalized, recombent patients. On the other hand, Na restriction induced a dramatic improvement in hyperkalemia (from 5.89 +/- 0.11 mEq/l to 4.79 +/- 0.08 mEq/l:; p less than 0.001) in 4 patients in whom the effect was studied in the outpatient state. Although the mean plasma aldosterone (PA) was significantly lower in the patient group than in the healthy group, during normal Na intake there was a considerable overlap. A clearer distintion was made by using the new index of PA per SK ratio expressing the diminution in the apparently normal PA when related to the abnormally high SK. During high Na intake, PA was definitely suppressed and during Na restriction there was a dramatic relief from suppression. The present studies confirmed the previously described phenomenon of "upright hyperkalemia" which may have played an additional role in the development of outpatient elevation of SK. The knowledge of the clinical syndrome of "outpatient hyperkalemia" may be important to single out certain cases of easily correctable insufficient (suppressed) aldosterone production.

Adult↗
PubMed1975

Hyperkalemia complicating splenic irradiation of chronic lymphocytic leukemia.

Hyperkalemia is an infrequent complication of the therapy of malignant disease. In previously reported cases, hyperkalemia following the institution of chemotherapy has been associated with acute renal failure. In this report, we present a patient with chronic lymphocytic leukemia who developed hyperkalemia following splenic irradiation. Necrosis of tumor cells, either as direct or an abscopal effect appears to be implicated as a cause of hyperkalemia. It seems appropriate to monitor potassium levels when therapy of a responsive tumor is instituted.

Enema↗
PubMed1975

Paradoxical glucose-induced hyperkalemia. Combined aldosterone-insulin deficiency.

Severe hyperkalemia associated with spontaneous hyperglycemia as well as with the intravenous infusions of glucose occurred in an insulin-requiring diabetic patient in the absence of potassium administration, the use of diuretics which inhibit urinary potassium excretion or acidemia. Metabolic balance studies revealed, in addition to diabets, the presence of isolated aldosterone deficiency of the hyporeninemic type. Intravenous glucose infusions (0.5 g/kg body weight) produced significant hyperkalemia but desoxycortisone acetate (DOCA) therapy (10 mg/day) prevented the glucose-induced hyperkalemia. In this patient, the serum potassium concentration increases after the intravenous infusions of glucose because there is insufficient aldosterone and insulin to reverse the transfer of potassium to the extracellular fluid which normally occurs after hypertonic infusions of glucose. Although DOCA replacement modifies the distribution of potassium in the extracellular fluid and blunts the hyperkalemic effect of intravenous infusions of glucose, a rise in the insulin level is required for the usual hypokalemic response to intravenously administered glucose. These studies illustrate the risk of raising blood glucose levels in patients with combined aldosterone and insulin deficiency and the tendency towards hyperkalemia in diabetic patients under certain clinical conditions.

Aldosterone↗
PubMed1976

Unusual electrocardiographic finding--bifascicular block due to hyperkalemia.

A unique case in which the patient had bifascicular block consisting of right bundle branch block and left posterior hemiblock as a result of marked hyperkalemia is presented. To our knowledge, this is the first reported case in which such unusual electrocardiographic abnormalities due to hyperkalemia were demonstrated. The electrocardiographic abnormalities produced by hyperkalemia in this case disappeared promptly by hemodialysis, as the serum potassium level returned to normal. It has been stressed that hyperkalemia should be considered as an important etiologic factor in the differential diagnosis of bundle branch block, hemiblocks and bifascicular block, particularly when these intraventricular blocks are produced suddenly.

Bundle-Branch Block↗
PubMed1978

Electrocardiographic changes simulating acute myocardial infarction caused by hyperkalemia: report of a patient with normal coronary arteriograms.

A patient is described with severe diabetic ketoacidosis and hyperkalemia who presented with an ECG resembling an acute anterior wall myocardial infarction. Treatment of hyperkalemia resulted in prompt return of the ECG towards normal. Subsequent work-up including exercise testing and selective coronary arteriography ruled out any significant coronary artery disease suggesting that the ECG changes were probably caused by hyperkalemia. While similar changes have rarely been described in the past, this would appear to be the first such case in whom coronary artery disease was ruled out by a negative exercise testing and coronary arteriography.

Coronary Angiography↗
PubMed1975

Atrioventricular and intraventricular conduction in hyperkalemia.

Twelve patients exhibited electrocardiographic evidence of fascicular block during hyperkalemia. Isolated left posterior hemiblock occurred in four, isolated left anterior hemiblock in two, right bundle branch block with left anterior hemiblock in two, right bundle branch block with left posterior hemiblock in one, left bundle branch block with abnormal left axis deviation in two and advanced atrioventricular block in one. In all seven patients with sinus rhythm the P-R interval shortened after correction of hyperkalemia. Electrophysiologic studies using His bundle recording and atrial pacing in one patient revealed intraatrial conduction delay and marked prolongation of conduction time in the His-Purkinje system. It is concluded that conduction defects in the specialized intraventricular conduction system are common in hyperkalemia and result in electrocardiographic patterns of fascicular block.

Adolescent↗
PubMedDate not supplied

Hyperkalemia: diagnosis and treatment.

We have considered a differential diagnosis of clinical hyperkalemia. The clinical signs and symptoms of patients with hyperkalemia are manifold and can involve many organ systems. The nonoliguric chronic renal failure patient with hyporeninemia and hypoaldosteronemia may have as one of his principal problems recurrent hyperkalemia. Treatment of this condition includes well-known modalities such as administration of calcium salts, NaHCO3, removal of potassium with resin or dialysis as well as placement of a transvenous pacemaker in anticipation of bradyarrhythmias or asystole.

Acidosis↗
PubMed1978

Glucose-induced hyperkalemia with normal aldosterone levels. Studies in a patient with diabetes mellitus.

A diabetic patient exhibited glucose-induced hyperkalemia despite normal plasma and urinary aldosterone levels. The patient received no diuretics, was not acidotic, and had a creatinine clearance of 39 ml/min. Insulin or pharmacologic doses of desoxycorticosterone acetate eliminated the glucose-induced hyperkalemia. Normal aldosterone levels may be insufficient to protect certain diabetic patients from glucose-induced hyperkalemia.

Aged↗
PubMed1978

Life-threatening hyperkalemia induced by arginine.

Marked hyperkalemia was observed during and immediately after an infusion of arginine monohydrochloride in two patients with severe hepatic disease and moderate renal insufficiency. Both patients had received brief courses of spironolactone before arginine treatment. In one of the patients, the hyperkalemia was associated with a fatal cardiac arrhythmia. Arginine has been shown to shift potassium from cells to the extracellular compartment, an effect directly related to its serum concentration. The profound hyperkalemia that occurred in these two patients is thought to be the result of an inability to metabolize the administered arginine and excrete the excess extracellular potassium. Caution is advised in administering arginine to patients with renal or hepatic insufficiency, or both.

Adult↗
PubMed1978

Familial hyperkalemia, hypertension, and hyporeninemia with normal aldosterone levels. A tubular defect in potassium handling.

A 52-year-old man had hypertension, persistent hyperkalemia, and hyperchloremic metabolic acidosis; renal and adrenal functions were normal. Four other members of the family have the same findings. The patient's plasma aldosterone (PA) level was within normal range, though plasma renin activity (PRA) was undetectable. The ability to conserve sodium with increased endogenous aldosterone levels, and the inability to increase potassium excretion while exogenous mineralocorticoid (fludrocortisone acetate) was administered, indicated a distal tubular defect in potassium handling. Effective reduction of the hyperkalemia by K+ -Na+ exchange resin also corrected the acidosis and the hyperchloremia, suggesting that hyperkalemia may cause metabolic acidosis.

Acidosis↗
PubMed1978

Paraplegia: succinylcholine-induced hyperkalemia and cardiac arrest.

The rapid development of hyperkalemia leading to cardiac arrest can occur in patients with spinal cord injuries and other conditions when succinylcholine is used during the induction of anesthesia. Three patients with thoracolumbar spinal cord injuries resulting in lower motor neuron lesions or lesions above the lower extremity motor units developed hyperkalemia followed by cardiac arrest after succinylcholine administration. The mechanism by which succinylcholine leads to hyperkalemia from denervated muscle is described and precautions to be taken are mentioned. Physicians caring for patients with denervated muscle due to spinal cord injuries should be aware of this danger and nondepolarizing muscle relaxants should be used instead of succinylcholine.

Adult↗
PubMed1978

Hyperkalemia after renal transplantation. Occurrence in a patient with insulin-dependent diabetes.

An insulin-dependent diabetic patient received a renal transplant from a living related donor without evidence of rejection. In the posttransplant period, his serum potassium concentration (3.7 to 6.7 mEq/liter) fluctuated widely with the serum glucose concentration (165 to 470 mg/dl) during the day. Serum glucose and potassium concentrations were directly correlated (r = .734, P less than .001). Other factors controlling the serum potassium concentration were examined. Plasma and urinary aldosterone levels were normal, plasma renin activity and aldosterone levels rose during upright activity, and urinary potassium excretion increased with the administration of exogenous mineralocorticoid. Thus, mineralocorticoid secretion and responsiveness were intact. These observations indicate that hyperkalemia in a diabetic patient can occur in the absence of a defect in potassium excretion and are consistent with the interpretation that insulinopenia, as evidenced by hyperglycemia, can result in hyperkalemia due to diminshed translocation of both potassium and glucose from the extracellular to the intracellular compartment.

Adult↗
PubMedDate not supplied

Glucose-induced paradoxical hyperkalemia in patients with suppression of the renin-aldosterone system: prevention by sodium depletion.

A paradoxical transitory elevation of serum potassium concentration after intravenous infusion of hypertonic glucose has been found in 6 renal and/or hypertensive patients with suppression of the renin-aldosterone system (RAS) while on high sodium intake. Sodium restriction induced a dramatic increase in plasma renin activity (PRA) and/or plasma aldosterone (PA) in every patient, a substantial fall in the elevated serum potassium levels in 4 out of the 6 patients and a marked increase in fractional potassium excretion. During sodium restriction the glucose-induced paradoxical transitory hyperkalemia was abolished. The study confirmed the important extrarenal influence of aldosterone in the maintenance of normal potassium level in the hyperosmolal extracellular fluid and showed that: i) high sodium intake may predispose to hazardous hyperkalemia after massive glucose loading in certain nondiabetic patients with liability to suppression of aldosterone; ii) sodium restriction abolishes the glucose-induced abnormal serum potassium response.

Adolescent↗
PubMed1975

Evidence for specialized atrioventricular conduction in hyperkalemia.

A patient who had chronic coarse atrial fibrillation developed severe hyperkalemia accompanied by total loss of fibrillatory waves while an irregularly irregular ventricular rhythm persisted. Correction of hyperkalemia resulted in prompt return of coarse atrial fibrillation. This sequence of events renders strong support to direct atrioventricular conduction through the specialized internodal tracts.

Aged↗