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Results for “Hyperkalemia”

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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↗

PubMed1991

The ability of physicians to predict hyperkalemia from the ECG.

STUDY OBJECTIVE: To determine whether physicians blinded to the serum potassium level can predict hyperkalemia (potassium concentration of more than 5.0 mmol/L) from the ECG. DESIGN: ECGs of patients at high risk for hyperkalemia were interpreted retrospectively by two physicians blinded not only to the specific clinical diagnosis of the patient and to their serum potassium measurement but also to each other's interpretation. The physicians predicted the presence or absence of hyperkalemia as well as the severity of hyperkalemia on a nominal scale (mild, moderate, or severe). SETTING: The emergency department of a university-affiliated urban county hospital. PATIENTS: Two hundred twenty consecutive patients admitted to the hospital from the ED with a diagnosis of renal failure or hyperkalemia. Eighty-seven patients had hyperkalemia, and 133 did not. RESULTS: The sensitivities of the readers for predicting hyperkalemia were .43 and .34, respectively (best positive predictive value, .65). The respective specificities for detecting hyperkalemia were .85 and .86 (best negative predictive value, .69). When only patients with moderate-to-severe hyperkalemia (potassium of more than 6.5 mmol/L) were analyzed, sensitivities were .62 and .55. The readers' ability to predict the severity of hyperkalemia was equally poor. CONCLUSION: The ECG is not a sensitive method of detecting hyperkalemia, even in high-risk patients. The specificity of the ECG is better for hyperkalemia, but empiric treatment of hyperkalemia based on the ECG alone will lead to mistreatment of at least 15% of patients.

Adult↗

PubMed1992

Hyperkalemia in very low birth weight infants.

PURPOSE: To assess the frequency and pathogenesis of hyperkalemia in the very low birth weight infant. METHODS: Infants who weighed less than 1000 gm at birth were prospectively entered into the study within 12 hours of birth. Potential risk factors for hyperkalemia were assessed. Body weight, fluid and electrolyte balance, serum levels of sodium and potassium, creatinine clearance, fractional sodium excretion, and urine sodium/potassium ratio were measured every 8 hours for 72 hours. Measurements of plasma renin, serum aldosterone, and plasma atrial natriuretic factor were made at study entry and repeated when hyperkalemia (serum potassium greater than 6.5 mmol/L) occurred or at 72 hours. Infants in whom hyperkalemia developed were compared with those in whom it did not. RESULTS: Thirty-one infants completed the study; hyperkalemia developed in 16 (51.6%). The only difference in the occurrence of perinatal complications was the more frequent occurrence of pH less than 7.20 in infants with subsequent development of hyperkalemia. Creatinine clearance, urine output, and potassium excretion were significantly lower in the hyperkalemia group during the first 24 hours. Serum potassium concentration at 24 hours was inversely related to urine output in the prior 24 hours. Fractional sodium excretion, urine sodium/potassium ratio, and levels of renin, aldosterone, and atrial natriuretic factor did not differ between groups. CONCLUSIONS: Hyperkalemia is a frequent complication in very low birth weight infants. Infants with low urinary flow rates during the first few hours after birth are at greatest risk for the development of hyperkalemia.

Aldosterone↗

PubMed1992

ECG changes under hyperkalemia with nephrectomy in the rat.

Electrolyte abnormalities have become an increasingly important cause of arrhythmias. Although the electrocardiographic (ECG) changes under hyperkalemia in the rat are poorly understood, it is conceivable that excess plasma potassium may also alter the cardiac excitations in the rat. Further, effects of hyperkalemia on ECG in the rat may differ from other species that have ST-segment and longer QT intervals in ECG. The present study was designed to determine the diagnostic criteria for ECG manifestations to various levels of plasma potassium concentration. For this purpose, hyperkalemia was induced by nephrectomy with and without infusions. Because it was difficult to produce various levels of plasma potassium concentration by only nephrectomy, we used two kinds of infusions to obtain especially moderate levels of nephrectomy-induced hyperkalemia. ECGs were recorded 24, 36, and 48 hours after nephrectomy. Plasma potassium concentration and number of abnormal ECGs were increased time-dependently. Increased T wave amplitude was present with mild hyperkalemia. The typical T wave change observed with so-called sinoventricular conduction levels of potassium concentration in species with long QT intervals did not occur in the rat. PR interval and QRS duration became slightly shorter within moderate hyperkalemia. P wave disappeared in most rats at potassium levels above 8.0 mEq/l. In advanced hyperkalemia (plasma potassium concentration above 7.5 mEq/l), conduction in all parts of the heart was suppressed. Moreover, sinoventricular conduction appeared. Thus, the diagnostic criteria for ECG manifestations to various levels of plasma potassium concentration in the rat were demonstrated.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1992

Hyperkalemia associated with ketorolac.

OBJECTIVE: To report and describe the apparent first case of hyperkalemia following intramuscular administration of ketorolac and to discuss the proposed mechanism of action. PATIENT: The patient was a 59-year-old man who developed hyperkalemia following a right upper lobectomy; he had received an intramuscular injection of ketorolac 30 mg for incisional pain. RESULTS: All possible causes of the hyperkalemia, including other drugs and intraoperative and postoperative events, were thoroughly evaluated and ruled out. Hyperkalemia has been reported in patients who have received other nonsteroidal antiinflammatory drugs (NSAIDs). The proposed mechanism of action for the occurrence of this hyperkalemia appears to be related to the suppression of prostaglandin synthesis. CONCLUSIONS: Considering the temporal sequence of events and drugs administered prior to the hyperkalemia in this patient and the hyperkalemic potential associated with other NSAIDs, ketorolac appears to be the precipitating agent. The possibility of hyperkalemia associated with the parenteral use of ketorolac may warrant practitioners to closely monitor the blood chemistry of patients receiving this agent.

Analgesics↗

PubMed1991

Endocrine crises. Hyperkalemia.

Clinical disorders causing hyperkalemia require a basic understanding of normal K homeostasis, which consists of external and internal K balances. The kidney is predominant in maintaining the external balance of K, and a number of mechanisms exist to provide a renal adaptation to defend against K excess. Likewise, several factors are known to modulate internal K balance--i.e., its distribution within the body. Some of these factors may provide defense against hyperkalemia before the kidneys have time to adapt. Potassium retention by the kidney causes hyperkalemia when renal failure is advanced, or earlier in the face of impaired tubular function in a variety of disorders. Hyperkalemia out of proportion to loss of renal function also occurs in the syndrome of hyporeninemic hypoaldosteronism. Drug-induced hyperkalemia is increasingly common and usually is caused by nonsteroidal anti-inflammatory drugs, angiotensin converting enzyme inhibitors, cyclosporine, or K-sparing diuretics. Clinical disorders of internal K imbalance include diabetes mellitus, systemic acidosis, and use of beta-blockers. Hyperkalemia is usually asymptomatic, but the danger of cardiac arrest or arrhythmia in severe hyperkalemia forces prompt clinical attention. Available treatment choices include agents that antagonize the effect of K on membrane potentials, redistribute it internally into cells, and remove it altogether from the body. The diagnostic work-up can then proceed, first by distinguishing renal and extrarenal causes, then by examining the roles of specific factors outlined in the section on normal K homeostasis.

Aged↗

PubMed1989

Hyperkalemia in diabetes mellitus. Effect of a triamterene-hydrochlorothiazide combination.

Hyperkalemia is known to occur with increased frequency in the patient with diabetes mellitus and in the elderly when agents that interfere with renal potassium excretion are employed, but the precise frequency has not been established. We employed data from a post-marketing surveillance trial following the introduction of a triamterene-hydrochlorothiazide (Maxzide) combination to estimate the frequency. In patients normokalemic at baseline, hyperkalemia developed with a frequency of 0.59% in 20,809 nondiabetics and in 1.08% of 922 diabetics. Hyperkalemia was threefold to fivefold more likely in those more than 60 years of age, and all of the excess hyperkalemia in diabetics occurred in the elderly. The severity of hyperkalemia was not influenced by the diabetes mellitus. Hypokalemia occurred with a frequency of about 5% and was not influenced by either age or diabetes. In patients who were hypokalemic prior to treatment, hypokalemia was corrected in more than two thirds and hyperkalemia occurred less frequently. Although hyperkalemia indeed occurs with increased frequency in the elderly diabetic when a potassium-sparing combination is employed, the frequency is not so great that such agents should be avoided routinely when their use could be beneficial. Renal function and serum potassium concentration should be assessed prior to instituting treatment and repeated within a few days and a few weeks thereafter in the patient at risk, especially when renal function is suspected, and in the elderly.

Diabetes Complications↗

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↗

PubMed1987

A rat model for hyperkalemia.

It is often necessary to have a small animal model for hyperkalemia for use in electrolyte and acid base experiments. In reviewing the literature, we found a paucity of such animal models, especially for acute hyperkalemia. We have had difficulty in inducing acute hyperkalemia in rats using potassium chloride alone either intravenously or intraperitoneally and felt the need for an easily reproducible small animal model for hyperkalemia. We gave experimental animals a combination of intraperitoneal amiloride 3 mg/kg and potassium chloride 2 meq/kg in two divided doses while control animals received only the potassium chloride. Initial serum potassiums were similar but at 2 hr, the experimental group had significantly higher serum potassium levels which were sustained throughout the 8 hr of the experiment. Arterial blood gas revealed no significant difference in blood pH values at all time points during the experiment. We conclude that the combination of amiloride and potassium chloride is useful to produce acute hyperkalemia in rats and that this hyperkalemia is sustained beyond 6 hr. This model is convenient for use in metabolic experiments requiring the use of acutely hyperkalemic rats.

Amiloride↗

PubMed1991

Heparin-induced hyperkalemia: a prospective study.

Heparin is frequently used for the prophylaxis and treatment of deep venous thromboembolism and it induces hypoaldosteronism leading to hyperkalemia, an uncommon adverse effect. In an intensive prospective drug monitoring study, 154 inpatients at the Internal Medicine Unit of Hospital Sotero del Río, Santiago, Chile, received heparin in the period between March and November 1990. Mean age of the patients was 65.8 +/- 12.9 years and 56.5% were female. Twenty-one (13.6%) patients developed heparin-induced adverse reactions. Thirteen events were hyperkalemia, 7 ecchymoses and 1 hematuria. The monitoring team and attending physicians have agreed to classify 9 heparin-induced hyperkalemia cases as probable and the other 4 as possible. No adverse reaction was fatal but 8 of the patients had severe hyperkalemia. Almost all reactions were dose-related. Hyperkalemia was more frequent in patients with diabetes mellitus, metabolic acidosis and long-term heparin therapy. The frequency of hyperkalemia did not correlate with age, sex, renal impairment or with previous use of anti-inflammatory drugs, heparin or aspirin.

Adolescent↗

PubMed1988

Early onset hyperkalemia in extremely low birth weight infants.

The incidence of hyperkalemia and associated clinical features in extremely preterm infants were determined by reviewing medical records of 32 infants with birth weights of less than or equal to 800 g born during a 1-year period. Hyperkalemia, defined as serum potassium concentration of greater than 6.5 mEq/L, occurred in 12 infants on the first day of life and in four others on the second day. Six infants (38%) had electrocardiographic abnormalities associated with hyperkalemia. Infants with hyperkalemia were less mature than infants with normal potassium levels. All infants of less than 25 weeks' gestation developed hyperkalemia. Fluid intakes and urine flow rates were lower and body weight loss greater during the first 24 hours of hospitalization for hyperkalemic infants. Hyperkalemia frequently occurs within the first 48 hours of life in extremely immature infants. Serum potassium should be monitored closely to avoid life-threatening cardiac arrhythmias in these infants.

Humans↗

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↗

PubMed1990

Ventilatory responses to hyperkalemia and exercise in normoxic and hypoxic goats.

The ventilatory response to moderate exercise is potentiated during hypoxia in goats, causing PaCO2 to decrease more from rest to exercise than in normoxia. We investigated the hypothesis that this response is due to the ventilatory stimulus provided by an interaction between exercise induced hyperkalemia and hypoxia. Plasma potassium concentration ([K+]), arterial blood gases and ventilation were measured in normoxia and hypoxia (PaO2 = 34-38 Torr) at rest and during steady-state exercise (5.6 kph; 5% grade) in seven goats. PaCO2 decreased during normoxic exercise (2.9 +/- 0.7 Tor; P less than 0.01), and decreased significantly more during hypoxic exercise (6.4 +/- 0.6 Torr; P less than 0.01). [K+] increased in both normoxic (1.0 +/- 0.1 mEq/L; P less than 0.01) and hypoxic (0.9 +/- 0.2 mEq/L; P less than 0.01) exercise, but these changes were not significantly different from each other. On a different day, resting goats were infused intravenously with 200 mM KCl for 5 min at a rate sufficient to obtain [K+] similar to exercise (8.6-12 ml/min) in normoxia and hypoxia. Hyperkalemia at rest caused similar PaCO2 decreases in normoxia (1.7 +/- 0.7 Torr; P less than 0.05) and hypoxia (1.7 +/- 0.5 Torr; P less than 0.01), but had no statistically significant effect on ventilation in either condition. These data indicate that hyperkalemia, at levels approximating those during moderate exercise, has a mild stimulatory effect on alveolar ventilation; however, hypoxia does not affect this response. We conclude that hyperkalemia does not provide sufficient ventilatory stimulation to account for exercise hyperpnea, nor does hypoxia potentiate the ventilatory stimulation from hyperkalemia at rest.

Animals↗

PubMed1987

Delayed fatal hyperkalemia in a patient with acute fluoride intoxication.

A 19-year-old man presented with acute fluoride poisoning. Initially his serum electrolytes were normal, but two hours later he developed ECG evidence of hyperkalemia followed by refractory ventricular fibrillation, suggesting that hyperkalemia may be important in the cardiotoxicity of acute fluoride intoxication. Treatment of fluoride-induced hyperkalemia consists of removal of fluoride from the body by dialysis, binding fluoride with aluminum or calcium, or enhancing fluoride excretion by inducing a metabolic alkalosis. Direct treatment of the hyperkalemia with glucose, insulin, and bicarbonate is ineffective. Quinidine may be an effective therapy for the hyperkalemia and ventricular irritability, but is as yet untested in human beings.

Adult↗

PubMed1990

Hyperkalemia in acute glomerulonephritis due to transient hyporeninemic hypoaldosteronism.

Transient hyperkalemia has been reported to occur in patients with acute glomerulonephritis, but the pathogenetic mechanism has not been investigated systematically. We studied the mechanism of hyperkalemia (5.7 to 6.7 mmol/liter) in four men with post-infectious glomerulonephritis. All four patients had clinical findings consistent with acute glomerulonephritis (edema, hypertension, proteinuria, hematuria, and an elevated ASO titer) and a renal biopsy performed in three of the patients confirmed the diagnosis. In comparison to normal subjects (N = 18), plasma aldosterone (5.4 +/- 1.6 vs. 22.8 +/- 2.6 ng/dl, P less than 0.005) and plasma renin activity (0.3 +/- 0.2 vs. 4.3 +/- 0.6 ng/ml/hr, P less than 0.005) were reduced. Hyperkalemia resolved within one to two weeks in two patients as the nephritis resolved and diuresis ensued, and aldosterone and renin levels obtained at follow-up visits were normal. Hyperkalemia persisted despite furosemide-induced diuresis in the other two patients, but resolved with fludrocortisone treatment. Thus, hyperkalemia in patients with acute glomerulonephritis is a manifestation, in part, of hyporeninemic hypoaldosteronism. It is ameliorated by mineralocorticoid therapy and improves spontaneously with resolution of the glomerulonephritis.

Acute Disease↗

PubMed1985

Drug-induced hyperkalemia.

After reviewing the available data on drug-induced hyperkalemia, we conclude that the situation has not improved since Lawson quantitatively documented the substantial risks of potassium chloride over a decade ago (90). As discussed, the risk of developing hyperkalemia in hospital remains at least at the range of 1 to 2% and can reach 10%, depending on the definition used (Table 2). Potassium chloride supplements and potassium-sparing diuretics remain the major culprits but they have been joined by a host of new actors, e.g., salt substitutes, beta-blockers, converting enzyme inhibitors, nonsteroidal antiinflammatory agents, and heparin, among others. Readily identifiable risk factors (other than drugs) for developing hyperkalemia are well-known but seem to be consistently ignored, even in teaching hospitals. The presence of diabetes mellitus, renal insufficiency, hypoaldosteronism, and age greater than 60 years results in a substantial increase in the risk of hyperkalemia from the use of any of the drugs we have reviewed. If prevention of hyperkalemia is the goal, as it should be, the current widespread and indiscriminate use of potassium supplements and potassium-sparing diuretics will need to end. We remain intrigued by Burchell's prescient pronouncement of over a decade ago that "more lives have been lost than saved by potassium therapy" (28).

Adrenergic Agonists↗

PubMed1991

Effects of chronic hyperkalemia on renal production and proximal tubule transport of ammonium in rats.

Free-flow micropuncture experiments were performed to examine directly the effects of chronic hyperkalemia on renal ammonium production, urinary ammonium excretion, and proximal convoluted tubule ammonium transport in the rat in vivo. Munich-Wistar rats were pair-fed either a control or a high-K+ diet for 6-11 days. Chronic K+ loading was associated with an increase in plasma K+ concentration and significant systemic metabolic acidosis. Renal blood flow did not differ in control and high-K+ rats. In the hyperkalemic rats, urinary ammonium excretion was reduced by 40% and whole kidney ammonium production was reduced by 50% compared with controls. In contrast, chronic hyperkalemia had no significant effect on net ammonium transport by either the early or late segment of the proximal convoluted tubule. Chronic hyperkalemia also had no effect on the absolute rate of ammonium delivery to early or late proximal convoluted tubule sites. These results indicate that a change in renal ammonium production does not necessarily correlate with a change in proximal tubule ammonium transport and that reduced urinary ammonium excretion in chronic hyperkalemia is not due to impaired secretion of ammonium by the proximal convoluted tubule. Chronic hyperkalemia may reduce ammonium excretion by decreasing transfer of ammonium from proximal tubules to collecting ducts in the renal medulla.

Ammonia↗

PubMed1988

Primary role of hyperkalemia in the acidosis of hyporeninemic hypoaldosteronism.

A 65-year-old woman with mild renal insufficiency had persistent hyperkalemia and hyperchloremic acidosis. Her plasma aldosterone level was relatively low for her hyperkalemia, and her urine pH was low. Fludrocortisone acetate administration corrected both hyperkalemia and acidosis by increasing urinary excretion of potassium and net acid, implicating deficient mineralocorticoid activity in the distal renal tubule in this patient. During this medication urinary ammonium excretion increased, but urine pH remained low, so that urinary titratable acid excretion did not decrease. On the other hand, correction of hyperkalemia by administration of a potassium-calcium exchange resin alone also resolved the acidosis by increasing urinary ammonium excretion. This increment exceeded the decrement of urinary titratable acid excretion, which was caused by raised urine pH secondary to increased urinary ammonium excretion, and resulted in increase of net acid excretion. Thus, in this patient, hyperkalemia appears to be a decisive causative factor in the acidosis, with deficient mineralocorticoid effect only contributing in part to the reduction of net acid excretion and the acidosis.

Acidosis, Renal Tubular↗