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PubMed2006

Hyperkalemia.

Hyperkalemia is a potentially life-threatening metabolic problem caused by inability of the kidneys to excrete potassium, impairment of the mechanisms that move potassium from the circulation into the cells, or a combination of these factors. Acute episodes of hyperkalemia commonly are triggered by the introduction of a medication affecting potassium homeostasis; illness or dehydration also can be triggers. In patients with diabetic nephropathy, hyperkalemia may be caused by the syndrome of hyporeninemic hypoaldosteronism. The presence of typical electrocardiographic changes or a rapid rise in serum potassium indicates that hyperkalemia is potentially life threatening. Urine potassium, creatinine, and osmolarity should be obtained as a first step in determining the cause of hyperkalemia, which directs long-term treatment. Intravenous calcium is effective in reversing electrocardiographic changes and reducing the risk of arrhythmias but does not lower serum potassium. Serum potassium levels can be lowered acutely by using intravenous insulin and glucose, nebulized beta2 agonists, or both. Sodium polystyrene therapy, sometimes with intravenous furosemide and saline, is then initiated to lower total body potassium levels.

Algorithms↗
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↗
PubMed1980

Hyperkalemia and hyperglycemic increments in plasma potassium in diabetes mellitus.

The frequency of persistent or intermittent hyperkalemia in patients with diabetes is unknown. In 405 predominantly insulin-treated patients, major hyperkalemia was not common (< 5.0 mEq/L in 2.5%). In ten insulin-treated patients sampled hourly from 8 AM through 8 PM, major intermittent hyperkalemia was not detected (< 4.8 mEq/L in all samples). However, mean plasma potassium values paralleled mean glucose values; these variables were significantly correlated in seven of ten patients. In contrast, there were no relationships between plasma potassium and plasma free insulin, glucagon, epinephrine, or norepinephrine values. We conclude that (1) hyperkalemia--fasting or intermittent--does not occur commonly in patients with diabetes, and (2) hyperglycemia, but not insulin or epinephrine lack or glucagon excess, appears to be a direct determinant of plasma potassium but is not a sufficiently potent determinant to commonly produce clinically important hyperkalemia in insulin-treated diabetic patients.

Adolescent↗
PubMed1981

[Electrophysiological study of cardiac effects of succinylcholine: role of vagal tone and hyperkalemia in anesthetized dog (author's transl)].

The effects of intravenously infused succinylcholine (SCh): 1 mg/kg/minute during 30 minutes were assessed in anesthetized dogs on spontaneous heart rate, conduction within the atrio-ventricular node and the His-Purkinje system and on atrial (AERP) and atrio-ventricular (AVERP) effective refractory periods with varying levels of vagal tone and under mild hyperkalemia. 1) The heart rate which was not affected by SCh in the absence of vagal tone was by contrast increased by 50 p. cent when vagal tone was maintained. Under hyperkalemia, the vagolysis-mediated tachycardia did not prove more marked. 2) The conduction velocity, which was never modified by SCh in either the atria or the His-Purkinje system, was always accelerated with vagal tone. This acceleration is directly related to the vagolytic properties of SCh, but also partly to a mild hyperkalemia. The changes of potassium blood levels tend to reverse the potassium outflow due to the parasympathetic neuromediator. 3) The AERP was was lengthened by SCh and hyperkalemia; the latter impaired the outflow of potassium ions responsible for repolarization. The AVERP was always shortened when the vagal tone is maintained, however less largely under mild hyperkalemia which limits SCh anticholinergic effect owing to its own anticholinergic action.

Anesthesia, General↗
PubMed1996

Hyperkalemia in the elderly: a group at high risk.

Hyperkalemia is a serious electrolyte disorder which appears to develop more commonly in the aged patient. The elderly may be predisposed to hyperkalemia as a result of underlying abnormalities in potassium homeostasis. These include inapparent renal insufficiency, tubulointerstitial disease in the kidney, disturbed aldosterone production, and abnormal salt and water balance. Several commonly prescribed medications may further disrupt potassium balance and promote the development of hyperkalemia in these patients. Trimethoprim-sulfamethoxazole, a commonly used antimicrobial agent, has recently been noted to cause hyperkalemia in the elderly, even with standard dosage. The elderly should be considered at high risk to develop hyperkalemia, especially when they are using certain medications. Potassium concentration should be monitored closely when these patients are hospitalized and/or treated with potassium-altering medications.

Aged↗
PubMed1996

Hyperkalemia: therapeutic options in acute and chronic renal failure.

Hyperkalemia is a life threatening emergency and warrants immediate treatment because of its deleterious cardiac consequences. Initial measures in mild cases include restriction and binding of dietary potassium, correction of metabolic acidosis and increasing urinary excretion by furosemide. In moderate and severe hyperkalemia infusion of glucose with insulin has been regarded as the standard medical treatment so far. However, recently also the beta 2 stimulatory drug salbutamol has been shown to be an effective agent to treat hyperkalemia by inducing a shift of potassium into the intracellular compartment. We treated 15 pediatric patients of different age groups (mean age 5.16, range 0.1-16 years) suffering from acute hyperkalemia (mean level 6.6, range 5.9-7.7 mmol/l) by means of a single infusion of salbutamol (5 micrograms/kg over 15 minutes). Serum potassium concentrations decreased significantly to 5.74 +/- 0.53 after 30 minutes and furthermore to 5.19 +/- 0.48 and to 4.92 +/- 0.53 mmol/l after 60 and 120 minutes, respectively (p < 0.001 at all stages compared to pre-treatment). Since no side effects occurred besides a slight increase of heart rate in 3 patients, we conclude that short-term intravenous salbutamol infusion is an effective, rapid, safe and predictable way to treat children of any age suffering from acute hyperkalemia and therefore has become the first line treatment in our center.

Acute Disease↗
PubMed1996

Trimethoprim-sulfamethoxazole: hyperkalemia is an important complication regardless of dose.

Trimethoprim-sulfamethoxazole is a frequently prescribed antibiotic with a wide spectrum of antimicrobial activity. As a result of the increasing number of AIDS patients requiring therapy for Pneumocystis carinii pneumonia, high dose trimethoprim-sulfamethoxazole use had dramatically increased. A previously unreported and potentially lethal adverse reaction associated with high dose trimethoprim-sulfamethoxazole therapy, hyperkalemia, subsequently developed. Recognition of this potassium disorder led to investigation and description of the mechanism by which trimethoprim-sulfamethoxazole induced hyperkalemia. Trimethoprim was found to act like the potassium-sparing diuretic amiloride and reduce renal potassium excretion. Subsequent to this work, a handful of cases noted the development of hyperkalemia with standard dose trimethoprim-sulfamethoxazole in elderly patients without evidence of an obvious defect in potassium homeostasis. A prospective surveillance study of patients treated with standard dose trimethoprim-sulfamethoxazole as compared to similar controls treated with other antibiotics confirmed the rise in potassium concentration associated with trimethoprim-sulfamethoxazole therapy. Patients with mild renal insufficiency were the only group at significant risk for more severe hyperkalemia. Hence, trimethoprim-sulfamethoxazole therapy can be complicated by hyperkalemia regardless of the dose employed.

AIDS-Related Opportunistic Infections↗
PubMed1997

Hyperkalemia and trimethoprim-sulfamethoxazole: a new problem emerges 25 years later.

Trimethoprim-sulfamethoxazole is a frequently prescribed antibiotic with a wide spectrum of antimicrobial activity. A previously unreported and potentially lethal adverse reaction associated with "high dose" trimethoprim-sulfamethoxazole therapy, hyperkalemia, was described. Subsequent to the descriptions of hyperkalemia with "high dose" trimethoprim-sulfamethoxazole, a handful of cases noted the development of hyperkalemia with "standard dose" trimethoprim-sulfamethoxazole in elderly patients without evidence of an obvious defect in potassium homeostasis. A surveillance study of patients treated with "standard dose" trimethoprim-sulfamethoxazole as compared to similar controls treated with other antibiotics confirmed the rise in potassium associated with trimethoprim-sulfamethoxazole therapy. Recognition of this potassium disorder led to investigation and description of the mechanism by which trimethoprim-sulfamethoxazole-induced hyperkalemia. Trimethoprim was found to act like the potassium-sparing diuretic amiloride and reduce renal potassium excretion. Hence, trimethoprim-sulfamethoxazole therapy was found to be associated with a new adverse reaction, hyperkalemia, nearly 25 years after its introduction into clinical practice as an antimicrobial agent.

Animals↗
PubMedDate not supplied

[Circulatory failure due to severe cardiac arrhythmia as a result of hyperkalemia in a very low birth weight infant].

BACKGROUND: Hyperkalemia is frequently seen during the first days of life in premature infants with a gestational age at birth less than 28 weeks. Normally, these high concentrations of potassium are well tolerated of the premature infants. In a few cases hyperkalemia leads to life-threatening cardiac arrhythmias. CASE REPORT: We report about a 800 grams weighing preterm infant born after 26 + 4 gestational weeks. 24 hours after birth the infant developed 2 : 1 atrioventricular block due to hyperkalemia with a heart rate about 75 bpm. The bradycardia continued about 45 minutes in spite of immediate therapy concomitant by circulatory failure that resulted in an intraventricular hemorrhage of grade III with periventricular intraparenchymal lesions. CONCLUSIONS: The case report demonstrates the variations of the electrocardiogram that can be found in preterm infants with hyperkalemia and their potential risks. Therapy of symptomatic hyperkalemia is not able to interrupt early a life-threatening circulatory failure in any case.

Bradycardia↗
PubMed1975

Geophagia. A cause of life-threatening hyperkalemia in patients with chronic renal failure.

Geophagia has been associated with life-threatening hyperkalemia in five patients with chronic renal failure. All five patients were black and had been born in the southeastern United States. Four had had frequent hyperkalemia requiring at least one hospitalization, and two had had hyperkalemia with serum potassium concentration as high as 9.8 mEq/liter, resulting in cardiac arrest in one and paralysis, disorientation, and cardiac arrythmia in the other. Since riverbed clay contains as much as 100 mEq of potassium in 100 gm of clay, much of which is exchangeable at acid pH, the mechanism of geophagia-induced hyperkalemia appears to be the absorption of potassium released from clay after ingestion. After discontinuing geophagia, no new hyperkalemic episodes occurred in these patients.

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↗
PubMed2005

Hyperkalemia induced failure of atrial and ventricular pacemaker capture.

Hyperkalemia is a life threatening metabolic condition. The common risk factors for hyperkalemia include renal insufficiency, use of angiotensin converting enzyme inhibitors, potassium supplementation and excessive consumption of potassium containing diet. A mild to moderate increase in serum potassium causes an increase in myocardial excitability, but further increase leads to impaired myocardial responsiveness, including that to pacing stimulation. Hyperkalemia has been reported to cause failure of atrial capture due to pacemaker exit block. We report a case where hyperkalemia resulted in failure of both the atrial and the ventricular pacemaker capture.

Electrocardiography↗
PubMed2006

Wide-complex tachycardia associated with severe hyperkalemia in three cats.

The well recognized cardiac effects of severe hyperkalemia include progressive rhythm and conduction disturbances such as bradycardia, spiked and narrow T waves, widening QRS complex, widening and flattening P wave, disappearance of the P wave, and cardiac arrest. Paradoxically, a heart rate greater than 200 beats/min may coexist with hyperkalemia in some cats. This report describes three cats with moderate to severe hyperkalemia and concurrent rapid heart rate. In each cat, the serum potassium (K(+)) concentration was > or =7.5 mEq/dl with a concurrent heart rate > 200 beats/min. In each cat, nine-lead electrocardiograms demonstrate an absence of P waves and a wide-complex tachycardia. Hyperkalemia should be considered in the differential diagnosis when a feline electrocardiogram demonstrates a wide-complex tachycardia without identifiable P waves.

Animals↗
PubMed2000

Drug-induced hyperkalemia: old culprits and new offenders.

Prescribed medications, over-the-counter drugs, and nutritional supplements are used by many patients. Although most of these products are well tolerated, drug-induced hyperkalemia may develop in patients with underlying renal impairment or other abnormalities in potassium handling. Drug-induced hyperkalemia most often occurs from impaired renal potassium excretion. However, disturbed cellular uptake of a potassium load as well as excessive ingestion or infusion of potassium-containing substances may also occur. Physicians must be aware of medications that can precipitate hyperkalemia, how these drugs induce alterations in potassium homeostasis, and the patient characteristics that increase the risk of hyperkalemia.

Dietary Supplements↗
PubMed2002

Aprikalim reduces the Na+-Ca2+ exchange outward current enhanced by hyperkalemia in rat ventricular myocytes.

BACKGROUND: [corrected] Aprikalim, an adenosine triphosphate (ATP) sensitive K+ (K(ATP)) channel opener, attenuates the elevation of intracellular Ca2+ concentration ([Ca2+]i) and improves the contractile functions after hyperkalemic and hypothermic cardioplegia. There is evidence that cardioplegia increases the Na+-Ca2+ exchange activity without affecting Ca2+ influx through L-type Ca2+ channels or Ca2+ content in the sarcoplasmic reticulum, the intracellular Ca2+ store. METHODS: We measured the Na+-Ca2+ exchange outward current with the patch-clamp technique in single rat ventricular myocytes exposed to hyperkalemia and hypothermia in the presence of aprikalim. The intracellular calcium concentration ([Ca2+]i) during cardioplegia, and the contractile function and [Ca2+]i transients induced by electrical stimulation or caffeine during rewarming and reperfusion in single ventricular myocytes were also determined. Contraction and [Ca2+]i were determined with video tracking and spectrofluorometry, respectively. RESULTS: Aprikalim, 100 micromol/L, the effect of which was blocked by glibamclamide, a K(ATP) inhibitor, significantly attenuated the hyperkalemia-elevated Na+-Ca2+ exchange current by 26% and 11% at 22 degrees C and 4 degrees C, respectively. Aprikalim also attenuated significantly the [Ca2+]i elevated during cardioplegia. Furthermore aprikalim significantly attenuated the reduction in amplitude and prolongation in duration of contraction of myocytes after cardioplegia. The effects of aprikalim mimicked those of nickle (Ni2+), a Na+-Ca2+ exchange blocker. The electrically or caffeine-induced [Ca2+]i transients were unaltered by cardioplegia or aprikalim. CONCLUSIONS: Aprikalim attenuates the Na+-Ca2+ exchange outward current elevated by hyperkalemia, which may attenuate the [Ca2+]i elevation during hyperkalemia and improve the contractile function after cardioplegia in the ventricular myocyte. The study provides further support that addition of a K(ATP) channel opener to the cardioplegic solution may produce beneficial effects in open heart surgery.

Adenosine Triphosphate↗
PubMed1990

Hyperkalemia in the elderly.

Physiologic and pathologic events that occur in patients as they grow older may result in distal renal tubular dysfunction, as well as decreased levels of plasma renin activity and plasma aldosterone. Such alterations result in a tendency toward hyperkalemia. A syndrome termed hyporeninemic hypoaldosteronism, associated with hyperkalemia, has been frequently described in elderly patients. The common occurrence of hyperkalemia in the elderly may be aggravated by the use of drugs that either further suppress renin and/or aldosterone or interfere with distal tubular potassium excretion. Some patients with hyporeninemic hypoaldosteronism respond to diuretic therapy. The recognition of the possible development of severe hyperkalemia in the elderly patient may avoid serious and even fatal complications of this electrolyte disorder.

Aged↗