Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “HYPOKALEMIA”

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
PubMed1998

Acute and chronic hypokalemia sensitize the isolated heart to hypoxic injury.

We examined the effects of acute and/or chronic hypokalemia on responses to 30 min of hypoxia and recovery in the isolated, perfused heart model. We found that both acute hypokalemia and chronic hypokalemia impaired contractility [expressed as maximum slope of pressure increase over time (dP/dt): 501 +/- 49 and 529 +/- 48 vs. 1,302 +/- 118 mmHg/s, P < 0.01] and recovery of ATP concentrations (determined with 31P NMR spectroscopy: 30 +/- 6 and 40 +/- 10 vs. 67 +/- 5% initial, P < 0.05) at 30 min of recovery. Moreover, the combination of acute hypokalemia and chronic hypokalemia had additive effects (dP/dt 166 +/- 15 mmHg/s and ATP 21 +/- 7% initial, both P < 0.01). We also measured cytosolic calcium with surface fluorescence spectroscopy after indo 1 loading. Acute hypokalemia and acute hypokalemia + chronic hypokalemia increased cytosolic calcium (averaged throughout the cardiac cycle) during and after hypoxia (390- to 460-nm ratio at 30 min of recovery: 0.46 +/- 0.07 and 0.65 +/- 0.07 vs. 0.18 +/- 0.03, P < 0.01), whereas control and chronic hypokalemia hearts had only small changes with hypoxia and recovery. Finally, when we examined mitochondria isolated from hearts perfused under experimental conditions, we found that chronic hypokalemia-alone mitochondria and chronic hypokalemia + acute hypokalemia mitochondria had marked impairment of state 3 respiration compared with control hearts (52 +/- 13 and 50 +/- 9 vs. 128 +/- 10 natm.min-1.mg protein-1 with succinate as substrate, P < 0.01), whereas acute hypokalemia mitochondria demonstrated only subtle changes. These data suggest that both acute hypokalemia and chronic hypokalemia impair cardiac responses to hypoxia. The mechanism may involve impairment of calcium metabolism, but cytosolic calcium alterations do not explain all of the metabolic and functional effects of acute hypokalemia and chronic hypokalemia in the setting of hypoxia.

Acute Disease↗
PubMed1992

Effect of bilateral stellectomy on electrical instability of the atrium in the dog with hypokalemia.

To investigate the effect of sympathetic nerve activity on electrical instability of the atrium in the presence of hypokalemia, open chest electrophysiological study was performed before and after bilateral stellectomy (BS) in 15 dogs with hypokalemia (hypokalemia group) and in 15 dogs with normokalemia (control group). Hypokalemia was created by infusion of 5.0 g/kg of polystyrene sulfonic acid calcium into the colon. Serum level of potassium was significantly lower in the hypokalemia group (2.94 +/- 0.52 mEq/L) than in the control group (4.86 +/- 0.51 mEq/L, P less than 0.01) before BS. There was no significant change in serum level of potassium in the two groups after BS. Incidence of electrically induced atrial fibrillation (AF) was significantly higher in the hypokalemia group (80%) than in the control group (13%, P less than 0.001) before BS. It was significantly reduced in the hypokalemia group (40%, P less than 0.05), but not in the control group (6%) after BS. Dispersion of effective refractory period of the atrium (delta ERP) was significantly greater in the hypokalemia group (26.1 +/- 2.8 msec) than in the control group (22.0 +/- 3.3 msec, P less than 0.005) before BS. It was significantly decreased to 23.1 +/- 3.2 msec in the hypokalemia group (P less than 0.001) and to 20.6 +/- 2.5 msec in the control group (P less than 0.01) after BS. Maximum conduction delay in the atrium (MaxCD) was 36.1 +/- 3.5 msec before and 36.2 +/- 4.1 msec after BS in the hypokalemia group and 31.1 +/- 4.2 msec before and 32.3 +/- 4.9 msec after BS in the control group. There was a significant difference in MaxCD between the two groups before BS. Atrial fibrillation threshold (AFT) was significantly lower in the hypokalemia group (3.9 +/- 0.7 mA) than in the control group (13.8 +/- 3.1 mA, P less than 0.001) before BS. It was significantly increased both in the hypokalemia group (6.5 +/- 1.3 mA, P less than 0.001) and in the control group (15.0 +/- 2.7 mA, P less than 0.005) after BS. It is concluded that sympathetic nerve activity may play some role in the increase in electrical instability of the atrium in the presence of hypokalemia.

Animals↗
PubMed1998

ECG changes during furosemide-induced hypokalemia in the rat.

Electrolyte abnormalities have become an increasingly important cause of arrhythmias owing to the widespread use of high-potency diuretics. Hypokalemia is one of the common complications of diuretic use. Although some studies of hypokalemia induced by furosemide as well as of potassium-deficient diets in the rat have been reported, the electrocardiographic (ECG) changes during hypokalemia in the rat are poorly understood. This study was designed to examine such changes. For this purpose, hypokalemia was induced by furosemide administration, and the diagnostic criteria for ECG manifestations of hypokalemia were determined. During hypokalemia, conduction in most parts of the heart was suppressed to an extent depending on plasma potassium concentration. Prolongation of the QT interval was also observed, which agrees with findings in humans and dogs. Furthermore, prolonged durations of the P wave and QRS complex were observed during hypokalemia in the rat. The extent of alteration of the PR interval induced by hypokalemia was less significant than that of P wave and QRS complex durations. These results suggest that the excitabilities of the myocardium in the atria and ventricles may be affected by extracellular potassium level rather than by the atrioventricular conduction system in the rat. Wave amplitude, except that of the P wave, was decreased by severe hypokalemia. These changes were not dependent on the plasma potassium concentration. Typical T wave changes observed with hypokalemia in humans and dogs did not occur in the rat. The ECG manifestations of acute hypokalemia in the rat did not include the typical T wave changes seen in species with ST-segment type ECGs; however, other ECG parameter changes occurring with hypokalemia were qualitatively similar to those in other species. These results may be useful for testing the toxicity of potassium-depleting drugs in the rat.

Animals↗
PubMed2002

Hypokalemia following trauma.

Frequent hypokalemia was noted immediately after trauma, and it was hypothesized that hypokalemia occurred more frequently in the more severely injured. A retrospective trauma registry and chart review was done on 546 trauma patients looking at admission potassium, a variety of lab tests related to potassium, specific injuries, hospital/ICU lengths of stay, and general patient demographics. Admission hypokalemia (K < 3.6 meq/l) was more frequent in those with closed head injuries (41.1% vs. 27.5%, P < .001) and in those who suffered spinal cord injuries (54.5% vs. 33.6%, P < .05). Hyperglycemia was more frequent with admission hypokalemia (45.2% vs. 29.7%, P < .001). Hypokalemia occurred more frequently in younger patients (28.6 vs. 37.7 y, P < .001). Also, the pediatric group, ages 5-14, had admission hypokalemia more frequently than those ages 15-59, or those ages > 59 (54.9% vs. 34.5% vs. 16.7%, P < .001). Glasgow Coma Scores (GCS) were significantly lower (12.0 vs. 13.5, P < .001) and Injury Severity Scores (ISS) were higher (17.4 vs. 13.4, P < .001), with admission hypokalemia. Additionally, hypokalemia was a positive predictor of ISS (P = .05). Hypokalemic patients more likely needed a ventilator, (26.6% vs. 16.5%, P < .01) but did not have significantly more ventilator days (P > .05). Subsequently, hypokalemic patients had longer ICU lengths of stay (LOS) (2.6 vs. 1.5 days, P < .005) and longer hospital LOS (8.5 vs. 5.6 days, P < .001). When stratified into categories of "severe": (K < 3.1 meq/l), "moderate": (K = 3.1-3.3 meq/l), and "mild": (K = 3.4-3.5 meq/l) hypokalemia, those with severe hypokalemia had significantly lower GCS (10.0 vs. 13.1, p < .05), higher serum glucose levels (167 vs. 137 mg/dl, P < .05), lower creatinine levels (.77 vs. .95 mg/dl, P < .05), and longer hospital lengths of stay (13.1 days vs. 7.6 days, P < .05 results).

Adolescent↗
PubMed1989

Hypokalemia in rats produces resistance to dysrhythmias under halothane anesthesia.

The arrhythmogenic threshold was investigated during acute and chronic hypokalemia under halothane anesthesia with an epinephrine challenge in the rat model. It was hypothesized that in the setting of severe hypokalemia, general anesthesia would be arrhythmogenic and would be exaggerated with increased levels of catecholamines. Rats were divided into four groups as follows: normokalemic control (group I, n = 10), acute hypokalemia with furosemide (group II, n = 16), acute hypokalemia with hyperventilation (group III, n = 18), and chronic hypokalemia induced by a low potassium (K+) diet (group IV, n = 22). There were no significant differences (P less than .05) in baseline K+ and arterial blood gases among the four groups. There was a significant difference between groups I and II and groups I and IV (P less than 0.05) in serum K+ values after the low K+ diet, but no differences were observed between groups II and IV or groups I and III in serum K+ levels. There was no significant difference in myocardial tissue K+ among the four groups. There was a significant difference in the arrhythmic dose of epinephrine among the four groups (P less than 0.05). Acute hypokalemia was more prone to dysrhythmias than chronic hypokalemia. However, compared with control, acute and chronic hypokalemia groups were resistant to dysrhythmias is probably based on compensatory mechanisms. The heart seems more resistant to K+ changes than skeletal muscle. This resistance is associated with compensation by the cardiac muscle sodium pump in the face of K+ depletion. Hypokalemia per se did not increase the incidence of dysrhythmias under halothane anesthesia in rats.

Acute Disease↗
PubMed2000

Older age and in-hospital development of hypokalemia from loop diuretics: results from a multicenter survey. GIFA Investigators. Multicenter Italian Pharmacoepidemiologic Study Group.

BACKGROUND: Hypokalemia is a common finding among older patients taking diuretic medications. However, it is not known whether older age per se carries an increased risk of hypokalemia, particularly during a patient's treatment with loop diuretics. METHODS: The association between age and incident hypokalemia was examined in 18,872 patients with normal baseline serum potassium enrolled during three yearly multicenter surveys; 4,035 patients started receiving loop diuretics during their hospital stay. Demographic variables, comorbid conditions, medications, and objective tests that were associated with incident hypokalemia in separate age- and sex-adjusted logistic regression models were examined as potential confounders. RESULTS: Among patients with normal baseline serum potassium, the factors of age, presence of coronary disease or diabetes, comorbidity, the use of ACE inhibitors, loop diuretics, digitalis, corticosteroids, or insulin, and baseline serum potassium were associated with incident hypokalemia in initial models. After these variables were adjusted for, age (for each decade, odds ratio = 1.30; 95% confidence interval = 1.17-1.46; p < .0001) was associated with incident hypokalemia. The use of parenteral (2.30; 1.53-3.46; p < .0001) but not oral (1.16; 0.79-1.69; p = .44) loop diuretics was associated with hypokalemia. Eventually, age was associated with hypokalemia when the summary regression model was analyzed in patients taking loop diuretics (1.33; 1.03-1.71; p = .027), as well as in those taking intravenous loop diuretics only (1.84; 1.25-2.70; p = .002). CONCLUSIONS: Older age is independently associated with the in-hospital development of hypokalemia, particularly among patients taking loop diuretics. Monitoring of serum potassium levels is therefore advisable when older patients are treated with these agents.

Age Factors↗
PubMed1995

Indapamide-induced severe hyponatremia and hypokalemia.

OBJECTIVE: To describe 2 patients with severe indapamide-induced hyponatremia and hypokalemia and to discuss the incidence and mechanisms of diuretic-induced hyponatremia and hypokalemia. CASE SUMMARY: Two women aged 60 and 62 years presented with severe hyponatremia (plasma sodium concentrations of 103-104 mmol/L) and hypokalemia (plasma potassium concentrations of 1.6-2.2 mmol/L) 5-6 weeks after they received indapamide 2.5 mg/d therapy for arterial hypertension. Central nervous system symptoms of hyponatremia were observed in both patients. One patient experienced severe postural hypotension, a plasma potassium concentration of 1.6 mmol/L, and electrocardiographic abnormalities consistent with hypokalemia. Hyponatremia was initially mistaken in this patient for the syndrome of inappropriate secretion of antidiuretic hormone (SIADH). Both patients recovered completely after withdrawal of indapamide therapy and correction of the hyponatremia and hypokalemia. DISCUSSION: Previous studies of administration of indapamide 2.5 mg/d for 10-24 months in hypertensive patients showed a low incidence (0.6-1.2%) of hypokalemia severe enough to require withdrawal of drug therapy. Serum sodium concentrations were unaltered in these studies. All case reports, except 1, of indapamide-induced electrolyte disturbances described only hypokalemia. CONCLUSIONS: Indapamide can cause both severe hypokalemia and hyponatremia. The predominant clinical features can be a result of severe hyponatremia. The latter can have diverse clinical presentations and may be mistaken for SIADH. As with other diuretics, plasma sodium and potassium concentrations must be monitored during indapamide therapy, especially in patients at risk for hyponatremia and hypokalemia.

Diabetes Mellitus, Type 2↗
PubMed1986

Hypokalemia and arrhythmias.

The focus of this article is hypokalemia, its electrophysiologic properties, and clinical arrhythmias. The effects of potassium on the electrophysiologic properties of the heart have been extensively studied and clearly are arrhythmogenic. Hypokalemia increases resting membrane potential and increases both the duration of the action potential and the duration of the refractory period, the latter to a greater degree than the former. This combination is conducive to the genesis of reentrant arrhythmias. Hypokalemia also increases threshold potential as well as automaticity, thus providing the context for automatic arrhythmias as well. Lastly, hypokalemia decreases conductivity, which also predisposes to arrhythmias of the reentrant type. The electrocardiographic criteria for hypokalemia include the presence of U waves greater than 1 mm and U waves larger than the T wave in the same lead (with associated ST-segment depression). Other criteria have been a T:U ratio of 1 or less and a U wave greater than 0.5 mm in electrocardiographic lead II or greater than 1.0 mm in lead V3. The relationship between hypokalemia and clinical arrhythmias has long been recognized. In 1949, Bellet et al reported extrasystoles with hypokalemic alkalosis that decreased with potassium administration. These observations were confirmed by several groups in the early 1950s. 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. These clinical observations were strengthened by the 1962 findings of Gettes et al, who employed microelectrode techniques to show that perfusion of low potassium solutions resulted in ventricular ectopic beats, ventricular tachycardia, and ventricular fibrillation. In more recent years, several studies have evaluated the relationship between potassium levels and arrhythmias in patients with and without hypertension who were receiving diuretic therapy. These studies have demonstrated that there is an increased incidence of ventricular arrhythmias associated with the hypokalemia induced by diuretic therapy, an observation with obvious clinical implications.

Action Potentials↗
PubMed2002

Ethnicity and unprovoked hypokalemia in the Atherosclerosis Risk in Communities Study.

BACKGROUND: Hypertension is more prevalent in the African American population when compared with the European American population in the United States. Unprovoked hypokalemia may lead to hypertension and is associated with several forms of recognized secondary hypertension. METHODS: We investigated the association of ethnicity with unprovoked hypokalemia in the second Atherosclerosis Risk in Communities (ARIC) study examination. Hypokalemia was defined as serum potassium <3.5 mmol/L. RESULTS: A statistically significant association was detected between ethnicity and unprovoked hypokalemia (odds ratio = 5.3; 95% confidence interval = 3.6, 7.7) with unprovoked hypokalemia more prevalent in African Americans both before and after adjustment for important covariates. The unadjusted prevalence for unprovoked hypokalemia was 2.6% for African Americans and 0.5% for European Americans. CONCLUSIONS: We found that the prevalence of unprovoked hypokalemia for African Americans in the ARIC cohort was more than five times that for European Americans. These data suggest that an increased awareness of hypokalemia and its etiology may be indicated for African Americans.

Arteriosclerosis↗
PubMed1987

Frequency of hypokalemia after successfully resuscitated out-of-hospital cardiac arrest compared with that in transmural acute myocardial infarction.

To evaluate the prevalence of hypokalemia in out-of-hospital cardiac arrest, the initial serum potassium and arterial pH values were reviewed from 138 consecutive patients resuscitated from cardiac arrest. For comparison, the same variables were reviewed for 62 consecutive patients who had transmural acute myocardial infarction (AMI) without cardiac arrest. The mean serum potassium level was lower after resuscitation from cardiac arrest (3.6 +/- 0.6 mEq/liter) than during AMI (3.9 +/- 0.5 mEq/liter) (p less than 0.005). The incidence of hypokalemia (potassium less than 3.5 mEq/liter) was greater in patients sustaining cardiac arrest (41%) than in patients who had AMI without cardiac arrest (11%) (p less than 0.001). Hypokalemia was common after cardiac arrest regardless of the occurrence of AMI at the time of arrest. Hypokalemia after cardiac arrest was independent of arterial pH, epinephrine or bicarbonate therapy during resuscitation, or prior therapy with diuretic drugs, digoxin or propranolol. In 10 patients with marked hypokalemia, the serum potassium level returned to normal rapidly (16 hours) during the hospitalization even though only 29% of the predicted potassium requirement was infused before its normalization. Thus, hypokalemia is prevalent immediately after out-of-hospital cardiac arrest, whereas it is uncommon in AMI in the absence of cardiac arrest. The cause and electrophysiologic consequences of this hypokalemia are unknown; in most cases, it is apparently caused by a shift of potassium from the intravascular compartment rather than a total body depletion of potassium.

Acute Disease↗
PubMed1986

Mechanism of cardiac arrhythmias induced by epinephrine in dogs with hypokalemia.

To investigate the mechanism of ventricular arrhythmias induced by epinephrine in dogs with hypokalemia, 30 adult mongrel dogs were separated into a control group (n = 13) and a hypokalemia group (n = 17). In the hypokalemia group, sodium polystyrene sulfonate (5 g/kg body weight) was infused into the colon. In both groups, the serum concentrations of sodium, potassium and calcium were measured every 15 minutes for 60 minutes. The mean (+/- standard deviation) serum potassium level of the hypokalemia group decreased significantly from 3.81 +/- 0.21 to 2.92 +/- 0.36 mEq/liter; there were no significant changes in other electrolytes. After 60 minutes, epinephrine (10 micrograms/kg) was injected intravenously in the hypokalemia and control groups, and the arrhythmia ratio (the number of ventricular ectopic beats divided by the total heart rate) was calculated for 5 minutes. Each group was further classified into subgroups of dogs with an arrhythmia ratio higher or lower than 10%. An arrhythmia ratio over 10% was observed in 7.7% of the control group and 53% of the hypokalemia group. Immediately after 5 minutes of epinephrine injection, myocardial mitochondria and plasma membrane fraction were prepared from each group. Mitochondrial calcium content and phospholipase activity of plasma membrane fraction were determined. Significant increases in both mitochondrial calcium content and phospholipase activity were observed in the dogs with hypokalemia and an arrhythmia ratio greater than 10%.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1989

Effects of somatostatin and oral potassium administration on terbutaline-induced hypokalemia.

Terbutaline, a beta 2-adrenergic agonist, has been shown to cause hypokalemia and an increase of plasma glucose and serum insulin concentrations. We considered that terbutaline-induced hypokalemia may be due to the insulin-induced shift of potassium (K+) from the extracellular to the intracellular space. If so, then inhibition of insulin secretion by somatostatin would prevent terbutaline-induced hypokalemia. Further, we wondered whether oral potassium pretreatment could prevent terbutaline-induced hypokalemia. Therefore, 10 healthy volunteers (5 men, 5 women; mean age, 23 yr +/- 3 SD) received either sodium chloride (NaCl) or somatostatin intravenously together with 0.25 mg terbutaline subcutaneously in a double-blind crossover design. On a third test day, they received 39 mval of K+ powder orally before terbutaline injection in an open trial. Terbutaline caused a significant decrease of K+ (from 3.96 +/- 0.08 to 3.3 +/- 0.13 mmol/L +/- SEM; p less than 0.0005), accompanied by a significant increase in plasma glucose (from 83 +/- 3.6 to 101 +/- 4.4 mg/dl +/- SEM; p less than 0.01) and serum insulin concentrations (from 11.7 +/- 0.9 to 19.9 +/- 1.1 microU/ml +/- SEM; p less than 0.001), confirming earlier data. Somatostatin pretreatment inhibited the terbutaline-induced hypokalemia; the small fall of K+ (from 3.7 +/- 0.08 to 3.5 +/- 0.2 mmol/L) was no longer significant. Insulin secretion was completely blocked by somatostatin, leading to an even more pronounced increase of blood glucose. Hypokalemia after terbutaline injection was not prevented by oral potassium pretreatment. In summary, the present findings confirm that terbutaline-induced hypokalemia is associated with increased plasma glucose and insulin levels.(ABSTRACT TRUNCATED AT 250 WORDS)

Administration, Oral↗
PubMed1995

Hypokalemia in outpatients with eating disorders.

OBJECTIVE: The literature on the prevalence and importance of hypokalemia in persons with eating disorders in contradictory and confusing. The authors investigated the frequency of hypokalemia and its relationship to symptoms in a group of outpatients with eating disorders. METHOD: Diagnostic evaluations and electrolyte studies were performed for 945 outpatients meeting the DSM-III-R criteria for eating disorders at the time of their intake evaluations at a suburban clinic for eating disorders. RESULTS: Clinically significant hypokalemia was comparatively rare. A total of 43 subjects (4.6%) were hypokalemic; of these, seven (0.7% of all subjects) were borderline hypokalemic (serum potassium = 3.4 mmol/liter). The hypokalemic subjects had a significantly lower mean weight and body mass index at entry than the normokalemic subjects. Significantly more of the hypokalemic subjects purged by abusing laxatives, either alone or with vomiting. The patients with restricting (nonpurging) anorexia nervosa, even those whose weights were very low, were generally normokalemic. CONCLUSIONS: The low frequency of hypokalemia in this group of eating disordered outpatients suggests that routine electrolyte determination is a poor screening tool for occult or denied bulimia. Hypokalemia occurred almost invariably in lower-weight bulimic (or anorectic/bulimic) patients who were vomiting and/or abusing laxatives. Indeed, the study suggests that hypokalemia in a patient with an eating disorder is virtually certain evidence that the patient is purging at least daily. In addition, it appears that a patient with purely restricting anorexia nervosa is not at risk for hypokalemia even if his or her weight is very low.

Adolescent↗