Higher Plasma Potassium Levels Research Articles

Risk Factors and Outcomes for Preoperative Asymptomatic Pulmonary Embolism in Patients Aged 60 Years and Over with Hip Fracture.

ObjectiveTo investigate the risk factors for, and outcomes of, preoperative asymptomatic pulmonary embolism (PE) in patients ≥60 years old following delayed operation for hip fracture.MethodsFrom March 2017 to December 2018, 90 patients aged ≥60 years with hip fracture who suffered a delay in surgery were recruited to this prospective study following admission to our hospital. Computed tomography pulmonary angiography (CTPA) was used to detect preoperative asymptomatic PE and calculated its incidence. Time from injury to admission, baseline characteristics, medical comorbidities, and blood biomarker levels were evaluated as potential risk factors. Logistic regression analysis was used to identify risk factors. Mortality and major bleeding events were recorded and compared between individuals with PE and without. Data were analyzed by t‐test, Mann–Whitney U test, χ 2 test, Fisher's exact test, and logistic regression analysis.ResultsThe incidence of preoperative asymptomatic PE was 18.9% (17/90 patients). In the univariate analysis, the risk factors for preoperative asymptomatic PE were male sex, hypertension, cerebrovascular accident, smoking, plasma D‐dimer level, potassium level, urea level, creatinine level, and cysteine level. Multivariate logistic regression analysis showed that the risk of preoperative asymptomatic PE was higher in patients with hypertension (odds ratio [OR] = 10.048; 95% confidence interval [CI], 1.118–90.333), cerebrovascular accident (OR = 20.135; 95% CI, 1.875–216.164), smoking (OR = 48.741; 95% CI, 4.155–571.788), high plasma D‐dimer levels (OR = 1.200; 95% CI, 1.062–157.300), and high plasma potassium levels (OR = 12.928; 95% CI, 1.062–157.300). All patients were followed up for 21.0 months (range, 2 to 36 months). Mortality within the first year postoperatively was higher in patients with PE (29.41% vs 9.59%, P = 0.046).ConclusionsIn view of the high incidence of preoperative asymptomatic PE and the inferior prognosis in individuals with PE, routine CTPA examination for preoperative asymptomatic PE could be useful for patients aged ≥60 years with hip fracture for whom surgery is delayed.

Early recognition of reverse pseudohyperkalemia in heparin plasma samples during leukemic hyperleukocytosis can prevent iatrogenic hypokalemia

ObjectivesTo investigate the cause of apparent hyperkalemia in leukemic heparin plasma. Design and methodsLithium heparin plasma and serum samples from a patient with chronic lymphocytic leukemia (CLL) with hyperleukocytosis were transported by either a pneumatic tube system or manual transport and analyzed either immediately or after 4h. ResultsPneumatic tube transported samples resulted in higher plasma potassium levels than manually transported samples. Serum potassium was lower than plasma potassium, confirming the suspicion of “reverse” pseudohyperkalemia. Letting the pneumatic tube transported samples stand on the bench for 4h before centrifugation surprisingly resulted in decreased or unchanged plasma potassium. ConclusionsThe reverse pseudohyperkalemia in heparin plasma samples from a CLL patient was caused by pneumatic tube transport. Our results suggest extracellular leakage of potassium, followed by active transport of potassium into intact leukemic cells. This is the first Swedish case of reverse pseudohyperkalemia in a CLL patient, where clinical suspicion of false hyperkalemia and awareness of the phenomenon lead to a rapid laboratory diagnosis. The demonstration of reverse pseudohyperkalemia prevented potentially dangerous medical interventions, such as potassium lowering treatment.

Pathogenesis of Hypertension: Interactions Among Sodium, Potassium, and Aldosterone

Arterial hypertension is a major cause of disease-related morbidity and mortality worldwide. It is nearly absent in populations that consume natural foods low in sodium. However, in industrial countries, where the individual intake of sodium is at least 10 times higher, the prevalence of hypertension is approximately 40%. Major population-based studies link a high-sodium and low-potassium diet to an increase in blood pressure. A hallmark of arterial hypertension is endothelial dysfunction characterized by decreased synthesis of nitric oxide (NO). Plasma sodium and potassium are major determinants for the mechanical stiffness of endothelial cells. High plasma sodium levels stiffen endothelial cells and block NO synthesis. Aldosterone is a prerequisite for this action. However, high plasma potassium levels soften endothelial cells and activate NO release. There is increasing evidence that sodium can be stored transiently in considerable amounts and osmotically inactive in the interstitium. Taken together, it is recommended to maintain plasma sodium levels in the low physiologic range and potassium levels in the high physiologic range while suppressing plasma aldosterone as much as possible. A restriction in sodium intake that is accompanied by increased intake of potassium can profoundly improve the prevalence of hypertension and cardiovascular disease.

Validation of A Paper Based Dietary Potassium Test for Adults with Chronic Kidney Disease

TEST FOR ADULTS WITH CHRONIC KIDNEY DISEASE Katherine Baczewski Mary Julius and Elizabeth Kern, Louis Stokes Cleveland Veteran Affairs Medical Center, Cleveland, Ohio High plasma potassium levels are common in patients with chronic kidney disease (CKD) and cause life threatening cardiac dysrhythmia. Self management by dietary restriction of potassium is critical. Currently, there is no valid instrument to quickly assess patient’s knowledge of dietary potassium. The purpose of this observational study was to develop and validate a novel paperbased test of knowledge of foods containing high versus low potassium (test), designed for clinical use in adult patients with CKD who need to restrict dietary potassium intake. The 21 item test allows individuals to choose from two food items, asking them to select the item lower in dietary potassium. Two forms (A) and (B) of the test were designed as parallel forms. Statistical analysis was determined using SAS, version 9.1. 34 participants with high knowledge and 34 participants with low knowledge of dietary potassium and 10 renal dietitians participated in the research by taking the potassium test. 10 renal dietitians also rated each item as essential/non-essential for patient knowledge.

Corticosteroid-dependent hypertension: environmental influences.

Hypertension is a major disease of later life affecting 25% of the adult population in the industrialized world with most hypertensive individuals diagnosed as having essential hypertension. Approximately one third of these patients have elevated blood pressure due to increased sodium and water retention by the kidney resulting in suppressed plasma renin and aldosterone concentrations with high urinary potassium excretion and low plasma potassium levels. Monogenic forms of corticosteroid-dependent hypertension are rare. However, the discovery of these disorders has revealed genes whose proteins play a key role in the regulation of sodium homeostasis. The impaired function of these proteins, due to altered protein expression or the presence of inhibitors, contributes to the development of corticosteroid-dependent hypertension. This article focuses on the potential impact of environmental influences on corticosteroid-dependent regulation of sodium homeostasis and the development of hypertension.

Corticosteroid-dependent hypertension: environmental influences.

Hypertension is a major disease of later life affecting 25% of the adult population in the industrialized world with most hypertensive individuals diagnosed as having essential hypertension. Approximately one third of these patients have elevated blood pressure due to increased sodium and water retention by the kidney resulting in suppressed plasma renin and aldosterone concentrations with high urinary potassium excretion and low plasma potassium levels. Monogenic forms of corticosteroid-dependent hypertension are rare. However, the discovery of these disorders has revealed genes whose proteins play a key role in the regulation of sodium homeostasis. The impaired function of these proteins, due to altered protein expression or the presence of inhibitors, contributes to the development of corticosteroid-dependent hypertension. This article focuses on the potential impact of environmental influences on corticosteroid-dependent regulation of sodium homeostasis and the development of hypertension.

Neonatal mortality following transfusion of red cells with high plasma potassium levels

The death of a neonatal infant following cardiac surgery and the transfusion of packed red cells (RBCs) with high plasma potassium levels is reported. The patient had been diagnosed at 2 weeks of age as having multiple cardiac malformations. During cardiopulmonary bypass surgery, multiple units of packed RBCs less than 5 days old were transfused. In response to a "stat" order and after depletion of stock units prepared for neonatal usage, a 32-day-old unit of packed RBCs was issued for transfusion. After approximately 60 mL was rapidly transfused from this unit, the patient experienced cardiac arrest. Serum potassium concentration after transfusion and before death was 8.9 mmol per L. Plasma potassium concentration in the remainder of the transfused packed RBC unit was approximately 60 mmol per L. A model was created to calculate the posttransfusion plasma potassium concentration, and close correlation was found between the model and the observed potassium concentration, which assumes that the potassium load had not yet been distributed to the extravascular and intracellular fluid compartments. It is concluded that the transfusion of relatively large volumes of RBCs be limited to fresh packed RBCs or to packed RBCs that have been saline washed, to minimize the complications of electrolyte disturbances.

Effects of chronic angiotensin converting enzyme inhibition on glucose tolerance and insulin sensitivity in essential hypertension.

The relation between the renin-angiotensin-aldosterone (RAA) system and carbohydrate metabolism and insulin sensitivity in essential hypertension has not been investigated systematically. Twenty nondiabetic patients (age, 49 +/- 1 years; body mass index (BMI), 26.1 +/- 0.4 kg/m2) with essential hypertension (blood pressure, 155 +/- 3/105 +/- 1 mm Hg) received an oral glucose tolerance test (OGTT) at the end of a 1-month placebo period and again monthly during 3 months of angiotensin converting enzyme (ACE) inhibition (cilazapril, 5 mg/day). Furthermore, a two-step euglycemic insulin clamp was performed after placebo and again at the end of treatment. Blood pressure fell by 7 +/- 4/10 +/- 3 mm Hg (p less than 0.001), while BMI remained stable. On the euglycemic clamp, insulin-mediated (plasma insulin, 470 pM) whole body glucose use averaged 42.5 +/- 1.6 mumol.min-1.kg-1 before and 43.6 +/- 1.9 after ACE inhibition (p = NS). Substrate concentrations and oxidative rates and energy expenditure (as estimated by indirect calorimetry) were not altered by ACE inhibition, either in the fasting state or in response to insulin. In contrast, oral glucose tolerance was significantly (p less than 0.05) improved after treatment (area under OGTT curve (AUC), 240 +/- 24 versus 282 +/- 23 mmol 2 hr.l-1). The latter change was associated with enhanced (+16%, p less than 0.05) insulin responsiveness to glucose (estimated as the insulin AUC divided by the glucose AUC) throughout the 3 months of ACE inhibition. At baseline, both the OGTT and the clamp had a marked hypokalemic effect (mean decrements in plasma potassium of 0.75 +/- 0.05 and 0.92 +/- 0.05 mmol/l, respectively) in association with plasma aldosterone reductions of 30% and 50%. Chronic ACE inhibition caused a further 20% (p less than 0.03) lowering of plasma aldosterone concentrations but attenuated insulin-induced hypokalemia. Plasma sodium, which was unaltered by the pretreatment tests, fell during the posttreatment tests (by 3 mmol/l, p less than 0.001). In the urine, the ratio of the fractional excretion of potassium to that of sodium was decreased by both oral glucose (-22%, p less than 0.01) and ACE inhibition (-21%, p less than 0.001). Higher plasma potassium levels before treatment predicted a better blood pressure response to ACE inhibition (r = 0.60, p less than 0.005).(ABSTRACT TRUNCATED AT 400 WORDS)

The Diurnal Rhythm of Plasma Potassium

Plasma potassium levels have been implicated in the genesis of cardiac arrhythmias, particularly in patients receiving diuretic therapy. The present study was undertaken to evaluate the stability of plasma potassium levels throughout a 28-h period. Normal volunteers (n = 8) and subjects with essential hypertension (n = 10) were studied in a clinical research center while receiving controlled dietary intakes. Plasma potassium followed a diurnal rhythm in both groups, with a peak level at 12 h and a trough level at 24 h. The average peak-to-trough difference was 0.62 +/- 0.05 mmol/L. Urinary potassium excretion also followed a diurnal rhythm, with the lowest excretory rate during the evening hours, when plasma potassium reached its nadir. Subjects with essential hypertension were restudied after 4 weeks of hydrochlorothiazide (50 mg/day) and then after an additional 4 weeks of hydrochlorothiazide (50 mg/day) and amiloride (5 mg/day). Hydrochlorothiazide alone reduced plasma potassium at all times of measurement without altering the diurnal rhythm. The combination of hydrochlorothiazide and amiloride resulted in higher plasma potassium levels in the morning, but did not significantly affect evening plasma potassium levels. The frequency of hypokalemia (K less than or equal to 3.0 mmol/L) was related to the time at which the plasma potassium was measured. We conclude that plasma potassium undergoes a diurnal rhythm and that diuretics shift this rhythm to uniformly lower values. This rhythm must be considered when defining the frequency of hypokalemia.

Hyperkalemia after irradiation of packed red blood cells: Possible effects with intravascular fetal transfusion

Plasma potassium, calcium, and albumin concentrations in irradiated blood, and in fetal blood before and after transfusion, were measured. Dangerously high plasma potassium levels were observed in some units of irradiated packed red blood cells (range, 13.9 to 66.5 mEq/L; mean, 44.7 mEq/L) and could be one possible explanation for the high incidence of fetal arrhythmia associated with fetal intravascular transfusion. There are many factors operative in the preparation of irradiated packed red blood cells that may predispose to high potassium levels: the age of the red blood cells, the number of procedures used to concentrate the blood, the duration of time elapsed from concentration, the duration of time elapsed from irradiation, and the hematocrit. Use of fresh blood, avoidance of multiple packing procedures, limiting the hematocrit in the donor unit to ≤80%, and minimizing the time between concentration, irradiation and transfusion may minimize the potassium levels, and therefore making an additional washing procedure unnecessary.

Mechanisms by which nephrectomy stimulates adrenal renin.

Renin has been identified in the adrenal gland by several investigators. Nephrectomy is the most potent stimulator of adrenal renin, and in the present study we investigated the mechanism by which nephrectomy stimulates adrenal renin. The pituitary plays a permissive role since hypophysectomy abolished the response of adrenal renin to nephrectomy (from 117.3 +/- 14.55 to 10.37 +/- 1.63 ng angiotensin I/mg protein/hr) and adrenocorticotropic hormone (ACTH) treatment restored the response to nephrectomy in hypophysectomized rats to 120 +/- 20.62 ng angiotensin I/mg protein/hr. However, large doses of ACTH given to intact rats did not increase adrenal renin to the high level observed after nephrectomy. Potassium also plays an important role, since prevention of hyperkalemia after nephrectomy by treatment with a cation exchange resin, sodium polystyrene sulfonate (Kayexalate), significantly reduced the adrenal renin response to nephrectomy. A third factor involved is the lack of negative feedback by plasma angiotensin II. Infusion of angiotensin II intraperitoneally prevented the rise in adrenal renin after nephrectomy (from 65.25 +/- 7.60 to 9.27 +/- 0.99 ng angiotensin I/mg protein/hr) despite an increase in plasma potassium and corticosterone. In conclusion, three factors influence the response of adrenal renin to nephrectomy: 1) the pituitary through the release of ACTH, 2) a direct stimulation by high plasma potassium levels, 3) the lack of angiotensin II feedback inhibition. Whether the high adrenal renin contributes to the high aldosterone observed in rats after nephrectomy remains to be established.

Effect of angiotensin converting-enzyme inhibition on potassium-mediated aldosterone secretion in essential hypertension

1. Eight patients with essential hypertension were challenged with an infusion of 32 mmol of potassium chloride in saline before and after control of their blood pressure by the angiotensin converting-enzyme (ACE) inhibitor enalapril. 2. The potassium infusion was associated with similar increases in plasma aldosterone before and during enalapril treatment, although absolute aldosterone levels were lower after enalapril treatment despite higher plasma potassium levels. 3. The handling of the potassium load was altered by ACE inhibition. The area under the curve of a plot of the increase in plasma potassium above baseline against time was greater during enalapril treatment than during treatment with placebo. 4. These observations contrast with data obtained in the dog and demonstrate that in patients with essential hypertension stimulation of aldosterone secretion by potassium is not abolished by chronic suppression of plasma angiotensin II; and although plasma aldosterone remains at a lower level, the homoeostasis of plasma potassium is only mildly impaired.

The effects of the increase of arterial potassium upon the excitability of normal and dystrophic myotonic muscles in man

Progressively increasing concentrations of potassium chloride were administered intra-arterially to patients affected with dystrophia myotonica (Steinert's disease) and to healthy volunteers before and after parenteral taurine treatment. Changes in the excitability of thenar eminence muscles were related to plasma potassium concentrations. A rise in the plasma potassium brought about a parallel increase of muscular excitability in normal individuals whilst in dystrophic myotonic patients it was associated with a two-phase phenomenon: the severity of myotonia first decreased and then, at higher plasma potassium levels, greatly worsened with the occurrence of spontaneous myotonic discharges. The administration of taurine, a membrane-stabilizing drug, considerably lowered the excitability of both normal and dystrophic myotonic muscles. The effects of potassium and taurine on muscular membrane conductance may explain the observed changes in muscular excitability.

Falsely high plasma potassium values in patients with hyperaldosteronism.

The common practice of encouraging forearm exercise as an aid to venepuncture is a potent source of erroneously high plasma potassium levels. This may be sufficient to obscure a suspicion of hyperaldosteronism, with possible serious repercussions in hypertensive patients, in whom the diagnosis of hyperaldosteronism has important therapeutic implications. Plasma is preferable to serum for potassium estimations, and forearm exercise should be avoided before venepuncture for potassium measurements.

Body water variations in manic-depressive psychosis.

Most of the water and electrolyte studies in mental illness have been carried out on patients suffering from periodic disorders and have been reviewed by Crammer (1962). Coppen and Shaw (1963) found increases in total body water and extracellular fluid and a decrease in residual sodium space on recovery from depression. Manic patients with a high vocal productivity were found by Anderson et al. (1964) to have a negative sodium balance, low plasma potassium levels and a positive potassium balance. Depressed patients with a low vocal productivity had a reduced rate of sodium loss and higher plasma potassium levels. Dawson et al. (1956) found extracellular expansion on spontaneous recovery from manic or depressive attacks. The purpose of the present study was to investigate variations in total body water and its distribution in manic-depressive psychosis. The investigation was complementary to a similar study of variations in body composition during recovery from depression reported by Hullin et al. (1967).

ROLE OF POTASSIUM IN EPINEPHRINE-INDUCED CARDIAC ARRHYTHMIAS

Five series of experiments have been performed to investigate a possible causal relationship between the induced hyperkalemia and epinephrin-induced ventricular arrhythmias in pentobarbital anesthetized dogs. It is concluded that no causal relationship exists on the basis of the following observations. The hyperkalemic response to epinephrine is not quantitatively correlated with the induction of arrhythmias, and the ability of subthreshold doses of epinephrine to induce arrhythmias is not potentiated by the injection of exogenous potassium unless the plasma levels attained are considerably above those occurring after an arrhythmia -inducing dose of epinephrine. The ability of isoproterenol to induce cardiac arrhythmias is not enhanced by the infusion of potassium to produce blood levels comparable to those resulting from an arrhythmia-inducing dose of epinephrine. Infusion of potassium chloride to produce blood levels comparable to those induced by a previously arrhythmia-inducing dose of epinephrine does not allow the production of arrhythmias after Dibenamine blockade. Exclusion of the liver from the circulation and consequent abolition of the epinephrine-induced hyperkalennia does not prevent the production of arrhythmias by epinephrine. It was observed that very high plasma potassium levels, above those resulting from an arrhythmia-inducing dose of epinephrine, can facilitate the production of arrhythmias. The administration of exogenous potassium is particularly effective when peak levels are reached early in the course of the epinephrine action before the beginning of the epinephrine hyperkalemia. After exclusion of the liver from the circulation, the animals become more sensitive to this action of potassium. In one case potassium infusion alone induced ventricular fibrillation.