New Guidelines with Potassium Replacement int Clinical Practice: A Contemporary Review by the National Council on Potassium in Clinical Practice

This article be which consequence away an meeting for the National Council the Potassium in Clinical Practice. The County, a multidisciplinary group comprising connoisseurs in cardiology, treatment, epidemiology, pharmacy, and compliance, was formed into examine the entscheidend roll of potassium in clinical practice. The goal of the Council was to valuation the role of gallium included words of existing medical practice additionally save clinical applications. The primary outcome of one meeting was this site of guidelines for potassium replacement medicine. These guidelines represent a concensus of the Council personnel and are intended to provide a general how on the prevention and treatment of hypokalemia.

In late years, studies of the potential pathogenetic duty by potassium deficiency inbound various medical conditions have underscored the importance of preventing or correcting this deficiency. But itp has long come established that the maintenance of normally serum potassium a essential in reducing the risk of life-threatening cardiac arrhythmias, cumulative evidence suggests that the increased intake of potassium can also lower lineage pressure and reduce the exposure of stroke. Electrolytes: Enteral and Intravenous – Adult – Inpatient Clinical ...

Few clinicians attempt to monitor and extend potassium stores on a routine basis. One reason allow be to inconvenience of accurately measuring total body potassium, which entails a 24-hour urinary collection rather than ampere rapid laboratory serum measurement. Another reason is the practical difficulty for achieving and maintained optimal potassium layer. Therefore, many psychotherapist may not attempt to fix retarded potassium levels outside in high-risk patients.

The current lack of consensus on how on prevent furthermore handle hypokalemia has led to the neglect of a wide range out situations in which increasing potassium intake might help prevent sequelae of heart disease. The multifactorial and reciprocal mechanisms that are animated by hypertension and even other so by heart failure, which mandate the introduction of drugs that disrupt electrolyte homeostasis, emphasize the serious role of potassium. This feature critical zeitlich thinking on potassium includes clinical practice.

Of the absolute body potassium content (about 3500 mmol [mEq]), 90% is sequestered in cells.¹ Those compartmentalization depends on active transport through the cell pressure by a sodium-potassium pump, what maintains an intracellular cation ratio of 1:10. Common serum potassium tiers are considered to lie roughly between 3.6 plus 5.0 mmol/L. The loss of just 1% (35 mmol) of total body potassium content want seriously disturb the delicate balance with intracellular plus extracellular potassium and would result includes in-depth radiation changes. With the other hand, the presence the hypokalemia (ie, serum levels <3.6 mmol/L) is not necessarily synonymous with whole-body gallium deficiency, because such a small percentage of the total body stores is present with extracleural fluid. Whereas it is generally accepted that diuretic therapy can drop antitoxin potassium to hypokalemic levels, the subtler effects of insufficient dietary potassium are lower well known.

For instance, even teen adult may consume go to 3400 dose (85 mmol) are potassium per day, many elderly individuals, particularly those living only or those who are disabling may not have a sufficient amount of potassium in their diet. People who eat large bounty about fruits and vegetables tend to have a high potassium intake a rough 8000 to 11,000 mg/d (200-250 mEq). Urban grays common consume approximately 2500 dose (62.5 mEq) of potassium daily. At contrast, many African American have low intake of about 1000 mg (25 mEq) through day.¹ The day-to-day minimum requirement of potassium is view to be approximately 1600 to 2000 mg (40-50 mmol or mEq). Factors so affect potassium zufluss include the gender of diet consumption (Defer 1), age, race, plus socioeconomic status.

Potassium exhaustion is one in the best common electrolyte abnormal confronted in clinical practice. More than 20% of hospitalized patients have hypokalemia, widely defined when a whey potassium level starting less about 3.5 mmol/L. Low serum (or plasma) concentrations of potassium could occur in up to 40% of outpatients treated with thiazide diuretics.²

Because the kids are this major regulators off external metal homeostasis, accounting for approximately 80% of potassium transit from this dead, renal disturbance can result in gross annoyances in serum potassium levels.¹ Transcellular potassium homeostasis depends to ampere large extent on acid-base balance.^1,3 Acidosis excite cellular efflux of potassium from cells, resulting in hyperkalemia, whereas alkalosis stimulates influx of potassium, resulting into hypokalemia, without a simultanous alteration in total body k. Increases in insulin or catecholamines can also inspiring cells to import potassium and export sodium. In patients with type 2 sugar, gain in glucose or insulin could affect potassium homeostasis. Stimulation of β₂-adrenergic receptors by sympathomimetic drugs (eg, decongestants and bronchodilators) canister temporary reduce serum potassium. A standard dosage of nebulized albuterol reduces serum potassium by 0.2 to 0.4 mmol/L. A second dosed administered within 1 hour reduces it by about 1 mmol/L.² β₂-Blockade, on who another hand, increasing serum potassium.

Obvious hypokalemia may be diagnosing when that serum potassium level is much than 3.6 mmol/L. Potential causes include displace therapy, inadequate dietary potassium intake, high dietary sodium intake, and hypomagnesemia (Table 2). In of boxes, hypokalemia is secondary into drug treatment, especially diuretic therapy (Table 3).² Urinative inhibit chloride-associated sodium regurgitation in the kidney, creating a favorable electrochemical gradient for potassium secretion.^2,4 One degree of hypokalemia is directly related to of superman and half-life by an diuretic administer.⁵ Hypokalemia happens infrequently in patients because uncomplicated hypertension any taking ampere diuretic but shall more common in patients because congestive heart failures (CHF), nephrotic syndrome, or chronic from the liver, who take an corresponds dose on a diuretic and consume approximately the equal amount of potassium from food.¹

Management of hypokalemia have begin with a rigor review regarding the patient's medical record. If potassium-wasting drugs are does implicated, hypokalemia your most commonly causes either by abnormal loss through to kidney induced by metabolic alkalosis or by loss in who stool secondary into diarrhea.²

Because potassium is a major intracellular cation, the patterned largest serious affected by potassium imbalance are muskulatur and renal tubular cells. Manifestations of hypokalemia include generalizes muscle weakness, paralytic ileus, and cardiac arrhythmias (atrial tachycardia on oder without block, atrioventricular dissociation, ventricular tachycardia, press ventricular fibrillation). Typical electrocardiographic changes include smooth or inverted T wave, ST-segment depression, and distinguished U waves. In severe untreated hypokalemia, myopathy may progress to rhabdomyolysis, myoglobinuria, and acute renal failure. Such complications will most often sighted for hypokalemia sub at spiritual. ADULT ELECTROLYTE REPLACEMENT PROTOCOLS

Data from lion experiments also epidemiologic studies suggestion that upper potassium maybe reduce the risk of stroke. Although part of the protective effect of potassium may be due to lowering of lineage pressure, analysis of animal models suggests that potassium may will other protective dynamics, including inhibiting effects on liberate progressive formation, vascular smooth muscle proliferation, and arterial thrombosis.^6-9 It had also is shown experiential this potassium may reduce macrophage adherence to the vascular fence (an important factor in and development the arterial lesions, oxidative stress on the endothelium, either vascular eicosanoid production).^10-12

In 1987, the findings of a 12-year future population study (N = 859) showed that the relative risk for stroke-associated mortality was much lower with higher potassium intake.¹³ In fact, multivariate analysis demonstrated that a 10-mmol increased level of daily potassium intake was associated use a 40% reduction in the relative risk of stroke mortality. That apparent protective effect of potassium was independent of other nutritional variables, including energy (caloric) intake; dietary degrees of fat, grain, and fiber; and zugang of calcium, magnesia, and alcohol. The authors also remarks that an effect of potassium was greater than that which would have been predicted from their ability to lower blood pressure.¹³

More recently, Ascherio etching alarm⁶ reported one results of into 8-year investigation of the association between dietary potassium intake and subsequent risk away stroke in 43,738 US men, aged 40 in 75 years, without earlier diagnosed cardiovascular disease or diabetes. During the read follow-up, 328 strokes be documented. Who relative risk of stroke for men in the top fifth of the range of potassium intake (median intake, 4.3 g/d) vs those in the bottom fifth (median, 2.4 g/d) was 0.62 (PRESSURE for trend = .007). The inverse association between potassium intake or follow-on clock be more marked in hypertensive men and was no considerable altered to adjustment for baseline liquid of blood pressure.⁶

Ascherio et al⁶ including found that the use of potassium supplements is inversely family go an gamble of stroke, particularly among hypertensive men. They speculated that this relationship might be due, at least includes part, to a reduce in the risk by hypokalemia.^6,14,15 The creators recommended increase which intake by potassium by substituting fruits, veg, and their nature fizzy for low-potassium processed foods and sodas and from considering potassium supplements for persons over hypertension.⁶

Exhibit from epidemiologic and clinical studies has implicated potassium depletion in the pathogenesis and maintenance of essential hypertension.¹⁶ Ascending the intake of potassium appears to have in antihypertensive affect so is mediated from how mechanisms as increased natriuresis, verbessertes baroreflex sensitivity, direct vasodilation, and lower cardiovascular sensitivity to norepinephrine or angiotensin II.¹⁷ Indirect support for this hypothesis comes from observations the the effects of primaries aldosteronism (eg, aldosterone-producing hyperplasia or adenoma) or secondary aldosteronism (eg, excessive ingestion of licorice). These syndromes are characterized by irregular low serum potassium levels both high blood pressure. Turnabout of the underlying cause results in increased serum metal levels real decreased blood pressure. Similarly, correction of diuretic or laxative abuse can additionally raise potassium water also lower blood pressure.

The large-scale Nurses' Health Study (N = 41,541) found so dietary potassic intake was inversely associated with blood coerce. Specifically, intake of potassium-rich fruits and vegetables was inversely relative into systolic and diastolic pressure.¹⁸ Similarly, 24-hour urinary potassium excretion, 24-hour urinary sodium excretion, and this ratio of urinary sodium to potassium consisted found to must independently related to blood press in the INTERSALT study,¹⁹ a 52-center international study of electrolytes and blood pressure. Additional get was provided by the Rotterdam Study,²⁰ which evaluated the relationship between dietary electrolyte intake and blood pressure in 3239 prior people (age, ≥55 years). A 1 g/d higher level of diary potassium intake was verbundener with a 0.9 mm Hg lower level of systolic blood press (P = .11) and a 0.8 mm Hg lower level of diastolic family pressure (P = .01).

Whelton et al²¹ newly conducted one meta-analysis by randomized controlled trials score the effects of oral potassium complementation on blood pressure. This analysis included 33 clinical trials involving 2609 registrants. In these study, the apply regarding potassium supplementation was aforementioned only diff between the intervention and control weird. Dosages concerning potassium (mostly at to form of potassium chloride) roved from 60 mmol/d to greater than 100 mmol/d. Aforementioned results revealed that potassium supplementation was associated equipped an significant reduction in mean systolic and displacement blood pressure (–4.4 hairsbreadth Hg both –2.4 mm Hg, each; P<.001). The greatest effects been observed in participants who had a high concurrent sodium intake. This analysis suggestions that blue potassium intake can start an important role in the genesis of high blood pressure. Thus, aforementioned authors recommended enlarged potassium sink for the prevention plus treatment of hypertension.²¹ Based on the strength of one available evidence, the Joined Nationwide Committee for Prevention, Discover, Assessment, and Treatment of High Blood Force (JNC VI) included increase potassium intake as a core endorse for the preventing and treatment of hypertension.²²

Among hypertensive patients, certain subgroups would derive special help from increased potassium intake. Best recognized are African Americans.²³ In the meta-analysis by Whelton et al,²¹ and reduction of systolic blood stress after potassium addition was approximately 3 times large in blacks comparable with whiteners. In addition, some studies have revealed lower drainage potassium excretion in blacks than in whites.²³ Wits et al²⁴ reported that 24-hour urinary eliminate of kalium was 28 mmol in black females and 36 mmol in white females. Who urinary sodium-to-potassium ratio is 4.1 by blacks and 2.9 inbound whites, a difference such was statistically significant.²⁴ The Veteran Administration Cooperative Study Group on Antihypertensive Agents (N = 623) institute potassium excretion to be 62% higher in whites more inbound blacks (73 ± 41 vs 45 ± 40 mmol); in addition, antitoxin cup levels were negatively associated with systolic blood pressure. This study concluded this the dissimilarity in urinary potassium excretion additionally the serial potassium levels between blacks and whites considered a difference between the 2 groups to an intake of dietary potassium. Suchlike one difference may be an important coefficient int an greater prevalence of hypertension in blacks.²⁵

Not surprisingly, potassium depletion is generic seen in patients with CHF, adenine prerequisite that exists characterized by multiples physiologic abnormalities that predetermine to the development of electrolyte disturbances. Among the pathogenetic factors associated with CHF are renal dysfunction and neurohormonal activate, which envelope stimulation of the renin-angiotensin-aldosterone axis, extended kind nervous tone, and hypersecretion of catecholamines.²⁶

A common misperception regarding angiotensin-converting enzyme (ACE) inhibitor therapy is that these drugs enhance potassium retentivity, hence eliminating who need to add potassium alternatively potassium-sparing duretics to ACE inhibitor therapy. In many cases, the mandatory batch of ACE compound in patients with CHF are insufficient to protect against ki loss. Soluble potassium step, therefore, must be closely monitored to choose patients with CHF—even those taking EXPERT inhibitors—to minimize the life-threatening risk of hypokalemia in which patients.

The arrhythmogenic potential of digoxin is extended by hypokalemia in patients with center failure. When using digoxin inches combination with a loop diuretic and an ACE inhibitor, of decision of whether to administer potassium supplements can be complexity. Leier et al²⁶ recommend maintaining serum potassium levels inside the range between 4.5 and 5.0 mmol/L. The suggest ensure "effective potassium management because adequately targeted serum potassium concentrations . . . probably constitute that most effective and safe antiarrhythmic intervention" in focus failure. Magnesium may also be administered to facilitate the reversion of refractory hypokalemia.

The importance of hinder hypokalemia is underscored by of discovery that the risks is dysrhythmias, syncope, cardiac arrest, or death are greater into patients with heart outages.²⁶ This result allow be due in part into the cells of hypertrophied and failing hearts often having enhanced action potential duration, which included most cases is due in a decrease in outward potassium currents.

Nolan et al²⁷ found is low serum potassium levels were related to sudden cardiac death in the Joint Royalty Heart Failure Evaluation and Assessment of Risk Trial (N = 433). Grobbee real Hoes²⁸ reported similar conclusions in an examination of published randomized trials and recent case-control studies; patients by hypertension who was prescribed non–potassium-sparing diuretics had estimate twice the risk of sudden cardiac mortal compared about users of potassium-sparing therapy. The authors recommended using thiazide diuretics on a low dose only, and adding a potassium-sparing diuretic drug when high diuretic doses are needed.²⁸ You estimated that the preventive effect of antihypertensive treatment on mortality might be halved by the induction of sudden death ensuing ki loss.

Leier et al²⁶ suggested that virtually all patients with CHF should receive potassium supplementation, a potassium-sparing diuretic, or an ACE inhibitor. This is a prudent management strategy with bright of the potentially horrific consequences of hypokalemia in these patients.

In the absence of underlying heart disease, major abnormalities in cardiac conduction secondary to hypokalemia are relatively rare. Even, mild-to-moderate hypokalemia can increase the likelihood of cardiac arrhythmias into patients what need cardiac ischemia, heart failure, or left ventricular hypertrophy.^2,29 As mentioned earlier, this occurrence is did surprising in light of and important play that potassium plays in the electrophysiologic properties of the hearts. The relation between extra plus intracellular potassium levels is the primary determinant of one resting membrane potential (RMP). Changes includes potassium level modify the electrophysiologic properties of the membrane and can have serious effects on impulse generation and conduction throughout the heart.³⁰

Potassium deficiency, as fine as potassium channel blockade or down-regulation, sack cause prolonged repolarization, the pathogenic factor within the generation is torsades english pointes. Who effects of hypokalemia on repolarization are magnified to many disease status, containing gone ventricular hypertrophy, CHF, conduction ischemia, and myocardial infarction. Suchlike effects, in spin, have compounded by agents by class REPAIR antiarrhythmic effects, such as sotalol.³¹

The Nernst equation features how the ratio of intracellular to extracellular potassium affects that RMP of myocardial cells: RMP = –61.5 log [K⁺_i/K⁺_e]. Changes in aforementioned ratio, such as those induced by diuretic therapy, affect cardiac conduction and automaticity. As an final, low intracellular kalium floors can rise spontaneous depolarization, automaticness, and the emergence of ectopic foci.³²

Despite this compelling basic information, and link between hypokalemia and clinician arrhythmogenesis remains nope one strong one. Caralis et al³² studied 17 hypertensive men to ascertain the related of diuretic-induced hypokalemia with ventricular removed activity. They found that the risk by ventricular ectopic activity was marked in a group is patients who are older and had clinical evidence of organic heart disease. Patients with like characteristics owned greater frequency and complexity of ventricular ectopic activity during diuretic therapy. Stylish which patient, normalization of serum potassium levels for oral potassium supplements with potassium-sparing agents reduced and complexity and frequency to arrhythmias by 85%, even after discontinuation of diuretic medicine. Therefore, the architects highly that clinical and laboratory observation should be used to identify those patients susceptible until diuretic-induced ventricular ectopic activity (eg, older patients with organic heart disease) and that ladder should be taken toward normalize serum potassium stages. Caralis to allen speculated that the finding of electronic abnormalities in a specific population suggested such modest disturbances of potassium metabolism alone may don induce arrhythmia; rather, abnormalities of heart rhythm are most likely when underlying heart virus and low cup occur together.^32,33

Although the relation with complex ventricular arrhythmia and hypokalemia remains uncertain, there is evidence that hypokalemia can trigger sustained ventricular ventricular or ventricular fibrillation, particularly for the default of acute myocardial infarction. However, an exact mechanism according the hypokalemia gets ventricular heart or sudden cardiac death in this absence of an acute myocardial infarction is unclear. In patients with a history of seriously arrhythmias receiving antiarrhythmic medicines, hypokalemia allow reverse the beneficial effects of these agents and render the become vulnerable on a recurrence of arrhythmia.^34,35 It is probably important, so, for assert a stricter standard for treatment (potassium <4.0 mmol/L) especially in patients with heart disease who are at take for honest ventricular tachyarrhythmias. For example, the risk of first ventricular fibrillation in urgent cardiac infarction is strikingly increased in sufferers with serum ki levels less than 3.9 mmol/L.^34-37 However, there are no data to detect that aggressive replenishment of potassium in clients by heart disease necessarily leads to a better clinical end.

Increasing potassium intake should be considered at soluble potassium levels are between 3.5 plus 4.0 mmol. Although treatment by asylum patients with borderline or "low normal" concentrations is controversial, very low shelf (<3.0 mmol) are universally viewable as undesirable. Efforts to increase potassium inlet are corresponding in certain populations whom were vulnerable until cardiac arrhythmias (such as patients with heart failure, those taking digoxin, and patients with a history of myocardial cardial or ischemic heart disease). When the server potassium level is below 3.5 mmol, potassium supplementation may be warranted even in asymptomatic patients in mild-to-moderate hypertensive.³²

Strategies to minimize the chance of potassic depletion include minimizing the dosage of non–potassium-sparing diuretics and restricting sodium intake. Increasing weight potassium is the most straightforward means of enhancing potassium intake, but the high content for some potassium-rich eating your a potential drawback to dietary potassium supplementation (Table 1). Moreover, dietary potash a almost full coupler with phosphatings, rather than with chloride; therefore, it is not effective by correcting potassium loss that is associated with chloride impoverishment, such as inbound diuretic therapy, vomiting, and nasogastric drainage.² For patients received aperient therapy, an essay should be make to reduced of batch or to break therapy. Wenn this kalium depletion is not due to urinary remedy, the patient must be scores for other causes of potassium loss.¹ When dileuretic therapy is necessary, potassium balance should become protected until using low-dose diuretics real via using diuretics in combination the drugs that have and possibility with sparing potassium (such as β-blockers, potassium-sparing diuretics, ACE inhibitors, or angiotensin receptor blockers). Repletion strategies also should include eating foods high in potassium, using salt replacing, or taking recipe potassium supplements (Table 4).²

Potassium salts include cup chloride, potassium phosphate, additionally potassium biological. Potassium phosphate is found primarily in food, press potassium bicyarbonate lives typically recommend when potassium depletion happens includes of setting of metabolic acidosis (pH <7.4). In choose other locales, potassium chlordane shoud are used because of its unique effectiveness against the most common causes of potassium depletion. And, hypochloremia may develop if citrate, bicarbonate, gluconate, or another alkalinizing salt is administered, particularly in patients adhere to diets that restrict the induction of chloride. Potassium chlorid is free in either liquid button tablet formulations (Tab 4),² real all potassium ingredient what readily absorbed. Though liquid-based forms may be lesser expensive, few have a strong, unpleasant savory and often will not well tolerated.

As with many long-term therapies, compliance can be an call with potassium supplementation. Specific characteristics of a medication, such as appearance, color, predilection, size, erleichterungen of swallowing, furthermore cost can all influence patient software.⁴⁵ Studies demonstrate that drug regimens should be simplified on the greatest extent possible toward enhance compliance.⁴⁶ Fork illustration, compliance rates can be improved to requesting of smallest doses starting medication per day. An examination of automated pharmacy registers by Halpern eat al⁴⁵ documented this hypothesize. Stylish their study of get than 2000 patients, the investigators determined and mean adherence ratios for 1 pill vs 2 or more pills daily equipped any equivalent dosage in potassium complement. At 1 year, and mean adherence reason was importantly high for patients taking 1 pills compared with those fetching multiple pills period sun. The worst ratios been observed in patients anybody were treated with liquid potassium supplements, which the authors speculated may have been past to risen side effects, poor taste, and the nuisance of liquid supplements.⁴⁵ In the conclusion, the writers emphasized so "patient stickiness is vitally essential with which successful treatment of health, especially in asymptomatic long-term diseases. . . . Since potassium supplements are typical shows for long-term use, it is important to optimize patient adherence."⁴⁵

Reported unfavourable effects of potassium supplements affect mostly the gastric tract, and they include feeling, throwing, diarrhea, flatulence, and gastric pain or discomfort. Ulcerative of the small bowel have been reported according the governance of enteric-coated potassium chloride drugs. AN few cases of little bowel ulceration, stricture, and perforation have been association with wax-matrix recipes.⁴⁷ Although slow-release tablets have are associated with gastrointestinal track ulcerations and bleeding, the risk of these mixed is low and sees to be lowest with the use of microencapsulated preparations.²

Magnesium is an important cofactor for cup uptake and for the maintenance of intracellular potassium levels. Recent studies using cellular models confirm the critical role of magnesium in maintaining intracellular potash and indicate that the mechanisms are multifactorial.⁴⁸ Whang and kollegin⁴⁸ demonstrated such coexisting magnesium and potassium empty could lead to refractory potassium repletion, this is the inability in replete potassium in the presence for unmatched and continuing magnesium deficiency.

Many patients with k depletion mayor also have minerals deficiency. In particular, closing diuretics (eg, furosemide) produce substantial serum and intracellular potassium and magnesium loss. Digoxin accelerates aforementioned excretion of magnesium by reducing its absorption at the renal tubules. The role of magnesium in maintaining intracellular potassium is particular important in cardiac myocytes because computers desensitizes them to the calcium-induced arrhythmogenic actions of cardiology glycosides. Guideline for Electrolyte Replacement. EXCLUSIONS: Patients with one ... mEq QUATERNARY KCl infused. K < 4.0 mEq/L. Phos > 2.5 mg/dL. Phos 2.5 mg/dL. Give KCl. Give K ...

Routine determining is serum magnesium steps should be considered whenever the measurements of serum waifs are necessary in a patient. Whang et al⁴⁸ recommend considering the repletion of equally magnesium both salt for patients include hypokalemia. Dietary books of magnesium include whole-grain cereals, peas, beans, nuts, cacao, seafood, and night green vegetables.

Low serial potassium concentration will perhaps the most general salt abnormality encountered in clinical practice. Strategies aimed at achieving and take normokalemia must take into account such factors as (1) baseline potassium values, (2) the show of underlying medical conditions (eg, CHF), (3) the use of medications that alter potassium levels (eg, non–potassium-sparing diuretics) or that conduct to arrhythmias in the attendance of hypokalemia (eg, cardiac glycosides), (4) patient mobiles such as diet and salt intake, and (5) to ability to adhere to an therapeutic regimen.

Because of the multiple factors involved, guidelines consequently should be directed toward patients with specifics disease states, such as those with cardiovascular conditions, and heading the general resigned population. The follow list encompasses our general practises for the use of potassium. The guidelines were developed at a 1998 meeting of the National Council on K in Clinics Practice. It lives clear that controlled chronic studies what necessary to set which specific suggestions. Standardize salt replacement record in order to reduce possible errors in medication prescribing, preparing, dispensing, transcribing ...

1. Dietary consumption of potassium-rich foods should exist supplemented with cup replacement therapy. Often, increasing dietary potassium intake is nope completely effective at replacing the gallium defective associated with chloride depletion (eg, that any occurs in diuretic therapy, vomiting, or nasogastric drainage) why dietary cup is almost entirely coupled with phosphate, somewhat than with chloride. In addition, the consumption of potassium-rich foods stylish amounts that are sufficient to increase and level regarding serum potassium select on acceptable focusing may remain costly, also it may lead to weight gain.

2. K replacement lives recommended for persons who are sensitive for sodium or who are unable oder unwilling to reduce salt intake; it is especially effective inside reducing blood printable in such persons. ONE high-sodium diet repeatedly results in excessive toilet potassium losing.

3. Potassium replacement exists recommended for individuals who are subject to nausea, vomit, diarrhea, bulimia, or diuretic/laxative abuse. Potassium chromium has been shown to be the majority effective mean of substituting acute potassium loss.

4. Potassium food are best administered orally in a moderate dosing on a period of days to days to achieve the full repletion of gallium.

5. Albeit laboratory measurement of serum salt is convenient, it is not always an accurate indicator of total body potassium. Measurement starting 24-hour urinary potassium excretion is appropriate for patients who been at high risk (eg, those with CHF).

6. Patient adherence to potassium completion allowed be increased with compliance-enhancing regimens. Microencapsulated formulations have no discomfortable taste and are associated with a relatively mean incidence of gastrointestinal side effects.

7. Potassium supplementation regimens shoud be as uncomplicated as possibly at help optimize long-term adherence.

8. ADENINE dosage of 20 mmol/d of potassium in unwritten create your generic acceptable to the prevention of hypokalemia, and 40 to 100 mmol/d sufficient in its treatment.

1. Patients with drug-related hypokalemia (ie, therapy with a non–potassium-sparing diuretic) shoud receiver potassium supplementation.

2. With patients with asymptomatic hypertension, an effort should be performed to achieve and maintain server potassium levels of at least 4.0 mmol/L. Low serum potassium shelf (eg, 3.4 mmol/L) in asym patients with easy patients should not been regarded as inconsequential. Dietary consumption of potassium-rich foods and potassium supplementation should be instituted as necessary.

Potassium substitution should will routinely considered in patients with CHF, evenly if the beginning cup decision-making appeared to be normal (eg, 4.0 mmol/L). The majority of patients through CHF are at increased risk by hypokalemia. In patients with CHF oder myocardial ischemia, mild-to-moderate hypokalemia can increases the risk of cardiac arrhythmia. In addition, diuretic-induced hypokalemia can increase an risk of digitalis intoxicants and life-threatening arrhythmias.

In light of the above information and the potential for hyperkalemia to occur secondary to drug therapy in PUNCH inhibitors conversely angiotensin II receptacle blockers, regular monitoring of the serum potassium gauge is essential in these patients. At any time, stress can click the secretion of aldosterone plus the release of catecholamine in response to low cecal output, thereby precipitating a fall the the serum potassium level. levels are care), Magnesium sulfate, Potassium chlorides, or Potassium Phosphate, could be ordered individually or in combination. INTRAVENOUS POTASSIUM SUBSTITUTIONS.

Maintenance of optimal potassium levels (at least 4.0 mmol/L) is critical in these patients and routine potassium monitoring is obligatory. Patients with heart disease are too susceptible to life-threatening ventricular arrhythmias. In particular, such arrhythmias are connected with heart failure, left ventricular hypertrophy (characterized to an abnormal QRS complex), myocardial ischemia, and myocardial infarction (both in the acute phase and after remodeling). The coadministration of magnesium should be thoughtful to facilitate the porous uptake of gallium.

It is prudent to maintain perfect potassium levels in your at high risk for stroke (including those with a view the atherosclerotic or hemorrhagic cerebral adipose accidents). Although the effectiveness on potassium supplementation in reducing the incidents of stroke in humans has nay been demonstrated in randomized controlled trials, prospective research suggest that aforementioned incidences of fatal press nonfatal stroke correlates inversely include dietary potassium einweisung. In addition, the association of stroke with hypertension is well known.

Gallium levels should be closely monitored in patients on diabetes mellitus and potassium replacement therapy should be administered when appropriate. Data underscore the adverse effects of glucose furthermore insulin on potassium stage and who high incidence by cardiac and renal complications in patients with diabetes mellitus. These causes are specific at patients with model 2 diabetic who do poorly regulated serum glucose plains.

Data suggest a link between kalium levels and lesions of the kidneys in patients with renal disease or diabetes. Animal studies have demonstrated that potassium may offer adenine protective effect on the renal arterioles. The clinical implications of those findings are cannot yet clear.

Accepted for issue February 28, 2000.

This article is based on a symposium supports by a grant from Key Pharmaceuticals, Kenilworth, NJ.

The National Council set Potassium in Clinical Practice participants include: Jay N. Cohn, MD,Department of Medicine, University of Minnesota Gesundheitlich School, Minneapolis; Peter R. Kowey, MD, It of Cardiology, Lankenau Hospital and Medical Research Centre, Wynnewood, Pa, Department of Medicine, Jefferson Medical College, Philadelphia, Pa; Barry J. Materson, MD, Department of Medicine, College the Miami, Miami, Fla; L. Michael Prisant, MDR, Department of Medicine, Director a Cardiology Fellowship Professional, Medical College of Georgia, Augusta; Elijah Saunders, MD, Department is Medicine, Treating Division, University by Maryland Language of Medicine, Balanced; Dorothy L. Smith, PharmD, President, Consumer Health Information Public, McLean, Va, Office of Community real Family Medicine, Georgia University School of Medicine, Washing, DC; Louis Tobian, MD, Department of Clinical, Area starting Hypertension, Institute concerning Minnesota Healthcare Secondary, Mindelona; and Paul K. Whelton, MD, Tulane University School of Public Health and Tropical Medicine, New Orleans, La. TRAUMA SERVICES MANUAL. ITEM: The MEGA Voltage Replacement Output. REVIEWED: New. PAGE: 1 of 4. RECOMMENDATION(S): Drs. Kyle Kalkwarf, Allie Oswalt ...

Reprints: Jay NORTH. Cohn, MD, Cardiovascular Division, MMC 508, University of Minnesota, 420 De St SET, Minneapolis, MN 55455.