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Clinical manifestations and

treatment of hypokalemia

Author Section Editor Deputy Editor

Burton D Rose, MD Richard H Sterns, MD Theodore W Post, MD

Last literature review version 17.1: January 2009 | This topic last updated:
January 24, 2009 (More)

INTRODUCTION — Although hypokalemia can be transiently induced by the entry of

potassium into the cells, most cases result from unreplaced gastrointestinal or urinary
losses [ 1,2] . (See "Causes of hypokalemia" ).

Potassium replacement is primarily indicated when potassium has been lost; it is also
given in some cases, such as hypokalemic periodic paralysis, when hypokalemia is due
to redistribution into the cells. However, potassium is given very cautiously in the latter
setting, if at all, since the hypokalemia is transient and the administration of too much
potassium can lead to rebound hyperkalemia when the process is corrected and
potassium moves back out of the cells.

Optimal therapy is dependent upon the severity of the potassium deficit. In addition,
somewhat different considerations are required to minimize continued urinary losses
due to diuretic therapy, or less often, primary hyperaldosteronism.

The clinical manifestations and treatment of hypokalemia will be reviewed here. The
causes and diagnosis of hypokalemia are discussed separately. ( See "Causes of
hypokalemia" and see "Diagnosis of hypokalemia" ).

MANIFESTATIONS OF HYPOKALEMIA — The severity of the manifestations tends to

be proportionate to the degree and duration of hypokalemia. Symptoms generally do
not become manifest until the serum potassium is below 3.0 meq/L, unless the serum
potassium falls rapidly or the patient has a potentiating factor such as a predisposition
to arrhythmia due to the use of digitalis. Symptoms usually resolve with correction of
the hypokalemia.

Severe muscle weakness or paralysis — Muscle weakness usually does not occur
at potassium concentrations above 2.5 meq/L if the hypokalemia develops slowly [ 3] .
However, significant weakness may occur with sudden decreases, as occurs in
hypokalemic periodic paralysis, although the cause of weakness in this disorder may
be more complex. ( See "Myopathies of systemic disease" , section on Hypokalemic
myopathy).

The pattern of weakness bears similarities to what is observed with hyperkalemia. It

usually begins with the lower extremities, progresses to the trunk and upper
extremities, and can worsen to the point of paralysis. ( See "Clinical manifestations and
extremities, and can worsen to the point of paralysis. ( See "Clinical manifestations and
treatment of hyperkalemia" ).

Hypokalemia can also result in the following:

Respiratory muscle weakness, which can be severe enough to result in

respiratory failure and death.

Involvement of gastrointestinal muscles, resulting in ileus and its associated

symptoms of distension, anorexia, nausea and vomiting.

Cramps, paresthesias, tetany, muscle tenderness and atrophy.

Cardiac arrhythmias and ECG abnormalities — A variety of arrhythmias may be

seen with hypokalemia. These include premature atrial and ventricular beats, sinus
bradycardia, paroxysmal atrial or junctional tachycardia, atrioventricular block, and
ventricular tachycardia or fibrillation [ 3] . Hypokalemia produces characteristic
changes on the ECG. There is depression of the ST segment, decrease in the
amplitude of the T wave, and an increase in the amplitude of U waves which occur at
the end of the T wave ( show ECG 1 ). U waves are often seen in the lateral precordial
leads V4 to V6. ( See "ECG tutorial: Miscellaneous diagnoses" , section on Hypokalemia).

There is large variability in the actual potassium concentrations that are associated
with progression of ECG changes. In a carefully controlled trial of thiazide therapy
(hydrochlorothiazide 50 mg/day), there was a two-fold increase in ventricular
arrhythmias (as detected by Holter monitoring) in the small proportion of patients in
whom the plasma potassium concentration fell to or below 3.0 meq/L [ 4] .

In addition, the presence of concomitant factors, such as coronary ischemia, digitalis,

increased beta adrenergic activity, and magnesium depletion, can promote
arrhythmias, the last two of which can further lower the plasma potassium
concentration:

Epinephrine released during a stress response (as with coronary ischemia)

drives potassium into the cells [ 5] . A similar effect can be seen with
bronchodilator therapy with a beta adrenergic agonist [ 6] . (See "Sympathetic
activity and potassium balance" ).

Diuretic-induced magnesium depletion can promote the development of

arrhythmias, particularly in patients also treated with drugs that prolong the QT
interval, a combination that can predispose to torsade de pointes ( show table 1 )
[7,8] . Hypomagnesemia can also increase urinary potassium losses and lower
the plasma potassium concentration. ( See "Acquired long QT syndrome" and
see "Signs and symptoms of magnesium depletion" ).

Rhabdomyolysis — Severe potassium depletion (serum potassium less than 2.5

meq/L) can lead to muscle cramps, rhabdomyolysis, and myoglobinuria [ 9,10] .
Potassium release from muscle cells normally mediates vasodilation and increased
blood flow to muscles during exercise. Decreased potassium release due to profound
hypokalemia may diminish blood flow to muscles in response to exertion. ( See
"Rhabdomyolysis" ).
Renal abnormalities — Hypokalemia can induce a variety of renal abnormalities
which are mostly reversible with potassium repletion. These include impaired urinary
concentrating ability (which may be symptomatic with nocturia, polyuria and
polydipsia), increased renal ammonia production due to intracellular acidosis,
increased renal bicarbonate reabsorption, and hypokalemic nephropathy [ 11-15] .
Hypokalemia may cause polydipsia, which may contribute to polyuria [ 16] . A more
comprehensive discussion of these abnormalities is presented elsewhere. ( See
"Hypokalemia-induced renal dysfunction" ).

PATHOGENESIS OF SYMPTOMS — The neuromuscular and cardiac symptoms

induced by hypokalemia are related to alterations in the generation of the action
potential [3] . The ease of generating an action potential (called membrane
excitability) is related both to the magnitude of the resting membrane potential and to
the activation state of membrane sodium channels; opening up of these sodium
channels, leading to the passive diffusion of extracellular sodium into the cells, is the
primary step in this process. According to the Nernst equation, the resting membrane
potential is related to the ratio of the intracellular to the extracellular potassium
concentration. A reduction in the plasma (extracellular) potassium concentration will
increase this ratio and therefore hyperpolarize the cell membrane (that is, make the
resting potential more electronegative). This increases sodium permeability, which
enhances membrane excitability.

In addition to increased cardiac automaticity (related to membrane excitability),

hypokalemia also delays ventricular repolarization. This prolongs the duration of the
relative refractory period, and predisposes to reentrant arrhythmias. ( See "Reentry
and the development of cardiac arrhythmias" ).

The renal effects of hypokalemia are related in part to decreased expression of

aquaporin-2, the antidiuretic hormone-sensitive water channel, interference with
sodium-potassium transport in the thick ascending limb, and increased intracellular
acidosis due to K+ movement out of cells followed by H+ entry into cells to maintain
electroneutrality. The pathogenesis of the hypokalemic nephropathy is not well
understood. ( See "Hypokalemia-induced renal dysfunction" ).

EVALUATION

Patient assessment — Monitoring of the ECG and muscle strength are indicated to
assess the functional consequences of the hypokalemia. At serum potassium
concentrations lower than 2.5 meq/L, severe muscle weakness, or marked
electrocardiographic changes are potentially life-threatening and require immediate
treatment. Immediate therapy is warranted if electrocardiographic changes or
peripheral neuromuscular abnormalities are present. ( See "ECG tutorial: Miscellaneous
diagnoses" , section on hypokalemia).

One problem with the assessment of serum potassium is that it is often unclear
whether the hypokalemia represents a chronic or an acute condition. A careful history
to assess the probable etiology of the hypokalemia is important. ( See "Diagnosis of
hypokalemia" ).

Potassium deficit — There is no strict correlation between the serum potassium

concentration and total body potassium stores, thus the total potassium deficit in
patients with hypokalemia due to potassium loss can only be approximated.

In chronic hypokalemia, a potassium deficit of 200 to 400 meq is required to lower the
serum potassium concentration by 1 meq/L [ 17] . Once the serum potassium level falls
to approximately 2 meq/L, continued potassium losses will not produce much more
hypokalemia due to release of potassium from the cell stores.

These estimates assume that there is a normal distribution of potassium between the
cells and the extracellular fluid, that is, there is no concurrent acid-base abnormality.
The most common settings in which this estimation does not apply is diabetic
ketoacidosis or nonketotic hyperglycemia, and in other conditions such as hypokalemic
periodic paralysis. ( See "Causes of hypokalemia" , section on Increased entry into
cells).

In diabetic ketoacidosis, hyperosmolality, insulin deficiency, and perhaps the acidemia

favor the movement of potassium out of the cells. As a result, patients with this
disorder may have a normal or even elevated serum potassium concentration at
presentation, despite having a marked potassium deficit due to urinary and
gastrointestinal losses [ 18] . In this setting, potassium supplementation is usually
begun once the serum potassium concentration is 4.5 meq/L or below, since the
administration of insulin and fluids often leads to a rapid reduction in the serum
potassium concentration. ( See "Treatment of diabetic ketoacidosis and hyperosmolar
hyperglycemic state in adults" ).

TREATMENT

Potassium preparations — An intravenous or oral potassium chloride preparation is

generally preferred over potassium citrate or potassium bicarbonate , in particular
among patients with metabolic alkalosis due to diuretic therapy, vomiting, and
hyperaldosteronism [ 19,20] . On the other hand, potassium citrate or potassium
bicarbonate is often preferred in patients with hypokalemia and metabolic acidosis.
This most often occurs in renal tubular acidosis and chronic diarrheal states.

Oral potassium chloride can be given in crystalline form ( salt substitutes), as a liquid,
or in a slow-release tablet or capsule. Salt substitutes contain 50 to 65 meq per level
teaspoon; they are safe, well tolerated and much cheaper than the other preparations,
and thus may be an option if cost is a concern [ 21] . In comparison, potassium
chloride solutions are often unpalatable, and the slow-release preparations can in rare
cases cause ulcerative or stenotic lesions in the gastrointestinal tract due to the local
accumulation of high concentrations of potassium [ 22] .

Increasing the intake of potassium-rich foods (such as oranges and bananas) is

generally less effective ( show table 2 ) [2,23] .

Intravenous administration — Potassium chloride can be given intravenously to

patients who are unable to eat or as an adjunct to oral replacement in patients who
have severe symptomatic hypokalemia.

In most patients, intravenous potassium is administered as an additive in intravenous

fluids at concentrations of 20 to 40 meq per liter of fluid through a peripheral vein. A
concentration up to 60 meq/L can also be used, but such higher concentrations are
often painful.

A saline rather than a dextrose solution is recommended for initial therapy, since the
administration of dextrose can lead to a transient 0.2 to 1.4 meq/L reduction in the
serum potassium concentration, particularly if only 20 meq/L of potassium chloride is
provided [ 2,24] . This effect, which can induce arrhythmias in susceptible patients
(such as those taking digitalis) [24] , is mediated by dextrose-stimulated release of
insulin, which drives potassium into the cells by enhancing the activity of the cellular
Na-K-ATPase pump [ 24,25] .

In patients who cannot tolerate large volumes of fluid, more concentrated solutions
(200 to 400 meq/L) can be infused into large veins in patients with severe symptomatic
hypokalemia [ 26-28] . The rate at which this can be given and the potential
complications of overly rapid therapy are described below. ( See "Severe hypokalemia"
below).

Ongoing losses and the steady state — The following recommendations for
potassium replacement assume that there are no ongoing losses (eg, vomiting,
diarrhea, nasogastric suction, diuretic therapy) and that the patient does not have a
chronic potassium wasting condition such as diuretic therapy, primary aldosteronism,
or Gitelman's disease:

Among patients with ongoing losses, the rate of potassium administration

recommended below must be increased by the rate of potassium loss to
produce the desired rate of potassium repletion.

Stable patients with chronic diuretic therapy (at a fixed dose), primary
aldosteronism, or Gitelman's syndrome typically do not develop progressive
hypokalemia because their increased urinary potassium losses are quickly
balanced by hypokalemia-induced potassium retention,establishing a new
steady state in which potassium output matches potassium intake, albeit at a
lower than normal plasma potassium concentration. In such patients, usual rates
of potassium repletion produce only modest elevations in serum potassium. As
soon as the serum potassium rises, there is less hypokalemia-induced
potassium retention and most of the administered potassium is excreted in the
urine. (See "Clinical features of primary aldosteronism" , section on The steady
state, and see "The steady state" ).

Correction of the hypokalemia in such patients usually includes a potassium-sparing

diuretic. A mineralocorticoid receptor antagonist ( spironolactone , eplerenone ) is
preferable to a sodium channel blocker ( amiloride , triamterene ) in patients with
primary aldosteronism since blockade of the effects of excess aldosterone on the heart
is an additional goal. ( See "Treatment of primary aldosteronism" ).

Caution — A potassium-sparing diuretic in combination with potassium supplements

should be used only with careful monitoring to prevent possible overcorrection and the
development of hyperkalemia.
This may be a particular problem in patients with moderately severe to severe heart
failure in whom several factors may act together to markedly reduce urinary
potassium excretion (decreased renal perfusion due to the fall in cardiac output,
therapy with an ACE inhibitor and/or angiotensin II receptor blocker, and therapy with
the aldosterone antagonists, spironolactone or eplerenone ). (See "Use of diuretics in
heart failure" , section Risk of hyperkalemia).

Mild to moderate hypokalemia — Most hypokalemic patients have a serum

potassium concentration between 3.0 and 3.5 meq/L; this degree of potassium
depletion usually produces no symptoms, except for patients with heart disease
(particularly if they are taking digitalis or undergoing cardiac surgery [ 29-31] ) or
patients with advanced cirrhosis. ( See "Diuretic-induced hypokalemia" ).

Treatment in this setting is directed toward replacing the lost potassium and toward
treating the underlying disorder (such as vomiting or diarrhea). Treatment is usually
started with 10 to 20 meq of potassium chloride given two to four times per day (20 to
80 meq per day), depending on the severity of hypokalemia and on whether
hypokalemia developed acutely or is chronic.

Sequential monitoring of the serum potassium is essential to determine continued

requirements, with frequency of monitoring dependent on the severity of hypokalemia.

Severe hypokalemia — Potassium must be given more rapidly to patients with

severe (serum potassium <2.5 to 3.0 meq/L) or symptomatic (arrhythmias, marked
muscle weakness) hypokalemia. However, caution must be exercised when repleting
potassium in patients with a concurrent disorder that, when treated, will tend to drive
potassium into the cells and worsen the hypokalemia. The two main examples are
insulin therapy in diabetic ketoacidosis or nonketotic hyperglycemia, and bicarbonate
therapy in metabolic acidosis.

Potassium repletion is most easily done orally. The serum potassium concentration can
transiently rise acutely by as much as 1 to 1.5 meq/L after an oral dose of 40 to 60
meq, and by 2.5 to 3.5 meq/L after 135 to 160 meq [ 32,33] ; the serum potassium
concentration will then fall back towards baseline, as most of the exogenous potassium
will then be taken up by the cells [ 34] . TA patient with a serum potassium
concentration of 2 meq/L, for example, may have a 400 to 800 meq potassium deficit
[17] .

Thus, potassium chloride can be given orally in doses of 40 to 60 meq, three to four
times/day. If tolerated, this should be continued until the serum potassium
concentration is persistently above 3.0 to 3.5 meq/L, and/or symptoms resolve;
thereafter, the dose and frequency of administration can be reduced to avoid gastric
irritation. (See "Mild to moderate hypokalemia" above ).

During repletion, frequent monitoring of the serum potassium concentration is

required, to ensure that potassium supplementation is continued until body stores are
repleted, and to avoid hyperkalemia.

During chronic replacement, serum potassium concentration should be monitored

approximately every three to four months, or if clinically indicated.

Intravenous therapy — Potassium chloride can be given intravenously as an

adjunct to oral replacement in patients who have severe symptomatic hypokalemia.
Potential constraints to intravenous therapy for severe hypokalemia include a potential
risk of volume overload in susceptible subjects and hyperkalemia due to excessive
repletion.

The necessity for aggressive intravenous potassium replacement has been reported
primarily in patients with diabetic ketoacidosis or nonketotic hyperglycemia who
present with hypokalemia due to marked potassium losses [ 35] . Treatment with
insulin and fluids will exacerbate the hypokalemia. Fortunately, these patients are also
quite volume depleted; thus, 40 to 60 meq/L of potassium chloride in half-isotonic
saline can usually be given to supply potassium and volume repletion, with a low risk
of pulmonary congestion in this setting.

Although isotonic saline is generally the initial replacement fluid used in treating
diabetic ketoacidosis or nonketotic hyperglycemia, the addition of potassium will make
this a hypertonic fluid (since potassium is as osmotically active as sodium), thereby
delaying reversal of the hyperosmolality that is primary responsible for neurologic
symptoms in this disorder. On the other hand, the combination of 40 to 60 meq of
potassium in half-isotonic saline is almost the osmotic equivalent of isotonic saline.
(See "Treatment of diabetic ketoacidosis and hyperosmolar hyperglycemic state in
adults").

The maximum recommended rate of intravenous potassium administration is 10 to 20

meq/h; higher rates of administration carry the risk of hyperkalemia [ 36,37] .
However, as much as 40 to 100 meq/h have been given to selected patients with
paralysis or life-threatening arrhythmias [ 27,35] . In this setting, solutions containing
as much as 200 to 400 meq of potassium per liter have been used; in clinical practice,
concentrations of 100 to 200 meq/L are used most commonly. These high
concentrations should be prepared as 10 to 20 meq of potassium in 100 mL of fluid to
avoid accidental administration of very large quantities of intravenous potassium [ 26] .
If high concentrations are used, an additional safety measure to avoid excess
potassium administration is use of an infusion pump. Potassium solutions with
concentrations over 60 meq/L are often painful, and should be infused into a large vein
(central vein) [ 26] .

Careful monitoring of the physiologic effects of severe hypokalemia (ECG

abnormalities, muscle weakness or paralysis) is essential, especially if a faster rate of
repletion is used (eg, over 20 meq/h). Once these problems are no longer severe, the
rate of potassium repletion should be slowed (to 10 to 20 meq/h), or changed to only
oral repletion, even if there is persistent hypokalemia.

Rapid intravenous administration of potassium is potentially dangerous. In settings of

potassium redistribution, even low rates of administration can result in hyperkalemia.
In a report of patients with hypokalemic thyrotoxic periodic paralysis (baseline serum
potassium concentration of 2.0 meq/L), administration of potassium at a rate of 10
meq/hour (80 meq/L) resulted in hyperkalemia (>5.5 meq/L) in 40 percent of patients,
which was complicated by electrocardiographic changes in half of the patients [ 38] .
(See "Causes of hypokalemia" , section on Hypokalemic periodic paralysis).

Hypomagnesemia — Hypokalemia is a common event in hypomagnesemic patients,

occurring in approximately one-half of cases. The hypokalemia in this setting is
relatively refractory to potassium supplementation and requires correction of the
magnesium deficit. ( See "Signs and symptoms of magnesium depletion" and see
"Diagnosis and treatment of hypomagnesemia" ).

SUMMARY AND RECOMMENDATIONS

General issues

Hypokalemia is most commonly due to urinary or gastrointestinal losses. In the

absence of a rapid decrease in potassium concentration or other risk factors such as
use of digitalis, clinical manifestations of hypokalemia are typically seen only if the
serum potassium is below 2.5 to 3.0 meq/L. ( See "Causes of hypokalemia" and see
"Manifestations of hypokalemia" above ).

Common acute manifestations are muscle weakness and electrocardiographic

changes. More prolonged hypokalemia can lead to rhabdomyolysis or renal
abnormalities. ( See "Manifestations of hypokalemia" above and see "Pathogenesis of
symptoms" above ).

The reduction in serum potassium allows only a rough approximation of whole body
losses. A fall in serum potassium from 4.0 to 3.0 meq/L represents an approximate
loss of 200 to 400 meq of potassium. ( See "Potassium deficit" above ).

This estimation does not apply to patients with transcellular potassium redistribution.
As examples:

Patients with diabetic ketoacidosis may have normal (or even high) plasma
potassium levels despite substantial potassium losses due to transcellular
potassium shifts, and the administration of insulin and fluids leads to a rapid
reduction in the serum potassium concentration and, in many cases,
hypokalemia. ( See "Treatment of diabetic ketoacidosis and hyperosmolar
hyperglycemic state in adults" ).

Hypokalemic periodic paralysis can lead to sudden reductions in serum

potassium due to potassium movement into the cells. Although there is no
potassium deficit, acute potassium therapy should be given in symptomatic
patients. Posttherapy hyperkalemia is common as the potassium that entered
the cells returns to the extracellular fluid [ 38] . (See "Causes of hypokalemia" ,
section on Hypokalemic periodic paralysis).

Acute replacement — The rapidity and method of potassium repletion is based upon
the severity of hypokalemia, the presence of associated conditions, the presence or
absence of signs and symptoms (cardiac conduction abnormalities, muscle weakness),
and whether continued losses are expected.

Monitoring — We recommend obtaining an ECG on all patients with hypokalemia,

although there is large variability in the potassium concentration associated with ECG
changes.

We recommend frequent monitoring of the serum potassium concentration to ensure

repletion, and to avoid hyperkalemia, with the frequency depending on the
aggressiveness of the repletion strategy.

The following recommendations for the rate of potassium replacement assume that
there are no ongoing losses (eg, vomiting, diarrhea, nasogastric suction, diuretic
therapy) and that the patient does not have a chronic potassium wasting condition such
as diuretic therapy, primary aldosteronism, or Gitelman's disease. ( See "Ongoing
losses and the steady state" above ).

Asymptomatic, potassium >3 meq/L — In the absence of ongoing losses, we

suggest administration of 10 to 20 meq of potassium chloride given two to four times
per day (20 to 80 meq per day), depending upon the severity of hypokalemia ( Grade
2B). (See "Mild to moderate hypokalemia" above ).

Patients with heart disease (particularly if they are taking digitalis or undergoing
cardiac surgery) or advanced cirrhosis may require more aggressive repletion. ( See
"Mild to moderate hypokalemia" above ).

In patients with concurrent metabolic acidosis, we suggest the use of potassium

bicarbonate or citrate ( Grade 2B ). (See "Potassium preparations" above ).

Mild to moderate symptoms, or potassium <3.0 meq/L — In the absence of

ongoing losses, we suggest oral administration of potassium chloride (40 to 60 meq
three to four times/day, total 120 to 240 meq), until the plasma serum potassium
concentration remains above 3.0 to 3.5 meq/L, and symptoms resolve ( Grade 2B ).
(See "Severe hypokalemia" above ).

Severe symptoms or unable to take oral medication — We recommend

intravenous potassium chloride in saline solution for patients with severe symptoms of
hypokalemia and in patients who are unable to take oral medications, especially if they
are also receiving insulin therapy for diabetic ketoacidosis or nonketotic
hyperglycemia, or bicarbonate therapy for metabolic acidosis ( Grade 1B ). (See
"Manifestations of hypokalemia" above and see "Intravenous therapy" above ).

When using intravenous potassium, we recommend the following ( see "Intravenous

therapy" above ):

Do not use a dextrose-containing solution, since the associated stimulation of

insulin secretion will drive potassium into the cells and limit acute correction of
the hypokalemia.

A maximal intravenous repletion rate in most cases of 10 to 20 meq/h, and

maximal concentration of 100 to 200 meq/L (prepared in 100 mL).

Follow the serum potassium concentration closely to avoid overcorrection.

Continuous ECG monitoring in patients receiving potassium at 10 to 20 meq/h or

faster.

Ongoing losses — We suggest the following alternatives for chronic replacement:

oral potassium chloride preparations, salt substitutes sprinkled on food (containing 50
to 65 meq potassium chloride per level teaspoon) which are substantially cheaper, or
the addition of a potassium sparing diuretic ( Grade 2B ). (See "Treatment of primary
aldosteronism" , for recommendations concerning the use of potassium-sparing
diuretics).

If a potassium-sparing diuretic is used in combination with potassium supplements, we

recommend close monitoring of potassium levels. This combination must be used with
extreme caution in patients with decreased kidney function and in patients on an ACE
inhibitor and/or angiotensin receptor blocker.

We suggest monitoring the serum potassium concentration approximately every three

to four months in all patients receiving chronic potassium supplementation, or if
clinically indicated.

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effects of an ACE inhibitor: results of the HOPE study. Clin Nephrol 2005;
63:181.
32. Keith, NM, Osterberg, AE, Burchell, HB. Some effects of potassium salts in man.
Ann Intern Med 1942; 16:879.
 33. Nicolis, GL, Kahn, T, Sanchez, A, Gabrilove, JL. Glucose-induced hyperkalemia
in diabetic subjects. Arch Intern Med 1981; 141:49.
34. Sterns, RH, Feig, PU, Pring, M, et al. Disposition of intravenous potassium in
anuric man: A kinetic analysis. Kidney Int 1979; 15:651.
35. Abramson, E, Arky, R. Diabetic acidosis with initial hypokalemia. Therapeutic
implications. JAMA 1966; 196:401.
36. Rose, BD, Post, TW, Clinical Physiology of Acid-Base and Electrolyte Disorders,
5th ed, McGraw-Hill, New York, 2001, pp. 870-875.
37. Seftel, HC, Kew, MC. Early and intensive potassium replacement in diabetic
acidosis. Diabetes 1966; 15:694.
38. Lu, KC, Hsu, YJ, Chiu, JS, et al. Effects of potassium supplementation on the
recovery of thyrotoxic periodic paralysis. Am J Emerg Med 2004; 22:544.

GRAPHICS
Hypokalemia

An increase in the amplitude of U waves, which occur at the end of the T

wave, are characteristic of hypokalemia.

Reported causes of the long QT syndrome

Congenital Antihistamines

Jervell and Lange-Nielsen Terfenadine

syndrome
Astemizole
Romano-Ward syndrome
Psychotropic drugs
Idiopathic
Thioridazine
Acquired Phenothiazines
Metabolic disorders
Tricyclic or tetracyclic antidepressants
Hypokalemia
Haloperidol and other batyrophenones
Hypomagnesemia
Selective serotonin reuptake inhibitors
Hypocalcemia
Risperidone
Starvation
 Starvation
Methadone
Anorexia nervosa
Other drugs
Liquid protein diets
Vasodilators - Prenylamine, bepridil,
Hypothyroidism mibefradil

Bradyarrhythmias Diuretics - Via electrolyte changes

(hypokalemia, hypomagnesemia)
Sinus node dysfunction
Serotonin antagonist - Ketanserin
AV block - second or third
degree Motility drugs - Cisapride, domperidone

Antiarrhythmic drugs Droperidol - may be safe at the low

doses used by anesthesiologists (0.625 to
Quinidine
1.25 mg)
Procainamide or
Ranolazine
N-acetylprocainamide
HIV protease inhibitors
Disopyramide
Miscellaneous - Organophosphate
Amiodarone
insecticides, probucol, cocaine, terodiline,
Sotalol papaverine, certain Chinese herbs,
chloral hydrate, arsenic trioxide, cesium
Dofetilide, ibutilide, azimilide, chloride, levomethadyl
sematilide
Other
Antimicrobial drugs
Myocardial ischemia or infarction
Erythromycin, clarithromycin,
telithromycin, azithromycin Intracranial disease
(minor)
HIV infection
Pentamidine
Hypothermia
Some fluoroquinolones (eg,
Connective tissue diseases with
sparfloxacin, gatifloxacin,
anti-Ro/SSA antibodies
levofloxacin, moxifloxacin)

Other - Spiramycin,
chloroquine, halofantrine
mefloquine

High potassium content foods

 Highest content (>25 meq/100 High content (>6.2
g) meq/100 g)
Dried figs Vegetables

Molasses Spinach

Seaweed Tomatoes

Very high content (>12.5 Broccoli

meq/100 g) Winter squash
Dried fruits (dates, prunes)
Beets
Nuts
Carrots
Avocados
Cauliflower
Bran cereals
Potatoes
Wheat germ
Fruits
Lima beans
Bananas

Cantaloupe

Kiwis

Oranges

Mangos

Meats

Ground beef

Steak

Pork

Veal

Lamb

Adapted from Gennari, FJ. N Engl J Med 1998; 339:451.

Grade 2B recommendation
A Grade 2B recommendation is a weak recommendation;
alternative approaches may be better for some patients under
some circumstances.
Explanation:

A Grade 2 recommendation is a weak recommendation. It means "this is our

suggestion, but you may want to think about it." It is unlikely that you should
follow the suggested approach in all your patients, and you might reasonably
choose an alternative approach. For Grade 2 recommendations, benefits and
risks may be finely balanced, or the benefits and risks may be uncertain. In
deciding whether to follow a Grade 2 recommendation in an individual patient,
you may want to think about your patient's values and preferences or about your
patient's risk aversion.

Grade B means that the best estimates of the critical benefits and risks come
from randomized, controlled trials with important limitations (eg, inconsistent
results, methodologic flaws, imprecise results, extrapolation from a different
population or setting) or very strong evidence of some other form. Further
research (if performed) is likely to have an impact on our confidence in the
estimates of benefit and risk, and may change the estimates.

Recommendation grades
1. Strong recommendation: Benefits clearly outweigh the risks and burdens
(or vice versa) for most, if not all, patients
2. Weak recommendation: Benefits and risks closely balanced and/or
uncertain

Evidence grades
A. High-quality evidence: Consistent evidence from randomized trials, or
overwhelming evidence of some other form
B. Moderate-quality evidence: Evidence from randomized trials with
important limitations, or very strong evidence of some other form
C. Low-quality evidence: Evidence from observational studies, unsystematic
clinical observations, or from randomized trials with serious flaws

For a complete description of our grading system, please see the UpToDate
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selecting "Policies".

Grade 1B recommendation
 A Grade 1B recommendation is a strong recommendation, and
applies to most patients. Clinicians should follow a strong
recommendation unless a clear and compelling rationale for an
alternative approach is present.
Explanation:

A Grade 1 recommendation is a strong recommendation. It means that we

believe that if you follow the recommendation, you will be doing more good than
harm for most, if not all of your patients.

Grade B means that the best estimates of the critical benefits and risks come
from randomized, controlled trials with important limitations (eg, inconsistent
results, methodologic flaws, imprecise results, extrapolation from a different
population or setting) or very strong evidence of some other form. Further
research (if performed) is likely to have an impact on our confidence in the
estimates of benefit and risk, and may change the estimates.

Recommendation grades
1. Strong recommendation: Benefits clearly outweigh the risks and burdens
(or vice versa) for most, if not all, patients
2. Weak recommendation: Benefits and risks closely balanced and/or
uncertain

Evidence grades
A. High-quality evidence: Consistent evidence from randomized trials, or
overwhelming evidence of some other form
B. Moderate-quality evidence: Evidence from randomized trials with
important limitations, or very strong evidence of some other form
C. Low-quality evidence: Evidence from observational studies, unsystematic
clinical observations, or from randomized trials with serious flaws

For a complete description of our grading system, please see the UpToDate
editorial policy which can be found by clicking "About UpToDate" and then
selecting "Policies".

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