2. Less than 3.5 mEq/L- (3.5 mmol/L)
Moderate hypokalemia- 2.5-3 mEq/L
Severe hypokalemia- less than 2.5 mEq/L
3. -most abundant intracellular cation
- important to normal cellular function
particularly of nerve and muscle cells
-regulated by specific ion-exchange pumps,
primarily by cellular, membrane-bound, sodium-
potassium adenosine triphosphatase (ATPase)
pumps
4. -obtained through the diet
-excreted via the kidney.
-Potassium homeostasis is maintained
predominantly through the regulation of
renal excretion
5. inadequate potassium intake
increased potassium excretion- most
common
shift of potassium from the extracellular to
the intracellular space
6. Common findings include weakness, fatigue,
constipation, ileus, and respiratory muscle
dysfunction.
Symptoms seldom occur unless plasma K+ is
less than 3.0 mmol/L.
8. Reduction of potassium losses
Replenishment of potassium stores
Evaluation for potential toxicities
Determination of the cause to prevent future
episodes
9. Daily excess intake of approximately 1
mEq/kg/day (60-100 mEq):
Ninety percent is excreted through the kidneys
10% is excreted through the gut
Potassium homeostasis is maintained
predominantly through the regulation of
renal excretion (collecting duct)
10. Aldosterone
High sodium delivery to the collecting duct
(eg, diuretics)
High urine flow (eg, osmotic diuresis)
High serum potassium levels
Delivery of negatively charged ions to the
collecting duct (eg, bicarbonate)
11. Absolute aldosterone deficiency or resistance
to aldosterone effects
Low sodium delivery to the collecting duct
Low urine flow
Low serum potassium levels
Renal failure
12. increase in osmolality exit from cells
acute cell/tissue breakdown releases
potassium into extracellular space
13. Kidneys adapt to acute and chronic alterations in
potassium intake:
When potassium intake is chronically high, potassium
excretion likewise is increased.
obligatory renal losses are 10-15 mEq/day
The kidney maintains a central role in the
maintenance of potassium homeostasis, even in
the setting of chronic renal failure.
In the presence of renal failure, the proportion
of potassium excreted through the gut increases.
The colon is the major site of gut regulation of
potassium excretion.
14. Potassium is predominantly an intracellular
cation; therefore, serum potassium levels
can be a very poor indicator of total body
stores.
15. Glycoregulatory hormones:
(1) Insulin enhances potassium entry into cells
(2) glucagon impairs potassium entry into cells
Adrenergic stimuli:
(1) Beta-adrenergic stimuli enhance potassium
entry into cells
(2) alpha-adrenergic stimuli impair potassium
entry into cells
pH:
(1) Alkalosis enhances potassium entry into cells
(2) acidosis impairs potassium entry into cells
16. Hypokalemia can occur via the following
pathogenetic mechanisms:
Deficient intake
Increased excretion
A shift from the extracellular to the intracellular
space
Although poor intake or an intracellular shift
by itself is a distinctly uncommon cause
17. The most common mechanisms leading to
increased renal potassium losses include
the following:
Enhanced sodium delivery to the
collecting duct, as with diuretics
Mineralocorticoid excess, as with
primary or secondary
hyperaldosteronism
Increased urine flow, as with an osmotic
diuresis
18. Gastrointestinal losses:
Diarrhea
Vomiting
nasogastric suctioning, also are common causes
of hypokalemia
Volume depletion leads to secondary
hyperaldosteronism enhanced cortical
collecting tubule secretion of potassium in
response to enhanced sodium reabsorption
Metabolic alkalosis increases collecting
tubule potassium secretion
19. Shift from extracellular to intracellular space
often accompanies increased excretion
potentiation of the hypokalemic effect of
excessive loss
Intracellular shifts of potassium
often are episodic
frequently are self-limited (ie., acute insulin
therapy for hyperglycemia)
20. Cardiovascular complications
Atrial and ventricular arrhythmias
Increased susceptibility to cardiac arrhythmias is
observed with hypokalemia in the following
settings:
Congestive heart failure
Underlying ischemic heart disease/acute myocardial
ischemia
Aggressive therapy for hyperglycemia, such as with
diabetic ketoacidosis
Digitalis therapy
Methadone therapy
Conn syndrome
21. Low potassium intake
hypertension and/or hypertensive end-organ
damage
altered vascular reactivity vasoconstriction
and impaired relaxation
Treatment of hypertension with diuretic
exacerbates the development of end-organ
damage by fueling the metabolic abnormalities
high risk for lethal hypokalemia under stress
conditions such as myocardial infarction, septic
shock, or diabetic ketoacidosis
22. Muscle weakness
Depression of the deep-tendon reflexes
Flaccid paralysis
Rhabdomyolysis (severe hypokalemia)
23. Nephrogenic diabetes insipidus-
Abnormalities of renal function often accompany
acute or chronic hypokalemia
Metabolic alkalosis from impaired
bicarbonate excretion
Cystic degeneration
Interstitial scarring
24. Decreased gut motility, which can lead to or
exacerbate an ileus
Hepatic encephalopathy in the setting of
cirrhosis
25. Dual effect on glucose regulation by
decreasing insulin release and peripheral
insulin sensitivity
Thiazide-associated diabetes mellitus
26. Inadequate potassium intake
Increased potassium excretion **
Shift of potassium from the extracellular to
the intracellular space
27. Eating disorders : Anorexia, bulimia,
starvation, pica, and alcoholism
Dental problems: Impaired ability to chew or
swallow
Poverty: Inadequate quantity or quality of
food (eg, "tea-and-toast" diet of elderly
individuals)
Hospitalization: Potassium-poor TPN
28. Mineralocorticoid excess (endogenous or
exogenous)
Hyperreninism from renal artery stenosis
Osmotic diuresis: Mannitol and
hyperglycemia can cause osmotic diuresis
Increased gastrointestinal losses
Drugs
Genetic disorders
32. Alkalosis (metabolic or respiratory)
Insulin administration or glucose
administration (the latter stimulates insulin
release)
Intensive beta-adrenergic stimulation
Hypokalemic periodic paralysis
Thyrotoxic periodic paralysis
Refeeding: This is observed in prolonged
starvation, eating disorders, and alcoholism
Hypothermia
33. Eating disorders (incidence of 4.6-19.7% in an
outpatient setting)
AIDS (23.1% of hospitalized patients)
Alcoholism (incidence reportedly as high as
12.6% [33] in the inpatient setting), likely from
a hypomagnesemia-induced decrease in
tubular reabsorption of potassium
Bariatric surgery
34. Therapeutic goals
Prevent life-threatening complications
(arrhythmias, respiratory failure, hepatic
encephalopathy)
Correct the K+ deficit
Minimize ongoing losses
Treat the underlying cause
35. K deficit= (desired k- actual k) x 100%
0.27
Estimation of K+ deficit
3.0 meq/L= total body K+ deficit of 200-400
meq/70kg
2.5 meq/L = 500 meq/70kg
2.0 meq/L = 700 meq/70kg
36. Oral therapy
Generally safer
Degree of K+ depletion does not correlate well
with the plasma K+
KCl is usually the preparation of choice
Kalium durule: 1 durule = 10 meqs KCl
KCl syrup: 1meq/mL
37. IV therapy
For severe hypokalemia or those who are unable
to take anything by mouth
Maximum rate at which potassium is infused into
peripheral veins is usually 10 meq/hr
Central – 20 meq/hr
Rate of infusion should not exceed 20 meq/hour
unless paralysis or malignant ventricular
arrhythmias are present
Hinweis der Redaktion
Hypokalemia is generally defined as a serum potassium level of less than 3.5 mEq/L (3.5 mmol/L). Moderate hypokalemia is a serum level of 2.5-3 mEq/L, and severe hypokalemia is a level of less than 2.5 mEq/L.
Potassium, the most abundant intracellular cation, is essential for the life of an organism. Potassium homeostasis is integral to normal cellular function, particularly of nerve and muscle cells, and is tightly regulated by specific ion-exchange pumps, primarily by cellular, membrane-bound, sodium-potassium adenosine triphosphatase (ATPase) pumps.
Potassium is obtained through the diet and excreted principally via the kidney. Potassium homeostasis is maintained predominantly through the regulation of renal excretion; the adrenal gland and pancreas also play significant roles (see Pathophysiology).
Hypokalemia may result from inadequate potassium intake, increased potassium excretion, or a shift of potassium from the extracellular to the intracellular space. Increased excretion is the most common mechanism. Poor intake or an intracellular shift by itself is a distinctly uncommon cause, but several causes often are present simultaneously.
The symptoms of hypokalemia are nonspecific and predominantly are related to muscular or cardiac function. Weakness and fatigue are the most common complaints.
Hypokalemia produces distinctive changes in the ST-T complex. The most common pattern seen is ST depressions with prominent U waves and prolonged repolarization. With hypokalemia, the U waves typically become enlarged and may even exceed the height of the T waves.
An electrocardiogram (ECG) may show atrial or ventricular tachyarrhythmias.
Pathophysiology
Gastrointestinal absorption of potassium is complete, resulting in daily excess intake of approximately 1 mEq/kg/day (60-100 mEq). Ninety percent of this excess is excreted through the kidneys, and 10% is excreted through the gut.
Potassium homeostasis is maintained predominantly through the regulation of renal excretion. The most important site of regulation is the collecting duct, where aldosterone receptors are present.
An acute increase in osmolality causes potassium to exit from cells. An acute cell/tissue breakdown releases potassium into extracellular space.
Renal factors in potassium homeostasis
Kidneys adapt to acute and chronic alterations in potassium intake. When potassium intake is chronically high, potassium excretion likewise is increased. In the absence of potassium intake, however, obligatory renal losses are 10-15 mEq/day. Thus, chronic losses occur in the absence of any ingested potassium.
The kidney maintains a central role in the maintenance of potassium homeostasis, even in the setting of chronic renal failure. Renal adaptive mechanisms allow the kidneys to maintain potassium homeostasis until the glomerular filtration rate drops to less than 15-20 mL/min.
Additionally, in the presence of renal failure, the proportion of potassium excreted through the gut increases. The colon is the major site of gut regulation of potassium excretion. Therefore, potassium levels can remain relatively normal under stable conditions, even with advanced renal insufficiency. However, as renal function worsens, the kidneys may not be capable of handling an acute potassium load.
Potassium distribution
Potassium distribution
Potassium is predominantly an intracellular cation; therefore, serum potassium levels can be a very poor indicator of total body stores. Because potassium moves easily across cell membranes, serum potassium levels reflect movement of potassium between intracellular and extracellular fluid compartments, as well as total body potassium homeostasis.
Several factors regulate the distribution of potassium between the intracellular and extracellular space, as follows:
Glycoregulatory hormones: (1) Insulin enhances potassium entry into cells, and (2) glucagon impairs potassium entry into cells
Adrenergic stimuli: (1) Beta-adrenergic stimuli enhance potassium entry into cells, and (2) alpha-adrenergic stimuli impair potassium entry into cells
pH: (1) Alkalosis enhances potassium entry into cells, and (2) acidosis impairs potassium entry into cells
Pathogenic mechanisms
Pathogenic mechanisms
Hypokalemia can occur via the following pathogenetic mechanisms:
Deficient intake
Increased excretion
A shift from the extracellular to the intracellular space
Although poor intake or an intracellular shift by itself is a distinctly uncommon cause, several causes often are present simultaneously.
Increased excretion
The most common mechanisms leading to increased renal potassium losses include the following:
Enhanced sodium delivery to the collecting duct, as with diuretics
Mineralocorticoid excess, as with primary or secondary hyperaldosteronism
Increased urine flow, as with an osmotic diuresis
Gastrointestinal losses, from diarrhea, vomiting, or nasogastric suctioning, also are common causes of hypokalemia. Vomiting leads to hypokalemia via a complex pathogenesis. Gastric fluid itself contains little potassium, approximately 10 mEq/L. However, vomiting produces volume depletion and metabolic alkalosis, which are accompanied by increased renal potassium excretion.
Volume depletion leads to secondary hyperaldosteronism, which in turn leads to enhanced cortical collecting tubule secretion of potassium in response to enhanced sodium reabsorption. Metabolic alkalosis also increases collecting tubule potassium secretion due to the decreased availability of hydrogen ions for secretion in response to sodium reabsorption.
Extracellular/intracellular shift
Hypokalemia caused by a shift from extracellular to intracellular space often accompanies increased excretion, leading to a potentiation of the hypokalemic effect of excessive loss. Intracellular shifts of potassium often are episodic and frequently are self-limited, as, for example, with acute insulin therapy for hyperglycemia.
Cardiovascular complications
Hypokalemia has widespread actions in many organ systems that, over time, may result in cardiovascular disease. Cardiovascular complications are clinically the most important harbingers of significant morbidity or mortality from hypokalemia.
Although hypokalemia has been implicated in the development of atrial and ventricular arrhythmias, ventricular arrhythmias have received the most attention.
Increased susceptibility to cardiac arrhythmias is observed with hypokalemia in the following settings:
Congestive heart failure
Underlying ischemic heart disease/acute myocardial ischemia
Aggressive therapy for hyperglycemia, such as with diabetic ketoacidosis
Digitalis therapy
Methadone therapy
Conn syndrome
Low potassium intake has been implicated as a risk factor for the development of hypertension and/or hypertensive end-organ damage. Hypokalemia leads to altered vascular reactivity, likely from the effects of potassium depletion on the expression of adrenergic receptors, angiotensin receptors, and mediators of vascular relaxation. The result is enhanced vasoconstriction and impaired relaxation, which may play a role in the development of diverse clinical sequelae, such as ischemic central nervous system events or rhabdomyolysis.
Treatment of hypertension with diuretics without due attention to potassium homeostasis exacerbates the development of end-organ damage by fueling the metabolic abnormalities. These patients are then at higher risk for lethal hypokalemia under stress conditions such as myocardial infarction, septic shock, or diabetic ketoacidosis.
Abnormalities of renal function often accompany acute or chronic hypokalemia. These may include nephrogenic diabetes insipidus. They also may include metabolic alkalosis from impaired bicarbonate excretion,as well as cystic degeneration and interstitial scarring.
***Diabetes insipidus
Diabetes insipidus is an uncommon condition in which the kidneys are unable to prevent the excretion of water.
Hypokalemia decreases gut motility, which can lead to or exacerbate an ileus. Hypokalemia also is a contributory factor in the development of hepatic encephalopathy in the setting of cirrhosis.
Hypokalemia has a dual effect on glucose regulation by decreasing insulin release and peripheral insulin sensitivity. Clinical evidence suggests that the hypokalemic effect of thiazide is the causative factor in thiazide-associated diabetes mellitus.[
As mentioned, hypokalemia can result from inadequate potassium intake, increased potassium excretion, or a shift of potassium from the extracellular to the intracellular space.
Increased excretion is the most common mechanism. Poor intake or an intracellular shift by itself is a distinctly uncommon cause, but several causes often are present simultaneously.
Inadequate potassium intake
Inadequate potassium intake may result from any of the following:
Eating disorders [11] : Anorexia, bulimia, starvation, pica, and alcoholism
Dental problems: Impaired ability to chew or swallow
Poverty: Inadequate quantity or quality of food (eg, "tea-and-toast" diet of elderly individuals)
Hospitalization: Potassium-poor TPN
Increased excretion of potassium, especially coupled with poor intake, is the most common cause of hypokalemia. Increased potassium excretion may result from any of the following:
Mineralocorticoid excess (endogenous or exogenous)
Hyperreninism from renal artery stenosis
Osmotic diuresis: Mannitol and hyperglycemia can cause osmotic diuresis
Increased gastrointestinal losses
Drugs
Genetic disorders
can result from vomiting, diarrhea, or small intestine drainage. The problem can be particularly prominent in tropical illnesses, such as malaria and leptospirosis.
Bartter syndrome is a group of autosomal recessive disorders characterized by hypokalemic metabolic alkalosis and hypotension.[18] Sensorineural hearing loss is also a feature of this syndrome. Mutations in 6 different renal tubular proteins in the loop of Henle have been discovered in individuals with clinical Bartter syndrome.
Gitelman syndrome
Gitelman syndrome is an autosomal recessive disorder characterized by hypokalemic metabolic alkalosis and low blood pressure. It is caused by a defect in the thiazide-sensitive sodium chloride transporter in the distal tubule, which is encoded by the SLC12A3 gene
Compared with Bartter syndrome, Gitelman syndrome generally is milder and presents later; in addition, Gitelman syndrome is complicated by hypomagnesemia, which generally does not occur in Bartter syndrome. Hypocalciuria is also frequently found in Gitelman syndrome, while patients with Bartter syndrome are more likely to have increased urine calcium excretion.
Liddle syndrome is an autosomal recessive disorder characterized by a mutation affecting either the beta or gamma subunit of the epithelial sodium channel in the aldosterone-sensitive portion of the nephron. Mutations to these genes lead to unregulated sodium reabsorption, hypokalemic metabolic alkalosis, and severe hypertension.
Gullner syndrome
This syndrome was described as being like Bartter syndrome, except that renal histology showed normal juxtaglomerular apparatus and changes to the proximal tubules.
Glucocorticoid receptor deficiencysyndrome is caused by mutations to the NR3C1gene and has different clinical manifestations in patients who are homozygous than it does in those who are heterozygous. Homozygotes for this condition display mineralocorticoid excess, hypertension, hypokalemia, and metabolic alkalosis. Heterozygotes may have increased plasma cortisol levels and generally do not have hypokalemia or metabolic alkalosis. However, several reports in the literature have described likely heterozygotes for this condition who have symptoms of either partial adrenal insufficiency or mild virilization in females.
Hypokalemic periodic paralysis types 1 and 2 are caused by mutations in theCACNL1A3 and SCN4A genes, respectively, and are both inherited in an autosomal dominant fashion. Patients with this disorder experience episodes of flaccid, generalized weakness, usually without myotonia. Patients will have hypokalemia during the flaccid attacks. The disorder is treated by administration of potassium and can be precipitated by a large glucose or insulin load, as both forms tend to drive potassium from the extracellular to the intracellular space.
Thyrotoxic periodic paralysis (TTPP) is a form of hypokalemic periodic paralysis in which episodes of weakness associated with hypokalemia are seen in individuals with hyperthyroidism. TTPP is most common in Asian males.
The mechanism by which hyperthyroidism produces hypokalemic paralysis is not yet understood, but theories include increased Na-K-ATPase activity, which has been found in patients with both thyrotoxicosis and paralysis. Three single-nucleotide polymorphisms in 3 different regions of the CACNA1S gene have been associated with increased rates of TTPP, compared with normal controls or patients with Graves disease.[28]
SeSAME syndrome In addition to seizures, sensorineural deafness, ataxia, mental retardation, and electrolyte imbalance, some patients with SeSAME syndrome will have short stature, salt craving with polydipsia, renal potassium and sodium wasting, and polyuria. Hypokalemia, hypomagnesemia, hypocalciuria, and metabolic alkalosis are seen.
This syndrome is caused by mutations in the KCNJ10 gene, which encodes an inwardly rectifying potassium channel. It is inherited in an autosomal recessive fashion.[29]
A shift of potassium to the intracellular space may result from any of the following:
Alkalosis (metabolic or respiratory)
Insulin administration or glucose administration (the latter stimulates insulin release)
Intensive beta-adrenergic stimulation
Hypokalemic periodic paralysis
Thyrotoxic periodic paralysis
Refeeding: This is observed in prolonged starvation, eating disorders, and alcoholism
Hypothermia