HYPOKALEMIA

Sheila Perillo, MDObstetrics and Gynecology

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

POTASSIUM -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

-obtained through the diet -excreted via the kidney. -Potassium homeostasis is maintained

predominantly through the regulation of renal excretion

HYPOKALEMIA

inadequate potassium intake increased potassium excretion- most

common shift of potassium from the extracellular

to the intracellular space

Common findings include weakness, fatigue, constipation, ileus, and respiratory muscle dysfunction.

Symptoms seldom occur unless plasma K+ is less than 3.0 mmol/L.

ECG changes

THE TREATMENT OF HYPOKALEMIA HAS 4 FACETS

Reduction of potassium losses Replenishment of potassium stores Evaluation for potential toxicities Determination of the cause to prevent

future episodes

PATHOPHYSIOLOGY

Daily excess intake of approximately 1 mEq/kg/day (60-100 mEq):Ninety percent is excreted through the

kidneys10% is excreted through the gut

Potassium homeostasis is maintained predominantly through the regulation of renal excretion (collecting duct)

POTASSIUM EXCRETION IS INCREASED BY THE FOLLOWING FACTORS: 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)

POTASSIUM EXCRETION IS DECREASED BY THE FOLLOWING FACTORS: Absolute aldosterone deficiency or

resistance to aldosterone effects Low sodium delivery to the collecting

duct Low urine flow Low serum potassium levels Renal failure

increase in osmolality exit from cells

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. 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.

POTASSIUM DISTRIBUTION

Potassium is predominantly an intracellular cation; therefore, serum potassium levels can be a very poor indicator of total body stores.

SEVERAL FACTORS THAT REGULATE THE DISTRIBUTION OF POTASSIUM BETWEEN THE INTRACELLULAR AND EXTRACELLULAR SPACE

Glycoregulatory hormones: (1) Insulin enhances potassium entry into cells (2) glucagon impairs potassium entry into cellsAdrenergic stimuli: (1) Beta-adrenergic stimuli enhance potassium

entry into cells (2) alpha-adrenergic stimuli impair potassium

entry into cellspH: (1) Alkalosis enhances potassium entry into cells (2) acidosis impairs potassium entry into cells

PATHOGENIC MECHANISMS Hypokalemia can occur via the following

pathogenetic mechanisms:Deficient intake Increased excretionA shift from the extracellular to the

intracellular space Although poor intake or an intracellular

shift by itself is a distinctly uncommon cause

INCREASED EXCRETION

The most common mechanisms leading to increased renal potassium losses include the following:Enhanced sodium delivery to the

collecting duct, as with diureticsMineralocorticoid excess, as with

primary or secondary hyperaldosteronism

Increased urine flow, as with an osmotic diuresis

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

EXTRACELLULAR/INTRACELLULAR SHIFT Shift from extracellular to intracellular

spaceoften 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)

COMPLICATIONS

Cardiovascular complicationsAtrial 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 

Low potassium intakehypertension and/or hypertensive end-

organ damagealtered 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

MUSCULAR COMPLICATIONS Muscle weakness Depression of the deep-tendon reflexes Flaccid paralysis Rhabdomyolysis (severe hypokalemia)

RENAL COMPLICATIONS

Nephrogenic diabetes insipidus- Abnormalities of renal function often

accompany acute or chronic hypokalemia Metabolic alkalosis from impaired

bicarbonate excretion Cystic degeneration Interstitial scarring

GASTROINTESTINAL COMPLICATIONS Decreased gut motility, which can lead

to or exacerbate an ileus

Hepatic encephalopathy in the setting of cirrhosis

METABOLIC COMPLICATIONS

Dual effect on glucose regulation by decreasing insulin release and peripheral insulin sensitivity

Thiazide-associated diabetes mellitus

ETIOLOGY Inadequate potassium intake Increased potassium excretion ** Shift of potassium from the extracellular

to the intracellular space

INADEQUATE POTASSIUM INTAKE

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

INCREASED POTASSIUM EXCRETION 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

GASTROINTESTINAL LOSS OF POTASSIUM Vomiting Diarrhea Small intestine drainage

DRUGS THAT CAN CAUSE HYPOKALEMIA INCLUDE THE FOLLOWING: Diuretics (carbonic anhydrase inhibitors, loop diuretics,

thiazide diuretics): Increased collecting duct permeability or increased gradient for potassium secretion can result in losses

Methylxanthines (theophylline, aminophylline, caffeine) Verapamil (with overdose) Quetiapine (particularly in overdose) Ampicillin, carbenicillin, high-dose penicillins Bicarbonate Antifungal agents (amphotericin B, azoles, echinocandins)  Gentamicin Cisplatin Ephedrine (from Ephedra; banned in the United States, but

available over the Internet)  Beta-agonist intoxication 

GENETIC DISORDERS Congenital adrenal hyperplasia (11-beta

hydroxylase or 17-alpha hydroxylase deficiency) Glucocorticoid-remediable hypertension Bartter syndrome Gitelman syndrome Liddle syndrome Gullner syndrome Glucocorticoid receptor deficiency Hypokalemic period paralysis Thyrotoxic periodic paralysis (TTPP) Seizures, sensorineural deafness, ataxia, mental

retardation, and electrolyte imbalance (SeSAME syndrome)

SHIFT OF POTASSIUM FROM EXTRACELLULAR TO INTRACELLULAR SPACE 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

OTHER FACTORS ASSOCIATED WITH A HIGH INCIDENCE OF HYPOKALEMIA INCLUDE THE FOLLOWING: 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 

TREATMENT Therapeutic goals

Prevent life-threatening complications (arrhythmias, respiratory failure, hepatic encephalopathy)

Correct the K+ deficitMinimize ongoing lossesTreat the underlying cause

TREATMENT K deficit= (desired k- actual k) x 100% 0.27

Estimation of K+ deficit3.0 meq/L= total body K+ deficit of 200-400

meq/70kg2.5 meq/L = 500 meq/70kg2.0 meq/L = 700 meq/70kg

TREATMENT Oral therapy

Generally saferDegree of K+ depletion does not correlate

well with the plasma K+KCl is usually the preparation of choiceKalium durule: 1 durule = 10 meqs KClKCl syrup: 1meq/mL

TREATMENT 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/hrRate of infusion should not exceed 20

meq/hour unless paralysis or malignant ventricular arrhythmias are present

TO GOD BE THE GLORY!