The document provides a comprehensive overview of hypokalemia, its causes, symptoms, and management strategies. It details the physiological role of potassium, factors influencing its homeostasis, and the common mechanisms leading to its deficiency. Treatment approaches include dietary supplementation, addressing underlying causes, and careful monitoring of potassium levels, especially in cases of severe hypokalemia.

1. Sheila Perillo, MD
Obstetrics and Gynecology

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.

7. ECG changes

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

29.  Vomiting
 Diarrhea
 Small intestine drainage

30.  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

31.  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)

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