potassium homeostasis, hypokalemia and potassium correction, electrolyte imbalance, management of hypokalemia,potassium deficit

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