HYPOKALEMIA
Salient Features 55 y/o male Diarrhea for several weeks to admission 3 days PTA: progressive weakness
Laboratory Findings:
Chemistry Profile
Actual Results Normal Values Remarks
Na+ 140 meq/L 136-145meq/L Normal
Cl- 110 meq/L 98-106 meq/L Increased
K+ 2. 0 meq/L 3.5-5.0 meq/L Decreased
Laboratory Findings:Arterial Blood Gas Profile:
Urine Potassium: 15 meq/L(NV: usually >15 meq/L)
Actual Results Normal Values Remarks
pH 7.28 7.38 - 7.44 Decreased
pCO2 39mmHg 35 - 45 mmHg Normal
HCO3 16 meq/L 21 - 30 meq/L Decreased
Guide Questions:
1.) Using an algorithm, discuss the diagnostic approach to hypokalemia. What is the cause of hypokalemia in this patient?
DIAGNOSTIC APPROACH TO HYPOKALEMIA
Urinary K+ Loss
<15 moml/d >15 mmol/d
Assess Acid-Base status Assess K+ secretion
Metabolic acidosis
Metabolic alkalosis
TTKG >4 TTKG <2
Lower GIT K+ loss
Remote diuretic useRemote vomitingK+ loss via sweat
Na+ wastingNephropathy
Osmotic diuresisDiuretic
Acid-Base status
Metabolic acidosis Metabolic alkalosis
HypertensionDiabetic ketoacidosisProximal Type 2 RTA
Distal Type 1 RTAAmphotericin B Mineralocorticoid excess
Liddle’s syndrome
VomitingBartter’s syndromeHypomagnesemia
Harrison’s Principles of Internal Medicine 16th ed. Vol.I, p.260
Causes of Hypokalemia
DecreaseIntake Increase Loss
Redistribution into Cells
A.Nonrenal
B.Renal
Causes of HypokalemiaI. Decreased intake
A. Starvation B. Clay Ingestion
II. Redistribution into Cells A. Acid-Base (Metabolic Alkalosis) B. Hormonal (Insulin, Beta agonist, Alpha
antagonist) C. Anabolic State (folic acid) D. Other (Hypothermia, Pseudohypokalemia)
Causes of Hypokalemia
III. Increased Loss
A. Nonrenal
1. Gastrointestinal Los (diarrhea)
2. Integumentary Loss (sweat)
B. Renal
Hypokalemia: Extrarenal loss
Cause of Hypokalemia in the patient:
Gastrointestinal losses diarrhea (secretory)
Urine potassium level less than 20 mEq/L suggests gastrointestinal loss
Stool has a relatively high potassium content, and fecal potassium losses could exceed 100 mEq per day with severe diarrhea.
Gastrointestinal Loss Hypokalemia is also due to increased K+
renal excretion Loss of Gastric contents results in volume
depletion and metabolic alkalosis, both of which promotes kaliuresis
Gastrointestinal Loss Stimulates aldosterone release=augments
K+ secretion by principal cells There is an increase in distal delivery of
NaHCO3 which enchances the electrochemical gradient favoring potassium loss in urine.
SIGNS & SYMPTOMS Fatigue Myalgia Muscular weakness & paralysis Hyporeflexia Dyspnea Arrhythmia Predispose to digitalis toxicity Constipation
SIGNS & SYMPTOMS
Risk of hyponatremia resultant confusion, headaches, & seizures
Irritable Nervousness anorexia Ileus
Adverse Medical Implications Muscle weakness and paralysis (more
negative resting membrane potential) Respiratory
Hypoventilation (due to respiratory muscle weakness or paralysis)
Gastrointestinal Paralytic ileus
Adverse Medical Implications Cardiac
ECG changes Due to delayed ventricular repolarization Early changes: flattening or inversion of T wave,
prominent U wave, ST-segment depression, prolonged QU interval
Severe K+ depletion: prolonged PR interval, decreased voltage and widening of QRS complex
A: Normal
B: flattening of T wave
C-F:U wave, ST-depression, prolonged QU interval
Adverse Medical Implications Cardiac
Increased risk for ventricular arrythmias Potential digitalis toxicity Risk for Hypertension
Exercising skeletal muscle insufficient blood flow increased risk for rhabdomyolysis
Metabolic acidosis (due to increased bicarbonate excretion)
Adverse Medical Implications Renal
Risk for renal cystic disease HypoK leads to increased ammoniagenesis which
may activate the complement system Mild Nephrogenic Diabetes Insipidus (NDI)
Defective activation of adenylate cyclase = decrease effect of vasopressin
Endocrine Glucose intolerance = due to decreased insulin
or insulin resistance
4. What is the significance of the urinary potassium
levels?
Potassium Regulation Kidney
K+ balance: Urinary K+ excretion= Dietary intake Decreased secretion: Low K+ diet, hypoaldosteronism,
acidosis, K+ sparing diuretics GIT
dietary K+ is absorbed in the small intestine by passive diffusion
K+ is secreted in the colon through aldosterone stimulation
in diarrhea, K+ secretion by the colon is increased
Urinary Potassium level NV = 25 - 100 meq/L patient has decreased urinary K+
(15meq/L) a decrease of:
<25meq/L - diarrhea >40meq/L - diuretics
What is the treatment?
TREATMENT
Therapeutic goals:
to correct the K+ deficit
to minimize on going losses
•It is safer to correct hypokalemia via oral route in order to prevent rebound hyperkalemia if given IV
•The plasma potassium concentration should be monitored frequently when assessing the response to treatment
TREATMENT
Emergency Treatment of Hypokalemia
A. Estimated Potassium Deficit
serum K <3 mEq/L= K deficit >300 mEq
serum K <2 mEq/L= K deficit >700 mEq
TREATMENT
B. Indications for Urgent Replacement
ECG abnormalities consistent with severe K+ depletion
myocardial infarction
hypoxia
digitalis intoxication
marked muscle weakness
respiratory muscle paralysis.
TREATMENT
IV infusion
- for severe hypokalemia or those who cannot take oral supplementation
- peripheral vein = 40 mmol/L (preferred) central vein = 60 mmol/L
- rate of infusion 20 mmol/hr - mixed in NSS
Continous ECG monitoring
Serum potassium determination every 3-6 hours
TREATMENT
Potassium chloride (KCl)
-drug of choice
- treat hypokalemia and metabolic alkalosis
Potassium bicarbonate and citrate
- more appropriate for hypokalemia associated with chronic diarrhea or RTA
Non-Emergency Treatment of Hypokalemia
-attempts should be made to normalize K+ levels if <3.5 mEq/L.
-oral supplementation is significantly safer than IV
-KCL elixir, 1-3 tablespoon every day.
TREATMENT
TREATMENT
ORAL ROUTE
1 mmol/L decrease in plasma K+ concentration
200-400mmol total body K+ deficit
=
Plasma levels <3 mmol/L require additional 600 mmol