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:
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
Urine Potassium: 15 meq/L
(NV: usually >15 meq/L)
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 K+ secretion
Assess Acid-Base status
Metabolic
acidosis
Lower GIT
K+ loss
Metabolic
alkalosis
TTKG >4
TTKG <2
Acid-Base status
Remote diuretic use
Remote vomiting
K+ loss via sweat
Metabolic acidosis
Diabetic ketoacidosis
Proximal Type 2 RTA
Distal Type 1 RTA
Amphotericin B
Harrison’s Principles of Internal Medicine 16th ed. Vol.I, p.260
Na+ wasting
Nephropathy
Osmotic diuresis
Diuretic
Metabolic alkalosis
Hypertension
Mineralocorticoid excess
Liddle’s syndrome
Vomiting
Bartter’s syndrome
Hypomagnesemia
Causes of Hypokalemia
Decrease
Intake
Increase Loss
A. Nonrenal
B. Renal
Redistribution into
Cells
Causes of Hypokalemia
I. 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

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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



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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


Mild Nephrogenic Diabetes Insipidus (NDI)


HypoK leads to increased ammoniagenesis which
may activate the complement system
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
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

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
TREATMENT
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
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