Hyperkalemia and
Hypokalemia
Ilan Marcuschamer M.D.
Hadassah University Hospital
Mount Scoppus
Potassium Balance
• K is the major intracelullar cation.
• It’s regulation is tightly regulated between
the IC and EC compartments.
• Gradient mantained by Na/K ATPase
• 3NaX2K Creates electric charge of
membrane: therefore Effects of abnormal
K tend to manifest in electrically active
tissues.
Potassium Balance
• Potassium Excretion:
- 80% Excreted via kidneys.
* Na delivery and urine flow in the distal and
collecting tubules favor excretion.
* Aldosterone directly stimulates the kidney to
excrete K
* Hyperkalemia increases aldosterone, which
increases K excretion.
- 15% Excreted via GI Tract (increases in RF)
- 5 % Excreted through sweat
Potassium Balance
• Abnormalities in Serum K may result
from Total body potassium depletion or
excess, or alterations in the flux
between IC and EC spaces.
* Because of obligatory potassium
losses, there is a minimum daily
requirement of 40 – 50 mEq of K.
Acid – Base effects
• Acidosis Shifts K out of cells resulting in
hyperkalemia.
• Alkalosis Shifts K into cells resulting in
hypokalemia.
Hormone effects
• Insuline and ß 2 agonists stimulates
cellular uptake of K.
• α Agonists will shift K out of cells
Hypokalemia - Basics
• In the abscense of acid – base disorders
or abnormal concentrations of insuline or
chatecolamines:
Hypokalemia almost always implies low
total body K.
• May result from inadequate daily intake.
• More commonly results when K losses
exceed potassium intake.
Hypokalemia – Clinical
Presentation
1.
Generalized muscle weakness, often mild and
limited to lower extremities.
2. Paralysis may develop
3. Smooth muscle of intestine may be affected with
development of paralytic ileus.
4. Cardiac electrical activity affected: Arrhythmias: Atrial
tachycardia, A-V disociation, VT, VF.
* Increased risk with high digoxin concentrations!
* May predispose to osmotic demyelinization seen with
hyponatremia treatment: If neurologically stable
patients, correct K before Na.
Hypokalemia: DD
Rule out inadequate intake
Consider Renal Losses
Consider GI Losses
Consider IC redistribution
• K wasting diuretics
• Diarrhea
• Alkalosis
•Non reabsorbable anions
•Vomiting
•Insuline admon
•Osmotic Diuresis
•Nasogastric Suction
•Hyperglycemia
•Mineralocorticoid excess
•Gastrointestinal fistula
•Beta stimulation
•Glucocorticoid excess
•Laxative abuse
•Hypomagnesemia
•Leukemia: 30%
•Gittelman, Bartter, Liddle
Sx.
Hypokalemia EKG Changes
Increased amplitude and width of the P wave
Prolongation of the PR interval
T wave flattening and inversion
ST depression
)best seen in the precordial leads( U waves Prominent
)long QT interval due to fusion of the T and U waves (= long QU interval Apparent)
Hypokalemia Treatment
• Degree?? Symptoms??
1. Investigate and treat underlying cause
2. Aggressive treatment to those with RF for
arrhythmia developing.
3. Prevent further losses
4. Moderate to Severe: -3 mEq/L
- Not severe/No symptoms: PO supplements.
- Severe/Symptoms: IV supplements.
Hyperkalemia - Basics
• Less common than hypokalemia, ussualy
implies some degree of RF.
- Diabetics are twice as likely to develop
hyperkalemia than non-diabetics.
• Sustained hyperkalemia rarely caused by
excess K intake alone: Kidney very efficient.
• Aldosterone protects against hypernatremia by
stimulating Renal K excretion
• Pseudohyperkalemia: Artifactual elevation in
sample when serum K usually normal.
Hyperkalemia – Clinical
presentation
• Related to K role in the membrane potential of cells:
Symptoms worse with acute development.
- Mild: 5-5.9 mEq/L usually asymptomatic
- Mod: Muscle weakness and paresthesias.
* >6.5 mEq/L Areflexia, muscle paralysis, respiratory
failure.
- Severe: Cardiac manifestations are the most life
threatening of hyperkalemia, but EKG changes are not
a sensitive marker for the presence of hyperkalemia.
* Bradycardia, A-V disociation, VT, VF may follow.
Hyperkalemia - DD
Rule peusohyperkalemia
Decreased K excretion
Increased K intake
• Decreased GFR
• K rich salt substitue
•Adrenal Insufficiency
• Blood transfusion
•Hyporeninemic
hypoaldosteronism RTA IV
• Potassium containing
medications
•Renal insensitivity to
aldosterone
•Drugs
EC K redistribution
• Celular lysis: (hemolysis,
tumor lysis,
rhabdomyolisis)
•Metabolic Acidosis
•Insulin deficient state
•Beta blockade (rare)
Food
1. White Beans
2. Darky leafy greens (spinach)
5. Pumpkin
4. Dried Apricots
7. Plain Yogurt
8. Avocadoes
3. Potatoes with skin
6. Plain Yogurt
9. Mushrooms
10. Bananas
Hyperkalemia EKG changes
Hyperkalemia treatment
• 3 steps involved: Degree? Symptoms?
1.
Decrease K Intake
- Look for ingestion of salt substitutes or K charged
medications or food.
- Avoid drugs than inhibit K excretion
2. Shift K Intracellularly (Mod to Severe/symptoms)
- Insuline with D50
- ß agonists
- Calcium administration stabilizes electrically active
membranes: First choice in arrhythmias
3. Reduce body stores of K
- Sodium Polystyrene sulfonate (Kayexalate)
- Potassium wasting diuretics or Urgent hemodyalisis
Rare Syndromes
• Bartter: Ascending think of Henle Loop
NaK2Cl
• Gittelman: Distal tubule – NaCl, Ca++
• Liddle: Colector: Resembling
hyperaldosteronism, with low aldosterone
and renine levels
• Gordon: Aldosterone resistance
• Conn: Aldosterone producing tumor