Hyperkalemia and Hypokalemia

Ilan Marcuschamer M.D.

Hadassah University HospitalMount 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 develop3. 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: DDRule out inadequate intake

Consider Renal Losses Consider GI Losses Consider IC redistribution

• K wasting diuretics

•Non reabsorbable anions

•Osmotic Diuresis

•Mineralocorticoid excess

•Glucocorticoid excess

•Hypomagnesemia

•Leukemia: 30%

•Gittelman, Bartter, Liddle Sx.

• Diarrhea

•Vomiting

•Nasogastric Suction

•Gastrointestinal fistula

•Laxative abuse

• Alkalosis

•Insuline admon

•Hyperglycemia

•Beta stimulation

Hypokalemia EKG Changes

Increased amplitude and width of the P wave Prolongation of the PR interval T wave flattening and inversion ST depression Prominent U waves (best seen in the precordial leads) Apparent) long QT interval due to fusion of the T and U waves (= long QU interval)

http://lifeinthefastlane.com/wp-content/uploads/2011/02/severe-hypok-1.7.jpg

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 - DDRule peusohyperkalemia

Decreased K excretion Increased K intake EC K redistribution

• Decreased GFR

•Adrenal Insufficiency

•Hyporeninemic hypoaldosteronism RTA IV

•Renal insensitivity to aldosterone

•Drugs

• K rich salt substitue

• Blood transfusion

• Potassium containing medications

• Celular lysis: (hemolysis, tumor lysis, rhabdomyolisis)

•Metabolic Acidosis

•Insulin deficient state

•Beta blockade (rare)

Food1. White Beans 2. Darky leafy greens (spinach) 3. Potatoes with skin

4. Dried Apricots 6. Plain Yogurt 5. Pumpkin

7. Plain Yogurt 8. Avocadoes 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 excretion2. Shift K Intracellularly (Mod to Severe/symptoms) - Insuline with D50 - ß agonists - Calcium administration stabilizes electrically active

membranes: First choice in arrhythmias3. 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