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Mohammad A. Alfuhaily, PhD د. محمد عبدالمحسن الفحيلي

Associate Professor

College of Applied Medical Sciences, Department of Clinical Laboratory Sciences

كلية العلوم الطبية التطبيقية
Building 24, Office 2299
مدونة

Electrolytes (Electric Lights)

-Electrolytes are inorganic compounds that dissociate in body fluids into ions (charged atoms) capable of conducting electricity and controlling fluid balance.

-Specimen: Heparin; SST; Serum; Urine. 

(1) Potassium (K+)

-Distribution:

*95% inside cells (most abundant intracellular cation)
*5% in blood ( narrow RR). 
(This is maintained by the Na/K pump)

-Sources:

*Vegetables (tomatoes, potatoes…)
*Fruits (orange, citrus fruits, banana…)
*Meat

-Functions:

*Maintenance of cellular membrane potential
*Transmission of action potential in nerve cells (transmission of nerve impulses)
*Homeostasis of cell volume

-Elimination:

*Kidney (filtered by glomerulus; active reabsorption in PCT and ascending limb of LoH; active secretion in the DCT and CD by aldosterone). 
*GIT

Hyperkalemia

*High blood K+ leads to depolarization of membrane potential of cells, which opens volume-gated sodium channels (tiny lil pores through which Na goes into the cell) not enough to generate an action potential. With time, these channels become refractory and need higher threshold to generate an action potential. As a result, nerve conduction to neuromuscular, gastrointestianl, and cardiac systems seizes (arrhythmia and asystole).
*Hemolysis = pseudohyperkalemia (excessive vacuum of blood draw; too fine needle gauge). Heparinized 2nd blood if suspected.

*Causes:

  • Decreased renal excretion due to renal failure (most common): Drugs; Addison’s and low cortisol lead to K retention
  • Excessive intake (uncommon unless renal function is impaiured).
  • Shift from IC space to EC space (from destruction “burns; surgery; trauma; rhabdomyolysis; heat stroke; seizures”, acidemia “mostly metabolic acidosis”, or low insulin production “block K entry to cell”). 

*Supportive Data: 

  • Urine (oliguria/anuria; fixed SG).
  • Renal function (serum Cr better than BUN).
  • ABG’s. 
  • Blood sugar.
  • Hemolysis “Hgb; CK; hematocrit”.
  • ECG & neuromuscular evaluation (none of your business).

*Management:

  • Hypertonic dextrose + regular insulin IV to shift K into cells
  • Na bicarbonate IV to shift K into cells
  • Ca gluconate IV to protect the heart
  • Beta agonist IV
  • Na polystyrene sulfonate (Kayexalate) orally, NG, or via enema for K elimination in the bowel
  • Hemodialysis to remove K from blood

Hypokalemia

-Mild with slow onset; may be asymptomatic with no effects.
-Cardiac: Decreased cell contractility; increased excitability; arrhytmias; hypotension; digitalis toxicity.
-ECG & neuromuscular evaluation.

*Causes:

  • Loss from GIT (vomiting; diarrhea; tap water enema; nasogastric suction; laxative abuse; eliostomy).
  • Low intake (K-restricted diets; malnutrition; anorexia nervosa; K-free IV solutions).
  • Shift from IC space to EC space (alkalosis; Rx of DKA by INS)
  • Excessive loss through kidneys (diuretics; steroids; beta agonists; osmotic diuresis from DKA; hyperaldosteronism as in Cushing) - Loss of concentrating ability; polyuria; nocturia; low SG

*Management:

  • IV pump of K (moderate or severe = given per hour if diluted appropriately: 10-40 mEq in 50-100 mL normal saline administered over 2-4 hours) while patient on cardiac monitor.
  • K-rich diet
  • Oral K causes GI upset, so give it with meals or extra fluids

(IV/IM K administration must be diluted 20-40 mEq/L fluid and infused with a continuous infusion pump (monitor closely for phlebitis and infiltration). 

(2) Sodium (Na+)

-Major extracellular cation.

Hypernatremia

-Potentially life-threatening due to brain damage caused by brain cell injury and intercranial hemorrhage.
-Risk of injury is compounded by the risk for fluid volume deficit (e.g., burns) that commonly accompanies hypernatremia.
-Higher serum Na+ = higher serum osmolality (commonly due to overall deficit in total body water). Hyperosmolality causes fluid to move out of the cell into the intravascular compartment (this fluid shift is called osmosis). So, fluid moves to the compartment where solute concentration is the greatest (serum) until the solute is dispersed equally. 
-In the brain, the fluid moves into the EC compartment, which causes the cells to shrink and become dehydrated. This shrinkage pulls the brain tissue away from the dome of the skull, which traumatizes small vessels around the affected brain tissue leading to intercranial hemorrhage. All in all, shrinkage + dehydration + bleeding = low cognitive abilities.
-Concurrent fluid volume deficit problem and neurological deterioration.
-Risk: Advanced age (low thirst response) and infancy (can’t communicate their need and they have a greater insensible water loss).

*Causes:

  • Low fluid intake (inadequate thirst mechanism “elderly” or inability to respond to thirst mechanism)
  • Water loss (ongoing in rapid breathing, fever, diapheresis; renal in diuretics Rx or abnormal development like osmotic diuresis seen in solute diuresis associated w/ hyperglycemia/DM).
  • Hormonal (low ADH as in diabetes inspidus “low water reabsorption in tubules and high urine output w/o Na”; high cortisol or aldosterone  leads to Na retention).
  • High intake (diet, IV, medics…).

*Management:

  • If acute with onset over 48 hours: Free water orally or 5% dextrose in water (D5W) IV infusion.
  • If chronic: slower (rapid fluid replacement can lead to cellular swelling, cerebral edema, and high intercranial pressure).
  • If fluid volume deficit is suspected (isotonic NaCl IV until bital signs are stable then change to D5W).
  • Medics: Diuretics (inhibit Na reabsorption in DCT = Na excretion); Vasopressin & ADH analogues (high water reabsorption). 

Hyponatremia

-Life-threatening (permanent brain damage). Severe if under 120 mEql/L.
-Low Na = low osmolality = fluid move into cells and they swell.

*Causes:

  • Total body water loss proportionately lower than Na loss.
  • Increase in total body water not accompanied by Na increase (most common). 
  • High ADH as in SIADH.
  • Low intake/Excess secretion.

*Risks:

  • Excessive use of hypotonic IV solutions.
  • Excessive oral water intake (high total body water).
  • Low intake. 
  • Vomiting & diarrhea (increases Na excretion).
  • Nasogastric suctioning (increases Na elimination).
  • Diuretics (Na loss is more than that of water).
  • Chronic renal insufficiency due to increased total body water.
  • Adrenal insufficiency due to Na loss more than water.
  • SIADH due to increased total body water related to increased ADH.
  • CHF due to fluid volume overload.
  • Disorder that redistrubite Na to the 3rd space (e.g., ascites).

*Supportive Data:

  • Urine Na+ & osmolality.
  • Serum osmolality.

*Management:

-Caution as pulmonary edema may result (fluid from IC to EC space).
-Normal saline and lactated ringers are hypertonic for hyponatremic patients.

  • Hypertonic NaCl solution IV (e.g., 3% NaCl).
  • Isotonic NaCl solution IV (0.9% NaCl or lactated ringers).
  • Oral fluid restriction, oral intake of Na-rich diet, and hemodialysis.
  • ADH-inhibiting drugs (e.g., lithium).

(3) Chloride (Cl-)

coming soon...