14 – Electrolytes and Acid-Base Flashcards
What are some mechanisms of change in electrolyte concentrations?
- Changes in free water (Na, Cl»K)
- Intake (K»Na, Cl)
- Translocation (K)
- Excretion/loss (Na, Cl, K)
Sodium
- Central role in water and osmotic regulation
o Primary determinant of ECF volume
o Interpret relative to hydration status - Main source is diet
- Regulated by kidney (aldosterone)
- Serum Na reflects total body Na (very little Na intracellularly)
Absolute hypernatremia: 3 causes
- *Na gain
- Iatrogenic (ex. hypertonic saline administration)
- Ingestion of high salt products (ex. salt water, playdough, paintballs)
- Hyperaldosteronism (rare)
Relative hypernatremia: various causes/when can it occur
- *hypotonic fluid/pure water loss or water deficit)
- Panting
- Extensive burns/cutaneous wounds
- Polyuria (ex. central or nephrogenic diabetes insipidus, kidney disease)
- Water deprivation
- Primary adipsia (rare)
- Occasionally GI disease (v/d)
What are the causes of hyponatremia?
- Decreased or inadequate dietary intake (large herbivores)
- Excess Na loss
- Volume overload
- Excessive water intake/overhydration
What are some things that can cause excessive Na loss?
- GI tract: vomiting, diarrhea
- Kidneys: hypoadrenocorticism, osmotic diuresis
- Skin: sweating in horses
- Third space: edema, ascites
- Milk: high yield dairy cows
What are some things that can cause volume overload?
- Congestive heart failure
- Advanced renal failure
What are some things that can cause excessive water intake/overhydration?
- Psychogenic polydipsia (rare)
- Hypotonic fluid administration
Chloride
- Main source is diet
- Regulated by kidneys
o Passive (alongside Na)
o Active (reabsorption) - Cl- changes typically PARALLEL Na changes unless acted on by acid-base disturbances
o Remember to “eyeball” Na/Cl for proportionality
K+ homeostasis
- Kidney is main regulatory of total body K
- 90% is intracellular
o Serum K is a POOR reflection of total body K
What is serum [K+] dependent upon?
- K intake
- Redistribution (between ECF and ICF)
- K output
o Urine: 90% (aldosterone)
o Digestive tract: 10%
o Sweat (HORSES!)
What are the K shifts in acid-base disorders?
- H and K are exchanged to maintain electroneutrality
- **Metabolic alkalosis=hypokalemia
o H shifts to blood, K goes into cells - *(bicarbonate loss) metabolic acidosis=hyperkalemia
o H shifts into cells, K goes into blood
What are the K shifts with insulin?
- Insulin promotes cellular uptake of K+
o Stimulates Na/K/ATPase pump in liver, muscle, adipose tissue - New diabetics may initially appear to have normal K
o BUT when starting insulin it may cause enough K to shift into cells to result in a rapid onset of hypokalemia (watch out for muscle weakness/hypoventilation)
What are the K shifts with tissue necrosis?
- Tissue necrosis can cause a release of IC K
o May result in hyperkalemia
o Usually seen with marked myocyte damage (capture myopathy, rhabdomyolysis)
What is hyperkalemic periodic paralysis (HYPP) of horses?
- Genetic defect in sodium channel of muscle cells in QHs and associated breeds
- K leaks from muscles through defective channels
- Intermittent episodes
- Variable serum K level
o Normokalmeic variants have been described
What are 2 types of pseudohyperkalemia?
- Delayed serum separation from cells or in vitro hemolysis
- Contamination with K EDTA anticoagulant
Delayed serum separation from cells or in vitro hemolysis (pseudohyperkalemia)
- K leaks out of leukocytes and platelets
o Especially in patients with leukocytosis or thrombocytosis - K leaks out of RBCs
o Cattle, horses, pigs, camelids
o Dogs: Akita, Shiba Inu, Korean breeds
o Reticulocytes have higher intracellular K (ex. in a patient with a regenerative anemia
Contamination with K EDTA anticoagulant (pseudohyperkalemia)
- Tend to see very high K+ (>20mEq/L) and concurrent hypocalemia (chelation)
