1.

Sodium, potassium, chloride

Sodium:

 Most abundant cation in ECF, strongly affects the distribution of water between ICF & ECF by
osmosis
 Functions: nerve conduction, part of the bicarbonate buffer system
 Excreted in urine & perspiration
 Normal intake occurs via table salts & as a constituent of the vast majority of dietary intake
 Reference values: 135-145 mmol/L
 Hypernatremia (Na+>145 mmol/L):
o Causes:
 Na+ content normal, H2O ↓: ↓ H2O intake (elderly, stroke), renal H2O loss
(diabetes insipidus, loop diuretics)
 Na+ content ↓, H2O ↓↓: excessive sweating/diarrhoea (children), osmotic
dieresis (diabetes mellitus)
 Na+ content ↑, H2O normal: Na+ administration (NaHCO3 for acidosis), near-
drowning in salt water, Conn’s syndrome (primary hyperaldosteronism),
Cushing’s syndrome (cortisol has weak mineralocorticoid activity)
o Clincal features:
 If there is H2O loss: dehydration
 If there is salt gain: ↑ jugular venous pressure, pulmonary edema
o Treatment:
 If pure H2O loss: p.o./i.v. 5% dextrose
 If Na+ & H2O loss: add Na+
 If salt poisoning: diuretics & water
 Hyponatraemia (Na+<135 mmol/L):
o The most frequent abnormality encountered
o Causes:
 Na+ deficit (hypovolemic): ↑ loss (vomiting, diarrhoea, GIT fistula,
hypoaldosteronism, thiazide diuretics)
 H2O retention:
 Edematous (hypervolemic): ↑ H2O intake (inappropriate i.v. saline),
↓ H2O excretion (congestive heart failure)
 Non-edematous (normovolemic): ↑ H2O intake (compulsive H2O
drinking), ↓ H2O excretion (SIADH)
o Clincal features:
 Na+ deficit: headache, nausea, ↓ consciousness, hypotension, ↑ pulse, ↓
urine output
 H2O retention: edema (pitting in lower extremities)
o Treatment:
 If hypovolemic: Na+ & H2O replacement
 If normovolemic: fluid restriction
 If hypervolemic: diuretics, fluid restriction
 Pseudohyponatremia:
 o Hyponatremia in patients with severe hyperproteinemia/hyperlipidemia
o ↑ protein/lipoprotein occupy more of the plasma volume & the water less
o Na+ is distributed in the water fraction only
o Patients have normal Na+ concentration in plasma water
o Many methods used in analytical instruments measure Na+ concentration in the
total plasma volume & take no account of a water fraction that occupies less of the
total plasma volume than usual

Potassium:

 Principal cation in the ICF

 Function: determines resting membrane potential of cells (nerve cells, muscle cells)
 Excreted in urine
 Reference values: 3.5-5.0 mmol/L
 Hyperkalemia (K+> 5.0 mmol/L):
o Causes:
 ↑ intake: any drugs given as K+ salts (e.g.: penicillin), blood products >5 days
old (stored RBCs release K+ down its concentration gradient)
 Redistribution of out cells: metabolic acidosis, damaged cells
(rhabdomyolysis, extensive trauma, tumour lysis syndrome), insulin
deficiency (because insulin stimulates cellular uptake of K+)
 ↓ excretion: renal failure (↓ GFR), hypoaldosteronism (ACE inhibitors,
angiotensin receptor blockers, spironolactone, adrenal insufficiency)
o Clinical features: ECG changes (tall ‘tented’ T waves, widening of QRS complex),
muscle weakness, paresthesia, arrhythmias, cardiac arrest
o Treatment:
 Insulin & glucose (to prevent hypoglycaemia)
 i.v. calcium gluconate (counteracts the effect of K+ on nerve & muscle cells)
 Oral administration of cation exchange resins (to stop slower rises in K+)
 Dialysis
 Hypokalemia (K+<3.5 mmol/L):
o Causes:
 ↑ losses: GIT (diarrhoea, vomiting), urinary tract (loop & thiazide diuretics,
mineralocorticoid excess, hypomagnesemia-interferes with renal K+
reabsorption)
 Redistribution into cells: metabolic alkalosis, insulin, refeeding (refeeding
syndrome: feeding of malnourished patients with high carbohydrate loads
→ insulin moves glucose, phosphate, magnesium & K+ into cells), β-agonism
(acute physiological stress, salbutamol, dobutamine)
 ↓ intake (rare because K+ is present in most foods)
o Clinical features: ECG changes (flattened T wave, prominent U wave), muscle
weakness, hyporeflexia, cardiac arrhythmias
o Treatment:
 Administration of K+ salts prophylactically in an enteric coating
 i.v. K+
  Pseudohyperkalemia: ↑ in the measured K+ due to K+ movement out of cells during/after
the drawing of the blood specimen (caused by hemolysis)

Chloride:

 Principal anion of the ECF

 Functions: role in acid-base balance of blood, water balance, saliva, sweat & gastric acid
formation
 Reference values: 97-108 mmol/L
 Hyperchloremia (Cl->108 mmol/L):
o Causes: diarrhoea (↓ HCO3-), renal tubular acidosis type III ((↓ HCO3-), overactivity
of parathyroid glands (↑ PTH → ↑ urinary excretion of HCO3-), carbonic anhydrase
inhibitors
o Often comorbid with diabetes/hyponatremia
o Clinical features:
 Usually asymptomatic
 If diabetic: hyperglycemia, Kussmaul’s breathing, thirst
o Treatment:
 If dehydrated: hydration
 If due to medications: alter/discontinue the medication
 If there is kidney disease: refer to nephrologist
 If there is endocrine dysfunction: refer to endocrinologist
 Hypochloremia (Cl-<97 mmol/L):
o Rarely occurs in the absence of other abnormalities
o If it occurs with metabolic alkalosis, it is often due to vomiting (loss of HCl)