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SODIUM Causes Cause

- sodium depletion (decreased intake) - loss of water or gain of sodium in excess of water
- sodium dilution (excess extracellular water; excessive oral
water intake or iatrogenic IV) Hypervolemic hyper Hypovolemic hyper
- untreated hyperglycemia/ mannitol administration Iatrogenic administration Nonrenal water loss (GI,
- For every 100 mg/dl increment in plasma glucose above of sodium or skin; thyrotoxicosis or
normal, plasma sodium should decrease by 1.6 meq/L mineralocorticoid excess impaired thirst)
- extreme elevations in plasma lipids and proteins Urine >20 meq/L < 15 meq/l
- Post-op patients prone to increased secretion of ADH (self- sodium
limiting) conc
Urine > 300 mOsm/L > 400 mosm L
Signs and symptoms osmolality
- CNS origin; oliguric renal failure
- Symptomatic hyponatremia does not occur until sodium serum Normovolemic: can be due to renal casuses or nonrenal water loos from
is <= 120 meq/l GI tract or skin

Systematic review Symptoms

- hyperosmolar causes should be easily excluded - occur in patients with impaired thirst or restricted access to fluid
- depletional (low urine sodium <20 meq/l) vs. dilutional (high urine - are rare until serum sodium >160 meq/l
sodium >20 meq/l) - CNS effects predominate; cellular dehydration; subarachnoid
hemorrhage; restleness and irritability, seizures, coma, death
- free water restriction (most cases); administer sodium (severe) Correction
- (+) CNS symptoms: 3% normal saline by no more than 1 meq/l/hr - In hypovolemic patients: restored with normal saline before
- asymptomatic: increase sodium by no more than 0.5 meq/l/hr to concentration abn is addressed
a max increase of 12 meq/l/day - once adequate volume is achieved, water deficit is replaced by
- chronic: slower correction hypotonic fluid (5% dextrose, 5% dextrose in ¼ normal saline,
enterally administered water
- for acute symptomatic hyper: achieve decrease in serum sodium of no
more thatn 1 meq/h and 12 meq/day
- for chronic hyper: slower correction bec rapid may lead to cerebral
edema and herniation
POTASSIUM More common Above normal range of 3.5 – 5.0 meq/l
(50-100 meq/d) Causes Causes
- inadequate K intake, excessive renal excretion, loss in GI - increased K intake (IV or oral, red cell lysis after transfusion)
secretions or intracellular shifts from metabolic alkalosis or - release of K from cells (rhamdomyolysis, hemolysis, crush injuries
insulin therapy - impaired excretion by kidneys
- drugs that incude magnesium depletion cause postassium - medications – K sparing diuretics, ACE inhibitors, NSAIDs
- Symptoms
- GI: nausea, vomiting, intestinal colic, diarrhea
Change in K associated with alkalosis = potassium decreases by - Neuromuscular: weakness to ascending paralysis, respi failure
0.3 meq/l for every 0.1 increase in pH above normal - CVS (ECG): high peak T waves, wide QRS, flat P, prolonged PR, sine
Correction: in cases where K deficiency is due to Mg depletion, wave formation, vfib
hypomagnesemia has to be corrected first
Symptoms Correction
- ECG: U waves, flat T, ST changes, arryhtmias - remove exogenous source of K (IV fluis; enteral parenteral
Correction - can be removed by cation exchange resin: Kayexalate (binds K
- K repletion in exchange for sodium)
- Oral repletion for mild asymptomatic - shift K intracellular with glucose and bicarbonate infusion
- IV repletion: no more than 10 meq.h - ECG changes are present: CaCl or Ca-gluconate
CALCIUM Serum calcium below 8.5 meq/l Above normal range of 8.5-10.5 meq/l
<1% in ECF Decrease ionized calcium below 4.2 mg/dl Increase in ionized calcium level above 4.2-4.8 mg/dl
3 forms: protein
(40%), Causes Causes
complexed to - pancreatitis, massive soft tissue infections, renal failure, - primary hyperparathyroidism
phosphates and pancreatic and small vowel fistuals, hypoparathyroidism,
other anions toxic shock syndrome, abn in mg, tumor lysis syndrome Symptoms
(10%), ionized - rarely results from decreased intake bec bone resoprtion (check book)
(50%) can maintain normal levels for prolonged periods - ECG: short QT, prolonged PR and QRS, increase QRS voltage,
flat and wide T, AV block à progress to complete heart block
Symptoms and cardiac arrest
- Chvostek’s sign – spasm from tapping facial nerve
- Trousseau’s – spasm from pressure applied to nerves and Correction
vessels of upper ex with BP cuff - Is reqd when hypercalcemia is symptomatic (exceeds 12 mg/dl)
- May lead to decreased cardiac contractility and heart filure - Replete assoc water deficit, induce brisk diuresis with normal
- ECG: prolonged QT, T wave inversion, heart block, vfib saline

- Asymptomatic: IV or oral alcium
- Acute symptomatic: IV 10% calcium gluconate to achieve
serum conc of 7-9 mg/dl


Primary divalent - decrease intake, intracellular shift, increase excretion - decreased urinary excretion, increased intake, endogenous
ICF anion; - decrease Gi uptake due to malabsorption or administration mobilization of phosphorous
abundant in of phosphate binders; decreased intake due to malnutrition - hypoparathyroidism
metabolically = chronic - hyperthyroidism
active cells - Acute cases: intracellular shifts in assoc with respi - clinical conditions that result in cell destruction causes release
alkalosis, insulin therapy, refeeding syndrome, hungry of endogenous phosphorous
bone syndrome - excessive administration through IV

Symptoms Most are asymptomatic; but prolonged hyperphosphatemia can lead to

- cardiac dysfunction and muscle weakness metastatic deposition of soft tissue calcium-phosphorous complexes

Correction Correction
- enteral and parenteral repletion - phosphate binders (Sucralfate or aluminum containing antacids
- if hypocalcemia coexist: calcium acetate
- Excretion may be aided by saline infusion
- Dialysis for patients with renal failure
MAGNESIUM Kidney is primarily responsible for Mg homeostasis through Rare
Dietary intake regulation by Ca/Mg receptors on renal tubular cells Mg containing antacids and laxatives can produce toxic levels in
approx. 20 meq/d patients with renal failure
1/3 is bound with Causes:
albumin Alterations of intake, renal excretion and pathologic losses Symptoms
- nausea, vomiting, neuromuscular dysfunction, impaired cardiac
Symptoms conduction
- neuromuscular and nervous system hyperactivity - ECG: (same with hyperkalemia); increased PR, wide QRS, high
- hyperactive reflexes, muscle tremors, tetany, positive T
chovsteks and trousseaus sign
- ECG: prolonged QT and PR, ST depression, flat or Correction
inverted P, torsade de pointes, arrhythmia - elimination of exogenous sources, correction of concurrent
volume deficits, correction of acidosis if present
Correction - Acute symptoms: calcium chloride (antagonize CV effects)
- oral repletion - Hemodialysis
- IV repletion
- 102 g of magnesium sulfate administed IV over 15 mins