electrolyte balance

sodium

Na- because water follows sodium

aldosterone and ANP (atrial natriuretic peptide hormone)

ADH

cerebral edema- because the brain is confined within the skull cerebral edema is poorly tolerated

imbalance in the amount of water vs imbalance in the amount of sodium

serum sodium less than 135

intracellular environment is hyperosmolar relative to the ECF, this leads to influx of water into the cell which leads to cerebral edema

the volume of water and the amount of solute (serum osmolarity)

280-285 mOsm/L

low measured serum sodium concentrations with normal serum osmolality (serum osmolality will decrease over time.)

can be caused from absorption of fluids when patient has procedure such as TURP or cystoscopy, endometrial ablation

greater than 285 mOsm/L

• serum sodium low, and osmolarity high
• results from presence of non-sodium solutes, holds water within ECF leads to dilutional hyponatremia

can be caused from glucose, mannitol, and glycine

presence of non sodium solutes that hold water within the ECF space, this leads to dilution causing hyponatremia.

• -in anesthesia usually results from absorption of large volumes of sodium free solutions (TURP, endometrial ablation)
• -may also accompany renal insufficiency or failure
• **treat the underlying hypotonic state, patient can become very confused

minimal symptoms, doesn't cross the BBB and is excreted with water in the urine

hyposomolality will develop as it is metabolized, can lead to cerebral edema

<280 mOsm/L

• low serum Na+ and low osmolality
• -likely to cause clinical manifestations
• -treatment depends on volume status

causes- diuretics, salt losing nephropathy, ketonuria, third spacing, adrenal insufficiency, vomiting, and diarrhea

tx-0.9 NS

causes- SIADH, renal failure, hypothyroidism, drugs, water intoxication

• treatment-
• Una>20 water restriction
• Una<10 hypertonic saline, fluid restriction, +/- loop diuretics

causes nephrotic syndrome, cirrhosis, congestive heart failure

tx- sodium and water restriction, +/- loop diuretics

neuro- cerebral edema, seizure, coma, agitation, confusion, headache

gi- anorexia, n/v

muscular- cramps and weakness

• is a neurological disease caused by severe damage of the myelin sheath of nerve cells in the brainstem
• -disorder of upper neurons, spastic quadiparesis, pesudobulbar palsy, and mental disorders
• -most patients at risk are those with hyponatremia more than 48 hours

is caused from to rapid of a correction of hyponatremia

• -controversy exists on how aggressive tx should be
• - rapid correction of serum sodium can lead to neuro disorder know as myelinolysis.
• -optimal tx must balance the risk of cerebral edema against the risk of myelinolysis
• -serum sodium should not be increased more than 1-2 meq/L/hr
• (infuse 3% saline at rate of 1-2 ml/kg/hr)

1-2 meq/L/hr

1-2 ml/kg/hr

>145

usually result of impaired water intake (ie- hospitalized patients, debilitated, mentally impaired, and intubated patients)

brain usually adapts by conserving intracellular solutes, allowing normal intracellular volume

rapid shrinking of the brain, traction on intracranial veins and venous sinuses, intracranial hemorrhage

cerebral edema

neuro- thrist, weakness, seizure, coma, intracranial bleeding, disorientation, hallucinations, irritability

cardiac- hypovolemia

renal- polyuria or oliguria, renal insufficiency

water and sodium gain, sodium gain> water gain

causes- excessive intake of sodium (IV or PO), mineralcorticoid excess

tx- administer loop diuretic

causes- diabetes insipidus, high insensible  loss

tx- correct water deficit (0.45 NS, D5W, or PO water)

water and sodium loss, water loss> than sodium loss

causes- diuretics, gi loss, respiratory and skin loss, adrenal insufficiency

tx- correct volume deficit with isotonic fluids until hemodynamically stable

• principle electrolyte of ICF
• -ratio of ICF to ECF potassium is largely responsible for the cells resting membrane potential
• -abnormal levels may be a result of an imbalance between the distribution or the total body store of potassium

aldosterone, epi, insulin, and intrinsic renal mechanisms

insulin and alkalosis promote movement of potassium into the cell

insulin and albuterol (beta 2 agonist) can put potassium into the cell

<3.5

• redistribution- alkalosis, insulin administration, beta agonists
• increased renal excretion- multiple drug use (diuretics, pcn, aminoglycosides, corticosteroids,) hyperaldosteronism, renal tubular acidosis, mag deficiency
• GI loss- diarrhea, gastric suctioning, villous adenoma, fistulas
• Inadequate intake- anorexia, alcoholism, debilitation

cardiac- st segment depression, widened QRS complex, flattened T waves, ventricular ectopy

neuro- weakness, decreased reflexes, confusion

renal- polyuria, concentrating defect

metabolic- glucose intolerance, potentiation of hypercalcemia, and hypomagnesemia

• iv replacement of potassium under continuous ECG monitoring
• -maximum rate of infusion 10-20 meq/hr
• -potassium chloride is preferred
• -cancellation of surgery not warranted based on low serum potassium
• --just replace it, recommend having an Iv only for potassium replacement, if given to fast can cause ectopy, always give on a pump

10-20 meq/hr

>5.0

**less common than hypokalemia (quite uncommon if no renal impairment) ** can be from overcorrection

cardiac- tall peaked T waves, widened QRS complex, ventricular dysrhythmia, cardiac arrest

neuro- muscle weakness, confusion, and parasthesias (same as hypo)

reverse membrane excitability- give 10 ml calcium chloride 10% over 10 minutes

• transfer extracellular potassium into cell
• -glucose and insulin (D10w+ 5-10 units insulin per 25-50 grams of glucose)
• -sodium bicarb (50-100 meq over 5-10 minutes)
• -beta 2 agonists (albuterol)

• remove potassium from the body
• -diuretics (loop or proximal)
• -potassium exchange resins (kaexylate, or lactulose)
• -hemodialysis (gold standard but difficult to do in OR, can be done in PACU)

***monitor serum potassium levels and ECG

redistribution- acidosis, hypertonicity, hemolysis, tissue necrosis, rhabdomyosis

decreased renal excretion- renal insufficiency and failure, postassium sparing diuretics, hypoaldosteronism, drugs (nsaids, beta blockers and ACEI)

excessive potassium intake- iv or po supplementation, excessive use of salt substitutes, rapid transfusion of banked blood

99% found in bone

regulated by parathyroid hormone and vitamin D

• importance
• -role as a 2nd messenger
• - for muscle contraction, release of hormones and neurotransmitters.

• coagulation of blood
• muscle funtion

50%

• 1.19-1.33 mmol/L (1.1-1.4)
• or
• 2.38-2.66 mEq/L

< 1.0 mmol/L

causes- hypoparathyroidism, pseudohypoparathyroidism, malabsorption, acute pancreatitis, malignancy, alkalosis, hyperphosphatemia, rhabdomyosis, chronic renal insuff, hypomagnesemia

• tx- calcium chloride- most bioavailable form of calcium (13.6 meq/gram)
• calcium gluconate- less irritating to vein (4.6 meq/gram) ** will have to give more of this, but this drug is used commonly in the OR

• cardiac- dysrhythmia, prolonged QT interval, T wave conversion, hypotension, decreased myocardial contractility
• pulmonary- laryngospasm, bronchospasm, hypoventilation
• neuro- cramps, muscle weakness, chvosteks sign (facial nerve is hyperirritable), trosseaus sign (spasm of arm when BP cuff inflated), seizure, numbness, tingling

> 1.5

causes- hyperparathyroidism, malignancy, thiazide diuretics, thyrotoxicosis, renal failure, excessive intake of calcium supplements

• tx- increased renal excretion
• --volume expansion with NS
• --loop diuretic

cardiac- HTN, heart block, shortened QT interval, dysrythmia

renal- hypercalcuria, polyuria

neuro- muscle weakness, decreased deep tendon reflex, sedation

gi- anorexia, pancreatitits

1.8-2.4

• second most abundant intracellular cation
• important co-factor in many enzymatic pathways
• regulated primarily by renal mechanisms, PTH and vitamin D play minor roles

• ECF=1-2%
• bone= 67%
• ICF=31%

<1.8

causes- inadequate intake (TPN, starvation, alcoholism) increased GI losses (diarrhea, fistulas, NG suctioning, vomiting, increased renal losses (diuretics, aminoglycosides) changes in distribution (pancreatitis, insulin, glucose, catecholamines)

• tx- 1-2 mag sulfate over 5 minutes (continuous ECG), followed by infusion of 1-2g/hr
• **monitor serum levels and avoid iatrogenic hypermagnesemia

cardiac- coronary vasospasm, dysrhythmia, v-fib, CHF, QT and PR prolongation, QRS widening

neuro- weakness, chvostek sign (facial nerve hyperirritable), trosseaus sign (spasm of forearm with inflation of BP cuff)

misc- hypocalcemia, hypokalemia, nausea, anorexia

>2.5 mg/dl

causes- renal failure, adrenal insuff, excessive mag administration (tx of preeclampsia, preterm labor, ischemic heart disease, cardiac dysrhythmia)

• tx- D/C mag administration
• if emergent use calcium as an antagonist

symptoms reflect depression of peripheral and central nervous system and are dose related

• 3-5= flushing, n/v
• 4-7=drowsiness, decreased deep tendon reflex, weakness
• 5-10=hypotension, bradycardia
• 10=respiratory depression
• 10-15= resp paralysis, coma
• 15-20=cardiac arrest