Electrolyte Balance

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Electrolyte Balance
2013-12-07 13:00:03
Anesthesia Final pg
Anesthesia Final pg. 4-9
Show Answers:

  1. What is the most abundant electrolyte in the ECF
  2. Which electrolyte is responsible for most of the osmotic activity in the ECF
    Na- because water follows sodium
  3. what regulates total body sodium
    aldosterone and ANP (atrial natriuretic peptide hormone)
  4. what hormone regulates sodium concentration
  5. what is one of the most significant consequences of hyponatremia
    cerebral edema- because the brain is confined within the skull cerebral edema is poorly tolerated
  6. imbalances in sodium reflect altered concentrations of sodium in water so this can be
    imbalance in the amount of water vs imbalance in the amount of sodium
  7. hyponatremia is classified as a sodium level
    serum sodium less than 135
  8. what is patho behind hyponatremia
    intracellular environment is hyperosmolar relative to the ECF, this leads to influx of water into the cell which leads to cerebral edema
  9. what must you consider when treating hyponatremia
    the volume of water and the amount of solute (serum osmolarity)
  10. serum osmolality of isotonic hyponatremia

    what is it and what causes it
    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
  11. serum osmolality of hypertonic hyponatremia

    what is it and what causes it
    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
  12. isotonic and hypertonic hyponatremia result from what
    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
  13. mannitol and hypertonic hyponatremia
    minimal symptoms, doesn't cross the BBB and is excreted with water in the urine
  14. glycine or sorbitol and hypertonic hyponatremia
    hyposomolality will develop as it is metabolized, can lead to cerebral edema
  15. hypotonic hyponatremia osmolality and what it is
    <280 mOsm/L

    • low serum Na+ and low osmolality
    • -likely to cause clinical manifestations
    • -treatment depends on volume status
  16. cause and treatment of hypovolemic hypotonic hyponatremia
    causes- diuretics, salt losing nephropathy, ketonuria, third spacing, adrenal insufficiency, vomiting, and diarrhea

    tx-0.9 NS
  17. causes and treatment of isovolemic hypotonic hyponatremia
    causes- SIADH, renal failure, hypothyroidism, drugs, water intoxication

    • treatment-
    • Una>20 water restriction
    • Una<10 hypertonic saline, fluid restriction, +/- loop diuretics
  18. causes and treatment of hypervolemic hypotonic hyponatremia
    causes nephrotic syndrome, cirrhosis, congestive heart failure

    tx- sodium and water restriction, +/- loop diuretics
  19. clinical manifestations of hyponatremia
    neuro- cerebral edema, seizure, coma, agitation, confusion, headache

    gi- anorexia, n/v

    muscular- cramps and weakness
  20. Central pontine myelinolysis or just myelinolysis is what and what is it caused from
    • 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
  21. treating 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)
  22. serum sodium should not be increased more than
    1-2 meq/L/hr
  23. 3% saline should not be infused faster than
    1-2 ml/kg/hr
  24. serum sodium in hypernatremia
  25. causes of hypernatremia
    usually result of impaired water intake (ie- hospitalized patients, debilitated, mentally impaired, and intubated patients)
  26. slow onset hypernatremia
    brain usually adapts by conserving intracellular solutes, allowing normal intracellular volume
  27. rapidly occurring hypernatremia
    rapid shrinking of the brain, traction on intracranial veins and venous sinuses, intracranial hemorrhage
  28. rapid correction of hypernatremia can lead to
    cerebral edema
  29. clinical manifestations of hypernatremia
    neuro- thrist, weakness, seizure, coma, intracranial bleeding, disorientation, hallucinations, irritability

    cardiac- hypovolemia

    renal- polyuria or oliguria, renal insufficiency
  30. hypervolemic hypernatremia causes and tx
    water and sodium gain, sodium gain> water gain

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

    tx- administer loop diuretic
  31. isovolemic hypernatremia causes and tx
    causes- diabetes insipidus, high insensible  loss

    tx- correct water deficit (0.45 NS, D5W, or PO water)
  32. hypovolemic hypernatremia causes and tx
    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
  33. Potassium
    • 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
  34. what is potassium regulated by
    aldosterone, epi, insulin, and intrinsic renal mechanisms
  35. beta-adrenergic stimulation and potassium
    insulin and alkalosis promote movement of potassium into the cell

    insulin and albuterol (beta 2 agonist) can put potassium into the cell
  36. serum potassium in hypokalemia
  37. causes of hypokalemia
    • 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
  38. hypokalemia clinical manifestations
    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
  39. tx of hypokalemia
    • 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
  40. maximum rate of infusion for potassium infusion
    10-20 meq/hr
  41. hyperkalemia serum level

    **less common than hypokalemia (quite uncommon if no renal impairment) ** can be from overcorrection
  42. clinical manifestations of hyperkalemia
    cardiac- tall peaked T waves, widened QRS complex, ventricular dysrhythmia, cardiac arrest

    neuro- muscle weakness, confusion, and parasthesias (same as hypo)
  43. treatment of hyperkalemia
    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
  44. hyperkalemia causative factors
    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
  45. calcium
    where is it found
    what is it regulated by
    importance to anesthesia
    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
  46. ionized calcium is physiologically active portion of circulating calcium.  it accounts for what percent of calcium in the ECF
  47. normal calcium levels
    • 1.19-1.33 mmol/L (1.1-1.4)
    • or
    • 2.38-2.66 mEq/L
  48. hypocalcemia is a ionized calcium level of
    < 1.0 mmol/L
  49. causes and treatment of hypocalcemia
    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
  50. hypocalcemia clinical manifestations
    • 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
  51. hypercalcemia serum level
    > 1.5
  52. causes and tx of hypercalcemia
    causes- hyperparathyroidism, malignancy, thiazide diuretics, thyrotoxicosis, renal failure, excessive intake of calcium supplements

    • tx- increased renal excretion
    • --volume expansion with NS
    • --loop diuretic
  53. hypercalcemia clinical manifestations
    cardiac- HTN, heart block, shortened QT interval, dysrythmia

    renal- hypercalcuria, polyuria

    neuro- muscle weakness, decreased deep tendon reflex, sedation

    gi- anorexia, pancreatitits
  54. normal serum level for magnesium
  55. magnesium
    • second most abundant intracellular cation
    • important co-factor in many enzymatic pathways
    • regulated primarily by renal mechanisms, PTH and vitamin D play minor roles
  56. distribution of magnesium in ECF, bone, and ICF
    • ECF=1-2%
    • bone= 67%
    • ICF=31%
  57. hypomagnesemia serum mag level
  58. causes and tx of hypomagnesemia
    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
  59. hypomagnesemia clinical manifestations
    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
  60. hypermagnesemia serum level
    >2.5 mg/dl
  61. causes and tx of hypermagnesemia
    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
  62. symptoms of hypermagnesemia
    symptoms reflect depression of peripheral and central nervous system and are dose related
  63. hypermagnesemia levels
    • 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