ECC1- Electrolytes

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  1. What is the equation for plasma osmolality?
    Plasma osmolality (mOsm/kg)= 2 (Na+K) + BUN (mg/dL)/ 2.8 + glucose (mg/dL)/18

    [sodium is the main component of osmolality]
  2. What is responsible for intracellular versus extracellular sodium?
    • Na+K+ATPase pump
    • extracellular Na+  is 14-15x intracellular conc
  3. Sodium is mostly ___________.
    extracellular
  4. How do kidneys control Na+ conc?
    • kidneys allows for Na-free water resorption when ADH (vasopressin) is released from the pituitary
    • ADH release is triggered when plasma [Na+] increases and in hypovolemia
    • ADH plugs aquaporins in distal tubule, allowing resorption of water only
  5. Na+ usually follows ________, which is...
    water; isotonic fluid loss and Na+ conc does not change
  6. What are the only ways to change Na+ conc? (4)
    • loss of free water
    • gain of free water
    • loss of hypertonic fluid (extremely rare)
    • gain of hypertonic fluid
  7. What are potential causes of loss of free water, leading to ___________? (7 causes)
    • hypernatremia
    • no access to water, CNS dz making patient less likely to seek  out water, diabetes insipidus and no access to water, fever, burns, panting/ tachypnea
  8. What are potential causes of gain of hypertonic fluid, leading to _________?  (3 causes)
    • hypernatremia
    • salt>water intake, salt intoxication, 7.5% NaCl administration
  9. What are potential causes of gain of free water, leading to __________? (5 causes)
    • hyponatremia
    • fluid therapy with hypotonic fluid, ADH secretion (d/t hypovolemia), high osmolality (hyperglycemia), renal failure, Addison's disease
  10. What is a significant Na+ change on bloodwork?
    1% Na+ variation is abnormal (Na+ is VERY tightly regulated)
  11. What is the treatment of hypernatremia?
    • treat primary cause (such as DI)
    • administer hypotonic fluids, D5W (dextrose  in 100% free water) OR 0.45% NaCl or Plasmalyte (needs double the fluid b/c not free water)
  12. How do you calculate the dose of hypotonic fluids to give a hypernatremic patient?
    water deficit= 0.6 x BWkg x [(Patient Na/ Normal Na)-1]

    Normal Na= 145mmol/L in dogs, 150mmol/L in cats
  13. How fast do you give hypotonic fluids in a hypernatremic patient?
    • if chronic changes, compensatory mechanisms are in place- 0.5mEq/L/hr
    • can be faster if known acuteness of disorder
  14. Why shouldn't you cause rapid changes in sodium concentration in a hypernatremic patient (ie. with fluid therapy)?
    free water deficit --> cell shrinkage--> production of iatrogenic osmoles--> return to normal cell volume w/ same Na conc--(overeager/aggressive/ freaked out clinician)--> too much fluids--> cell swelling and lysis
  15. What is the treatment for hyponatremia?
    • Treat the primary cause!!
    • If hypovolemia- give enough fluids of any kind IV
    • If renal disease- manage accordingly
    • If Addison's- mineralocorticoids
    • If syndrome of inappropriate ADH secretion (SIADH)- stop fluids and maybe give diuretics
    • If d/t DM/DKA- treat hypovolemia and hyperglycemia
  16. What is syndrome of inappropriate ADH secretion (SIADH)?
    ADH secretion when it should not be in critically ill patients...not well understood
  17. How do you determine the fluid dose for a hyponatremic patient?
    • ΔNa+chart?chf=bg,s,00000000&cht=tx&chl=%5Cfrac%7B(Fluid%20Na-%20Patient%20Na)%7D%7B(0.6%20x%20BW)%2B1%7D&chs=336x86
    • 0.9%NaCl is 155 mmol/L of Na
  18. How fast should you give fluids to a hyponatremic patient?
    no faster than 0.5mmol/L/hr
  19. Why shouldn't you cause rapid change in Na+ conc in a hyponatremic patient (ie. with fluids)?
    free water excess --> cell swelling--> get rid of idiogenic osmosis--> return to normal cell volume--(overeager/aggressive/ freaked out clinician)--> too much fluids--> cell shrinkage and cell death
  20. What acute and delayed reactions can occur as a result of administering fluids too quickly to a hyponatremic patient?
    • Acute: cerebral swelling or shrinkage--> seizures, changes in mentation
    • Delayed: central pontine myelinolysis/ osmotic demyelination syndrome d/t quick rise in Na conc--> myelin loss in brain--> lethargy, weakness, ataxia, hypermetria [no good txt]
  21. Potassium is mostly __________.
    intracellular
  22. Potassium has a very narrow ___________.
    therapeutic range
  23. Potassium conc contributes to ___________.
    resting membrane potential/ cell excitability
  24. How is K+ regulated endogenously? (5)
    • excreted by renal (90%) and GI (10%) system
    • hyperK--> increased conc gradient in distal nephron and kaliuresis
    • aldosterone--> secretion of K+ in distal nephron
    • distal tubular flow washes out K+
  25. K+ conc is influences by what other molecules in the body? (4)
    insulin, H+ conc, beta-adrenergic activity, diuretics
  26. What are causes of hyperkalemia? (5)
    • oliguria/ anuria (renal failure)
    • urinary obstruction/ rupture
    • pseudohypoaldosteronism (Trichuris infection, third spacing)
    • Increased intake (overzealous high K+ IV)
    • tissue catabolism/ reperfusion
  27. How is hyperK+ diagnosed? (3)
    • serum K+ level
    • ECG- brady, spiked T waves, wide QRS, absent p waves, increase P-R interval, "sine wave"
    • PE- bradycardia, hypothermia in blocked cats
  28. How is hyperkalemia treated? (5)
    • calcium gluconate (cardioprotective- does not lower K+ conc)
    • IV fluids (if able to urinate)- dilution
    • insulin and dextrose- pushes K+ intracellularly
    • bicarb- pushed K+ intracellularly
    • dialysis
  29. What are causes of hypokalemia? (12- 4 categories)
    • renal loss: diuretics, renal insufficiency, hyperaldosteronism, fluid therapy, metabolic acidosis, hypomagnesemia 
    • translocation of K+: insulin/ dextrose therapy, beta-adrenergic toxicity (albuterol), hypothermia, metabolic alkalosis
    • increased GI loss: vomiting and diarrhea
    • decreased intake: rare
  30. How is hypokalemia diagnosed? (2)
    • serum K+ levels
    • PE: neck ventroflexion
  31. How is hypokalemia treated?
    KCl in fluids NOT FASTER THAN 0.5mEq/kg/hr and monitor patient
  32. Briefly describe hypercalcemia.
    • neoplasia, vitamin D toxicity, hyperparathyroidism
    • Ca-Ph >60-70 risk for organ mineralization
    • IV fluids with 0.9% NaCl, furosemide, steroids
  33. Briefly describe hypocalcemia.
    • eclampsia
    • supplement with calcium gluconate slowly
  34. Briefly describe hypomagnesemia.
    • grass tetany, critically ill patients
    • Treat with IV magnesium sulfate or chloride or use plasmalyte/normosol R
  35. In order for fluid to move between the ICF and ECF, then...
    there must be changes in osmolality.
  36. In orer for fluid to move between the interstitial fluid compartment and the intravascular fluid, then...
    there must be changes in starling's forces

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Author:
Mawad
ID:
323159
Filename:
ECC1- Electrolytes
Updated:
2016-09-13 03:05:06
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vetmed ECC1
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vetmed ECC1
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