9 Fluid and Electrolytes Flashcards
Total body water (TBW): fraction of body weight that is water and then further breakdown
2/3 (M ~2/3, F a little less, infants a little more) … 2/3 of water is intracellular (mostly muscle) and 1/3 extracellular … (of the extracellular) 2/3 is interstitial and 1/3 is plasma
TBW: roles of proteins vs Na
determines plasma/interstitial oncotic P vs intra/extracellular osmotic P
TBW: what determines plasma/interstitial compartment oncotic pressures?
proteins
TBW: what determines intracellular/extracellular osmotic pressure?
Na
TBW: MC cause of V overload
iatrogenic
TBW: first sign of V overload
weight gain
TBW: what releases H2O?
cellular catabolism releases a significant amnt
plasma osmolarity calculation
(2xNa) + (gluc/18) + (BUN/2.8) … normal is 280-295 … water goes from low solute conc (i.e. low osm) to high
electrolyte contents of different fluids … NS, 3%NS, LR
0.9% NS = NaCl 154 … 3% NS = NaCl 513 … LR (ionic composition of plasma) Na 130, K 4, Ca 2.7, Cl 105, bicarb 28
V replacements: estimate amnts
4cc/kg/hr for first 10kg …. 2 for the the next 10 … 1 for each kg after that
V replacements: best indicator of sufficient V replacement
UOP
V replacements: fluid loss w open abdomean
0.5-1.0L/h plus measured blood loss (usually don’t replace blood until >500cc)
V replacements: insensible fluid losses amnt and source
10cc/kg/day, 75% skin, 25% respiratory, pure water
V replacements: what replacement fluids are used after major adult GI surgery
intraop and 1st 24 hours after - use LR … after 24hrs switch to D5 1/2 NS + 20K (b/c 5% dextrose stimulates insulin release, leading to amino acid uptake and protein synthesis, prevents catabolism)
V replacements: amnt of glucose and calories in D5 fluids @ 125/hr
150g glucose (525 kcal/day)
GI fluid secretion: amnt from GI system (easy way to remember)
biliary system, panc, duo are all 500-1000mL/day …. stomach 1-2L/day
GI fluid secretion: normal Na and K requirements
Na 1-2mEq/kg/day … K is 0.5-1.0
GI electrolyte losses: sweat
hypotonic, Na conc 35-65
GI electrolyte losses: saliva
K, highest conc of K in the whole body
GI electrolyte losses: stomach
H and Cl
GI electrolyte losses: pancreas
HCO3
GI electrolyte losses: bile
HCO3
GI electrolyte losses: small intestine
HCO3, K
GI electrolyte losses: large intestine
K
GI electrolyte losses: HCO3 soures
panc, bile, small intestine (w K)
GI electrolyte losses: K sources
saliva (highest conc of K in body), small bowel, large bowel
GI electrolyte losses: replacement fluid for gastric losses
D5 1/2 NS w 20mg K
GI electrolyte losses: replacement fluid for panc/biliary/small intestine losses
LR and HCO3
GI electrolyte losses: replacement fluid for large intesting losses
LR and K
GI electrolyte losses: replacement for GI losses (V)
1:1
GI electrolyte losses: fluids for dehydration (i.e. marathon runner)
NS
GI electrolyte losses: UOP replacement
None needed, >0.5cc/kg/hr is normal post op diruesis (Dr. Hines says typically seen on POD 2-3)
K: normal range
3.5-5.0
K: hyperK dx
typically in renal failure patients, EKG shows peaked T
K: hyperK tx
(1) Ca gluconate (membrane stabilizer for the heart) … (2) sodium bicarb (causes alkalosis, K/H exchange, drives K into cells), insulin (10U) w 1 amp 50% dextrose (more K driven into cells) … (3) kayexelate (more long term, take K out of body) … (4) dialysis if refractory
K: hypoK EKG changes and mgmt
T waves diappear (usually in the setting of overdiuresis) … may need to correct mag before K
Na: normal range
135-145
Na: hyperNa cause, px, mgmt
2/2 dehydration … restlessness, irritability, seizures … correct slowly w D5 water to avoid brain swelling
Na: hypoNA causes, px, mgmt
2/2 fluid overload are SIADH … HA, n/v, seizures … correct slowly (no more than 1mEq/hr) to avoid central pontine myelinolysis
Na: impact of hyperglycemia
hyperglycemia causes pseudohyponatremia … for each 100 increment of glucose over normal, add 2 to Na
Ca: normal range
normal 8.5-10.0, ionized 4.4-5.5
Ca: hyperCa - value and sx
Ca >13 or ionized >6-7 for sx … causes lethargy
Ca: hyperCa - MC causes (benign and malignant)
hyperparathryoidism and breast cancer
Ca: hyperCa - tx
NS at 200-300cc/hr w Lasix
Ca: hyperCa - what to avoid?
LR b/c contains K … thiazide diuretics b/c retain Ca
Ca: hyperCa - mgmt of pts w malignant disease
mithramycin, calcitonin, alendronic acid, dialysis
Ca: hypoCa - amnts
Ca <8, ionized <4
Ca: hypoCa - px
hyperreflexia, Chovstek’s sign (tapping on face produces twitching), perioral tingling and numbness, Trosseau’s sign (carpopedal spasm), prolonged QT intervals … can occur after parathyroidectomy
Ca: hypoCa - replacement
may need to fix Mag first
Ca: hypoCa - protein adjustment for Ca
(protein i.e. albumin) … for every 1g decrease in protein add 0.8 to Ca
Mag: normal range
2.0-2.7
Mag: need to replete this before repleting what?
K and Ca
Mag: hyperMag px and tx
lethargic state, usually in renal failure pts taking Mag containing products … tx w Ca
Mag: hypoMag px (and typical setting)
usually after massive diuresis, chronic TPN without mineral replacement, EtOH abuse … similar sx to hypoCa - hyperreflexia, Chovstek’s sign (tapping on face produces twitching), perioral tingling and numbness, Trosseau’s sign (carpopedal spasm), prolonged QT intervals
metabolic acidosis: anion gap calculation and normal
nL <10-15 … Na - (HCO3 + Cl)
metabolic acidosis: high anion gap acidosis causes
MUDPILES - Methanol, Uremia, DKA, Par-aldehydes, Isoniazid, Lactic acidosis, Ethylene glycol, Salicylates
metabolic acidosis: normal anion gap acidosis causes
usually loss of Na/HCO3 (i.e. ileostomies, small bowel fistulas)
metabolic acidosis: tx
treat the underlying cause, keep pH > 7.2 with bicarb, severely low pH can impact the myocardial contractility
metabolic alkalosis: typical cause
usually contraction alkalosis
describe acid/base abnormality seen w NGT suction, plus tx and mechanism
hypochloremic hypokalemic metabolic alkalosis w paradoxical aciduria … tx w NS (need to correct the Cl deficit) … mech: (1) loss of H and Cl from stomach leads to hypochloremia and alkalosis, (2) loss of water causes kidneys to reabsorb Na in exchange for K (Na/K ATPase) thus losing K (i.e. hypoK), (3) Na/H exchanger activated to reabsorb water also K/H exchanger activated to reabsorb K leads to paradoxical acirduria
acid/base abnL: respiratory and renal compensation
resp - CO2 regulation, takes minutes … renal - HCO3 regulation, takes hours to days
acid/base abnL: Winters formula
PCO2 = 1.5 x HCO3 + 8 … +/- 2 = expected CO2 compensation in the setting of metabolic acidosis
acute renal failure: FeNa formula and use
(urine Na / Cr) / (plasma Na / Cr), best test for azotemia
acute renal failure: prerenal findings
fena <1%, urine Na <20, BUN/Cr >20, Uosm >500
acute renal failure: how much renal mass must be damaged before there’s an increase in BUN or Cr
70%+
acute renal failure: prevent damage 2/2 contrast dyes
prehydration is best prevention, HCO3 and N-acetylcysteine
acute renal failure: myoglobin mech of damage and tx
myoglobin is converted to herrihemate in acidic environment –> toxic to renal cells … tx = alkalinize urine
tumor lysis syndrome: mechanism
release of purines and pyrimidines –> increase PO4 and uric acid, decrease Ca … leads to inc BUN and Cr (renal damage), EKG changes
tumor lysis syndrome: tx
hydration (best) … rasburicase (converts uric acid into inactive metabolite allantoin) … allopurinol (dec uric acid production) … diruetics … alkalinize urine
vit D (cholecalciferol): production
skin: UV converts 7-dehydrocholesterol to cholecalciferol –> cholecalciferol goes to liver to +25-OH –> to kidney for +1-OH –> now active vitamin D –> increases Ca-binding protein and leads to increased intestinal absorption of Ca
chronic renal failure: lab findings
(1) anemia 2/2 low erythropoietin … (2) decrease active vit D (dec 1-OH hydroxylation) leads to decreased Ca reabsorption from the gut and decreased Ca-binding protein
transferrin and ferritin
transferrin is Fe transporter … ferritin is storage form of Fe