Acid Base Flashcards
anion gap
Na- (HCO3 + Cl)
*adding acid consumes HCO3, therefore increasing anion gap
three types of buffers
bicarb
phosphate (buffering causes bone loss)
proteins (mostly albumin–H displaces Ca and Na)
factors that change the gap
increase- acid load
decrease- hypoalbuminemia
acute compensation for respiratory acidosis
1 meq/L per 10 mmHg increase in PCO2
chronic compensation in respiratory acidosis
3-4 meq/L per 10 mmg increase in PCO2
respiratory compensation for metabolic acidosis
1.2 mmHg per 1 mEq/fall
winter’s formula
calculates expected PCO2 (is compensation adequate?)
=(1.5*[HCO3-]+8) +/-2
delta delta rule
if change in anion gap doesnt equal change in hco3, an additional acid-base disorder may be present
hyperchloremic metabolic acidosis is either__ or __
retention of HCL or bicarb loss
reasons for high anion gap metabolic acidiosis
MUD PILES methanol uremia DKA paraldehyde INH lactic acidosis ethylene glycol salicylate
osmolar gap
measured posm-calculated posm
calculated posm
2Na + glu/18 +BUN/2.8 + EtOH/4.6
if osmolar gap is high
intoxication with unmeasured osmoles
causes of increased osmole gap with acidosis
mud piles
causes of increased osmolal gap without acidosis
DELLPIM diethyl ether ethanol lipidemia lithium toxicity proteinemia isopropanolol mannitol
change in anion gap greater than change in bicarb
metabolic alkalosis present
change in anion gap less than change in bicarb
hypercholermic metabolic acidosis present
renal tubular acidosis presents as
hypercholermic acidosis
distal RTA
inability to excrete H+
proximal RTA
inability to reabsorb HCO3
urine anion gap
(Na+K)-Cl
kidney excretes acid as
NH4Cl
negative urine ion gap
expected in metabolic acidosis with healthy kidney
positive urine anion gap
distal RTA
TYPE 1 RTA
impaired H+ secretion in DISTAL tubulue
type 1 urine pH
> 5.5
causes of RTA 1
idiopathic
drugs- isofamide, amphoB, Lithium
hypercalciuria (damages distal nephron)
obstructive uropathy
RTA 1 labs
low urine pH
positive UAG
hypokalemia
type 2 RTA
cant reabsorb HCO3-
acidosis in RTA 2
less severe
labs in type 2 RTA
> 5.5 pH
UAG -
bicarb stays 12-18 because hits tmax
hypokalemia
how to distinguish rta 2 from diarrhea
load with bicarb- shoudl immediately cause bicarburia
tx or rta 2
lots of bicard
type 4 RTA
hypercholremic acidosis with hyperkalemia
decreased aldosterone effect
causes of type IV RTA
decreased aldo production aldo ressitance (ENAC blocked by K sparring diuretics, bactrim, pseudo hypoaldo because decreased distal Na low) defects in Enac
labs type 4 RTA
low bicarb
pH>5.5 in urine
hyperkalemia (should be suspected when hyperkalemic but no increased effort to excrete (urine K is normal))
drug for hypoaldosteronism
fludocortisones
acute metabolic comp for resp alkalosis
-2 mEq/L per -10 mmHg
chronic respiratory alkalosis compensation
-4 per -10
what makes you immediately thing salicylate toxicity
respiratory alkalosis with elevated AG acidosis
mechanism of salicylate toxicity
hyperventilation because of salicylate acid–>rep alklaosis
also direct stim of resp center–>further hypervent–>lots of resp alklaosis
compensation for metabolic alkalosis
+0.7 mmHg per 1 mEq/L
contraction alkalosis
volume depeletion with Cl-containing fluid will stimulate an increase in Na reabs (via aldo)..since Cl- isnt pressent HCO3 will go with it
milk-alkali syndrome
ingestion of HCO3 or CO3 alone is not enough to make alklaosis, but if you do it with calcium (tums, dairy, etc) you will inhibit distal HCO3 excretion
tx metabolic acidosis
remove offending agent or block affected channels
