3&4 - Metabolic Acidosis Flashcards Preview

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Flashcards in 3&4 - Metabolic Acidosis Deck (18):

effects of acidemia

dec Hgb affinity for O2
impairs bone structure/formation
dec contractility of heart
dec excitability of brain > metabolic encephalopathy
dec peripheral vascular resistance
inc K levels


effects of alkalemia

Hgb binds O2 strongly
dec resp center > hypoventilation
inc irritability > arrhythmias and seizures
dec ionized Ca > weakness
dec K levels


AG =

Na - (Cl + bicarb)


nl AG



2 main causes of normal anion gap metabolic acidosis

renal and GI bicarb wasting


stepwise approach for acid base problems (6)

look at pH > acidemic or alkalemic
primary disorder metabolic or resp?
calc AG and dAG
calc dBicarb
adequate compensation?
simple or mixed?


dBicarb - how to calc and what does it tell you

24 (nl) - patient's bicarb
if dAG = dBicarb, pt as simple AG metabolic acidosis. If not, something else is going on to make you lose/gain more bicarb


winters formula

expected pCO2 = (bicarb * 1.5) + 8 +/- 2


"golden rule" of acid base

under no circumstances can secondary response bring pH back to normal > normal pH means pt is normal or has opposing disorders


lactic acidosis - what causes it

type A - poor tissue perfusion (shock, cardiac failure, mito enzyme defect

type B - perfusion ok, but malignancy, liver or renal failure, seizures, drugs etc cause it


lactic acidosis - tx

tx underlying condition - esp restore perfusion
bicarb therapy if pH < 7.1 to get them up to 7.2
(lactate is "potential" bicarb > will normalize eventually, dont want to overshoot)



due to insulin deficiency and stressors - like infection, MI, etc
bicarb only used if severe b/c ketones are "potential" bicarb


alcoholic ketoacidosis

predominantly beta hydroxy butyrate - not picked up by dipsticks
hypoglycemia, low insulin after drinking
tx - volume replacement w/ saline and glucose


ethylene glycol acidosis mech

in anti freeze
metab to variety of acids
early ingestion - just causes osmolar gap, after metabolized causes anion gap acidosis


ethylene glycol tox tx

fluids, thiamine
fomepizole or ethanol to compete w/ alcohol dehydrogenase


causes of metab alkalosis

exogenous bicarb
loss of acid (vomiting, NG suction)
dec ECF volume / normal BP (secondary hyperaldosterone)
ECF expansion / HTN


maintenance phase of alkalosis

persistent hyperaldosterone state / continued acid loss or alkali therapy
causes chloride depletion from H loss in type A cells and bicarb retention in type B cells


tx of metab alkalosis

if volume contracted - "chloride sensitive" > replenish volume w/ normal saline

if volume overloaded / ECF expanded > tx primary disorder that caused high RAAS state, replace K