3&4 - Metabolic Acidosis

Question 1

effects of acidemia

Answer 1

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

Question 2

effects of alkalemia

Answer 2

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

Question 3

AG =

Answer 3

Na - (Cl + bicarb)

Question 4

nl AG

Answer 4

~10

Question 5

2 main causes of normal anion gap metabolic acidosis

Answer 5

renal and GI bicarb wasting

Question 6

stepwise approach for acid base problems (6)

Answer 6

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

Question 7

dBicarb - how to calc and what does it tell you

Answer 7

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

Question 8

winters formula

Answer 8

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

Question 9

“golden rule” of acid base

Answer 9

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

Question 10

lactic acidosis - what causes it

Answer 10

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

Question 11

lactic acidosis - tx

Answer 11

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)

Question 12

DKA

Answer 12

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

Question 13

alcoholic ketoacidosis

Answer 13

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

Question 14

ethylene glycol acidosis mech

Answer 14

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

Question 15

ethylene glycol tox tx

Answer 15

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

Question 16

causes of metab alkalosis

Answer 16

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

Question 17

maintenance phase of alkalosis

Answer 17

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

Question 18

tx of metab alkalosis

Answer 18

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