3&4 - Metabolic Acidosis Flashcards

1
Q

effects of acidemia

A
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
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2
Q

effects of alkalemia

A
Hgb binds O2 strongly
dec resp center > hypoventilation
inc irritability > arrhythmias and seizures
dec ionized Ca > weakness
dec K levels
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3
Q

AG =

A

Na - (Cl + bicarb)

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4
Q

nl AG

A

~10

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5
Q

2 main causes of normal anion gap metabolic acidosis

A

renal and GI bicarb wasting

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6
Q

stepwise approach for acid base problems (6)

A
look at pH > acidemic or alkalemic
primary disorder metabolic or resp?
calc AG and dAG
calc dBicarb
adequate compensation?
simple or mixed?
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7
Q

dBicarb - how to calc and what does it tell you

A

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

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8
Q

winters formula

A

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

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9
Q

“golden rule” of acid base

A

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

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10
Q

lactic acidosis - what causes it

A

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

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11
Q

lactic acidosis - tx

A

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)

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12
Q

DKA

A

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

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13
Q

alcoholic ketoacidosis

A

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

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14
Q

ethylene glycol acidosis mech

A

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

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15
Q

ethylene glycol tox tx

A

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

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16
Q

causes of metab alkalosis

A

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

17
Q

maintenance phase of alkalosis

A

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

18
Q

tx of metab alkalosis

A

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