ACID-BASE Flashcards

1
Q

– ratio that is constant and about equal to 20 to maintain a normal pH

A

bicarbonate to CO2

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2
Q

Respiratory acidosis occurs when –depressing the pH

A

PCO2 rises relative to bicarbonate,

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3
Q

response to respiratory acidosis

A

kidney retains bicarbonate to buffer and excretes more hydrogen ions

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4
Q

dangerous acidosis (significant organ injury)

A

< 7.1

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5
Q

dangerous alkalosis (significant organ injury)

A

> 7.6

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6
Q

normal pH

A

7.4

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7
Q

normal pCO2

A

40

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8
Q

normal bicarbonate

A

24

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9
Q

why is an alteration of PCO2 is always considered the primary process?

A

respiratory compensation is faster than renal compensation

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10
Q

acidosis: high CO2

A

respiratory acidosis

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11
Q

acidosis: low HCO3-

A

metabolic acidosis

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12
Q

respiratory alkalosis

A

low CO2

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13
Q

metabolic alkalosis

A

high HCO3-

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14
Q

anion gap

A

measured cations - measured anions = NA- (chloride and bicarbonate)

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15
Q

normal anion gap

A

12 +/- 4

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16
Q

effect of low albumin to anion gap

A

low anion gap (albumin and other blood proteins = negative charge)

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17
Q

serum anion gap falls – for every 1 g/dL reduction in albumin

A

2.5

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18
Q

methanol

A

anion gap acidoses

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19
Q

uremia

A

anion gap acidoses

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20
Q

diabetic ketoacidosis

A

anion gap acidoses

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21
Q

paraldehyde

A

anion gap acidoses

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22
Q

iron, isoniazid, inhalants

A

anion gap acidoses

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23
Q

lactic acid

A

anion gap acidoses

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24
Q

ethylene glycol, ethanol (alcoholic ketoacidosis)

A

anion gap acidoses

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25
Q

salicylates (aspirin), solvents, starvation (ketoacidosis)

A

anion gap acidoses

26
Q

most common anion gap acidoses

A

lactic acid

27
Q

primary mech by which anion gap acidosis occurs

A

organic acid accumulation

28
Q

hyperalimentation (TPN, IV fluids, excess CL-)

A

non-anion gap acidosis

29
Q

acetazolamide (carbonic anhydrous inhibitor)

A

non-anion gap acidosis

30
Q

renal tubular acidosis

A

non-anion gap acidosis

31
Q

diarrhea

A

non-anion gap acidosis

32
Q

Addison’s disease

A

non-anion gap acidosis

33
Q

spironolactone

A

non-anion gap acidosis

34
Q

small bowerl fistulas

A

non-anion gap acidosis

35
Q

main cause of non-anion gap acidosis

A

loss of bicarbonate, accumulation of chloride or failure of kidney to excrete acid

36
Q

for every change in 10 in pCO2 –> acutely pH will change by

A

0.08

37
Q

for every change in 10 in pCO2 –> chronic pH will change by –

A

0.03

38
Q

acidosis – in minute ventilation

A

decrease

39
Q

alkalosis – in minute ventilation

A

increase

40
Q

acute acidosis due to –

A
  1. V/Q mismatch due to dead space or shunt

2. apnea/hypopnea

41
Q

diseases that lead to V/Q mismatch –> acidosis

A

pneumonia, edema, hemorrhage, mucus plug

bronchospasm (asthma, COPD)

42
Q

acute alkalosis due to –

A

tachypnea (neurogenic, pain, psychogenic)

43
Q

chronic acidosis due to –

A

hypoventilation syndrome, air trapping (COPD), restrictive lund disease

44
Q

chronic alkalosis is –

A

rare

45
Q

Winter’s formula gives you

A

expected PCO2 for any given serum bicarbonate

46
Q

Winter’s forumla helps determine if the – is appropriate or inappropriate.

A

amount of compensation

47
Q

fatal acidosis

A

pH < 6.9

48
Q

fatal alkalosis

A

ph > 7.9

49
Q

primary determinant when interpreting acid-base disorder will be –

A

pCO2

50
Q

pH drop and increased pCO2

A

acute respiratory acidosis

51
Q

chronic compensated respiratory acidosis

A

with time, kidney accumulates bicarbonate to normalize (increase pH)

52
Q

pH rise and decreased pCO2

A

acute respiratory alkalosis

53
Q

why is acute respiratory alkalosis not clinically relevant?

A

body can’t maintain high minute ventilation long enough to keep pCO2 low

54
Q

chronic, compensated respiratory alkalosis by kidney is –

A

not common

55
Q

acute metabolic acidosis

A

pH drop, normal pCO2, [HCO3-] drop

56
Q

respiratory compensation for acute metabolic acidosis

A

pCO2 drops

57
Q

why is respiratory compensation for acute metabolic acidosis not sustainable long term

A

body can’t maintain high minute ventilation (respiratory fatigue limits this)

58
Q

acute metabolic alkalosis

A

pH rise, normal pCO2, [HCO3-] rise

59
Q

respiratory compensation for acute metabolic alkalosis is clinically uncommon but nevertheless it is –

A

hyperventilate and reain CO2 which decrease pH

60
Q

most clinical practice

A

metabolic compensation for chronic respiratory disorders and rapid respiratory compensation for acute metabolic disorders (not sustainable long term)