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PHRM 864 > Acid Base Kania > Flashcards

Acid Base Kania Flashcards

1
Q

normal pH

A

7.35-7.45

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2
Q

what pHs are incompatible with life

A

<6.7
>7.7

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3
Q

acidemia is considered what pH

A

<7.35

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4
Q

HCO3 is what

A

bicarb

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5
Q

H2CO3 is what

A

carbonic acid

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6
Q

metabolic disorders involve changes in what

A

H+ and HCO3 (bicarb)

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7
Q

respiratory disorders involve changes in what

A

CO2

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8
Q

kidneys compensate what disorders

A

respiratory

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9
Q

lungs compensate what disorders

A

metabolic

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10
Q

Henderson hasselbach equation

A

pH = pKa + log (base/acid)

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11
Q

pKa of carbonic acid

A

6.1

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12
Q

normal PaCO2

A

35-45 mmHg (40)

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13
Q

normal HCO3 (bicarb)

A

22-26 mEq/L (24)

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14
Q

normal PaO2

A

95-100 mmHg

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15
Q

normal SaO2

A

95% +

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16
Q

acidemia adverse events cardiovascular

A

decreased CO
impairment of cardiac contractility
increased pulmonary vascular resistance and arrythmias
hyperventilation
SOB

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17
Q

acidemia adverse events metabolic

A

insulin resistance
anaerobic glycolysis inhibition
hyperkalemia

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18
Q

acidemia adverse events CNS

A

coma
altered mental status

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19
Q

alkalemia sx cardiovascular

A

decreased coronary blood flow
ateriolar constriction
decreased anginal threshold (risk MI)
arrythmias
decreased respirations (hypoventilation)

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20
Q

alkalemia sx metabolic

A

decreased K+, Ca and Mg
stimulation anaerobic glycolysis

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21
Q

alkalemia sx CNS

A

decreased cerebral blood flow
lethargy, delirium, stupor
seizures

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22
Q

how is acid generated in us (3)

A

diet: 1 meq consumed per day
aerobic metabolism glucose
non volatile acids: anaerobic/lactic

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23
Q

4 mechanisms of acid regulation

A
  1. buffering systems
  2. renal regulation
  3. ventilatory regukation
  4. hepatic regulation
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24
Q

what is a buffer

A

ability of a weak acid and its base to resist change in pH with addition of a strong acid or base

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25
Q

what are the three main buffers

A

bicarb/carbonic acid
phosphate
protein

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26
Q

onset and capacity of bicarb buffer

A

rapid onset
intermediate capacity

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27
Q

when acid is added to bicarb buffer, what happens with breathing

A

more exhalations, getting rid of CO2

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28
Q

which buffer is present extracellularly more than any other buffer

A

bicarb

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29
Q

onset and capacity of phosphate buffer

A

intermediate onset
intermediate capacity

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30
Q

which types of phosphates more useful

A

intracellular organic phosphates

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31
Q

onset and capacacity of protein buffer

A

albumin/hemoglobin
rapid onset
limited capaccity
VERY FAST

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32
Q

two main purposes of kidney in acid regulation

A

reabsorb filtered HCO3- (hold on to bicarb)
excrete H+ ions released from nonvolatile acids (generate bicarb)

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33
Q

how much bicarb filtered through kidney daily

A

4,000-4,500 mEq daily

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34
Q

how much bicarb reabsorbed by proximal tubule

A

85-90%

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35
Q

how much bicarb reabsorbed by distal tubule / collecting duct

A

10-15%

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36
Q

how much HCO3- in the urine

A

basically none

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37
Q

what happens if we limits H+ secretion in proximal tubule lumen

A

bicarb losses in urine

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38
Q

carbonic anhydrase inhibitors do what

A

block carbonic anhydrase
CO2 and H2O dont get back to tubular cell
losses of bicarb in the urine, metabolic acidosis

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39
Q

bicarb generation onset and capacithy

A

delayed onset
large capacithy

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39
Q

bicarb generation happens where

A

distal tubule

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40
Q

describe how bicarb is made from ammoniagenesis

A

carbonic acid splits into H+ and HCO3
H+ forms ammonium and is excreted
HCO3 gets into bloodstream and is new

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41
Q

how much bicarb is made from ammoniagenesis

A

40 mEq/day can be increased to 300 mEq/day

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42
Q

how much bicarb made from HPO42 titratable activity

A

30 mEq/day, cant be increased

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43
Q

how does titratable activity with phos work

A

HPO4 combines with H+ and HCO3 formed is in bloodstream

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44
Q

distal tubular hydrogen ion secretion makes up what percent of acid excretion

A

50%

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45
Q

ventilatory regulation, onset and capacity

A

rapid onset
large capacity

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46
Q

how does ventilatory regulation work

A

chemoreceptors detect increase in PaCO2 and increase rate and depth of ventilation

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47
Q

hepatic regulation: oxidation of proteins generates what

A

HCO3- and NH4+

48
Q

if liver stops urea synthesis, what can happen

A

metabolic alkalosis
(urea is acidic)

49
Q

metabolic acidosis primary change and compensation

A

change: decreased HCO3-
compensation: decreased PaCO2

50
Q

metabolic alkalosis primary change and compensation

A

change: increased HCO3-
compensation: increased PaCO2

51
Q

respiratory acidosis change and compensation

A

change: increased PaCO2
compensation: increased HCO3-

52
Q

respiratory alkalosis change and compensation

A

change: decreased PaCO2
compensation: decreased HCO3-

53
Q

respiratory compensation speed

A

rapid

54
Q

renal compensation speed

A

3-5 days for max effect

55
Q

does compensation correct pH?

A

no, moves it towards normal

56
Q

types of metabolic acidosis

A

anion gap
non-anion gap

57
Q

metabolic acidosis characterized by what 3 things

A

pH <7.35
PaCO2 decreased (35-45 normal)
decreased HCO3- (<24)

58
Q

anion gap equation

A

anion gap = Na - (Cl + HCO3-)

59
Q

normal anion gap rnage

A

3-11 mEq/L

60
Q

patho of non-anion gap metbaolic acidosis

A

loss of plasma HCO3- replaced by Cl-

61
Q

non anion gap metabolic acidosis GI bicarb loss causes

A

diarrhea
pancreatic fistula/biliary drainage (rich in HCO3)

62
Q

non anion gap metabolic acidosis renal bicarb loss causes

A

type II renal tubular acidosis (proximal can’t reabsorb H+)
usually from toxins like metals, carbonic anhydrase, drugs)
causes reduced reabsorptive threshold for HCO3 in proximal tubule)

63
Q

type II renal acidosis occurs where

A

proximal tubule
can’t reabsorb as much HCO3-

64
Q

type I renal tubule acidosis occurs where

A

distal tubule

65
Q

non anion gap metabolic acidosis renal H+ excretion reduction causes

A

type I renal tubule acidosis: inc in K+ excretion, hypokalemia
type IV renal tubule acidosis: hypoaldosterone hyperkalemia
chronic renal failure

66
Q

what is type I renal tubule acidosis

A

in distal tubule
hypokalemia - increase in K+ excretion
H+ cant be pumped into tubule lumen

67
Q

what is type IV renal tubule acidosis

A

in distal tubule
hyperkalemia
hypoaldosteronism (H+ retention)

68
Q

what happens in chronic renal failure

A

less H+ secretion
less amonia production
therefore less HCO3 produced

69
Q

what can acid and chloride administration from TPN or Cl admin cause?

A

non-anion gap metabolic acidosis

70
Q

causes of anion gap metabolic acidosis

A

M - methanol intoxication
U - uremia
L - lactic acidosis
E - ethyleneglycol
P - aldehyde ingestion
A - aspirin / salicylates
K - ketoacidosis
I - infection

71
Q

what is the delta gap equation

A

difference between patient’s anion gap and the normal anion gap

72
Q

when do we measure delta gap

A

only in anion gap above normal

73
Q

how do we use delta gap

A

add it to the pts HCO3, it should be in normal range
- if HCO3 isnt in normal range after adding then they have a metabolic alkalosis as well

74
Q

what is the most common cause of anion gap acidosis

A

lactic acidosis

75
Q

what causes lactic acidosis (9)

A

shock
drugs/toxins
seizures
leukemia
hepatic failure
renal failure
diabetes
malnutrition
rhabdomyolysis

76
Q

drugs that cause lactic acidosis

A

ethanol
metformin
linezolid
propofol
topirimate
propylene glycol
NRTIs

77
Q

what does salicylate toxicity present as?

A

respiratory alkalosis - respiratory drive stimulation
metabolic acidosis - organic acid accumulation

78
Q

methanol/ ethylene ingesetgion from what substances

A

cleaning supplies
paint

79
Q

lactic acidosis symptoms

A

Kussmaul respirations - breathing fast and deep
flushing, tachycardia
N/V
lethargic / coma
hyperkalemia
bone demineralization in chronic RTAs

80
Q

when do we use bicarb therapy

A

treat underlying cause
pH < 7.1
hyperkalemia
overdose
in a code

81
Q

does bicarb therapy reduce morbidity and mortatlity

A

no evidence

82
Q

bicarb therapy how to calculate dose

A

(o.5 x IBW) x (12- HCO3-) mult by 1/3-1/2
IBW = 50+ 2.3 (in over 60)

83
Q

how much bicarb given during cardiac arrest

A

1 mEq/kg

84
Q

what might we need to supplement in cardiac arrest

A

K+

85
Q

what happens with Hg if we have too much bicarb

A

Hg saturation increases
oxygen not released to tissues
decreased cerebral blood flow

86
Q

what happens with bicarb overload

A

hypernatremia
CSF acidosis
hypokalemia
hypocalcemia

87
Q

chronic bicarb therapy / metabolic acidosis therapy dose

A

average 1-3 mEq/kg

88
Q

is veverimer used

A

no, FDA denied

89
Q

metabolic alkalosis marked by what

A

pH >7.45
high HCO3-
high PaCO2 compensatory hypoventilation

90
Q

metabolic alkalosis rise in HCO3 comes from what

A

loss of acid from GI tract
administration of bicarb
contraction alkalosis (loss Cl- rich fluid and HCO3 poor fluid)

91
Q

metabolic alkalosis kidney impairment

A

renal impairment in HCO3 excretion
volume and chloride depletion
decrease in blood volume
proximal tubule capcity increases so we hang on to more bicarb

92
Q

types of metabolic alkalosis

A

saline responsive
saline resistant

93
Q

saline responsive alkalosis Cl level

A

Cl in urine < 10-20 mEq/L

94
Q

saline responsive alkalosis causes (3)

A

diuretics
vomiting / NG suction
bicarb administration

95
Q

how do diuretics cause alkalosis

A

aldosterone release increases bicarb reabsoption and generation
hypokalemia because K moves out
hypo chloremic state because bicarb absorbed instead with Na

96
Q

in alkalosis and diuretics, without Cl - Na is reabsorbed with ____

A

bicarb

97
Q

what is an example of exogenous bicarb administration

A

blood transfusion - citrate breaks down into bicarb

98
Q

in metabolic alkalosis, what happens with Na

A

reabsoprtion increased in distal and proximal tubule

99
Q

saline resistant alkalosis urinary chloride level

A

> 20 mEq/L

100
Q

key difference with saline resistant alkalosis vs saline responsive

A

no chloride depletion

101
Q

causes of saline resistant alkalosis

A

increased mineralocorticoid activity
hypokalemia
renal tubular chloride wasting (Bartters)

102
Q

symptoms of metabolic alkalosis

A

muscle cramps
dizziness
hypoxia, confusion, seizures
arrythmias

103
Q

treatment of metabolic alkalosis

A

treat underlying cause
fluid replacement
carbonic anhydrase inhibitor
HCl acid
ammonium chloride

104
Q

use fluid replacment for alkalosis with caution in what pts

A

HF
renal / hepatic failure

105
Q

who should get carbonic anhydrase inhibitors in metabolic alkalosis

A

sodium responsive pts who cant tolerate fluids / sodium

106
Q

carbonic anhydrase drug, dose and what it should be given with

A

acetazolamide 250-375 mg
given with potassium

107
Q

when should HCl be given

A

metabolic alkalosis sodium responsive
- cant tolerate sodium
- severe bicarb
- severe HF
- others not working

108
Q

who should not get ammonium chloride

A

hepatic / renal failure

109
Q

treatment for saline resistant alkalosis

A

decrease mineralocorticoid
supplement potassium
potassium sparing diuretic: spironolactone

110
Q

respiratory acidosis classified by what

A

pH < 7.35
CO2 increased
HCO3 increased compensatory

111
Q

causes of respiratory alkalosis

A

not breathing out
asthma
choking
aspiration
overdose
sleep apnea
trauma
CNS infection
PE
mechanical vent
Guillian-Barre syndrome

112
Q

symptoms of respiratory acidosis

A

SOB
dyspnea
drowsiness
tachycardia
coma / seizure

113
Q

treatment of respiratory acidosis

A

correct underlying cause
mechanical vent or oxygen

114
Q

respiratory alkalosis characterized by what

A

pH >7.45
decreased PaCO2
decreased HCO3

115
Q

causes of respiratory alkalosis

A

anxiety
trauma
salicylate intoxication
high altitude

116
Q

symptoms of respiratory alkalosis

A

lightheadedness
decreased cerebral blood flow
N/V

117
Q

treatment of respiraotry alkalosis

A

underlying cause
sedation
paralysis
vent

118
Q
A

PHRM 864 (23 decks)

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