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APEX > Unit 9 - Acid Base > Flashcards

Unit 9 - Acid Base Flashcards

1
Q

details how PaCO2 and HCO3- influence pH

A

Henderson-Hasselbach equation

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2
Q

most important buffer system in the blood

A

bicarb

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3
Q

2nd most important buffer in the blood

A

Hgb

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4
Q

renal compensation of buffers

A
  • Reabsorption of filtered bicarb
  • Removal of titratable acids (non-volatile acids)
  • Formation of ammonia
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5
Q

why is acidosis often accompanied by hyperkalemia

A

H+ is transported into cells, K+ is transported out of cells

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6
Q

normal anion gap

A

8-12 mEq/L

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7
Q

anion gap =

A

Na+ - (Cl + HCO3)

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8
Q

causes of increased anion gap metabolic acidosis

A

MUDPILES
Methanol
Uremia
DKA
Paraldehyde
Isoniazid
Lactate
Ethanol, ethylene glycol
Salicylates

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9
Q

examples of increased lactate assoc with increased anion gap metabolic acidosis

A

sepsis
decreased O2 delivery
cyanide poisoning

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10
Q

causes of normal anion gap metabolic acidosis

A

HARDUP
Hypoaldosteronism
Acetazolamide
Renal tubular acidosis
Diarrhea
Uterosigmoid fistula
Pancreatic fistula

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11
Q

time it takes for compensation of respiratory vs metabolic disorders

A
  • Compensation for metabolic disorders is rapid (over several minutes) due to changes in minute ventilation
  • Compensation for respiratory disorders is slow (over several days) due to change in H+ excretion in urine
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12
Q

how does the body compensate for respiratory acidosis

A

increased HCO3-

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13
Q

how does the body compensate for respiratory alkalosis

A

decreased HCO3-

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14
Q

how does the body compensate for metabolic acidosis

A

decreased PaCo2

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15
Q

how does the body compensate for metabolic alkalosis

A

increased PaCO2

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16
Q

5 questions to ask when evaluating a blood gas

A
  1. is the pH normal
  2. is the PaCO2 normal
  3. is the HCO3- normal
  4. has compensation occured
  5. if there’s metabolic acidosis, is the anion gap normal or increased
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17
Q

CV effects of acidosis

A

↑ P50 (right = release)
↑ SNS tone
↑ risk dysrhythmias
↓ contractility
Direct myocardial depression

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18
Q

CNS effects of acidosis

A

↑ cerebral blood flow
↑ ICP

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19
Q

pulmonary effects of acidosis

A

↑ PVR

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20
Q

CV effects of alkalosis

A

↓ P50 (left = love)
↓ coronary blood flow
↑ risk dysrhythmias

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21
Q

CNS effects of alkalosis

A

↓ cerebral blood flow
↓ ICP

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22
Q

pulm effects of alkalosis

A

↓ PVR

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23
Q

electrolyte changes assoc with alkalosis

A

hypokalemia
↓ ionized calcium

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24
Q

pH that indicates need for mechanical ventilation

A

< 7.2

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25
Q

PaCO2 =

A

CO2 production / alveolar ventilation

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26
Q

3 etiologies of respiratory acidosis

A
  1. increased CO2 production
  2. decreased CO2 elimination
  3. rebreathing
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27
Q

Most common cause of resp acidosis

A

hypoventilation

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28
Q

causes of ↑ CO2 production

A
  • sepsis
  • overfeeding
  • MH
  • intense shivering
  • prolonged seizure activity
  • thyroid storm
  • burns
29
Q

causes of ↓ CO2 elimination

A
  • airway obstruction
  • ↑ Vd
  • ↑ Vd/Vt
  • ARDS
  • COPD
  • respiratory center depression
  • drug overdose
  • inadequate NMB reversal
30
Q

in acute resp acidosis, every 10 mmHg increase in PaCO2 = pH increase by ____

A

for every 10 mmHg increase in PaCO2, pH increases by 0.08

31
Q

in chronic resp acidosis, every 10 mmHg increase in PaCO2 = pH increase by ____

A

for every 10 mmHg increase in PaCO2, pH decreases by 0.03

32
Q

why is resp acidosis assoc with hypoxemia

A

Alveolar nitrogen is inert – concentration remains constant

↑ Alveolar CO2 displaces alveolar O2 = arterial hypoxemia

33
Q

why does P50 increase with respiratory acidosis

A

Curve shifts to the right – releases more O2 to tissues

Partially compensates for hypoxemia

34
Q

why is cardiac and smooth muscle depression assoc with respiratory acidosis

A

Acidosis inside muscle affects contractile protein & enzymatic function

myocardial depression, vasodilation

35
Q

SNS effects of respiratory acidosis

A

SNS stimulation - CO2 activates

unless acidosis is severe, offsets smooth muscle depression

36
Q

effects of SNS stim with resp acidosis

A
  • Tachycardia = ↑ myocardial O2 consumption & ↓ delivery
  • Vasoconstriction = ↑ SVR = ↑ myocardial O2 consumption
  • Dysrhythmias, prolonged QT
  • Oculocardiac reflex is more common following precipitating event
37
Q

why is K+ increased in respiratory acidosis

A
  • Activates H+/K+ pump
  • Buffers CO2 acid in exchange for releasing K+ into plasma
38
Q

why is Ca2+ increased in resp acidosis

A

Ionized Ca2+ competes with H+ for binding sites on plasma proteins

Acidosis: plasma proteins buffer H+ and release Ca2+ = ↑ inotropy

39
Q

ICP with resp acidosis

A

increased
* CO2 freely diffuses across BBB
* Decreased CSF pH = ↓ cerebrovascular resistance = ↑ CBF & vol.

40
Q

when does CO2 narcosis occur

A

PaCO2 > 90 mmHg

41
Q

how does hypercarbia affect pulmonary vs peripheral blood vessels

A

opposite effect on pulmonary blood vessels vs. peripheral blood vessels
* In the lungs, CO2 is a direct-acting vasoconstrictor - can cause pHTN and ↑ RV workload

42
Q

when does respiratory alkalosis occur

A

when alveolar ventilation exceeds CO2 production

43
Q

etiologies of resp alkalosis

A
  • Iatrogenic: mechanical ventilation - most common
  • Hypoxia (high altitude, low FiO2, profound anemia)
  • Pain/anxiety
  • Pregnancy
  • Drugs: progesterone, salicylates
  • Pulmonary embolism
  • Reduced mechanical dead space with same alveolar ventilation (removing HME, changing from mask to ETT)
44
Q

how does the body compensate for respiratory alkalosis

A

kidneys excrete HCO3- to return pH to normal

This may take several days

45
Q

how does the body compensate for respiratory alkalosis

A

kidneys excrete HCO3- to return pH to normal

This may take several days

46
Q

CV effects of resp alkalosis

A
  • Dysrhythmias
  • Decreased coronary blood flow
  • Decreased myocardial contractility
  • Decreased P50 (left shift)
47
Q

CNS effects of resp alkalosis

A
  • Inhibition of respiratory drive
  • Cerebral vasoconstriction (↓ CBF and ↓ ICP)
  • Neuronal irritability
  • Confusion
48
Q

electrolyte changes with resp alkalosis

A

Decreased serum K+
Decreased serum Ca2+

49
Q

best treatment for resp alkalosis

A

reverse underlying cause

  • In spontaneously ventilating patient, treat with sedation (concern when pH > 7.6)
  • In mechanically ventilated patient, treat by reducing minute ventilation on the ventilator
50
Q

causes of metabolic acidosis

A

accumulation of nonvolatile acids, loss of bicarbonate, or large volume resusication with sodium chloride solution

51
Q

anion gap =

A

major cations - major anions
or
([Na+] – [Cl-] + [HCO3-])

52
Q

is accumulation of acids assoc with gap or non-gap metabolic acidosis

A

gap

53
Q

is loss of bicarb/ECF dilution caused by gap or non gap acidosis

A

non gap

54
Q

how does the body compensate for metabolic acidosis

A

eliminate CO2 by increasing minute ventilation

55
Q

PaCO2 decreases by ____ mmHg for every HCO3- decrease of ____ mEq/L

A

PaCO2 decreases by 1-1.5 mmHg for every HCO3- decrease of 1 mEq/L

56
Q

when should bicarb be admin with metabolic acidosis

A

generally useful in non-gap acidosis (most etiologies produce bicarb loss)

controversial in gap acidosis

Best used for gap as a temporary measure if pH < 7.2 and patient is hemodynamically unstable

57
Q

treatment of uremia or drug-induced gap acidosis

A

dialysis

58
Q

what causes metabolic alkalosis

A

increased bicarbonate and/or loss of nonvolatile acids

59
Q

etiologies of metabolic alkalosis assoc with addition of HCO3-

A

bicarb admin
massive transfusion

(liver converts transfusion preservatives to HCO3)

60
Q

etiologies of metabolic alkalosis assoc with addition of HCO3-

A

bicarb admin
massive transfusion

(liver converts transfusion preservatives to HCO3)

61
Q

etiologies of metabolic alkalosis assoc with loss of nonvolatile acid

A
  • Loss of gastric fluid (most common): vomiting, NG suction
  • Loss of acid in urine
  • Diuretics
  • ECF depletion = increased Na+ reabsorption
62
Q

causes of metabolic alkalosis assoc with increased mineralocorticoid activity

A

Cushing’s syndrome
Hyperaldosteronism

63
Q

how does the body compensate for metabolic alkalosis

A

body will retain CO2 by reducing minute ventilation

64
Q

PaCO2 increases by ____ for every HCO3- increase of 1 mEq/L

A

0.5-1 mmHg

65
Q

treatment of metabolic alkalosis

A

fix underlying cause
* Acetazolamide (carbonic anhydrase inhibitor): increases renal excretion of HCO3-
* Spironolactone (mineralocorticoid antagonist)
* Dialysis

66
Q

acid base disturbance assoc with large volume NS resuscitation

A

hyperchloremic metabolic acidosis

67
Q

why do salicylates cause metabolic acidosis

A

inhibit krebs cycle

68
Q

when should bicarb be given for anion gap metabolic acidosis

A

temporary measure if pt’s pH is < 7.2 and hemodynamically unstable

bicarb can cause intracellular acidosis in the setting of inadequate ventilation/perfusion

APEX (54 decks)

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