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Fall'20 Pharmacology III > Pharm Acid/Base > Flashcards

Pharm Acid/Base Flashcards

1
Q

Acidity of solution reflects its

A

hydrogen ion content

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2
Q

PH stands for

A

Potential of hydrogen

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3
Q

causes for metabolic alkalosis

loss of acid from extracellular space examples

A

loss of gastric fluid- vomiting, NG drainage

loss of acid into urine- diuretic administration, hyperaldosteronism

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4
Q

causes for metabolic alkalosis

excessive HC03 loads

A

NaHCO3 administration
Lactate, acetate, citrate administration
Alkali administration to patients with renal failure
Abrupt correction of chronic hypercapnia

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5
Q

respiratory alkalosis

A

Hyperventilation-Increase in minute ventilation to level greater than that required to excrete the metabolic production of CO2

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6
Q

respiratory acidosis

A

Hypoventilation-Occurs when minute ventilation is insufficient to eliminate CO2 production without an increased capillary-alveolar CO2 gradient

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7
Q

metabolic acidosis is normally accompanied by compensatory

A

hyperventilation

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8
Q

in metabolic acidosis the significant reduction of PH

A

increased PVR
reduced myocardial contractility
decreased SVR
impaired response to CV system to endogenous or exogenous catecholamines

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9
Q

what compensatory mechanism is immediate

A

buffer system

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10
Q

the buffer system is followed by

A

respiratory

renal system- renal is slow and more effective

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11
Q

when the patient is acidosis- what happens to opioids, sedatives and anesthetic agents

A

sedatives and anesthetic agents on the CNS are potentiated

nonionized form of opioids increases and more penetrates the brain

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12
Q

what neuromuscular blocker do we avoid in the acidotic patient

A

succinylcholine in the acidotic patient with hyperkalemia

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13
Q

respiratory or metabolic acidosis augments nondepolarizing NMB agents?

A

respiratory acidosis

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14
Q

what are the circulatory depressant effects of volatile and IV anesthetics for the acidotic patient

A

exaggerated

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15
Q

what acid-base imbalance prolongs the duration of opioid induced respiratory depression

A

respiratory alkalosis

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16
Q

what electrolyte abnormality may precipitate severe arrhythmias in alkalemia

A

hypokalemia

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17
Q

especially during hypotension cerebral ischemia can occur from marked reduction in cerebral blood flow- what acid base imbalance is this

A

alkalemia

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18
Q

normal clearance maintains serum concentrations of lactate at

A

0.5-1mmol/L

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19
Q

where is most lactate cleared

A

by the liver

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20
Q

in the liver what three things does lactate undergo

A

oxidation
gluconeogenesis
eventual conversion to bicarbonate

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21
Q

lactate undergoes both passive diffusion and active transport into the liver via

A

monocarboxylate transporter

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22
Q

active transport becomes saturated as serum lactate concentrations >

A

2.5mmol/L

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23
Q

severe reduction in hepatic blood flow will do what to hepatic lactate clearance

A

decrease

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24
Q

lactate acid is a strong acid and therefore dissociates almost completely under physiologic conditions into the

A

lactate anion

and

hydrogen ion

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25
Q

when does lactate accumulation occur

A

mainly during anaerobic glycolysis

generated under normoxic conditions

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26
Q

in the critically ill patient lactate production may increase while lactate clearance is impaired- meaning…

A

lactic acidosis may occur

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27
Q

a serum lactate ___ upon admission is an independent predictor of mortality in critically ill patients

A

> 1.5mmol/L

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28
Q

failure to decrease lactate concentration to less than or equal to ___24 hours after admission is also associated with significant mortality

A

1.0mmol/L

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29
Q

this investigational drug decreases concentration of lactate

A

dichloroacetate (DCA)

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30
Q

dichloroacetate decreases concentration of lactate in what 4 situations

A

malaria
DKA
burns
cardiogenic shock

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31
Q

DCA activates

A

activates the mitochondrial pyruvate dehydrogenase complex, thus accelerating the irreversible oxidation of lactate via pyruvate to acetyl CoA which then enters the Krebs cycle

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32
Q

The buffer:

A

tris (hydroxymethyl) aminomethane or THAM can be used to treat metabolic acidosis and does not generate carbon dioxide

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33
Q

Lactic Acidosis

A

It may be useful as an alternative to sodium bicarbonate to treat metabolic acidosis in pts who are hypernatremic

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34
Q

When cause of metabolic acidosis is unclear measure:

A

Serum lactate
BUN,
Creatinine
Glucose

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35
Q

If this does not identify the etiology then:

Send serum for toxicology to measure:

A

Salicylates
Methanol
Ethylene glycol

36
Q

large volume infusion of isotonic saline may result in

A

hyperchoremic metabolic acidosis

37
Q

Dilutional acidosis also occurs when the plasma pH is decreased by extracellular volume expansion with chloride-containing solution such as NS

A

Dilutional acidosis also occurs when the plasma pH is decreased by extracellular volume expansion with chloride-containing solution such as NS

38
Q

ph of water at 37 degrees celsius is 6.8- what does this mean

A

any increase in the free water volume of the body will contribute to acidosis.

39
Q

normal saline is commonly thought of as physiologic. why

A

because it has an osmolarity close to that of plasma and does not lyse RBC

40
Q

what is the PH of normal saline? as it contains more chloride and slightly more sodium

A

5.7

41
Q

infusion of a large volume of NS will increase ___

A

plasma chloride concentrations to a relatively greater degree than sodium concentrations

42
Q

chloride is a

A

strong acid (proton donor)

43
Q

sodium is a

A

strong base (hydroxyl donor)

44
Q

BE is a calculation (not measured) from an algorithm baed on measured

A

bicarb and PH

45
Q

does base excess distinguish among the possible causes of metabolic acidosis

A

no

46
Q

anion gap normal

A

6-10 mEq/L

47
Q

acute respiratory acidosis or alkalosis what happens to BE

A

it does not change.

48
Q

respiratory acidosis in the presence of metabolic acidosis the BE is

A

<0

49
Q

if underlying issues was metabolic alkalosis BE=

A

BE>0

50
Q

mixed respiratory and metabolic acidosis is a common clinical problem - how do we guide treatment

A

BE can be a guide to treatment

51
Q

does base excess distinguish among the possible causes of metabolic acidosis

A

no

52
Q

major extracellular anions (-)

A

chloride and bicarbonate

53
Q

the major extracellular cation is

A

sodium

54
Q

is potassium measured in its anion gap

A

calculation varies from institution

55
Q

k -ca- mg is grouped into

A

unmeasured cations

56
Q

anion gap refers solely to the differences in concentrations between

A

anions and cations

57
Q

electroneutrality occurs when

A

the concentrations of the combined unmeasured anions exceed that of the unmeasured cations by the same amount

58
Q

Anion Gap

A

“Anion Gap” refers solely to the differences in concentration between the traditionally measured anions and cations.

59
Q

Strong Ion Gap (SIG):

strong cations

A

compares excess measured serum concentrations of strong cations (NA+, K+, Mg++, Ca++)

60
Q

Strong Ion Gap (SIG): strong anions

A

(Cl-, HCO3-, albumin, phosphate).

61
Q

what can strong ion gap do

A

differentiate between dilution acidosis to acidosis due to tissue hypo perfusion

62
Q

normal anion gap metabolic acidosis

A

diarrhea
pancreatic fistula
renal tubular acidosis
intoxication ammonium chloride, acetazolamide, toluene.
hyperchoremic acidosis (excess saline administration)

63
Q

increased anion gap

A

lactic acidosis
ketoacidosis
chronic renal failure accumulation of sulfates, phosphates, urea.
intoxication organic acids (salicylate, ethanol, methanol, formaldehyde, ethylene glycol, paraldehyde) INH, sulfates, metofrmin
massive rhabdomyolysis

64
Q

metabolic alkalosis is commonly

A

iatrogenic

65
Q

causes of metabolic alkalosis

A 
vomiting with excess hydrochloride acid
ng suction
chronic administration of diuretics
hypoalbuminemia
excess secretion of aldosterone
66
Q

a loss of free water (PH 6.8) will cause a

A

volume contraction alkalosis

67
Q

treatment of metabolic alkalosis

A

treat underlying cause

68
Q

hospital cause of metabolic alkalosis

A

excess administration of sodium bicarbonate

69
Q

when is respiratory acidosis compensated-

how does respiratory compensation occurs

A

within 6-12 hours

increased secretion of hydrogen ions with a resulting increase in the plasma bicarbonate concentration.

70
Q

correction of chronic respiratory acidosis is

A

iatrogenic hyperventilation.

acute metabolic alkalosis. because increased plasma bicarbonate is not promptly eliminated by the kidneys

71
Q

compensation of respiratory alkalosis

A

decreased reabsorption of bicarbonate ion from renal tubules.

72
Q

compensation for metabolic acidosis

A

stimulates alveolar ventilation, which causes rapid removal of carbon dioxide

73
Q

the respiratory compensation for metabolic acidosis is only partial - what does the PH do

A

Ph remains somewhat below normal

74
Q

metabolic alkalosis compensation

A

diminishes alveolar ventilation

75
Q

metabolic alkalosis and metabolic acidosis- the respiratory compensation is only ever

A

partial

76
Q

during cardiopulmonary bypass- what happens to c02 and ph

A

ph will increase to 7.6 and c02 becomes more soluble.

77
Q

in PH stat we give c02 via

A

the oxygenator

78
Q

who do we give co2 in PH stat

A

in pediatric cardiac surgeries

79
Q

what is a negative outcomes oh PH state

A

microemboli

80
Q

what is the Main goal of PH stat

A

to provide co2 for cerebral vasodilation
to combat the leftward shift of the oxyhemoglobin during hypocarbia and hypothermia and alkalosis. so the addition of the PH stat strategy will help the oxygen unload the hemoglobin

81
Q

who do we use alpha stat on

A

adult cardiopulmonary bypass

82
Q

does alpha stat have microemboli

A

no because supplemental carbon dioxide is not administered

83
Q

does alpha stat have temperature correction

A

no

84
Q

what is the alpha stat strategy

A

seek to optimize enzyme function during hypothermia.

85
Q

the objective of alpha stat is to

A

maintain biologic neutrality by preserving the alpha imidazole and protein charge state OH/H ratio.

Fall'20 Pharmacology III (14 decks)

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