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Acid/base/electrolytes/fluids > Acid-base disorders > Flashcards

Acid-base disorders Flashcards

1
Q

In the most general terms what causes metabolic acidosis?

A

Endogenous acid production or loss of bicarbonate.

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2
Q

What is the normal bicarbonate range?

A

22 - 26mEq/L

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3
Q

What is often seen on physical exam in patients with metabolic acidosis?

A

Compensatory tachypnea

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4
Q

What is one of the first laboratory signs of acidosis?

A
  • low bicarbonate
  • normal homeostasis acidosis is buffered by kidneys via H+ excretion and bicarbonate reabsorption and regeneration
  • when this system is overwhelmed (uses up all bicarbonate) acidosis occurs
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5
Q

What other lab/ ABG value directly correlates with bicarbonate?

A

Base deficit

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6
Q

What blood gas abnormalities are seen in metabolic acidosis?

A

pH < 7.35
PCO2 < 35
HCO3 < 22/normal
BDE </= -3

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7
Q

What blood gas abnormalities are seen in metabolic alkalosis?

A

pH > 7.45
PCO2 > 40-45
HCO3 > 26
BDE >/= 3

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8
Q

What blood gas abnormalities are seen in respiratory acidosis?

A

pH < 7.35
PCO2 > 45
HCO3 > 26
BDE -

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9
Q

What blood gas abnormalities are seen in respiratory alkalosis?

A

pH > 7.45
PCO2 < 35
HCO3 < 22
BDE -

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10
Q

What are causes of anion gap acidosis?

A

Methanol
Uremia
DKA
Paraldehyde
Infection
Lactate
Ethanol
Salicylates

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11
Q

Is the ABG or the BMP/CMP a more accurate assessment of plasma bicarbonate?

A

BMP/CMP
-bicarbonate on the blood gas is a calculated value where it is actually measured in chemistry values

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12
Q

What is the base deficit/excess?

A

Calculated value of the amount of strong acid or base required to bring 1L blood in vitro at temp 38C and PCO2 40mmHg to pH 7.4
-approximates the severity of acidosis
-only useful in metabolic derangements

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13
Q

What is the anion gap?

A

The difference in concentration between routinely measured cations (Na+ and K+) and anions (Cl- and HCO3-)

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14
Q

What is the normal anion gap range?

A

8-12mEq/L

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15
Q

How is lactate produced?

A

In anaerobic glycolysis through the reduction of pyruvate by lactate dehydrogenase

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16
Q

How is lactate cleared?

A

Mostly hepatic some renal and other organs

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17
Q

What lactate isomers is tested on routine labs?

A

L- lactate

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18
Q

Where is D- lactate thought to be produced?

A

GI tract through metabolism via gut bacteria breakdown of carbohydrates

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19
Q

When should you consider D-lactate acidosis?

A

In anion gap acidosis in setting of intestinal disease and confusion especially if it happens after a carb load

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20
Q

Between lactate and base deficit which is a better predictor of mortality?

A

Lactate
-Elevated lactate correlates w/ higher mortality and longer length of stay
-BDE showed no correlation w/ mortality

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21
Q

What are some non-focal ischemia causes of lactic acidosis?

A

-lung injury/ARDS
-asthma d/t elevated oxygen demand and liver ischemia
-seizures
-pheochromocytoma
-burns
-neuroleptic malignant syndrome
-cardiopulmonary bypass d/t inadequate perfusion causing a shock like state
-use of epinephrine d/t potentiation of tissue malperfusion
-liver mets
-metformin (and other biguanides)
-malnutrition (d/t thiamine and biotin deficiency which are required for pyruvate metabolism, if it isn’t broken down it accumulates and leads to lactate)

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22
Q

What is type A lactic acidosis?

A

Due to hypoperfusion or hypoxemia

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23
Q

What is type B lactic acidosis?

A

Lactic acidosis in the absence of hypoperfusion and hypoxemia

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24
Q

From an acid/base status what occurs when GFR < 25mL/min?

A

Impaired renal acidification, reduced bicarbonate reabsorption, impaired renal homeostatis all leading to metabolic acidosis

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25
Q

What test can be ordered to help determine if ketoacidosis is the cause of anion gap acidosis?

A

beta-hydroxybuterate

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26
Q

What is the treatment for DKA?

A

-low-dose insulin infusion to correct hyperglycemia and electrolyte abnormalities (ie. total body potassium depletion)
-continue until gap has improved not just hyperglycemia
-adequate fluid resuscitation as hyperglycemia has an osmotic diuresis effect

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27
Q

What is the treatment for alcoholic or starvation ketoacidosis?

A

-treat electrolyte derrangements
-glucose in an isotonic solution
-avoid refeeding syndrome

28
Q

Alcohols can cause an anion gap and what else?

A

osmolar gap

29
Q

What are the common causes of non-gap acidosis?

A

-renal tubular acidosis
-GI losses (diarrhea and proximal fistula)
-iatrogenic (TPN, NS, medications)

30
Q

What is the general cause of RTA types 1 and 4?

A

reduced ammonia production

31
Q

What is the general cause of RTA type 2?

A

-impaired chloride resorption
-part of Fanconi syndrome

32
Q

How do you treat RTA?

A

-treat the underlying cause
-prevent hypercalciuria
-in types 1 and 2: NaHCO3 or citrate and hyperkalemia management
-type 4: furosemide and treatment of adrenal insufficiency, alkalinization is less commonly needed

33
Q

What is the treatment of non-gap acidosis d/t GI losses?

A

-these large fluid shifts result in a relative loss of Na compared w/ chloride (gut lumen has high levels of Na and HCO3)
-this discrepancy is exacerbated by NS resuscitation
-control the losses and resuscitate w/ LR to avoid hyperchloremia

34
Q

What are the ventilation changes seen as a result of respiratory compensation to metabolic acidosis?

A

-get a respiratory alkalosis
-increased minute ventilation d/t increased tidal volume and tachypnea
-tachypnea can get to dangerous and unsustainable rates

35
Q

Approximately when is maximal respiratory compensation to metabolic acidosis?

A

12-24hrs

36
Q

How do you calculate the expected compensation of metabolic acidosis?

A

Winter’s formula
PCO2(expected) = (1.5 x HCO3) +8
-if measured PCO2 is higher than this there is a superimposed respiratory acidosis
-if measured PCO2 is lower than this there is a superimposed respiratory alkalosis

37
Q

What is the theoretical limit of respiratory compensation for metabolic acidosis?

A

PCO2 15mmHg

38
Q

What effects does acidemia have on the CV system?

A

-venodilation
-arterioconstriction
-conduction abnormalities
-decreased inotropy
-splanchnic vasoconstriction

39
Q

What is the direct effect of acidemia on the pulmonary system?

A

respiratory depression
-however compensation of metabolic acidosis does lead to an increase in minute ventilation

40
Q

What electrolyte changes are seen d/t acidemia?

A

-hyperkalemia
-hypercalcemia
-hyperuricemia

41
Q

What are some of the causes of metabolic alkalosis?

A

-GI losses (gastric drainage and emesis)
-villous adenomas that are chloride secreting not bicarb secreting
-laxative abuse
-diuretics (furosemide, chlorothiazide)
-mineralocorticoid excess
-exogenous NaHCO3
-citrate excess from pRBC transfusions
-bone lytic conditions

42
Q

What cluster of electrolyte abnormalities are seen in patients with large upper GI losses?

A

hypokalemic, hypochloremic, metabolic alkalosis

43
Q

How do you treat metabolic alkalosis due to GI losses?

A

-NS or potassium chloride
-severe forms might need hydrochloric acid
-make sure you also watch and replete potassium, many of these mechanisms lead to potassium losses as well

44
Q

How do you treat metabolic alkalosis due to mineralocortic excess?

A

spironolactone

45
Q

What do blood transfusion w/ pRBC cause metabolic alkalosis?

A

the citrate is metabolized to bicarbonate

46
Q

What is the timeframe needed for respiratory compensation of metabolic alkalosis?

A

it’s almost immediate

47
Q

What is the equation to predict the expected PCO2 rise due to respiratory compensation of metabolic alkalosis?

A

PCO2 = 0.9 x (HCO3) + 9
-if PCO2 is lower there is a superimposed respiratory alkalosis

48
Q

What are soem of the deleterious effects of metabolic alkalosis?

A

-increased hemoglobin-oxygen affinity
-vasoconstriction (especially cerebral)
-calcium wasting
-hypokalemia
-hypomagnesemia

49
Q

What is the treatment for metabolic alkalosis?

A

-volume expansion
-if patient can’t tolerate volume expansion consider chloride loading w/ KCl
-acetazolamide, but careful
-mitigate acid production in upper GI losses w/ H2 blockers or PPIs

50
Q

What do you have to be careful of if giving acetazolamide for metabolic alkalosis?

A

-first this is a carbonic anhydrase inhibitor
-causes bicarbonate diuresis
-but it leads to hypokalemia and hypercapnia

51
Q

What type of base deficit/excess do you seen in respiratory acidosis?

A

neither

52
Q

What is the hallmark diagnostic feature of respiratory acidosis?

A

PCO2 elevation to > 45

53
Q

A bicarbonate level of what is suggestive of chronic respiratory acidosis?

A

> 26mEq/L

54
Q

What is the most common cause of respiratory acidosis through hypoventilation seen in the SICU?

A

overdosing narcotics, benzodiazepines, sleep aids, axiolytics

55
Q

What is the hallmark diagnostic feature of respiratory alkalosis?

A

PCO2 decrease < 22mEq/L

56
Q

What are some causes of central hyperventilation?

A

-sepsis
-hepatic failure
-pregnancy
-salicylate poisoning

57
Q

What is the acid/base disorder seen in ethylene glycol poisoning?

A

metabolic acidosis

58
Q

What type of shift on the oxyhemoglobin curve is seen as blood is warmed (what what does this do to the PaO2)?

A

rightward shift
-increases PaO2

59
Q

What type of shift on the oxyhemoglobin curve is seen in hypothermia?

A

leftward shift
-so a hypothermic pt who has their blood sample warmed for the ABG will have a higher PaO2 on the ABG than exists in vivo

60
Q

How do you calculate the O2 content?

A

O2 content = 1.34(Hgb)(%sat) + (0.003)(PaO2)
-Hgb g/dL
-PaO2 mmHg

61
Q

How does the CO2 concentration effect cerebral vessels?

A

-hypercapnia dilates cerebral vessels
-hypocapnia constricts cerebral vessels

62
Q

What is the proposed mechanism in which acute increases in CO2 leads to decreased consciousness?

A

-leads to intraneuronal acidosis
-excessive cerebral blood flow
-rising intracranial pressure

63
Q

What two types of renal tubular acidosis can cause metabolic acidosis d/t inability to secrete a normal dietary acid load?

A

-type 1 (distal) RTA
-type 4 RTA (hypoaldosteronism)

64
Q

What type of renal tubular acidosis can cause metabolic acidosis d/t an increased H+ load or HCO3 loss?

A

type 2 (proximal) RTA

65
Q

What are the benefits of permissive hypercapnia?

A

-reduces tissue metabolixm
-improves surfactant function
-prevents nitration of proteins

66
Q

What are the intracranial effects of hypocapnia?

A

-reduces total cerebral blood flow
-raises neuronal pH
-reduces ionized Ca causing disturbances in cortical and peripheral nerve function

67
Q
A

Acid/base/electrolytes/fluids (3 decks)

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