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

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28
Q

Alcohols can cause an anion gap and what else?

A

osmolar gap

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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)

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30
Q

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

A

reduced ammonia production

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31
Q

What is the general cause of RTA type 2?

A

-impaired chloride resorption
-part of Fanconi syndrome

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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

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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

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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

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35
Q

Approximately when is maximal respiratory compensation to metabolic acidosis?

A

12-24hrs

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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

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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

To maintain a pH 7.4 what mut the ratio of HCO3 to (0.03 x PaCO2) be?

A

20:1

68
Q

What equation can given the predicted PaCO2 of a given HCO3 in metabolic acidosis?

A

PaCO2 = (1.5 x HCO3) + (8 +/- 2)
-if PaCO2 is more than this value pt has both met acidosis and resp acidosis
-if PaCO2 is less than this value pt has met acidosis and resp alkalosis

69
Q

What equation can given the predicted PaCO2 of a given HCO3 in metabolic alkalosis?

A

PaCO2 = (0.7 x HCO3) + (20 +/- 1.5)
-if PaCO2 is more than this value pt has both met alkalosis and resp acidosis
-if PaCO2 is less than this value pt has met alkalosis and resp alkalosis

70
Q

What are the 4 basic mechanisms that can lead to metabolic acidosis?

A

-bicarbonate consumption from decreased H+ excretion
-bicarbonate consumption from increased H+ production
-bicarbonate loss
-bicarbonate dilution

71
Q

What causes an anion-gap acidosis versus a non-anion gap acidosis

A

-AG is the addition of fixed acids
-nonAG is the loss of bicarb

72
Q

What is the principal early manifestation of metabolic acidosis?

A

increased minute ventilation from increased tidal volume

73
Q

Why is the a loss of vasomotor tone and reduction of myocardial contractility for pH < 7.2?

A

catecholamine resistance develops

74
Q

Above what pH can you see ventricular irritability in metabolic alkalosis?

A

> 7.55

75
Q

How much should the PaCO2 increase for every 1mMol/L increase in HCO3 in metabolic alkalosis?

A

PaCO2 should increase by 0.7mmHg

76
Q

What should be the increase in HCO3 for every 1mmHg PaCO2 increase in acute respiratory acidosis? In chronic?

A

-acute = 3-4mEq/L
-chronic = 0.3mEq/L

77
Q

Which respiratory compensation is more common in hypercapnea and metabolic aciosis, increased tidal volume or increased respiratory rate?

A

increased tidal volume
-Kassmual respiration
-if acidemia is severe can reach 30L/min
-starts in 1-2 hours after onset of acidemia and reaches peak at 12-24hrs

78
Q

What is the equation to calcuate the expected PaCO2 d/t respiratory compensation in response to metabolic acidosis?

A

PaCO2 = 1.5 x measured HCO3 +8 (+/-2)

79
Q

What are potential indications for direct treatment of metabolic acidosis (and not just treating the cause)?

A

-pH < 7.1
-overt physiologic compromise attributable to acidosis
-excessive work of breathing required to maintain pH > 7.2

80
Q

How do you approximate the HCO3 deficit for HCO3 dosing?

A

HCO3 deficit = (0.5 x total body water) x (24 - HCO3)

81
Q

Reduced amounts of which electrolytes can inhibit the excretion of excess HCO3?

A

Hypokalemia hypomagnesemia hypochloremia

82
Q

What is the effect on the adrenal glands due to volume depletion?

A

Hyperaldosteronism (HCO3 retention K loss)
-aldosterone also promotes Na reabsorption leading to higher rates of Na+ for H+ exchange which worsens alkalosis

83
Q

What are the chloride responsive causes of metabolic alkalosis?

A
  • volume depletion
  • vomiting/diarrhea
  • NGT suctioning
  • diuretics (loop and thiazide type)
  • post-hypercapnia
  • medications (PCN)
84
Q

What are the chloride resistant causes of metabolic alkalosis?

A

-hyperaldosteronism
-exogenous steroids
-Cushing syndrome
-alkali ingestion

85
Q

What diuretic is preferred in pts in an edematous state (HF, cirrhosis, nephritis syndrome) to prevent metabolic alkalosis?

A

Acetazolamide
-dose 125 - 500mg
-carbonic anhydrase inhibitor that increases renal excretion of NaHCO3

86
Q

What are the causes of respiratory acidosis due to inhibition of the medullary respiratory center?

A

Acute
- meds (opiates, anesthetics, sedatives)
- oxygen in someone who has chronic hyperopia
- cardiac arrest
- OSA

Chronic
- obesity (Pickwickian syndrome)
- CNS disease
- metabolic alkalosis

87
Q

What are the causes of respiratory acidosis due to disorders of the chest wall?

A

Acute
- muscle weakness (MG, Guilain-Barre, hypokalemia, hypophosphatemia)

Chronic
- muscle weakness (SCI, ALS, MS, polio, myxedema)
- kyphoscoliosis
- extreme obesity

88
Q

What are the causes of respiratory acidosis due to gas exchange disorders?

A

Acute
- exacerbation of lung disease
- ARDS
- cardiogenic pulmonary edema
-PTX

Chronic
- COPD
- extreme obesity

89
Q

What are the causes of respiratory acidosis due to upper airway obstruction?

A
  • aspiration
  • OSA
  • laryngospasm
90
Q

What are symptoms of acute respiratory acidosis?

A
  • HA
  • blurred vision
  • restlessness
  • anxiety
  • tremors
  • asterixis
  • delirium
  • somnolence
  • CSF pressure can be elevated causing papilledema
  • hypotension if pH<7.1
91
Q

What are causes of respiratory alkalosis?

A
  • CNS disorders
  • agitation
  • pain
  • inappropriate mechanical ventilation
  • hypoxemia
  • restrictive diseases