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ABGs > Overview (Cameron's) > Flashcards

Overview (Cameron's) Flashcards

1
Q

What are the indications for an arterial blood gas?

A
  • To assess gas exchange and ventilation
    • To monitor gas exchange and ventilation in response to interventions/therapy
    • Identification of acid-base disorders
    • Monitoring of acid-base disorders in response to interventions/therapy
    • Identification of dyshaemoglobinaemias
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2
Q

What are complications of arterial cannulation?

A

Haematoma, local infection, bleeding, sepsis, pseudoaneurysm formation

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3
Q

Describe the normal reference ranges for pH, paO2, pCO2, HCO3- and base excess at an fiO2 of .21

A

pH 7.35-7.45, paO2 80-100, paCO2 35-45, HCO3- 22-26, base excess -2 to +2

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4
Q

What equation describes the oxygen content in blood?

A
  • Arterial oxygen content = Hb x oxygen saturation x 1.39 (paO2 x 0.0031)
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5
Q

Is paO2 or oxygen saturation more important when it comes to oxygen delivery to the tissues?

A
  • Oxygen saturation

* Arterial oxygen content = Hb x oxygen saturation x 1.39 (paO2 x 0.0031)

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6
Q

How is hypoxaemic respiratory failure defined?

A

A clinically significant decreased in PaO2 usually to be less than 60 mmHg

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7
Q

Why is a PaO2 value of 60 important with regards to the oxygen-Hb dissociation curve?

A

For any drop in PaO2 below 60 the oxygen saturation falls precipitously with any further decrease in PaO2

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8
Q

What are four factors that cause the oxygen dissociation curve to move left and right?

A

Temperature, acidosis/alkalosis, PaCO2 and 2, 3-DPG

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9
Q

What changes to the four factors that shift the oxygen dissociation curve move the curve left?

A

Decrease in PaCO2, fall in temperature, alkalosis and fall in 2,3-DPG concentration

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10
Q

What changes to the four factors that shift the oxygen dissociation curve move the curve right? What is the result?

A
  • Increase in PaCO2, temperature rise, acidosis and increases in 2, 3-DPG concentration
    • Facilitates more effective delivery of oxygen to peripheral tissues which is beneficial in the presence of hypoxia
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11
Q

What is the PaO2 when approx 50% of haemoglobin is saturated with oxygen?

A
  • 26.6 mmHg
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12
Q

How can you evaluate a patient’s oxygenation from an ABG?

A
  • PAO2 = FiO2 (Patm - PH2O) - (PaCO2)/R

* where Patm = 760, pH2O = 47 and R = 0.8

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13
Q

What is a normal range for the P(A-a)O2? What increases it?

A
  • P(A-a)O2 = Age/4 + 4

* Increases in cigarette smoking, increasing fiO2 and advanced age

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14
Q

What are the 5 possible causes for hypoxaemia?

A
  • Decreased inspired fractional oxygen (high altitudes)
    • Impaired diffusion - interstitial fibrosis thickens the membrane (rare, because diffusion usually is done in 1/3 of the circulatory time available)
    • Shunting
    • Ventilation-perfusion (V/Q) mismatch
    • Hypoventilation
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15
Q

What are the different types of shunts?

A
  • Extrapulmonary - acquired or congenital cardiac abnormalities - septal defects
    • Intrapulmonary - severe pneumonia, atelectasis, pulmonary AV malformation, hepatopulmonary syndrome
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16
Q

Under normal physiology what is the V/Q ratio normally? Why?

A

V/Q ratio is normally 0.8. This is because perfusion is more pronounced at the lung bases and ventilation is more pronounced at the lung apices

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17
Q

What are non-perfused alveolar units referred to as?

A

Physiological dead space

18
Q

Give an example where the V/Q ratio is 0 and one where the V/Q ratio is infinity.

A

V/Q ratio of 0 occurs in shunt (alveoli are not ventilated but are perfused)

V/Q ratio of infinity occurs in fully ventilated but unperfused alveoli (massive PE)

19
Q

How can you pick up a V/Q mismatch clinically?

A

Increased alveolar-arterial PO2 gradient

20
Q

What does the alveolar gas equation tell us about the relationship between oxygen and carbon dioxide partial pressures?

A
  • Significant alveolar hypoventilation can result in proportional decrease in alveolar oxygen
    • Thus, an increase in PaCO2 will be associated with a decrease in PAO2
21
Q

How can you determine if hypoxaemia is secondary to hypercapnoea/hypoventilation or due to a V/Q mismatch/shunt?

A
  • If the (A-a)PO2 is normal - secondary to hypercapnoea

* If increased - secondary to shunt or V/Q mismatch

22
Q

What is a recommended approach to the evaluation of respiratory failure using ABGs?

A
  1. Confirm hypoxaemia - PaO2 <60 +/- SaO2 <90%
    1. Establish if there is an increased alveolar-arterial oxygen tension gradient (A-a)O2 (PAO2 = fiO2 (713) - PaCO2/0.8)
    2. Is there evidence of hypoventilation? PaCO2 is <50 there is alveolar hypoventilation
    3. Hypoxic altitude if hypoxaemia, normal (A-a)PO2 and the PaCO2 is not elevated
    4. Is the hypoxaemia entirely accounted for by hypoventilation (CNS depression, respi mm failure)? –> the (A-a)PO2 gradient is normal (<15) in this case. If the (A-a)O2 gradient is elevated (>15) then pneumonia/ARDS are likely causative
    5. If PaCO2 is normal, hypoxaemia is present and there is a raised (A-a)O2 gradient then response to oxygen discriminates between shunt and V/Q mismatch (shunt - does not improve, V/Q mismatch - does improve)

(Insert flow chart)

23
Q

Fill in the primary acid-base disorder table:

A
  • Respiratory acidosis: ↓ pH, ↑ CO2, ↑ bicarbonate compensation
    • Respiratory alkalosis: ↑ pH, ↓ CO2, ↓ bicarbonate compensation
    • Metabolic acidosis: ↓ pH, ↓ HCO3, ↓ CO2 compensation
    • Metabolic alkalsosis: ↑ pH, ↑ HCO3, ↑ CO2 compensation
24
Q

Describe the recommended approach to acid-base disorders:

A
  1. Determine if there is alkalaemia or acidaemia present
    1. Determine the primary disturbance - is it respiratory or metabolic. Established by assessing the relationship between the pH and pCO2 direction of change
    2. Assess whether the primary disturbance has been compensated (the 6 formulae…). If the anticipated compensation is not present, it is likely that a mixed acid-base disorder exists
    3. Calculate the anion gap in the presence of metabolic acidosis (high or normal)
    4. If there is an increased anion gap present then determine the delta ratio to establish if there is a mixed acid-base disorder
    5. Identify the ‘initiating factor’ if the gas reflects a metabolic alkalosis + a reason for the kidney not to be excreting bicarb appropriately

(Insert picture)

25
Q

What is the formula to predict compensation for metabolic acidosis?

A

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

26
Q

What is the formula to predict compensation for acute respiratory acidosis?

A

For every 10 mmHg increase in PCO2 the HCO3- should increase by 1 mmol/L

27
Q

What is the formula to predict compensation for chronic respiratory acidosis (> 3-5 days)?

A

For every 10 mmHg increase in the PCO2 the HCO3- should increase by 3-4 mmol/L over 4 days

28
Q

What is the formula to predict compensation for metabolic alkalosis?

A

PaCO2 = 0.8 x HCO3- + 20

29
Q

What is the formula to predict compensation for acute respiratory alkalosis?

A

For every 10 mmHg decrease in PCO2 the HCO3- should decrease by 1 mmol/L

30
Q

What is the formula to predict compensation for chronic respiratory alkalosis?

A

For every 10 mmHg decrease in PCO2 the HCO3- should decrease by 2 mmol/L

31
Q

What are the causes of high anion gap metabolic acidosis? Give examples.

A
  • Lactic acidosis and ketoacidosis
    • Shock, hypoxia, liver failure, sepsis, haem malignancies, renal failure, thyroid storm, drug induced, inborn errors of metabolism (G6PD), diabetic/alcoholic/starvation ketoacidosis
32
Q

List 5 drugs that may cause a high anion gap metabolic acidosis:

A

Paracetamol, biguanides, cocaine, diethyl ether, adrenaline, ethanol, ethylene glycol, isoniazide, methanol, antiretroviral therapy, salbutamol

33
Q

What are the causes of normal anion gap metabolic acidosis?

A
  • Renal bicarbonate loss: tubulo-interstitial renal disease, renal tubular acidosis types 1, 2 and 4
    • GI bicarbonate loss: diarrhoea, colostomy, ileostomy, enteric fistulas, use of ion-exchange resins
    • Drugs: carbonic anhydrase inhibitors (acetazolamide)
    • Endocrine: hypoaldosteronism, hyperparathyroidism
    • Excess chloride: rapid sodium chloride infusion
34
Q

How do you calculate the anion gap?

A

Anion gap = [Na+] - [Cl-] +[HCO3-] = 12 +/- 2

35
Q

What must you automatically think of if you have a patient with a high anion gap? What else will be true in this circumstance?

A
  • A toxic ingestion of methanol or ethylene glycol should be suspected if there is no lactic or ketoacidosis clinically
    • A high osmolal gap (>10 mmol/L)
36
Q

What is a high osmolal gap and how do you calculate it?

A
  • > 10 mmol/L
    • Osmolal gap = measured - calculated serum osmolality
    • Osmlolal gap = measured osmolality - 2x [Na] + glucose + urea –> if this is higher than 10 it is high
37
Q

What is the delta ratio, how do you calculate it and what is its use?

A
  • Delta ratio is used to establish if there is a mixed acid-base disorder when there is a raised anion gap
    • Delta ratio = (measured anion gap - 12) ÷ (24 - [HCO3-]
    • Magnitude of the delta ratio can range from <0.4 to >2 and allows a differential diagnosis in metabolic acidosis to be refined
38
Q

How do you interpret the delta ratio and what do different values mean?

A
  • <0.4 = normal anion gap hyperchloraemic metabolic acidosis
    • <1 = combine high and normal anion gap acidosis
    • 1-2 = isolated high anion gap metabolic acidosis
    • > 2 = mixed high anion gap metabolic acidosis and alkalosis
39
Q

What are the possible causes of metabolic alkalosis?

A
  • GI hydrogen ion loss (NG suction, vomiting, villous adenomas, gastrocolic fistulae, chloride-loosing diarrhoea)
    • Renal hydrogen loss (loop/thiazide diuretics, hypocalcaemia, Bartter or Gitelman syndrome)
    • Transcellular hydrogen ion shift into cells (hypokalaemia)
    • Exogenous alkali (NaHCO3- administration, gluconate, acetate, citrate load with massive transfusion, excess antacids/milk alkali syndrome)
    • Contraction alkalosis (sweat loss in CF, loop/thiazides, achlorhydria, factitious diarrhoea including laxative abuse)
    • Endocrine (cushings, exogenous steroids, primary aldosteronism, mineralocorticoid excess)
40
Q

What can be said about the difference between ABG and VBG pCO2?

A
  • pCO2 is approximately 3-8 mmHg higher on a VBG

* When in doubt and clinical decisions hinge on pCO2 on a VBG –> do an ABG

41
Q

What needs to happen in order for metabolic alkalosis to be sustained? Causes?

A

Kidneys need to be unable to lose excess bicarbonate - usually secondary to hypovolaemia or reduced effective arterial blood volume (heart/liver failure), chloride depletion, hypokalaemia, renal impairment

42
Q

Which of the causes of metabolic alkalosis is not fluid/saline responsive?

A
  • Endocrine causes and Barrter’s/Gitelman’s syndromes

* Endocrine causes include exogenous steroids, Cushing’s, primary aldosteronism, mineralocorticoid excess

ABGs (2 decks)

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