Interpretation of lung function and ABG Flashcards

The normal flow volume loop, changes in spirometry in restrictive and obstructive pathology, interpretation of an ABG, acid-base disturbance and compensation

1
Q

Normal flow-volume loop

A
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2
Q

Flow-volume loop in obstructive small airways disease

A

Initial ‘scalloping of the expiratory loop’ - while FVC (amplitude) is mostly retained - then as degree of obstruction progresses the amplitude falls due to dynamic airway collapse resulting in a fall in VC

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3
Q

Grading of severity of obstruction

A
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4
Q

Flow-volume loop in restrictive airways disease

A

Shape/morphology of the loop is preserved but amplitude is reduced. NB spirometry can only suggest restriction - need confirmation by measuring lung volumes

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5
Q

Flow-volume loop in fixed large airway obstruction e.g. circumferential invading tumours of trachea, tracheal stenosis following prolonged intubation

A

Limitation to both inspiration and expiration - resulting in plateauing of both the expiratory and inspiratory limbs of the loop

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6
Q

Flow-volume loop in variable obstruction of large airways (e.g. tracheal polyps, non-circumferential tumours with vocal cord paralysis) where the obstruction is intra-thoracic

A
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7
Q

Flow-volume loop in variable obstruction of large airways where the obstruction is extra-thoracic

A
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8
Q

Why perform an ABG?

A

1) To accurately assess causes of SOB or hypoxia
- by allowing calculation of Alveolar-arterial gradient i.e. A-a gradient, which is a global assessment of pulmonary gas exchange
- since normal O2 sats do NOT exclude a problem with ventilation!

2) Determine acid-base balance and assess for cause of acidaemia or alkalaemia

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9
Q

Step-wise approach to ABG interpretation (with regards to assessing causes of hypoxia, SOB)

A

1) Understand the indication - why was the test performed?
2) Ensure accurate record of the FiO2 at time of testing
3) pH n = 7.35-7.45, outside these is acidaemia and alkalaemia
4) PaO2 n = 80-100mmHg
5) PaCO2 n = 35-45mmHg
6) HCO3- n = 24-25mmol/L
7) O2 Sats (Hb) n = >94% NB: check against finger sats, if gas value is significantly lower consider accidental venous sampling
8) Na, K, Cl
9) Others - gluc, lactate

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10
Q

Validating an ABG sample

A

1) Calculate the hydrogen ion concentration using Henderson-Hasselbach equation

[H+] = 24 (PaCO2/ [HCO3-])

If the pH obtained differs substantially from the calculated value consider a sampling or analysis error and recollect

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11
Q

Calculating A-a gradient (Alveolar-arterial gradient)

When an ABG is obtained at Fi02 RA i.e. 21% the A-a gradient can be used to assess the ability of the oxygen to transfer from the alveolus into the bloodstream effectively. So… if A-a gradient is normal this argues AGAINST any parenchymal lung disease and point towards hypoventilation as a cause of the hypoxia

A

A-a at FiO2 0.21 at sea level = (150- (1.25PaCO2)) - Pa O2

Normal ~ (Age in years/4) + 4

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12
Q

When does respiratory acidosis occur?

A

When ventilation is inadequate to eliminate PCO2 at the same rate it is produced by the tissues

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13
Q

Compensation rules for respiratory acidosis

A

Acute response (mins to hrs):
[HCO3-] increases by 1mmol/L for every 10mmHg rise in PaCO2

Chronic response:
[HCO3-] increased by 4mmol/L for every 10mmHg rise in PaCO2

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14
Q

When does respiratory alkalosis occur?

A

When ventilation occurs at a level that eliminates CO2 in excess of that produced by metabolism

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15
Q

Compensation rules for respiratory alkalosis

A

Acute response (mins to hrs):
[HCO3-] decreases by 2mmol/L for every 10mmHg rise in PaCO2

Chronic response:
[HCO3-] decreased by 5mmol/L for every 10mmHg rise in PaCO2

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16
Q

When does metabolic alkalosis occur?

A

Through excessive loss of acidic fluid (e.g. prolonged vomiting), or excessive consumption of alkaline substances (e.g. Milk alkali syndrome via excessive ingestion calcium carbonate)

17
Q

Compensation rules for metabolic alkalosis

A

NB: all respiratory compensation is acute

Via hypoventilation, PaCO2 increases by 0.7mmHg for each mmol/L decrease in [HCO3-]

18
Q

When does metabolic acidosis occur?

A

Through excessive ACCUMULATION of acidic fluid
- can be endogenous e.g. increased [H+] associated with sepsis
- can be exogenous e.g. ethanol, methanol, salicylates

or

Through excessive LOSS of alkaline substances e.g. prolonged diarrhoea

19
Q

Compensation rules for metabolic acidosis

A

Occurs via hyperventilation

PaCO2 decreases by 1.2mmHg for each 1 mmol/L decrease in [HCO3-]

20
Q

Winter’s Formula - what is it used for?

A

Used in metabolic acidosis
Uses the patient’s HCO3- level to calculate what the appropriate respiratory compensation should be if this was a PURE metabolic acidosis - if it does not match with this, it means there might also be a primary respiratory issue i.e. acidosis or alkalosis going on

21
Q

Winter’s formula

A

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

If:
Measured CO2 = expected = appropriate respiratory compensation is occurring

Measured CO2 > expected = inadequate compensation or concurret respiratory acidosis

Measured CO2 < expected = concurrent respiratory alkalosis

22
Q

Normal anion gap calculation

A

([Na+] + [K=]) - ([Cl-] +[HCO3-]) = ~11 (largely attributable to the presence of albumin which is neg charged)

23
Q

What is the anion gap calculation used for?

A

For analysing whether a metabolic acidosis is due to a HAGMA or NAGMA as specific conditions fall into either category and this is useful for diagnosing the CAUSE of a metabolic acidosis

24
Q

Examples of NAGMA

A

Diarrhoea
Renal wasting
Chloride excess

25
Q

Examples of a HAGMA

A

Ketones
ETOH
Methanol
Uraemia
Ethylene glycol (antifreeze)
Isoniazid
Salicylates

26
Q
A