ABG

Question 1

5 step approach to interpretation of ABGs

Answer 1

1. How is the patient?
2. Is the patient hypoxaemic?
   the Pa02 on air should be >10 kPa
3. Is the patient acidaemic (pH <7.35) or alkalaemic (pH >7.45)
4. Respiratory component: What has happened to the PaCO2?
   PaCO2 > 6.0 kPa suggests a respiratory acidosis (or respiratory compensation for a metabolic alkalosis)
   PaCO2 < 4.7 kPa suggests a respiratory alkalosis (or respiratory compensation for a metabolic acidosis)
5. Metabolic component: What is the bicarbonate level/base excess?
   bicarbonate < 22 mmol/l (or a base excess < - 2mmol/l) suggests a metabolic acidosis (or renal compensation for a respiratory alkalosis)
   bicarbonate > 26 mmol/l (or a base excess > + 2mmol/l) suggests a metabolic alkalosis (or renal compensation for a respiratory acidosis)

Question 2

normal pH range

Answer 2

7.35 - 7.45

Question 3

normal PaO2 range

Answer 3

10.7 - 13.3 kPa

Question 4

Normal PaCO2 range

Answer 4

4.7 - 6.0 kPa

Question 5

normal HCO3 range

Answer 5

22 - 26 mmol/L

Question 6

Base excess normal range

Answer 6

-2 to +2

Question 7

Lactate normal range

Answer 7

0.5-1 mmol/L

Question 8

what does a low PaO2 indicate?

Answer 8

A low PaO2 indicates hypoxia and respiratory failure

Question 9

what is type 1 resp failure? pathophysiology?

Answer 9

low PaO2, normal PaCO2 (1 thing wrong)
pH likely normal

ventilation/perfusion (V/Q) mismatch

As a result of the VQ mismatch, PaO2 falls and PaCO2 rises. The rise in PaCO2 rapidly triggers an increase in a patient’s overall alveolar ventilation, which corrects the PaCO2 but not the PaO2 due to the different shape of the CO2 and O2 dissociation curves. The end result is hypoxaemia (PaO2 < 8 kPa /60mmHg) with normocapnia (PaCO2 < 6.0 kPa / 45mmHg).¹

Reduced ventialtion and normal perfusion:
- pulmonary oedema
- bronchoconstriction
- pneumonia

Reduced perfusion with normal ventilation:
- pulmonary embolism

Question 10

what is type 2 resp failure? pathophysiology?

Answer 10

low PaO2, high PaCO2 (2 things wrong)

alveolar hypoventilation

eg:
- Pulmonary disease (COPD, asthma, pulmonary fibrosis, obstructive sleep apnoea)
- Reduced respiratory drive – can be a result of sedentary drugs, trauma or CNS tumour
- Neuromuscular disease – e.g. cervical cord lesion, diaphragmatic paralysis, polio, myasthaenia gravis
- Thoracic wall disease - e.g. Flail chest, kyphoscoliosis, hyperinflation, large pleural effusions, obesity, and thoracoplasty

Question 11

When to suspect resp acidosis? causes?

Answer 11

low pH
raised PaCO2

things that cause type 2 resp failure
- Pulmonary disease (COPD, asthma, pulmonary fibrosis, obstructive sleep apnoea)
- Reduced respiratory drive – can be a result of sedentary drugs, trauma or CNS tumour
- Neuromuscular disease – e.g. cervical cord lesion, diaphragmatic paralysis, polio, myasthaenia gravis
- Thoracic wall disease - e.g. Flail chest, kyphoscoliosis, hyperinflation, large pleural effusions, obesity, and thoracoplasty

Question 12

resp acidosis with metabolic compensation makes you think?

Answer 12

During an acute episode of respiratory acidosis, bicarbonate cannot be produced fast enough to compensate for the rising carbon dioxide.

Raised bicarbonate indicates that the patient chronically retains CO2. Their kidneys have responded by producing additional bicarbonate to balance the acidic CO2 and maintain a normal pH. This is seen in patients with chronic obstructive pulmonary disease (COPD). In an acute exacerbation of COPD, the kidneys cannot keep up with the rising level of CO2, so the patient becomes acidotic despite having higher bicarbonate than someone without COPD.

Question 13

when to suspect respiratory alkalosis? causes?

Answer 13

high pH
low PaCO2

This is due to hyperventilation

Respiratory alkalosis occurs when a patient has a raised respiratory rate and “blows off” too much CO2. They are breathing too fast and getting rid of too much CO2. There will be a high pH (alkalosis) and a low PaCO2.

Anxiety (i.e. panic attack) - will have high PaO2
Pain: causing an increased respiratory rate.
Hypoxia: resulting in increased alveolar ventilation in an attempt to compensate.
Pulmonary embolism - will have low PaO2
Pneumothorax
Iatrogenic (e.g. excessive mechanical ventilation)

Question 14

how to tell the difference between resp alkalosis caused by hyperventilation syndrome vs PE

Answer 14

Patients with a PE will have a low PaO2, whereas patients with hyperventilation syndrome will have a high PaO2.

Question 15

when to suspect metabolic alkalosis? cuases?

Answer 15

high pH
high HCO3- or high base excess

loss of H+
- diarrhoea + vomiting
- burns
- increased action of aldosterone (conns, liver cirrhosis, HF)

excess of HCO3-
- diuretics esp loop and thiazide
- ingestion of alkalotic substances

Question 16

when to suspect metabolic acidosis? causes?

Answer 16

low pH
low HCO3 / low BE

ABCD LKTR

Addisons
Bicarbonate loss (diarrhoea / renal failure)
Chloride excess
Drugs (acetazolomide diuretic)

Lactate
Ketones
Toxins
Renal failure (can’t excrete H+ well)

Question 17

what helps you differnetiate causes of metabolic acidosis? how do you do it?

Answer 17

calculating anion gap

Anion gap formula: Na+ – (Cl– + HCO3–)
The normal anion gap varies with different assays but is typically between 4 to 12 mmol/L.

High anion gap = increase in organic acids that aren’t accounted for in the equation

Question 18

anion gap formula

Answer 18

Na+ – (Cl– + HCO3–)

Question 19

what is a anion

Answer 19

negatively charged chemical species

Question 20

what is a cation

Answer 20

positively charged chemical species

Question 21

when to suspect mixed repiratory and metabolic acidosis

Answer 21

↓ pH
↑CO2
↓HCO3–

Causes of mixed respiratory and metabolic acidosis include:
Cardiac arrest
Multi-organ failure

Question 22

when to suspect mixed respiratory and metabolic alkalosis

Answer 22

↑ pH
↓ CO2
↑ HCO3–

Causes of mixed respiratory and metabolic alkalosis:
Liver cirrhosis in addition to diuretic use
Hyperemesis gravidarum
Excessive ventilation in COPD

Question 23

What would an ABG show acute asthma

Answer 23

The more severe the obstruction, the lower the PaO2 will be

Low CO2 and resulting respiratory alkalosis suggests that the patient is breathing hard and blowing of CO2

Normal CO2 suggests the patient may be tiring and is a sign of life-threatening asthma

High CO2 is a sign of near-fatal acute asthma as the patient is no longer breathing well. if the patient becomes hypercapnic they are likely to become acidotic. In very severe cases this can result in metabolic acidosis.

Question 24

signs of co2 retention

Answer 24

Confusion – as a result of peripheral vasodilation
Asterixis (renal failure, type 2 resp failure, liver failure)
Warm extremeties
Bounding pulse
Morning headache – CO2 particularly high at these times.

Question 25

if someone with copd and co2 retention needs treatment for type 2 resp failure

Answer 25

in an acute setting, if unknown or very unwell give 15L 100% O2 NRM

if known retentive:
Give controlled oxygen therapy, starting at 24% O2
Recheck the ABG after 20 minutes – if the PaCO2 is steady or lower, then you can increase the O2 to 28%.
If the PaCO2 has risen >1.5kPa– then consider giving a respiratory stimulant such as doxapram (1.5-4mg/min IV) or assisted ventilation.
You can also see CO2 retention as physical signs – the patient will become drowsy and confused
If this fails consider intubation / ventilation

Question 26

pathophysiology respiratory failure in copd

Answer 26

Significant ventilation/perfusion mismatching with a relative increase in the physiological dead space leads to hypercapnia and hence acidosis. This is largely the result of a shift to a rapid shallow breathing pattern and a rise in the dead space/tidal volume ratio of each breath. This breathing pattern results from adaptive physiological responses which lessen the risk of respiratory muscle fatigue and minimise breathlessness.

Question 27

how may diuretics cause metabolic alkalosis

Answer 27

Normal kidneys are very effective at excreting bicarbonate. Diuretics prevent the re-absorption of sodium from the renal tubule, and thus they promote sodium loss. The normal mechanism for recovering this sodium, involves an exchange with bicarbonate, and thus the ability of the renal tubule to excret bicarbonate is reduced.

Question 28

aldosterone and metabolic pH disturbance

Answer 28

aldosterone is responsible for the resorption of Na and H2O, and the excretion of K+ and Cl-

sodium reabsorption in the distal tubule is linked with acid/hydrogen ion (H+) secretion

high aldosterone –> lots of H+ secreted = metabolic alkalosis

low aldosterone eg addisons–> H+ not secreted = metabolic acidosis

Question 29

when to be concerned about type 2 resp acidosis? when not to be?

Answer 29

acute ie no raise in HCO3-

acute on chronic ie raised HCO3- but still low pH

not concerned if chronic type 2 resp failure ie fully compensated resp acidosis - make target sats 88-92