Arterial blood gas Flashcards

1
Q

How is a Modified Allen’s test performed?

A
  1. Patient clenches fist
  2. Apply pressure over the radial and ulnar artery to occlude both vessels
  3. Ask patient to open hand which should now appear blanched.
  4. Remove pressure from the ulnar artery whilst maintaining pressure over radial artery
  5. If there is adequate perfusion from ulnar artery, normal colour should return within 5-15 seconds.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What is the importance of Modified Allen’s test in an ABG?

A

Assess the collateral arterial supply of the hand from the ulnar artery i.e., to make sure the hand isn’t completely reliant on the radial artery for its blood supply, in which case sampling should be avoided.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What is the technique for doing an ABG?

A
  1. Remove equipment from packaging, attach needle to pre-heparinised ABG syringe, position hand with wrist extended by 20-30 degrees
  2. Palpate radial artery and identify a distal site where artery is most pulsatile
  3. Clean area for 30 seconds and allow to dry
  4. Wash hands again and don an apron and gloves
  5. Administer subcutaneous lidocaine and aspirate to ensure not in a blood vessel before injecting the LA. Allow at least 60 seconds for the LA to work
  6. Flush through the heparin from the syringe of the ABG
  7. Palpate radial artery around 1cm proximal to the planned puncture site
  8. Hold ABG syringe like a dart and insert at 30-45 degrees angle
  9. Advance needle towards pulsation until you feel sudden reduction in resistance and see flashback. The syringe should now fill in a pulsatile manner
  10. Once required amount of blood has been collected, remove the needle and apply firm pressure.
  11. Gauze, discard needle, place cap on ABG syringe and expel any air from the sample if present
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What are the indications for an ABG? (x7)

A

To assess oxygenation levels, respiratory derangements, metabolic derangements, acid-base status, carboxyhaemoglobin in CO poisoning, assess lactate (for sepsis), and gain preliminary results for electrolytes and Hb.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What are the contraindications of ABG? (x4)

A

Peripheral vascular disease, cellulitis surrounding site, and arteriovenous fistula in situ are absolute contraindications. Impaired coagulation is a relative contraindication.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What are sources of sampling error in ABGs? (x3)

A

Presence of air in the sample distorts blood gases, an improper quantity of heparin in syringe, delay in specimen delivery (increases paCO2)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What are the complications of an ABG? (x5)

A

Haematoma, nerve damage, arteriospasm, arterial aneurysm, vaso-vagal response of fainting

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What is the normal range for pH in an ABG?

A

7.35-7.45

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What is the normal range for pCO2 in an ABG?

A

4.5-6.0 kPa

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What physiological factors result in low pCO2? (x2)

A

Large tidal volume, increased RR.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What is the normal range for pO2 in an ABG?

A

10-14 kPa

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What is the normal range for HCO3 in an ABG?

A

22-26 mmol/l

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What is the buffer equation that controls pH in the blood?

A

CO2 + H2O <=> H2CO3 <=> HCO3- + H+ catalysed by carbonic anhydrase

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What is the normal range for BE in an ABG?

A

-2 to +2

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What is the normal range for lactate in an ABG?

A

0.5-1 mmol/l but less than 2 when acutely ill.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

How is lactate produced?

A

By-product of anaerobic respiration. Therefore, it is raised in exercise, hypoxia and ischaemia.

17
Q

What drugs induce hyperlactatemia?

A

Metformin.

18
Q

What is the normal range for Hb in an ABG?

A

115-160 g/l

19
Q

What is the normal range for Na+ in an ABG?

A

135-145 mmol/l

20
Q

What is the normal range for K+ in an ABG?

A

3.5 – 5.5 mmol/l

21
Q

What is the normal range for Ca2+ in an ABG?

A

1.10 – 1.35 mmol/l

22
Q

How must serum calcium be corrected? Note about ABG?

A

Corrected for amount of albumin present in the blood as calcium is protein bound in circulation. ABG samples will not correct this since it does not measure serum albumin.

23
Q

!!! What happens to serum calcium in acid-base disturbances? How does this manifest physically?

A

Acidosis increases ionised calcium levels due to DECREASED protein binding. Opposite trend in alkalosis. In alkalosis, patients may experience peri-oral paraesthesia which is caused by a reduction in calcium dissociation (hypocalcaemia).

24
Q

What is the normal range for Cl in an ABG?

A

95 – 105 mmol/l

25
Q

What is FO2Hb?

A

Fractional haemoglobin – measure of how much of the Hb is oxyHb.

26
Q

What is FCOHb?

A

Fractional carboxyhaemoglobin – measure of how much of the Hb has CO bound reversibly to it

27
Q

How much added affinity does CO have to Hb compared with oxygen?

A

x200

28
Q

What is FMetHb?

A

Fractional methaemoglobin – formed when ferrous iron ions (Fe2+) in the heme groups are oxidised to ferric iron (Fe3+). Methaemoglobin is unable to combine with oxygen.

29
Q

How do you interpret an ABG? (x7)

A
  1. Introduce
  2. pH
  3. Metabolic vs respiratory
  4. Compensation?
  5. If respiratory, acute or chronic?
  6. Respiratory failure?
  7. Anion gap?
30
Q

How do you introduce an ABG? (x4 parts)

A

State what the investigation is (ABG), who from, date and time taken, and whether they were on breathing air or oxygen delivery.

31
Q

What characterises acute and chronic respiratory acidosis/alkalosis?

A

Acute sees no alteration in bicarbonate levels. In chronic cases, the kidney will attempt to buffer the pH abnormalities by increasing/decreasing bicarbonate. If there is significant increase/decrease, then the event is chronic.

32
Q

What are the signs of Type 1 respiratory failure on an ABG?

A

Reduction in oxygen content of the blood less than 8 kPa.

33
Q

What are the signs of Type 2 respiratory failure on an ABG?

A

Reduction in oxygen content of the blood less than 8 kPa and rise in CO2 content above 6 kPa.

34
Q

!!! How does the mechanism and aetiology of Type 1 and Type 2 respiratory failure differ?

A

Type 1 is a failure of oxygen transfer from the air to blood; Type 2 is a failure of ventilation due to inability of lungs to move air in and out effectively. Type 1 is caused by pneumonia (failure of oxygen to get to and through alveoli), PE (failure of blood to pass through some lung tissue), and pulmonary fibrosis (failure of oxygen to diffuse through fibrosed lung). Type 2 is caused by opiate overdose (reduced RR), COPD (excess mucus and airway resistance), and neuromuscular disease (MND or Guillain-Barre syndrome).

35
Q

What is the anion gap? Significance?

A

Difference between the measured cations (Na+, K+) and anions (Cl-, HCO3-). The total number of cations should be equal to the total number of anions, but the ABG doesn’t measure all types of ions. As such, the anion gap represents these missing or unmeasured anions. The anion gap is calculated with a metabolic acidosis to help work out underlying aetiology.

36
Q

What is the normal range for anion gap?

A

6 – 12 mEq/l

37
Q

What are the causes of a raised anion gap acidosis?

A

MUD PILES: methanol, uraemia, diabetic ketoacidosis, paracetamol, iron/isoniazid (antibiotic), lactate, ethanol/ethylene glycol, salicylates (aspirin)

38
Q

What is normal anion gap acidosis? Doesn’t make sense to me!

A

Acidosis but normal anion gap due to loss of bicarbonate levels. As there is only one other buffering ion (chloride), the acidosis must be compensated for by increasing chloride. This is known as hyperchloremic acidosis. HCO3 can be lost through diarrhoea, or due to drugs which increases excretion.