ABGs

 

• Indications

  • New hypoxia.
  • Suspected pH change.
  • Acutely unwell patient.

  Parameters and their significance

  • pH: is there acidosis/alkalosis?
  • PaCO2: opposite to pH if respiratory cause e.g. ↓pH and ↑CO2 = respiratory acidosis.
  • PaO2: hypoxaemia is <8 kPa, and <10.5 kPa is abnormal ('mild' hypoxaemia). If on oxygen therapy, should be around 10 below FiO2.
  • HCO3-: matches pH if metabolic cause e.g. ↓pH and ↓HCO3 = metabolic acidosis.
  • Base excess: how much H+ needed to return pH to 7.35. Normal range is -2 to 2. High when HCO3- is high, and vice versa, but also takes into account other bases.

  Procedure

  1. Wash hands, get equipment, and get consent. Make note of oxygen therapy and O2 sats.
  2. Some recommend using Allen's test to check the collateral ulnar circulation. However, it is not in BTS guidelines and a number of studies have found that the test is of little utility.
  3. Offer local anaesthesia.
  4. Palpate pulse, clean area, don gloves.
  5. Insert needle at 30-45° and allow to fill.
  6. Remove, cover needle, and apply pressure to site with gauze or cotton wool for 5 minutes to reduce haematoma.
  7. Dispose of needle, expel bubbles, and check results. Sats should match those of the finger probe; lower levels suggests venous sample.

  Minimizing the pain of ABGs

  ABGs hurt and shouldn't be done unless they're needed. Do VBGs where possible, and offer local anaesthesia if not.

  Venous blood gas (VBG):

  • VBGs hurt much less, and give an accurate measure of pH, HCO3- (venous is around 1 mmol/L higher than arterial), and lactate. So if that's what you need to know (e.g. in DKA, sepsis), they are preferable.
  • In general, VBGs cannot accurately measure PaO2 and PaCO2, though there is evidence that they can rule out hypercapnia in COPD (if PvCO2 <6 kPa). You can roughly estimate the arterial PaCO2 by subtracting 0.7 kPa from the venous PvCO2.

  Local anaesthesia:

  • BTS guidelines say that local anaesthesia should be offered for all ABGs, except in emergencies or if the patient is unconscious.
  • Give 0.1-0.2 ml of 1% lidocaine via subcutaneous injection with an insulin syringe, aspirating before injecting. Warming the lidocaine and injecting slowly reduce the sting. Allow 60-90 seconds for it to take effect before doing the ABG.

• Respiratory failure

  Definitions

  • Respiratory failure: PaO2 <8 kPa.
  • Hypoxia: inadequate tissue oxygenation.
  • Hypoxaemia: low arterial O2 levels.
  • Can have hypoxia without hypoxaemia. There are 4 types of hypoxia: cytotoxic (e.g. cyanide), anaemic, hypoxic hypoxia (ventilation problem), or stagnant (shock).

  Type 1 respiratory failure

  • PaO2 <8 kPa + PaCO2 <6 kPa (normocapnia), due to impaired oxygenation.
  • Hyperventilation may occur in response, leading to low CO2.
  • May respond to CPAP.

  Causes

  • ↓Alveolar ventilation. Due to alveolar collapse or congestion – pulmonary oedema, pneumonia, atelectasis (e.g. pneumothorax), ARDS, pulmonary haemorrhage – or airway obstruction (asthma, COPD, foreign body). Causes ↓V/Q, or in its extreme form, 'shunt' (V/Q = 0).
  • ↓Alveolar perfusion: PE. Causes ↑V/Q , or in its extreme form, 'dead space' (V/Q = ∞).
  • ↓O2 intake: hypoventilation or low FiO2 (high altitude).
  • Right to left cardiac shunt (aka anatomic shunt).

  Type 2 respiratory failure

  • PaO2 <8 kPa + PaCO2 >6 kPa (hypercapnia), due to impaired ventilation. Some definitions do not require hypoxia to be present.
  • Causes: COPD, opiate OD, respiratory muscle failure. May be seen in severe asthma when respiratory effort begins to fail.
  • May respond to BIPAP.
  • 'Chronic retainer': long-term respiratory acidosis (e.g. in COPD) which has been metabolically compensated leading to normal pH. Acute decompensation is when pH becomes acidotic.

• Metabolic acidosis and the anion gap

  The anion gap

  The anion gap estimates unmeasured ions (e.g. sulfates, proteins, ketoacids) to differentiate causes of metabolic acidosis. The formula is:

  Anion gap = Measured cations (Na+ ± K+) – Measured anions (HCO3- + Cl-)

  Normal range is 12±4 (Na+ only) or 16±4 (Na+ + K+). The fact that the normal range is +ve means there are usually more -ve than +ve unmeasured ions, hence 'anion' gap.

  Raised anion gap acidosis

  Due to ↓HCO3- without concurrent ↑Cl-. Caused by RAISED-MC:

  • Renal failure.
  • Aspirin, Amitriptyline (and other TCAs).
  • Infection (sepsis), Ischaemia, Iron, Isoniazid.
  • Starvation ketoacidosis.
  • Ethanol (via ↑lactate or ketoacidosis), Ethylene glycol.
  • DKA
  • Methanol, Metformin.
  • Cyanide, Carbon monoxide.

  Normal anion gap acidosis

  Due to hyperchloraemic acidosis. Caused by NORMAL:

  • NOrmal saline excess.
  • Renal tubular acidosis.
  • Mineralocorticoid antagonists e.g. spironolactone.
  • Addison's, Acetazolamide.
  • Loose stools.

• Metabolic alkalosis

  ↑HCO3- due to loss of H+ or gain of HCO3-.

  Causes

  H+ loss:

  • GI: vomiting
  • Kidneys: loop/thiazide diuretics → ↓K+ → ↓H+. Other causes of hypokalaemia can also cause metabolic alkalosis.

  HCO3- gain:

  • Excess intake: milk-alkali syndrome, antacids.
  • Rapid correction of chronic ↑CO2.