arterial and venous blood gases (ABGs/VBGs)

see also:

• clinical procedures in the ED
• acid-base physiology
• hypoxia
• Life in the fast lane blog (2010) - sometimes it is dangerous to attempt to normalise ABG abnormalities, consider these examples

• arterial blood gas is a sampling of arterial blood taken from either a direct needle aspirate of an artery, or from an arterial line (“art line”)
• it can provide valuable information on the acid-base status, ventilation status (via interpretation of the pCO2 level) and oxygenation.
• in addition, many ABG analyser machines also provide measures of Na, K, Hb, and ionised calcium.

• suspected carbon monoxide poisoning (assuming the analyzer has CoHB read outs)
• COPD exacerbation - moderate to severe with suspicion of carbon dioxide narcosis
• Critically unwell patients.
• Diabetic Ketoacidosis including suspected.
• Hyperkalaemia including suspected - although a serum U&E is cheaper and may be more appropriate
• Ischaemic bowel including suspected - although a serum lactate is cheaper and may be more appropriate
• Overdose with suspected acid-base disturbance e.g. toxic alcohol, massive / delayed paracetamol toxicity.

• a venous blood gas may provide you with sufficient data to assist your decision making and with less pain and risk to the patient.

• free flowing venous blood can be used if following taken into account:
  • pCO2 higher in venous by 7-8mmHg;
  • pH lower by 0.3-0.4;
  • calculated actual bicarb. higher by 1.8mM;

• patients with coagulopathy or likely to undergo thrombolysis may result in difficult to control local bleeding
• patients with inadequate collateral arterial supply eg. absent ulnar artery are at risk of arterial insufficiency if the artery is damaged.

• patients who are likely to need multiple ABGs may benefit from an arterial line which will also provide more accurate blood pressure recording, particularly those at risk of becoming hypotensive such as cardiogenic or septic shock.

• pH, PCO2, Cl-, Na+, K+, can be measured directly but the following need to be calculated:
  • Actual Bicarbonate:
    • from H-H equation above (ie. from pH & pCO2);
  • Std. Bicarbonate:
    • the bicarbonate level adjusted if pCO2=40:
      • the pt. where CO2 titration line intersects the bicarb. scale on Siggaard-Andersen curve nomogram;
  • CO2 titration line:
    • determined by buffer levels;
  • Base excess:
    • amount of acid or base that would restore 1L of blood to normal acid-base at pCO2=40;
    • about 1.2 x std. bicarb. deficit;
  • Anion gap:
    • = Na+ + K+ - Cl- - bicarbonate;
    • see anion gap
    • Normal = 9mEq/L (6-14mEq/L) if Cl determined using the newer ion-selective methods
    • NB. normally, divalent ions are approximately balanced out & so are ignored (ie. Ca, Mg, HPO4, SO4)
    • normal anion gap consists mainly of the net anionic nature of serum albumin
    • raised in:
      • ketoacidosis;
      • lactic acidosis;
      • other organic anions raised (see under metabolic acidosis with raised anion gap);
      • decr. plasma K+, Ca++, Mg++;
      • severe alkalaemia with dehydration (this causes a greater anionicity of higher [albumin] when pH is high)
    • lowered in:
      • incr. plasma K+, Ca++, Mg++;
      • decr. plasma albumin;
    • is there a mix of high anion gap and normal anion gap?
      • The Delta Gap ratio = (increase in Anion Gap / decrease in bicarbonate)
        • 0 - 0.4 = Normal anion gap metabolic acidosis
        • 0.4 - 0.8 = Normal + high anion gap metabolic acidosis
        • 0.8 - 2.0 = High Anion gap metabolic acidosis
        • >2.0 = (Metabolic acidosis + respiratory acidosis) or (Metabolic acidosis + metabolic alkalosis)

• if pH > 7.4 then primary alkalosis;
• if pH < 7.4 then primary acidosis;

• look at pCO2:
  • determine pH if pCO2=40 by:
  • adding 0.1 to pH for every 12mmHg reduction in pCO2 from 40;
  • subtracting at same rate for levels > 40;
  • if resulting pH > 7.40 then there is a metabolic alkalosis and if less then there is a metabolic acidosis;

• look at pCO2:
  • if pCO2>40, then there is resp. acidosis which is:
    • compensatory if there is a primary alkalosis;
    • primary event if there is a primary acidosis;

• PaCO2 (normal = 40) should have changed to compensate & should be:
  • equal to last 2 digits of pH (ie. 7.XX rule)
• also:
  • CO2 falls by 1 for each 1.3 fall in HCO3
  • CO2 rises by 6 for each 10 rise in HCO3

• HCO3 (normal = 24) should have changed to compensate & for each change of 10mmHg PaCO2 should change (to a max. of ~31-32) according to 1-2-3-4 rule:
  • 1mM for acute resp. acidosis
  • 2mM for acute resp. alkalosis
  • 3.5mM for chronic resp. acidosis (eg. COAD)
  • 4-5mM for chronic resp. alkalosis (eg. high altitude, pregnancy)
• also:
  • change in [H+] per unit change in PCO2:
    • resp. acidosis: acute = 0.8; chronic = 0.3;
    • resp. alkalosis: acute = 0.8; chronic = 0.17;

• look at anion gap to exclude presence of co-existing increased anion gap metabolic acidosis (eg. lactic acidosis)
• if raised anion gap consider checking osmolal gap & measuring lactic acid +/- salicylate, etc
• in general, only one primary respiratory condition exists at one time EXCEPT for chronic respiratory acidosis with superimposed acute respiratory alkalosis.

• if pH is normal:
  • PaCO2 low ⇒ metabolic acidosis + resp. alkalosis
    • eg. sepsis, liver disease, salicylate OD
  • PaCO2 normal:
    • ⇒ no acid-base disturbance
    • ⇒ metabolic acidosis + metabolic alkalosis
      • normal anion gap ⇒ vomiting & diarrhoea
      • raised anion gap:
        • ⇒ ketoacidosis or uraemia + vomiting
        • ⇒ lactic acidosis + diuretic Rx
  • PaCO2 raised ⇒ metabolic alkalosis + resp. acidosis
    • eg. chronic lung disease + diuretic Rx

• 2 possible combinations:
  • metabolic acidosis + metabolic alkalosis + resp. alkalosis:
    • ethanol abuser with ketoacidosis, vomiting, febrile, agitated with delirium tremens
      • ⇒ hypocapnia (not compensatory), alkalaemia, raised anion gap
  • metabolic acidosis + metabolic alkalosis + resp. acidosis:
    • COAD pt Rx with frusemide & has developed worsening hypoxia & lactic acidosis
      • ⇒ severe hypercapnia, mild acidaemia, raised anion gap, severe hypoxaemia