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abg

arterial blood gases (ABGs)

introduction

  • 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.
  • the procedure is quite painful and risks local haematoma and arterial damage.

before you do an ABG

do you really need to do one?

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

is it safe to do one?

  • 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.

should you place an arterial line first?

  • 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.

what are these results?

  • 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;
      • 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)

interpretation of blood gas results

Step 1: Look at pH:

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

Step 2: Is the primary process respiratory or metabolic?

Technique I:
  • 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;
Technique II:
  • 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;

Step 3: is the degree of compensation appropriate?

if primary metabolic condition:
  • 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
if primary respiratory condition:
  • 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;

Step 4: is there a mixed disorder where 2 or more primary acid-base abnormalities co-exist?

  • 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.
double acid-base disturbances:
  • if pH is normal:
    • PaCO2 low ⇒ metabolic acidosis + resp. alkalosis
      • eg. sepsis, liver disease, salicylate OD
    • PaCO2 normal:
      • ⇒ no acid-base disturbance
        • 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
triple acid-base disturbances:
  • 2 possible combinations:
      • ethanol abuser with ketoacidosis, vomiting, febrile, agitated with delirium tremens
        • ⇒ hypocapnia (not compensatory), alkalaemia, raised anion gap
      • COAD pt Rx with frusemide & has developed worsening hypoxia & lactic acidosis
        • ⇒ severe hypercapnia, mild acidaemia, raised anion gap, severe hypoxaemia
abg.txt · Last modified: 2013/08/15 17:45 (external edit)