A Practical Approach To Blood Gasses (Acid Base Disorders)

Many textbooks and online resources contain too much information as the physiology of blood gasses is scarily complex (the exact physiology of metabolic alkalosis is still poorly understood). Thankfully, it's not nearly as difficult in clinical practice. Here is a method of interpreting blood gas (ABG/VBG) results; sans minutiae; with an easy-to-understand logical approach focusing on distilled, clinically-relevant axioms.

pH 7.35-7.45
CO2 35-45 mmHg
HCO3 22-30mmol/l
Anion Gap 15
Base Excess -3 to +3

1) Is it acidaemia (<7.35) or alkalaemia (>7.45)?
Acidosis is a pathological process causing the blood to become more acidic. You can have an acidosis and alkalosis simultaneously and have a normal pH. Hence the terms acidaemia and alkalaemia are more suitable.

2) Is it metabolic or respiratory in origin?
CO2 = acid, generally respiratory in origin.
HCO3 = base, generally metabolic in origin.
Acidaemia can be either caused by low HCO3 or high CO2. Inversely, alkalaemia can either be caused by high HCO3 or low CO2.

3) Are there excess organic acids? Check the Anion Gap! Na+K-Cl-HCO3
This figure tells you if there is extra acid, loss of bicarbonate, or both. Note that albumin is an anion that contributes significantly to the normal AG of 15. Hypoalbuminaemia causes the AG to be skewed lower. Infusing a patient with HCl will not increase the AG! Organic acids have anions that bind to HCO3 but the anions themselves are not counted in the equation. That's why the AG is useful. If AG>30, metabolic acidosis is present fullstop.

4) Just losing HCO3, without any excess organic acids (normal AG)?
GIT secretions are generally rich in HCO3, and diarrhea will cause the kidneys to compensate by adsorbing more Cl. In renal tubular acidosis, the kidneys dont readsorb enough HCO3 and retains too much Cl.

4) Look at the base excess (+-3) for severity of the metabolic disturbance.
This is simply the amount of acid (base if negative) required to bring the pH back to 7.4 in vitro, independent of pCO2.
BE +5 suggests mild metabolic alkalosis.
BE -12 suggests severe metabolic acidosis.

5) A simple way to look at compensation
Respiratory disturbances will change pCO2 (away from pCO2=40). The body uses HCO3 as a buffer, and hence HCO3 will rise/fall to counteract the gain/loss of CO2. 1425AcidBase. Remember...1.4.2.5.Acid.Base. In the chronic setting the body logically has more time to increase the HCO3 concentration so the second number is for chronic while the first is for acute.

• Acidosis: Every 10 pCO2 up, 1 or 4 HCO3 up.
  
• Alkalosis: Every 10 pCO2 down, 2 or 5 HCO3 down.

Metabolic disturbances on the other hand tend to be compensated by changing the pCO2. The rule of thumb for the change in pCO2 is even simpler to remember.

• The last two numbers of pH. eg. pH7.30, expect pCO2=30

In Practice:

Watch out for FALLING BICARBONATE / TACHYPNOEA in all patients
Because metabolic acidosis cannot be ignored. Do ABGs/VBGs. if pCO2 is not elevated...and HCO3 is low, then there is a metabolic acidosis.

• High AG (organic acids present): Left - Lactate; Total - Toxins (salicylates); Knee - Ketones; Replacement - Renal Failure
  
• Low Look at the AG equation. A metabolic acidosis (read: drop in HCO3) with a normal anion gap can only exist if Cl goes up. Thats why a normal AG metabolic acidosis is also known as a hyperchloremic metabolic acidosis. Think diarrhoea and RTA.
  

Credits:
This article is loosely based on a lecture (Approach to Acid-Base Disorders) by Dr Tim Crozier at Maroondah Hospital, Ringwood, VIC Australia.