I’m going to focus on Arterial blood gases here. Venous gases are close enough in well people, but beware in critical illness there is divergence between arterial and venous samples, particulary in CO₂, lactate and pH.

Method

• Oxygenation – IF FiO₂ present, determine A-a gradient
  • Calculated alveolar oxygen tension: A = (760 – 47) x FiO₂ – 1.25 x CO₂ **
    or
    A = 713 x FiO₂ – 1.25 x CO₂
  • A-a gradient = A – a(measured PaO₂)
  • Normal A-a gradient (conservatively) is < (age / 4) + 4 or, increases by 1 for every decade of life
    • Think of it as ~10 at age 20, and ~20 by the time you reach 100
  • ** technically the 1.25 x CO2 is actually (CO2 / RQ) where RQ is the respiratory quotient (usually 0.8), but honestly who has the time?

• pH

• Primary process
  • Respiratory or metabolic?
  • Physiological acid/base processes never overcompensate

• Compensation – Boston rules (main alternative is Copenhagen method)
  • Respiratory -osis (“1425”)
    • Acute Acid-: “up 1:10”
      Expected HCO₃^– = [1 x (PaCO₂ – 40) / 10] + 24
    • Chronic Acid-: “up 4:10”
      Expected HCO₃^– = [4 x (PaCO₂ – 40) / 10] + 24
    • Acute Alkal-: “down 2:10”
      Expected HCO₃^– = [2 x (PaCO₂ – 40) / 10] + 24
    • Chronic Alkal-: “down 5:10”
      Expected HCO₃^– = [5 x (PaCO₂ – 40) / 10] + 24
  • Metabolic -osis
    • Acid-: Expected PaCO₂ = (1.5 x HCO₃^–) + 8
    • Alkal-: Expected PaCO₂ = (0.7 x HCO₃^–) + 20

• Anion Gap?
  • AG = Na – (HCO₃^– + Cl^–)
  • Normal = 12 +/- 4
  • ** Albumin adjustment
    • Albumin makes up ~75% of the anion gap. Reduced albumin means the Anion Gap goalposts shift! Normal AG reduces by 1, for every 4g/L reduction in albumin below 40
    • Phosphate also significantly affects the AG, but it’s a smaller component so I choose to ignore it for now (well, technically the normal AG is Alb/4 + 1.5xPO₄^3-, but you didn’t hear it from me)
    • if you think about it… of the normal deficiency of anions (12, usually)…
      • 40 albumins make up 10 anions
      • 1.0 phosphates make up 1.5 anions
      • and the last 0.5 is made up of random piddly anions

• Delta Gap?
  • DG = (AG – 12) / (24 – HCO₃^–)
  • “A over B, Up over Down”
  • Interpretation:
    • < 0.4: Hyperchloraemic NAGMA (in addition to the HAGMA)
      Significant drop in bicarb without a change in anion gap. Remember AG = Na – (Cl^– + HCO₃^–) therefore if AG is not much different from normal, and HCO₃^– has dropped, then Cl^– must be high!
    • 0.4 – 0.8: HAGMA + NAGMA
      Often DG <1 in renal failure
    • 1-2: Pure HAGMA
    • >2: pre-existing metabolic alkalosis
      i.e. the HCO₃^– started high, and even though it’s dropped, it’s still closer to normal than it would have been without the met alk

• Osmolarity / Osmolar gap?
  • OG = Calculated Osmolar Gap (OG_c) – Measured Osmolar Gap (OG_m)
  • OG_c = 2 x Na⁺ + Urea + BSL + ETOH(mmol/L)
  • Converting ETOH
    • so, ETOH(%) = ETOH(g/dL)
    • ETOH(mg/dL) = ETOH(g/dL) x 1000
    • ETOH(mmol/L) = [1000 x ETOH(%)] / 4.6
    • Alternatively, ETOH(mmol/L) = 217 x ETOH(%)
  • Therefore, alternate formula: OG_c = 2 x Na⁺ + Urea + BSL + [217 x ETOH(%)]
  • Therefore, if we have Urea, BSL and ETOH(%) we can calculate the expected osmolarity
  • Normal OG <10
  • NB we calculate osmolaRity (by volume) but measure osmolaLity (by weight) so it’s all a bit silly, but the gap helps nonetheless

• Significant electrolyte changes
  • Sodium correction in hyperglycaemia – Pseudohyponatraemia
    • Corrected sodium = measured sodium, plus 1/3 of the glucose change above 5
      or, in formula format:
      cNa⁺ = mNa⁺ + [(BSL – 5) / 3]
  • Hypocalcaemia can suggest ethylene glycol intoxication if the other prerequisites are there (HAGMA, OG>10)

Differential Diagnosis

HAGMA (CATMUDPILES or LTKR)

NAGMA (CAGE, ABCD, HARDUPS, USEDCRAP or PANDARUSH)
(shamelessly pilfered from various sources such as LITFL, Deranged Physiology and my own training programme. You should really visit those sites, as they’re much better.)

LAGMA (BLUE)

• Bromide overdose (pseudohyperchloraemia)
• Low albumin, low phosphate (but if you consider this to simply change the definition of ‘normal’ then it doesn’t really fit here)
• Unmeasured cations (Multiple myeloma, raised Ca²⁺, raised Mg²⁺, Lithium overdose, Polymixin B)
• Errors in measurement (raised Na⁺, raised lipids, raised viscosity, iodide ingestion)

Metabolic Alkalosis (CLEVERR)

• Contraction (volume)
• Licorice / diuretics
• Endocrine (hyperaldosteronism [Conn’s synd], Bartter’s, Cushing’s)
• Vomiting / NG suction (chloride loss)
• Excess alkali (antacids, milk-alkali syndrome, dialysis)
• Refeeding alkalosis
• Renal bicarbonate retention (hypochloraemia, hypokalaemia, chronic hypercapnoea)

Acute Respiratory Acidosis (many causes, here are a few)

• Obtundation
• Opiates
• Obstructive lung disease (exac COPD, asthma)

Chronic Respiratory Acidosis (many, here are a few)

• Chronic obstructive lung disease
• Neuromuscular disorders eg CIDP/MG

Acute Respiratory Alkalosis (CHAMPS)

• CNS disease (raised ICP)
• Hypoxia (altitude, anaemia, VQ mismatch)
• Anxiety
• Mechanical hyperventilation
• Progesterone, pregnancy
• Sepsis, salicylates, other toxins (nicotine, xanthines)

Chronic Respiratory Alkalosis (not many; here are most of them, some are just the acute ones, for longer)

• rare, also can be fully metabolically compensated (unique, amongst acid-base disorders)
• Chronic hypoxaemia
  • Congenital heart disease
  • Chronic altitude compensation
• Hyperthyroidism