Lab case 357 interpretation


PH = 7.025, that is severe acidaemia.

pCO2 = 116 mmHg, so we have respiratory acidosis.

Next, we calculate the compensation. For acute respiratory acidosis, we expected HCO3 to increase by 1 (from 24), for every 10 pCO2 above 40.

Accordingly, expected HCO3 (if the case was acute) should be: 24 + [(116 – 40) x 0.1] = 31.6

(for chronic respiratory acidosis, we expect HCO3 to increase by 4 for every 10 pCO2 higher than 10. According to that, the expected HCO3 if this case was chronic = 24 + 76 x 0.4 = 54.4).

Our HCO3 is 28.9 (we are going to use a value of 29 for the ease of calculation), slightly to the acidic side but we can argue that it is within accepted range.

Usually, we calculate the anion gap to check for the presence of HAGMA.

AG for this patient = Na – (Cl + HCO3) = 144 – (105 + 29) = 10, that is with in normal range. ?????

Other abnormal findings:

  • Hb = 198 g/L (high)
  • Glucose = 10 mmol/L (deranged random blood sugar. Expected with the release of stress hormones).
  • Lactate = 7.6, that is very high. (severe hyperlacataemia).

This is another case of reconsider calculation and assess the patient further:

These calculations don’t fit with the PH level that we have. If the case was just well compensated acute respiratory acidosis we should expect the PH to be close to normal. (The whole function of the Buffers systems is to bring PH back to normal).

On further history taking, that patient was alcoholic with history of metastatic cancer. He didn’t look after himself. He was brought after witnessed hypoxic cardiac arrest (secondary to an overdose). He had ROSC after 1 cycle.


Patient was started on BiPAP, and repeat VBG in 2 hours showed the following:

Ph = 7.22

pCO2 = 81

HCO3 = 32

Na = 142

Cl = 105

Lactate = 3.1


While the respiratory acidosis has improved, his bicarbonate level went higher. That will make us think that this patient’s bicarbonate is usually higher than normal (With treatment of respiratory acidosis, we expect the blood gases to get to what is normal for the patient).

Now we can say that that patient had severe respiratory acidosis with combined metabolic acidosis and alkalosis.

  • Acute respiratory acidosis is caused by respiratory arrest secondary to the overdose
  • Metabolic acidosis is caused by high lactate secondary to poor tissue perfusion during the arrest.
  • The metabolic acidosis cause is not clear yet. However, it looks like chloride-resistant (we need to check urinary chloride to confirm that.).


Repeat blood gases in 2 days showed the following

PH = 7.55

pCO2 = 38

HCO3 = 34

Na = 144

K = 3

Cl = 106

Lactate = 1.3

Creatinine = 42

Albumin = 32

Mg = 0.52


**** Bicarbonate retention alkalosis (Chloride-resistant -Urine chloride > mmol/L)

Shift of hydrogen ions into intracellular space – Seen in

  • ypokalemia. Due to a low extracellular potassium concentration, potassium shifts out of the cells. In order to maintain electrical neutrality, hydrogen shifts into the cells, raising blood pH.
  • Hyperaldosteronism – Loss of hydrogen ions in the urine occurs when excess aldosterone (Conn’s syndrome) increases the activity of a sodium-hydrogen exchange protein in the kidney. This increases the retention of sodium ions whilst pumping hydrogen ions into the renal tubule. Excess sodium increases extracellular volume and the loss of hydrogen ions creates a metabolic alkalosis. Later, the kidney responds through the aldosterone escape to excrete sodium and chloride in urine.
  • Excess glycyrrhizin consumption
  • Low levels of magnesium in the blood
  • Severely high levels of calcium in the blood
  • Bartter syndrome and Gitelman syndrome – syndromes with presentations analogous to taking diuretics characterized with normotensive patients
  • Liddle syndrome – a gain of function mutation in the genes encoding the epithelial sodium channel (ENaC) which is characterized by hypertension and hypoaldosteronism.
  • 11β-hydroxylase deficiency and 17α-hydroxylase deficiency – both characterized by hypertension
  • Aminoglycoside toxicity can induce a hypokalemic metabolic alkalosis via activating the calcium sensing receptor in the thick ascending limb of the nephron, inactivating the NKCC2 cotransporter, creating a Bartter’s syndrome like effect.

From the list above, this patient had low K, Low Mg and Low albumin. All these are potential causes of metabolic alkalosis. This patient is alcoholic with metastatic cancer. The final conclusion was refeeding syndrome.