A 69 year old patient had a cardiac arrest soon after return to the ward following an operation.
Resuscitation was commenced and included intubation and ventilation. Femoral arterial blood gases
were collected about five minutes after the arrest. Other results: Anion gap 24, Lactate 12 mmol/l.
Firstly: Initial clinical assessment
The expected result here would be a mixed disorder with respiratory acidosis
(due inadequate ventilation) and a lactic acidosis (related to poor perfusion).
Secondly: The acid-base diagnosis
pH: The pH is extremely low (severe acidaemia) so a severe acidosis is present
Pattern: The combination of a high pCO2 and a low bicarbonate means that a mixed disorder
is present: there must be 2 or more primary acid-base disorders present. This pattern is found with
a combined acidosis: metabolic acidosis (low bicarbonate) and a respiratory acidosis (high pCO2).
Clues: The anion gap result confirms a high anion gap acidosis and the high lactate
level confirms this as a severe lactic acidosis.
Compensation: Consider the expected
pCO2 for the metabolic acidosis: By the one & a half plus 8 rule (rule 5): Expected pCO2 =
(1.5 x 14 + 8 ) = 29mmHg. The actual pCO2 of 82 mmHg is very much higher which confirms the
presence of a co-existent respiratory acidosis. The pCO2 level of 82 mmHg is so high that a
respiratory acidosis must be present. (In exceptional cases of severe metabolic alkalosis a pCO2 of 86mmHg has
Formulation: A severe mixed acidosis due to lactic acidosis and respiratory acidosis.
Confirmation: Nil else is required. There should be clinical evidence to support
the conclusion of poor peripheral perfusion. If not, then an ischaemic gut cause should be
considered but there is no evidence of this here. Compared to standard
normal values, the anion gap has increased by 12 & the bicarbonate level has decreased by
10 so the delta ratio is 12/10 = 1.2 - this is consistent with a high anion gap acidosis.
Finally: The Clinical Diagnosis
Cardiac arrest with low cardiac output and tissue hypoperfusion causing a severe
lactic acidosis. Ventilation is depressed causing a respiratory acidosis.
The pCO2 of 82mmHg is too high to have developed from a level of 40 mmHg in 5 minutes.
An elevated pCO2 must have been present before the arrest. Inadequate ventilation in this
pre-arrest phase may have been related to several factors, in particular inadequate
reversal of neuromuscular paralysis, airway obstruction in a supine sedated patient
or acute pulmonary oedema.
The hypercapnia would have been associated with hypoxaemia and this would have
contributed to the arrest. The high pO2 level on the gases is due to the high inspired
oxygen fraction as such a level is not possible when breathing room air.