A 66 year old man had a postoperative cardiac arrest.
Past history is of hypertension treated with an ACE inhibitor. There is no past history of ischaemic heart disease. ECG shows sinus rhythm with lateral T-wave flattening. Biochemistry is normal. Preoperative anaesthetic assessment of patient status was ASA class 2.
During a septoplasty, his ST segments became acutely depressed up to 2.4 mm and BP fell to 85-90 systolic. BP recovered with volume loading and IV ephedrine but ST segments remained depressed. Following reversal and extubation, he was transferred to ICU for overnight monitoring. On arrival in ICU, BP 90/50, pulse 80/min, resp rate 16/min and SpO2 99%. During handover to ICU staff, he developed ventricular fibrillation which reverted to sinus rhythm with a single 200J countershock. Soon after, blood gases were obtained from a radial arterial puncture:
Arterial Blood Gases
pCO2 55.4 mmHg
pO2 144 mmHg
HCO3 24.3 mmol/l
Biochemistry Results: Na+ 138, K+ 4.7, Cl- 103, urea 6.4 & creatinine 0.07 (all in mmol/l)
The assessment uses the structured approach outlined in section 9.1 and elaborated in subsequent sections.
The history suggests several possibilities:
Any of these disorders could be present (except of course that there cannot be both a respiratory acidosis and respiratory alkalosis at the same time). The options cited may seem too many but consideration of the history suggests that it is realistic.
Some things are obviously excluded (for example, a metabolic alkalosis would seem very unlikely as there is no history of vomiting or diuretic use; there is nothing to suggest ketoacidosis, acidosis due to toxins or hyperchloraemic acidosis due to diarrhoea or renal tubular acidosis; there is no history of chronic respiratory disease and chronic respiratory acidosis).
The full list of what is unlikely is longer and perhaps less important than considering what could be present but sometimes you will find something quite unexpected and will have to consider unexpected possibilities. Now lets look at the gases systematically.
The analysis continues with the structured approach outlined in section 9.2
1. pH: An acidaemia is present so there must be an acidosis present.
2. Pattern: An acidaemia with the pattern of elevated pCO2 and normal HCO3 is consistent with an acute respiratory acidosis.
3. Clues: The anion gap is about 11 which is normal so no evidence of a high anion gap acidosis.
4. Compensation: For an acute respiratory acidosis, the '1 for 10' rule (rule 1) is used: the expected HCO3 is 24 + 1.5 = 25.5mmol/l. The actual value is only about one mmol/l different so there is no evidence of a co-existent metabolic acid-base disorder. Note that the selection of rule 1 over rule 2 is based entirely on our assessment of the clinical details that there is no chronic respiratory problem.
5. Formulation: Acute respiratory acidosis. No evidence of a metabolic acid-base disorder.
6. Confirmation: There is no specific test to confirm this diagnosis.
Acute respiratory acidosis following resuscitation from postop ventricular fibrillation.
Respiratory acidosis is almost always due to decreased alveolar ventilation though the rare possibility of CO2 overproduction due to malignant hyperthermia should always be kept in mind in the anaesthetic context. There is no evidence of this here.
The history strongly suggests intra-operative myocardial ischaemia and the decision to monitor postoperatively in ICU turned out to be a good decision. What was the cause of the hypoventilation? The residual depressant effects of the Anaesthetic agents is considered the most likely cause but the possibility of inadequate reversal of neuromuscular blockade should also be considered in this context.
It is possible that if the patient also had both a metabolic acidosis and a metabolic alkalosis (in addition to the acute respiratory acidosis), then these could have counterbalancing effects on the actual [HCO3]. This situation is excluded because there is no supportive evidence from either the history (no vomiting or diuretic use) or other investigations (normal anion gap & chloride levels) of either metabolic disorder. As a general rule, it is not wise to chase alternative diagnoses which have no supportive evidence.
If the patient is hypoventilating, why is the pO2 elevated?
This is because the patient is breathing a high inspired oxygen concentration. If the patient was breathing room air (FIO2 = 0.21), then a depression of alveolar pO2 must occur if the pCO2 is elevated (as predicted from the alveolar gas equation). Most ill patients in hospital are breathing supplemental oxygen so it is common for the pO2 to be elevated on blood gas results.