You're a part of the advanced life support team, arriving at the sleep lab in the small hours of the morning. Worried staff narrate a story of a morbidly obese sleep apnoea patient who presented for a sleep study and has been observed all night with continuous pulse oximetery.
Prolonged apnoeic pauses were witnessed, with desaturation into the 60s. However, each time the patient snored back into life after a few seconds.
However, recently the saturation probe had become dislodged, and in spite of fiddling with it the sleep lab staff could not get it to read a "realistic" result. A resident had collected an arterial blood gas, "to make sure". The pulse oximeter continued to offer very depressing numbers. Concerned that they may be real, the staff attempted to rouse the patient - and could not.
The resident returned with this blood gas.
It would be laughable to discuss these at any great length. The hypoxia is profound. sO2 is reported as 8.7%. The FShunte suggests that the vast majority of the blood is travelling through a poorly ventilated area of the lung; or rather, that the lungs are not being ventilated at all. The A-a gradient suggests that hypoventilation alone does not completely explain the hypoxia; probably some atelectatic collapse or negative pressure pulmonary oedema are contributing.
There is a mild acidaemia; the pH is 7.253.
The pCO2 is high, likely contributing to the acidosis.
The Actual Base Excess is negative, suggesting a metabolic acidosis - however, this is still within a normal range of values. The respiratory acidosis is therefore probably the primary problem.
Copenhagen interpretation of acid-base compensation:
The Actual Base Excess is slightly negative, but still within the normal acceptable limits. On this basis, one would be forced to conclude that this patient's acidaemia is caused primarily by a respiratory acidosis with a negligible contribution from a metabolic acidosis.
Boston interpretation of acid-base compensation:
This ABG machine has been set up to report the standard bicarbonate, which is of course useless for assessment of compensation. The calculated actual bicarbonate is 27mmol/L. The bicarbonate expected from the "1 for 10" rule is 26.3mmol/L, and therefore the respiratory acidosis is reasonably well compensated (and of course that does not mean that the pH should have returned to normal).
Using the actual bicarbonate value, the anion gap is 7.9 - actually lower than the expected value.
The albumin was 40- with this value, the "normal" anion gap should be 12.
This suggests that whatever little metabolic acidosis is present, it represents a normal anion gap acidosis, due to the slightly raised chloride.
There is a normal p50(st) and an abnormally raised p50; the difference can be accounted for by the acidosis and hypercapnea, given that the dyshaemoglobin levels are within the expected range.
This severely hypoxic patient appears particularly well adapted to severe hypoxia. The haemoglobin level is 214; with this degree of polycythaemia the oxygen content of his blood could be 287ml/L with an sO2 of 100%. However, at this saturation, the oxygen content of blood is around 25.3ml/L. Thus in order to meet with a normal resting metabolic demand (lets say, an O2 requirement of 3ml/kg/min) this 180kg patient would require a minimum cardiac output of 21.3 L/min.
So, what the hell happened here? Well. Subsequent detective work had revealed that the patient, anxious of sleeping in a strange place, had snuck some sedating antihistamines (Phenergan) into the sleep lab, and self-administered a nice big dose without the knowledge of the sleep lab staff.
Anyway. Cardiac arrest was diagnosed. The initial rhythm was bradycardic PEA; the rate was apparently about 20. With intubation and fresh oxygen, circulation was rapidly restored.