Question 9.2

You are asked to review a 44 year old male known epileptic following a prolonged generalised tonic-clonic convulsion. He is intubated and ventilated. Arterial blood gas analysis is as follows:

Test	Value	Normal Range
FiO2	0.5
pH*	7.15	7.35 – 7.45
pCO2	35 mmHg (4.6 kPa)	35 – 45 (4.6 – 6)
pO2*	105 mmHg (14 kPa)	75 – 98 (10 – 13)
HCO3-*	10.3 mmol/l	22 – 26

a) List the abnormalities on the blood gas and give the most likely cause of each abnormality.

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College Answer

a) List the abnormalities on the blood gas and give the most likely cause of each abnormality.

•    Metabolic acidosis – lactic acidosis secondary to prolonged seizures
•    Respiratory acidosis (or inadequate compensation) – central hypoventilation or inadequate mechanical ventilation
•    Increased A-a gradient - aspiration pneumonia

Discussion

Let us dissect these results systematically.

The A-a gradient is high:
PAO2 = (0.5 × 713) - (35 × 1.25) = 312.75
Thus, A-a = ( 312.75 - 105) = 207.75mmHg.
In fact, the PaO₂/FiO₂ ratio is (105/0.5) = 210, which puts this man's hypoxia in a "mild ARDS" category by the 2012 Berlin definition.
There is acidaemia
The PaCO2 is compensatory
The SBE is not offered, but the bicarbonate is low, suggesting a severe metabolic acidosis
The respiratory compensation is inadequate - the expected PaCO₂ = (10.3 × 1.5) + 8 = 23.5 mmHg, and thus there is also a respiratory acidosis
The anion gap cannot be calculated.

The college suggests the following explanations for this gas:

Hypoxia = aspiration
Hypercapnea = obtundation
Metabolic acidosis = seizure-associated rise in lactate.

This explanation is certainly within reason. One could even get into a discussion about MELAS. Often in the postictal state there is still appropriate respiratory compensation for the lactic acidosis, with most postictal patients averaging a PaCO₂ around 17mmHg in a 1977 study of post-seizure lactic acidosis. However, postictal hypopnoea is a known cause of respiratory acidosis after a seizure, and may be a factor in SUDEP - Sudden Unexplained Death in Epilepsy.

To consider alternative explanations, this mixed acid-base disturbance can also be accounted for by the complications of toxic alcohol ingestion, a hypoglycaemic episode, opiate overdose, and numerous others.

References

Pavlakis, Steven G., et al. "Mitochondrial myopathy, encephalopathy, lactic acidosis, and strokelike episodes: a distinctive clinical syndrome." Annals of neurology 16.4 (1984): 481-488.

Orringer, Carl E., et al. "Natural history of lactic acidosis after grand-mal seizures: a model for the study of an anion-gap acidosis not associated with hyperkalemia." New England Journal of Medicine 297.15 (1977): 796-799.

Bateman, Lisa M., Mark Spitz, and Masud Seyal. "Ictal hypoventilation contributes to cardiac arrhythmia and SUDEP: Report on two deaths in video‐EEG–monitored patients." Epilepsia 51.5 (2010): 916-920.

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