Discussion

The relationship between non-perfusion and hypoxic brain injury explains why few patients survive post cardiac arrest with a pH of <6.8.1 A few cases of survival with good neurological outcome exist below this level, mostly in young adults. The lowest published arterial pH of an adult who survived cardiac arrest with normal neurology is 6.33. This was a 24-year-old male in a near-drowning where relative hypothermia may have provided neuroprotection.1 Two further reports exist of survival with no neurological deficit, in normothermic adults with a lower pH than in our patient. Case 1 (pH 6.54) was that of a 54-year-old woman who had an out-of-hospital arrest and was subsequently found to have a hepatic rupture.2 Case 2 (pH 6.6) was that of a 35-year-old man who had an in-hospital arrest with adult pyloric stenosis.3 There are numerous reports of survivors with a lower pH (<6.61) without cardiac arrest who made a good neurological recovery.2

The metabolic acidosis post cardiac arrest is due to imbalance between tissue oxygen supply and demand. This may be compounded by respiratory acidosis due to hypoventilation from respiratory arrest, difficulty in manual ventilation because of poor airway maintainance, atelectasis or intrapulmonary shunt with increased ventilation–perfusion mismatch due to poor lung perfusion during cardiopulmonary resuscitation. Hyperlactaemia reflects tissue ischaemia and low available ATP levels and contributes around 50% of the post-arrest metabolic acidosis.

In shock a raised lactate (>10 mmol/l) is associated with high mortality (83%). Lactate increases progressively through cardiac arrest and remains high through resuscitation. Lactate has been suggested as a predictor of downtime during cardiopulmonary arrest and as a determinant of prognosis. Lower lactate at return of spontaneous circulation and effective clearance of lactate by metabolism at 12 h post arrest is associated with more favourable outcome. With increasing lactate, functional neurological recovery is more likely to be unfavourable. Only at very high levels (>16.3 mmol/l) could unfavourable neurological recovery be detected, with 100% specificity but low sensitivity (16%) (n=167 out-of-hospital arrests).4 This suggests lactic acidosis is not a reliable indicator of severity of cerebral hypoxia in individuals. Most work on the physiology of cardiac arrest in humans is based on out-of hospital cardiac arrest, where a prolonged time without cardiopulmonary resuscitation and cerebral anoxia may occur and may not accurately model the situation of witnessed arrest in the emergency department.

Our patient suffered a cardiac arrest in hospital, with severe acidosis at return of spontaneous circulation. He survived without any neurological impairment. We are aware of only three cases with a complete recovery with a lower temperature corrected pH. Profound acidosis is often interpreted by physicians as reflecting a prolonged period of circulatory standstill that inevitably leads to hypoxic brain injury. Our case illustrates that this assumption may be wrong when the majority of the metabolic acidosis has accumulated due to relative circulatory insufficiency before arrest and there is prompt recognition and resuscitation from cardiac arrest.