Search

Background We present a patient who received cerebral oximetry monitoring during targeted temperature management (TTM) post-cardiac arrest and discuss its potential in the early detection of cerebral hypoperfusion and implications on haemodynamics and ventilatory management. Case summary A 60-year-old Chinese male was admitted for acute pulmonary oedema with Type 2 respiratory failure. He failed an initial trial of non-invasive ventilation and was planned for intubation and mechanical ventilation. However, the patient suffered a pulseless electrical activity cardiac arrest peri-intubation. He was started on our institution’s protocolized post-cardiac arrest care bundle, which included cerebral regional oxygen saturation (rSO2) monitoring and TTM. Initial arterial blood gas (ABG) post-return of spontaneous circulation showed severe respiratory acidosis, and the patient was sedated, paralyzed, and ventilator settings optimized. Repeat ABG showed resolution of respiratory acidosis. However, a drop in rSO2 to 35% was subsequently noted. Ventilator settings were quickly adjusted, and dobutamine was started to improve global and cerebral perfusion. These measures improved cerebral rSO2 to more than 50%. Patient was cooled for 24 h and gradually rewarmed. He was later extubated with a cerebral performance category of 1 and is now on outpatient follow-up. Discussion During post-cardiac arrest care, there are many factors which can contribute to a decrease in cerebral blood flow. Therapeutic hypothermia and ventilation strategies, including the use of neuromuscular blocking agents, can both reduce pCO2 which is a major regulator of cerebrovascular tone. Accidental hypocapnia can lead to adverse cerebral vasoconstriction and hypoperfusion. Without cerebral oximetry, cerebral ischaemia may not be detected early and can potentially result in secondary brain injury.