Measurement of the saturation of brain effluent blood gives a global estimate of cerebral oxygenation. It may provide clinicians with information to assist in reducing secondary insults to the brain with potential benefits to a range of patients with actual or potential acute brain injury such as trauma and cardiac bypass procedures. The technology to continuously measure this variable is simple to use but requires attention to detail; it is limited in its ability to detect discrete regions of ischaemia or hyperaemia unless these are of sufficient magnitude to influence the saturation of brain effluent blood. There are few complications that result from this invasive technique and they are usually of a minor nature. The technique also enables research opportunities from the ability to sample blood as it leaves the cranium. Poor outcomes are seen in patients with traumatic brain injury who exhibit either reduced or increased cerebrovenous oxygen saturation and it remains to be seen if detection and correction of these anomalies will produce patient benefits.

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Cardiac injury and pulmonary oedema occurring after acute neurological injury have been recognised for more than a century. Catecholamines, released in massive quantities due to hypothalamic stress from subarachnoid haemorrhage (SAH), result in specific myocardial lesions and hydrostatic pressure injury to the pulmonary capillaries causing neurogenic pulmonary oedema (NPO). The acute, reversible cardiac injury ranges from hypokinesis with a normal cardiac index, to low output cardiac failure. Some patients exhibit both catastrophic cardiac failure and NPO, while others exhibit signs of either one or other, or have subclinical evidence of the same. Hypoxia and hypotension are two of the most important insults which influence outcome after acute brain injury. However, despite this, little attention has hitherto been devoted to prevention and reversal of these potentially catastrophic medical complications which occur in patients with SAH. It is not clear which patients with SAH will develop important cardiac and respiratory complications. An active approach to investigation and organ support could provide a window of opportunity to intervene before significant hypoxia and hypotension develop, potentially reducing adverse consequences for the long-term neurological status of the patient. Indeed, there is an argument for all SAH patients to have echocardiography and continuous monitoring of respiratory rate, pulse oximetry, blood pressure and electrocardiogram. In the event of cardio-respiratory compromise developing i.e. cardiogenic shock and/or NPO, full investigation, attentive monitoring and appropriate intervention are required immediately to optimise cardiorespiratory function and allow subsequent definitive management of the SAH.