Pulmonary and cardiac sequelae of subarachnoid haemorrhage: time for active management?
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.
University of Dundee, Department of Anaesthesia, Ninewells Hospital, Dundee DD1 9SY, UK. csmacmillan@doctors.org.uk
C S A
CS
Macmillan
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IS
Grant
P J D
PJ
Andrews
D000818:Animals; D002395:Catecholamines / Q000502:physiology; D003422:Critical Care / Q000379:methods; D004562:Electrocardiography; D019317:Evidence-Based Medicine; D006331:Heart Diseases / Q000209:etiology*; D006439:Hemodynamics; D006801:Humans; D007031:Hypothalamus / Q000503:physiopathology; D009206:Myocardium / Q000473:pathology; D011654:Pulmonary Edema / Q000209:etiology* / Q000503:physiopathology / Q000628:therapy; D013222:State Medicine; D020206:Subarachnoid Hemorrhage, Traumatic / Q000150:complications* / Q000503:physiopathology / Q000628:therapy; D014019:Tissue Donors; D006113:United Kingdom; D018754:Ventricular Dysfunction
D002395:Catecholamines