Multiple forms of brain damage, primarily, subarachnoid haemorrhage (SAH) are frequently accompanied by neurogenic myocardial injury with changes in the electrocardiogram, accompanied by the release of markers of myocardial injury. This form of cardiac dysfunction is thought to be mediated by cellular toxicity associated with catecholamine release. Central nervous system damage in the course of intracranial haemorrhage may, in a similar pathogenic pathway, lead to neurogenic lung injury. Up to this day, little is known whether the extent of brain damage in patients with SAH correlates with the degree of neurogenic myocardial injury. Moreover, it remains unknown what is the full clinical picture and duration of this type of myocardial injury and how often it co-occurs with neurogenic lung injury. Such analysis is a fundamental and most important step in optimising the treatment of these patients.~Methods: In this prospective observational study the authors aim to recruit 30 patients with subarachnoid haemorrhage, requiring hospitalization in the Intensive Care Unit. The patients will be monitored for elevation in cardiac damage markers (hs-TnT, CPK, CK-MB, NT-proBNP) and worsening of respiratory conditions, defined by need for more invasive ventilation parameters, and subsequent changes in arterial blood gas. The above mentioned parameters will be assessed every 12 hours. Additionally, the patients will be screened for an elevation in catecholamine metabolite (metanephrine) concentration in 12-hour urine collection.~Hypothesis to be tested: Myocardial and lung injury in SAH patients is timely-associated with an increase in metanephrine concentration in urine.
Up to this day, little is known whether the extent of brain damage in patients with SAH correlates with the degree neurogenic myocardial injury and neurogenic lung injury.~This is a prospective observational study designed to asses relationship between catecholamine surge and development of myocardial and lung injury in subarachnoid haemorrhage patients.