Pulmonary and cardiac sequelae of subarachnoid haemorrhage: time for active management?

Abstract

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.

Effects of energy drinks on blood pressure, heart rate, and electrocardiographic parameters: An experimental study on healthy young adults

“…Given that any dynamic ST-T change could reflect a probable subendocardial damage, our findings of more frequent post-consumption ST-T changes are of high clinical importance. Accordingly, it might be hypothesized that excessive catecholamine release after the consumption of energy drinks is the responsible mechanism for the significant ST-T changes, an issue which is similar to the “catecholamine storm” theory for ECG changes after subarachnoid hemorrhage (33-35). Yet, larger clinical trials are needed to support that claim.…”

The Relationships Between BNP and Neurocardiac Injury Severity, Noninvasive Cardiac Output, and Outcomes After Aneurysmal Subarachnoid Hemorrhage

“…After aneurysmal subarachnoid hemorrhage (aSAH), neurocardiac injury occurs in 31–48% of patients (Cremers et al, 2016; Hravnak et al, 2009; Frangiskakis et al, 2009). It is widely accepted that neurocardiac injury is caused by an acute release of catecholamines that results from elevated intracranial pressure post-hemorrhage (Salem et al, 2014 Bank et al, 2005; Macmillan, Grant, & Andrews, 2002). Manifestations of neurocardiac injury often include cardiac arrhythmias, widened QT intervals, depressed cardiac output and ejection fraction on echocardiogram, and elevated serum cardiac troponin I (cTnI) (Hravnak et al, 2009).…”

Impairment of cardiac metabolism and sympathetic innervation after aneurysmal subarachnoid hemorrhage: a nuclear medicine imaging study

“…The most widely accepted theory for SAH-induced neurogenic myocardial stunning is the ‘catecholamine hypothesis’. The release of massive quantities of catecholamines following aneurysm rupture results in specific myocardial lesions [37]. …”