title: Cardiac Dysfunction After Neurologic Injury: What Do We Know and Where Are We Going?
abstract: Recent literature has implicated severe neurologic injuries, such as aneurysmal subarachnoid hemorrhage, as a cause of cardiac dysfunction, impaired hemodynamic function, and poor outcomes. Mechanistic links between the brain and the heart have been explored in detail over the past several decades, and catecholamine excess, neuroendocrine dysfunction, and unchecked inflammation all likely contribute to the pathophysiologic process. Although cardiac dysfunction has also been described in other disease paradigms, including septic shock and thermal injury, there is likely a common underlying pathophysiology. In this review, we will examine the pathophysiology of cardiac dysfunction after neurologic injury, discuss the evidence surrounding cardiac dysfunction after different neurologic injuries, and suggest future research goals to gain knowledge and improve outcomes in this patient population.
authors.affiliation: Department of Anesthesiology and Pain Medicine, University of Washington, Seattle, WA; Harborview Injury Prevention and Research Center, University of Washington, Seattle, WA. Electronic address: vkrish@u.washington.edu.
authors.forename: Vijay
authors.initials: V
authors.lastname: Krishnamoorthy
authors.affiliation: Department of Anesthesiology and Pain Medicine, University of Washington, Seattle, WA.
authors.forename: G Burkhard
authors.initials: GB
authors.lastname: Mackensen
authors.affiliation: Department of Medicine, University of Washington, Seattle, WA; Harborview Injury Prevention and Research Center, University of Washington, Seattle, WA.
authors.forename: Edward F
authors.initials: EF
authors.lastname: Gibbons
authors.affiliation: Department of Anesthesiology and Pain Medicine, University of Washington, Seattle, WA; Harborview Injury Prevention and Research Center, University of Washington, Seattle, WA.
authors.forename: Monica S
authors.initials: MS
authors.lastname: Vavilala
mesh_terms: D001926:Brain Death / Q000378:metabolism; D000070642:Brain Injuries, Traumatic / Q000150:complications / Q000378:metabolism; D009202:Cardiomyopathies / Q000209:etiology / Q000378:metabolism; D002395:Catecholamines / Q000378:metabolism; D002494:Central Nervous System Infections / Q000150:complications / Q000378:metabolism; D004827:Epilepsy / Q000150:complications / Q000378:metabolism; D006331:Heart Diseases / Q000209:etiology* / Q000378:metabolism; D006801:Humans; D017682:Myocardial Stunning / Q000209:etiology / Q000378:metabolism; D009422:Nervous System Diseases / Q000150:complications* / Q000378:metabolism; D020521:Stroke / Q000150:complications / Q000378:metabolism; D013345:Subarachnoid Hemorrhage; D054549:Takotsubo Cardiomyopathy / Q000209:etiology / Q000378:metabolism
chemical_list: D002395:Catecholamines
keywords: cardiomyopathy; critical care; neurology
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