Cardiac Dysfunction After Neurologic Injury: What Do We Know and Where Are We Going?

Chest. 2016 May;149(5):1325-31. doi: 10.1016/j.chest.2015.12.014. Epub 2015 Dec 28.

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.

Keywords: cardiomyopathy; critical care; neurology.

Publication types

  • Review
  • Research Support, N.I.H., Extramural

MeSH terms

  • Brain Death / metabolism
  • Brain Injuries, Traumatic / complications
  • Brain Injuries, Traumatic / metabolism
  • Cardiomyopathies / etiology
  • Cardiomyopathies / metabolism
  • Catecholamines / metabolism
  • Central Nervous System Infections / complications
  • Central Nervous System Infections / metabolism
  • Epilepsy / complications
  • Epilepsy / metabolism
  • Heart Diseases / etiology*
  • Heart Diseases / metabolism
  • Humans
  • Myocardial Stunning / etiology
  • Myocardial Stunning / metabolism
  • Nervous System Diseases / complications*
  • Nervous System Diseases / metabolism
  • Stroke / complications
  • Stroke / metabolism
  • Subarachnoid Hemorrhage
  • Takotsubo Cardiomyopathy / etiology
  • Takotsubo Cardiomyopathy / metabolism

Substances

  • Catecholamines