Can Levosimendan Be a Treatment Option in Subarachnoid Hemorrhage?


Mengi T., Yilmaz B., GÖKMEN A. N., KOCA U.

TURKISH JOURNAL OF INTENSIVE CARE-TURK YOGUN BAKIM DERGISI, vol.16, no.2, pp.50-57, 2018 (ESCI) identifier

  • Publication Type: Article / Review
  • Volume: 16 Issue: 2
  • Publication Date: 2018
  • Doi Number: 10.4274/tybd.05025
  • Journal Name: TURKISH JOURNAL OF INTENSIVE CARE-TURK YOGUN BAKIM DERGISI
  • Journal Indexes: Emerging Sources Citation Index (ESCI), TR DİZİN (ULAKBİM)
  • Page Numbers: pp.50-57
  • Keywords: Subarachnoid hemorrhage, traumatic, aneurysm, intracranial vasospasm, critical care, levosimendan, neurogenic stress cardiomyopathy, CEREBRAL-BLOOD-FLOW, TAKOTSUBO CARDIOMYOPATHY, CLINICAL CHARACTERISTICS, HYPERVOLEMIC THERAPY, CARDIOGENIC-SHOCK, CARDIAC INJURY, VASOSPASM, HYPERTENSION, OXYGENATION, DYSFUNCTION
  • Dokuz Eylül University Affiliated: Yes

Abstract

Despite improvements in medical and surgical treatment, aneurysmatic subarachnoid hemorrhage (SAH) remains one of the main causes of early mortality. Cardiac and pulmonary complications are the main causes of mortality. One of the most severe cardiac complications is neurogenic stress cardiomyopathy. Left ventricular dysfunction which is seen in neurogenic stress cardiomyopathy, although it is usually reversible within a few days, can cause severe hypotension, pulmonary edema and cardiogenic shock. Traditional treatment of heart failure after SAH is based on the use of noradrenaline, dobutamine and high volume of fluids. However, it is difficult to treat reduced cardiac output in SAH. Because, myocardial cells are already under stress due to increased adrenergic stimulation. The use of exogenous catecholamines may cause additional neurocardiogenic damage in myocardial cells, excessive calcium burden, decreased cerebral blood flow, and delayed cerebral ischemia.