Editorial Views  |   March 2017
Anesthetics, the Ryanodine Receptors, and the Heart
Author Notes
  • From the Department of Anesthesia, Critical Care and Pain Medicine, Massachusetts General Hospital, Boston, Massachusetts; and Harvard Medical School, Boston, Massachusetts.
  • Corresponding article on page 495.
    Corresponding article on page 495.×
  • Accepted for publication June 16, 2016.
    Accepted for publication June 16, 2016.×
  • Address correspondence to Dr. Hobai: ihobai@partners.org
Article Information
Editorial Views / Cardiovascular Anesthesia
Editorial Views   |   March 2017
Anesthetics, the Ryanodine Receptors, and the Heart
Anesthesiology 3 2017, Vol.126, 373-375. doi:10.1097/ALN.0000000000001520
Anesthesiology 3 2017, Vol.126, 373-375. doi:10.1097/ALN.0000000000001520
CARDIOVASCULAR complications are still a major cause of perioperative mortality and morbidity.1  Myocardial ischemia, arrhythmias, and cardiac pump failure usually harm patients with preexisting cardiac disease and/or during extreme hemodynamic challenges. To prevent these complications, a substantial body of research aims to understand the effects exerted by anesthetic agents on the heart. We have learned that volatile anesthetics usually depress cardiac contractility,2  especially at large doses, and in patients with preexisting cardiomyopathy. We know that volatile anesthetics are also protective during ischemia/reperfusion injury, a phenomenon known as anesthetic-induced preconditioning.3  General anesthesia prolongs the electrocardiogram QT interval4  and is potentially arrhythmogenic. But are these effects similar for equianesthesthetic doses of various agents? In other words, are some anesthetics better than others at protecting the heart?
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