Abstract
Low cardiac output syndrome frequently complicates the post-operative care of infants and children following cardiac surgery. The onset of low cardiac output follows a predictable course in the hours following cardiopulmonary bypass, as myocardial performance declines in the face of an elevated demand for cardiac output. When demand outstrips supply, shock ensues, and early recognition and intervention can decrease mortality. Multifactorial in etiology, this article will discuss the pathophysiology of low cardiac output syndrome, including myocardial depression following bypass, altered cardiac loading conditions, and inflammation driving a hypermetabolic state. Contributions from altered neurohormonal, thyroid, and adrenal axes will also be discussed. Sources included the clinical experiences of four cardiac intensivists, supported throughout by primary sources and relevant reviews obtained through PubMed searches and from seminal textbooks in the field. This article addresses the second of eight topics comprising the special issue entitled “Pharmacologic strategies with afterload reduction in low cardiac output syndrome after pediatric cardiac surgery”.
Keywords: Cardiopulmonary bypass, low cardiac output syndrome, cardiopulmonary interactions, adrenal axis, thyroid axis.
Current Vascular Pharmacology
Title:Pathophysiology of Post-Operative Low Cardiac Output Syndrome
Volume: 14 Issue: 1
Author(s): Conrad L. Epting, Mary E. McBride, Eric L. Wald and John M. Costello
Affiliation:
Keywords: Cardiopulmonary bypass, low cardiac output syndrome, cardiopulmonary interactions, adrenal axis, thyroid axis.
Abstract: Low cardiac output syndrome frequently complicates the post-operative care of infants and children following cardiac surgery. The onset of low cardiac output follows a predictable course in the hours following cardiopulmonary bypass, as myocardial performance declines in the face of an elevated demand for cardiac output. When demand outstrips supply, shock ensues, and early recognition and intervention can decrease mortality. Multifactorial in etiology, this article will discuss the pathophysiology of low cardiac output syndrome, including myocardial depression following bypass, altered cardiac loading conditions, and inflammation driving a hypermetabolic state. Contributions from altered neurohormonal, thyroid, and adrenal axes will also be discussed. Sources included the clinical experiences of four cardiac intensivists, supported throughout by primary sources and relevant reviews obtained through PubMed searches and from seminal textbooks in the field. This article addresses the second of eight topics comprising the special issue entitled “Pharmacologic strategies with afterload reduction in low cardiac output syndrome after pediatric cardiac surgery”.
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Cite this article as:
Epting L. Conrad, McBride E. Mary, Wald L. Eric and Costello M. John, Pathophysiology of Post-Operative Low Cardiac Output Syndrome, Current Vascular Pharmacology 2016; 14 (1) . https://dx.doi.org/10.2174/1570161113666151014123718
DOI https://dx.doi.org/10.2174/1570161113666151014123718 |
Print ISSN 1570-1611 |
Publisher Name Bentham Science Publisher |
Online ISSN 1875-6212 |
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