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J Thorac Cardiovasc Surg. 2014 Dec;148(6):3166-71.e1-4. doi: 10.1016/j.jtcvs.2014.05.044. Epub 2014 May 21.

Right ventricular architecture responsible for mechanical performance: unifying role of ventricular septum.

Author information

1
Department of Cardiothoracic Surgery, University of California, Los Angeles, David Geffen School of Medicine, Los Angeles, Calif. Electronic address: gbuckberg@mednet.ucla.edu.
2
Department of Pediatrics and Cardiovascular Research Institute, University of California, San Francisco, School of Medicine, San Francisco, Calif.

Abstract

The right ventricle (RV) is composed of a free wall containing a wrap-around circumferential muscle at its base and a septum composed of helical fibers that are oblique and cross each other at 60° angles. This structure is defined by the helical ventricular myocardial band and defines RV function because the wrap-around transverse fibers constrict or compress to cause the bellows motion responsible for 20% of RV output, whereas the oblique fibers determine shortening and lengthening that produces 80% of RV systolic function. Clinical shortening is quantified by tricuspid annular plane systolic excursion and measured by echocardiography. Destruction of the free wall by electrocautery or patch replacement does not alter RV function if the septum is intact. Conversely, septal damage causes RV dysfunction if pulmonary vascular resistance is increased. The interaction between structure and function to cause RV failure and how these factors become corrected is defined for RV failure, RV relationship to LV failure, resynchronization, pacing, RV dysplasia, left ventricular assist device, intraoperative septal injury during myocardial protection, the septal role in tricuspid insufficiency, pharmacologic decisions on altering pulmonary vascular resistance in RV failure, congenital heart disease, and adult heart disease is considered in this overview. These structure-function relationships emphasize why clinical decisions must be based on knowledge of normality, recognizing how disease offsets normality, and introducing actions that rebuild normality.

PMID:
24973008
DOI:
10.1016/j.jtcvs.2014.05.044
[Indexed for MEDLINE]
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