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Ann Thorac Surg 2006;82:995
© 2006 The Society of Thoracic Surgeons
Paediatric Cardiac Surgery, Bristol Royal Hospital for Children, Upper Maudlin St, Bristol BS2 8BJ, United Kingdom
(Email: andrew.parry{at}ubht.swest.nhs.uk).
The contribution of the right ventricle to maintaining cardiac output has long been underestimated compared with the left. Historically, this has been truer of adult clinicians, although with increasing experience of transplantation and left ventricular assist devices, the importance of the right ventricle is being better appreciated. For those attending patients with congenital heart lesions this is less true, however. It has long been observed that patients who have had chronic volume loading of the right ventricle often require a higher central venous pressure than expected after bypass to maintain cardiac output.
This study by Szabó and colleagues [1] gives some scientific basis to these clinical pragmatisms. After the exposure of the right ventricle to a volume load for 3 months, during which time right ventricular failure developed, the shunt was removed and hemodynamic studies of the right ventricle undertaken. This demonstrated increased right ventricular systolic and end-diastolic pressures and volumes, although contractile function was maintained. When a pressure load of 35 mm hg and then 55 mm Hg was acutely imposed, however, differences in the way the normal and volume loaded ventricles responded were observed. Although cardiac output was maintained and stroke work increased in both groups, the mechanism for achieving this was different. The control group had increased contractility, whereas output in the study group was maintained by increasing end-diastolic pressure and volume (the Frank-Starling mechanism).
Care must be exercised in extrapolating these data to the clinical situation. It is somewhat surprising that no differences in right ventricular diastolic function due to volume overload were demonstrated, which may reflect the relatively short duration of right ventricular volume overload. It would be interesting to know whether the duration of volume overload impacted on right ventricular diastolic function (as is suggested from human studies) and subsequently the response of the right ventricle to increasing afterload. It would also be interesting to determine whether the right ventricle recovers from these immediate effects of volume overload with time.
In the possible clinical scenario in which short-term right ventricular volume loading is experienced and then corrected (young infants with left to right shunts), many developmental adaptive mechanisms are still active within the myocardium that are likely to affect the tolerance of a "chronically" volume-loaded right ventricle to increased afterload, and these may overshadow the mechanisms identified in this study. Yet knowing whether the same right ventricle maladaption pertains could add weight to the argument for very early age of repair in these children.
This laboratory study provides us with some understanding of the mechanisms of the right ventricular dysfunction that occurs after chronic volume overload. Knowing this mechanism will allow us to tailor our interventions to combat these changes and improve clinical management of these patients.
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