(Circulation. 1999;100:211-214.)
© 1999 American Heart Association, Inc.
Correspondence |
Department of Cardiovascular and Pediatric Cardiac Surgery, Marie Lannelongue Hospital, Paris-Sud University, Paris, France
| Introduction |
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Two fundamental observations might be drawn from the article by Shekerdemian et al1 concerning the physiological study of the Fontan circulation:
1. Stroke volume increase, as an adaptation of cardiac output, is difficult to obtain. One of the suggested explanations is that "the total afterload limits the potential for an increase in stroke volume."1 The total afterload of a Fontan circulation, which is equal to the total vascular resistances, or more precisely, to total impedance, may effectively lead to hemodynamic instability.2 By analogy with the study on preload, afterload, and cardiac output relationship,3 stroke volume may be preserved during afterload increase, thus requiring a preload elevation. Conversely, with constant preload, stroke volume decreases when afterload increases. It is a matter of heterometric autoregulation within a range of ventricular function curves.3 Thus, the adaptation of stroke volume will be more difficult in the presence of an excessive afterload increase, depending on the level of pulmonary vascular resistance or a ventricular dysfunction.
2. Conversely, a negative pressure ventilation may generate an
important stroke volume increase. The authors1 stated that
"presumably there must lie a plateau beyond which cardiac output can
no longer continue to improve" when negative pressure ventilation is
used. The main reported consequence of negative ventilation is a venous
return variation.4 Guyton's venous return
curves5 actually admit a "plateau" effect. Reduction
of intrathoracic pressure during negative pressure ventilation
increases the pressure gradient between intrathoracic venae cavae and
peripheral vascular beds, thus optimizing preload over
Guyton's venous return
Department of Paediatrics, Royal Brompton Hospital, London, England
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