(Circulation. 1999;100:211-214.)
© 1999 American Heart Association, Inc.
Correspondence |
Cardiopulmonary Interactions After Fontan Operations
Department of Cardiovascular and Pediatric Cardiac Surgery, Marie Lannelongue Hospital, Paris-Sud University, Paris, France
 |
Introduction |
|---|
 Top Introduction ReferencesIntroduction References |
|---|
To the Editor:
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 curve, accounting for an important stroke volume increase. There is a threshold beyond which venous return can no longer be increased whatever the negative pressure ventilation intensity because intrathoracic venae cavae pressure would be lower than atmospheric pressure.4
Fontan circulation studies should therefore benefit from the inclusion of Guyton's concept2 5 on the equilibrium point between ventricular function and venous return curves. As discussed in the hemodynamic comparison between partial or total Fontan circulations,2 reported results1 emphasize that ventricular function and venous return curves seem to be interdependent variables of the Fontan circulation.
|
References |
|---|
|
TopIntroductionReferencesIntroduction References |
|---|
1. Shekerdemian LS, Bush A, Shore DF, Lincoln C, Redington AN. Cardiopulmonary interactions after Fontan operations: augmentation of cardiac output using negative pressure ventilation. Circulation. 1997;96:3934–3942.
2.
Macé L, Dervanian P, Weiss M, Daniel JP, Losay
J, Neveux JY. Hemodynamics of different degrees of
right heart bypass: experimental assessment. Ann Thorac
Surg. 1995;60:1230–1237.
3. Sagawa K. Analysis of the ventricular pumping capacity as a function of input and output pressure loads. In: Reeve EB, Guyton AC, eds. Physical Bases of Circulatory Transport: Regulation and Exchange. Philadelphia, Pa: WB Saunders; 1967:141–149.
4. Skaburskis M, Rivero A, Fitchett D, Zidulka A. Hemodynamic effects of continuous negative chest pressure ventilation in heart failure. Am Rev Respir Dis. 1990;141:938–943.[Medline] [Order article via Infotrieve]
5.
Guyton AC. Determination of cardiac output by equating
venous return curves with cardiac response curves. Physiol
Rev. 1955;35:123–129.
Response
Department of Paediatrics, Royal Brompton Hospital, London, England
|
Introduction |
|---|
|
TopIntroductionReferencesIntroduction References |
|---|
We would like to thank Macé and colleagues for their additional comments related to our observations.1 A low-resistance unobstructed pulmonary circuit, sufficient preload, adequate systemic ventricular function, and physiological afterload are the key determinants of pulmonary blood flow and hence cardiac output of Fontan patients. In the acute postoperative period, these factors can be labile or simply suboptimal, and conventional methods of maintaining preload can ultimately result in fluid overload and lead to ventricular dysfunction. Manipulation of stroke volume is ideally aimed at improving pulmonary blood flow without adversely affecting ventricular function or systemic vascular resistance.
We agree that negative pressure ventilation (NPV) could theoretically compromise systemic ventricular function by increasing afterload.2 We did not directly measure intrathoracic pressure, and so in the absence of transmural pressure data, we can only assume that any effect of NPV on afterload was clinically insignificant and was exceeded by its beneficial influence on diastolic pulmonary blood flow. We have previously shown that acute transition to the Fontan circulation is associated with maintained systolic function3 and is characterized by profound changes in diastolic function consequent on the reduction in preload.4
A negative intrapleural pressure accelerates systemic venous return by
increasing the pressure gradient between the intrathoracic and
extrathoracic veins. We previously reported an improvement in cardiac
output of 
11% in nonbypass patients receiving NPV, and in the same
study, we showed an increase of 28% in postbypass patients after
biventricular surgery.5 We suggested that this
improvement was achieved by augmentation of venous return (along the
principles of Guyton) and that this effect was more marked in
postbypass patients who were likely to be more sensitive to the
detrimental effects of intermittent positive pressure ventilation on
venous return.
Macé and colleagues have rightly pointed out that the augmentation of venous return is ultimately limited by collapse of intrathoracic veins as the right atrial pressure approaches zero. Although the pulmonary artery pressure and hence, right atrial pressure fell in our patients, at no point in the respiratory cycle did these pressures fall to atmospheric or below. The Fontan circulation in particular is likely to be relatively resistant to this phenomenon because of the high baseline preload that exists in these patients. Indeed, the potential improvement that could be achieved by this adjustment of cardiopulmonary interaction in the Fontan circulation may be even greater than that which we demonstrated in our study.
|
References |
|---|
|
TopIntroductionReferencesIntroduction References |
|---|
1. Shekerdemian LS, Bush A, Shore DF, Lincoln C, Redington AN. Cardiopulmonary interactions after Fontan operations: augmentation of cardiac output using negative pressure ventilation. Circulation. 1997;96:3934–3942.
2.
Peters J, Fraser C, Sturat RS, Baumgartner W, Robotham
JL. Negative intrathoracic pressure decreases independently left
ventricular filling and emptying. Am J
Physiol. 1989;257:H120–H131.
3. Penny DJ, Lincoln C, Shore DF, Xiao HB, Rigby ML, Redington AN. The early response of the systemic ventricle during transition to the Fontan circulation: an acute hypertrophic cardiomyopathy? Cardiol Young. 1992;2:78–84.
4.
Penny DJ, Rigby ML, Redington AN. Abnormal patterns of
intraventricular flow and diastolic
filling after the Fontan operation: evidence for incoordinate
ventricular wall motion. Br Heart J. 1991;66:375–378.
5.
Shekerdemian LS, Bush A, Shore DF, Lincoln C, Petros
AJ, Redington AN. Cardiopulmonary interactions in healthy
children and children after surgery for simple cardiac defects: a
comparison of positive and negative pressure ventilation.
Heart. 1997;78:587–593.
| |||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||