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J Thorac Cardiovasc Surg 2003;125:219-220
© 2003 The American Association for Thoracic Surgery
Letters to the Editor |
Cardiac Surgical Department, Royal Group of Hospitals, Belfast, Northern Ireland BT12 6BA, United Kingdom
To the Editor:
I read with interest the article by Klima and associates
1 published in the January 2002 issue of the Journal. This work represents another valuable contribution by Vlahakes and his coworkers to the understanding of the pathophysiologic mechanisms that underlie right ventricular (RV) failure.
The model used in this study comprised an isovolumetric contracting right ventricle in which the preload was varied by means of incremental increases in volume of an intracavity latex balloon. Systemic arterial pressure and coronary perfusion were maintained by cardiopulmonary bypass support with or without left ventricular (LV) ejection. RV performance was assessed by maximum developed pressure during contraction.
From these experiments the authors suggest that ventricular interaction as opposed to RV free-wall perfusion is the most significant determinant of maximal RV performance. It is difficult to see how this conclusion can be reached from the data they present. In fact, they identified no significant difference in RV performance in terms of maximum developed RV pressure or RV dP/dt when the left ventricle was ejecting or completed offloaded. A myocardial perfusion-limiting phenomenon occurring at maximum RV volume appears a more likely explanation.
The authors found that, at the point of maximum RV preload, the maximum RV developed pressure is correlated with systemic arterial pressure (independent of LV loading) (their Figure 3). It is possible that at this point of RV dilation the increase in RV diastolic pressure is sufficient to critically limit RV myocardial perfusion and subsequent variation in the systemic pressure will produce a corresponding change in contractility. This would be consistent with the findings by Sunagawa and associates, 2 who identified a similar linear relationship between coronary artery pressure and the slope of the end-systolic pressure-volume relationship under conditions of critical perfusion. With increasing RV distention and rise in RV diastolic pressure, increased wall tension will occur with the potential for ischemia of the subendocardium (free wall and septal). In addition, the increased oxygen demand required at the higher developed RV pressure will contribute to myocardial ischemia when perfusion becomes marginal.
In the authors' Figure 4, maximal RV developed pressure increases with increasing RV balloon volume up to 60 mL and then declines thereafter (defined as the point of RV failure). This curve has the appearance of a Frank-Starling relationship whereby the performance of the ventricle is enhanced by the increased ventricular volume. Further increments in RV volume result in RV failure, indicated by a reduction in the maximum RV developed pressure. The authors' discussion does not clarify what the potential and likely mechanisms for RV failure are beyond this ventricular volume. This volume could represent the peak of the Starling curve, that is, the sarcomere length at which the maximum crossbridge/actin interaction occurs. Alternatively, it may result from inadequate myocardial perfusion. It is interesting right coronary artery flow decreased significantly after RV failure.
To gain further insight and in attempt to resolve these issues, the authors could easily construct an RV diastolic pressure-volume curve (this would have to be repeated by distending the balloon alone, so that the contribution of the balloon to the total compliance is determined). An acute increase in pressure-volume gradient with the higher ventricular volumes may indicate a reduction in RV driving pressure, which will reduce coronary artery flow 3 and render the subendocardium vulnerable to ischemia.
Furthermore, the authors identified that maximum RV developed pressure occurs at higher ventricular volumes if the left ventricle is ejecting rather than empty. LV ejection potentially may contribute two benefits: First, the filling of the LV cavity during diastole will maintain RV geometry. (This was indicted in the article by the displacement of the septum with LV filling, Figure 5). This more physiologic shape in diastole may affect the compliance of the right ventricle with subsequent beneficial effects on wall tension and subendocardial perfusion. Again, the use of the diastolic pressure-volume curve may identify this. Second, LV ejection will add pulsatility to the systemic arterial supply, which may allow greater perfusion at marginal pressure gradients.
References
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