The right heart in a biventricular circulation

Division Head, Cardiology, The Hospital for Sick Children, Toronto, Canada
Andrew Redington

The effects of the left ventricle on the right ventricle
The‘cross-talk’between the normal left and right ventricles was beautifully demonstrated by the work of Damiano and colleagues in 1991. In an experimental model, they showed the relative contributions of the left ventricle to right ventricular contractile performance and vice versa. Their model was an electrically isolated but mechanically contiguous system. Ventricular pressure was measured in the right and left ventricle with ipsilateral or contralateral ventricular pacing. Fig. 1 shows the results (redrawn from Damiano et al). Pacing of the ipsilateral ventricle led to the expected rise in ventricular pressure. During right ventricular pacing, the change in left ventricular pressure is modest, suggesting relatively little contribution of right ventricular myocardial contraction to left ventricular mechanical force generation. However, in the top right hand panel, the effect of left ventricular contraction on right ventricular pressure generation can be seen. Pacing of the left ventricle leads to a robust pressure waveform within the right ventricle. This presumably reflects the effect of septal and free wall contraction on RV geometry as a result of circumferential shortening of the left ventricle in response to pacing. Confirmation of this hypothesis can be drawn from the work of Hoffman and colleagues. In their experiments, they replaced the right ventricular free wall with a non-contractile patch. Again, left ventricular contraction led to a near normal right ventricular pressure development, even in the absence of exclusively‘right ventricular’myocardium. It has been estimated that one quarter to one third of the external mechanical work performed by the right ventricle is a direct result of left ventricular contractile work. Clearly therefore, any abnormality of left ventricular performance is likely to reduce intrinsic right ventricular efficiency also. Conversely, increased left ventricular contractility might be expected to impose additional effects on the right side of the heart. The work of Karunanithi and co-workers is interesting in this regard. They showed that right ventricular stroke volume increases in response to an abrupt change in left ventricular afterload. Presumably, homeometric LV adaptation leads to increased right ventricular shortening via a cross-talk mechanism. So far however, this interaction has rarely been, intentionally, reported as a therapeutic mechanism.
The effects of the right ventricle on left ventricular performance
The studies by Damiano, discussed above, suggest that in health, right ventricular contractile work adds little to left ventricular performance. It is becoming increasingly clear however, that abnormalities of right heart function can negatively impact on left ventricular contractile performance. The mechanisms for these adverse interactions are both via series and parallel effects. Clearly any perturbation which leads to a reduction in right ventricular cardiac output, will have a series effect, in terms of left ventricular preload and output. Equally important causes of dysfunction are manifest via parallel mechanisms. In this situation, abnormal right heart dilatation, right ventricular pressure overload, etc. have direct effects on left ventricular geometry and subsequently on its systolic and diastolic performance. Often the relative contribution of these series and parallel effects are difficult to separate in the clinical or experimental situation. For example in the experiment by Hoffman, described above, not only was it shown that left ventricular contractile performance contributed to right ventricular work (in the absence of a contractile right ventricular free wall) but also, as the right ventricle dilated (as the non-contractile patch was enlarged), left ventricular pressure development fell. Whether this was a result of adverse ventriculo-ventricular interactions, in a parallel fashion, or a series effect, because of reduced right ventricular cardiac output, could not be answered in this study. We therefore investigated this phenomenon in a porcine model of acute right heart dilatation induced by local right ventricular free wall ischemia. Using conductance catheter measurements, we were able to measure load independent indices of contractile performance in both the right and left ventricle. In this model acute right ventricular dilatation led to a fall in left ventricular contractile performance as assessed by preload recruitable stroke work and end systolic elastance. This was presumably related to changes in ventricular geometry and adverse crosstalk, undermining left ventricular contractile performance. This was substantiated by our finding that these effects were exaggerated in the presence of an intact pericardium. Indeed, relief of pericardial constraint mitigated against the changes in left ventricular volume (imposed by right heart dilatation) but were still associated with reduced intrinsic contractile performance.
Such interactions are not confined to the experimental laboratory however. It is becoming increasingly apparent that congenital heart diseases, as natural models of abnormal right heart hemodynamics, are characterized by adverse ventriculo-ventricular interactions. Taking tetralogy of Fallot as an example, it is now clear that left ventricular dysfunction is linearly associated with right heart dysfunction. While the fundamental mechanisms remain to be explored, there is a loose relationship between right and left ventricular ejection fraction in these patients, and those with poor left ventricular function, in association with right heart dilatation, have worse long term outcomes. It is important to remember that not only are geometric considerations important, but abnormalities of ventricular coordination, in terms of the timing of contraction and relaxation, may also impose a significant burden on biventricular performance. Calabro’s group have recently shown that interventricular dyssynchrony (presumably as a consequence of the right bundle branch block - itself a surrogate of right heart dilation) is an important predictor of both exercise performance and the presence of ventricular arrhythmia. While representing another manifestation of abnormal cross-talk, the issues of ventricular synchronization represent a possible therapeutic target. Resynchronization of intraventricular incoordination is now of proven benefit to the ischemic and dilated cardiomyopathies in the structurally normal heart. There are few data regarding either intra or interventricular resynchronization in congenital heart disease, but the registry data appear to be promising, and in individuals, the beneficial effects may be profound.
There are many other ways in which the right and left ventricles may interact in congenital heart disease. The influence of septal position and its relationship to tricuspid valve function, in the setting of congenitally and surgically corrected transposition will be discussed elsewhere. Similarly, the adverse effects of‘isolated’right heart diseases, such as Ebstein’s anomaly of the tricuspid valve, on biventricular performance are becoming increasingly understood. All of these interactions are further impacted by the relationship between the right heart and its pulmonary vascular bed. Indeed, a full description of right heart function is incomplete without assessing the influence of cardiopulmonary interactions.