The average cardiac output from the RV must, of course, essentially equal the cardiac output from the left heart. Nonetheless, the mechanism by which this is achieved is very different. The RV performs approximately one-quarter of the external mechanical work compared with its left ventricular (LV) counterpart. External mechanical work is a function of stroke volume and developed ventricular pressure, and is more accurately described as the area enclosed by the ventricular pressure–volume curve. Figure 26.1 shows a schematic comparison of left and right ventricular (RV) pressure–volume curves. Not only is the developed pressure substantially lower in the RV but its trapezoidal shape still further reduces the amount of work performed on the circulation to generate the cardiac output. The LV essentially works as a square wave pump, its stroke work being reasonably well represented as a direct product of its stroke volume and developed pressure (stroke work = stroke volume × peak left ventricular pressure – minimum left ventricular pressure). Because of its ability to eject blood into the pulmonary circulation during both pressure rise and pressure fall (1), the external work performed by the RV cannot be described using such a simple derivation. Furthermore, it can be seen that small changes in hemodynamics might impose a major change to global workload of the RV. Indeed, small changes in RV afterload can lead to major changes in workload and the shape of the pressure–volume characteristics to mirror the LV (2).

The trapezoidal shape of the RV pressure–volume relationship is exquisitely matched to the low hydraulic impedance imposed by the pulmonary vascular bed. Unlike the systemic vascular resistance, which reflects a dynamic balance between vasodilatory and vasoconstrictor influences, the pulmonary vascular bed appears to be maximally vasodilated. The low pulmonary vascular resistance requires a healthy endothelium and normal lung function for its integrity. In health, additional inhaled nitric oxide, for example, fails to lower the pulmonary vascular resistance, suggesting pulmonary endothelial vasodilatory capacity is at its maximum (3). This is a markedly different mechanism to that of the systemic vascular bed where a wide portfolio of vasodilatory substances can lower its resistance. The pulmonary vascular bed is also uniquely affected by external factors. The status of lung inflation, even the normal circulation, has major effects on the pulmonary vascular resistance and hemodynamic function. Normal respiration, ventilating around
functional residual capacity, minimizes the pulmonary vascular resistance. Underinflation of the lungs leads to an increased pulmonary vascular resistance, as a result of atelectasis and secondary alveolar hypoxemia, and overinflation of the lungs leads to an increase, secondary to alveolar stretch and direct vascular compression (Fig. 26.2) (4). Both should be avoided whenever RV afterload needs to be minimized.

Descent of the diaphragm during normal inspiration leads to a modest fall in pleural pressure (3 to 5 cm of water) (5) and a concomitant rise in intra-abdominal pressure. These two changes lead to increased venous return and an increased RV stroke volume, in accord with the Frank–Starling mechanism. There is thus a waxing and waning of cardiac output of approximately 10% to 15% during the cardiac cycle (6).

The classic experiments of Cournand in the 1940s (7) were interpreted as confirmation that right heart filling and cardiac output were related to intrathoracic pressure. Positive pressure ventilation via a mask in conscious volunteers led to a fall in cardiac output of approximately 10% to 15%. This was initially thought to be entirely due to changes in systemic venous return (and reduced ventricular preload) imposed by a raised mean intrathoracic pressure. It has subsequently become clear that reduced preload, as a result of increased airway pressure, is not the whole story. In an elegant series of experiments in dogs, Henning (8) showed that restoration of preload during positive pressure ventilation failed to restore cardiac output to its baseline levels. The persistent reduction in RV stroke volume, despite normalized preload, suggested an adverse effect on intrinsic RV performance. It was hypothesized that the RV shows signs of reduced systolic function, even under the circumstances of a modest hemodynamic burden imposed by lung hyperinflation, as a result of increased afterload occurring via the mechanism described in Figure 26.2. No matter what the mechanism, however, the functional implications of these changes are not simply theoretic. In a study of children undergoing cardiac catheterization performed by Shekerdemian et al. (9), a negative pressure cuirass device was used to mimic normal ventilation to compare the effects of positive and negative pressure ventilation on cardiac output. In essentially normal children having undergone closure of a small arterial duct, for example, there is an approximate 16% fall in cardiac output, simply as a result of a modest rise in mean airway pressure (to ∼8 cm of water) secondary to positive pressure ventilation. These adverse hemodynamic effects of increased RV afterload (negative cardiopulmonary interactions) become even more important when the right heart circulation is affected by congenital heart disease.

The potential for beneficial and adverse cardiopulmonary interactions is greater when the right heart is intrinsically abnormal because of congenital anomalies or is primarily affected by surgery. There are two circumstances in which these concepts are exemplified, those patients with abnormal RV diastolic function and those with exclusion of the RV from the venopulmonary circulation.