In the model, the cardiac outputs of the right and left ventricles vary directly with their respective filling pressures. Normally, the outputs of both ventricles are equal at 5 L/minute. The right ventricle's pumping action causes the pressure in the pulmonary artery to exceed the pressure in the pulmonary veins, resulting in fluid flow through the pulmonary vascular resistance at a rate of 5 L/minute. 

When the right ventricle stops pumping, the systemic venous and pulmonary arterial systems, along with the right ventricle itself, become a passive conduit with a large compliance. As a result, pulmonary arterial pressure decreases rapidly and systemic venous pressure rises to approximately 5 mm Hg. At this low pressure, however, fluid flows from the pulmonary arteries to the pulmonary veins at a significantly reduced rate.

At the onset of right ventricular arrest, the left ventricle continues to pump fluid from the pulmonary veins to the systemic arteries at the control rate of 5 L/minute, which is much higher than the rate at which blood returns to the pulmonary veins after the right ventricle stops functioning. Consequently, pulmonary venous pressure drops sharply, affecting the preload for the left ventricle and causing left ventricular output to abruptly decrease to a steady-state value of around 2.5 L/minute. This reduction in left ventricular output then leads to a rapid decrease in systemic arterial pressure.

In summary, the cessation of right ventricular pumping significantly reduces cardiac output, systemic arterial pressure, and pulmonary venous pressure. These effects can be reversed by increasing the fluid volume in the system. Adding fluid until pulmonary venous pressure (left ventricular preload) returns to its control value restores cardiac output and systemic arterial pressure to almost normal levels, but results in abnormally elevated systemic venous pressure. If left ventricular function is normal, adding a normal left ventricular preload evokes normal left ventricular output. The increase in peripheral resistance caused by the addition of pulmonary vascular resistance to systemic vascular resistance does not pose a serious burden on left ventricular pumping capacity. However, in the absence of right ventricular function, normal pulmonary blood flow is not achieved unless the usual pulmonary arteriovenous pressure gradient of approximately 10 to 15 mm Hg is maintained. Thus, systemic venous pressure must exceed pulmonary venous pressure by this amount.
Fig. 19.13 . In the model, the right and left ventricles generate cardiac outputs that vary directly with their respective filling pressures. Under control conditions (when the right ventricle is functioning normally), the outputs of the left and right ventricles are equal (5 L/ minute). The right ventricular pumping action causes the pressure in the pulmonary artery (not shown) to exceed the pressure in the pulmonary veins (Ppv) by an amount that forces fluid through the pulmonary vascular resistance at a rate of 5 L/minute. When the right ventricle ceases pumping (arrow 1 in
Fig. 19.13 ), the systemic venous and pulmonary arterial systems, along with the right ventricle itself, become a common passive conduit with a large compliance. When the right ventricle ceases to transfer blood actively from the systemic veins to the pulmonary arteries, pulmonary arterial pressure (Ppa) decreases rapidly (not shown) and systemic venous pressure (Psv) rises rapidly to a common value (≈5 mm Hg). At this low pressure, however, fluid flows from the pulmonary arteries to the pulmonary veins at a greatly reduced rate.
At the start of right ventricular arrest, the left ventricle is pumping fluid from the pulmonary veins to the systemic arteries at the control rate of 5 L/minute, which greatly exceeds the rate at which blood returns to the pulmonary veins once the right ventricle ceases to operate. Hence, pulmonary venous pressure (Ppv) drops sharply. Because pulmonary venous pressure is the preload for the left ventricle, left ventricular (cardiac) output drops abruptly as well and attains a steady-state value of approximately 2.5 L/minute. This effect in turn leads to a rapid reduction in systemic arterial pressure (Psa). In short, stoppage of right ventricular pumping markedly curtails cardiac output, systemic arterial pressure, and pulmonary venous •Fig. 19.13 Changesincardiacoutput,systemicarterialpressure(Psa),systemicvenouspressure(Psv),andpulmonaryvenouspressure(Ppv)evokedbysimulatedrightventricular(RV)failureandbysimulatedinfusionoffluidinthecirculatorymodelshownin
Fig.19.12 .Atarrow 1, thepumpingactionoftherightventriclewasdiscontinued(simulatedRVfailure),andtherightventricleservedonlyasalow-resistanceconduit.Atarrow 2, thefluidvolumeinthesystemwasexpanded,andtherightventriclecontinuedtoserveonlyasaconduit.(ModifiedfromFureySA,etal.Am Heart J. 1984;107:404.)
Fig. 19.13).
Most of the hemodynamic problems induced by inactivation of the right ventricle can be reversed by an increase in the fluid (blood) volume of the system (arrow 2 in
Fig.
19.13). If fluid is added until pulmonary venous pressure (left ventricular preload) is raised to its control value, cardiac output and systemic arterial pressure are restored almost to normal, but systemic venous pressure is abnormally elevated. If left ventricular function is normal, adding a normal left ventricular preload evokes normal left ventricular output. The 10% increase in peripheral resistance caused by adding the pulmonary vascular resistance to that of the systemic vascular resistance does not impose a serious burden on left ventricular pumping capacity.
When the right ventricle is inoperative, however, pulmonary blood flow is not normal unless the usual pulmonary arteriovenous pressure gradient (≈10 to 15 mm Hg) prevails. Hence, systemic venous pressure (Psv) must exceed pulmonary venous pressure (Ppv) by this amount.