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.