High systemic venous pressure can lead to the accumulation of tissue fluid (edema) in dependent regions of the body, which is commonly observed in patients with right ventricular heart failure. The left ventricle alone can adequately provide sufficient blood flow to all tissues in the body, making the operation of both ventricles in series unnecessary for this function. The primary role of the right ventricle is to prevent an increase in systemic venous (and pulmonary arterial) pressure, which would be required to push the normal cardiac output through the pulmonary vascular resistance. By preventing an abnormal rise in systemic venous pressure, a healthy right ventricle prevents the development of extensive edema in dependent areas of the body.

Clinically, right ventricular heart failure can occur due to occlusive disease predominantly affecting the coronary vessels supplying the right ventricle. Although these vessels are less commonly affected compared to those supplying the left ventricle. Acute right-sided heart failure results in significant reductions in cardiac output and arterial blood pressure, and the primary treatment involves blood or plasma infusion. In certain cases of congenital cardiac defects such as severe narrowing of the tricuspid valve or underdevelopment of the right ventricle, surgical bypass of the right ventricle (by connecting the right atrium to the pulmonary artery) may be performed. The effects of acute right-sided heart failure or right ventricular bypass are similar to those predicted from analysis of the model shown in Figure 19.13.

The control of cardiac output depends on stroke volume and heart rate. Although previous analysis has focused on the control of stroke volume, the role of heart rate has not been considered. Altering heart rate affects the other factors (preload, afterload, and myocardial contractility) that determine stroke volume, making the analysis of its effect on cardiac output complex. For example, an increase in heart rate shortens the duration of diastole, reducing ventricular filling (preload). If a change in heart rate directly influenced cardiac output, it would also alter arterial pressure (afterload). Additionally, an increase in heart rate enhances myocardial contractility by increasing the net influx of calcium ions into myocardial cells.

Extensive research has been conducted to investigate the effects of heart rate changes on cardiac output, yielding results similar to those depicted in Figure 19.14. As atrial pacing frequency gradually increases, stroke volume progressively decreases due to reduced ventricular filling. However, the change in stroke volume is not inversely proportional to the change in heart rate since the direction of the change in cardiac output is strongly influenced by the actual heart rate. For instance, as pacing frequency increases from 50 to 100 beats per minute, the rise in heart rate augments cardiac output. This is because cardiac output (Qh) is the product of stroke volume (SV) and heart rate (HR), and the decrease in stroke volume over this frequency range must be proportionately smaller than the increase in heart rate.

Between approximately 100 and 200 beats per minute, changes in pacing frequency do not significantly affect cardiac output.
Maintenance of high systemic venous pressure may lead to the accumulation of tissue fluid (edema) in dependent regions of the body, a characteristic finding in patients with right ventricular heart failure. With this information, the principal function of the right ventricle may be characterized as as follows. From the viewpoint of providing sufficient flow of blood to all tissues in the body, the left ventricle alone can carry out this function. Operation of the two ventricles in series is not essential to provide adequate blood flow to the tissues. The crucial function of the right ventricle is to prevent the rise in systemic venous (and pulmonary arterial) pressure that would be required to force the normal cardiac output through the pulmonary vascular resistance. A normal right ventricle, by preventing an abnormal rise in systemic venous pressure, prevents the development of extensive edema in dependent regions of the body.
Clinically,right ventricular heart failure maybecausedbyocclusivediseasepredominantlyofthecoronaryvesselstotherightventricle.Thesevesselsareaffectedmuchlesscommonlythanthevesselstotheleftventricle.Themajorhemodynamiceffectsofacuteright-sidedheartfailurearepronouncedreductionsincardiacoutputandarterialbloodpressure,andtheprincipaltreatmentisinfusionofbloodorplasma.Bypassoftherightventricle(byanastomosisoftherightatriumtothepulmonaryartery)maybeperformedsurgicallyinpatientswithcertaincongenital cardiac defects, suchasseverenarrowingofthetricuspidvalveormaldevelopmentoftherightventricle.Theeffectsofacuteright-sidedheartfailureorrightventricularbypassaredirectionallysimilartothosepredictedpreviouslyfromanalysisofthemodelshownin
Fig.19.13
Role of the Heart Rate in Control of Cardiac Output
Cardiac output is the product of stroke volume and heart rate. Analysis of the control of cardiac output has thus far been restricted to the control of stroke volume, and the role of heart rate has not been considered. Analysis of the effect of a change in heart rate on cardiac output is complex because a change in heart rate alters the other three factors (preload, afterload, and myocardial contractility) that determine stroke volume (see
Fig. 19.1 ). An increase in heart rate, for example, shortens the duration of diastole. Hence, ventricular filling is diminished; that is, preload is reduced. If an increase in heart rate altered cardiac output, arterial pressure would change; that is, afterload would be altered. A rise in heart rate would increase the net influx of Ca++ per minute into myocardial cells (see also ), and this influx would enhance myocardial contractility.
The effects of changes in heart rate on cardiac output have been studied extensively, and the results are similar to those shown in
Fig. 19.14 . As atrial pacing frequency is •Fig. 19.14 Changesinstrokevolume(A) andcardiacoutput (B) inducedbychangesintherateofatrialpacing.(RedrawnfromKumadaM,etal.Jpn J Physiol. 1967;17:538.) gradually increased, stroke volume progressively diminishes (see
Fig. 19.14A ). The decrease in stroke volume is caused by the reduced time for ventricular filling. The change in stroke volume is not inversely proportional to the change in heart rate because the direction of the change in cardiac output (Qh) is markedly influenced by the actual heart rate (see
Fig. 19.14B ). For example, as pacing frequency is increased from 50 to 100 beats/minute, the increase in heart rate augments Qh. Because Qh = SV × HR, the decrease in stroke volume (SV) over this frequency range must be proportionately less than the increase in heart rate (HR).
Over the frequency range from approximately 100 to 200 beats/minute, however, cardiac output is not affected significantly by changes in pacing frequency (see
Fig.