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.