Electrical stimulation of the cardiac sympathetic nerves can produce Fig. 19.7. When the neural stimulation is limited to the heart, it does not affect the vascular function curve. Therefore, only one vascular function curve is necessary for this hypothetical intervention (see Fig. 19.7).

In the control state of the model, point A in Fig. 19.7 represents the equilibrium values for cardiac output and Pv. Stimulation of the cardiac sympathetic nerves increases cardiac output abruptly to point B due to enhanced myocardial contractility. However, this elevated cardiac output leads to a net transfer of blood from the veins to the arteries of the circuit, resulting in a subsequent decrease in Pv to point C. The reduction in Pv then causes a slight decrease in cardiac output. However, the cardiac output remains high enough to affect the net transfer of blood from the veins to the arteries, causing both Pv and cardiac output to gradually decrease until reaching a new equilibrium point, point D. This point is located at the intersection of the vascular function curve and the new cardiac function curve, and it is above and to the left of the control equilibrium point (point A). This demonstrates that sympathetic stimulation can induce greater cardiac output despite the lower level of Pv (see Fig. 19.8).

The model in this chapter mimics the biological response to enhancement of myocardial contractility. As shown in Fig. 19.8, stimulation of the sympathetic nerves innervating the heart results in a quick rise in cardiac output (aortic flow) followed by a gradual decrease to a steady-state value significantly higher than the control level. This increase in aortic flow is accompanied by reductions in right and left atrial pressures.

Changes in blood volume do not directly impact myocardial contractility but do influence the vascular function curve as depicted in Fig. 19.4. To understand the effects of changes in blood volume on cardiac output and Pv, the appropriate cardiac function curve is plotted along with the control and experimental states' vascular function curves (see Fig. 19.9). When blood volume increases due to a blood transfusion, the equilibrium point (point B in Fig. 19.9) representing the values of cardiac output and Pv after transfusion lies above and to the right of the control equilibrium point (point A). Thus, transfusion increases both cardiac output and Pv. On the other hand, hemorrhage has the opposite effect. Mechanistically, changes in ventricular filling pressure (Pv) resulting from changes in blood volume alter cardiac output by affecting the sensitivity of the contractile proteins to the concentration of intracellular Ca++ (see section). Increases or decreases in venomotor tone elicit responses similar to those induced by increases or decreases in total blood volume.

After a blood transfusion, the vascular function curve is shifted to the right in Fig. 19.9. Consequently, both cardiac output and venous pressure increase, as indicated by the translocation of the equilibrium point from point A to point B.
Fig. 19.7 can be produced by electrical stimulation of the cardiac sympathetic nerves. When the effects of such neural stimulation are restricted to the heart, the vascular function curve is unaffected. Therefore, only one vascular function curve is needed for this hypothetical intervention (see
Fig. 19.7
During the control state of the model, the equilibrium values for cardiac output and Pv are designated by point A in
Fig. 19.7 . Cardiac sympathetic nerve stimulation abruptly raises cardiac output to point B because of the enhanced myocardial contractility. However, this high cardiac output causes an increase in the net transfer of blood from the veins to the arteries of the circuit, and as a consequence, Pv subsequently begins to fall (to point C). The reduction in Pv then leads to a small decrease in cardiac output. However, cardiac output is still sufficiently high to effect •Fig. 19.8 Duringelectricalstimulationofthecardiacsympatheticnervefibers,aorticbloodflow(cardiacoutput)increased,whereaspressuresintheleftatrium(PLA)andrightatrium(PRA)diminished.Thesedataconformtotheconclusionsderivedfrom
Fig.19.7 ,inwhichtheequilibriumvaluesofcardiacoutputandvenouspressureareobservedtoshiftfrompointAtopointD(i.e.,cardiacoutputincreased,butcentralvenouspressuredecreased)duringcardiacsympatheticnervestimulation.(RedrawnfromSarnoffSJ,etal.Circ Res. 1960;8:1108.) the net transfer of blood from the veins to the arteries of the circuit. Thus both Pv and cardiac output continue to fall gradually until a new equilibrium point (point D) is reached. This equilibrium point is located at the intersection of the vascular function curve and the new cardiac function curve. In
Fig. 19.7 , point D lies above and to the left of the control equilibrium point (point A) and indicates that sympathetic stimulation can evoke greater cardiac output despite the lower level of Pv.
The biological response to enhancement of myocardial contractility is mimicked by the hypothetical change predicted by the model in this chapter. As depicted in
Fig. 19.8 , sympathetic nerves innervating the heart are stimulated during the time denoted by the double-headed arrow. During neural stimulation, cardiac output (aortic flow) rises quickly to a peak value and then falls gradually to a steady-state value significantly higher than the control level. The increase in aortic flow is accompanied by reductions in right and left atrial pressures.
Changes in blood volume do not directly affect myocardial contractility, but they do influence the vascular function curve in the manner shown in
Fig. 19.4 . Thus to understand how changes in blood volume affect cardiac output and Pv, the appropriate cardiac function curve is plotted along with the vascular function curves that represent the control and experimental states (
Fig. 19.9 ). When blood volume is increased by a blood transfusion, the equilibrium point (point B in
Fig. 19.9 ), which denotes the values of cardiac output and Pv after transfusion, lies above and to the right of the control equilibrium point (point A). Thus transfusion increases both cardiac output and Pv. Hemorrhage causes the opposite effect. Mechanistically, the change in ventricular filling pressure (Pv) evoked by a given change in blood volume alters cardiac output by changing the sensitivity of the contractile proteins to the prevailing concentration of intracellular Ca++ (see ). For reasons explained earlier, pure increases or decreases in venomotor tone elicit responses that are like those evoked by increases or decreases, respectively, in total blood volume.
•Fig. 19.9 Afterabloodtransfusion,thevascularfunctioncurveisshiftedtotheright.Therefore,bothcardiacoutputandvenouspressureareincreased,asdenotedbytranslocationoftheequilibriumpointfrompointAtopointB.–2 A B 1086420 0 2 4 6 8 10 Central venous pressure (mm Hg) Transfusion ControlCardiac output (L/min)