The variations in total blood volume affect the vascular function curve. When there is no cardiac output, mean circulatory pressure is solely dependent on total vascular compliance and blood volume. Hypervolemia (expanded blood volume) leads to an increase in mean circulatory pressure, while hypovolemia (diminished blood volume) causes a decrease. This relationship is shown in Fig. 19.4, where mean circulatory pressure is 5 mm Hg after hemorrhage, 9 mm Hg after transfusion, and 7 mm Hg at normal blood volume (normovolemia or euvolemia).

Changes in venomotor tone have a similar effect on the vascular function curve as changes in blood volume. In Fig. 19.4, the transfusion curve can also represent increased venomotor tone, while the hemorrhage curve can represent decreased tone. In the case of sudden occlusion of a major coronary artery, cardiac output may abruptly decrease. Myocardial infarction (death of myocardial tissue) usually results in acute heart failure accompanied by a fall in arterial blood pressure and a rise in Pv. Fig. 19.4 also shows that the cardiac output at which Pv = 0 varies directly with blood volume. As a result, the maximal value of cardiac output becomes more limited as the total blood volume is reduced. However, the pressure at which the veins collapse (illustrated by the sharp change in slope of the vascular function curve) is not significantly affected by changes in blood volume. This pressure depends only on the ambient pressure surrounding the central veins, which is the pleural pressure in the thorax.

Under nervous and humoral control, the pressure within the vascular system increases as smooth muscle tension in the vascular walls increases. Arteriolar tone (changes in peripheral resistance) has no significant effect on mean circulatory pressure, while changes in venous tone can significantly alter it. Mean circulatory pressure rises with increased venomotor tone and falls with diminished venomotor tone.

In experiments, the mean circulatory pressure approximately 1 minute after abrupt circulatory standstill is usually higher than 7 mm Hg, even with normal blood volume. This elevation is attributed to generalized venoconstriction caused by cerebral ischemia, activation of chemoreceptors, and reduced excitation of baroreceptors. If resuscitation is unsuccessful, this reflex response subsides as central nervous activity ceases, and mean circulatory pressure usually falls to a value close to 7 mm Hg.

Certain regions of the body experience greater venoconstriction than others, which serve as blood reservoirs. In humans, the skin's vascular bed is one of the major blood reservoirs. Hemorrhage triggers significant subcutaneous venoconstriction, resulting in the pale appearance of the skin. This diversion of blood from the skin allows for perfusion through more vital regions of the body. The vascular beds of the liver, lungs, and spleen also serve as important blood reservoirs. However, the volume changes in the spleen are less extensive compared to other organs. The changes in the vascular function curve caused by alterations in arteriolar tone are depicted in Fig. 19.5 "Effectsofarteriolardilationandconstrictiononthevascularfunctioncurve."
The vascular function curve is affected by variations in total blood volume. During circulatory standstill (zero cardiac output), mean circulatory pressure depends only on total vascular compliance and blood volume. For a given vascular compliance, mean circulatory pressure is increased when blood volume is expanded (hypervolemia) and is decreased when blood volume is diminished (hypovolemia). This relationship is illustrated by the y-axis intercepts in
Fig.
19.4 , in which mean circulatory pressure is 5 mm Hg after hemorrhage and 9 mm Hg after transfusion, in comparison with a value of 7 mm Hg at normal blood volume (normovolemia or euvolemia).
The effects of changes in venomotor tone on the vascular function curve closely resemble those of changes in blood volume. In
Fig. 19.4 , for example, the transfusion curve could also represent increased venomotor tone, whereas the hemorrhage curve could represent decreased tone. During
Cardiacoutputmaydecreaseabruptlywhenamajorcoronaryarterysuddenlybecomesoccluded.Theacute heart failure thatoccursasaresultofmyocardial infarction (deathofmyocardialtissue)isusuallyaccompaniedbyafallinarterialbloodpressureandariseinPv.In
Fig.19.4 itisalsoapparentthatthecardiacoutputatwhichPv= 0variesdirectlywithbloodvolume.Therefore,themaximalvalueofcardiacoutputbecomesprogressivelymorelimitedasthetotalbloodvolumeisreduced.However,thePvatwhichtheveinscollapse(illustratedbythesharpchangeinslopeofthevascularfunctioncurve)isnotsignificantlyalteredbychangesinbloodvolume.Thispressuredependsonlyontheambientpressuresurroundingthecentralveins.Ambientpressureisthepleuralpressureinthethorax(see circulatory standstill, for a given blood volume, the pressure within the vascular system rises as smooth muscle tension exerted within the vascular walls increases (these contractile changes in arteriolar and venous smooth muscle are under nervous and humoral control). The fraction of the blood volume located within the arterioles is very small, whereas the blood volume in the veins is large percentage of total blood volume (see
Table 15.1 ). Thus changes in peripheral resistance (arteriolar tone) have no significant effect on mean circulatory pressure, but changes in venous tone can alter mean circulatory pressure appreciably. Hence, mean circulatory pressure rises with increased venomotor tone and falls with diminished venomotor tone.
In experiments, the mean circulatory pressure attained approximately 1 minute after abrupt circulatory standstill is usually substantially above 7 mm Hg, even when blood volume is normal. The elevation to this pressure level is attributable to the generalized venoconstriction that is caused by cerebral ischemia, activation of chemoreceptors, and reduced excitation of baroreceptors. If resuscitation fails, this reflex response subsides as central nervous activity ceases, and mean circulatory pressure then usually falls to a value close to 7 mm Hg.
Venoconstriction is considerably greater in certain regions of the body than in others. In effect, vascular beds that undergo significant venoconstriction constitute blood reservoirs. The skin’s vascular bed is one of the major blood reservoirs in humans. Blood loss evokes profound subcutaneous venoconstriction, which gives rise to the characteristically pale appearance of the skin in response to hemorrhage. Diversion of blood away from the skin frees several hundred milliliters of blood that can be perfused through more vital regions of the body. The vascular beds of the liver, lungs, and spleen are also important blood reservoirs. In humans, however, the volume changes in the spleen are considerably less extensive (see also the sections “ •Fig. 19.5 Effectsofarteriolardilationandconstrictiononthevascularfunctioncurve.
The changes in the vascular function curve induced by alterations in arteriolar tone are depicted in