At the start of cardiac arrest, there is no blood flow (Qh = 0) and the volume of blood in the arteries (Va) and veins (Vv) remains relatively unchanged. As a result, arterial pressure (Pa) and venous pressure (Pv) are the same as in Fig. 19.2A (Pa = 102 and Pv = 2). This creates a pressure gradient of 100 mm Hg between the arteries and veins, leading to a flow rate (Qr) of 5 L/minute through the peripheral resistance of 20 mm Hg/L/minute. Even though cardiac output (Qh) is 0 L/minute, blood continues to flow through the microcirculation (Qt) due to the potential energy stored in the arteries from previous pumping action. Initially, this transfer of blood from arteries to veins occurs at a steady-state rate, even though the heart can no longer transfer blood from veins to arteries.

As cardiac arrest persists, blood flow through the resistance vessels causes a progressive decrease in arterial blood volume and a corresponding increase in venous blood volume. The elastic nature of the arteries and veins leads to a gradual decline in arterial pressure and a gradual rise in venous pressure. This process continues until arterial and venous pressures equalize, as shown in Fig. 19.2C. At this equilibrium state, the flow rate from arteries to veins through the resistance vessels (Qr) is 0 L/minute, as is Qh.

When the effects of cardiac arrest reach this equilibrium state, the pressure in the arteries and veins depends on their relative compliance. If arterial compliance (Ca) and venous compliance (Cv) are equal, the decline in Pa is equal to the rise in Pv because the decrease in arterial volume matches the increase in venous volume. In this case, both Pa and Pv would reach an average value of 52 mm Hg, as calculated from Fig. 19.2A. However, in living individuals, arterial and venous compliance are not equal. Veins are much more compliant than arteries, with a compliance ratio (Cv/Ca) of approximately 19 as assumed in the model in Fig. 19.2. Consequently, when cardiac arrest reaches equilibrium in a person, the pressures in the arteries and veins are much lower than the average value of 52 mm Hg. The transfer of blood from arteries to veins at equilibrium leads to a significant fall in arterial pressure, approximately 19 times greater than the rise in venous pressure. In Fig. 19.2C, Pv increases by 5 mm Hg (to 7 mm Hg), while Pa decreases by 95 mm Hg (19 × 5 mm Hg). This equilibrium pressure, which occurs in the absence of flow, is referred to as mean circulatory pressure or static pressure. The static pressure reflects the total blood volume in the system and the overall compliance of the system.

The example of cardiac arrest helps in understanding the vascular function curve, represented in Fig. 19.3. The curve plots cardiac output (independent variable along the x-axis) against Pv (dependent variable along the y-axis). Key points on this curve can be derived from the example shown in Fig. 19.2. One such point is A in [Fig. 19.3].
Effects of Cardiac Arrest on Arterial and Venous Pressure
Fig. 19.2B depicts the circulation at the very beginning of an episode of cardiac arrest; that is, Qh = 0. In the instant immediately after arrest of the heart, the volume of blood in the arteries (Va) and veins (Vv) has not had time to change appreciably. Because arterial pressure and venous pressure depend on Va and Vv, respectively, these pressures are identical to the respective pressures in
Fig. 19.2A (i.e., Pa = 102 and Pv = 2). This arteriovenous pressure gradient of 100 mm Hg forces a flow rate (Qr) of 5 L/minute through the peripheral resistance of 20 mm Hg/L/minute. Thus although cardiac output (Qh) at that point is 0 L/ minute, the rate of flow through the microcirculation (Qt) is 5 L/minute because the potential energy stored in the arteries by the preceding pumping action of the heart causes blood to be transferred from arteries to veins. This transfer occurs initially at the control (steady-state) rate, even though the heart can no longer transfer blood from the veins to the arteries.
As cardiac arrest continues, blood flow through the resistance vessels causes the blood volume in the arteries to decrease progressively and the blood volume in the veins to increase progressively at the same absolute rate. Because the arteries and veins are elastic structures, arterial pressure falls gradually, and the venous pressure rises gradually. This process continues until arterial and venous pressures become equal (see
Fig. 19.2C ). Once this condition is reached, the rate of flow (Qr) from the arteries to the veins through the resistance vessels is 0 L/minute, as is Qh.
When the effects of cardiac arrest reach this equilibrium state (see
Fig. 19.2C ), the pressure attained in the arteries and veins depends on the relative compliance of these vessels. If arterial compliance (Ca) and venous compliance (Cv) are equal, the decline in Pa is equal to the rise in Pv because the decrease in arterial volume would be equal to the increase in venous volume (according to the principle of conservation of mass). Both Pa and Pv would attain the average of their combined values in
Fig. 19.2A ; that is, Pa = Pv = (102 + 2)/2 = 52 mm Hg. However, Ca and Cv in a living person are not equal. Veins are much more compliant than arteries; the compliance ratio (Cv/Ca) is approximately 19, the ratio assumed for the model in
Fig. 19.2 . When the effects of cardiac arrest reach equilibrium in an intact subject, the pressure in the arteries and veins is much lower than the average value of 52 mm Hg that occurs when Ca and Cv are equal. Hence, transfer of blood from arteries to veins at equilibrium induces a fall in arterial pressure 19 times greater than the concomitant rise in venous pressure. As
Fig. 19.2C shows, Pv would increase by 5 mm Hg (to 7 mm Hg), whereas Pa would fall by 95 (i.e., 19 × 5) mm Hg (to 7 mm Hg). This equilibrium pressure, which prevails in the absence of flow, is referred to as either mean circulatory pressure or static pressure. The pressure in the static system reflects the total blood volume in the system and the overall compliance of the system.
•Fig. 19.2 A toD, Simplifiedmodelofthecardiovascularsystem,consistingofapump,arterialcompliance(Ca),peripheralresistance,andvenouscompliance(Cv).
The example of cardiac arrest aids in the understanding of the vascular function curve. The clinician can now begin to assemble a vascular function curve (
Fig. 19.3 ). The independent variable (plotted along the x-axis) is cardiac output, and the dependent variable (plotted along the y-axis) is Pv. Two important points on this curve can be derived from the example in
Fig. 19.2 . One point (A in