Cardiovascular Physiology
Integration of Cardiovascular Function:
Regulation of Systemic Arterial Pressure
In Chapter 1 we described the fundamental components of
all refl ex control systems: (1) an internal environmental vari-
able maintained at a relatively stable level, (2) receptors sensi-
tive to changes in this variable, (3) afferent pathways from the
receptors, (4) an integrating center that receives and integrates
the afferent inputs, (5) efferent pathways from the integrating
center, and (6) effectors the efferent pathways “direct” to alter
their activities. The control and integration of cardiovascular
function will be described in these terms.
The major cardiovascular variable being regulated is the
mean arterial pressure in the systemic circulation. This should
not be surprising because this pressure is the driving force for
blood fl ow through all the organs except the lungs. Maintaining
it is therefore a prerequisite for ensuring adequate blood fl ow to
these organs.
The mean systemic arterial pressure is the arithme-
tic product of two factors: (1) the cardiac output and (2) the
total peripheral resistance (TPR),
which is the sum of the
resistances to fl ow offered by all the systemic blood vessels.
Mean systemic
Total peripheral
arterial pressure =
These two factors, cardiac output and total peripheral
resistance, set the mean systemic arterial pressure because they
determine the average volume of blood in the systemic arteries
over time, and it is this blood volume that causes the pres-
sure. This relationship cannot be emphasized too strongly:
All changes in mean arterial pressure must be the result of
changes in cardiac output and/or total peripheral resistance.
Keep in mind that mean arterial pressure will change only if
the arithmetic product of cardiac output and total peripheral
resistance changes. For example, if cardiac output doubles and
total peripheral resistance decreases 50 percent, mean arterial
pressure will not change because the product of cardiac out-
put and total peripheral resistance has not changed. Because
cardiac output is the volume of blood pumped into the arter-
ies per unit time, it is fairly intuitive that it should be one of
the two determinants of mean arterial volume and pressure.
The contribution of total peripheral resistance to mean arte-
rial pressure is less obvious, but it can be illustrated with the
model introduced previously in Figure 12–33.
As shown in
Figure 12–49
, a pump pushes fl
uid into a
container at the rate of 1 L/min. At steady state, fl
uid also
leaves the container via outfl ow tubes at a total rate of 1 L/min.
Therefore, the height of the fl
uid column (
), which is the
driving pressure for outfl ow, remains stable. We then disturb
the steady state by dilating outfl ow tube 1, thereby increasing
its radius, reducing its resistance, and increasing its fl ow. The
total outfl ow for the system immediately becomes greater than
1 L/min, and more fl uid leaves the reservoir than enters from
the pump. Therefore, the volume and, thus, the height of the
fl uid column begin to decrease until a new steady state between
595 ml
468 ml
170 ml
133 ml
1 L/min
Steady state
Organ blood
1 L/min
200 ml
1.275 L/min
Outflow > Inflow
1 L/min
1 L/min
New steady state
1 L/min
Figure 12–49
Dependence of arterial blood pressure upon total arteriolar resistance. Dilating one arteriolar bed affects arterial pressure and organ blood fl ow
if no compensatory adjustments occur. The middle panel indicates a transient state before the new steady state occurs.
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