Cardiovascular Physiology
Cardiovascular Patterns in Health and Disease
Hemorrhage and Other Causes
of Hypotension
The term
means a low blood pressure, regardless
of cause. One general cause of hypotension is a loss of blood
volume, as for example in a hemorrhage, which produces
hypotension by the sequence of events shown previously in
Figure 12–52. The most serious consequences of hypotension
are reduced blood fl ow to the brain and cardiac muscle.
The immediate counteracting response to hemorrhage is
the arterial baroreceptor refl ex, as summarized in Figure 12–56.
Figure 12–58
, which shows how fi ve variables change
over time when blood volume decreases, adds a further degree
of clarifi cation to Figure 12–56. The values of factors changed
as a direct result of the hemorrhage—stroke volume, cardiac
output, and mean arterial pressure—are restored by the baro-
receptor refl ex toward, but not all the way to, normal. In con-
trast, values not altered directly by the hemorrhage but only by
the refl ex response to hemorrhage—heart rate and total periph-
eral resistance—increase above their pre-hemorrhage values.
The increased peripheral resistance results from increases in
sympathetic outfl ow to the arterioles in many vascular beds but
not those of the heart and brain. Thus, skin blood fl ow may
decrease considerably because of arteriolar vasoconstriction—
this is why the skin becomes cold and pale. Kidney and intes-
tinal blood fl ow also decrease because the usual functions of
these organs are less immediately essential for life.
A second important type of compensatory mechanism
(one not shown in Figure 12–56) involves the movement of
interstitial fl uid into capillaries. This occurs because both the
drop in blood pressure and the increase in arteriolar constric-
tion decrease capillary hydrostatic pressure, thereby favoring
the absorption of interstitial fl uid (
Figure 12–59
). Thus, the
initial event—blood loss and decreased blood volume—is in
large part compensated for by the movement of interstitial
uid into the vascular system. This mechanism, referred to as
can restore the blood volume to virtually
normal levels within 12 to 24 hours after a moderate hem-
orrhage (
Table 12–6
). At this time, the entire restoration of
blood volume is due to expansion of the plasma volume and,
thus, the hematocrit actually decreases.
The early compensatory mechanisms for hemorrhage
(the baroreceptor refl
exes and interstitial fl uid absorption) are
highly effi
cient, so that losses of as much as 1.5 L of blood—
approximately 30 percent of total blood volume—can be sus-
tained with only slight reductions of mean arterial pressure or
cardiac output.
We must emphasize that absorption of interstitial fl
the extracellular fl
uid. Ultimate
Restoration of
arterial pressure
toward normal
Plasma volume
Fluid absorption
from interstitial
(Fig. 12-56)
Stroke volume
Heart rate
Cardiac output (SV x HR)
Total peripheral resistance
Mean arterial pressure
(CO x TPR)
Figure 12–58
Five simultaneous graphs showing the time course of cardiovascular
effects of hemorrhage. Note that the entire decrease in arterial
pressure immediately following hemorrhage is secondary to the
decrease in stroke volume and, thus, cardiac output. This fi
emphasizes the relative proportions of the “increase” and “decrease”
arrows of Figure 12–56. All variables shown are increased relative to
the state immediately following the hemorrhage, but not necessarily
to the state prior to the hemorrhage.
Figure 12–59
The autotransfusion mechanism compensates for blood loss by
causing interstitial fl uid to move into the capillaries.
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