Page 110 - Cardiac Nursing

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86 PA R T I / Anatomy and Physiology
2
1
RELATION BETWEEN CARDIAC
OUTPUT AND CENTRAL VENOUS
V
2
PRESSURE—RETROGRADE
VERSUS ANTEGRADE MODELS
V
1 In the 1950s, Guyton et al. 236–238 developed a model in which
Venous volume central venous pressure was presumed to affect cardiac output in
a retrograde fashion. However, an opposing conceptualization is a
model of the anterograde relationship between cardiac output and
central venous pressure, that is, cardiac output affects central ve-
nous pressure. 70,239,240 A recent point–counterpoint discussion
has failed to resolve these opposing models, with issues around the
concept of mean circulatory pressure, the clarification of the com-
ponents of the pressure gradient (mean circulatory pressure vs.
V
o
right atrial pressure) and its effect on cardiac output, and the ap-
O P 1 P 2 plication of the models in static versus dynamic states. 241–245
Venous transmural pressure There are several implications of this discussion for clinical
practice. For example, does increasing heart rate increase cardiac
■ Figure 3-13 Typical volume–pressure curve of an isolated vein.
P
P
V
V
Dashed lines (1 and 2) show the compliance ( V/ P) at two venous output? In experiments, an increase in cardiac output secondary
P
transmural pressures, P 1 and P 2 P . Note that compliance varies with to an increase in heart rate was limitedby a decrease in central ve-
172
pressure, being greatest at the lower pressures (line 1) and decreasing nous pressure. Consideration of the resistive and capacitive
V V
as the pressure increases (line 2). V 0 is the unstressed volume, which is properties of the arteries and veins within the context of an ante-
the volume contained at 0 transmural pressure. The change in volume grade model may help to explain this effect. 99,168 In response to
from V 2 to V 1 is the passive effect of changing pressures from P 2 P to P 1 . increasedbloodflow (increased cardiac output), transmuralpres-
P
V V
V V
Note how changing cross-sectional geometry contributes to passive sure in the veins rises, and thus their volume rises as well. The
emptying. (From Rowell, L. B. [1986]. Human circulation: Regulation consequent shift in blood volume from the central to the periph-
during physical stress [p. 46]. New York: Oxford University Press.) 73,168,169
eral veins lowers the central venous pressure. If cardiac
output continues to increase, the central venous pressure ap-
not initially distended compared with the volume expansion that proaches 0 mm Hg, and eventually the central venous vasculature
would occur if the veins were fully distended with decreased com- collapses, making it impossible to increase cardiac output further.
pliance. Conversely, passive vasoconstriction translocates a larger This inverse relationship constitutes an autolimitation on our
volume of blood to the central circulation when venular volume ability to increase cardiac output when there is no extra cardiac
is normal or increased, in contrast to a situation such as hemor- force available to match increased venous return with cardiac out-
rhage, in which the volume is already diminished (e.g., no further put. Factors that offset this autolimitation and allow us to stand
volume to move into the central circulation). and exercise are the muscle pump and the respiratory pump.
The passive effects of an alteration in blood flow on venous
volume are exemplified in a study that evaluated the effect of a Muscle Pump
pacing-induced increase or decrease in cardiac output on central
venous pressure. 169 A decrease in cardiac output, which resulted in Initially when standing, there is an immediate translocation of
a 17-mm Hg decrease in arterial pressure, was associated with a 500 to 700 mL of blood to the periphery, which causes a decrease
3.9-mm Hg increase in central venous pressure. The increase in cen- in central venous pressure and cardiac output and if allowed to
tral venous pressure reflects the decrease in venous flow and trans- continue could cause a person to faint. To offset this effect, con-
mural pressure associated with the decrease in cardiac output and the traction of the skeletal muscles in the legs causes compression of
resultant passive recoil of the veins and the translocation of their the veins and generates a gradient for flow between the venous
blood centrally. The relation between venous volume and cardiac beds and the right atrium, which can expel blood against the
output is addressed further in the sections on the relation between 100 mm Hg venous hydrostatic pressure that develops during
cardiac output and central venous pressure, and the Krogh model. quiet standing. The muscle pump, with a pumping capability
The dominance of passive venous volume mobility can be al- equal to that of the left ventricle, is so important (particularly with
tered in conditions such as hemorrhage, in which active venocon- exercise) that it is often referred to as the “second heart.” 73,246,247
striction of the richly innervated splanchnic veins can also play a Clinically, encouraging the patient to actively contract their calf
role in the translocation of blood back to the central circula- muscles when arising from bed will augment the muscle pump
tion. 99,233,234 In a study that examined the effects of a 27% de- and potentially decrease the risk for orthostasis.
crease in cardiac output, with and without the presence of reflexes,
active constriction of the splanchnic veins accounted for 21% of Respiratory Pump
the translocated blood volume, whereas passive vasodilation ac-
counted for the remaining 79%. 235 Thus, when active and passive The respiratory pump augments the effect of the muscle pump on
effects are combined, the passive effects of decreased blood flow venous bloodflow. 248,249 The pressure difference promoting flow
on venous volume mobility exceed the effect of simultaneous ac- from the venules to the right atrium is affectedby changes in in-
tive venoconstriction. 70,235 trathoracic and intra-abdominal pressures. During inspiration,