Page 109 - Cardiac Nursing

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C HAPTER 3 / Regulation of Cardiac Output and Blood Pressure 85
Metabolic Hypothesis the latter cases, external compression may decrease blood flow be-
The metabolic hypothesis is based on the idea that the concentra- low a physiologically safe level.
tion of metabolites and metabolic substrates (e.g., ATP, potas-
sium, hydrogen, O 2 , CO 2 , adenosine) in the interstitial space
controls vascular tone. In this case, the vascular smooth muscle VENOUS SYSTEM
acts as a chemosensor. According to this hypothesis, a decrease in
blood flow leads to an increase in the local concentration of a The primary functions of the venous system are to return blood
metabolite and causes vasodilation and increased blood from the capillaries to the heart and to serve as a reservoir that
flow. 223,226 For example, red blood cells release ATP in response counterbalances the transient imbalance between cardiac output
to increased oxygen demand. Increased venular ATP may trigger and venous return. However, because of its capacious nature, the
an upstream response that causes arteriolar vasodilation. 224,227,228 venous system serves not only as a reservoir, storing approximately
The metabolic hypothesis has been suggested as a mechanism for 70% of the total blood volume (approximately 33% of total blood
autoregulation in organs or tissues where the primary function of volume is stored in the splanchnic bed—liver, stomach, spleen,
blood supply is to support local metabolism. In this case, there is and intestines), but also as a buffer against changes in cardiac out-
a close relation between blood flow and metabolic needs. How- put and blood pressure. The venous system plays both an active
ever, in organ systems with high blood flow (e.g., kidney, skin), (venoconstriction) and, more importantly, a passive role in the
where blood flow occurs in excess of metabolic needs, there is a maintenance of thoracic blood volume.
limited relationship between blood flow and metabolism, 99 and
the metabolic hypothesis as a factor in the autoregulatory control Neurohumoral Stimulation
of blood flow has not been supported. A combination of meta-
bolic and myogenic responses generate autoregulatory flow The only neural control of veins is through the -adrenergic fibers
changes despite the opposing effects of shear. 224 of the sympathetic nervous system. 231 Release of norepinephrine
An important point is that metabolic autoregulation is not the from -adrenergic fibers causes constriction in the splanchnic and
same as metabolically induced active and reactive hyperemia (in- cutaneous veins, whereas withdrawal of sympathetic stimulation
creased blood flow), which occur in response to increased meta- results in passive vasodilation. The cutaneous veins are densely in-
bolic demand (e.g., intestinal vasculature during digestion or car- nervated with -adrenergic receptors, predominantly postsynaptic
diac and skeletal muscle during activity) or interruption of blood 2 -receptors. 68,232 There is limited -adrenergic stimulation in
flow to a vascular bed, respectively. 223 Active hyperemia is the the cutaneous veins and the veins of the skeletal muscle and the
adaptive increase in blood flow in response to changes in the local small venules have virtually no innervation. Epinephrine is the
metabolic rate caused by variation in the functional activity of the primary humoral factor that affects the veins, with actions on cu-
surrounding cells. In response to this change in functional status, taneous vessels and, more importantly, splanchnic vessels. Given
the vascular resistance decreases almost immediately. In addition, the preponderance of -adrenergic receptors on the veins, epi-
there is an increase in the number of perfused capillaries (capillary nephrine stimulation causes venoconstriction.
recruitment) in response to metabolic stimulation. The magni-
tude of the reactive hyperemia response depends on the duration Passive Versus Active Effects
of the vascular obstruction and the metabolic rate of the given vas- Neurohumoral stimulation primarily affects the most capacious vol-
cular bed. Unlike “pure” metabolic autoregulation, this response ume reservoirs (splanchnic and cutaneous venous bed). The ques-
is a combination of three components: (1) passive changes in ves- tion is whether translocation of blood from the venous system is
sel diameter caused by a change in transmural pressure; (2) a myo- primarily the consequence of active venoconstriction or of the pas-
genic response to the change in transmural pressure; and (3) a sive effects that stem from the substantial changes in venous trans-
metabolic component. 223,229,230 mural pressure caused by arteriolar vasoconstriction or vasodilation.
Changes in upstream arteriolar tone alter downstream venous
Tissue Pressure Hypothesis transmural pressure and the volume of blood that flows through
The tissue pressure hypothesis states that an increase in external the venous system. For example, arteriolar vasodilation increases
pressure (e.g., interstitial pressure) decreases transmural pressure blood flow into the highly capacious postcapillary venous beds,
(pressure inside minus pressure outside the vessel), which passively and the increase in their transmural venular pressure passively ex-
decreases the vessel diameter and decreases flow. 223 The effect of pands their volume. Given that total blood volume is constant, an
external compression on blood flow normally occurs during ven- increase in blood volume in the peripheral venous system means a
tricular systole, when the coronary arteries are compressed. Clini- decrease in the volume of the central veins that fill the heart. Con-
cally, the effect of transmural compression is more likely to be ob- versely, vasoconstriction decreases flow into the postcapillary ve-
served in organs constrained in a rigid container (e.g., brain, nous system, venous transmural pressure decreases, and the elastic
where increased cerebrospinal fluid pressure may compress cere- recoil of the veins passively expels their volume toward the central
bral vessels) or a stiff capsule (e.g., kidney). 99,223 In the lung, vas- thoracic veins. 231
cular compression caused by increased external (alveolar) pressure, The magnitude of passive change in venous transmural
such as with the application of high levels of positive end-expiratory pressure depends on where the changes occur along the venous
pressure, may also affect blood flow. volume–pressure curve. For example, as demonstrated in Figure
Under physiological conditions, tissue pressure probably does 3-13, at a low venous transmural pressure, the pressure–volume
not play a major role in the control of blood flow, but it may be curve is steep. A small change in distending pressure causes a large
particularly important under pathological conditions such as change in volume, that is, arteriolar vasodilation, which increases
edema, hemorrhage into the interstitial space, or cellular swelling venous blood flow and venous transmural pressure, which causes
caused by injury or hypoxemia (compartment syndrome). 223 In a larger increase in venous volume expansion when the veins are