Page 108 - Cardiac Nursing

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84 PA R T I / Anatomy and Physiology
also affects large-artery distensibility. 217,218 The reduction or ab-
sence of tonic nitric oxide release causes increased mean arterial Resistance
blood pressure and may be a cause of pathological conditions
characterized by increased blood pressure. 218,219
As demonstrated in Figure 3-11, active and passive vasomotion
occurs around the basal and resting tone of the vascular bed. Four
terms define this vasomotion 99,220 : Blood flow
1. Active vasoconstriction, which is mediated by sympathetic stimu- Blood flow (Resistance --)
lation, is the increase in vascular resistance above the basal level.
2. Passive vasodilation, in contrast to active vasoconstriction, is the Autoregulatory
reduction in vascular resistance back to the basal level caused by range
the withdrawal of the sympathetic stimulation associated with
active vasoconstriction. In some vascular beds, resistance may
be increased above basal tone by tonic sympathetic stimulation.
This increase in vascular tone is referred to as resting tone. Pas- 60 150
sive vasodilation is most easily seen in vascular beds with in- Blood pressure (mm Hg)
creased resting tone (e.g., acral regions). ■ Figure 3-12 A schematic representation of autoregulation. The
3. If a vascular bed has high basal tone, active vasodilation, which is blood flow is relatively constant between an arterial pressure of 60 and
a decrease in vascular resistance below the level maintained by 150 mm Hg because of an active increase in resistance. Below a mean
basal tone, may occur (i.e., vasodilation beyond that which exists pressure of 60 mm Hg and above 150 mm Hg, the flow is directly re-
after all neural and hormonal influences are removed). In this lated to pressure.
case, the vasodilation is not merely the result of withdrawal of
sympathetic tone, because this action causes passive vasodilation. terioles or precapillary vascular segments control the number of
4. Passive vasoconstriction is caused by withdrawal of the stimula- open capillaries and are under sympathetic nervous system and lo-
tion causing active vasodilation. 221
cal control. Local control mechanisms (autoregulation) that af-
The skeletal muscle arterioles have a high basal tone and therefore fect the terminal arterioles may have a substantial influence on ex-
are capable of a wide range of vasoconstriction and vasodilation, change vessel pressures and flows and on the vascular tissue
because there is an increased level of basal tone to be modulated. exchange of fluid and solutes.
In contrast, the renal vasculature has a low basal and resting tone
that can be markedly increased through sympathetic stimulation, Autoregulation
but has little capability to undergo active vasodilation because
there is so little basal tone to inhibit. Autoregulation, which appears to occur in all organs except the
lung, is the intrinsic tendency of an organ or vascular bed to main-
tain constant blood flow through alteration in its arteriolar tone,
LOCAL REGULATION OF despite changes in arterial pressure. Autoregulation can occur in
SYSTEMIC MICROVASCULAR some organs over a range of perfusion pressure of 60 to 80 mm
Hg to an upper limit of 150 mm Hg (Fig. 3-12), and is inde-
BEDS pendent of neural and hormonal control. There are three hy-
potheses to explain autoregulation: the myogenic, metabolic, and
Arteriolar resistance vessels are partially constricted under normal tissue pressure hypotheses. 222,223 It appears that none of these
circumstances by a tonic rhythmic myogenic tone, and this level mechanisms works in isolation and, as described later, the tissue
of tone is modulated by neurogenic or other factors that cause ac- pressure hypothesis may apply only in pathological conditions. A
tive vasoconstriction or vasodilation. In the intact organism, recent model suggests that myogenic and metabolic regulations
blood flow and vascular hydrostatic pressure in the microvascula- overcome myogenic (shear-induced) effects. 224
ture of each organ system are controlled by complex interrelations
among the effects of physical factors, locally released substances, Myogenic Hypothesis
circulating hormones, and above all by neurotransmitters secreted The myogenic hypothesis refers to the acute reaction of a blood
in response to central activation of the sympathetic nervous sys- vessel to a change in intraluminal pressure. For example, increas-
tem. The relative predominance of local versus centrally mediated ing intraluminal pressure between 20 and 120 mm Hg causes a
control of the microvascular bed varies among vascular beds, and pressure-induced stretch in vascular smooth muscle, which results
it also varies among resistance, precapillary, and postcapillary in vasoconstriction and a decrease in the flow. 222,225 However,
blood vessels within a given vascular bed. above an intraluminal pressure of 140 mm Hg the blood vessels
The large- and medium-sized arterioles, which are the pre- dilate. 224 Shear stress, which is also associated with increased pres-
dominant sites of vascular resistance, are primarily under the con- sure, causes an increase in the release of endothelial niric oxide
trol of the sympathetic nervous system and centrally mediated and subsequent vasodilation (see Chapter 2). Conversely, when
neurohumoral factors (e.g., angiotensin II). These vascular seg- the intraluminal pressure is decreased, the stimulus for the myo-
ments are influential in the control of arterial blood pressure and, genic response is decreased, the vessel dilates, and blood flow is re-
by virtue of their position; they control the total amount of blood turned toward control levels. Recent research suggests that, in iso-
entering a specific vascular area; and therefore, the distribution of lation the myogenic response exerts only a small autoregulatory
blood flow between the different vascular beds. The terminal ar- response. 224