Page 107 - Cardiac Nursing

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C HAPTER 3 / Regulation of Cardiac Output and Blood Pressure 83
LONG-TERM CONTROL OF
BLOOD PRESSURE
The mechanism for the long-term control ofblood pressure has
traditionally been considered to involve fluid volume regulation,
with the mechanism being renal pressure diuresis–natriure-
sis. 200,201 There are alternative models which suggest that volume
diuresis–natriuresis and centralbaroreceptors play a role in long-
term blood pressure control. This section presents the pressure di-
uresis–natriuresis model, introduces the alternative models of
long-term arterialblood pressure control, anddiscusses the im-
portance ofbasal tone on the maintenance ofblood pressure.
Pressure Diuresis–Natriuresis Model
The classic model of long-term blood pressure control is based on
the principle that arterial pressure is maintained at a level required
by the kidneys to excrete a volume of urine approximately equiv-
alent to the daily fluid intake (minus extrarenalfluidlosses). 200,202
The kidneys sense a change in blood volume through the arterial Figure 3-11 Schematic of active and passive changes in vascular
pressure. 200,203 According to this model, that arterial pressure and resistance. The vascular bed is tonically constricted (basal tone) as a
not fluid volume is sensed is demonstrated in disease processes as- result of neurohumoral and local factors (autoregulation). In addi-
tion, some vascular beds have a higher level of tone (resting tone) in-
sociated with a combination of increased extracellular volume and dicating sympathetic nervous system stimulation. Passive vasodilation
decreased arterial pressure (e.g., heart failure or cirrhosis with as- is the passive release of sympathetic nervous system stimulation,
cites). In these cases, the kidneys retain fluiddespite expanded dilating the vessel toward basal tone. Passive vasoconstriction is the
fluid volume. Based on this hypothesis, an increase in renal per- release of active vasodilatory stimuli. Active vasodilation is vascular di-
fusion pressure causes a decrease in sodium reabsorption and an lation below basal tone and active vasoconstriction is constriction above
increase in sodium and water excretion. This model may involve basal tone. (Courtesy of Loring B. Rowell, University of Washington,
autoregulation of renal medullary bloodflow, although the exact Seattle, WA.)
mechanism remains unknown. 201,204 According to this model, as
long as sodium and water intake remained stable, the enhanced been proposed, with the primary goal of maintaining cerebral blood
sodium excretion will decrease extracellular volume and blood flow. 212,213 The paraventricular nuclei in the hypothalamus may
volume, and arterialpressure will decrease. Additionally, an in- also play a role in modulating renal sympathetic nerve activity. 8
crease in systemic vascular resistance and subsequent increase in
renal perfusion pressure would not cause a long-term increase in
arterial pressure, unless renalfunction was impaired. 200 Basal Tone
All arterioles exhibit a basal level of vasoconstriction or tone. Basal
Alternative Models of Long-Term tone, which is the intrinsic level of vascular tone, is independent
Blood Pressure Control of neural or humoral influences and serves as the baseline around
which neural or humorally mediated vasoconstriction or vasodila-
An alternative model for long-term blood pressure control sug- tion occurs (Fig. 3-11). Basal tone varies among organs; it is low-
gests that the pressure diuresis–natriuresis mechanism may play est in the kidneys and highest in the skeletal muscles, heart, and
less of a role under normal circumstances than previously concep- brain. 214 The maintenance of arteriolar tone through tonic rhyth-
tualized; rather that volume diuresis–natriuresis may be the pri- mic vasoconstriction is essential for the maintenance of blood
mary mechanism for long-term blood pressure role. 205 According pressure. For example, it is estimated that if this basal myogenic
to this model sodium excretion is based on extracellular volume, tone were eliminated, a minimal cardiac output of 60 to 75 L/min
with the renin system playing a key role. would be required to maintain a normal blood pressure. 99,214 In
Another model suggests that while the sympathetic nervous sys- contrast, if the sympathetic input associated with resting tone
tem, through the sinoaortic baroreceptor reflex, plays the primary were withdrawn, the blood pressure would decrease only from
role in the rapid regulation of blood pressure it may also play a role 100 to 86 mm Hg. This small decrease in blood pressure occurs
in long-term blood pressure control. 206–208 The clinical importance because the vascular bed with the highest resting tone (skeletal
of the involvement of the sympathetic nervous system in long-term muscle) normally receives only 15% of the cardiac output.
blood pressure control may be in the development to hypertension. Nitric oxide (eNOS and nNOS) affects basal arteriolar and
Resetting of the baroreflex at a higher pressure threshold may limit microvascular tone, with a greater effect in larger resistance vessels
their ability to buffer changes in blood pressure and increased sym- ( 200 m) than in smaller resistance vessels ( 200 m). 215,216
pathetic nervous system activity at any given pressure. 209,210 Fur- Recent research suggests that nNOS generated nitric oxide is im-
ther research is needed to support this model. 206,211 portant for the regulation of basal vasomotor tone, which influ-
Baroreflex independent control of the blood pressure via a cen- ences blood pressure, and eNOS generated nitric oxide affects the
tral baroreceptor (rather than a pressor–sensor in the kidney) has dynamic alterations in blood flow distribution. 215 Nitric oxide