Page 102 - Cardiac Nursing

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78 PA R T I / Anatomy and Physiology
20 hemorrhage, the change in intrathoracic volume alters the arterial
systolic blood pressure, which decreases arterial baroreceptor stimu-
lation, and leads to increased vasopressin secretion. 109
0 50 Natriuretic Peptides
Arterial pressure (Δ%) –20 Vasopressin 30 There are three natriuretic peptides (A, B, and C) that contribute
40
Pressure
to the regulation of blood pressure and electrolyte and volume
110,111
112
homeostasis.
and brain
Atrial natriuretic peptide (ANP)
–40
natriuretic peptide (B-type natriuretic peptide [BNP]) are released
20
from granules in the atria and ventricles in response to increased
stretch (increased preload and afterload) and hormonal stimuli
–60
10
(e.g., angiotensin II, glucocorticoids, endothelin I, cate-
cholamines). 113,114 Of note, factors that stimulate BNP release
0
–80 may be different in a normal versus hypertrophied ventricle and
C 5 10 15 20 25 30 after myocardial infarction, with hypoxia acting independent of
Hemorrhage (mL/kg) ventricular dilation to stimulate BNP release. 113 The actions of
■ Figure 3-8 Mean percentage changes in arterial blood pressure BNP are similar to ANP. C-type natriuretic peptide is widely dis-
and in plasma vasopressin concentration in response to blood loss tributed in the brain, kidneys, lungs, heart, and endothelial cells,
(0.5 mL/kg/min) in a group of 12 dogs; the maximal volume of blood and is released in response to shear stress. Dendroaspis natriuretic
withdrawn was 30 mL/kg. (Redrawn from Shen, Y.-T., Cowley, peptide has been recently discovered; however, its exact mecha-
A. W., J., & Vatner, S. F. [2001]. Relative roles of cardiac and arterial nism remains to be determined.
baroreceptors in vasopressin regulation during hemorrhage in con- The heart has endocrine functions 113 via the cardiac natri-
scious dogs. Circulation Research, 68, 1422; from Koeppen, B. M., & uretic peptides (ANP and BNP) that bind with natriuretic peptide
Stanton, B. A. [2008]. Berne and Levy Physiology [6th ed.]. Philadel-
phia: Mosby Elsevier.) receptors A and B (NPR-A and NPR-B) and cause diuresis and
natriuresis. These actions subsequently decrease preload and
blood pressure. 115 Preload reduction may occur because of shift-
The sensitivity of the baroreceptor system is less than that of the ing of fluid from the intravascular to the extravascular space (in-
osmoreceptors, as demonstrated by the large (5% to 10%) iso- creased vascular endothelial permeability) and possibly increased
osmotic change in plasma volume required before vasopressin se- capillary hydrostatic pressure along with natriuresis. 110,116 Addi-
cretion is altered. However, during hemorrhage (plasma volume tionally, ANP and BNP decrease sympathetic tone to the periph-
decreased by 5% to 10%), plasma levels of vasopressin are in- eral vasculature both centrally and peripherally, inhibit the RAAS
creased, in some cases 100-fold 107 (Fig. 3-8). In this case, vasopressin by inhibiting angiotensin II-stimulated sodium and water trans-
acts in a manner similar to renin and norepinephrine, causing vaso- port in the proximal tubules, inhibit endothelin-1 production,
constriction and playing a supporting role to the sympathetic nerv- improve ventricular relaxation, and lower the activation threshold
ous system in the maintenance of blood pressure. The primary reflex for the vagal afferents, which suppresses the reflex tachycardia and
controllers of the plasma volume-mediated release of vasopressin are vasoconstriction associated with the decrease in preload and car-
the arterial baroreceptors and not the cardiac receptors. 70,108 In diac output 117,118 (Fig. 3-9). In severe heart failure, increased
Increased atrial stretch
Other stimuli (Ang ll) STROKE
HYPERTENSION
Gene alterations
ANP Extravascular fluid shift
Vagal afferent activity
Diuresis
natriuresis
Renin, aldosterone
Sympathetic activity
AVP Apoptosis
Ang ll actions Antigrowth effect

Cardiac afterload Vasodilation Cardiovascular remodeling Cardiac filling pressure

■ Figure 3-9 Schematic representation of the regulation and function of atrial natriuretic peptide (ANP).
Along with the classical circulatory effects, the new emerging functional properties of the atrial natriuretic pep-
tides are shown. AVP, vasopressin; ANG II, angiotensin II. (From Rubattu, S., & Volpe, M. [2001]. The atrial
natriuretic peptide: A changing view. Journal of Hypertension, 19, 1925.)