Page 95 - Cardiac Nursing

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C HAPTER 3 / Regulation of Cardiac Output and Blood Pressure 71
reflex bradycardia and hypotension that occur during coronary an- medulla, which is responsible for sympathetic efferent activity; (2)
giography, particularly during injection of contrast material into the the nucleus ambiguus or “cardioinhibitory center” of the medulla,
arteries that supply the inferoposterior surface of the left ventricle which is the location of the cell bodies of the vagal parasympa-
(e.g., circumflex, right coronary artery). 19 thetic nerves; and (3) the median preoptic nuclei, which affect the
In severe aortic stenosis, some patients experience exertional release of vasopressin. The output from the medulla depends on
syncope and even sudden death. The probable mechanism of the the perturbation of the system (i.e., an increase or decrease in
syncope is an exercise-induced increase in left ventricular pressure, blood pressure). From the central nervous system, the efferent arm
which is extreme because of high aortic valve resistance, despite a of the rapid control of blood pressure operates through the auto-
decrease in aortic blood pressure. This high left ventricular pressure nomic nervous system. From the carotid sinus, afferent input to
stimulates the ventricular baroreceptors and is manifested by a the nucleus tractus solitarius in the medulla is through the carotid
Bezold-Jarisch response. 20–23 Once these patients undergo surgical sinus nerve (nerve of Hering), which joins the ninth cranial nerve
correction of the stenosis, however, the normal sympathetic vaso- (glossopharyngeal). The sensory input from the aortic arch is
constrictor response to exercise is restored. Similarly, in patients through the 10th cranial nerve (vagus). Through synaptic con-
with hypertrophic cardiomyopathy, this abnormal response may be nections to areas located in caudal and rostral ventrolateral
the cause of syncope, exercise-induced paradoxical peripheral va- medulla and nucleus ambiguus, sympathetic and parasympathetic
sodilation, or sudden cardiac arrest. 24–26 Finally, in cases of severe output, respectively, is modified by afferent feedback from the
hemorrhage or during head-up tilt (particularly in patients receiv- baroreceptors. Output from the lateral ventrolateral medulla,
ing a concurrent infusion of isoproterenol), the ventricular depres- which is directly projected to spinal sympathetic outflow via the
sor reflex is thought to be initiated by the acute distortion of the bulbospinal (or medullospinal) tract, is responsible for maintain-
ventricular mechanoreceptors by a forceful ventricular contraction ing tonic sympathetic activity, and thus resting arterial blood
on a relatively empty ventricle or simply forceful contraction pressure. 37,38 In addition, baroreceptor signals are transmitted to the
27
alone. In a trauma model, inhibition of Bezold-Jarisch mediated forebrain. Paraventricular nuclei in the forebrain play a role in the
bradycardia with -adrenergic blockade may aid in resuscitation. 28 release of vasopressin in response to a sustained decrease in blood
pressure and increased osmolarity (or hypernatremia) and influ-
Chemoreceptors ences the sympathoexcitatory vasomotor neurons in the
medulla. 39,40 The excitation or inhibition of the sympathetic and
Peripheral chemoreceptors located in the carotid and aortic bod- parasympathetic systems depends on the direction of the change
P P in arterial blood pressure. An example of the reflex response (in-
P
ies are sensitive to decreased arterial PaP O 2 or an increase in Pa CO2

or [H ], whereas central chemoreceptors, which are located in the creased parasympathetic activity in the heart and sympathetic ac-
P
P . 29 Stimulation of these tivity in the heart and vasculature) to increased blood pressure is
medulla are sensitive to increased Pa CO 2
receptors leads to hyperventilation and sympathetic activation, summarized in Figure 3-3. 41 Of clinical importance, the barore-
which causes vasoconstriction in most vascular beds, except the ceptor reflex is reset at a higher point in hypertension, which is as-
brain and heart. While an increase in blood pressure is an out- sociated with adrenergic overdrive, decreased ability of cardiopul-
come of the chemoreflex, an increase in baroreceptor stimulation monary receptors to control renin release and altered control of
(i.e., increased arterial blood pressure) inhibits the chemoreflex re- blood pressure and blood volume. 42
sponse. Conversely, the chemoreflexes potentiate the baroreflex-
mediated vasoconstriction in response to decreased arterial blood
pressure. 30 In hypertension and sleep apnea, the peripheral AUTONOMIC NERVOUS SYSTEM
chemoreflex response to hypoxemia is enhanced, with a resultant REGULATION
increase in sympathetic activation. Of clinical importance, there is
a strong relationship between hypertension and sleep apnea (i.e., The autonomic nervous system, which is one branch of the pe-
individuals with sleep apnea have a high prevalence of hyperten- ripheral nervous system, is responsible for coordination of body
sion). 31 In heart failure, both the peripheral and central chemore- functions that ensure homeostasis. The autonomic nervous system
flex responses may be enhanced, as manifested by increased sym- is further divided into two major components: the sympathetic
pathetic activation. 32 This enhanced response may contribute to nervous system and the parasympathetic nervous system (Fig. 3-4).
genesis of sleep apnea in these patients, which is associated with a
poorer prognosis. 33–35 (See Chapter 8 for discussion of the rela- Sympathetic Nervous System
tionship between sleep apnea and cardiovascular disease.)
Efferent projections from the hypothalamus and medulla termi-
nate in the intermediolateral cells located in the gray matter of the
CENTRAL NERVOUS SYSTEM thoracic and lumbar (thoracolumbar) sections of the spinal col-
REGULATION umn (specifically, T-1 to L-2). Hence, the sympathetic nervous
system is often referred to as the thoracolumbar division of the au-
The nucleus tractus solitarius is an ovoid area located in the tonomic nervous system. The neuronal cell bodies, which are lo-
medulla that receives efferent input from cardiovascular, respira- cated in the spinal column, are generally the origin of short pre-
tory, and gastrointestinal sites (see Fig. 3-1). The nucleus tractus ganglionic efferent fibers that innervate postsynaptic sympathetic
solitarius serves as the first relay station for reflexes (e.g., barore- neurons located in three general groupings of ganglia (a group of
ceptor reflex, central and peripheral arterial chemoreceptors, and nerve cell bodies). The paravertebral ganglia are located in a bilat-
skeletal muscle receptors [ergoreceptors]) that control circulation eral chain-like structure adjacent to the spinal column. This chain
and respiration. 36 From the nucleus tractus solitarius, there are extends from the superior cervical ganglia, located at the level of
multiple projections to areas such as: (1) the ventrolateral the bifurcation of the carotid artery, to ganglia located in the