Page 93 - Cardiac Nursing

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CHAPTER
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R R R R Regulation of Cardiac Output and
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Elizabeth J. Bridges
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Thiis chapter reviews thhe neurohhumorall controll fof thhe cardiovas-
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Th di In Input to thhe central neervous system from the ventriicular re-
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cu cularr system ass it relates to thee rapidd andd more long-term control ce ceptors, which are seensitive to mechanical and chemical stimuli, is
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of cardiac output and blood pressure and the local control of through nonmyelinatted vagal afferentss (C fibers). In response to
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bl bloodd flflow ((autoregulatoryy, metabolic, autacoid)). Sever lal m dod lels an increase iin ventricular pressure, the mechanoreceptors were
of cardiac function are presented, including the relationship be- previously thought to stimulate a depressor response (decreased
tween cardiac output and central venous pressure, the Krogh heart rate/vasodilation). The depressor reflex causes a decrease in
model of the effect of distribution of blood volume on cardiac heart rate, and may play a role in the alteration in vascular tone; 5
output, and the arterial baroreflex responses to decreased and in- although this response is less than the vascular response induced
creased blood pressure. by increases in carotid or coronary arterial pressure. The ventricu-
lar mechanoreceptors appear to play a role only in protection from
gross overdistention, possibly during myocardial ischemia. 6,7
AFFERENT INPUT AND Chronic activation of cardiac receptors in heart failure cause in-
RECEPTOR creased activation of hypothalamic paraventricular neurons,
which may contribute to resetting of the baroreceptor reflex and a
Arterial Baroreceptors sustained increase in sympathetic activation. 8
The arterial baroreceptors are responsible for the reflex control of Bezold-Jarisch Reflex
blood pressure. These baroreceptors are undifferentiated nerve The Bezold-Jarisch reflex, which is the most commonly used model
fibers located in the adventitia of the carotid sinus (at the bifurca- to explain the triggering of vasovagal (neurocardiogenic) syncope, is
tion of the carotid artery) and the aortic arch (between the arch of manifested as a triad of symptoms (bradycardia, apnea, and hy-
9
the aorta and the bifurcation of the subclavian artery; Fig. 3-1). The potension). Neurocardiogenic syncope is thought to occur as a re-
receptors are mechanoreceptors that respond to distortion or a sult of excessive venous pooling and a decrease in peripheral venous
change in transmural pressure or stretch of the vascular bed in return. The decreased venous return leads to a hypercontractile state
which they are located. For example, the carotid baroreceptors are that stimulates the cardiac mechanoreceptors (particularly those in
10
sensitive to external compression or massage, both of which unload the inferoposterior wall of the left ventricle). This hypercontrac-
them (decrease transmural pressure). Although baroreceptors are of- tile state mimics hypertension and causes a paradoxical inhibitory
ten referred to as “pressoreceptors,” they in fact do not sense pres- or depressor reflex causing a vagally mediated decrease in heart rate
sure directly, but instead only indirectly through change in stretch. and withdrawal of sympathetic stimulation to the peripheral vascu-
The baroreceptors respond to two types of input: static input lature with subsequent vasodilation. 11 Stimulation of this reflex
(i.e., mean arterial pressure) and phasic input (i.e., pulsatile may occur with pathological conditions, such as myocardial infarc-
changes). Therefore, the baroreceptors are responsive to mean ar- tion, administration of thrombolytic therapy, hemorrhage, aortic
terial pressure, pulse pressure, and the number of pulses per stenosis, or syncope. It is important to note that vasovagal syncope
1
minute (e.g., heart rate). The static response has a threshold ef- may also occur in patients with transplanted (denervated) hearts;
fect, that is, below a certain threshold of mean arterial pressure thus, factors other than those traditionally attributed to the Bezold-
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(20 to 50 mm Hg), the receptor stops firing. Above this threshold Jarish reflex must be considered. Figure 3-2 characterizes the nu-
there is an increase in rate of receptor firing in proportion to the merous putative causes of vasovagal syncope. During an acute in-
increase in mean pressure, until a plateau of the output is reached feroposterior myocardial infarction (particularly because of right
at saturation. The phasic response increases when the rate of coronary artery occlusion) and at the time of reperfusion of these
change of pressure rises (increasing pressure) and decreases when infarctions, the transient bradycardia observed is thought to be a
the rate of change in pressure decreases. manifestation of the depressor effect of vagal receptors located in
the inferoposterior wall of the left ventricle. 12 Recent research also
Cardiopulmonary Receptors suggests that this response occurs with more proximal lesions in-
volving the right ventricle. 13 During ischemia, these receptors,
Cardiopulmonary or low-pressure baroreceptors are located in the which are mechanosensitive or chemosensitive, may be distorted by
atria, ventricles, and pulmonary arteries and veins, with the car- bulging of the ventricular wall during systole 14 or by the presence
A
diac baroreceptors providing the primary afferent input for the va- of reactive oxygen species, serotonin, bradykinin, thromboxane A 2 ,
gal cardioreflex. 2,3 The properties of the cardiopulmonary barore- or adenosine. 15–17 During thrombolytic therapy, the occurrence of
ceptors are similar to those of the arterial baroreceptors, that is, a vagally mediated bradycardia may be an indicator of reperfusion
decrease in transmural pressure in the chamber or vessel results in and sustained vessel patency, particularly with an inferior myocar-
a decrease in the firing rate of receptors, and vice versa. dial infarction. 18 These receptors are also thought to mediate the
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