CHAPTER 33
Cardiovascular Regulatory Mechanisms 561response to abrupt changes in blood volume, cardiac output,
or peripheral resistance during exercise.
Blood pressure initially rises dramatically after bilateral sec-
tion of baroreceptor nerves or bilateral lesions of the NTS.
However, after a period of time, mean blood pressure returns
to near control levels, but there are huge fluctuations in pres-
sure during the course of a day. Removal of the baroreceptor
reflex prevents an individual from responding to stimuli that
cause abrupt changes in blood volume, cardiac output, or
peripheral resistance, including exercise and postural changes.
A long-term change in blood pressure resulting from loss of
baroreceptor reflex control is called
neurogenic hypertension.
ATRIAL STRETCH RECEPTORS
The stretch receptors in the atria are of two types: those that dis-
charge primarily during atrial systole (type A), and those that
discharge primarily late in diastole, at the time of peak atrial fill-
ing (type B). The discharge of type B baroreceptors is increased
when venous return is increased and decreased by positive-
pressure breathing, indicating that these baroreceptors respond
primarily to distention of the atrial walls. The reflex circulatory
adjustments initiated by increased discharge from most if not all
of these receptors include vasodilation and a fall in blood pres-
sure. However, the heart rate is increased rather than decreased.
CARDIOPULMONARY RECEPTORS
Receptors in the endocardial surfaces of the ventricles are ac-
tivated during ventricular distention. The response is a vagal
bradycardia and hypotension, comparable to a baroreceptor
reflex. Left ventricular stretch receptors may play a role in the
maintenance of vagal tone that keeps the heart rate low at rest.
Various chemicals are known to elicit reflexes due to activa-
tion of cardiopulmonary chemoreceptors and may play a role
in various cardiovascular disorders (see Clinical Box 33–2).VALSALVA MANEUVER
The function of the receptors can also be tested by monitoring
the changes in pulse and blood pressure that occur in responseFIGURE 33–7
Baroreflex-mediated lowering of the heart
rate during infusion of phenylephrine in a human subject.
Note
that the values for the RR interval of the electrocardiogram, which are
plotted on the vertical axis, are inversely proportionate to the heart
rate.
(Reproduced with permission from Kotrly K et al: Effects of fentanyl-diazepam-
nitrous oxide anaesthesia on arterial baroreflex control of heart rate in man. Br J
Anaesth 1986;58:406.)
18001600140012001000800
600
80 100 120 140 160
Systolic pressure (mm Hg)Slope = 33.3 ms mm Hg−^1
Threshold = 124 mm HgRR interval (ms)CLINICAL BOX 33–2
Cardiopulmonary Chemosensitive Receptors
For nearly 150 years, it has been known that activation of
chemosensitive vagal C fibers in the cardiopulmonary re-
gion (eg, juxtacapillary region of alveoli, ventricles, atria,
great veins, and pulmonary artery) causes profound brady-
cardia, hypotension, and a brief period of apnea followed by
rapid shallow breathing. This response pattern is called the
Bezold–Jarisch reflex
and was named after the individuals
who first reported these findings. This reflex can be elicited
by a variety of substances including capsaicin, serotonin,
phenylbiguanide, and veratridine in cats, rabbits, and ro-
dents. Although originally viewed as a pharmacologic curi-
osity, there is a growing body of evidence supporting the
view that the Bezold–Jarisch reflex is activated during cer-
tain pathophysiologic conditions. For example, this reflex
may be activated during myocardial ischemia and reperfu-
sion as a result of increased production of oxygen radicals
and by agents used as radio-contrast for coronary angiogra-
phy. This can contribute to the hypotension that is fre-
quently a stubborn complication of this disease. Activation
of cardiopulmonary chemosensitive receptors may also be
part of a defense mechanism protecting individuals from
toxic chemical hazards. Activation of cardiopulmonary re-
flexes may help reduce the amount of inspired pollutants
that get absorbed into the blood, protecting vital organs
from potential toxicity of these pollutants, and facilitating
the elimination of the pollutants. Finally, the syndrome of
cardiac slowing with hypotension
(vasovagal syncope)
has
also been attributed to activation of the Bezold–Jarisch re-
flex. Vasovagal syncope can occur after prolonged upright
posture that results in pooling of blood in the lower extrem-
ities and diminished intracardiac blood volume (also called
postural syncope
). This phenomenon is exaggerated if
combined with dehydration. The resultant arterial hypoten-
sion is sensed in the carotid sinus baroreceptors, and affer-
ent fibers from these receptors trigger autonomic signals
that increase cardiac rate and contractility. However, pres-
sure receptors in the wall of the left ventricle respond by
sending signals that trigger paradoxical bradycardia and de-
creased contractility, resulting in sudden marked hypoten-
sion. The individual also feels lightheaded and may experi-
ence a brief episode of loss of consciousness.