Book Text

Cardiac Reflexes

Cardiac reflexes are fast-acting reflex loops between the heart and the central nervous system (CNS) that contribute to the regulation of cardiac function and maintenance of physiologic homeostasis. Specific cardiac receptors elicit their physiologic responses by various pathways. Cardiac receptors are linked to the CNS by myelinated or unmyelinated afferent fibers that travel along the vagus nerve. Cardiac receptors can be found in the atria, ventricles, pericardium, and coronary arteries. Extracardiac receptors are located in the great vessels and the carotid artery. Sympathetic and parasympathetic nerve inputs are processed in the CNS. After central processing, efferent fibers to the heart or the systemic circulation will provoke a particular reaction. The response of the cardiovascular system to efferent stimulation varies with age and duration of the underlying condition that elicited the reflex in the first instance.

Baroreceptor Reflex (Carotid Sinus Reflex)

The baroreceptor reflex is responsible for the maintenance of blood pressure. This reflex is capable of regulating arterial pressure around a preset value through

Figure 18-18 Anatomic configuration of the baroreceptor reflex. Pressure receptors in the wall of the carotid sinuses and aorta detect arterial pressure changes in the circulation. These signals are conveyed to afferent receptive regions of the medulla through the Hering and vagus nerves. Output from effector portions of the medulla modulates peripheral tone and heart rate. The increase in blood pressure results in increased activation of the reflex (right), which effects a decrease in blood pressure. (From Campagna JA, Carter C: Clinical relevance of the Bezold-Jarisch reflex. Anesthesiology 98:1250–1260, 2003.)

a negative feedback loop ( Fig. 18-18 ). ^[65] ^[66] In addition, the baroreceptor reflex is capable of establishing a prevailing set point for blood pressure when the preset value has been reset because of chronic hypertension. Changes in blood pressure are monitored by circumferential and longitudinal stretch receptors located in the carotid sinus and aortic arch. The nucleus solitarius located in the cardiovascular center of the medulla receives impulses from these stretch receptors through afferents of the glossopharyngeal and the vagus nerves. The cardiovascular center in the medulla consist of two functionally different areas: the area responsible for increasing blood pressure is located laterally and rostrally, whereas the area responsible for lowering blood pressure is located centrally and caudally. The latter area also integrates impulses from the hypothalamus and the limbic system. Typically, stretch receptors are activated if systemic blood pressure is greater than 170 mm Hg. The response of the depressor system includes decreased sympathetic activity leading to a decrease in cardiac contractility, heart rate, and vascular tone. In addition, activation of the parasympathetic system further decreases the heart rate and myocardial contractility. Reverse effects are elicited with the onset of hypotension.

The baroreceptor reflex plays an important role during acute blood loss and shock. However, the reflex arch loses its functional capacity at a blood pressure less than 50 mm Hg. Hormonal status and therefore sex differences have been implicated in altered baroreceptor responses.^[67] Furthermore, volatile anesthetics (in particular, halothane) inhibit the heart rate component of this reflex.^[68]

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Concomitant use of calcium channel blockers, angiotensin-converting enzyme inhibitors, or phosphodiesterase inhibitors will lessen the cardiovascular response of raising blood pressure through the baroreceptor reflex. This lessened response is achieved by either their direct effects on the peripheral vasculature or, more importantly, their interference with CNS signaling pathways (calcium, angiotensin).^[69] Patients with chronic hypertension often exhibit perioperative circulatory instability as a result of a decrease in their baroreceptor reflex response.

Chemoreceptor Reflex

Chemosensitive cells are located in the carotid bodies and the aortic body. These cells respond to changes in pH status and blood oxygen tension. At an arterial partial oxygen pressure (PaO₂ ) of less than 50 mm Hg or in conditions of acidosis, the chemoreceptors send their impulses along the sinus nerve of Hering (a branch of the glossopharyngeal nerve) and the 10th cranial nerve to the chemosensitive area of the medulla. This area responds by stimulating the respiratory centers and thus increasing the ventilatory drive. In addition, activation of the parasympathetic system ensues and leads to a reduction in heart rate and myocardial contractility. In the case of persistent hypoxia, the CNS will be directly stimulated, with a resultant increase in sympathetic activity.

Bainbridge Reflex

The Bainbridge reflex is elicited by stretch receptors located in the right atrial wall and the cavoatrial junction. An increase in right-sided filling pressure sends vagal afferent signals to the cardiovascular center in the medulla. These afferent signals inhibit parasympathetic activity, thus increasing the heart rate. Acceleration of the heart rate also results from a direct effect on the SA node by stretching the atrium. The changes in heart rate are dependent on the underlying heart rate before stimulation.

Bezold-Jarisch Reflex

The Bezold-Jarisch reflex responds in the triad of hypotension, bradycardia, and coronary artery dilatation to noxious ventricular stimuli sensed by chemoreceptors and mechanoreceptors within the LV wall.^[66] The activated receptors communicate along unmyelinated vagal afferent type C fibers. These fibers reflexively increase parasympathetic tone. Because it invokes bradycardia, the Bezold-Jarisch reflex is thought of as a cardioprotective reflex. This reflex has been implicated in the physiologic response to a range of cardiovascular conditions such as myocardial ischemia or infarction, thrombolysis, or revascularization and syncope. Natriuretic peptide receptors stimulated by endogenous ANP or BNP may modulate the Bezold-Jarisch reflex. Thus, the Bezold-Jarisch reflex may be less pronounced in patients with cardiac hypertrophy or atrial fibrillation.^[70]

Valsalva Maneuver

Forced expiration against a closed glottis produces increased intrathoracic pressure, increased central venous pressure, and decreased venous return. Cardiac output and blood pressure will be decreased after this (Valsalva) maneuver. This decrease will be sensed by baroreceptors and reflexively result in an increase in heart rate and myocardial contractility through sympathetic stimulation. When the glottis opens, venous return increases and causes the heart to respond by vigorous contraction and an increase in blood pressure. This increase in blood pressure will in turn be sensed by baroreceptors, thus stimulating the parasympathetic efferent pathways to the heart.

Cushing's Reflex

The Cushing reflex is a result of cerebral ischemia caused by increased intracranial pressure. Cerebral ischemia at the medullary vasomotor center induces an initial activation of the sympathetic nervous system. Such activation will lead to an increase in heart rate, blood pressure, and myocardial contractility in an effort to improve cerebral perfusion. As a result of the high vascular tone, reflex bradycardia mediated by baroreceptors will ensue.

Oculocardiac Reflex

The oculocardiac reflex is provoked by pressure applied to the globe of the eye or traction on the surrounding structures. Stretch receptors are located in the extraocular muscles. Once activated, stretch receptors will send afferent signals through the short and long ciliary nerves. The ciliary nerves will merge with the ophthalmic division of the trigeminal nerve at the ciliary ganglion. The trigeminal nerve will carry these impulses to the gasserian ganglion, thereby resulting in increased parasympathetic tone and subsequent bradycardia. The incidence of this reflex during ophthalmic surgery ranges from 30% to 90%. Administration of an antimuscarinic drug such as glycopyrrolate or atropine reduces the incidence of bradycardia during eye surgery (also see Chapter 65 ).