reflexStimulus ResponseAnesthesia considerations

Cardiac output regulationWhen neither the contractility nor the HR is compromised, this mechanism ensures that the return of blood flow to the heart will maintain CO.Many of the factors that affect CO also affect the MAP. Some of the reflexes are listed below and they alter the CO are described.

Baroreceptor reflexHypertension resulting in baroreceptor stimulation; carotid baroreceptors send afferent response via hering and glossopharyngeal nerves (CNIX); aortic baroreceptors send afferent response via the vagus nerve (CNX)Decrease heart rate, decreased contractility, peripheral vasodilation from efferent response via the vagus nerve (CNX)The baroreceptor response is inhibited by volatile anesthetic agents in a dose-dependent manner and results in a decreased ability of the baroreceptors to respond to BP changes when these agents are used.

Valsalva maneuverForced expiration against a closed glottis mediated via baroreceptorsDecreased heart rate, decreased contractility, peripheral vasodilation from efferent response via the vagus nerve (CNX)Epidural anesthesia can be used. General anesthesia is preferred. If hypotension occurs during anesthesia, alpha-agonists such as phenylephrine can help. Titration of anesthetic agents and adequate volume loading is essential to safely conduct anesthesia in this clinical setting.

Oculo cardiac reflexTraction on the extraocular muscles (especially medial rectus) or pressure on the globe causes an afferent response via the trigeminal nerve (CNV) and results in an efferent vagal response via the vagus nerve (CNX)Bradycardia, hypotension, and arrhythmias Response can be inhibited by an anticholinergic agent (atropine or glycopyrrloate)

Celiac reflexTraction or pressure on structures within abdominal and thoracic cavities causes vagal nerve stimulationBradycardia, hypotension and apnea.Clinically, the celiac reflex can be initiated indirectly as a result of a pneumoperitoneum. Celiac reflex is frequently resolved by stopping the initiating stimulus.

Bainbridge reflexHypervolemia, increased venous return causes stimulation of atrial stretch receptorsIncreased HR, decreased BP, decreased systemic vascular resistance, diuresis.This reflex relates to the characteristic but paradoxical slowing of the heart seen with spinal anesthesia. Blockade of the sympathetic nervous system at T1-T4 levels ablates the efferent limb of the cardiac accelerator nerves. (therefore, unopposed vagus to cause bradycardia.) The primary defect in the development of spinal hypotension is a decrease in venous receptors to cause bradicardia. Reflex tachycardia is the usual response to hypotension or acidosis from other causes. Drug of choice for bradycardia is isoproterenol which causes an increase in the discharge rate of the donor SA node by direct ction.

Cushing reflexIncreased intracranial pressure resulting in cerebral ischemiaSympathetic nervous stimulation resulting in increased BPUse medications to decrease ICP or correction of ICP via other methods for example mannitol and decrease cerebral ischemia to correct cushing reflex.

Chemoreceptor reflexDecreased oxygen saturation, increased CO2, increased hydrogen ion concentration; peripheral chemoreceptors located in the carotid body and aortic arch. Increased respiratory drive, increased blood pressure This reflex can be inhibited by the volatile anesthetic agents in a dose-dependent manner. Thus if residual volatile agent is present during the emergence from anesthesia, the threshold for breathing will be increased, necessitating a higher PaCO2 prior to spontaneous respirations.