Carotid sinus reflex

Drugs related to PCP are known to alter the carotid sinus reflex. Mechanical stimulation of the carotid sinus in the neck normally results in a slowing of heart rate and a decrease in blood pressure. Carotid sinus stimulation, coupled with the effects of PCP on blood vessels, might result in a marked fall in the blood pressure that could lead, ultimately, to death. Individuals intoxicated with PCP may be at a higher risk to complications of carotid compression neck holds. Hence, additional cases would be expected to become medicolegal issues. 

To reduce severe bradycardia in hyperactive carotid sinus reflex... 

To reduce severe bradycardia in hyperactive carotid sinus reflex Diagnostically in Wolff-Parkinson-White syndrome, to restore the PRS complex to normal duration... 

Marked reflex vagal discharge sometimes accompanies the pain of myocardial infarction and may result in sufficient depression of sinoatrial or atrioventricular node function to impair cardiac output. Parenteral atropine or a similar antimuscarinic drug is appropriate therapy in this situation. Rare individuals without other detectable cardiac disease have hyperactive carotid sinus reflexes and may experience faintness or even syncope as a result of vagal discharge in response to pressure on the neck, eg, from a tight collar. Such individuals may benefit from the judicious use of atropine or a related antimuscarinic agent. 

The cardiovascular effects of muscarinic receptor antagonists are of limited clinical application. Atropine may be considered in the initial treatment of patients with acute myocardial infarction in whom excessive vagal tone causes sinus or nodal bradycardia. Dosing must be judicious doses that are too low can cause a paradoxical bradycardia excessive doses will cause tachycardia that may extend the infarct by increasing demand. Atropine occasiormlly is useful in reducing the severe bradycardia and syncope associated with a hyperactive carotid sinus reflex. Atropine will protect the SA and AV nodes from the effects of excessive ACh in instances of poisoning with anticholinesterase pesticides. 

Our laboratory has recently investigated the reflex effects of carotid sinus hypertension on the coronary circulation (Ito and Feigl, 1984a). The carotid sinuses were vascularly isolated and perfused with a servo controlled pressure pump. The aortic depressor nerves were cut bilaterally to prevent aortic arch baroreceptor reflexes from buffering carotid sinus reflexes. The left main coronary artery was perfused at constant pressure, and the ventricles were paced at a constant rate following the production of heart block in a closed-chest preparation. Aortic pressure was stabilized with a pressure reservoir and propranolol was administered to block reflex sympathetic effects to the myocardium. Step increases in carotid sinus pressure resulted in graded reflex coronary vasodilation accompanied by increases in coronary sinus oxygen tension. Atropine administration demonstrated that the major portion of the reflex vasodilation was due to parasympathetic activation. These results indicate that parasympathetic coronary vasodilation is part of the carotid sinus baroreceptor reflex. 

The regulation of the total peripheral resistance also involves the complex interactions of several mechanisms. These include baroreflexes and sympathetic nervous system activity response to neurohumoral substances and endothelial factors myogenic adjustments at the cellular level, some mediated by ion channels and events at the cellular membrane and intercellular events mediated by receptors and mechanisms for signal transduction. As examples of some of these mechanisms, there are two major neural reflex arcs (Fig. 1). Baroreflexes are derived from high-pressure barorecep-tors in the aortic arch and carotid sinus and low-pressure cardiopulmonary baroreceptors in ventricles and atria. These receptors respond to stretch (high pressure) or... 

Loss of plasma volume leads to a decrease in MAP. Baroreceptors located in the aortic and carotid sinuses detect this fall in MAP and elicit reflex responses that include an increase in the overall activity of the sympathetic nervous system. Sympathetic stimulation of the heart and blood vessels leads to an increase in cardiac output (CO) and increased total peripheral resistance (TPR). These adjustments, which increase MAP, are responsible for the short-term regulation of blood pressure. Although increases in CO and TPR are effective in temporary maintenance of MAP and blood flow to the vital organs, these activities cannot persist indefinitely. Ultimately, plasma volume must be returned to normal (see Table 19.1). 

A decrease in plasma volume leads to decreased MAP, which is detected by baroreceptors in the carotid sinuses and the arch of the aorta. By way of the vasomotor center, the baroreceptor reflex results in an overall increase in sympathetic nervous activity. This includes stimulation of the heart and vascular smooth muscle, which causes an increase in cardiac output and total peripheral resistance. These changes are responsible for the short-term regulation of blood pressure, which temporarily increases MAP toward normal. 

The answer is a. (Katzung, p 240.) Older therapies—all designed to favor parasympathetic control of rhythm—include digoxin, propranolol, edrophonium, and vasoconstrictors. The vasoconstrictor phenylephrine (given by intravenous bolus) causes stimulation of the carotid sinus and reflex vagal stimulation of the atria. More recently, adenosine has been favored over verapamil, which is also very effective but slower acting... 

Figure 8. Cardiovascular effects of clonidine (St 155) in an anaesthetized dog. Upper curve, blood pressure, heart frequency. Lower curve, nictitating membrane. At the whole dots carotid sinus occlusion reflex was elicited (11).

This area is also involved in the carotid sinus occlusion reflex, which can be blocked by clonidine, as already mentioned. Recently HAEUSLER (30) has shown that the action of clonidine bears similarity to a central activation of the depressor baroreceptor reflex which was elicited by electrical stimulation of the sinus nerves. 

Any sudden alteration in the mean arterial blood pressure tends to produce compensatory reflex changes in heart rate, contractility, and vascular tone, which will oppose the initial pressure change and restore the homeostatic balance. The primary sensory mechanisms that detect changes in the mean arterial blood pressure are stretch receptors (baroreceptors) in the carotid sinus and aortic arch. 

Atropine can be useful in patients with carotid sinus syncope. This condition results from excessive activity of afferent neurons whose stretch receptors are in the carotid sinus. By reflex mechanisms, this excessive afferent input to the medulla oblongata causes pronounced bradycardia, which is reversible by atropine. 

Afferent neurons The afferent neurons (fibers) of the autonomic nervous system are important in the reflex regulation of this system, for example, by sensing pressure in the carotid sinus and aortic arch and signaling the CNS to influence the efferent branch of the system to respond (see below). 

Reflex arcs Most of the afferent impulses are translated into reflex responses without involving consciousness. For example, a fall in blood pressure causes pressure-sensitive neurons (baroreceptors in the heart, vena cava, aortic arch, and carotid sinuses) to send fewer impulses to cardiovascular centers in the brain. This prompts a reflex response of increased sympathetic output to the heart and vasculature, and decreased parasympathetic output to the heart, which results in a compensatory rise in blood pressure and tachycardia (see Figure 3.5). 

Nicotine introduced into perfused sahne solution flowing through the isolated carotid bodies promotes respiratory stimulation and bradycardia. The same phenomena occur if the carotid sinus is painted with nicotine. The reflex action of nicotine through the sinus and aortic sensory mechanisms has also been recognized by Gollwitzer-Meyer (52). 

Due to its marked variability, it is impossible to state quantitatively whether stimulation by caffeine is affected by sino-aortic denervation. It is clear, however, that good stimulation can be obtained with caffeine in an animal after section of the aortic and carotid sinus nerves. These experiments seem to prove that caffeine acts centrally but they do not eliminate some shght reflex effects by way of the sino-aortic nerves. 

Baroreceptor reflex The neuronal homeostatic mechanism that the body uses to maintain blood pressure constant the sensory limb originates in the baroreceptors of the carotid sinus... 

Baroreceptor reflex Primary autonomic mechanism for blood pressure homeostasis involves sensory input from carotid sinus to the vasomotor center and output via the parasympathetic and sympathetic motor nerves... 

Shoukas, A.A., Brunner, M.J., Frankie, A.E., Greene, A.S., and Kallman, C.H. 1984. Carotid sinus baroreceptor reflex control and the role of autoregulation in the systemic and pulmonary arterial pressure-flow relationships of the dog. Circ. Res. 54 674-682. 

Shoukas, A.A. and Sagawa, K. 1973. Control of total systemic vascular capacity by the carotid sinus baroreceptor reflex. Circ. Res. 33 22. 

Shoukas, A.A. 1993. Overall systems analysis of the carotid sinus baroreceptor reflex control of the circulation. Anesthesiology 79 1402. 

Haase, E. and Shoukas, A. A. 1991. The role of the carotid sinus baroreceptor reflex on pressure and diameter relations of the microvasculature of the rat intestine. Am. J. Physiol. 260 H752. 

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