Baroreceptors

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Baroreceptors

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Baroreceptors

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Baroreceptor reflex is a regulatory system of mean arterial pressure through baroreceptors located in the walls of the carotid sinus, the , and large arteries of the neck and thorax.

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A 27-year-old man is involved in a motor vehicle accident and sustains massive blood loss. He is promptly brought to the emergency department. Initial survey shows an agitated, pale, diaphoretic young man. His initial blood pressure is holding steady at 100/70 mm Hg, but the trauma team is concerned about developing shock. Which of the following pathways is involved in the afferent limb of the physiologic response maintaining this patient's blood pressure?  

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Content Reviewers:

Rishi Desai, MD, MPH

“Baro-“ means pressure or stretch, so baroreceptors are special nerve cells or receptors that sense blood pressure, by the way that the walls of the blood vessels stretch. That information is sent from the baroreceptors to the brain to help keep blood pressure balanced.

Alright, baroreceptors are actually groups of nerve endings located within the blood vessel walls. and they can be classified into two types based on their location: the arterial ones and the cardiopulmonary ones. The arterial baroreceptors can be found on the wall of the aortic arch as well as on the wall of the carotid sinus, which is basically a bulge of the internal carotid artery just above its split from the common carotid artery in the neck. In the aortic arch, these nerve endings join up to form the vagus, or tenth (X) cranial nerve, and in the carotid sinus, they form the glossopharyngeal, or ninth (IX) cranial nerve. Both of these cranial nerves travel up towards the brainstem, carrying information about the stretch they sense in the arteries. They synapse at the nucleus tractus solitarius in the medulla oblongata of the brainstem, which then relays the information to the cardiovascular centers. The cardiovascular centers are areas in the lower one-third of the pons and medulla oblongata of the brainstem, responsible for the autonomic or involuntary control of the cardiac and vascular function. They do that by coordinating the sympathetic and parasympathetic branches of the autonomic nervous system. There are two main cardiovascular centers - the first is the vasomotor control center, which controls the diameter of the blood vessels, using the sympathetic nerve fibers to cause vasoconstriction. The second is the cardiac control center, which is further divided into the cardiac accelerator and cardiac decelerator centers. The cardiac accelerator center speeds up the heart rate and increases cardiac contractility through the sympathetic outflow tract, while the cardiac decelerator center slows down the heart rate through the parasympathetic outflow tract. Notice that both the sympathetic and parasympathetic system affect the heart rate, but that only the sympathetic system has an effect on the diameter of the blood vessels and the contractility of the heart muscle. This whole process is known as the baroreceptor reflex, or baroreflex in short, and takes place in seconds to minutes, allowing us to rapidly adjust our blood pressure.

Okay, so, as blood pulses through the carotid sinus and the aortic arch, the arterial walls get stretched out and in response, the baroreceptors start firing more nerve impulses up to those cardiovascular centers. The higher the pressure, the higher the frequency of nerve impulses. So, let’s say you’re running to catch the bus and your blood pressure rises. The increased pressure stretches the walls of the aortic arch and the carotid sinus, and the baroreceptors start firing at an increased frequency. The glossopharyngeal and vagus nerve carry that increased signal to the cardiovascular centers of the brainstem. To bring the pressure back down to normal, these centers inhibit the sympathetic and stimulate the parasympathetic nervous systems. Specifically, the vasomotor center decreases the vasoconstrictive effect of the sympathetic nervous system. In other words, the arterioles dilate, decreasing total peripheral arterial resistance, and there’s decreased constriction of veins, which allows blood to pool in the periphery rather than returning to the heart. Decreased venous return means there’s less preload - less diastolic filling of the heart - and that also decreases cardiac output. Meanwhile, remember that the cardiac accelerator center is also inhibited, reducing the sympathetic effect on the heart, and letting the heart work slower and less forcefully, in other words decreasing the heart rate and contractility, while the cardiac decelerator center is activated, boosting the parasympathetic effects on the heart, which again slows down the heart rate. Combined, these effects result in a decreased cardiac output (CO). Since blood pressure (BP), roughly equals cardiac output (CO) times total peripheral resistance (TPR), the decrease in cardiac output CO and the decrease in total peripheral resistance (TPR) means that blood pressure (BP) will decrease back down to normal as well. Hopefully, by that point, you’ve made the bus!

On the flip side, let’s say that you’re in a terrible traumatic accident and start losing a lot of blood, causing your blood pressure to fall. The decreased pressure causes the walls of the aortic arch and carotid sinus to become less stretched, and the baroreceptors start firing less frequently. The glossopharyngeal and vagus nerve carry that decreased signal to the cardiovascular centers of the brainstem. To bring the pressure back up to normal, these centers stimulate the sympathetic and inhibit the parasympathetic nervous systems. Specifically, the vasomotor center increases the vasoconstrictive effect of the sympathetic nervous system. In other words, the arterioles narrow, increasing total peripheral arterial resistance, and there’s increased constriction of veins, which returns more blood to the heart rather than allowing it to pool in the periphery. Increased venous return means there’s more preload, and that also increases cardiac output. Meanwhile, remember that the cardiac accelerator center is also stimulated, increasing the sympathetic effect on the heart, and letting the heart work faster and more forcefully, in other words increasing the heart rate and contractility, while the cardiac decelerator center is deactivated, reducing the parasympathetic effects on the heart, which again speeds up the heart rate. Combined, these effects result in an increased cardiac output (CO) and an increase in total peripheral resistance (TPR) which raises the blood pressure (BP) back to normal. In this case, these changes can save your life.