Baroreceptor Reflex - Neuroscience
Here, we will learn the neuroanatomy and neurophysiology of the baroreceptor reflex.
Start a table.
Denote that blood pressure (specifically, Mean Arterial pressure (MAP), which is the driving force for blood flow, is regulated by two main mechanisms:
The Baroreceptor Reflex, which is fast-acting (within seconds) and acts via changes in –
Cardiac Output (stroke volume x heart rate)
Total Peripheral Resistance (a measure of arteriolar constriction): like a faucet that regulates pressure from a hose.
The kidney's renin-aldosterone-angiotensin system, which acts slowly and via blood volume changes.
Now, let's draw some of the key involved structures.
First, draw the heart; aorta and aortic arch; and the common carotid artery — include its bifurcation into the internal carotid and external carotid arteries.
Then, draw a vertical snippet of the spinal cord.
Draw an expanded axial section of the medulla.
Now, let's draw the specific components of the cardiovascular reflex.
First, draw the carotid sinus at the origin of the internal carotid artery.
Then, draw aortic arch baroreceptors in the aortic arch.
They are mechanoreceptors, which respond to stretch changes in the arterial vasculature due to changes in blood pressure.
Also, add the carotid body at the bifurcation of the common carotid artery and the aortic bodies below the arch of the aorta.
They are chemoreceptors that respond to arterial oxygen and carbon dioxide levels and blood acidity; they are important cardiovascular receptors but have much little to do with the baroreceptor reflex, itself.
Show that we'll indicate parasympathetic elements in green and sympathetic elements in blue.
Next, draw the solitary tract nucleus within the medial dorsal medulla.
Draw nucleus ambiguus (the cardioinhibitory center) in front of it.
Then, draw the ventrolateral medulla vasomotor area, which comprises areas A1 (the cardiac accelerator center) and C1 (the vasoconstrictor center).
Now, show that the glossopharyngeal nerve (CN 9) projects from the carotid sinus to the solitary tract nucleus.
And that the vagus nerve (CN 10) projects from the aortic arch baroreceptors to the solitary tract nucleus.
Then, show that the solitary tract nucleus excites the cardioinhibitory center, which produces parasympathetic branches that project via the vagus nerve to the heart to produce:
Heart rate deceleration and reduced stroke volume.
Now, let's turn our attention to the sympathetic nervous system.
Create a box for the sympathetic ganglia (paravertebral and prevertebral).
Show that the vasomotor center provides tonic sympathetic stimulation to the spinal cord (the intermediolateral cell column from T1 to L2).
Then, show that presynaptic sympathetic branches innervate the sympathetic ganglia.
And show that post-synaptic sympathetic nerve fibers innervate the heart to produce:
Heart rate acceleration and increased stroke volume.
Now, draw a blood vessel in its resting state.
Show that the parasympathetic and sympathetic nerve fibers pass through the cardiac plexus prior to their synapsis in the heart, itself.
Show that sympathetic innervation of the vessel produces vasoconstriction (which increases total peripheral resistance).
To better understand this draw a section of the aorta.
Show a series of organs (like buckets).
Show a few arteries emerge from it in parallel.
Now add variable arteriolar resistance to each artery (like a faucet); show greater degrees of resistance from top to bottom.
Then, show the resultant flow, which is variable.
Indicate that as a result the organs, receive variable amounts of blood.
Thus, one mechanism to adjust blood flow is via arteriolar constriction (peripheral resistance).
Next, draw the kidneys.
Show that sympathetic innervation to the renin-angiotension-aldosterone system adjusts blood pressure via a slow mechanism, that works through change in blood volume.
Now, show that the brain modulates the solitary tract nucleus: after all, we can affect our heart rate through our own conscious fear and anxiety. (Key modulators include the hypothalamus and amygdala, and parabrachial pontine nucleus).
Lastly, let's examine what occurs in sudden low blood pressure (such as from hemorrhage (blood loss) or orthostasis (a drop in blood pressure upon standing).
A drop in blood pressure produces a drop in baroreceptor activity, which triggers an increase in sympathetic activity and a decrease in parasympathetic activity, which produces an increase in cardiac output and vessel constriction (total peripheral resistance).
And, as shown at the beginning, indicate that when they increase, so does blood pressure – in this case back to normal (the set-point).
A simple way to test the cardiovascular response is by varying your pulse. Take your pulse and get a good sense of your heart rate. Then, take a deep breath and hold it for 5 or 6 seconds. Your heart rate should speed up because when you inhale deeply, you open up lung tissue and shunt blood into the lung capillaries, which reduces your effective circulating blood volume (ie, your stroke volume).
Cardiac output is stroke volume multiplied by heart rate; therefore, to compensate for a decreased stroke volume, your heart rate increases (typically by 8 beats per minute).
An additional, slower response to a reduced stroke volume is to increase the effective circulating blood volume, itself. For instance, when we stand, blood pools in our veins, so after we stand upright for a full minute, T5 sympathetic splanchnic fibers command our abdominal vessels to shunt roughly 1.5 units of blood from our abdomen into our peripheral vasculature. Because there is a delay in the shunting of blood between systems, when we check orthostatic blood pressure, we must wait at least a few minutes in between measuring supine and standing blood pressure (and possibly longer, even).
Practical Electrophysiology
edited by Jasbir S. Sra, MD, Masood Akhtar, MD, Andrea Natale, MD, David J. Wilber, MD
Basic Neurosciences with Clinical Applications
By Eduardo E. Benarroch