Mean arterial pressure
Mean arterial pressure (MAP), also called perfusion pressure, is taken as the pressure difference between arteries and veins. Blood pressure regulation is performed to maintain MAP.
The MAP determines the amount of oxygen and nutrients delivered by the blood vessels and the waste transported out of the tissues.
regulation of blood pressure
The body has the ability to counteract short- and long-term changes in blood pressure. Long-term pressure changes cause the body to respond by activating the renin-angiotensin system.
Rapid/short-term changes in blood pressure force the body to activate the following receptors:
- Baroreceptors are present in the arch of the aorta and in the carotid sinus.
- Chemoreceptors are present in the carotid arteries, the aortic arch, and the medulla oblongata.
- Atrial receptors are located in the wall of the right atrium.
Baroreceptor
Baroreceptors are pressure-sensitive bodies. They are also called stretch receptors. They are modified nerve endings attached to the cytoskeleton present in nerve endings. The receptors are sensitive to rapid compensations in arterial pressure. Baroreceptors are densely located in the walls of the aortic arch and carotid sinus. The carotid sinus is located at the base of the internal carotid artery at the bifurcation of the common carotid artery. The chest area is slightly expanded because the tunica media, which is usually muscle, is relatively thin. The tunica adventitia, on the other hand, is thicker than normal. This is the layer of blood vessels where the nerve receptors are located. The same applies to the location of the baroreceptors in the aortic arch.
For example, rapid changes in pressure may occur in a person who has stood up and suddenly sits down. During the process, a large amount of blood moves from the peripheral to the central regions of the body. Consequently, a large volume of blood enters the heart and this volume overload or increased preload causes the heart to increase its cardiac output. A simultaneous increase in blood pressure is also observed with an increase in cardiac output. Baroreceptors register the increase in blood pressure.
Likewise, when a person suddenly rises from a sitting position, the baroreceptors register a drop in blood pressure. Increased blood pressure in the blood vessels causes these receptors to stretch, leading to the movement of sodium ions into the nerve endings, triggering an action potential.
These baroreceptors have a basic firing pattern. This means that they have an intrinsic potential to generate action potentials at a specific frequency at any time. This rate increases when the baroreceptors receive a stretch stimulus that is secondary to an increase in arterial pressure. The carotid arteries increase their rate of pulse generation when the pressure within them rises above 50 mm Hg. Below this pressure threshold, the carotid baroreceptors do not trigger an action potential. On the other hand, the aortic arch can register drops in blood pressure of up to 30 mm Hg. The upper limit of blood pressure, after which the rate of the action potential stops increasing, is 175 mmHg. Normal MAP is calculated to be 93 mmHg. It is believed that at this pressure the baroreceptors are most sensitive, and even small changes in pressure result in rapid firing of action potentials.
When the blood pressure is below 30 mm Hg, the chemoreceptors come into play..Chemoreceptors work by sensing the arterial concentration of carbon dioxide, oxygen, Ph, and other metabolites. You will not see any changes in blood pressure.
Barorezeptorreflex
The baroreceptor reflex, like other reflex arcs, consists of three units:
- Afferent nerves that carry impulses from receptors
- central unit
- An efferent nerve that innervates the effector.
Afferent impulses from the carotid sinus are transmitted by the Herring nerve, a branch of the glossopharyngeal nerve (CN-9). For baroreceptors in the aortic arch, the vagus nerve (CN-10) is the afferent nerve that transmits impulses to the spinal cord. Both the vagus nerve and the glossopharyngeal nerve transmit impulses to baroreceptors in the nucleus of the solitary tract. These nuclei are located in the medulla oblongata of the spinal cord and are tasked with processing incoming afferent impulses. Also within the medulla and lower third of the pons are the vasoconstrictor center, vasodilator center, and cardioinhibitory center. These centers receive processed impulses from the solitary tract nucleus and from here efferent impulses arise in the form of sympathetic and parasympathetic nerves. Impulses are sent to the heart via the parasympathetic vagus nerve. Sympathetic impulses travel through the medial-lateral segment of the spinal cord, giving rise to efferent motor spinal nerves that enter the sympathetic ganglion, which runs parallel to the spinal cord. Postganglionic sympathetic nerves innervate the heart and peripheral vessels. Another preganglionic sympathetic nerve also innervates the adrenal medulla, resulting in the release of epinephrine and norepinephrine, which further contribute to increased sympathetic activity. The end result is an increase or decrease in blood pressure, correcting the change in the body's hemodynamics. This phenomenon is also known as the clogging effect as the pressure change is dampened and returns to normal. The vagus and glossopharyngeal nerves are called damper nerves for the same reason.
Factors responsible for changing mean arterial pressure
MAP = heart rate x heart output
Yes, CO = SV (systolic volume) x TPR (total peripheral resistance)
Therefore MAP = FC x SV x TPR
Stroke volume is altered by changing the contractility of the heart muscles. The sympathetic nerves that innervate the heart muscles affect stroke volume. The parasympathetic nerves that innervate the SA and AV nodes are responsible for generating changes in heart rate. TPR can be increased or decreased by changing the diameter of the peripheral vasculature, which is under the control of the sympathetic nervous system.
Effects of baroreceptors under different conditions
Due to changes in blood pressure.
- reduced blood pressure: A reduction in blood pressure leads to a reduction in the number of afferent impulses from the baroreceptors. Sympathetic activity will increase and, as a result, RPT, HR, and stroke volume will also increase. At the same time, the parasympathetic input decreases. All of these changes will bring your blood pressure back to normal.
- Elevated blood pressure: This happens in situations such as sports or stress. Elevated blood pressure leads to stretching of the stretch receptors. This increases the frequency of the afferent impulses. The sympathetic supply will decrease and the parasympathetic system will take over. Eventually, blood pressure will drop back to normal.
Due to changes in cardiac output.
- decreased cardiac output: Occurs with vomiting, diarrhea, bleeding, etc. As a result, both the volume and the pressure of the blood decrease. It decreases the emission of afferent impulses from the baroreceptors. As a result, sympathetic spillover occurs, leading to an increase in HR, TPR, and SV. Due to an increase in these parameters, blood pressure returns to normal.
- Increased cardiac output: There is increased impulse production from the baroreceptors due to the stretch caused by the increased blood volume. This increased afferent input from the baroreceptors leads to PANS activation. Once activated, the parasympathetic nervous system lowers blood pressure to normal.
Massaging the carotid artery
By physically massaging the carotid arteries, the pressure on the baroreceptors present there is increased. The carotid baroreceptors respond by increasing the firing rate of the afferent impulse. The sympathetic is turned off and the parasympathetic is activated. This leads to a reduction in the body's blood pressure.
Carotid massage, which activates the parasympathetic nervous system, increases the AV node refractory period, thereby reducing AV nodal conduction and ultimately heart rate. For this reason, carotid sinus massage is always the first menu applied in the treatment of paroxysmal supraventricular tachycardia.
Carotid stenosis
Stenosis of the carotid arteries proximal to the sinus or obstruction of the carotid arteries due to atherosclerosis causes the baroreceptors to register a drop in pressure. Hence the activation of the sympathetic system follows. Increased sympathetic activity causes a consequent increase in blood pressure. This increase in blood pressure can lead to hypertension in a normal person.
The baroreceptor responses are summarized in the table below.
It is important to understand that baroreceptor control of blood pressure is a short-term regulation of blood pressure. Any short-term disturbance is treated by the baroreceptor response, while long-term blood pressure control is managed by the RAAS (renin-angiotensin-aldosterone system).
Baroreceptors also have the ability to adapt to chronic changes in blood pressure. When the mean pressure changes to a new value over time, the baroreceptors start using that MAP as a reference. All subsequent blood pressure changes are corrected to the new baseline MAP value.