Tag: Neural Regulation Of Cvs

Neural Regulation Of Cvs

Neural Regulation Of Cvs


NEURAL REGULATION OF CVS

CARDIOVASCULAR CONTROL CENTER

  • Neural cardiovascular regulatory mechanisms consist of,
  • Medullary cardiovascular center.
  • Its afferents & efferents.

1. MEDULLARY CARDIOVASCULAR CENTER:

  • Consist of,
  • Vasomotor Center (VMC).
  • Cardiovagal/Cardio-Inhibitory Center.
  • Both these centers act together to maintain BP.

1a. VASOMOTOR CENTER (VMC):

  • Also referred as “Medullary Sympathetic Center”.
  • Since it controls spinal sympathetic neuron output.

DIVISIONS:

2 areas- 

“Pressor area”:

  • Located in Rostral Ventrolateral Medulla (RVLM).
  • Increases spinal sympathetic output.

“Depressor area”:

  • Located in Caudal Ventrolateral Medulla (CVLM).
  • Reduces spinal sympathetic output.
  • Normally, pressor area effect predominates.
  • VMC frequently used synonymously with pressor area.
  • I.e., RVLM.
EFFECTS:
  • VMC stimulation (Specifically pressor area) 
  • Increases sympathetic discharge causing, 
  • Vasoconstriction.
  • Thus, increased BP
  • “Chronotropic effect” 
  • (Increased heart rate).
  • “Ionotropic effect” 
  • (Increased force of cardiac conduction).
  • “Dromotropic effect” 
  • (Increased conduction).
  • “Bathmotropic effect” 
  • (Increased automaticity).

2. CARDIO-VAGAL CENTER/CARDIOINHIBITORY CENTER:

  • Also referred as “Medullary Parasympathetic Area”.
  • Sends parasympathetic efferents discharge to heart causing,
  • Vasodilatation.
  • Negative Chronotropic Effect 
  • (Decreased heart rate).
  • Decreased BP.
  • Decreased cardiac output.

Under resting conditions, 

  • Neurons of pressor area of VMC have an inherent tonic discharge in vasomotor nerve supplying blood vessels.
  • Whereas on heart have predominating vagal (Parasympathetic) effect.

3. AFFERENT FROM HIGHER CENTERS:

  • Vasomotor center (VMC) receives afferent fibers from cerebral cortex.
  • Both directly & via hypothalamus (cortico-hypothalamic pathways).
  • Responsible for change in BP & heart rate.
  • Due to emotional stress.
  • Also during voluntary actions.
REGULATION OF VMC:
  • VMC tone regulatory through various reflexes.

REFLEXES:

1.  BARORECEPTOR REFLEX:

  • Type of Mechanoreceptors.
  • Located in adventitia of carotid artery & aorta, at specialized locations called “Sinuses”.

Carotid Sinus –

  • Little bulge at internal carotid artery root.
  • Just above the bifurcation of common carotid artery.
  • Innervated by sinus nerve, branch of glossopharyngeal (IX cranial) nerve.

Aortic arch:

  • Mechanoreceptors.
  • Stretch receptors (similar to carotid sinus).
  • Innervated by aortic nerve, branch of Vagus (X cranial) nerve.
  • Theses nerves from carotid sinus & from aortic sinus together referred as “Sinoaortic nerves”
  • Are afferents of cardiovascular nerves buffering abrupt BP change. 
  • Hence, “Buffer Nerves”.
FUNCTIONS:
  • Baroreceptors are highly sensitive to any change in mean blood pressure. 
  • Sinoaortic nerves discharge rhythmically & synchronous with the pressure fluctuation during systole & diastole.
  • Respond to BP changes between 70 mm Hg & 150 mm Hg.
EFFECTS OF BARORECEPTOR REFLEX:

1. ON INCREASED BP:

Increased BP Stimulates Baroreceptors & their afferents (through sinoaortic nerves).

In turn, stimulate nucleus of tractus solitarius (NTS).


Inhibits VMC pressor area. i.e., Rostral Ventrolateral Medulla (RVLM) → Decreased sympathetic outflow.

Hence, decrease vasomotor tone & vasodilation.

Vasodilation reduces BP helping hemostasis.

Activated NTS also stimulates nucleus ambiguous (cardioinhibitory center) of medulla.

Increases parasympathetic (vagal) output through vagus  → Decreases heart rate, cardiac output, & BP eventually.

  • Also, baroreceptor stimulation weakly inhibits respiration.

2. ON DECREASED BP:

Decreased BP (Eg: While changing posture from lying down to standing.

On standing up, blood pools in lower limb veins by gravitational effect.

Central venous pressure & venous return decrease.

Causes fall in stroke volume & systolic BP.

Resulting in decreasing baroreceptors discharge rate → Thus, decreases inhibitory influence on pressor area of VMC.

Increases vasomotor tone → Causing Vasoconstriction → Increases BP.

Simultaneously inhibits vagal nucleus ambiguous → Increases heart rate, stroke volume & eventually BP.

Hence, BP fall due to postural change transient.

3. ON PRESSURE:

3a. VALSALVA’S MANEUVER:

  • Baroreceptor reflex elicited by applying pressure on carotid sinus/“Carotid massage”,
  • Ie., Pressure application on area of neck overlying carotid sinus.
  • Also activated by wearing tight collor pressing upon carotid sinus.
  • Resulting in reflex hypotension & fainting.
  • Referred as “Carotid sinus syncope”.
  • This reflex increase in vagal discharge to AV node is of therapeutic value in controlling supraventricular tachycardia.

3b. ON RATE OF PRESSURE CHANGE:

  • At rest, arterial baroreceptors are stimulated during systolic upstroke of pressure pulse wave.

II. CHEMORECEPTOR REFLEX:

  • Activation of chemoreceptors in carotid & aortic body – 
  • By PaOreduction.
  • Also, by increased PaCO2 & pH.
FUNCTIONS:
  • Primarily concerned with pulmonary ventilation regulation.
  • Causes generalized vasoconstriction.
  • Due to increasd vasomotor tone.

Ultimate effect of chemoreceptor stimulation is,

  • Vasoconstriction.
  • Increased BP.
  • Tachycardia.
APPLIED PHYSIOLOGY:
  • Sinus & aortic nerve contain both baroreceptor & chemoreceptor afferents.

Regulation of BP in severe hypotension:

  • Ie., below 70mm Hg
  • By chemoreceptor reflex.
  • Regulation of BP below 40mm Hg.
  • By CNS ischemic response.
  • Resulting in direct VMC stimulation & increase in BP
  • Regulation of BP between 70-150 mm Hg:
  • By Baroreceptor mechanism

On bilateral sectioning of sinus & aortic nerves:

  • In normal & in mild hypotensive animals causes,
  • Elevation of BP & heart rate.
  • In severe hypotensive animals,
  • Produces further fall in BP.
  • Since baroreceptor discharge is already absent.
  • Also, this sectioning abolishes chemoreceptor drive as well.

On Proximal clamping of common carotid:

  • Increases blood pressure, heart rate, & respiratory rate.
  • Due to stimulation of both chemoreceptor & baroreceptor.
  • Chemoreceptor stimulation – 
  • Is due to reduced perfusion of carotid bodies
  • Baroreceptor inhibition – 
  • Is due to reduced pressure in carotid sinus.

On Bilateral clamping of carotid arteries:

  • Decreases BP, heart rate & respiratory rate.
Exam Question
 

NEURAL REGULATION OF CVS

  • Vasomotor Center (VMC) & Cardiovagal/Cardio-Inhibitory Center act together to maintain BP.
  • “Pressor area” of VMC, located in Rostral Ventrolateral Medulla (RVLM).
  • Under resting conditions, neurons of VMC pressor area have an inherent tonic discharge in vasomotor nerve supplying blood vessels.
  • Vasomotor center (VMC) receives afferent fibers from cerebral cortex, both directly & via hypothalamus (cortico-hypothalamic pathways.
  • Receptors for baroreceptor reflex process is located in the adventitia of carotid artery & aorta, at specialized locations called “Sinuses”.
  • Baroreceptors are highly sensitive to any change in mean blood pressure.
  • Respond to BP changes between 70 mm Hg & 150 mm Hg.
EFFECTS OF BARORECEPTOR REFLEX:

1. ON INCREASED BP:

Increased BP → Stimulates Baroreceptors & their afferents (through sinoaortic nerves).

In turn, stimulate nucleus of tractus solitarius (NTS).


Inhibits VMC pressor area. i.e., Rostral Ventrolateral Medulla (RVLM) —-> Decreased sympathetic outflow.

Hence, decrease vasomotor tone & vasodilation.

Vasodilation reduces BP helping hemostasis.

Activated NTS also stimulates nucleus ambiguous (cardioinhibitory center) of medulla.

Increases parasympathetic (vagal) output through vagus → Decreases heart rate, cardiac output, & BP eventually.

2. ON DECREASED BP:

Decreased BP (Eg: While changing posture from lying down to standing.

Central venous pressure & venous return decrease.

Causes fall in stroke volume & systolic BP.

Eventually increases heart rate, stroke volume & BP ultimately.

  • Valsalva’s maneuver is activated by “Carotid massage”.
  • This reflex increase in vagal discharge to AV node is of therapeutic value in controlling supraventricular tachycardia.
  • At rest, arterial baroreceptors are stimulated during systolic upstroke of pressure pulse wave.

Regulation of BP in severe hypotension:

  • Ie., below 70mm Hg
  • By chemoreceptor reflex.

Regulation of BP below 40mm Hg.

  • By CNS ischemic response.

Regulation of BP between 70-150 mm Hg:

  • By Baroreceptor mechanism.

Bilateral section of sinus & aortic nerves,

  • In normal and mild hypotensive animals causes, 
  • Elevation of BP & heart rate.
  • In severe hypotensive animals,
  • Further fall in BP.

Proximal clamping of common carotid causes

  • Increased blood pressure, heart rate, & respiratory rate.
  • Bilateral clamping of carotid arteries causes, 
  • Decreased BP, heart rate & respiratory rate.
Don’t Forget to Solve all the previous Year Question asked on Neural Regulation Of Cvs

Neural Regulation Of Cvs

NEURAL REGULATION OF CVS

Q. 1

Vasomotor centre of medulla is associated with?

 A

Acts with the cardiovagal centre to maintain B.P.

 B

Independent of corticohypothalamic inputs

 C Influenced by baroreceptors not chemoreceptors
 D

Essetially silent in sleep

Q. 1

Vasomotor centre of medulla is associated with?

 A

Acts with the cardiovagal centre to maintain B.P.

 B

Independent of corticohypothalamic inputs

 C Influenced by baroreceptors not chemoreceptors
 D

Essetially silent in sleep

Ans. A

Explanation:

Acts with the cardiovagal centre to maintain B.P. (Ref Ganong 23/e p556]

  • Neural regulation of the blood pressure is brought about by 2 different centres located in medulla – Vasomotor centre which control the sympathetic outflow, and Cardiovagal centre which controls the parasympathetic outflow.
  • TheVasomotor centre and the Cardiovagal centre act together to maintain the B.P. (Note that many books do not make the distinction between the vasomotor and cardiovagal centre and collectively use the term vasomotor centre for all the neurons in medulla that control the B.P.

Vasomotor centre

Cardio vagal centre

Vasomotor centre is group of neurons located in Rostral

Cardiovagal centre lies in the nucleus ambiguous.

Ventrolateral Medulla (RVLM) associated with sympathetic

It sends parasympathetic impulses to the heart via the

discharge controlling the cardiovascular system.

vagus(note that blood vessels receive only

The sympathetic discharge from vasomotor centre goes to

sympathetic impulses whereas heart receives both

heart and blood vessels resulting in:

sympathetic and parasympathetic supply).

Increased heart rate (Chronotropic effect)

This results in:

– Increased force of cardiac contraction (Inotropic effect)

– Decreased heart rate

– Increased rate of transmission in the cardiac conductive

– Decrease cardiac output

tissue (Dromotropic effect)

– Decreased B.P.

– Vasoconstriction

(this leads to increased stroke volume and increased BP)

 

  • The vasomotor centre receive inputs from Corticohypothalmic fibres

            Corticohypothalmic .fibres are descending tracts to the vasomotor area from the cerebral cortex (particularly the limbic cortex) that relay in the hypothalamus. These fibers are responsible .for the blood pressure rise and            tachycardia produced by emotions such as sexual excitement and anger.

  • The vasomotor centre is not silent during sleep The vasomotor centre neurons arc tonically active and discharge rhythmically.
  • The vasomotor centre receives inputs from baroreceptors and also from chemoreceptors.

The baroreceptors are stretch receptors in the walls of carotid sinus and aortic arch. The baroreceptors are stimulated by distention of the structures in which they are located, and so they discharge at an increased rate when the pressure in these structures rises. Increased baroreceptor discharge inhibits the tonic discharge of sympathetic nerves and excites the vagal innervation of the heart. These neural changes produce vasodilation, venodilation, a drop in blood pressure. bradycardia, and a decrease in cardiac output.

Chemoreceptors are located in carotid and aortic bodies. These receptors are primarily activated by a reduction in partial pressure of oxygen (Pa02), but they also respond to an increase in the partial pressure of carbon dioxide (PaCO2) and pH. Chemoreceptors exert their main effects on respiration; however, their activation also leads to vasoconstriction. Heart rate changes are variable and depend on various factors, including changes in respiration.

Factors Affecting the Vasomotor centre (RVLM)

Direct stimulation

CO2

Hypoxia

Excitatory inputs

Cortex via hypothalamus

Mesencephalic periaqueductal gray

Brain stein reticular formation

Pain pathways

Somatic afferents (somatosympathetic reflex)

Carotid and aortic chemoreceptors

Inhibitory inputs

Cortex via hypothalamus

Caudal ventrolateral medulla

Caudal medullary raphe nuclei

Lung inflation afferents

Carotid, aortic, and cardiopulmonary baroreceptors

  • Thus we see that the cardiovascular system is under neural influences of medulla, which in turn receive feedback from sensory receptors in the vasculature (eg, baroreceptors). An increase in neural output from the brain stem to sympathetic nerves leads to a decrease in blood vessel diameter (arteriolar constriction) and increases in stroke volume and heart rate, which contribute to a rise in blood pressure. This in turn causes an increase in baroreceptor activity, which signals the vasomotor centre to reduce the neural output to sympathetic nerves.

Also know:

  • The neurons of vasomotor centre secrete excitatory transmitter- glutamate (and not epinephrine)
  • Inflation of the lungs causes vasodilation and a decrease in blood pressure. This response is mediated via vagal afferents from the lungs that inhibit vasomotor discharge.
  • In general, stimuli that increase the heart rate also increase blood pressure, whereas those that decrease the heart rate lower blood pressure. However, there are exceptions, such as the production of hypotension and tachycardia by stimulation of atrial stretch receptors and the production of hypertension and bradycardia by increased intracranial pressure (Cushing reflex).
  • Cushing reflex: Increase in intracranial pressure compromises the blood supply to the vasomotor neurons, and the resulting local hypoxia and hypercapnia increase discharge from the vasomotor centre. This results in rise in systemic arterial pressure (Cushing reflex) which tends to restore the blood flow to the medulla. Over a considerable range, the blood pressure rise is proportional to the increase in intracranial pressure. The rise in blood pressure causes a reflex decrease in heart rate via the arterial baroreceptors. This is why bradycardia rather than tachycardia is characteristically seen in patients with increased intracranial pressure.

Q. 2

Massage of the carotid sinus results in all of the following, EXCEPT:

 A

Increased pressure at the carotid sinus baroreceptors

 B

Decreased firing rate of the carotid sinus fibers

 C

Decreased firing rate of cardiac sympathetic fibers

 D

Increased firing rate of the vagus nerve

Q. 2

Massage of the carotid sinus results in all of the following, EXCEPT:

 A

Increased pressure at the carotid sinus baroreceptors

 B

Decreased firing rate of the carotid sinus fibers

 C

Decreased firing rate of cardiac sympathetic fibers

 D

Increased firing rate of the vagus nerve

Ans. B

Explanation:

Increased baroreceptor pressure causes an increase in the firing rate of the carotid sinus nerve (afferent) that inhibits the medullary vasomotor center. Consequently, both a decrease in sympathetic tone and an increases in vagal discharge (efferent) contribute to the fall in heart rate and arterial blood pressure following carotid sinus massage. When performing this maneuver on your patients or peers, be prepared for cardiac sinus arrest and avoid vigorous massage, which might dislodge an embolus and cause permanent neurological damage.
 
Ref: Quinn J. (2011). Chapter 56. Syncope. In J.E. Tintinalli, J.S. Stapczynski, D.M. Cline, O.J. Ma, R.K. Cydulka, G.D. Meckler (Eds), Tintinalli’s Emergency Medicine

Q. 3

Which of the following statements about vasomotor centre (VMC) is TRUE?

 A

It is essentially silent in sleep

 B

Independent of cortico hypothalamic inputs

 C

Influenced by baroreceptor signals but not by chemo-receptors

 D

Acts along with the cardio vagal centre (CVC) to maintain Blood pressure.

Q. 3

Which of the following statements about vasomotor centre (VMC) is TRUE?

 A

It is essentially silent in sleep

 B

Independent of cortico hypothalamic inputs

 C

Influenced by baroreceptor signals but not by chemo-receptors

 D

Acts along with the cardio vagal centre (CVC) to maintain Blood pressure.

Ans. D

Explanation:

The main control of blood pressure is exerted by a group of neurons in the medulla called as vasomotor center. CVC controls the parasympathetic flow which functionally interacts with VMC in maintaining the blood pressure.

Ref: Review of Medical Physiology By William F Ganong, 23rd Edition, Page 478; Textbook of Medical Physiology By Guyton and Hall, 10th Edition, Page 191

 


Q. 4

Discharge from Baroreceptors causes inhibition of

 A

Caudal Ventrolateral Medulla

 B

Caudal Ventrolateral Medulla

 C

Nucleus ambiguous

 D

Nucleus tractus solitarus

Q. 4

Discharge from Baroreceptors causes inhibition of

 A

Caudal Ventrolateral Medulla

 B

Caudal Ventrolateral Medulla

 C

Nucleus ambiguous

 D

Nucleus tractus solitarus

Ans. B

Explanation:

B i.e. Rostral Ventrolateral Medulla


Q. 5

Baroreceptor stimulation produces:

 A

Decreased heart rate & BP

 B

Increased heart rate & BP

 C

Increased cardiac contractility

 D

All

Q. 5

Baroreceptor stimulation produces:

 A

Decreased heart rate & BP

 B

Increased heart rate & BP

 C

Increased cardiac contractility

 D

All

Ans. A

Explanation:

A i.e. Decreased HR & BP

Baroreceptors are the stretch receptors in the walls of heart & blood vessels eg carotid sinus & aortic arch receptors, receptors in walls of atria at enterance of SVC, IVC & pulmonary veins and receptors in pulmonary circulation (cardio- pulmonary receptors). These are stimulated by distension of the structure in which they are located 1/t vagal innervation of heart and producing vasodilation, venodilation, a drop in BP, bradycardia & decrease cardiac outputQ.


Q. 6

Baroreceptor are ‑

 A

Carotid body

 B

Carotid sinus

 C

Aortic body

 D

None

Q. 6

Baroreceptor are ‑

 A

Carotid body

 B

Carotid sinus

 C

Aortic body

 D

None

Ans. B

Explanation:

Ans. is ‘b’ i.e., Carotid sinus

  • Baroreceptors are mechanoreceptors that are located in the adventia of carotid artery and aorta, at specialized locations called sinuses.

1) Carotid sinus is a little bulge at the root of internal carotid artery, located just above the bifurcation of the common carotid artery. It is innervated by the sinus nerve, a branch of glossopharyngeal (IX cranial) nerve.

2) Aortic arch (aortic sinus) also contains mechenoreceptors (stretch receptors) which are similar to carotid sinus receptors. However, their afferent nerve fibers travel in the aortic nerve, a branch of Vagus (X cranial) nerve.

The sinus nerve (from carotid sinus) and aortic nerve/vagal fibers (from aortic sinus) are together called `Sino­aortic nerves’. They, together, are also refered to as ‘Buffer nerves’ because they are the afferents of cardiovascular reflexes that buffer abrupt changes in blood pressure.


Q. 7

Signal from Baroreceptors goes to ‑

 A

Caudal ventrolateral medulla

 B

Rostral ventrolateral medulla

 C

Nucleus of tractus solitarius

 D

None of the above

Q. 7

Signal from Baroreceptors goes to ‑

 A

Caudal ventrolateral medulla

 B

Rostral ventrolateral medulla

 C

Nucleus of tractus solitarius

 D

None of the above

Ans. B

Explanation:

Ans. is ‘b’ i.e., Rostral ventrolateral medulla

Baroreceptors are mechanoreceptors that are located in the adventia of carotid artery and aorta, at specialized locations called sinuses.

1) Carotid sinus is a little bulge at the root of internal carotid artery, located just above the bifurcation of the common carotid artery. It is innervated by the sinus nerve, a branch of glossopharyngeal (IX cranial) nerve.

2) Aortic arch (aortic sinus) also contains mechenoreceptors (stretch receptors) which are similar to carotid sinus receptors. However, their afferent nerve fibers travel in the aortic nerve, a branch of Vagus (X cranial) nerve.

The sinus nerve (from carotid sinus) and aortic nerve/vagal fibers (from aortic sinus) are together called `Sino­aortic nerves’. They, together, are also refered to as ‘Buffer nerves’ because they are the afferents of cardiovascular reflexes that buffer abrupt changes in blood pressure.

Baroreceptors are highly sensitive to any change in mean blood pressure. Sinoaortic nerves (buffer nerves) normally discharge rhythmically, synchronous with the pressure fluctuation during systole and diastole. They respond to BP changes between 70 mm Hg and 150 mm Hg. When BP rises, baroreceptors are stimulated and their afferents (through sinoaortic nerves) stimulate nucleus of tractus solitarus (NTS) which inturn inhibits the pressor area ofVMC, i.e., Rostral ventrolateral medula (RVLM). This results in decreased sympathetic outflow and therefore decreases in vasomotor tone and vasodilation. Vasodilation brings down the BP, thereby helping hemostasis. Activated NTS also stimulates nucleus ambiguous (cardioinhibitory center) of medulla, which increases parasympathetic (vagal) output, through vagus, that decreases heart rate. Reduction in heart rate reduces the cardiac output, which also reduces BP. Baroreceptor stimulation also weekly inhibits respiration.

When BP falls, for instance while changing the posture from lying down to standing, reverse change takes place. When a person stands up, his blood is pooled in the veins of lower limbs by the effect of gravity. Central venous pressure and venous return decrease, which causes a fall in stroke volume. Hence the systolic BP falls. As a result, the discharge rate of baroreceptors decreases leading to a decrease in the inhibitory influence on the pressor area of VMC. Hence vasomotor tone increases, leading to vasoconstriction, and consequently an increase in BP. Simultaneously, the nucleus ambiguous of the vagus is also inhibited, increasing the heart rate and consequently stroke volume and eventually BR Thus fall in BP due to change ofposture is very brief (Transient).


Q. 8

Clamping of the carotid arteries below (proximal) the carotid sinus is likely to produce:

 A

Increase in vasomotor centre activity

 B

Increase in discharge of carotid sinus afferent nerves

 C

Decreased heart rate and blood pressure

 D

Baroreceptor adaptation

Q. 8

Clamping of the carotid arteries below (proximal) the carotid sinus is likely to produce:

 A

Increase in vasomotor centre activity

 B

Increase in discharge of carotid sinus afferent nerves

 C

Decreased heart rate and blood pressure

 D

Baroreceptor adaptation

Ans. A

Explanation:

Ans. a. Increase in vasomotor centre activity

  • Clamping of the carotid arteries proximal to the carotid sinus elevates the blood pressure and heart rate because the procedure lowers the pressure in the carotid sinus (Baroreceptor reflex


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