Cardiovascular regulation

D R . V . S I N G H C H A U H A N
( O R T H O . S U R G E R Y )
F A C I L I T A T O R : D R . M F D I N
Cardiovascular Regulation
Dr. V Chauhan - Cardiovascular Regulation - 22/01/13

At a Glance
 Need for CVS Control
 Role of Kidney in regulation (Done earlier)
 Control Systems
1. Humoral
a. Vasodilators
b. Vasoconstrictors
c. Ions
2. Neuronal
3. Local
a. Acute
b. Long Term

Need for Control
 To increase blood supply to active tissues
 Exercise
 Redistribution of blood
 To increase/decrease heat loss from body as per req.
 Circulatory adjustments
 During routine CVS stresses e.g change in posture, meals, sleep
 Maintenance of adequate flow to vital organs
 Brain, Kidneys, Heart at all times

Circulatory Adjustments
 Control of Blood Volume
 Control of Arterial Pressure
BP
CO TPR
SV HR
EDV ESVDistensibility
Filling Time Filling Pressure Contractility

What is regulated
 Cardiac Performance
 Alterations in activity of heart
 Chronotrophic Action
o Effect on HR
 Ionotrophic Action
o Effect on force of contraction
 Dromotrophic Action
o Effect on conduction of impulses through the heart
 Bathmotrophic Action
o Effect on excitability of cardiac muscle

What is Regulated
 Blood Vessel Performance
 Alterations in diameter of arterioles
 Change in PR and also hydrostatic pressure in capillaries
 Alterations in diameter of veins
 Change in venous pressures…..change in Venous return & CO

Humoral
 Neural
 Local

Humoral Control
 Important Factors
 Circulatory Vasodilators
 Kinins
 ANP (Atrial Natriuretic Peptide)
 Circulatory Vasoconstrictors
 Catecholamines
 Angiotensin II
 Vasopressin
 Ions and other chemical factors

Circulatory Vasodilators
1. Kinin
• Peptides
• Include
 Bradykinin
 Lysyl- Bradykinin
• Functions
 Vasodilation
 Relax Vascular SM via NO & increase capillary
permeability
 Role in regulating blood flow esp to skin, salivary glands &
GIT glands
 May play a role in thermoregulatory vascular
adjustments.

Circulatory Vasodilators
 ANP
 Secreted by heart and antagonises the actions of various
vasoconstrictors hence lowers BP
 Exact role not known but,
 Kidney
 Increases Sodium ion excretion
 Increases capillary permeability…extravasation….decreased BP
 Relaxes vascular SM in arterioles and venules
 Inhibit Renin secretion & counteract pressor effect of
Catecholamines and Angiotensin 1
 Brain
 Effects opposite to that of Angiotensin 1….Lowers BP, promotes
Natriuresis
 Found in areas concerned with neural regulation of CVS

Circulatory Vasoconstrictors
 Catecholamines
 Released on sympathetic stimulation
 Include
 Epinephrine
 Norepinephrine

 Epinephrine
 Stimulate both alpha & beta adrenergic receptors
 Alpha – Vasoconstriction in skin & Splanchnic areas
 Beta – Dilatation of vessels in skeletal muscles, Liver &
coronary arteries.
 Beta receptor induced vasodilation is more dominant than
alpha receptor induced vasoconstriction.
 Net effect – Slight lowering of PR….decrease in DBP

 Norepinephrine
 Generalised vasoconstrictor effect….alpha>beta
 Increases PR & raises DBP
 Direct cardiac stimulation has negligible effect since it has
negligible effect on beta receptors

Humoral Control
 Important Factors
 Circulatory Vasodilators
 Kinins
 ANP (Atrial Natriuretic Peptide)
 Circulatory Vasoconstrictors
 Catecholamines
Angiotensin II
 Vasopressin
 Ions and other chemical factors

Renin Angiotensin System
 Renin
 Secreted by JG Apparatus cells of Kidney into blood
 Secretion stimulated by fall in BP
Angiotensinogen Angiotensin 1 Angiotensin 2
 Effects of Angiotensin II
 Vasoconstriction
 4-8 times more potent than norepinephrine
 Decrease in salt & water excretion by kidneys…..retention of salt and
water……increase in ECF vol…..increase in arterial pressure over
period of hours and days.
 Long term control of arterial pressure
Renin ACE

 Effect of Angiotensin II
 Stimulation of thirst
 Leads to increased consumption of water hence increased blood
volume
 Long term control of BP

Vasopressin
 A.k.a Anti Diuretic Hormone
 Mainly affects water reabsorption in renal tubules
 Production –
 Concentration rises to high levels after severe
haemorrhage after which it starts having a
vasocontrictive effect.

Ions and other chemical factors
 Alter local blood flow
 Calcium – Vasoconstriction
 Potassium – Vasodilation
 Hydrogen ion – Vasodilation
 CO2 – Vasodilation in most tissues, marked in brain
 Glucose and other vasoactive substances when
increased will increase osmolarity….Vasodilation
 Magnesium – Poweful Vasodilator

Dr. V Chauhan - Cardiovascular Regulation -
22/01/13

 Humoral
Neuronal
 Local

Neuronal Control
 Responds within seconds
 Components
 Medullary Cardiovascular Control Centres
 Medullary Sympathetic Centre (VASOMOTOR CENTRE)
 Medullary Parasympathetic Centre (NUCLEUS AMBIGUOUS)
 Medullary Relay Centre for Cardiorespiratory & Afferents
(NUCLEUS OF TRACTUS SOLITARIUS)

 Components
 Autonomic NS supplying The Heart & Blood Vessels
 Regulation by medullary control centres exerted through the ANS
 Sympathetic – Imp in controlling circulation
 Parasympathetic – Contributes to regulation of Heart Fxn
 Afferent Impulses to Medullary Centre
 From higher centres and a large number of other areas
 Skeletal Muscles + Nerves in controlling BP

Medullary Cardiovascular Centres
22/01/13

Vasomotor Centre
 Primary cardiovascular regulatory centre
 Location……………Medulla Oblangata (?Lower Pons)
 Has following areas
 Pressor Area
 Location – RVLM (Rostral Ventro Lateral Medulla)
 Content – Glutaminergic neurons
 Exert excitatory effect on thoracolumbar spinal sympathetic
neurons
 Depressor Area

Vasomotor Area
 Stimulation of Pressor area
 Arteriolar constriction…….increase in systemic BP
 Venoconstriction……decreases blood stored in venous
reservoir and increases venous return
 +ve Chronotrophic effect (Increase in HR)
 +ve Ionotrophic effect (Increase in force of contraction)
 Neurons here discharge rhythmically in a tonic fashion to
excite sympathetic preganglionic neurons hence continuous
signals passed to sympathetic vasocontrictive nerve fibres

 Blockage of this tone (e.g. by spinal anaesthesia)
leads to dilatation of blood vessels ….decrease in BP

 Depressor Area
 Location – CVLM (Caudal Ventro Lateral Medulla)..bilaterally
 Stimulation
 Decrease in sympathetic activity due to inhibition of tonically
discharging impulses of pressor area.
 Hence
 Arteriolar dilatation
 Venodilatation
 Decrease in HR
 Decrease in force of contraction

Medullary Parasympathetic Centres
 Previously – Cardio inhibitory centre
 Specific name – Nucleus Ambiguus
 Neurons here not tonically active
 Receive afferents VIA Nucleus Tractus Solitarius
 Sends inhibitory pathway in form of vagal fibres to the
heart
 Decreases Heart Rate
 Decreases Force of Contraction

Medullary Relay Station for Cardioresp. Afferents
 Aka – Nucleus Tractus Solitarius of Vagus nerve
 Receive Afferents from most baroreceptors &
Chemoreceptors
 Relays to Vasomotor centre & Nucleus Ambiguus

Neuronal Control
 Components
 Medullary Cardiovascular control centres
Autonomic NS supplying The Heart &
Blood Vessels
 Afferent Impulses to Medullary Centre

Autonomic supply to the Heart
 Sympathetic
 Parasympathetic
 Sympathetic supply
 From spinal sympathetic centre
 Neurons located in intermediolateral horns of spinal cord
 Extends from T1 – L2
 Pre Ganglionic Fibres……small, myelinated
 Post Ganglionic Fibres….Long, Unmyelinated
 Sympathetics from Rt – SA node
 Sympathetics from Lt – AV node

Autonomic Supply to Heart
22/01/13

 Stimulation of sympathetic supply increases
 HR (+ve Chronotropic)…Increases rhythmicity of SAN
 Conductance (+ve Dromotropic)
 Excitability (+ve Bathmotropic)
 Force of contraction (+ve ionotropic)

 Parasympathetic Supply
 Through both Vagii.
 Preganglionic fibres……long, myelinated
 From nucleus ambiguus
 Postganglionic fibres….Small, unmyelinated
 Distributed to Atria, SAN, AVN and AV Bundle.
 N/B – No vagal motor fibres to ventricles
 Rt Vagus – mainly SAN
 Lt Vagus - AVN

Decrease in :
. HR
. Impulse conduction
. Excitability of Atria
. Force of contraction of atria
22/01/13

Autonomic Nerve Supply to Blood Vessels
 Has 2 types of effects
 Vasoconstrictive & Vasodilative
 Vasoconstrictive
 By sympathetic fibres supplying blood vessels
 From intermediolateral horns in T1-L2 spinal segment
 Fibres have Norepinephrine, sometimes Neuropeptide
 Stimulation,
 Arteriolar constriction
 Increased PR hence Increased DBP
 Venoconstriction
 Decreased venous capacity hence increased venous return

Autonomic Supply to Blood Vessels
 Vasodilator Effect
 Decrease in discharge of noradrenergic vasoconstrictor nerves
 Parasympathetic Vasodilator Nerves
 Play limited role in control of general circulation
 Only contribute to pleasure & fulfilling important biological fxns
 Sympathetic cholinergic vasodilator nerves
 Neurotransmitter – Acetylcholine & VasoInhibitory Peptide (VIP)
 Fibres not tonically active and get activated only in biological
stresses e.g during exercise, childbirth, & help in blood flow

Autonomic supply to Blood Vessels
22/01/13

Neuronal Control
 Components
 Medullary Cardiovascular control centres
 Autonomic NS supplying The Heart & Blood Vessels
Afferent Impulses to Medullary Centre

Afferent Impulses to medullary centres
 Afferent Impulses from Higher Centres controlling
vasomotor centres
 Afferent impulses from Respiratory centres
 Cardiovascular Reflex Mechanisms
 Baroreceptor reflex
 Chemoreceptor reflex
 Direct effects on Vasomotor Area
 Cushings Reflex
 CNS ischemia response

Afferents from Higher Centres
 Cerebral cortex
 Influence on Limbic system results in
 Tachycardia & HTN in sexual excitation and Anger
 Bradycardia & Fainting in sudden emotional shock
 Reticular formation of pons, mesencephalon &
diencephalon influence vasomotor area
 E.g Pain causes increase in BP

Afferents from Respiratory Centres
 These change vagal tone
 Lead to Sinus Arrhythmia (alterations that occur
during forced breathing).....?normal in young children
 During Inspiration
 Afferents inhibit cardiac vagal centre hence decrease in vagal
tone & Sinus tachycardia
 During Expiration
 Increased vagal tone and Sinus bradycardia
 (Resp centres stop sending inhibitory impulses)

Cardiovascular Reflex Mechanisms
 Almost all are negative feedback reflex mechanisms
 Include
 Baroreceptor mechanisms
 Chemoreceptor mechanisms

Baroreceptor Reflex Mechanism
 Stretch receptors a.k.a Mechano/Pressure receptors
 Location – Walls of heart and Large blood vessels
 Classification (Functional vs Anatomical)
High Pressure Baroreceptors Low Pressure Baroreceptors
-Monitor Arterial Circulation
-Location
-Carotid Sinus
-Aortic Arch
-Wall of Left Ventricle
-Root of Subclavian
-Junction of thyroid artery
with the common carotid
-A.k.a cardiopulmonary receptors
-Location
-Pulmonary receptors
-Walls of pulm. Trunk &
its divisions
- Atrial receptors
-Wall of right & left Atria
-Entrance of Sup & inf
vena Cava
-Entrance of pulm. veins

Anatomical Classification
Arterial
Systemic
Pulmonary
Cardiac
Atrial
Ventricular
22/01/13

Baroreceptor Reflex
 Reflexes initiated
 Signals enter Tractus Solitarius of medulla
 Secondary signals inhibit vasoconstrictor centre of medulla
and excite vagal parasympathetic centre
 Effect
 Vasodilation of veins and arterioles
 Decrease in heart rate & force of contraction.
 Reflex usually responds much more to a rapidly
changing pressure than stationary

Baroreceptor Reflex
 Fxn of baroreceptors during change of posture
 On standing, arterial pressure in upper body & head decreases.
Immediate Baroreceptor reflex leads to strong sympathetic
discharge. Minimizes decrease in pressure in upper body
 Pressure Buffer Fxn
 Reduces minute by minute variations in BP occurring with
daily routine activity.
 Opposes either increase or decrease in BP
 Nerves from baroreceptors called buffer nerves

Baroreceptor Reflex
 Baroreceptor Resetting
 In 1-2 days to whatever pressures that are exposed (adaptive)
 Therefore has NO ROLE in long term regulation.
 E.g. in Chronic HTN, mech. reset to maintain an elevated BP
 Volume Reflex
 Example of Atrial & Pulm artery reflexes.
 Stretch of atria….Reflex dilatation of afferent arterioles in
Kidney
 Also, Signals sent to Hypothalamus to decrease ADH secretion
 Hence increased blood volume reduced back to normal

Chemoreceptor Reflexes
 Responds to Excess CO2, H+ and Decreased O2
 Not a powerful BP controller in normal range of Bp since are
not stimulated fully until <60mmHg Bps
 Location
 Carotid Bodies and Aortic bodies (adj. to arch of aorta)
 Functions
 Respiratory control
 Cardiovascular control
 Hypoxia
 Increase chemoreceptor discharge…..hyperventilation + VMC
excitation………peripheral vasoconstriction + Increase BP
 Hypotension due to severe haemorrhage
 Increase discharge……………increases BP

Direct Effect on Vasomotor Area
 Cushings Reflex
 Increase in ICP = Compression of arteries in brain & blood supply to vasomotor
centres.
 Resulting hypoxia + Hypercapnea = Increased VMC discharge = Increased BP =
Restoration of supply to medulla
 Increase in BP also causes reflex bradycardia via baroreceptor response
 CNS ischemic response
 Accumulation of CO2/Lactic acid that excites VMC
 Stimulation leads to vasoconstriction and immediate rise in BP
 Acts as emergency arterial pressure control syst.
 If rise in pressure doesn’t relieve the ischemia, neural cells become inactive (within
3-10min)

 Humoral
 Neuronal
Local

Acute /Short term control
 Within seconds
 Involves
 Autoregulation
 Metabolic theory/vasodilator theory
 Oxygen lack theory
 Myogenic Theory
 Endothelial Secretions
 Prostacyclin
 NO
 Endothelins

Role of vasodilator metabolites
(Metabolic/vasodilator theory)
 Accumulation = Increased blood flow
 Potassium and Lactate ions cause vasodilation
 Adenosine may play a role in vasodilation
 Decreased oxygen tension & pH = Vasodilation
 Increased pCO2 = direct dilation action of CO2, more
pronounced in skin and brain.
 Increased temp = Vasodilator effect

 Therefore, any vasodilator m/lite which accumulates
in tissues during active metabolism will produce
autoregulation.
 By causing increased flow, O2 and other nutrients
provided to tissues. Allows for vasoconstriction and
normal flow despite increased pressures

Myogenic theory
 Sudden stretch of small blood vessels causes Smooth
Muscles of vessels to contract.
 Increase in BP that stretches blood vessels may cause
reactive vascular constriction that decreases blood
flow nearly back to normal

Role of Substances released by endothelium
 Prostagladin and Thromboxane A2
 Prostacyclin – Vasodilation
 TxA2 – Vasoconstriction
 Endothelin Derived Relaxing Factor (EDRF)
 A.k.a Nitric Oxide
 Vasodilation
 Leads to eventual production of cGMP = Relaxation of vascular
smooth muscle by decreasing intracellular Calcium ion conc.
 Endothelins
 Vasoconstriction (Most potent agent)

Other specific local measures
 Tuboglomerular feedback mechanism
 Composition of fluid in early distal tubule detected by Macula
Densa.
 When too much filters from blood, feedback constriction of
afferent arterioles by macula densa hence decrease of renal
blood flow
 CO2 and H+ concentrations controlling blood flow to
brain
 Increase in dilation of cerebral blood vessels = rapid washout
of excess ions and CO2

Long Term Control
 Days/Months
 Required by
 Ischemic Tissues
 Tissues that grow rapidly
 Tissues becoming chronically hyperactive.
 Pattern and Vasculature Affected
 Increase in physiological size of vessel in tissue &
also number of blood vessels at times
 Low oxygen major factor in stimulating increased
vascularity

 Angiogenesis
 Factors
 VEGF – Vascular Endothelial Growth Factor
 FGF - Fibroblast Growth Factor
 Angiogenin
 Development of collateral blood vessels occur

References
 Guyton, Hall. Textbook of Medical Physiology, 10th
Edition
 Ganong F. Review of Medical Physiology, 22nd
Edition
 Khurana I. Textbook of Medical Physiology, 2nd
Edition
 en.wikipedia.org

Cardiovascular regulation

Recommended

Recommended

More Related Content

What's hot

What's hot (20)

Similar to Cardiovascular regulation

Similar to Cardiovascular regulation (20)

Recently uploaded

Recently uploaded (20)

Cardiovascular regulation

Editor's Notes