Cardiac innervation seminar by Dr Manish Ruhela, SMS Medical College,jaipur
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Transcript of Cardiac innervation seminar by Dr Manish Ruhela, SMS Medical College,jaipur
Dr Manish Ruhela
CARDIAC INNERVATION
The nerve supply of the heart is derived from –
1. The cardiac plexus formed by the sympathetic and parasympathetic(vagal) fibers and
2. Baroreceptors and chemoreceptors ( cardiac reflexes)
SYMPATHETIC CONTRIBUTION The preganglionic sympathetic fibres innervating the heart
are the axons of cells located in the lateral grey columns ofT1-T5 segments of the spinal cord.
They are myelinated preganglionic fibres and they leave thecord in the ventral roots of the corresponding spinal nervesand enter to adjacent ganglia in the paravertebralsympathetic trunk.
The postganglionic axons are unmyelinated or thinlymyelinated, and those for the heart run in the variouscardiac branches of the sympathetic trunks.
Thus in the sympathetic component of the autonomicnervous system the synapses between pre- and post-ganglionic neurons are often at considerable distances fromthe structure innervated, e.g. some of the cardiacpostganglionic fibres arise in the superior cervical gangliaand are lengthy.
By contrast parasympathetic postganglionic fibres areshort.
PARASYMPATHETIC CONTRIBUTION
The parasympathetic innervation arrives to the heart bymeans of branches of the vagus nerve.
The preganglionic vagal fibers flow from the brain stem,particularly from the bulbus (nucleus ambiguus, reticularnucleus and dorsal nucleus of vagus).
These nuclei are elongated columns of cells lying in themedulla oblongata.
The cardiac fibres are conveyed to their terminations in thevagus nerves and their branches, and they end by formingsynapses with postganglionic neurons in ganglia in thecardiac plexus or in the wall of the heart.
Synaptic relays close to or within the viscus supplied arecharacteristic of parasympathetic innervation and inconsequence parasympathetic postganglionic fibres arerelatively short compared with their sympatheticcounterparts, and more circumscribed in theirdistribution.
This is one reason why parasympathetic effects are morelocalized than sympathetic effects.
Anatomical Differences in Sympatheticand Parasympathetic Divisions
Length of postganglionic fibers Sympathetic – long postganglionic fibers
Parasympathetic – short postganglionic fibers
Branching of axons
Sympathetic axons – highly branched
Influences many organs
Parasympathetic axons – few branches
Localized effect
Copyright © 2005 Pearson Education, Inc., publishing as Benjamin Cummings
Anatomical Differences in Sympatheticand Parasympathetic Divisions
Copyright © 2005 Pearson Education, Inc., publishing as Benjamin Cummings
Anatomical Differences in Sympatheticand Parasympathetic Divisions
Copyright © 2005 Pearson Education, Inc., publishing as Benjamin Cummings
Basic pathways involved in the medullary control of heart by the vagus nerves
Neurotransmitters of Autonomic Nervous System
Neurotransmitter released by preganglionic axons Acetylcholine for both branches (cholinergic)
Neurotransmitter released by postganglionic axons Sympathetic – most release norepinephrine (adrenergic)
Parasympathetic – release acetylcholine
Copyright © 2005 Pearson Education, Inc., publishing as Benjamin Cummings
Cardiac Plexuses
Both the parasympathetic and sympathetic nerves form thesuperficial and deep cardiac plexuses
Superficial cardiac plexus - situated below the archof aorta in front of the right pulmonary artery, it is formedby – The superior cardiac branch of superior cervical ganglion of the left
sympathetic chain and
The cardiac branches from inferior cervical region ( inferior cervicalnerves ) of the left vagus nerve.
It gives branches to The deep cardiac plexus
The right coronary artery ( coronary plexus ) and
The left anterior pulmonary plexus.
Deep cardiac plexus - situated in front of the bifurcation of
trachea and behind the arch of aorta, it is formed by –
The cardiac branches of superior,middle & inferior cervical ganglia
& T 1 to T4/T5 ganglia of Rt & Lt sympathetic chain.
The inferior cervical ganglion & 1st thoracic ganglion are fused to
form a stellate ganglion.
Superior cardiac branches of vagus and recurrent laryngeal nerves of
both sides except inferior cardiac branches of Lt vagus (those which
form the superficial plexus).
Rt & Lt halves of plexus supplies branches to the corresponding
coronary and pulmonary plexus. Separate branches are given to
atria.
Peculiarities of nerve supply to the heart
Nerve supply Features1. Sympathetic innervation More at the base than the apex
2. Vagal activity Greater in posterior and inferior wall
3. Rt sympath. and vagus Affect SA node > AV node
4. Lt sympath. and vagus Affect AV node > SA node
Cardiac innervation
Sympathetic nerve – noradrenergic fiber; Parasympathetic
nerve- cholinergic fiber
Noradrenergic sympathetic nerve
to the heart increase the cardiac rate (chronotropic effect)
the force of cardiac contraction (inotropic effect).
Cholinergic vagal cardiac fibers decrease the heart rate.
CARDIAC RECEPTORS
Most important adrenoreceptor is heart is B1
B2 adrenoreceptor in heart has similar cardiac effect B1
Prejunctional a2 adrenoreceptor inhibit NE release
Prejunctional b2 adrenoreceptor facilitate NE release
Prejunctional M2 adrenoreceptor inhibit NE release
Right atrium – 74% b1 and 26% b2
Ventricles – 86% b1 and 14% b2
Control of heart activity by vasomotor
center(medulla oblongata) Lateral portion of vasomotor center transmit excitatory signals through sympathetic
fibers to heart to increase its rate and contractility.
Medial portion of vasomotor center transmit inhibitory signals through
parasympathetic vagal fibers to heart to decrease its rate and contractility. Neurons,
which give impulses to the heart, have constant level of activity even at rest, which is
characterized as nervous tone.
Receives input from higher centers, monitoring blood pressure and dissolvedgas concentrations.
Autonomic Innervation of the Heart
Figure 20.21
Cardiac Reflex Fast acting reflex loops between the heart and CNS
Regulates cardiac function
Maintains physiologic homeostasis
Cardiac receptors are linked to CNS by myelinated / unmyelinated afferents of vagus nerve
Cardiac receptors are present in Atria
Ventricles
Carotid bodies
Aorta
Cardiac Reflex
Reflexes originating in cardiac sensory receptors canbe classified according to various characteristics :
1 ) location of the receptors. for example, atrial or ventricular,
2) types of afferent fibers. for example myelinated versus nonmyelinated,
3) pathways of the afferent fibers for example. in
vagal or sympathetic nerves.
4) natural stimuli to the reflex , for example mechanosensitiveversus chemosensitive. and
5) cardiovascular effects. for example inhibition or excitation.
Cardiac receptor
Myelinated / unmyelinated afferent of vagus nerve
Central processing of sympathetic and parasympathetic nerve input in the CNS
Efferent fibres
Heart or systemic circulation
Particular reaction
Cardiovascular Reflexes Baroreceptor reflex (pressure receptor reflex)
Chemoreceptor reflex
Bainbridge atrial reflex (volume reflex) (atrial stretch reflex)
Bezold-Jarisch reflex (cardiopulmonary reflex)
Oculocardiac reflex (trigeminovagal reflex)
Cushing’s reflex
Valsalva maneuver
Afferent fibres of cardiac receptors (in vagus nerve)
Myelinated fibres (25%) Unmyelinated fibres (75%)
Present in walls of atria and
atriocaval junction
Present in walls of all cardiac
chambers
Baroreceptor Reflex (carotid sinus reflex)
initiated by stretch receptors, called baroreceptors Baroreceptors are present in
Carotid sinus Aortic arch Walls of right atrium at the entrance of SVC and IVC Walls of left atria at the entrance of pulmonary vein
These receptors in low pressure part of the circulation are called as cardiopulmonary receptors
They are stimulated by distension of the structure in which they are located
pressure in these structures are associated with discharge rate
Baroreceptor areas in the carotid sinus and aortic arch
Carotid sinus
At the bifurcation of the common carotid arteries
the root of internal carotid artery shows a little bulge
has stretch receptors in the adventitia
are sensitive to arterial pressure fluctuations
Afferent nerves from these stretch receptors travel in the carotid sinus nerve which is a branch of the glossopharyngealnerve (IXth cranial nerve)
Aortic Arch baroreceptors are also
present in the adventitia of the arch of aorta
have functional characteristics similar to the carotid sinus receptors.
their afferent nerve fibers travel in the aortic nerve,
branch of the vagus nerve. (Xth cranial nerve)
Baroreceptor system for controlling BP
Baroreceptor- reflex mechanism
Triggering factor( increased pressure )
Stimulates baro receptors in carotid sinus and aortic arch
information carries through Glossophrayngeal nerve ,Vagal nerve
Processing in medullary vasomotor centre
Increases parasympathetic tone, inhibition of sympathetic tone
Decreases heart rate, Stroke volume and vasodialation
Buffer nerves activity
The carotid sinus nerves and vagal fibers from the aortic arch are commonly called the buffer nerves
At normal blood pressure levels, the fibers of the buffer nerve discharge at a low rate.
When the pressure in the sinus and aortic arch rises, the discharge rate increases;
when the pressure falls, the rate declines.
Importance of the baroreceptor reflex
To keep the arterial pressure relatively constant
Short term regulation of blood pressure in the range of 70 mmHg to 150 mmHg, maintain the mean blood pressure at about 100 mmHg
Pressure buffer system – reduce the BP fluctuation during the daily events, such as changing of the posture, respiration and excitement
Baroreceptors are compromised by autonomic neuropathy and denervated heart ( Transplanted heart ).
Baroreceptor Resetting
Baroreceptor will adapt to the long term change of blood
pressure.
That is, if the blood pressure is elevated for a longer time, as in
chronic HTN, the set point will transfer to the elevated mean blood
pressure
So there is decrease baroreceptor response in pts with chronic HTN
This makes the baroreceptor system unimportant for long-
term regulation of arterial pressure
Baroreflex failure
Baroreflex failure lead to loss of response to arterial baroreceptorstimulation and failure of neural regulation of BP.
Damage to afferent neuronal input ( vagus and glossophrayngealnerves) or from damage to brainstem nuclei due to variouscauses( surgery, radiation therapy, CVA).
Clinical presentation can vary over time, and acute episodesduring waking hours may mimic a pheochromocytoma; severehypotension and bradycardia may occur during sleep.
Chemoreceptor Reflex Chemoreceptors are sensitive to the changes in blood chemistry.
main function is to keep the alveolar pCO2 at a normal level of40mmHg and also maintains arterial pO2,pCO2 and pH.
Mediated by two types chemoreceptors
Peripheral chemoreceptors
Carotid bodies
Aortic bodies
Central chemoreceptors
Medulla (associated with cardiovascular control “centers”)
Sinus nerve of Hering (branch of 9th cranial nerve) and vagus nerve
Peripheral Chemoreceptors
Present in carotid & aortic bodies
2 mm in size
Supplied with abundant blood flow through a small nutrient artery (senses changes in BP)
Rich sensory innveration
Rate of response is fast
Chemoreceptor areas in carotid and aortic bodiesCAROTID
BODY
AORTIC
BODY
Carotid bodies
2 in number
2 mg weight
Highest blood flow – 2000 ml/100 g/min
Present at bifurcation of each common carotid artery
Innervated by sinus nerve (branch of 9th nerve)
Aortic bodies
1-3 in numbers
Adjacent to aorta
Near the aortic arch
Near root of subclavian artery
Innervated by 10th nerve
Respiratory control by peripheral chemoreceptors in the carotid and aortic bodies
Central chemoreceptoprs – medulla (slow response)
Cardiac control centres in medulla oblongeta
Cardioaccelerator stimulatory
centre (VMC)
Cardioaccelerator inhibitory
centre (CIC)
Sympathetic stimulation Parasympathetic stimulation
Central & peripheral chemoreceptors respond to changes in chemical composition of blood or surrounding fluid
Central chemoreceptors respond only to acidosis (H⁺)
Peripheral chemoreceptors are sensitive to changes in arterial O2 and CO2 tension and to pH
Increasingly important when mean arterial pressure falls below 60 mmHg (i.e. when arterial baroreceptor firing rate is at minimum)
PaO2 < 50 mmHg / acidosis / PaCO2
Stimulate chemoreceptor in carotid & aortic bodies
Sinus nerve of Hering & vagus nerve
Medullary vasomotor centres
Stimulate respiratory centres
Directly stimulates sympathetic system
pulm ventilation(rate & depth)
BP
Indirectly catecholamine secretion from the adrenal medulla
BP
BAIN BRIDGE ATRIAL REFLEX
Receptors- Cardiac baroreceptors located in the walls of heart (
subendocardial distribution)
Anatomy
Primarily mediated through vagal myelinated afferent fibres;
activation of sympathetic afferent fibers may also occur. Increased
right atrial pressure directly stretches the SA node and enhances
its automaticity, increasing the heart rate.
Stimulus
Increased vagal tone and distention of the right atrium or central
veins.
Bainbridge Atrial Reflex(atrial stretch reflex, volume reflex)
right sided filling pressure
Stimulates stretch receptors present in right atrial wall & cavoatrial junction
Vagal myelinated afferent fibres
Cardiovascular center of medulla
Inhibit parasympathetic activity
HR
Directly stimulates SA node
HR
Stretching of atria
Efferents of vagus nerve
Reflex depends upon the preexisting heart rate
With slow heart rate, it causes progressive tachycardia
With pre-existing tachycardia, there is no effect
Denervation of vagi to heart eliminate this reflex
Clinical significance-
It helps prevent collection of blood in veins, atria andpulmonary circulation
It inhibits ADH release and promote secretion of ANP
When blood volume is increased, the Bainbridge reflex isdominant, when it is decreased, baroreceptor reflex isdominant
Bezold-Jarisch reflex(cardiopulmonary reflex)
Reflex triggered by
Intracoronary injection of serotonin, nicotine, capsaicin
Coronary ischemia (MI)
Bradykinin, PGI2, Arachidonic acid
Ventricular distension
Thrombolysis
Revascularization
BEZOLD-JARISCH REFLEX
Anatomy
Ventricular chemoreceptor and mechano-receptors withafferent pathway in unmyelinated vagal C fibres
Stimulus
Noxius stimuli to either ventricle, associated withmyocardial ischaemia, profound hypovolemia, coronaryreperfusion
Bezold-Jarisch reflex(cardiopulmonary reflex)
Triggering factors
Stimulates cardiopulmonary chemoreceptors and mechanoreceptors of LV wall
Unmyelinated vagal afferent type C fibres
Inhibit medullary vasomotor centre
parasympathetic tone
Triad of – bradycardia, hypotension, peripheral vasodilatation
Response
Hypotension, bradycardia, parasympathetically inducedcoronary vasodilatation and inhibition of sympatheticoutflow from vasomotor centres
Clinical significance
Reperfusion of previously ischemic tissue elicits reflex
Thus, Bezold Jarisch reflex may be less pronounced inpatients with cardiac hypertrophy
Bezold-Jarisch reflex
MI / Coronary reperfusionMolecules generated during ischemia and reperfusion such as free
radicals and PG
Stimulate cardiac inhibitory receptors(present in inferior & posterior walls of heart)
Hypotension Bradycardia and renal
vasodilatation
Sudden cardiac death Decreases myocardial oxygen
demand and augments renal
perfusion (protective reflex)
Oculocardiac Reflex(Trigemino-vagal Reflex, Aschner Phenomenon, Aschner Reflex, Aschner Dagini Reflex)
Reflex triggered by Pressure on globe Traction on the extraocular muscle (esp. medial rectus
muscle) as in strabismus surgery Ocular trauma Severe pain Orbital compression due to hematoma or edema Procedures under topical anaesthesia Orbital injections Hypercapnia or hypoxemia Fentanyl
Pressure on the globe of the eye or traction on the extraocular muscles
Stimulates stretch receptors of extraocular muscle
Afferents of short and long ciliary nerves
Ciliary ganglion
Ophthalmic division of trigeminal nerve
Gasserian ganglion
Sensory nucleus of trigeminal in the floor of 4th ventricle
Efferents of vagus nerves (vagal cardiac depressor nerve)
Parasympathetic stimulation
Bradycardia / hypotension / asystole / AV block / ventricular ectopy
Oculocardiac reflex
Treatment
Immediate
Cessation of manipulation
IV atropine
Lignocaine infiltration – near extrinsic muscles in case of recurrence
IV epinephrine 6-12 mg for hypotension
Prevention
Indicated in patients with h/o conduction block, vaso-vagal responses or b-blocker therapy
Premedication with anti-cholinergics (atropine or glycopyrrolate) (block efferent pathway)
Retrobulbar block with 1-3 ml of 1-2% lidocaine
Reponses ceases with repeated stimulation
Reflex is more sensitive in neonates and children, especially
during squint surgery
Clinical significance
Demonstrated in 30-90% of patients undergoing ophthalmic
surgery
Transient cardiac arrest may occur as 1 in 2200 strabismus
surgeries
Cushing ReflexReflex activated by
Cerebral edema
Hematoma – subdural, epidural, contusion, ICH
Depressed skull fracture
Hydrocephalus
Venous sinus thrombosis
IC-SOL: Tumor, hematoma, abscess
Brainstem compression
Acute traumatic brain injury
Neuroendoscopy
CSF pressure / ICT
Compression of cerebral arteries
Cerebral ischemia at the medullary VMC ( CO2 in blood, lactic acid in VMC)
Sympathetic stimulation
HR, BP, myocardial contractility improve cerebral perfusion
Stimulaes baroreceptors
Reflex bradycardia
Stimulates vasoconstrictor and cardioaccelerator neurons in VMC
Clinical significance:-
Triad of HTN, bradycardia and apnea
Seen in 33% of patients with ICT
Occurrence of bradycardia & HTN is used as warning sign
of ICT during neuroendoscopy
Treatment
Treated by measures to reduce ICP rather than pharmacological treatment of HTN
Elevate head to 30-45°
Avoid hypoxia (pO2 <60 mmHg)
Ventilate to normocarbia (pCO2 35-40 mmHg)
Sedation
Drain 3-5 ml CSF if ventriculostomy present
Hyperosmolar agents – mannitol, urea, glycerol
3% NaCl infusion
Barbiturates – thiopentone
Systemic diuretics – furosemide, ethacrynic acid
steroids – dexamethasone
Forced expiration against a closed glottis (after full inspiration)
Valsalva Maneuver
Intrathoracic pressure ( BP initially)
VR, CO
BP
Inhibit baroreceptors
Sympathetic stimulation
HR
myocardial contractility
Compression of veins ( CVP)
Opening of glottis (return of intrathoracic pressure to normal)
VR
myocardial contractility
BP
Stimulates baroreceptors
Stimulates parasympathetic efferent pathways to the heart
BP, HR
Phase I
Transient rise in BP due to increased intra-thoracic and intra-abdominal pressure
Phase II
Fall of BP followed by recovery
Increased HR due to sympathetic activation
Phase III
Fall in BP due to release of intrathoracic pressure
Phase IV
Increase in BP due to “overshoot” of cardiac output into a vasoconstricted peripheral circulation
Fall in HR with transient bradycardia, in the normal state, until after the BP overshoot
Valsalva ratio
Stimulus Expiration of 40 mmHg for 15 sec
Afferent Baroreceptors, glossopharyngeal, vagus nerves
Central Nucleus tactus solitarus
Efferent Vagus and sympathetic nervous system
Response HR & BP changes
• VR=Max HR/min HR
• A normal VR indicates an intact baroreceptor mediated increase and
decrease in HR
• A decreased VR reflects baroreceptror and cardiovagal dysfunction
• Normal value is a ratio of >1.21
In sympathectomized patients, HR changes occur since
baroreceptors and vagi are intact.
In autonomic insufficiency HR changes does not occur.
Transplanted heart (Denervated heart)
In cardiac transplantation, the vagus nerve and the cervical and thoracic sympathetic cardiac nerves are severed when the donor heart is removed.
These nerves will not generate, and they will not be reanastomosedwith the same nerves in the recipient.
Functional changes in transplanted heart occur both at rest and with activity and exercise. At the same time, some areas of cardiac physiology remain unchanged or minimally altered.
Normal Cardiac function in the Denervated heart The basic contractility of myocardium and intrinsic control
system remains intact. Starling effect remains intact (with increased venous
return, contractile force of myocardium will increase,causing increase in the stroke volume and cardiac output).
Anrep effect retained (with a rise in aortic pressure –afterload, the contractile force of myocardium willincrease, causing an increase in stroke volume and cardiacoutput).
Bowditch effect retained (an increased heart rate willaugment the contractile force of myocardium, againincreasing the cardiac output).
Altered Cardiac function in the Denervated heart
Does not experience anginal pain because the cervicalsympathetic cardiac efferent fibers are no longer intact.
Because the heart normally is more influenced by the PNS,the transplant recipient has a higher rate at rest comparedwith the normal heart( 90-110 bpm).
The denervated heart exhibits increased electrical stabilityand is much less susceptible to ventricular arrhythmias(VT/VF).
Ventricular fibrillation in denervated heart often is a signof significant rejection.
The valsalva maneuver and carotid sinus massage, both whichnormally decrease heart rate, have no effect on the heart rate of thedenervated heart.
Cardiac function with exercise:- With exercise, heart rate rises much more slowly because this
change is dependent on increased catecholamine levels rather thanneural system.
Hormonal system is much slower than the neural system and 5 – 10minutes warm-up period is essential for pt, without a gradualwarm-up cardiac output might not be able to deliver sufficientoxygen to exercising muscles , leading to exercise intolerance andultimately collapse of pt.
Pt with denervated heart never reaches normal peak HR withexercise.
Denervated heart is electrically stable and may be lessprone to ST segment deviation during exercise, even ifmyocardium becomes ischemic.
Recovery time after exercise is longer for the transplantedheart pt, HR decreases slowly because the re-uptake of thecatecholamines is a gradual process . A planned 5 – 10 minscool down period is important.
The absence of meaningful cardiac autonomic inputto the heart has imp implications forpharmacologic responses :-
Drugs with cardiac actions that depend on autonomicreflexes (e.g. atropine) are ineffective in altering HR.
for same reason, opioid induced bradycardia is absent.
Drugs that are direct agonist to beta adrenergic receptors(e.g. epinephrine ) are chosen when treating bradycardia.
Cardiac innervation may occur over time. Incomplete and unpredictable sympathetic reinnervation
Clinical determinants of reinnervation include time from transplant,
young age of the donor,
fast uncomplicated surgery, and
low rejection frequency.
The restoration of sympathetic innervation isassociated with improved contractility and HRresponse to exercise.
Sympathetic reinnervation may occur before, or inabsence of parasympathetic reinnervation. However, while parasympathetic reinnervation has been demonstrated in
animals, only sympathetic reinnervation has been demonstrated in humancardiac transplants.
THANKS
Cardiovascular Tests Used
Valsalva maneuver The subject sits quietly and then blows into a mouthpiece at a
pressure of 40 mmHg for 15 s.
The heart rate normally increases during the maneuver, followed by a rebound bradycardia after release.
The ratio of the longest R-R interval shortly after the maneuver to the shortest R-R interval during the maneuver is then measured.
We routinely express the result, the Valsalva ratio, as the mean ratio from three successive Valsalva maneuvers.
Normal ratio - ≥ 1.21
Heart rate response to standing up-
Subject lie quitely on couch and then stands –up.
Norm al response is immediate increase in HR maximal at about the
15th beat after starting to stand, followed by a relative bradycardia, max
around the 30th beat. This can be quantified as the 30:15 ratio, which
is the ratio of longest R-R interval around the 30th beat and shortest R-R interval around the 15th beat.
Normal ratio - ≥1.04
Blood pressure response to standing up
The blood pressure is measured using a standard sphygmomanometer
while the subject is lying down, and again after standing up.
The difference in systolic blood pressure is taken as the measure of postural blood pressure change.
Normal value of fall in SBP ≤ 10 mmHg
Blood pressure reponse to sustained handgrip –
Handgrip is maintained at 30% of the maximum voluntary contractionusing a handgrip dynamometer up to a maximum of 5 min, and theblood pressure measured each minute.
The difference between the diastolic blood pressure just before releaseof handgrip, and before starting, is taken as the measure or response.
Normal rise in diastolic BP - ≥ 16 mmHg
Heart rate response to deep breathing –
The subject sits quietly and then breathes deeply and evenly at 6 breaths/min.
The maximum and minimum heart rates during each breathing cycle are measured, and the mean of the differences during three successive breathing cycles are taken to give the max.-min. HR.
Normal value - ≥ 15