DR ADITYA SAROHA

ST. STEPHEN’S HOSPITAL

ANESTHESIA DEPARTMENT

Is a hollow, pyramidal shaped , fibromuscular organ lying obliquely behind sternum in middle mediastinum.

Males – 300gms females-250gms

Enclosed by pericardium.

It is a fibroserous sac which encloses heart and roots of great vessels.

Outer- fibrous pericardium and inner- serous pericardium

Serous pericardium is further divided into parietal layer and visceral layer (aka epicardium)

Pericardial cavity filled with serous fluid lies between parietal and visceral pericardium.

Fibrous and parietal pericardium are sensitive to pain and supplied by PHRENIC nerve

Epicardium is supplied by autonomic nerves and is not sensitive to pain.

Right border – right atrium

Left border – mainly by left ventricle and partly left auricle

Inferior border- mainly right ventricle and partly left ventricle

Upper border- mainly left atrium and partly left atrium

Apex – left ventricle.

Anterior surface(sternocostal surface)-mainly right ventricle(major) and right auricle & partly by left ventricle and left auricle.

Inferior(diaphragmatic) surface- left 2/3rd by left ventricle and right 1/3rd by right ventricle.

Base(posterior) surface- mainly by left atrium and partly by right atrium

Right surface-mainly right atrium Left surface- mainly left ventricle and left

auricle

Right border:- from 3rd to the 6th rib 1.25cm to the right side of the sternum.

Apex:- left 5th intercostal space 9cm from the midline.

Left border:-from the apex to the 2nd

intercostal space 1.25cm lateral to the sternum.

Total four chambers- two atrias and two ventricles.

Atria

◦ Thin-walled upper chambers

◦ Separated by atrial septum

◦ Right side of septum has oval depression, fossa

ovalis cordis, remnant of the foramen ovale

◦ Act as receiving chamber for blood returning from

the body and lungs

Thinnest walls

Crista terminalis- ridge of smooth muscle extending from SVC to IVC.

Divided by crista terminalis in rough anterior part and posterior smooth part.

Rough anterior part is aka atrium proper( pectinate part)

Posterior smooth part has openings of-SVC , IVC, coronary sinus , thebesian veins , anterior cardiac vein and right marginal vein.

SA NODE situated in upper part of crista terminalis.

Interatrial septal region-

Develops by approximation of embryonic septum primum and septum secundum.

Important features are fossa ovalis, limbusfossa ovalis, triangle of koch( contains AV NODE)

Left atrium

Fossa ovalis

Right atrium

Atrial septum

Epicardium

Myocardium

Endocardium

Ventricles

◦ Lower chambers which make up the bulk of the

muscle mass of the heart

◦ Left ventricle 2/3 larger than right ventricle

◦ Right ventricle is a thin-walled and oblong, like

pocket attached to left ventricle

◦ Both ventricles have papillary muscles attached

atrioventricular wall on one side and to chordae

tendinae on other side which are further

attached to AV valves

Ventricles

◦ Contraction of left ventricle pulls in right

ventricle, aiding its contraction (termed left

ventricular aid)

◦ Separated by intraventricular septum

Right ventricle

Left ventricle

Intraventricular septum

Superior vena cava

Inferior vena cava

Tricuspid valve

◦ Separates right atrium from right ventricle

Pulmonic semilunar valve

◦ Separates right ventricle from pulmonary artery

Bicuspid (mitral) valve

◦ Separates left atrium from left ventricle

Aortic semilunar valve

◦ Separates left ventricle from aorta

Blood flow from right ventricle to lungs Blood flow from left ventricle to aorta

Chordae tendineae cordis

◦ Anchor free ends of A-V valves to papillary

muscles

◦ Prevent A-V valves from pushing upward into atria

during ventricular contraction

SA node:-65% RCA.35% LCA

AV node:- 90% RCA10% LCA

Branch of Anterior Aortic sinus of Ascending aorta.

COURSE---Rt ant coronary sulcus(rt AV groove)—winds around inferior border & reaches Rt posterior coronary sulcus—Post IV groove & ends with anastomosing LCA.

BRANCHES-

1. Acute marginal

2. Posterior IV( descending) artery(85-90%)

3. Rt conus (infundibular) artery(aka 3rd coronary artery

4. Nodal br to SA node(65%)

5. Small branches like atrial,ant ventricular,post ventricular.

SUPPLIES-

1. Rt atrium & part of left atrium.

2. Most of rt ventricle( except area around Anterior IV groove) & small part of lt ventricle adjoining post IV groove..

3. Posterior one-third of IV septum.

4. Whole conducting system except rt bundle br & lt br of AV bundle.

5. SA node(65%)

6. AV node(90%)

Larger in diameter then RCA

Arise from left aortic sinus of ascending aorta.

COURSE--- it enters in AV groove & continues as circumflex artery which runs in LT ANT coronary sulcus---LT POST coronary sulcus & near post IV groove terminates by anastomosis with RCA.

BRANCHES-1. Anterior IV ( descending) artery2. Circumflex artery.3. Left diagonal artery.4. Obtuse marginal artery.5. Left conus artery.6. Nodal br for SA node(35%)

SUPPLIES-1. Mostly lt atrium2. Most of lt ventricle( except around post IV

groove) & small part of rt ventricle adjoining Ant IV groove.

3. Ant 2/3rd of ventricular septum.4. Rt bundle br & lt br of AV bundle.5. SA node in 35% cases.

Determined by artery which give the posterior IV br.

85-90% population – rt dominance.

10-15 % population- lt dominance because post IV br comes from circumflex artery which is a br of LCA

CO-DOMINANCE / BALANCED PATTERN-branches of both RCA & LCA run in post IV groove.

LAD( ANTERIOR IV ) ARTERY- most commonly involved in thrombotic occlusion leading to infarction of ANTERIOR WALL of left ventricle, APEX of heart, ANT 2/3 rd of IV septum. AKA as WIDOW’S ARTERY.

POSTERIOR IV ARTERY(RCA)- 2nd most common to be involved and it involves INFERIOR/ POSTERIOR WALL of lt & rt ventricle and POST 1/3rd of IV septum.

CIRCUMFLEX CORONARY ARTERY-(br of LCA)-3rd most common , causes infarction of LATERAL WALL of lt ventricle except apex

Mainly three systems

1) Coronary sinus and its tributeries

2) Anterior cardiac vein

3) Venae cordis minimae

It opens in posterior wall of rt atrium---b/w IVC & tricuspid orifice

Opening guarded by THEBESIAN valves– it prevents regurgitataion of blood into coronary sinus during atrial systole.

TRIBUTARIES—1. Great cardiac vein- lies in ant IV groove,left

marginal vein drain into it.2. Middle cardiac vein- lies in post IV groove3. Post vein of left ventricle4. Small cardiac vein- lies in post part of coronary

sulcus, right marginal may drain here but mostly it opens into rt atrium directly

5. Oblique vein of rt atrium

ANTERIOR CARDIAC VEIN– drains into rt atrium piercing rt atrial anterior surface close to sulcus terminalis.

VENAE CORDIS MINIMI- aka as smallest cardiac vein or thebesian vein.

- these are small multiple veins present in all four chambers of heart

NOTE- all veins drain into coronary sinus except anterior cardiac vein, venae cordis minimi and often rt marginal vein ( they drain directly into rt atrium)

parasympathetic by vagus (cardio-inhibitory), sympathetic by T1 to T5(cardio-stimulatory)

SUPERFICIAL CARDIAC PLEXUS- lies in front of rt pulm artery and below arch of aorta.

It is formed by- sup cervical cardiac br of lt sympathetic chain and inferior cervical br of left vagus.

DEEP CARDIAC PLEXUS- lies in front of bifurcation of trachea behind arch of aorta.

It is formed by all sympathetic and parasympathetic cardiac branches except those forming superficial plexus.

Afferents carrying pain sensation due to ischemia pass through sympathetic cardiac fibres and reach T1 to T5 cord segments of left side.

Since these dorsal root ganglia also receive sensory impulses from medial side of arm,forearm,upper front of chest.

Because of this common sensory supply cardiac ischemic pain is referred to these areas via T1 to T4 splanchanic nerves.

Made up of specialized myocardium (cardiac muscle)

SA NODE

located in upper part of crista terminalis at junction of SVC & Rt atrium.

It is pacemaker of heart as it generates impulse at rate of 70 – 100 beats per minute.

Supplied by nodal br of RCA(65%) and LCA(35%).

Supplied by rt vagus and rt sympathetic system as it develops from rt sided structures of embryo.

AV –NODE It lies in rt atrial floor near inter-atrial septum

in triangle of koch. Supplied by AV nodal br of RCA. Develops from lt side of heart – so supplied

by lt vagus and left sympathetic chain.AV BUNDLE/ BUNDLE OF HIS Arises from AV node and it crosses AV ring(

annulus fibrosus). Divides into right and left branches in

muscular septum. Has dual blood supply from AV nodal br(RCA)

& Ant descending br of LCA

Made of fibrous ring surrounding orifices of AV valves, pulmonary, aortic orifices along with adjoining masses of fibrous tissue.

TENDON OF INFUNDIBULUM- B/W pulmonary and aortic ring

TRIGONUM FIBROSUM DEXTRUM- b/w AV ring (mitral & tricuspid) & aorta.

TRIGONUM FIBROSUM SINISTRUM- B/W aortic and mitral rings.

VALVE DIAMETER AREA SURFACE MARKING AUSCULTATORY AREA

PULMONARY 2.5 cm Sternal end of left 3rd

costal cartilage(upper border)

Left 2nd

intercostal space near sternum

AORTIC 2.5 cm 2.6-3.5 cm2

Sternal end of 3rd left costal cartilage (lower border)

Right 2nd

intercostal space near sternum

MITRAL 3cm 4-6 cm2

Sternal end of left 4th

costal cartilageCardiac apex(just medial to mid-clavicularline in left 5th

intercostal space)

TRICUSPID 4cm Right half of sternum along 4th,5th

intercostal space

Right lower end of sternum

ELECTROPHYSIOLOGY OF HEART

Tissue Conduction rate (m/s)

SA node .05

Atrial pathways 1

AV node .05

Bundle of His 1

Purkinje 4

Ventricular muscle 1

SA NODE- located at superolateral wall of rt atrium, at junction of SVC with rt atrium

INTERNODAL ATRIAL PATHWAYS- 3 strips

1. Anterior(bachman)

2. Middle(wenkebach)

3. Posterior(thorel)

AV NODE- located in rt posterior portion of interatrial septum.

BOH divides in IV septum into right and left bundle( ant & post fascicles)

AUTOMATICITY- capability of spontaneous excitation, SA node maximum

SA NODE 70-80/ MIN

AV NODE 40-60/MIN

BOH 40/MIN

PURKINJE SYSTEM 24/MIN

OVERRIDE SUPRESSION-SA node have highest automaticity, so it paces all other cardiac fibres and suppress their intrinsic activity.

CONDUCTION OF CARDIAC IMPULSE-SA node—interatrial pathways--AV node—BOHis—Purkinje system—ventricular myocardium—depolarization at Left IV septum—right side across mid portion of septum–- down the septum—apex—impulse returns along vent walls to AV groove—from endocardial to epicardial surface.

Last part to be depolarized– POSTERO-BASALportion of left ventricles, pulmonary conus, upper most portion of septum.

Repolarization from epicardial surface to endocardial surface.

AV NODAL DELAY-1. 0.1- 0.13 secs

2. Time taken by impulse to travel across AV node.

3. It ensures that atria complete systolic contraction & empties completely before ventricular contraction starts.

4. Parasympathetic - AV node excitation & nodal delay–- heart rate

5. Sympathetic -- AV node excitation & nodal delay--- heart rate.

Small size of AV NODAL fibres.

Fewer gap junctions– leading to impaired conduction.

Slow response action potential at AV node.

Phase 0- Rapid depolarization- fast Na channel opening

Phase 1- Initial rapid repolarisation – closure of fast Na channels

Phase 2- Plateau phase- opening of voltage gated slow Ca channels causing Ca influx.

Phase 3- Final repolarisation – opening of K channels

Phase 4- Resting phase- phase of RMP

RMP -65mV

Even in resting phase RMP moves towards depolarization WITHOUT STIMULUS from nerves, hormones etc.

So slowly it reaches threshold automatically and AP is fired

So b/w two AP’s slow & gradual depolarization occurs which is k/a PACEMAKER POTENTIAL/ PREPOTENTIAL.

Unsteady RMP- because of which they generates RHYTHMIC IMPULSE SPONTANEOUSLY.

Rapid repolarization & plateau phase are absent.

Late rapid depolarization is slow.

PREPOTENTIAL/PACEMAKER POTENTIAL1. Aka slow depolarization2. Initial part is because of funny(F) channels- Na

influx3. Later part is because of T TYPE Ca channels-

Ca2+ influx DEPOLARIZATION PHASE1. Prepotential reaches threshold slowly and AP’s

is fired2. Mainly because of L TYPE Ca channels opening

leading to Ca influx. REPOLARIZATION- K channel efflux

SA node – right vagus

AV node- left vagusPARASYMPATHETIC STIMULATION( VAGAL)

SYMPATHETIC STIMULATION

-VE CHRONOTROPIC +VE ( RATE)

-VE DROMOTROPIC +VE (CONDUCTION)

INCRESED REFRACTORY PERIOD DECREASED

NIL +VE IONOTROPIC(FORCE)

NIL +VE BATHMOTROPIC( AUTOMATICITY)

Refers to interval b/w onset of one heart beat to onset of next.

VENTRICULAR SYSTOLEISOVOLUMETRIC CONTRACTION- Volume constant Pressure slowly increases- causing AV valve bulge(

C wave of JVP) At the end- semilunar valves opens.VENTRICULAR EJECTION Semilunar valves opens– ejection begins Rapid ejection phase and slow ejection phase Rapid ejection – AV ring gets pulled down– atria

dilates– sharp fall in atrial pressure---X-DESCENTin JVP

PROTODIASTOLE

Very short phase.

Ventricles start relaxing– sharp fall in ventricular pressure---semilunar valves are still open---column of blood in aorta/pulmartery tries to fall in ventricle----semilunar valve close– second heart sound(S2)

Also associated with rise in atrial pressure –-v wave in JVP

VENTRICULAR DIASTOLE

ISOVOLUMETRIC RELAXATION

b/w closure of semilunar valves and opening of AV VALVES

No change in volume.

Ventricles relax and pressure drops.

Ends with AV valve opening.

RAPID VENT FILLING

Initial ventricular filling after AV valve opens.

Contributes to 70% of vent filling.

Results in sharp fall of atrial pressure– Y descent in JVP.

DIASTASIS

Non- turbulent vent filling after initial rapid filling phase.

LAST RAPID FILLING PHASE

AKA atrial systole

Sharp rise in atrial pressure

Coincide with a- wave in JVP

NORMAL HEART RATE 75/ MIN

NORMAL CARDIAC CYCLE 0.8 sec

ISOVOLUMETRIC CONTRACTION 0.05 sec

RAPID VENTRICULAR EJECTION 0.11 sec

SLOW VENTRICULAR EJECTION 0.14 sec

PROTODIASTOLE 0.04 sec

ISOVOLUMETRIC RELAXATION 0.06 sec

RAPID VENTRICULAR FILLING 0.1 sec

DIASTASIS 0.2 sec

ATRIAL SYSTOLE 0.1 sec

Duration of isovolumetric contraction importance but not easy to measure.

Various indices used to measure it.

Via help of ECG, phonogram, carotid pulse (indicating aortic pressure change)

ELECTROMECHANICAL SYSTOLE(QS2)- time interval b/w onset of QRS complex and closure of aortic valves(S2)

-- ECG and phonocardiogram required

LEFT VENTRICULAR EJECTION TIME(LVET)-

Time b/w beginning of carotid pressure rise to dicrotic notch (incisura)

Only carotid pulse recording is required.

PRE EJECTION SYSTOLE-

Difference b/w QS2 & LVET

Gives duration of electromechanical events preceding systolic ejection.

All 3- ECG, phonocardiogram, carotid pulse tracing are required.

Normal PEP/LVET- 0.35

If left ventricular function impaired this ratio increases without change in QS2

Aorta pressure

Maximum- 120 mm Hg & minimum- 80 mmHg

Dicrotic notch- recorded in early down stroke of aortic pressure curve, corresponds to Aortic valve closure(S2)

Relationship b/w vent pressure & volume during cardiac cycle.

WIDTH OF LOOP- diff b/w end-diastolic volume & end-systolic volume aka STROKE VOLUME.

AREA under loop- ventricular stroke work or external cardiac work

LEFT SHIFT- when less volume is handled by same pressure ex-

1. Compliance is decreased2. Increased contractility- sympathetic

stimulation/ pressure overload(aortic stenosis)

3. Concentric hypertrophy. RIGHT SHIFT- volume overload ex- MR,AR

S1 S2 S3 S4

PROLONGED(0.15 sec)

Shorter( 0.12 sec) Soft,low pitched Aka atrial sound

Low pitched 24-45 Hz

High pitched 50 Hz

Very low frequency(20 Hz)

LUB sound DUB sound Can be normal in young adults andchildrenOld ages- heart failure

Cannot be heard with stethoscope

Closure of AV valves

Closure of semilunar valves

First Rapid filling of ventricle

Due to last rapid filling of ventricle( atrial systole)

Normally 5 litres/ min C.O.= stroke volume **heart rate C.O. Of right ventricle = C.O. Of left ventricle CARDIAC INDEX-1. cardiac output per minute per body surface area in

meter square2. Relatively constant3. Normal value- 3.2 L/min/ m2 STROKE VOLUME-1. Amount of blood pumped by left ventricle in each

cycle.2. Can also be defined as diff b/w end diastolic and

end systolic volume3. Normal value- 70ml

EJECTION FRACTION-

1. % of end diastolic volume that is ejected by ventricle in each cardiac systole.

2. Normally- around 60%

3. Valuable index for ventricular function

4. Calculated by stroke volume/end diastolic volume **100

CARDIAC OUTPUT MEASURMENT

1. Fick principle method

2. Dye( indicator dilution method)- based on stewart hamilton principle.

3. Thermodilution method

4. Combining doppler technique and ECHO

5. Cineradiography technique.

Mainly depends on STROKE VOLUME & HEART RATE

FACTORS AFFECTING STROKE VOLUME

Preload – degree of ventricular filling during diastole & is determined by venous return.

INCREASED PRELOAD DECREASED PRELOAD

Inc blood volume Dec blood volume

Inc venous tone Dec venous tone

Inc pumping action of skeletal muscle

Dec pumping action

Inc –ve intrathoracic pressure

Dec –ve intrathoracic pressure

Lying down position Sitting or standing position

Inc sympathetic discharge

Dec sympathetic discharge

Contractility of ventricles- determined by sympathetic discharge, circulating catecholamines.

Afterload- peripheral resistance offered to ventricular pumping action.

Decreased peripheral resistance –increased cardiac output- ex-

1. Exercise2. AV fistula, shunt3. Severe anemia (vasodilation because of anemia

hypoxia).4. Thyrotoxicosis- vasodilation because of

increased BMR.5. Wet beri-beri

FACTORS AFFECTING HEART RATE-

1. Predominantly neurohormonal factors.

2. Increased heart rate– increased cardiac output.

3. If heart rate > 180/min– decreased end-diastolic volume- decreased cardiac output.

C.OUTPUT- NO CHANGE

INCREASE DECREASE

MODERATE CHANGE IN ENVIRONMENTAL CONDITIONS

ANXIETY & EXCITMENT(50-100%)

SITTING OR STANDING UP FROM LYING DOWN POSITION(20-30%)

SLEEP EATING(30%) ARRYTHMIAS

EXERCISE(UPTO 700%) HEART DISEASE

PREGNANCY

EPINEPHRINE

Lateral pressure exerted by column of blood on arterial wall.

Mostly measured in mm/hg SI unit – newton /meter square aka pascal(Pa) B.P. In mm hg = 7.5* B.P. In kPa PULSE PRESSURE- systolic BP – diastolic BP

normally- 40 mm hg MEAN BP- 2/3rd diastolic BP + 1/3rd systolic

pressuremajor determinant of adequate blood flow to tissues.

Systolic BP determined by stroke volume. Diastolic BP determined by peripheral resistance.

SYMPATHETIC-

From rt side- SA node, lt side- AV node

Supplies epicardium mostly.

Effects- positive ionotropic, chronotropic,dromotropic,bathmotropic.

also decrease refractory period of all cardiac cells

Act via Nor-adrenaline.

PARA-SYMPATHETIC

Via vagus

SA node- rt vagus

AV node- lt vagus

Mostly endocardium in distribution.

Effects- -ve chronotropic, dromotropic

Via – acetylcholine

No negative ionotropic effect— because vagal fibres do not innervate myocardial cells of ventricles.

NOTE- without any innervation, intrinsic heart rate – 100/min but normally vagal tone is dominating, so stays at 70/min.

Sympathetic - Main supply of blood vessels.

Causes vasoconstriction---inc peripheral resistance---inc BP---dec venous capacitance.

Via nor-epinephrine.

Some fibres causes vasodilatation via Ach ex-arterioles to skeletal system....k/a sympathetic cholinergic fibres.

Para-sympathetic- Mostly no supply to vessels except vessels of

salivary glands,pancreas,external genitalia,brain,bladder,rectum,tongue.

Causes vasodilatation.

MEDULLARY CENTRES

VMC(VASOMOTOR CENTER)-

Control output of spinal sympathetic neurons– includes pressor area and depressorarea.

Pressor area is in ROSTRAL VENTROLATERAL MEDULLA(RVLM)– increase sympathetic discharge.

Depressor area is in CAUDAL VENTEROLATERAL MEDULLA(CVLM)– decrease sympathetic discharge.

CARDIO-VAGAL CENTER( INHIBITORY CENTER) AKA medullary parasympathetic area(

NUCLEUS AMBIGOUS) It sends parasympathetic efferents via vagus.

NOTE- in resting condition- neurons of pressor area of VMC have inherent tonic discharge in vasomotor nerve supplying blood vessel whereas on HEART vagal effect predominates.

From higher centre VMC receive afferent fibres from cerebral cortex both DIRECTLY as well as VIA HYPOTHALAMUS (cortico-hypothalamic pathways)

These are mechanoreceptors located in adventitia of carotid artery and aorta k/a sinus.

Carotid sinus- at the root of Internal carotid artery just above bifurcation of common carotid artery & its afferents travels via SINUS NERVE( br of Glossopharyngeal nerve)

AORTIC SINUS- located in aortic arch & afferent via AORTIC N. ( br of vagus nerve)

Together both nerves k/a SINO-AORTIC NERVE/ BUFFER NERVES.

BARORECEPTORS-1)sensitive to change in MEAN BP2)Respond b/w 70-150 mm Hg 3)When BP increase--- receptors stimulated---

stimulates nucleus tractus solitarus----causesa) inhibition of pressor area of VMC(RVLM)b) increased parasympathetic output via

stimulating nucleus ambigus.c) weakly inhibits respiration.

4) Effect of posture on BP is compensated by baroreceptors reflex within 15 seconds.

5) VALSALVA’s MANEUVER- pressure on carotid sinus--- inc baroreceptors discharge & reflex inc in vagal discharge to AV node---- dec heart rate.

(basis of carotid sinus syncope)

Present in carotid body & aortic body. Mainly activated by decreased PaO2 & also by

increased PaCO2 & pH Regulates- pulmonary ventilation( mainly) &

generalised vasoconstriction If stimulated it causes-1)increased pulmonary

ventilation and respiratory rate.2)vasoconstriction3) Increased BP4) Tachycardia

Mainly act when BP < 70 mmHg

B/L SECTION OF AORTIC AND SINUS NERVES-Normal individuals- inc heart rate

and BPHypotensive individuals- further

decrease in BP & heart rate PROXIMAL CLAMPING OF COMMON CAROTID

– causes chemoreceptors stimulation ( dec perfusion) & baroreceptors inhibition( dec pressure in carotid sinus) leading to INCREASED HEART RATE, BP, RESPIRATORY RATE

B/L DISTAL CLAMPING OF COMMON CAROTID ARTERY – baroreceptors stimulation-decreased heart rate , BP.

PULMONARY ARTERY BARORECEPTORS- low pressure receptors located in walls of pulmonary trunk, right & left pulmonary artery

CARDIAC BARORECEPTORS- In wall of heart Subendocardially vagus nerve TYPES-1. ATRIAL STRETCH RECEPTORS 2. VENTRICULAR STRETCH RECEPTORS.

k/a low pressure receptors

Classified as receptors with

1. Large myelinated efferent fibres- located at venoatrial junction, further divided into ATRIO-CAVAL receptors( at junction of SVC & IVC with rt atrium) and PULMONARY VENO-ATRIAL receptors( junction of pulmonary vein into lt atrium).

2. NON-MYELINATED FIBRES- throughout atria & inter-atrial septum

On the basis of discharge pattern further divided into TYPE A( during atrial systole) &

TYPE B(during atrial diastole)

As low pressure receptors they have important role to minimize arterial pressure changes in blood volume.

BAIN BRIDGE REFLEX-(ATRIAL REFLEX control of heart rate) increased venous return leads to tachycardia ex- rapid infusion of saline.

ATRIAL CONTROL OF BLOOD VOLUME(VOLUME REFLEX)- any volume overload causes DIURESIS via atrial stretch receptors by increasing ANP & inhibition of ADH secretion from pitutary.

Located in left ventricular & IV septum.

On injection of certain drugs ex serotonin, nicotine into left coronary artery- causes APNEA,BRADYCARDIA,HYPOTENSION......k/s BEZOLD-JARISH REFLEX or CORONARY CHEMOREFLEX.

This regulation has slow onset but has long lasting effect on CVS

Classification-VASOCONSTRICTORS VASODILATORS

Nor-adrenaline Kinins( bradykinin & lysylkinins)

Adrenaline PGE2, PGI2

ADH(vasopressin) VIP

Angiotensin-II ANP

Endothelins(from brain,kidney,intestine)

Nitrous oxide

PGF2

Thromboxane A2