2. Is a hollow, pyramidal shaped , fibromuscular
organ lying obliquely behind sternum in
middle mediastinum.
Males – 300gms females-250gms
Enclosed by pericardium.
3. 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.
4. 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.
5. 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
6. 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.
7. Total four chambers- two atrias and two
ventricles.
8. 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
9. 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.
10. Interatrial septal region-
Develops by approximation of embryonic
septum primum and septum secundum.
Important features are fossa ovalis, limbus
fossa ovalis, triangle of koch( contains AV
NODE)
12. 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
13. Ventricles
◦ Contraction of left ventricle pulls in right
ventricle, aiding its contraction (termed left
ventricular aid)
◦ Separated by intraventricular septum
20. 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.
21. 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%)
22. 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.
23. BRANCHES-
1. Anterior IV ( descending) artery
2. 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 atrium
2. 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.
24. 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.
25. 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
26. Mainly three systems
1) Coronary sinus and its tributeries
2) Anterior cardiac vein
3) Venae cordis minimae
27. 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 groove
3. Post vein of left ventricle
4. 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
28. 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)
29. 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.
30. 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.
31. 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.
32. 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
33. 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.
34. 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 cartilage
Cardiac
apex(just medial
to mid-clavicular
line in left 5th
intercostal
space)
TRICUSPID 4cm Right half of sternum
along 4th,5th
intercostal space
Right lower end
of sternum
37. Tissue Conduction rate (m/s)
SA node .05
Atrial pathways 1
AV node .05
Bundle of His 1
Purkinje 4
Ventricular muscle 1
38. 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)
39. 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
40. 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-BASAL
portion of left ventricles, pulmonary conus,
upper most portion of septum.
Repolarization from epicardial surface to
endocardial surface.
41. 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.
42. Small size of AV NODAL fibres.
Fewer gap junctions– leading to impaired
conduction.
Slow response action potential at AV node.
43.
44. 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
45. 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.
46. Unsteady RMP- because of which they
generates RHYTHMIC IMPULSE
SPONTANEOUSLY.
Rapid repolarization & plateau phase are
absent.
Late rapid depolarization is slow.
47.
48. PREPOTENTIAL/PACEMAKER POTENTIAL
1. Aka slow depolarization
2. Initial part is because of funny(F) channels- Na
influx
3. Later part is because of T TYPE Ca channels-
Ca2+ influx
DEPOLARIZATION PHASE
1. Prepotential reaches threshold slowly and AP’s
is fired
2. Mainly because of L TYPE Ca channels opening
leading to Ca influx.
REPOLARIZATION- K channel efflux
49. SA node – right vagus
AV node- left vagus
PARASYMPATHETIC STIMULATION(
VAGAL)
SYMPATHETIC STIMULATION
-VE CHRONOTROPIC +VE ( RATE)
-VE DROMOTROPIC +VE (CONDUCTION)
INCRESED REFRACTORY PERIOD DECREASED
NIL +VE IONOTROPIC(FORCE)
NIL +VE BATHMOTROPIC(
AUTOMATICITY)
50. Refers to interval b/w onset of one heart beat to
onset of next.
VENTRICULAR SYSTOLE
ISOVOLUMETRIC 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-DESCENT
in JVP
51. PROTODIASTOLE
Very short phase.
Ventricles start relaxing– sharp fall in
ventricular pressure---semilunar valves are
still open---column of blood in aorta/pulm
artery tries to fall in ventricle----semilunar
valve close– second heart sound(S2)
Also associated with rise in atrial pressure –-
v wave in JVP
52. 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.
53. 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
55. 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
56. 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
57. 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)
60. 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 decreased
2. Increased contractility- sympathetic
stimulation/ pressure overload(aortic
stenosis)
3. Concentric hypertrophy.
RIGHT SHIFT- volume overload ex- MR,AR
61. 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 and
children
Old 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)
62. 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 square
2. Relatively constant
3. 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 volume
3. Normal value- 70ml
63. 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.
64. 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
65. 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. Exercise
2. AV fistula, shunt
3. Severe anemia (vasodilation because of anemia
hypoxia).
4. Thyrotoxicosis- vasodilation because of
increased BMR.
5. Wet beri-beri
66. 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
67. 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
pressure
major determinant of adequate blood flow to
tissues.
Systolic BP determined by stroke volume.
Diastolic BP determined by peripheral resistance.
68. 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.
69. 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.
70. 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.
71. MEDULLARY CENTRES
VMC(VASOMOTOR CENTER)-
Control output of spinal sympathetic
neurons– includes pressor area and depressor
area.
Pressor area is in ROSTRAL VENTROLATERAL
MEDULLA(RVLM)– increase sympathetic
discharge.
Depressor area is in CAUDAL
VENTEROLATERAL MEDULLA(CVLM)– decrease
sympathetic discharge.
72. 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)
73. 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.
74. BARORECEPTORS-
1)sensitive to change in MEAN BP
2)Respond b/w 70-150 mm Hg
3)When BP increase--- receptors stimulated---
stimulates nucleus tractus solitarus----causes
a) 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)
75. 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)vasoconstriction
3) Increased BP
4) Tachycardia
Mainly act when BP < 70 mmHg
76. B/L SECTION OF AORTIC AND SINUS NERVES-
Normal individuals- inc heart rate
and BP
Hypotensive 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.
77. 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.
78. 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)
79. 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.
80. 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.
81. 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
