1. Coronary Circulation
Physiology Seminar
18/04/2013
©Dr. Anwar Siddiqui

2. CORONARY CIRCULATION
• CONSIST OF
1) Arterial supply
2) Venous drainage
3) Lymphatic drainage

3. ARTERIAL SUPPLY
• The cardiac muscle is supplied by
two coronary arteries the right and
left coronary arteries.
• Both arteries arises from the sinuses
behind the cusps of the aortic valves
at the root of the aorta.

5. RT. CORONARY ARTERY
• Smaller than left coronary
artery.
• Arises from anterior
coronary sinus.

6. COURSE:
• Emerges from the surface of heart
between pulmonary trunk and right
auricle.
• Winds round the inferior border to
reach the diaphragmatic surface to
reach the posterior inter-ventricular
groove.
• Terminates by anastomising with left
coronary artery

7. BRANCHES
• Large Branches
– marginal
– Post-interventricular
• Small branches:
– Right atrial
– Infundibular
– Nodal – in 60% cases
– Terminal

8. Anterior schematic diagram of heart shows course of dominant right
coronary artery and its tributaries. AV = atrioventricular, PDA =
posterior descending artery, RCA = right coronary artery, RV = right
ventricular, SA = sinoatrial

9. AREAS OF DISTRIBUTION
• Right atrium
• Ventricles
– Greater part of right ventricle, except
the area adjoining the anterior inter-
ventricular groove.
– A small part of the left ventricle
adjoining the posterior
interventricular groove.
• Posterior part or the inter-ventricular
septum
• Whole of the conducting system of the
heart except a part of the left branch of
AV bundle. The SA node is supplied by
left coronary artery in 40% cases

10. LEFT CORONARY ARTERY
• Larger than the right
coronary artery.
• Arises from left
posterior aortic
sinus.

11. COURSE
• Runs forward and to the left and emerges
between the pulmonary trunk and the left
auricle.
• Here the anterior inter-ventricular branch is
given .
• The further continuation of the left coronary
artery is sometimes called the circumflex
artery.
• After giving off the anterior interventricular
branch it runs into the left anterior coronary
sulcus.
• It winds around the left border and near
posterior interventriular groove it terminates
by anastomosing with the right coronary
artery.

12. BRANCHES:
• Large Branches:
– Anterior interventricular
– Branch to the diaphragmatic surface of the
left ventricle
• Small Branches:
― Left atrial
― Pulmonary
― Terminal

13. Dominant left coronary artery anatomy. Left anterior oblique schematic
diagram of dominant left coronary artery anatomy, including left
anterior descending artery and left circumflex artery tributaries, is
shown. AVGA = atrioventricular groove artery, PDA = posterior
descending artery.

14. Areas of distribution
• Left atrium
• Ventricles:
− Greater part of left ventricle, except the
area adjoing the posterior interventricular
groove.
− A small part of right ventricle adjoining the
anterior interventricular groove.
• Anterior part of interventricular septum.
• Part of left branch of AV bundle

15. COLLATERAL CIRCULATION
• Cardiac anatomosis: The two coronary
arteries anastomose in the myocardium.
• Extra cardiac anastomosis: The coronary
arteries anastomose with the
• Vasa vasorum of the aorta,
• Vasa vasorum of pulmonary arteries,
• Internal thoracic arteries
• The bronchial arteries
• Phrenic arteries.
• These channels open up in the emergencies
when the coronary arteries are blocked.

16. CORONARY ARTERY DOMINANCE
• The artery that gives the posterior
interventricular artery determines the coronary
dominance.
• If the posterior interventricular artery is supplied
by the right coronary artery (RCA), then the
coronary circulation can be classified as "right-
dominant".
• If the posterior interventricular artery is supplied
by the circumflex artery (CX), a branch of the left
artery, then the coronary circulation can be
classified as "left-dominant".
• If the posterior interventricular artery is supplied
by both the right coronary artery (RCA) and the
circumflex artery, then the coronary circulation
can be classified as "co-dominant".

17. FUNCTIONAL DIVISION
• Large coronary arteries(epicardial cortonary
arteries) - lies on epicardial surface,
– conduct blood with little resistance.
• Small coronary arteries – descends into
myocardium, are of two types:
– subepicardial vessels and
– subendocardial vessels.
• Small coronary arteries are the principle
resistance vessels of the heart, change in
their diameter regulate the coronary blood
flow

18. VENOUS DRAINAGE OF THE
HEART
• The venous drainage of
the heart is by three
means:
– Coronary sinus.
– Anterior cardiac veins
– Venae Cordis minimae.

19. CORONARY SINUS
• This is the largest of vein of heart situated in
the left posterior coronary sulcus. It is about
3 cm long and ends by opening into the
posterior wall of the right atrium.
• Its tributaries are:
−Great cardiac vein: It enters the left end
of the coronary sinus.
−Middle cardiac vein: It accompanies the
posterior interventricular artery and
joins the right end of the coronary sinus.
−Small cardiac vein: It accompanies the
right coronary artery and joins the right
end of the coronary sinus.

20. − Posterior vein of left ventricle: It runs on the
diaphragmatic surface of the left ventricle and
ends in the middle of the coronary sinus.
− Oblique vein of left atrium ( of Marshall): It runs
on the posterior surface of the left atrium, joins
the left end of coronary sinus and develops from
the left common cardinal vein.
− The right marginal vein: It accompanies the
marginal branch of the right coronary artery.

21. ANTERIOR CARDIAC VEIN
3 to 4 small veins run on the anterior wall of
the right ventricle, open directly into the right
atrium.
VENAE CORDIS MINIMAE
(also called smallest cardiac veins, venae cardiacae minimae, or
Thebesian veins)
• Numerous small veins present in all 4
chambers of heart which open directly into the
cavities.
• The Thebesian venous network is considered
an alternative (secondary) pathway of venous
drainage of the myocardium. It is named after
German anatomist Adam Christian Thebesius,
who described them in a 1708 treatise called
Disputatio medica inauguralis de circulo
sanguinis in corde.

22. Lymphatics of heart
• Lymphatics of the heart accompany
the coronary arteries and form 2
trunks.
• Right trunk ends in brachiocephalic
nodes and the left trunk into the
tracheobronchial lymph nodes at the
bifurcation of the trachea.

23. PECULIARITIES OF COR.CIRCULATION
• BF during diastole
• End arteries
• High capillary density
• High 02 extraction
• Regulation is mainly by metabolites
• Anatomical anastomosis
• The coronary vessels are susceptible to degeneration
and atherosclerosis.
• There is evident regional distribution: The
subendocardial myocardial layer in the left ventricle
receives less blood, due to more myocardial
compression (but this is normally compensated during
diastoles by V.D). However, this renders this area more
liable to ischemia and infarction

24. CORONARY BLOOD FLOW
(CBF):
• The resting coronary blood flow is
about 225 ml/min., which is about
0.7 – 0.8 ml/gm of heart muscle, or 4-
5 % of the total cardiac output.
• In severe muscular exercise, the work
of the heart increased and the CBF
may be increased up to 2 liters/
minute

25. FACTORS REGULATING
CORONARY BL.FLOW
• Physical
• Chemical
• Neural
• Hormonal
• Reflex

26. PHYSICAL FACTOR
Aortic blood pressure:
• CBF is directly proportional to aortic
blood pressure, especially the diastolic
aortic pressure , most of CBF occur
during diastole.
• When diastolic pressure decreases e.g.
aortic incompetence or when MAP is
decreased e.g. shock or aortic stenosis,
the CBF decreases.
• Blood flow to the endocardial regions is
more severely impaired than is that to
the epicardial regions of the ventricle

27. Heart Rate:
• Excessive in the heart rate e.g.
paroxysmal tachycardia diastolic period
coronary filling (as it occurs mainly during
ventricular diastole) CBF.
Cardiac Output:
• CBF is directly proportional to COP i.e. COP CBF
COP CBF
• Increased cardiac output BP in aorta + reflex
inhibition of the vagal vasoconstrictor tone (a nrepis
reflex) coronary vasodilatation CBF.

28. • C.B.F. occurs mainly during diastole due
to compression of coronary blood vessels
during systole by the contracted muscle
fibers.
During systolic phases
C.B.F. is less than that during
diastole. With minimal blood
flow during iso volumetric
contraction phase. (due to
compression of coronary blood
vessels with low aortic pressure).
During diastolic phases
C.B.F. is more than that during
systole.With maximal blood flow
during iso volumetric relaxation
phase. (due to dilated coronary blood
vessels with high aortic pressure).

29. CHEMICAL FACTORS:
Metabolic factors:
cardiac metabolism O2tension (local hypoxia),
CO2, K+, lactic acid & adenosine in the cardiac
muscle coronary vasodilatation CBF.
O2 lack (hypoxia) is the most effective coronary
vasodilator. It produces coronary vasodilatation
through:
• Direct action on coronary blood vessels and
• Release of chemical substances such as adenosine (from
ATP) which is a potent coronary vasodilator.
Drugs:
• Nitrites, angised, aminophylline, caffeine &
Khellin are coronary vasodilator coronary
vasodilatation CBF.

30. NERVOUS FACTORS:
Direct effect:
• Parasympathetic: vagus has very slight distribution to
coronary, so its stimulation has slight dilator effect.
• Sympathetic: Both alpha and Beta receptors exist in the
coronary vessels. Sympathetic stimulation causes slight
direct coronary constriction.
Indirect effect:
• Plays a far more important role in normal control of
coronary blood flow than the direct. Sympathetic
stimulation increase both heart rate and myocardial
contractility, as well as its rate of metabolism leading to
dilatation of coronary blood vessels. The blood flow
increase proportional to the metabolic need of heart
muscle

31. HORMONAL FACTOR
• Thyroxin cardiac metabolism
coronary vasodilator CBF.
• Vasopressin (antidiuretic hormone)
coronary vasoconst CBF.

32. REFLEX CONTROL
• Anrep’s reflex: Increased venous return
causes increased pressure in right atrium,
leading to reflex increase in CBF e.g. during
muscular exercise.
• Gastro-coronary reflex: Distention of the
stomach with heavy meal causes reflex
vasoconstriction of coronary blood vessels
decreasing CBF.

33. Coronary Autoregulation
• If there is sudden change in aortic pressure,
coronary vascular resistance will adjust
itself proportionally within few seconds; so
that a constant blood flow is maintained.
• Range of autoregulation: 60 – 140 mmHg.
Mechanism:
• Myogenic response: an increase in passive
stretch, caused by increased perfusion
pressure, causes active smooth muscle
contraction.

34. • Chemical theory:
• Decrease perfusion pressure leads to
Increase adenosine & Decreased oxygen
which causes Vasodilatation and
increase CBF
• Endothelium derived relaxation factor
(EDRF):
• Hypoxia, ADP, VIP, muscular exercise
(increase distention force), stimulate vascular
endothelium to secrete EDRF, which is a
potent vasodilator, that causes coronary
dilatation and increase CBF.

35. Applied aspects

36. CORONARY ARTERY DISEASE
ANGINA PECTORIS
• Angina Pectoris means severe chest pain (usually
retrosternal i.e. behind the sternum) due to
ischemia of the cardiac muscle.
• Angina pectoris is usually due to narrowing of the
coronary arteries ischemia.
• When the coronary artery is only partly obstructed
(by spasm or atherosclerosis) and the coronary
blood flow is only moderately reduced, symptoms
of ischemia appears only when cardiac work is
increased by effort, exercise, excitement, food or
severe cold, or anemia and relived by treatment.
• Pain is due to accumulation of pain producing
substances in the myocardium such as, P factor,
lactic acid, histamine, K, and Kinins.

37. • MYOCARDIAL INFARCTION
• Myocardial Infarction means necrosis of a part of the
myocardium due to
− Severe & prolonged ischemia due to narrowing of
the coronary arteries.
− Occlusion of one of the coronary arteries or its
branches by coronary thrombosis severe
ischemia.
• Myocardial Infarction produces also chest pain
which is more severe than that of angina and it
cannot be relieved by rest or coronary VD drugs.
• It is usually complicated by fatal ventricular
fibrillation.

39. Coronary bypass operation

40. Angioplasty

41. A Presentation By DR ANWAR H SIDDIQUI, JR, Physiology