Dr Prafull Turerao,

1. Coronary circulation
Dr Prafull H Turerao.
D.Y.Patil Medical College, Kolhapur
Tutor, Department of Physiology.

2. Specific Learning Objective
• Coronary blood vessels
• Coronary blood flow: characteristic features
• Measurement of coronary blood flow
• Regulation of coronary blood flow
• Factors affecting coronary blood flow
• Coronary artery disease

4. Physiologic Anatomy of the Coronary
Blood Supply
• The main coronary arteries lie on the surface
of the heart and smaller arteries then
penetrate from the surface into the cardiac
muscle mass.
• It is almost entirely through these arteries
that the heart receives its nutritive blood
supply.

5. • Only the inner 1/10 millimeter of the
endocardial surface can obtain significant
nutrition directly from the blood inside the
cardiac chambers, so this source of muscle
nutrition is minuscule.

6. CORONARY BLOOD VESSELS
• Two coronary arteries (right and left) arise
from the root of ascending aorta and supply
blood to the myocardium.

7. Right coronary artery
Right coronary artery supplies blood to the
• Right ventricle,
• The right atrium,
• The posterior part of left ventricle,
• The posterior part of interventricular septum
• And major portion of the conducting system
of heart including SA node.

8. Left coronary artery
Left coronary artery supplies blood mainly to
• The anterior part of left ventricle,
• Left atrium,
• Anterior part of the interventricular septum
• And a part of the left branch of bundle of His.

9. Distribution of Blood Supply
• Predominant supply by the right coronary
artery described above is seen in about 50%
individuals.
• In 20% individuals the predominant supply to
myocardium is by left coronary artery.
• In 30% individuals it is the balanced supply,
i.e. equal supply by the two arteries.

10. End arteries.
• Normally, the coronary arteries appear to
function as end arteries.
• However, the presence of an arterial plaque
or occlusion allows the anastomoses present
between vessels to become functional.
• That is why they are also known as functional
end arteries and not true end arteries.

11. These anastomoses are of two types:
• Cardiac anastomoses are those which are
present between branches of two coronary
arteries and between the branches of
coronary artery and deep venous system.

12. • Extracardiac anastomoses include those
present between the branches of coronary
arteries and vessels lying near the heart.
• Such as vasa vasora of aorta, vasa vasora of
pulmonary arteries, intrathoracic arteries,
bronchial arteries and phrenic arteries.

13. Coronary Veins
• Coronary sinus is a wide vein about 2 cm
long, which drains most of the venous blood
from the myocardium (mainly left ventricle)
into the right atrium.
• Its tributaries are the great cardiac vein, the
small cardiac vein, the posterior vein of left
ventricle and the oblique vein of left ventricle

14. • Anterior cardiac vein draining venous blood
mainly from the right ventricle opens directly
into the right atrium.

15. • Thebesian veins and coronary-luminal vessels
(connections between the coronary vessels
and the lumen of heart) constitute the deep
venous system.
• These vessels drain only less than 10% of the
venous blood from the myocardium directly
into the various cardiac chambers,
contributing to an anatomic shunt effect.

16. Coronary Blood Flow
• A continuous flow of blood to the heart is
essential to maintain an adequate supply of
O2 and nutrients.
• The resting coronary blood flow in the resting
human being averages 70 ml/min/100 g heart
weight, or about 225 ml/min, which is about
4 to 5 percent of the total cardiac output.

17. • Three to six fold increase in the coronary
blood flow may occur during exercise.

18. • Oxygen consumption by the myocardium is
very high (8 mL/min/100 g at rest).
• Because of this, even at rest 70–80% of the
oxygen is extracted from each unit of the
coronary blood as compared to the whole
body (average of 25%) oxygen extraction at
rest.

19. • The increased oxygen demand of the
myocardium during exercise is met with by
almost total (nearly 100%) extraction of
oxygen and by manifold increase in the
coronary blood flow

21. Phasic Blood Flow
• During systole, the tension developed in the left
ventricle is so high that it has throttling effect on
the branches of the coronary arteries penetrating
through them
• As a result, the average blood flow through the
capillaries of left ventricles falls to the extent
that during isometric contraction phase, the
blood flow to the left ventricle practically ceases,
i.e. becomes zero.

22. • During diastole, the cardiac muscles relax and
blood flow increases. Thus, most of the
coronary blood flow (over 70%) occurs during
diastole .

24. • Subendocardial region of the left ventricle
receives no blood supply during systole so this
region is particularly vulnerable to ischaemia
and is the most common site of myocardial
infarction.

25. • Minimum diffusion distance between the
capillaries and myocardial cells is 20% shorter
in the subendocardial region of left ventricle
(16.5 μm) as compared to the epicardial
region (20.5 μm).
• Myoglobin content (O2 storage pigment) is
higher in the subendocardial region than the
epicardial region of the left ventricle.

26. • This is true in spite of the fact that this region
has been provided with following
compensatory (protective) mechanisms:
Capillary density in subendocardial region of
left ventricle is much higher (1100
capillaries/mm2) than the epicardial region
(750 capillaries/mm2).

27. • The coronary blood flow shows changes
during phases of the cardiac cycle.
• The blood flow is determined by the balance
between pressure head (i.e. aortic pressure)
• And the resistance (i.e. extravascular pressure
exerted by the myocardium on the coronary
vessels) offered to the blood flow during
various phases of cardiac cycle

28. MEASUREMENT OF CORONARY BLOOD
FLOW
Nitrous oxide method (Kety method)
• Principle - Nitrous oxide method is the most
common method used for measuring coronary
blood flow. It gives almost accurate value and
is based on the Fick’s principle

29. • Procedure - The individual is made to inhale a
mixture of 15% nitrous oxide and air for 10
min.
• During inhalation of gases, serial samples of
arterial and coronary sinus venous blood
(through a catheter introduced) are taken at
fixed intervals for 10 min.

30. • The coronary blood flow (CBF) is then
determined from the amount of nitrous oxide
taken up per minute (N2O/ min) and the
difference of nitrous oxide content of arterial
(A) and venous (V) blood, i.e.
• CBF = N2O taken up/min
(A − V)

31. Radionuclides utilization technique
• Principle - The radioactive tracers are pumped
into cardiac muscle cells by the enzymes Na+–
K+ ATPase and equilibrate with the
intracellular K+ pool.
• Distribution of radioactive tracers is directly
proportional to myocardial blood flow and
this forms the basis of this technique

32. • Procedure. Radionuclide such as thallium-201
(201T1) is injected intravenously.
• After 10 min, the amount of 201T1 taken up
by the myocardial cells is then measured with
the help of gamma-scintillation camera over
the chest.
• The amount of coronary blood flow is
calculated from these values. Areas of
ischaemia are detected by their low uptake.

33. Newer methods
Coronary angiographic technique
• Coronary angiography when combined with
measurement of 133Xe washout using a
multiple crystal scintillation camera.
Electromagnetic flowmeter technique
• This technique is employed in animals to
measure the coronary blood flow.

34. REGULATION OF CORONARY BLOOD
FLOW
Autoregulation.
• Coronary circulation shows well developed
phenomenon of autoregulation
• 60-200 mmHg

35. Role of local metabolites
• Metabolic local factors are the most important
factors which regulate the coronary blood flow.
• Direct effect of O2. It has been proposed that a
decrease in the tissue PO2 could also act directly
on the arterioles and cause vasodilation.
• Oxygen Demand as a Major Factor in Local
Coronary Blood Flow Regulation

36. Role of adenosine (Berne’s hypothesis)
• Adenosine is considered the major factor in
production of coronary vasodilation during
hypoxic states.
• In myocardial ischaemia, either due to
generalized hypoxia or due to increased
myocardial metabolism the intracellular
myocardial adenine nucleotides are degraded
to adenosine.

37. • The adenosine is capable of crossing
myocardial cell membrane producing an
extremely strong vasodilator response

38. • Role of other local metabolites. Hydrogen
ions, bradykinin, CO2 and prostaglandins are
the other suggested vasodilator substances

39. Nervous control mechanism
• Autonomic nerves control the coronary blood
flow directly as well as indirectly.

40. Direct nervous control
• Parasympathetic nerve fibres to coronary
vessels through vagus are so less that the
parasympathetic stimulation has very little
direct effect, causing vasodilation

41. • Sympathetic nerve fibres extensively
innervate the coronary vessels.
• The transmitters released at their nerve
endings are epinephrine and norepinephrine.
• The coronary vessels contain both α and β
receptors.
• The net result of direct effect of sympathetic
stimulation is vasoconstriction.

42. Indirect nervous control
• Sympathetic stimulation causes increase in
the heart rate and increase of force of
contraction of the heart.
• Thus, an increased activity of heart helps
conversion of ATP to ADP which by producing
coronary vasodilation increases the coronary
blood flow.

43. • Parasympathetic stimulation causes
decreased heart rate and decreased force of
contraction of heart. Thus, indirectly the
coronary blood flow is reduced.

44. FACTORS AFFECTING CORONARY
BLOOD FLOW
Mean aortic pressure.
• This is the force for driving blood into the
coronary arteries. Rise in mean aortic pressure
increases the blood flow and vice versa.
Emotional excitement.
• During emotional excitement states, such as
fright, auditory and olfactory stimuli, the CBF
is increased due to increased sympathetic
discharge

45. Muscular exercise.
• Normal CBF at rest is about 70 mL/100 g
tissue/min. During exercise, CBF increases
about four times because of sympathetic
stimulation by the following mechanisms:
• Increased activity of heart
• Increased cardiac output (> 5 folds)
• Increase in mean arterial pressure

46. Hypotension.
• There occurs reflex increase in noradrenergic
discharge during hypotension which produces
coronary vasodilation to increase CBF.
• This effect is observed secondary to the
metabolic changes in the myocardium at a
time when there occurs vasoconstriction of
splanchnic, renal and cutaneous vessels

47. Hormones affecting CBF are:
• Thyroid hormones increase CBF because of
increase in metabolism.
• Adrenaline and noradrenaline cause increase
in CBF indirectly.
• Acetylcholine may increase CBF by its action
on heart similar to parasympathetic
stimulation.
• Pitressin is known to decrease CBF by
increasing coronary resistance.
• Nicotine is reported to increase CBF through
the liberation of norepinephrine.

48. Heart rate.
• When heart rate is increased, stroke volume
decreases, therefore, phasic CBF and O2
consumption per beat also decreases.
Effect of ions.
• Potassium ions (K+) in low concentration cause
dilatation of coronary vessels increasing CBF,
whereas high K+ ion concentration causes
constriction of coronary vessels decreasing CBF.

49. Metabolic factors.
• Increased metabolism of the heart increases
O2 consumption leading to relative hypoxia.
Hypoxia causes vasodilation due to direct
effect and also due to release of adenosine
leading to increased CBF.
Temperature.
• Hyperthermia increases metabolism and so
causes increase in the CBF, while hypothermia
decreases metabolic rate and thus decreases
CBF as well.

50. CORONARY ARTERY DISEASE
• Coronary artery disease (CAD) also known as
ischaemic heart disease results due to the
insufficient coronary blood flow.
• It is a condition associated with development of
atherosclerosis in the coronary arteries, which
supply the heart muscles (myocardium). With
atherosclerosis, the arterial wall is hardened and
its lumen becomes narrow due to plaque
formation

51. Angina pectoris
• Definition. Angina pectoris refers to a
transient form of myocardial ischaemia,
especially occurring during increased Oxygen
demand (e.g. during exercise) in patients with
coronary artery disease having about 60–70%
narrowing of coronary arteries.
• Superadded thrombus formation causing
incomplete coronary occlusion results in an
unstable angina.

52. Characteristic features.
• Typically, the angina is described as a feeling
of uncomfortable pressure, fullness,
squeezing or pain in the substernal region,
which may be localized or may be referred to
the inner border of left arm, neck or jaw.
• Pain occurs due to accumulation of anoxic
myocardial metabolites and factor P which
stimulates pain nerve endings.

54. Myocardial infarction
• Myocardial infarction (MI) or acute myocardial
infarction (AMI), commonly known as a ‘heart
attack’ refers to a degree of myocardial
ischaemia (due to interruption of blood
supply) that causes irreversible changes
(necrosis i.e. cell death or infarction) in the
myocardium.

55. Signs and symptoms
• Sudden severe chest pain is a classical
symptom of MI. Pain lasts for more than 30
min and typically may radiate to left arm and
left side of neck.
• Pain occurs due to the anoxic metabolites and
necrotic tissue products.
• Associated symptoms with pain, often
complained by patients are shortness of
breath, nausea, vomiting, palpitation,
sweating and anxiety (often described as a
sense of impending doom).

56. • Approximately 25% of all myocardial infarction
are ‘silent’ i.e. without chest pain or other
symptoms. Silent MI usually occurs in
diabetics with associated autonomic
neuropathy in elderly.

57. Diagnosis of MI is made by triad of:
• Typical signs and symptoms associated with ECG
changes seen on serial tracings and Changes in
serum levels of certain enzymes and proteins
(cardiac biomarkers).
• ECG changes in myocardial infarction are very
important to diagnose, localize the area of
infarction and to know the duration of infarction.
Typical ECG changes (hallmark) seen in MI
include:
• Elevation of ST segment in the leads overlying
the infarct area and
• Depression of ST segments in the reciprocal
leads.

58. “Coronary steal" syndrome
Value of Rest in Treating Myocardial Infarction
• The degree of cardiac cellular death is
determined by the degree of ischemia and
the workload on the heart muscle.
• When the workload is greatly increased, such
as during exercise, in severe emotional strain,
or as a result of fatigue, the heart needs
increased oxygen and other nutrients for
sustaining its life.

59. Collateral Circulation
Lifesaving Value of Collateral Circulation in the
Heart
• The degree of damage to the heart muscle
caused either by slowly developing
atherosclerotic constriction of the coronary
arteries or by sudden coronary occlusion is
determined to a great extent by the degree of
collateral circulation that has already developed
or that can open within minutes after the
occlusion

60. • Furthermore, anastomotic blood vessels that
supply blood to ischemic areas of the heart must
also still supply the areas of the heart that they
normally supply.
• When the heart becomes excessively active, the
vessels of the normal musculature become
greatly dilated.
• This allows most of the blood flowing into the
coronary vessels to flow through the normal
muscle tissue, thus leaving little blood to flow
through the small anastomotic channels into the
ischemic area so that the ischemic condition
worsens. This condition is called the "coronary
steal" syndrome.

61. Treatment
Treatment with Drugs
• Several vasodilator drugs, when administered
during an acute anginal attack, can often give
immediate relief from the pain. Commonly
used short-acting vasodilators are
nitroglycerin and other nitrate drugs.

62. Coronary Angioplasty
• In this procedure a small balloon-tipped
catheter, about 1 millimeter in diameter, is
passed under radiographic guidance into the
coronary system and pushed through the
partially occluded artery until the balloon
portion of the catheter straddles the partially
occluded point.
• Then the balloon is inflated with high
pressure, which markedly stretches the
diseased artery.

63. Surgical treatment
• A surgical procedure was developed in the
1960s, called aortic-coronary bypass, for
removing a section of a subcutaneous vein
from an arm or leg and then grafting this vein
from the root of the aorta to the side of a
peripheral coronary artery beyond the
atherosclerotic blockage point.
• One to five such grafts are usually performed,
each of which supplies a peripheral coronary
artery beyond a block.

64. References
• Textbook of Medical Physiology – Guyton And
Hall 13th Edition
• Textbook of Physiology – A K Jain 6th Edition
• Medical Physiology For Undergraduate Students –
Indu Khurana 1st Edition
• Images – Net source

65. Thank You.