The coronary circulation supplies blood to the heart muscle. The right and left coronary arteries branch to form a dense capillary network around each cardiac muscle cell. Coronary blood flow is regulated by metabolic demand of the heart as well as mechanical factors related to the cardiac cycle. During systole, compressive forces within the heart reduce coronary flow, while flow increases during diastole when the vessels dilate. Multiple chemical and neural factors also control resistance within the coronary vasculature to match blood supply with myocardial oxygen requirements. Imbalances can lead to ischemia if demand outpaces supply.

1. Anatomy Of Coronary Circulation
AND
Factors Affecting It.
Myocardial Oxygen Supply &
Demand.

2. Epicardial Vessel
Subepicardium
Subendocardium
Myocardium
Pericardium
(Epicardium)

3. Coronary Vascular
Resistance
Epicardial conductance vessels
Only a small % of resistance normally
Stenotic lesions
Intramyocardial vessels (arterioles)
Contribute most to total coronary vascular
resistance

4. Capillary Density in the Heart

5. CORONARY CIRCULATION
BLOOD SUPPLY OF THE HEART:
Arterial supply:
- The cardiac muscle is supplied by the first two branches
of the aorta i.e. right & left coronary arteries.
- The coronary arteries branch freely to form a rich
capillary network.
- There is about one capillary for each cardiac muscle
fiber.

6. Coronary arteries are functional end arteries.
Anastomatic connections bet. the small branches of
the two coronary arteries and bet. the coronary
arterioles and extra cardiac arterioles.
These anatomizes are not sufficient to supply the
cardiac muscle with blood if one of the coronary
arteries is occluded.
Thus, occlusion of a large branch of the coronary
artery e.g. by coronary thrombosis  necrosis
(=death) of the muscle supplied by that branch.

7. Venous Drainage:
Coronary venous drainage occurs through two
systems:
1) Superficial system: It is formed of coronary sinus
and anterior cardiac veins that open into the right
atrium.
2) Deep system: which drains the rest of the heart. It is
formed of thebasian veins and arterio-sinusoidal
vessels that open directly into the heart chamber.

8. CHARACTERISTICS OF THE
CORONARY CIRCULATION
1) It is very short and very rapid (so it is essential to the
heart).
2) The blood flow in this circulation occurs mainly during
cardiac diastole (75%)
3) There is no efficient anastomoses between the coronary
vessels.
4) It is a rich circulation (5% of the CO while the heart
weight is 300gm).

9. 5) Its regulation is mainly by metabolites and not
neural
6) The capillary permeability is high (the cardiac lymph
is rich in protein)
7) The coronary vessels are susceptible to
degeneration and atherosclerosis.

10. CORONARY BLOOD FLOW
Under resting conditions coronary blood flow
(CBF) in the human heart is about 250 ml/ minute
(=5% of the cardiac output).
In severe muscular exercise, the work of the
heart increased and the CBF may be increased
up to 2 liters/ minute.

11. Coronary Inflow (arterial) occurs mainly during
diastole, because during systole the coronary
arteries are mechanically compressed by the
contracting myocardium, i.e.
Systole of the heart   coronary inflow
Diastole of the heart   coronary inflow

12. Coronary Outflow (venous) occurs mainly
during systolic due to compression of the
coronary veins by the contracting myocardium.
During diastole coronary outflow  and veins are
filled.
Normal diastolic blood pressure is important for
coronary filling because filling of coronary
arteries occurs mainly during ventricular
diastolic.

13. Coronary Arterial System
Right & Left

14. RIGHT CORONARY ARTERY
Arises from the ant. Coronary sinus of valsalva just above the
ant. Cusp of aortic valve .
Passes bet. Pulmonay trunk & rt. Atrium.
Desends in the rt. Part of AV groove/sulcus.
In 80% continues as post. Inter-ventricular artery (PDA).
And anastamosis with ant. Inter-ventricular artery (br. Of LCA)

15. Before entering the AV groove gives SA nodal artery in
60%.
AV nodal branch in 90% (br. Of PDA)
Acute Marginal Branch – runs to the apex –ant. Wall of
right ventricle
PDA gives of Septal branches– Post. 1/3 inter-ventricular
septum
PDA gives off br. to post. Of right ventricle.
PDA gives off anastamotic br. with LCX & ant. Inter-
ventricular A.
Brach to Post. Medial papillary muscle of left ventricle.

16. LEFT CORONARY ARTERY
Arises from the Post. Aortic sinus of valsalva.
Passes behind the Pulmonary trunk & left atrial
appendage (1-2cm).
Divides in the space between Aorta & pulmonary
artery into:-
1) Left ant. Inter-ventricular (LAD)
2) Circumflex Artery

17. LAD- Left Ant. Descending Artery :-----
Runs in Ant. Inter-Venticular Sulcus.
Turns sharply at the apex to anastomose with PDA.
Supplies apical portion of both ventricles.
Gives off Diagonal Braches – Left ventricular lateral wall.
Gives off a branch to Antero-lateral papillary muscle of R
ventricle
Gives off Septal Branches–Ant. 2/3 inter-ventricular septum
( In 1%Left coronary artery is absent – both branches originate from the aorta
via separate Ostia)

18. LCX- Circumflex Artery:----
Arises at right angle to LCA near the base of left atrial
appendage.
Runs in the left part of AV groove around the left border of heart.
Ends on the post surface of heart by anastamosing with RCA.
In Av groove lies close to the annulus of mirtal valve.
Gives off Atrial circumfles artery – Left atrium.
Gives off Obtuse Marginal Br. At left border –Post surface LV
In less than 40% SA Nodal br. Arises from LCX.

20. VENOUS DRAINAGE OF HEART
- Veins follow the arteries but different names.
- 2/3 of venous return via Coronary sinus & Ant. Cardiac
Vein.
- Remaining by small veins – Venae Cordae Minimae-
directly into the cavity of heart.

22. Coronary Sinus
2.25 cm wide channel – continuation of Great Cardiac
Vein
Runs L-R in the Post. Portion of coronary groove on the
Post. Surface of heart.
Opening located bet. Right AV orifice & IVC.
Receives blood from ---
Great cardiac vein, Oblique vein, Post. Vein of left
ventricle from the left side.

23. Great Cardiac Vein
Begins at the apex
Ascends in Ant.inter-ventricular groove along with LAD artery
Drains areas supplied by LCA
Receives tributaries –
Left ventricular surface via Ant. Inter-ventricular Vein
Left marginal vein (follows marginal branch of the
circumflex artery)
Left posterior vein

24. Middle & Small Cardiac Vein
Middle cardiac vein :- begins at apex – Ascends in the post.
Inter-ventricular groove along with PDA.
Empties into the right side of coronary sinus.
Small Cardiac Vein :- is a continuation of right marginal vein.
Runs along the lower border of heart.
Empties into coronary sinus but may drain directly into right
atrium.
Both drain areas supplied by Right Coronary Artery

25. Oblique vein –
Descends on the back of left atrium.
Opens into the left side of coronary sinus.
Remnant of left superior vena cava.
Anterior Cardiac Vein –
Crosses the ant. Inter-venticular groove over RCA.
Opens directly into right atrium.
Drains most of ant. Surface of heart.

26. Venae Cordae Minimae / "lesser" venous system
Thebesian veins drain blood from the capillary bed into
the ventricular cavity.
Arterioluminal vessels drain blood directly from the
arteries into ventricles without traversing capillary beds.
Venoluminal vessels form direct communications with the
coronary veins, shunting blood from these vessels into
the ventricular cavities.
(this coronary venous blood draining directly into LV
contributes to fixed shunt & to dilution of oxygenated
blood)

27. Factors Affecting
Coronary Blood Flow

28. The amount of blood passing through
the coronary vessels (CBF) is directly
proportional to the work done by the heart
i.e.
 cardiac work   CBF
and
 cardiac work   CBF.

29. The following factors modify the CBF:
1) Nervous Factors:
The effect of the autonomic nerves to the heart on the
coronary arteries is indirect through their effect on cardiac
metabolism i.e.
a) Stimulation of sympathetic 
 cardiac metabolism  coronary vasodilatation 
CBF.
b) Stimulation of parasymp   cardiac metabolism 
coronary vasoconst.   CBF.

30. 2) Chemical Factors:
a) Metabolic factors:
 cardiac metabolism   O2 tension (local hypoxia), 
CO2,  K+, lactic acid & adenosine in the cardiac muscle
 coronary vasodilatation   CBF.
 cardiac metabolites  active hyperemia during 
cardiac activity = auto regulation of 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.

31. b) Drugs:
Nitrites, aminophylline, caffeine & Khellin
are coronary vasodilator  coronary
vasodilatation   CBF.
c) Hormones
Thyroxin   cardiac metabolism 
 coronary vasodilator   CBF.
Vasopressin (antidiuretic hormone) 
coronary vasoconst   CBF.

32. 3) Mechanical factors (=effect of cardiac cycle):
-Ventricular systole   of the intra-myocardial
pressure  compression of the coronary
vessels   CBF mainly in the left coronary
artery (due to stronger cont of the left vent.)
-CBF  during ventricular diastole (maximal at
the end of isometric relaxation).

33. 4) Other Factors:
a) Heart Rate:
Excessive  in the heart rate   diastolic period
  coronary filling (as it occurs mainly during
ventricular diastole)   CBF.
b) Cardiac Output:
CBF is directly proportional to COP i.e.
 COP   CBF
 COP   CBF

34. c) Blood Pressure:
CBF is directly proportional to aortic BP
especially diastolic
 diastolic pressure   CBF
and
 diastolic aortic pressure (as in aortic
regurgitation)   CBF

35. Determinants of coronary blood
flow
- Coronary perfusion pressure
- Perfusion Time
- Vessel wall diameter

36. Coronary Perfusion Pressure
Pressure gradient that drives blood through
the coronary circulation.
Coronary Perfusion Pressure =
Diastolic BP – LVEDP (or PCWP)

37. Perfusion Time
Increased heart rate ---
Decreases Diastole Time ---
Reduces Perfusion Time

38. Vessel wall diameter
Substances having DIRECT effect on coronary
Vasculature…
Constriction Dilation
prostaglandin H2 prostacyclin (PGI2)
thromboxane A2 endothelium-derived relaxing factor
(NO)
peptide endothelin protein C
Alpha-1 tissue-type plasminogen activator
Calcium channel blockers
ACE Inhibitors
Beta-2
H+, K+, Histamine
Adenosine

39. Factors affecting coronary vasomotor tone.
α = alpha receptor, β = beta receptor, M = muscarinic receptor, AT =
angiotensin receptor, ET = endothelin receptor, EDRF=endothelium
derived relaxant factor

40. Regulation of Coronary
Blood Flow

41. Coronary Blood Flow
1) Metabolic control
2) Autoregulation
3) Endothelial control of coronary
vascular tone
4) Extravascular compressive forces
5) Neural control

42. Vascular
Resistance
Coronary
Blood
Flow
Heart Rate
Contractility
Systolic Wall
Tension
O2-
Carrying
Capacity
SUPPLY DEMAND
Diastolic
Phase
Metabolic
Control
Auto regulation
Extravascular
Compressive
Forces
Neural
Control
Endothelial
Control

43. Regulation of
Coronary Blood Flow

44. Metabolic Control
Coronary circulation is exquisitely sensitive
to myocardial tissue oxygen tension
Increased oxygen demand results in a
lower tissue oxygen tension. This causes
vasodilation and increased blood flow via-
Adenosine
Nitric oxide
Prostaglandins
K+
ATP channels

45. Metabolic Control of Blood Flow
Lack of oxygen?
Formation of vasodilators?
Combination of both??
Metarteriole
Precapillary
Sphincter
Capillary
Relaxation of smooth muscle
Increased Blood Flow

46. Auto regulation
Ability of a vascular network to maintain constant
blood flow over a range of arterial
pressures.( 60–140 mm Hg)
Beyond this range flow becomes pressure- dependent
Autoregulation is an independent determinant of
CBF
The set point at which CBF is maintained
depends on MVO2

47. Coronary Perfusion Pressure
Flow
Auto regulation
Normal
Autoregulation
Maximal Available
Coronary Blood Flow
Autoregulation in
Anemia or LVH
60 140

48. Endothelial Control of
Coronary Vascular Tone

50. When Damage to Endothelium Occurs--
Damage to endothelial cells will lead to:
Decreased Nitric Oxide and Prostacyclin
production
Increased Endothelin production
This will lead to:
Vasoconstriction
Vasospasm
Thrombosis

51. Neural Control
Coronary blood flow is controlled
predominantly by local
metabolic, autoregulatory, and
endothelial factors
Neural control of the coronary circulation
complements the above local effects

52. Neural Control
Sympathetic Control
Alpha = constrict coronary vessels
Beta = dilate coronary vessels
Beta1 in conduit arteries
Beta2 in resistance arterioles
Parasympathetic Control
Acetylcholine
Vasodilation in healthy subjects
Vasoconstriction in patients with atherosclerosis

54. Extravascular Compressive Forces
The heart influences its blood supply by
the squeezing effect of the contracting
myocardium on the blood vessels
coursing through the heart.

55. Extravascular Compressive Forces
Left Ventricle
Early Systole > Initial Flow Reversal
Remainder of Systole > Flow follows aortic
pressure curve, but at a much reduced pressure
Early Diastole > Abrupt pressure rise (80-90% of
LV flow occurs in early diastole)
Remainder of Diastole > Pressure declines
slowly as aortic pressure decreases

56. Extravascular Compressive Forces

57. Extravascular Compressive Forces
Right Ventricle
Lower pressure generated by thin right
ventricle in systole.
No reversal of blood flow during early
systole.
Systolic blood flow constitutes a much
greater proportion of total blood flow.

59. Transmural Distribution of Myocardial Blood
Flow
Extravascular compressive forces are greater in the
subendocardium (inner) and least near the subepicardial
layer (outer)
Under normal resting conditions this does not impair
subendocardial blood flow as increased flow during diastole
compensates
Subendocardial to subepicardial ratio: 1.25/1
Due to preferential dilatation of the subendocardial vessels
secondary to increased wall stress and, therefore, increased
MVO2 in the subendocardium

60. Transmural Distribution of Myocardial Blood
Flow
The subendocardium is more susceptible
to ischemia than the mid-myocardium or
subepicardium.
Epicardial coronary stenoses are
associated with reductions in the
subendocardial to subepicardial flow
ratio.

61. Coronary Flow Reserve
Difference between baseline blood flow
and maximal flow
Usually measured following pharmacologic
coronary vasodilation
In the absence of coronary artery
disease, maximal flow is 4 – 5 times as
great as at rest.
Coronary flow reserve decreases with
increasing severity of coronary artery
disease.

63. Myocardial Oxygen Supply
Determined by –
1) Coronary Perfusion Pressure.
2) Oxygen Carrying Capacity of Blood
3) Heart rate - diastolic time
4) Coronary artery diameter

64. Resting O2 Consumption of
Various Organs

65. Myocardial Oxygen Supply
Oxygen Content of Blood
O2 Content =
(1.36 x Hb x % Saturation) + (pO2 x 0.003)
O2 delivered to myocardium =
O2 content x coronary blood flow

66. Myocardial Oxygen Supply
Oxygen Extraction
The heart extracts oxygen to a greater extent
than any other organ
Coronary sinus pO2 value is normally in range
of 20-22 mmHg (% sat = 32-38%)
Can only minimally increase O2 extraction
Increases in O2 demand must be met by
increased coronary blood flow

67. Myocardial Oxygen Demand

68. Myocardial Oxygen
Consumption
Oxygen consumption is defined as the
volume of oxygen consumed per minute
(usually expressed per 100 grams of
tissue weight)

69. Myocardial Oxygen Demand
is Related to Wall Stress
LaPlace’s Law
h
Pr

Wall Stress
P
r
Wall Stress
h

70. Factors Increasing
Myocardial Oxygen Consumption
Increased Heart Rate
Increased Inotropy (Contractility)
Increased Afterload
Increased Preload
Changes in preload affect myocardial oxygen
consumption less than do changes in the other factors

71. Oxygen Cost of Myocardial
Work
Pressure work is much more costly than
volume work for the heart
Pressure work = increasing arterial pressure
at a constant cardiac output
Volume work = increasing cardiac output
while maintaining a constant pressure

72. Volatile anaesthetics & coronary circulation
Volatile anesthetics cause direct coronary artery
vasodilation in vitro.
myocardial oxygen consumption (MVO2 )--heart
rate, preload, afterload, and inotropic state, cause
coronary vasoconstriction in vivo via metabolic
autoregulation
Direct and indirect actions ultimately determines the net
effect.
Halothane produces coronary artery dilation in arteries
larger than 2000 um.

73. Halothane – direct myocardial depression – dec.BP
Coronary Blood flow dec. coz of low BP
But O2 demand also decreases so CPP maintained
Isoflurane causes vasodilation of predominantly small
(<900 um) canine epicardial coronary arteries.
Isoflurane, desflurane, and sevoflurane little cardiac
depression.
Enflurane – same profile as Halothane.

74. Coronary Artery Steal
Absolute decrease in collateral dependent myocardial
perfusion at the expense of an increase in blood flow to a
normally perfused area of myocardium, as may follow the
drug-induced vasodilation of coronary arterioles
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