Coronary circulation

Physiology of Coronary Circulation,Factors affecting it.First MBBS Lecture

2. Left

3. Coronary Circulation
Two coronary arteries(Rt & Lt)
Arises from the root of aorta
Supply blood to myocardium.

6. Left Coronary artery

11. Coronary Circulation
RCA → post.
Interventricular branch
→marginal br.
LCA → Ant.
Interventricular branch
→ circumflex
→marginal br.

15. RIGHT CORONARY
LEFT CORONARY
CONUS ACUTE MARGINAL POSTERIOR DESCENDING ARTER
LCMA LCX LAD OM PL OM 1 2

19. Left Coronary Artery

20. Left Coronary Artery

26. External Heart: Posterior View
Figure 18.4d

27. Coronary Circulation: Venous
Supply
Figure 18.7b

32. Coronary Circulation
RCA –supply blood to-
-RV, RA,
-post. Part of I.V.
septum
-major part of
conducting system
including SAN
LCA supply blood to --
-LV, LA,
-ant. Part of I.V. septum
-part of Lt. bundle branch

34. Coronary Circulation
All major arteries travel in epicardium
therefore called as superficial vessels.
They subdivide & send penetrating
branchesthrough the myocardium.

38. Characteristics of coronary
Circulation
Blood flow variations in coronaries
-In 50% individuals RCA has greater
flow
-In 20% LCA, &
-In 30% flow is equal in both LCA &RCA

39. Characteristics of coronary
Circulation
Normal blood flow at rest –250 ml ( 70ml / 100
gm / mt )
–@ 5% of CO
During exercise –3-6 fold increase in flow
LV blood flow –80 ml / 100 gm / mt
RV blood flow –40 ml / 100 gm / mt
LA blood flow –20 ml / 100 gm / mt
RA blood flow –10 ml / 100 gm / mt

40. Characteristics of coronary
Circulation
O
2consumption of myocardium
Very high -@ 8 ml / 100 gm / mt at rest
Other tissues extract 25% O
2 / unit of blood
But myocardium extract 70-80% O
2 / unit of
blood
During exercise O
2 extraction reaches to
100 % & B. flow also increases.

41. Comparison of oxygen supply & consumption by
myocardium and other body tissues
Oxygen content Other tissues Myocardium
-Arterial 19 ml % 19 ml %
-Venous 14 ml % 06 ml %
AV Difference 05 ml % 13 ml %
Coefficient of O
2utilization 5/19 x100 13/19 x 100
= 26 % = 69%
O
2saturation of venous blood 14/19 x100 06/19 x 100
= 74 % = 31 %
pO
2 40 mm Hg < 20 mm Hg

42. Phasic changes in coronary blood flow
Myocardial blood flow depends upon
-pressure head i.e. aortic pressure
-resistance offered to blood flow during
various phases of cardiac cycle.

49. Blood flow to LV during systole
Like sk. Muscle myocardium
compresses coronary
vessels during systole.
LV pressure (121) > aortic
pr. (120).
So LV blood flow practically
ceases to LV (max during
isovolumetric contraction
phase) especially in
subendocardial portion. So
this part is prone to
ISCHEMICchanges.
Epicardial parts do receive
some B. flow during systole.

50. Blood flow to LV during diastole
Myocardial muscles
relax during diastole &
B.flow rises(max
during isovolumetric
relaxation phase)
Aortic pr. > LV pr. so
blood flow rises

51. Right coronary blood flow
Left coronary blood flow
*The peak left coronary flow
occurs at the end of isovolumetric
relaxation
*

52. Blood flow to RV, RA & LA
Rt. coronary blood flow shows similar
phasic changes as in Lt. coronary A.
Pressure in aorta > RV & in aorta > RA
during systole so coronary flow in these
three parts is not appreciably reduced.
Thus blood flow to RV, RA & LA occurs
both during systole & diastole.

53. Applied aspects
Subendocardial parts are more prone to ischemic
changes as during systole blood flow ceases to
LV
In AS (aortic stenosis) LV pressure > aorta
causing severe compression of coronaries.during
systole leading to ischemic changes.
In CHF, venous pr. > aortic pr. In diastole causing
decreased coronary perfusion pr. & low coronary
blood flow.

54. Regulation of coronary blood flow
Three mechanisms
1. Local control mechanism
2.Nervous control mechanism
3. Neuro -hormonal control

55. 1. Local control mechanism
a. Autoregulation
b. Role of local metabolites
c. Role of endothelial cells

56. a. Autoregulation
It is the ability of tissues/organ to maintain a
relatively constant blood flow over a wide
range of arterial blood pressure.
By
Adjusting vascular resistance according to
changes in arterial pressure.

58. a. Autoregulation
Autoregulation is well developed in –
-Kidney
-Heart
-Brain
-Sk. Muscles & mesentary

60. a. Autoregulation
Two mechanisms –
(i) Metabolic theory
↓ BP → ↓ B. flow → ↑ local accumulation of
vasodilator subs. e.g.CO2,
B.flow comes H+, adenosine, NO, PG,
to normal K+, PO4--, ↑ O2
↓ resistance art. dilatation

61. a. Autoregulation
(ii) Myogenic theory
Vascular smooth muscles respond to wall
tension depends on art. Pressure & radius.
↑ BP → ↑ stretching of wall → VSM contracts
↓
↓ BP ← ↓ B. flow ← narrowing of lumen

62. Reactive hyperemia
Definedas increased blood flow to the
organ/tissues after the removal of blockage
in a previously blocked artery.
Magnitudeof reactive hyperemia depends
on –duration of occlusion
Causeof R. hyperemia –adenosine
release

63. b. Role of local metabolites
Atrestmyocardium extracts 60 -70 % O
2
from Hb.
So not much additional O
2can be provided to
myocardium unless blood flow increase due to
vasodilation.
Causeof vasodilation –Adenosine release in
hypoxic states. Most imp. factor
B. flow ↑ ― myocardial O
2 consumption ↑(linear
relation)

65. b. Role of local metabolites
Direct effect of ↓ pO
2
on arterioles
vasodilation
Role of other metabolites -H
+
, NO, PG,
adenosine, CO
2 etc. are vasodilators.

66. Role of endothelial cells
Endo. Cells release several vasodilators
e.g. EDRF, prostacyclin (PGI2) & EDHF
Endo. Cells also release several
vasoconstrictors e.g. endothelin-1(ET-1),
Angiotensin II, EDCF.

67. Nervous control
ANS control CBF –
a. Directly
b. Indirectly
a.Direct nervous control is exerted via
symp. & parasymp effects on coronary
vessels.
b.Indirect nervous control is exerted via
symp. & parasymp effects on heart.

68. Direct nervous control
Parasymp.nervesto coronaries are too less there
fore have a negligible effect.
Symp.Nervesextensively innervates coronary
vessels.
Receptors–α-present mainly on epicardial vessels
β-present mainly on intramuscular
vessels
NT-NE reacts with α→ vasoconstriction
-E reacts with β→ vasodilation
Net effectis vasodilatation

69. Indirect Nervous control
Through action on heart
Symp. Stimulation → ↑ HR & force of contr
↓
↑B. flow ← ADP cause ← ADP ← ATP
vasodilation conversion
Parasymp. Stimulation produce opp. effect

70. Neuro –hormonal control
ATP →vasoconstriction (P1 receptors)
→ vasodilation (P2 receptors)
NPY (neuropeptide Y) →vasoconstriction
CGRP (calcitonin gene related peptide)
&
Substance P →vasodilation

75. Coronary Artery Disease

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Coronary Artery Disease
Coronary artery disease is one of the most common
and serious effects of aging.
Fatty deposits build up in blood vessel walls and
narrow the passageway for the movement of blood.
The resulting condition, called atherosclerosis often
leads to eventual blockage of the coronary arteries
and a “heart attack”.

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