Coronary Circulation

 Two coronary arteries(Rt & Lt)

 Arises from the root of aorta
 Supply blood to myocardium.
Coronary Circulation
 RCA → post.
Interventricular branch
→marginal br.
 LCA → Ant.
Interventricular branch
→ circumflex
→marginal br.
External Heart: Posterior View

Figure 18.4d
Coronary Circulation: Venous
Supply

Figure 18.7b
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
Coronary Circulation
 All major arteries travel in epicardium
therefore called as superficial vessels.
 They subdivide & send penetrating
branches through the myocardium.
 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
 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
 Characteristics of coronary
Circulation
O2 consumption of myocardium
 Very high - @ 8 ml / 100 gm / mt at rest
 Other tissues extract 25% O2 / unit of blood
 But myocardium extract 70-80% O2 / unit of
blood
 During exercise O2 extraction reaches to
100 % & B. flow also increases.
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 O2 utilization 5/19 x100 13/19 x 100
= 26 % = 69%
O2 saturation of venous blood 14/19 x100 06/19 x 100
= 74 % = 31 %
pO2 40 mm Hg < 20 mm Hg
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.
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
ISCHEMIC changes.
 Epicardial parts do receive
some B. flow during systole.
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
 * The peak left coronary flow
occurs at the end of isovolumetric
relaxation

*
Left coronary blood flow

Right coronary blood flow

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.
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.
Regulation of coronary blood flow
 Three mechanisms
1. Local control mechanism
2.Nervous control mechanism
3. Neuro - hormonal control
1. Local control mechanism
 a. Autoregulation
 b. Role of local metabolites
 c. Role of endothelial cells
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.
a. Autoregulation
Autoregulation is well developed in –
- Kidney
- Heart
- Brain
- Sk. Muscles & mesentary
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

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
Reactive hyperemia
 Defined as increased blood flow to the
organ/tissues after the removal of blockage
in a previously blocked artery.
 Magnitude of reactive hyperemia depends
on – duration of occlusion
 Cause of R. hyperemia – adenosine
release
b. Role of local metabolites
 At rest myocardium extracts 60 - 70 % O 2
from Hb.
 So not much additional O2 can be provided to
myocardium unless blood flow increase due to
vasodilation.
 Cause of vasodilation – Adenosine release in
hypoxic states. Most imp. factor
 B. flow ↑ ― myocardial O2 consumption ↑(linear
relation)
b. Role of local metabolites
 Direct effect of ↓ pO2 on arterioles
vasodilation
 Role of other metabolites - H+, NO, PG,
adenosine, CO2 etc. are vasodilators.
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.
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.
Direct nervous control
 Parasymp.nerves to coronaries are too less there fore
have a negligible effect.
 Symp. Nerves extensively 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 effect is vasoconstriction
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
Neuro – hormonal control
 ATP → vasoconstriction (P1 receptors)
→ vasodilation (P2 receptors)
 NPY (neuropeptide Y) → vasoconstriction
 CGRP (calcitonin gene related peptide)
&
 Substance P → vasodilation