Coronary Circulation Physiology
Coronary Circulation Physiology
Coronary Circulation Physiology
Lesson outcomes
Explain haemodynamic basis of fluctuation in
coronary blood flow in the left and right
ventricles during a cardiac cycle
Describe neural and chemical control of
coronary blood flow
Explain the interaction between systemic
regulatory mechanisms (sympathetic nervous
system) and the local auto-regulatory
mechanisms (metabolites) in the control of
coronary blood flow
Introduction
About one third of all deaths in industrialized
countries of the Western world result from
coronary artery disease, and almost all elderly
people have at least some impairment of the
coronary artery circulation
For this reason, understanding normal and
pathological physiology of the coronary
circulation is one of the most important subjects
in medicine
%
% cardiac
body
output @
weigh rest
t
Normal flow
Maximal flow
(ml/min per
100 g)
(ml/min per
100 g)
Heart
0.5
80
400
Brain
14
55
150
40
18
60
10
150
0.5
20
400
600
Skeleta
l
muscle
Skin
Kidney
s
Autonomi
c Nervous
System
(direct
and
indirect
effects)
Local
Pressure
changes
in
Ventricula
r walls
during
Cardiac
Cycle
Neural
Haemodynamic
Regulatory Mechanisms
Myocardi
al Oxygen
demand
and Local
Metabolit
es
Haemodynamic
Coronary capillary blood flow in the ventricle
muscle falls to a low value during systole, which
is opposite to flow in vascular beds elsewhere in
the body. The reason for this is strong
compression of the left ventricular muscle
around the intramuscular vessels during systolic
contraction
During diastole, the cardiac muscle relaxes and
no longer obstructs blood flow through the left
ventricular muscle capillaries, so blood flows
rapidly during all of diastole
Haemodynamic
Blood flow through a particular segment of
coronary artery depends on the gradient
between the aortic pressure and that segment
of the coronary artery
The intra-ventricular pressure decreases
progressively as it moves away from the point of
application, compressing maximally the
endocardial arteries and minimally the
epicardial arteries
10
Neural
Stimulation of the autonomic nerves to the
heart can affect coronary blood flow both
directly and indirectly
The direct effects result from action of the
nervous transmitter substances acetylcholine
from the vagus nerves and norepinephrine and
epinephrine from the sympathetic nerves on the
coronary vessels themselves.
Indirect effects result from secondary changes
in coronary blood flow caused by increased or
decreased activity of the heart
11
Neural
Parasympathetic
stimulation
Sympathetic
stimulation
Cardiac Muscle
HR,
Contractility
HR,
Contractility
Coronary
Vessels
Dilated (weak
effect)
Constricted ()
Dilated (2)
12
1 and 2
Receptors in
Ventricles
Indirect
Effects:
Vasodilation
of Coronary
Arteries
HR
Force
of
Contractio
n
Sympathetic
How?
Direct Effects:
Vasoconstricti
on of
Coronary
Arteries
Receptors in
Coronaries
Vasoconstric
tion
Receptors in
Coronaries
Vasodilation
13
Neural
The indirect effects, which are mostly opposite
to the direct effects, play a far more important
role in normal control of coronary blood flow
Thus, sympathetic stimulation increases both
heart rate and heart contractility and increases
the rate of metabolism of the heart. In turn, the
increased metabolism of the heart sets off local
blood flow regulatory mechanisms for dilating
the coronary vessels, and the blood flow
increases approximately in proportion to the
metabolic needs of the heart muscle
14
Autoregulation
The capacity of tissues to regulate their
own blood flow
Well developed in the:
Heart (myocardium)
Brain
Kidneys
Exercising skeletal muscles
Theories of autoregulation:
Myogenic theory
Metabolic theory
15
Local (Autoregulation)
Blood flow through the coronary system is
regulated mostly by local arteriolar vasodilation
in response to the nutritional needs of cardiac
muscle
That is, whenever the vigor of cardiac
contraction is increased, the rate of coronary
blood flow also increases
Blood flow in the coronary arteries usually is
regulated almost exactly in proportion to the
need of the cardiac musculature for oxygen
16
Local (Autoregulation)
The exact means by which increased oxygen
consumption causes coronary dilation has not been
determined
It is speculated by many research workers that a
decrease in the oxygen concentration in the heart
causes vasodilator substances to be released from the
muscle cells
A substance with great vasodilator propensity is
adenosine
In the presence of very low concentrations of oxygen in the
muscle cells, a large proportion of the cells ATP degrades to
adenosine monophosphate; then small portions of this are further
degraded and release adenosine into the tissue fluids of the
heart muscle, with resultant increase in local coronary blood flow
17
Local (Autoregulation)
Adenosine is not the only vasodilator product
that has been identified
Other Vasodilator Metabolites (VDMs) include
adenosine phosphate compounds, potassium
ions, hydrogen ions, carbon dioxide,
prostaglandins, and nitric oxide
18
Overall effect
Sympathetic activity directly causes coronary
vasoconstriction; at the same time, it causes
increased heart rate and contractility raising
cardiac work and metabolism
Increased production of vasodilator metabolites
(VDMs)
The effect of VDMs eventually overcomes the
direct coronary vasoconstrictor effect of
sympathetic nervous system
Thus the net effect of sympathetic activity is
coronary vasodilation secondary to increased
metabolic activity
19
20
Ischaemic Heart
Disease
21
22
Coronary angiography
Coronary angiography
involves the injection of a
radiocontrast dye into
the left and right
coronary arteries. X-ray
images are taken from
various angles in order to
observe fully any
narrowings. This
information may be
useful in assessing the
degree toShows
whichthe
vessels
anatomy of
may be narrowed
coronary vessels
23
Doppler ultrasonography
A non-invasive
alternative, Doppler
ultrasonography,
measures the direction
and speed of blood flow
and has more commonly
been used to evaluate
the degree of impairment
in patients with heart
failure. It can also be
used to evaluate blood
flow in the coronary
vessels.
Thank you
SufyanAkram@imu.edu.m
y
DID: 03 2731 7480
Ext: 2773
Faculty area 2 @ Level
2
25