Download Coronary Circulation

Coronary Circulation
Dr. Meg-angela Christi Amores
Physiologic Anatomy
• main coronary arteries lie on the surface
• smaller arteries then penetrate from the
surface into the cardiac muscle mass
Physiologic Anatomy
– left coronary artery supplies mainly the anterior
and left lateral portions of the left ventricle
– right coronary artery supplies most of the right
ventricle as well as the posterior part of the left
ventricle
Coronary Circulation
• coronary venous blood flow from the left
ventricular muscle returns by way of the
coronary sinus
• most of the coronary venous blood from the
right ventricular muscle returns through small
anterior cardiac veins
Variations in Blood Flow in Different
Tissues and Organs
ORGAN
PERCENT
Brain
14
Heart
4
Bronchi
2
Kidneys
22
Liver
27
Muscle
15
Bone
5
Skin
6
Thyroid
1
Adrenal glands
0.5
Others
3.5
The resting coronary blood flow in the human being averages about 225 ml/min
Coronary Circulation
• In exercise, heart in the young adult increases
its cardiac output fourfold to sevenfold
• Work output of heart increases 6 – 9fold
• Coronary blood flow increases 3 – 4fold
• "efficiency" of cardiac utilization of energy
increases to make up for the relative
deficiency of coronary blood supply
• coronary capillary blood flow in the left ventricle
• muscle falls to a low value during systole
– reason for this is strong compression of the left ventricular
muscle around the intramuscular vessels during systolic
contraction.
Control of Coronary Blood Flow
• Local Muscle Metabolism
– Primary controller of coronary blood flow
– local arteriolar vasodilation in response to cardiac
muscle need for nutrition
– whenever the vigor of cardiac contraction is
increased, regardless of cause, the rate of
coronary blood flow also increases
Control of Coronary Blood Flow
• Oxygen Demand
– Blood flow in the coronaries usually is regulated
almost exactly in proportion to the need of the
cardiac musculature for oxygen
– 70 per cent of the oxygen in the coronary arterial
blood is removed as the blood flows through the
heart
– coronary blood flow does increase almost in direct
proportion to any additional metabolic
consumption of oxygen
Mechanism
• decrease in the oxygen concentration in the heart
causes vasodilator substances to be released
• very low concentrations of oxygen in the muscle
cells, large proportion of the cell's ATP degrades to
adenosine monophosphate
• further degraded and release adenosine into the
tissue fluids of the heart muscle
• resultant increase in local coronary blood flow
Nervous Control Of Coronary blood
Flow
• Stimulation of AUTONOMIC nerves
– Affect coronary blood flow DIRECTLY and
INDIRECTLY
– Direct:
• Acetylcholine from VAGUS nerves and EPINEPHRINE or
NOREPINEPHRINE from sympathetic nerves
– Indirect:
• secondary changes in coronary blood flow caused by
increased or decreased activity of the heart
• Plays more important role in NORMAL control
Direct effect on Coronary Vasculature
• acetylcholine released by parasympathetic
stimulation has a direct effect to dilate the
coronary arteries
• distribution of parasympathetic (vagal) nerve
fibers to the ventricular coronary system is not
very great
• more extensive sympathetic innervation
Direct effect on Coronary Vasculature
• sympathetic transmitter substances
norepinephrine and epinephrine can have
either vascular constrictor or vascular dilator
effects, depending on the presence or
absence of constrictor or dilator receptors
• constrictor receptors -alpha receptors
• dilator receptors - beta receptors
• epicardial coronary vessels have a
preponderance of alpha receptors
Special Features of Cardiac Muscle
• under resting conditions
– consumes fatty acids to supply most of its energy
instead of carbohydrates
• under anaerobic or ischemic conditions
– must call on anaerobic glycolysis mechanisms for
energy
– Consumes large amounts of glucose
– Forms large amounts of LACTIC ACID - causes of
cardiac pain
• To be continued.....
Ischemic Heart Disease
• HYPOXEMIA vs ISCHEMIA
• What is hypoxemia?
– Decreased oxygen concentration in the blood
• What is ischemia?
– Diminished coronary blood flow
Ischemic Heart Disease
• most common cause of death in Western culture
• results from insufficient coronary blood flow
• Atherosclerosis is most frequent cause
– people who eat excessive quantities of cholesterol
– Sedentary lifestyle
– large quantities of cholesterol gradually become
deposited beneath the endothelium
– invaded by fibrous tissue and frequently become
calcified
Ischemic Heart Disease
• Acute coronary occlusion
– most frequently occurs in a person who
already has underlying atherosclerotic
coronary heart disease
– The atherosclerotic plaque can cause a local
blood clot called a thrombus
– clot breaks away from its attachment on the
atherosclerotic plaque – embolus
– that local muscular spasm of a coronary artery
also can occur
Collateral Circulation
• In a normal heart, almost no large communications exist
among the larger coronary arteries
• anastomoses do exist among the smaller arteries sized 20 to
250 micrometers in diameter
• When a sudden occlusion occurs in one of the
larger coronary arteries, the small anastomoses
begin to dilate within seconds
• diameters of the collateral vessels do not enlarge
much more for the next 8 to 24 hours
• collateral flow does begin to increase, doubling
by the second or third day and often reaching
normal or almost normal coronary flow within
about 1 month
• When atherosclerosis constricts the coronary
arteries slowly over a period of many years
rather than suddenly, collateral vessels can
develop at the same time while the
atherosclerosis becomes more and more
severe
Myocardial Infarction (MI)
• area of muscle that has either zero flow or so
little flow that it cannot sustain cardiac muscle
function is said to be infarcted
• after infarction occurs, small amount of
collateral blood seeps, lead to overfilling of
stagnant blood
• LAST amount of oxygen is used,
• Muscle becomes bluish
Causes of death after MI
• (1) decreased cardiac output;
• (2) damming of blood in the pulmonary blood
vessels and then death resulting from
pulmonary edema;
• (3) fibrillation of the heart; and, occasionally,
• (4) rupture of the heart
Cardiogenic shock
• heart becomes incapable of contracting with
sufficient force to pump enough blood into
the peripheral arterial tree
• always occurs when more than 40 per cent of
the left ventricle is infarcted
• death occurs in about 85 per cent of patients
Damming of venous blood
• Mostly in the lungs
• acute pulmonary edema
Fibrillation of ventricles
• Tendency is great if the infarct is large
• Dangerous times:
– during the first 10 minutes after the infarction
– 1 hour or so later and lasting for another few
hours
• Causes: loss of K, injury current, powerful
sympathetic reflex, cardiac muscle weakness
dilates ventricles
Rupture of infarcted area
• dead muscle fibers begin to degenerate
• heart wall becomes stretched very thin
• systolic stretch becomes greater and greater
until finally the heart ruptures
• Lead to cardiac tamponade
• compression of the heart from the outside by blood
collecting in the pericardial cavity
MI
• Normally, a person cannot "feel" his or her
heart
• ischemia causes the muscle to release acidic
substances, such as lactic acid
Angina Pectoris
• hot, pressing, and constricting Cardiac pain
that appears with exertion
• whenever the load on the heart becomes too
great in relation to the available coronary
blood flow
• felt beneath the upper sternum over the heart
• Radiates to left arm and left shoulder but also
frequently to the neck and even to the side of
the face
Surgical Treatment
• Aortic-Coronary Bypass Surgery
• Coronary Angioplasty