
Lect. 18
The Coronary Circulation
Objectives:
1. Describe the intrinsic mechanisms involved in the outoregulation
of coronary blood flow.
2. ?????????????
Arterial supply:
Immediately after aorta leaves left ventricle, it gives right and left
coronary arteries.
The left coronary artery passes under the left auricle and divides into two
branches:
The anterior interventricular artery; travels down the anterior
interventricular sulcus toward the apex. It gives smaller branches to
the interventricular septum and anterior walls of both ventricles.
Clinically, this vessel is also called the left anterior descending
(LAD) artery.
The circumflex artery; continues around the left side of the heart in
the coronary sulcus. It supplies blood to the left atrium and
posterior wall of the left ventricle.
The right coronary artery supplies the right atrium, continues along the
coronary sulcus under the right auricle, and then gives two branches:
The marginal artery supplies the lateral aspect of the right atrium
and ventricle.
The
posterior
interventricular
artery
travels
down
the
corresponding sulcus and supplies the posterior walls of both
ventricles.
An interruption of the blood supply to any part of the myocardium can
cause necrosis within minutes. A fatty deposit or blood clot in the
coronary artery can cause a myocardial infarction (MI). The coronary
circulation has a defense against such an occurrence by mean of the
anastomoses where two arteries come together and combine their flow to
supply distal tissue. Thus, if one artery becomes obstructed, blood
continues to reach myocardial tissue through the alternative route. The
most important anastomoses is the point at which the circumflex artery
and right coronary artery meet on the posterior side of the heart; they
combine their blood flow into the posterior interventricular artery.
Another is the meeting of the anterior and posterior interventricular
arteries at the apex of the heart.
Venous Drainage:

Venous Drainage refers to the route by which blood leaves an organ.
After flowing through capillaries of the myocardium, a bout 20% of the
coronary blood empties directly from small veins into the right ventricle.
The other 80% return to the right atrium by:
The great cardiac vein.
The middle cardiac vein.
The coronary sinus; collects blood from the upper veins and
smaller cardiac veins. It passes across the posterior aspect of the
heart in the coronary sulcus and empties blood into the right
atrium.
Factors affecting the coronary blood flow:
The coronary blood flow is affected by four types of factors:
Metabolic factors:
The coronary blood flow is regulated mainly by the metabolic needs of
the heart (metabolic autoregulation). Any increase in metabolic activity
leads to a parallel increase in coronary blood flow. This is induced by
coronary vasodilation. Coronary vasodilation during high metabolic
activity is caused by:
Local hypoxia, hypoxia is a strong coronary vasodilator.
Adenosine is a strong coronary vasodilator released by cardiac
cells. It is probably the main coronary vasodilator during high
cardiac activity.
Lactic acid, Hypercapnia, Endothelial-derived relaxing factor
(EDRF), increased extracellular K
+
level, Prostaglandins,
Histamine, and H+ ion.
All these factors are released during the normal metabolic reactions of the
myocardial cells causing some degree of coronary vasodilation. With
increased metabolic activity they are released in higher amounts leading
to more dilation. During low activity periods of the heart, the amount of
released metabolites decreases. This leads to coronary vasoconstriction
and reduction in coronary blood flow.
Mechanical factors:
The phase of the cardiac cycle: The left ventricle gets its blood
supply mainly during diastole. The highest coronary flow occurs
during the isometric relaxation phase. During the isometric
contraction phase, the left ventricular myocardial fibers squeeze the

coronary vessels between them, stopping the blood flow in them.
The aortic pressure: As the aortic pressure is the perfusion pressure
for the coronary blood flow, acute changes in aortic blood pressure
are accompanied with parallel changes in the coronary blood flow.
However, if the change is long lasting, the tone of the coronary
vessels is readjusted to maintain adequate coronary flow regardless
of the pressure level (autoregulation of the coronary blood flow).
The heart rate: An increase in the heart rate influences the coronary
blood flow in two opposite ways:
It decreases the diastolic period, so decreasing the coronary
blood flow.
It increases the metabolic activity, so increasing the coronary
blood flow.
A decrease in heart rate decreases the metabolic activity and
decreases the amount of vasodilator metabolites.
Nervous factors:
Sympathetic stimulation has a direct vasoconstrictor effect on the
coronary vessels by stimulating the α-adrenergic receptors. In vivo,
however, sympathetic stimulation increases the metabolic activity of the
heart which has a strong dilator effect on the coronaries. So, the net effect
of sympathetic stimulation is coronary vasodilation.
Parasympathetic vagal stimulation dilates the coronaries, but because it
decreases the heart rate, metabolic activity decreases and coronary flow
decreases.
Hormonal factors:
Noradrenaline is secreted by the sympathetic nerves and the
adrenal medulla. It is a strong vasoconstrictor of the coronaries by
stimulating the α-adrenergic receptors.
Adrenaline is secreted by the adrenal medulla during the alarm
response. It stimulates the α- receptors as well as the metabolic
activity of the heart leading to coronary vasodilation.
Vasopressin (also called antidiuretic hormone - ADH). It is a
hormone secreted by the posterior pituitary gland in response to
hypovolemia or plasma hypertonicity. It is a strong vasoconstrictor
of all vessels including the coronaries. It acts on blood vessels only
when found in high concentrations. In lower concentrations, it acts

only on the kidney to conserve water.
Angiotensin II is formed during hypotension, hypovolemia,
hyponatremia or renal ischemia. It is a powerful constrictor of
vessels including the coronaries.
Coronary anastomoses and angiogenesis:
With sudden occlusion of a coronary artery, the small anastomoses dilate
within few seconds (metabolic autoregulation). These vessels supply
about 15% of the basal blood supply to the ischemic area. Angiogenesis
is stimulated by the severe local hypoxia. New vessels appear and start to
allow blood flow after 8-24 hours. After 24-48 hours, the blood flow to
the ischemic area reaches 30-40% of the basal level. Angiogenesis
continues at a lower rate afterwards to take the flow back to the normal
basal level in about one month. Further increase in local blood flow
occurs by more angiogenesis if the metabolic needs of the heart are
increased.
CHARACTERISTICS OF CORONARY CIRCULATION:
It is a very short, very rapid circulation.
It is a very rich circulation. The heart weighs about 320 gm {~
0.5%
of
the body weight), and receives 200 mL blood/min (~ 4% of the
cardiac
output). There is one capillary for each myocardial fiber.
It is the only circulation where blood flow occurs mainly during
diastole.
It is regulated mainly by the amount of metabolites released from
the
cardiac muscle cells (metabolic autoregulation), not by autonomic
nerve
supply.
High capillary permeability, the lymph from the heart contains 4%
proteins.
Very low venous O
2
reserve. So, any increase in the metabolic
activity
of
the heart should be accompanied by a parallel increase in coronary
blood
flow.
OXYGEN CONSUMPTION OF THE HEART:

The normal heart, during rest, consumes 25 mL O
2
/min {8 mL/100
gm/min). This is the "resting O
2
consumption". It may increase up to 150
mL/min with maximum exertion. The metabolic reactions in the heart are
mostly aerobic. That is why the cardiac performance is rapidly and
seriously deteriorated in hypoxia.
OXYGEN SUPPLY TO THE HEART
The O
2
content of arterial blood is 19.5 mL/dL. So, the coronary blood
flow (200 mL/rain) supplies the heart with 39 mL O
2
/min. This is called
the "resting total Oj supply" to the heart. The heart normally extracts 12.5
mL O2 /dL of coronary blood supply, i.e. an O2 extraction coefficient of
65%.
When the metabolic activity of the heart increases, the heart can extract
up to 15.5 mL O2 /dL of coronary blood supply, i.e. an O2 extraction
coefficient of 80%. The maximum volume of O2 that can be extracted by
the heart from the coronary blood flow is called the "effective O2 supply"
to the heart (« 150 mL).
under nonphysiological conditions, e.g. coronary atherosclerosis where
coronary vessels can not dilate to the normal maximal limits, the increase
in the coronary blood flow does not match the metabolic activity he heart
and an increase in heart rate results in coronary insufficiency.
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