The Coronary Circulation
Arterial supply:
immediately after the aorta leaves the 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 off 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 a
coronary artery can cause a myocardial infarction (MI), the sudden tissue.
The coronary circulation has a defense against such an occurrence by
mean of the anastomoses where two arteries come together and combine
their blood flow to supply distal tissue.. Thus, if one artery becomes
obstructed, some blood continues to reach myocardial tissue through the
alternative route. The most important anastomosis 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, about 20%
of the coronary blood empties directly from small veins into the right
ventricle. The other 80% returns 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 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. In the right ventricle, the contraction of
the myocardial fibers is weaker. It does not stop the flow in the right
coronary vessels, so the flow in them is continuous throughout the cardiac
cycle.
• The aortic pressure: As 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 periods 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. This decreases the
coronary blood to parallel the decrease in cardiac metabolism.
Nervous factors:
Sympathetic stimulation has a direct vasoconstrictor effect on the
coronary vessels by stimulating the
ߙ -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
ߙ -adrenergic receptors. It is a weaker stimulant of myocardial
metabolism. The net effect is a weak coronary vasoconstriction.
• Adrenaline is secreted by the adrenal medulla during the alarm
response. It stimulates the
ߙ - and B-adrenergic 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 hypovolemic or
plasma hyperonicity. 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,
hypernatremia 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 hack 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.
The cerebral circulation
Physiological anatomy:
The brain is supplied by the internal carotid and vertebral arteries,
which form the circle of Willis, From each side of the circle arise three
cerebral arteries; anterior, middle and posterior. They run along the
convex surface of the cerebral hemispheres to supply the cerebral cortex
and send deep branches to supply the subcortical structures.
With the exception of the circle of Willis, there is no anastomosis
between the intracranial arteries, but some anastomoses exist between the
smaller arterioles. Still, these anastomoses are inadequate to nourish the
brain tissue when an arterial branch is occluded. That is why the cerebral
arteries are considered functionally as end- arteries.
The superficial and deep veins drain the cerebral blood into the
large venous sinuses which exist between the folds of the dura mater. The
venous sinuses are prevented from collapse by the tough structure of the
dura and the attachment of their walls to the bones of the skull. The
cerebral venous blood is drained from the sinuses by the jugular veins,
mainly the internal jugular in man.
In contrast to the arterial supply, the cerebral venous system
contains plenty of anastomoses between the superficial and deep veins,
and between the intra- and extra cranial veins. That is why occlusion of
the internal jugular veins does not arrest the cerebral venous return, even
if it is bilateral.
Autoregulation of the cerebral blood flow:
A sudden rise in the arterial blood pressure (ABP) leads to transient
increase in the cerebral blood flow. If the rise in pressure is maintained,
autoregulation mechanisms operate to restore the cerebral blood flow
back to its normal basal level within 1-2 minutes. The cerebral blood flow
is autoregulated in the blood pressure range of 70-140 mmHg in normal
persons or up to 180 mmHg in hypertensive persons. The cerebral blood
flow is regulated in response to a rise in ABP by the following
mechanisms:.
1. Myogenic vasoconstrictor response; caused b the increased tension in
the vascular wall.
2. Metabolic vasoconstriction response; caused by washing out the
vasodilator metabolites released by brain metabolism.
3. Neurosympathetic response; sympathetic stimulation constricts the
cerebral blood vessels.
A fall in the ABP leads to the opposite mechanisms with a resultant
vasodilation to maintain a constant blood flow rate.
Control of the cerebral blood flow:
Three main control mechanisms regulate adjust the cerebral blood
flow:
Nervous control:
The cerebral blood vessels receive sympathetic nerve supply from
the cervical division of the sympathetic nervous system. It constricts the
large and intermediate arteries during sympathetic activity. Under
ordinary conditions, the vasoconstrictor effect of the sympathetic nerves
on
cerebral
vessels
is
overridden
by
the
autoregulation
mechanisms.However, sympathetic cerebral vasoconstriction is strong
and is very important in the following conditions:
•In severe muscular exercise when arterial blood pressure rises to very
high levels. Vasoconstriction of the large and intermediate vessels
protects the small vessels and prevents their rupture.
•After rupture of a small cerebral vessel, e.g. cerebral stroke,subdural
hematoma or brain tumour. Sympathetic reflexes cause severe
constriction of the large arterial supply to limit the intracranial bleeding.
Metabolic control:
The blood flow to the brain is regulated mainly by its own
metabolism.The cerebral vessels are characterized by being extremely
sensitive to hypoxia, hypercapnia and acidosis, which produce marked
vasodilation of the cerebral vessels and increase the cerebral blood flow.
Hypercapnia increases the H
2
CO
3
and H
+
levels in blood. CO
2
has no
direct vasodilator effect. It is the H
+
ion produced by the hypercapnia
which dilates thevessels.
Physical control: (by the intracranial pressure)
The intracranial cavity has a fixed volume because it is enclosed in
the rigid bones of the skull. It contains the brain, whose volume is
approximately 1500 mL, plus 75 mL of blood and 75 mL of cerebrospinal
fluid (CSF). Because the brain tissue and fluids are incompressible, the
total volume of the blood, the CSF and the brain is constant at any time. It
follows that:
1. Any rise in the intracranial pressure compresses the cerebral vessels
and reduces the cerebral blood flow. A drop in the intracranial pressure
expands (dilates) the vessels and: increases the cerebral blood flow.
2. Any change in the venous pressure immediately causes a similar
change in the intracranial pressure which influences the cerebral blood
flow.