Coronary circulation

Introduction

• The heart is supplied by two coronary arteries, right and

left, arising from the root of the ascending aorta.
Right coronary artery:
• Traverse along the A-V sulcus to the back of the heart, and
gives out several descending branches to both ventricles.
• Terminates by anastomosing with left coronary artery.
• Supplies:
– Whole of rt. Atrium
– Greater part of rt. ventricle
– A small part of ventricle near posterior inter-ventricular groove.
– Posterior part of inter-ventricular septum, and
– Major portion of the conducting system of the heart, including
SAN(60 % cases).
Left coronary artery:
• Anterior descending branch or anterior interventricular,
runs in the interventricular groove to reach the apex of the
heart and gives out septal branches.
• Left circumflex branch which runs in A-V groove to the left
and proceeds downwards as posterior descending branch.
• Supplies:
– Whole of the left atrium
– Greater part of left ventricle
– A small part of right ventricle near anterior interventricular
septum, and
– Anterior part of inter-ventricular septum
– A part of the left branch of bundle of His (A-V bundle).
• In 20% individuals myocardium is predominantly supplied by
left coronary artery; in 50% individuals supplied by right
coronary artery; and in 30% individuals it is balanced by
supplied by both.
• The left coronary artery supplies mainly the anterior surface
and left lateral portions of the left ventricle.
• The right coronary artery supplies most of the right ventricle
as well as the posterior part of the left ventricle in 80 to 90
per cent of people.
• The main coronary arteries lie on the surface of the heart and
smaller arteries then penetrate from the surface into the
cardiac muscle mass.
• Only the inner 1/10 millimeter of the endocardial surface can
obtain significant nutrition directly from intra-chamber blood.
• Normally, the coronary arteries are end arteries.
• However, the functional anastomoses are present and become
active under abnormal condition like ischaemia heart diseases.
• These anastomoses are of two types:
Cardiac anastomosis:
• Between branches of one coronary artery with that of the other.
• Branches of coronary arteries and branches of deep system of veins
Extra cardiac anastomosis : anastomosis between coronary arteries
and vessels lying outside the heart:
• Vasa-vasora of aorta
• Vasa-vasora of pulmonary arteries
• Intra thoracic arteries
• Bronchial arteries
• Phrenic arteries
 Coronary artery dominance
• The artery that gives the posterior inter-ventricular
artery branch determines the coronary dominance.
• If the posterior inter-ventricular artery is supplied by
the right coronary artery (RCA), then the coronary
circulation can be classified as "right dominant".
•If the posterior inter-ventricular artery is supplied by the
circumflex artery (CX), a branch of the left artery, then the
coronary circulation can be classified as "left-dominant".
• If the posterior inter-ventricular artery is supplied by
both the right coronary artery (RCA) and the circumflex
artery, then the coronary circulation can be classified as
"co-dominant".
 Functional division
• Large coronary arteries(epicardial coronary arteries) -
lies on epicardial surface,
– conduct blood with little resistance.
• Small coronary arteries – descends into myocardium, are
of two types:
– sub-epicardial vessels and
– sub-endocardial vessels.
• Small coronary arteries are the principle resistance
vessels of the heart, change in their diameter regulate the
coronary blood flow
 Venous Drainage

• It is divided into two systems:

Superficial system: lies beneath the epicardium and it ends in
– Coronary sinus: largest vein and drains blood from myocardium
and ends in posterior wall of right atrium.
– Great cardiac vein: drains blood from left heart and ends in the
coronary sinus
– Anterior cardiac vein: receives blood mainly from the
myocardium and opens directly in the anterior wall of right
atrium.
Deep system: arise within myocardium from the fine
branches of coronary arteries, and opens directly into the
cardiac chambers via 3 sets of vessels:
– Arterio sinusoidal vessels
– luminal vessels
– Thebesian vessels.
 Lymphatics of Heart
• Lymphatics of the heart accompany the
coronary arteries and form 2 trunks.
• Right trunk ends in brachiocephalic nodes and
the left trunk into the tracheobronchial lymph
nodes at the bifurcation of the trachea.
Pecularities of coronary circulation
• BF during diastole
• End arteries
• High capillary density
• High 02 extraction
• Regulation is mainly by metabolites
• Functional anastomosis
• The coronary vessels are susceptible to degeneration and
atherosclerosis.
• There is evident regional distribution: The sub-endocardial
myocardial layer in the left ventricle receives less blood, due
to more myocardial compression (but this is normally
compensated during diastoles). However, this renders this
area more liable to ischemia and infarction
 Coronary blood flow (CBF)
• The resting coronary blood flow is about 250ml/min., which is
about 60 – 80 mL/100gm/min of heart muscle, or 4- 5 % of the
total cardiac output.
• In severe muscular exercise, the work of the heart increased by
6-9 folds and the CBF may be increased by 3-4 folds, up to 2
liters/ minute.
• 02 consumption (VO2) of the myocardium is very high (19-6=13
mL/dL).
• CBF fluctuates with each cardiac cycle, which is more notable in
LV where 80% flow occurs during diastole, 20% in systole. This
fluctuation along the phases of cardiac cycle is called phasic
coronary flow.
• In the heart, ventricular action affects the coronary circulation :
– By altering the aortic pressure
– By altering the extra-vascular pressure which varies with systole, exerting a
variable degree of compression on the coronary vessels.
• Therefore, CBF shows strong phasic variation with reference to
cardiac cycle.
• Pressure difference between aorta and LV is very small during systole,
therefore blood flows to sub-endocardial portion of LV only in
diastole.
• However, pressure gradient is more in superficial portion of LV to
permit some flow in this region throughout the cardiac cycle.
• Blood flow to RV and atria occurs both during systole and diastole.
• Systole : Aorta= 120, LV= 121, RV =25
• Diastole : aorta= 80, LV= 0, RV= 0
• In the coronary sinus the outflow of blood gradually arises from the
isovolumetric ventricular contraction phase and reaches its peak
during ‘ protodiastole’ phase and then falls.
 Clinical importance

• Variation in CBF wit heart rate.

• Sub-endocardial portion of LV is more prone to
myocardial infarction.
• In aortic stenosis:
– The pressure in the LV must be greater than that in the aorta
to eject blood.
– Therefore, coronaries are severely compressed during systole
hence lead to MI due to compression of coronaries and more
oxygen demand by ventricular muscles.
• In congestive cardiac failure, increase in venous pressure
decrease aortic diastolic pressure. Thus effective
coronary perfusion pressure falls and CBF decreases.
Compensatory mechanism in sub-endocardial portion of LV

• Sub-endocardial portion of the myocardium in

LV posses more capillaries density ( 1100
capillaries/mm2) than superficial layers (750
capillaries/mm2).
• Deep layers has minimum diffusion ( about
16.5 µm) than superficial (20.5 µm).
• Myoglobin is higher in deep layer.
FACTORS REGULATING CORONARY BL.FLOW
• Physical
• Chemical
• Neural
• Hormonal

Coronary circulation is controlled almost entirely by local metabolic factors (hypoxia

and adenosine) ; sympathetic nerves plays a minor role.
 Physical factors
Aortic blood pressure:
• CBF is directly proportional to aortic blood pressure,
especially the diastolic aortic pressure , most of CBF
occur during diastole.
• When diastolic pressure decreases when MAP is
decreased e.g. shock or aortic stenosis, the CBF
decreases.
• Blood flow to the endocardial regions is more severely
impaired than is that to the epicardial regions of the
ventricle
Heart Rate:
• • Excessive↑ in the heart rate e.g. paroxysmal
tachycardia→ ↓diastolic period→ ↓coronary filling (as it
occurs mainly during ventricular diastole)→ ↓CBF.
Cardiac Output:
• CBF is directly proportional to COP i.e. ↓COP→↓ CBF ;↑COP→
↑CBF
• Increased cardiac output→↑BP in aorta + reflex inhibition
of the vasoconstrictor tone →coronary vasodilatation→↑
CBF.
C.B.F. occurs mainly during diastole as there is compression of
coronary blood vessels during systole by the contracted
muscle fibers.
Temperature:
• Hyperthermia increases body metabolism and CBF
increases to maintain normal O2 requirement.
• Hypothermia, markedly decreases body metabolic
rate, O2 requirement decreases and CBF
decreases.
Anaemia: increases CBF
• Causes hypoxia in cardiac tissue, which causes
release of adenosine
• A compensatory increase in heart rate produces
metabolic hypoxia.
 NERVOUS FACTORS:
Direct effect:
• Parasympathetic: vagi are not poven to supply the coronary, but its
stimulation has slight dilator effect.
• Sympathetic: Both alpha and Beta receptors exist in the coronary vessels.
Sympathetic stimulation causes slight direct coronary constriction.
– the epicardial coronary vessels have a preponderance of alpha receptors, whereas the
intramuscular arteries may have a preponderance of beta receptors.
Indirect effect:
• Plays a far more important role in normal control of coronary blood flow
than the direct.
Sympathetic stimulation increase both heart rate and myocardial
contractility, as well as its rate of metabolism leading to dilatation of
coronary blood vessels.
The blood flow increase proportional to the metabolic need of heart
muscle
HORMONAL FACTOR
• Thyroxine increases the cardiac metabolism,
thus causes coronary vasodilation and increases
CBF.
• Vasopressin (antidiuretic hormone) coronary
causes vasoconstriction and decreases CBF.
 Coronary auto regulation
• If there is sudden change in aortic pressure,
coronary vascular resistance will adjust itself
proportionally within few seconds; so that a
constant blood flow is maintained.
• Range of autoregulation: 60 – 140 mmHg.
Mechanism:
• Myogenic response: an increase in passive
stretch, caused by increased perfusion pressure,
causes active smooth muscle contraction.
Chemical theory:
• Decrease perfusion pressure or hypoxia leads to
Increase adenosine which causes Vasodilatation
and increase CBF
Endothelium derived relaxation factor (EDRF):
• Hypoxia, ADP, muscular exercise, stimulate
vascular endothelium to secrete EDRF, which is a
potent vasodilator, that causes coronary dilatation
and increase CBF.
 Coronary artery disease
ANGINA PECTORIS
• Angina Pectoris means severe chest pain (usually retrosternal i.e.
behind the sternum) due to ischemia of the cardiac muscle.
• Angina pectoris is usually due to narrowing of the coronary arteries
ischemia.
• When the coronary artery is only partly obstructed (by spasm or
atherosclerosis) and the coronary blood flow is only moderately
reduced, symptoms of ischemia appears only when cardiac work is
increased by effort, exercise, excitement, food or severe cold, or anemia.

• Pain is due to accumulation of pain producing substances in the

myocardium such as, P factor, lactic acid, histamine, K, and Kinins.
pain is usually relieved by rest or drugs.
 MYOCARDIAL INFARCTION
• Myocardial Infarction means necrosis of a part of the myocardium
due to
− Severe & prolonged ischemia due to narrowing of the coronary
arteries.
− Occlusion of one of the coronary arteries or its branches by
coronary thrombosis leading to severe ischemia.
• Most common cause of MI is rupture of an atherosclerotic plaque
or hemorrhage into coronary arteries.
• Myocardial Infarction produces also chest pain which is more
severe than that of angina and it cannot be relieved by rest or
coronary VD drugs.
• It is usually complicated by fatal ventricular fibrillation.
• Common site for development of plaque is in first few
centimeters of the coronary artery.
• There is a strong positive correlation between atherosclerosis and
circulating homocysteine( damage endothelial cells).
– Converted to methionine in the presence of folate and Vit B12.
– Both vitamins lowers the incidences of coronary artery diseases.
• Atherosclerosis has an important inflammatory component and
there is a positive correlation between increased levels of C-
reactive protein and MI.
• Some serum enzymes plays an important role in the diagnosis of
MI. The enzymes most commonly measure are:
– MB isomer of creatine kinase ( CK-MB)
– Troponin I and T
– Lipoprotein a
• In ECG, there ST elevation in the lead overlying the infracted area.