Coronary Circulation

Physiology Seminar18/04/2013

PowerPoint® Seminar Slide Presentation prepared by Dr. Anwar Hasan Siddiqui, Senior Resident, Dep't of Physiology, JNMC

©Dr. Anwar Siddiqui

CORONARY CIRCULATION

• CONSIST OF 1) Arterial supply

2) Venous drainage

3) Lymphatic drainage

ARTERIAL SUPPLY

• The cardiac muscle is supplied by two coronary arteries the right and left coronary arteries.

• Both arteries arises from the sinuses behind the cusps of the aortic valves at the root of the aorta.

RT. CORONARY ARTERY

• Smaller than left coronary artery.

• Arises from anterior coronary sinus.

COURSE:• Emerges from the surface of heart

between pulmonary trunk and right auricle.

• Winds round the inferior border to reach the diaphragmatic surface to reach the posterior inter-ventricular groove.

• Terminates by anastomising with left

coronary artery

BRANCHES• Large Branches

– marginal– Post-interventricular

• Small branches:– Right atrial – Infundibular– Nodal – in 60% cases– Terminal

Anterior schematic diagram of heart shows course of dominant right coronary artery and its tributaries. AV = atrioventricular, PDA = posterior descending artery, RCA = right coronary artery, RV = right ventricular, SA = sinoatrial

AREAS OF DISTRIBUTION• Right atrium• Ventricles– Greater part of right ventricle, except the

area adjoining the anterior inter-ventricular groove.

– A small part of the left ventricle adjoining the posterior interventricular groove.

• Posterior part or the inter-ventricular septum

• Whole of the conducting system of the heart except a part of the left branch of AV bundle. The SA node is supplied by left coronary artery in 40% cases

LEFT CORONARY ARTERY

• Larger than the right coronary artery.

• Arises from left posterior aortic sinus.

COURSE• Runs forward and to the left and emerges

between the pulmonary trunk and the left auricle.

• Here the anterior inter-ventricular branch is given .

• The further continuation of the left coronary artery is sometimes called the circumflex artery.

• After giving off the anterior interventricular branch it runs into the left anterior coronary sulcus.

• It winds around the left border and near posterior interventriular groove it terminates by anastomosing with the right coronary artery.

BRANCHES:• Large Branches:

– Anterior interventricular– Branch to the diaphragmatic surface of the

left ventricle• Small Branches:

― Left atrial― Pulmonary― Terminal

Dominant left coronary artery anatomy. Left anterior oblique schematic diagram of dominant left coronary artery anatomy, including left anterior descending artery and left circumflex artery tributaries, is shown. AVGA = atrioventricular groove artery, PDA = posterior descending artery.

Areas of distribution• Left atrium• Ventricles:

−Greater part of left ventricle, except the area adjoing the posterior interventricular groove.

−A small part of right ventricle adjoining the anterior interventricular groove.

• Anterior part of interventricular septum.• Part of left branch of AV bundle

COLLATERAL CIRCULATION• Cardiac anatomosis: The two coronary arteries

anastomose in the myocardium.

• Extra cardiac anastomosis: The coronary arteries anastomose with the

• Vasa vasorum of the aorta,• Vasa vasorum of pulmonary arteries,• Internal thoracic arteries• The bronchial arteries• Phrenic arteries.

• These channels open up in the emergencies when the coronary arteries are blocked.

CORONARY ARTERY DOMINANCE

• The artery that gives the posterior interventricular artery determines the coronary dominance.

• If the posterior interventricular artery is supplied by the right coronary artery (RCA), then the coronary circulation can be classified as "right-dominant".

• If the posterior interventricular 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 interventricular 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

cortonary arteries) - lies on epicardial surface,– conduct blood with little resistance.

• Small coronary arteries – descends into myocardium, are of two types: – subepicardial vessels and – subendocardial vessels.

• Small coronary arteries are the principle resistance vessels of the heart, change in their diameter regulate the coronary blood flow

VENOUS DRAINAGE OF THE HEART

• The venous drainage of the heart is by three means: – Coronary sinus.

– Anterior cardiac veins

– Venae Cordis minimae.

CORONARY SINUS• This is the largest of vein of heart situated in

the left posterior coronary sulcus. It is about 3 cm long and ends by opening into the posterior wall of the right atrium.

• Its tributaries are:−Great cardiac vein: It enters the left end of

the coronary sinus.−Middle cardiac vein: It accompanies the

posterior interventricular artery and joins the right end of the coronary sinus.

−Small cardiac vein: It accompanies the right coronary artery and joins the right end of the coronary sinus.

−Posterior vein of left ventricle: It runs on the diaphragmatic surface of the left ventricle and ends in the middle of the coronary sinus.

−Oblique vein of left atrium ( of Marshall): It runs on the posterior surface of the left atrium, joins the left end of coronary sinus and develops from the left common cardinal vein.

−The right marginal vein: It accompanies the marginal branch of the right coronary artery.

ANTERIOR CARDIAC VEIN3 to 4 small veins run on the anterior wall of the right ventricle, open directly into the right atrium.

VENAE CORDIS MINIMAE(also called smallest cardiac veins, venae cardiacae minimae, or Thebesian veins)

• Numerous small veins present in all 4 chambers of heart which open directly into the cavities.

• The Thebesian venous network is considered an alternative (secondary) pathway of venous drainage of the myocardium. It is named after German anatomist Adam Christian Thebesius, who described them in a 1708 treatise called Disputatio medica inauguralis de circulo sanguinis in corde.

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.

PECULIARITIES OF COR.CIRCULATION

• BF during diastole• End arteries • High capillary density• High 02 extraction• Regulation is mainly by metabolites • Anatomical anastomosis• The coronary vessels are susceptible to degeneration

and atherosclerosis.• There is evident regional distribution: The

subendocardial myocardial layer in the left ventricle receives less blood, due to more myocardial compression (but this is normally compensated during diastoles by V.D). However, this renders this area more liable to ischemia and infarction

CORONARY BLOOD FLOW (CBF):

• The resting coronary blood flow is about 225 ml/min., which is about 0.7 – 0.8 ml/gm of heart muscle, or 4- 5 % of the total cardiac output.

• In severe muscular exercise, the work of the heart increased and the CBF may be increased up to 2 liters/ minute

FACTORS REGULATING CORONARY BL.FLOW

• Physical • Chemical • Neural • Hormonal • Reflex

PHYSICAL FACTORAortic 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 e.g. aortic incompetence or 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 vagal vasoconstrictor tone (a nrepis reflex) coronary vasodilatation CBF.

• C.B.F. occurs mainly during diastole due to compression of coronary blood vessels during systole by the contracted muscle fibers.

During systolic phases C.B.F. is less than that during diastole. With minimal blood flow during iso volumetric contraction phase. (due to compression of coronary blood vessels with low aortic pressure).

During diastolic phases C.B.F. is more than that during systole.With maximal blood flow during iso volumetric relaxation phase. (due to dilated coronary blood

vessels with high aortic pressure).

CHEMICAL FACTORS:Metabolic factors:

cardiac metabolism O2tension (local hypoxia), CO2, K+, lactic acid & adenosine in the cardiac muscle coronary vasodilatation CBF.

O2 lack (hypoxia) is the most effective coronary vasodilator. It produces coronary vasodilatation through:

• Direct action on coronary blood vessels and

• Release of chemical substances such as adenosine (from ATP) which is a potent coronary vasodilator.

Drugs:

• Nitrites, angised, aminophylline, caffeine & Khellin are coronary vasodilator coronary vasodilatation CBF.

NERVOUS FACTORS:

Direct effect:• Parasympathetic: vagus has very slight distribution to

coronary, so its stimulation has slight dilator effect.• Sympathetic: Both alpha and Beta receptors exist in the

coronary vessels. Sympathetic stimulation causes slight direct coronary constriction.

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

• Thyroxin cardiac metabolism coronary vasodilator CBF.

• Vasopressin (antidiuretic hormone) coronary vasoconst CBF.

REFLEX CONTROL

• Anrep’s reflex: Increased venous return causes increased pressure in right atrium, leading to reflex increase in CBF e.g. during muscular exercise.

• Gastro-coronary reflex: Distention of the stomach with heavy meal causes reflex vasoconstriction of coronary blood vessels decreasing CBF.

Coronary Autoregulation• 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 leads to

Increase adenosine & Decreased oxygen which causes Vasodilatation and increase CBF

• Endothelium derived relaxation factor (EDRF): • Hypoxia, ADP, VIP, muscular exercise (increase

distention force), stimulate vascular endothelium to secrete EDRF, which is a potent vasodilator, that causes coronary dilatation and increase CBF.

Applied aspects

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 and relived by treatment.

• Pain is due to accumulation of pain producing substances in the myocardium such as, P factor, lactic acid, histamine, K, and Kinins.

• 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 severe ischemia.

• 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.

Coronary bypass operation

Angioplasty

A Presentation By DR ANWAR H SIDDIQUI, JR, Physiology