Coronary Circulation in Human Beings: Anatomy and Factors | Biology

In this article we will discuss about:- 1. Anatomical Considerations of Coronary Circulation 2. Methods of Studying Coronary Circulation 3. Normal Values of Coronary Circulation 4. Ventricular Action Affects Coronary Circulation 5. Circulatory Status of the Cardiac Muscle under Certain Diseased Conditions

Anatomical Considerations of Coronary Circulation:

Blood supply to the heart is mainly carried out by the two coronary vessels, e.g., right and left coronary arteries arising from the sinuses behind the cusps of the aortic valve at the root of the aorta. Both the arteries are patent throughout the cardiac cycle as the eddy currents keep the cusps of the valve away from the orifices of the arteries.

The left coronary artery gives off the anterior descending and the left circumflex branch. The latter runs along the atrioventricular groove to the left and proceeds downwards as the posterior descending branch. The anterior descending branch runs downwards up to the apex. The right coronary artery gives off several descending branches on both ventricles (Figs. 7.97 & 7.98).

The venous blood from the myocardium is chiefly returned through two systems superficial venous system and deep venous system.

Predominance of the coronary artery supply is seen in about 50% of human heart by the right coronary artery; and in about 20% of human heart by the left coronary artery and in about 30% of cases by both coronary arteries. According to Schlesinger the last group in which the nature of supply is not made predominantly by either right or left coronary artery is least vulnerable to the cardiovascular disorder. The right and left coronary arteries break up into a large number of capillaries.

The superficial venous system lies beneath the epicardium and consists of:

(a) The coronary sinus, draining mostly the blood from the left coronary artery, partly from the right coronary artery, and ends ultimately in the posterior part of the right atrium;

(b) The great cardiac vein, draining blood from the left heart, ends in the coronary sinus;

(c) The anterior cardiac veins which are generally 2 to 3 in number, draining blood mostly from the right heart and partly from the left heart, end directly into the right atrium. The deep venous system arises within the substance of the myocardium and ends directly into the cavity of the right heart by the Thebesian, luminal and sinusoidal vessels.

Normally, the coronary arteries are end arteries though the functional anastomoses are present and become active under un-physiological state.

These anastomoses are between (a) branches of one coronary artery with that of the other, (b) Thebesian vessesls and cavity of the heart, (c) arterioluminal and arteriosinusoidal vessesl with the cavity of the heart, and (d) extracardiac anastomoses (Fig. 7.99).

Heart muscle has a rich blood supply. The total capillary length per cu.mm of cardiac tissue is about 11 metres (Rabbit). It is known that each fibre in the adult human heart receives one capillary twig, whereas in foetal life one capillary twig supplies four to six muscle fibres.

Methods of Studying Coronary Circulation:

The coronary blood flow and the oxygen usage of the heart can be studied by the Pitot tube, orificemeter, electromagnetic flowmeter, thermostromuhr and also, by the use of nitrous oxide gas. Nitrous oxide method (Fick principle) gives almost accurate values. The subject inhales a mixture of 15% of nitrous oxide and air for 10 minutes.

The amount of nitrous oxide taken up per minute is determined. Several samples of blood are taken from an artery and from a catheter introduced into the mouth of the coronary sinus at intervals during inhalation of nitrous oxide by the subject and their nitrous oxide content is determined. The arteriovenous difference of nitrous oxide is then calculated.

Coronary inflow is then determined with the help of Fick principle:

Normal Values of Coronary Circulation:

i. During rest for each 100 gm of the left ventricle, the left coronary inflow varies from 65 to 85 ml per minute. The arteriovenous O₂ difference is very high and is about 10 to 15 ml per 100 ml. So the extraction of O₂ by the cardiac muscle is very high.

ii. During heavy exercise minute volume increases about ten times, and coronary inflow also rises ten folds, i.e., about 2 litres. The O₂ usage of the heart is very high. The blood in the anterior cardiac veins or in the coronary sinus shows 20% saturation with O₂. During exercise, heart consumes about 250 ml of O₂ per minute (same as the resting O₂ consumption of the whole body). The arteriovenous O₂ difference of heart is about 10-15% (skeletal muscle – 5-6%). This is equivalent to a minute flow of about 2 liters of blood through the coronary vessels.

Ventricular Action Affects Coronary Circulation:

Ventricular action affects coronary circulation in two ways:

(a) By altering the aortic pressure, and

(b) By exerting a variable degree of compression on the coronary vessels.

The following phases are seen (Fig. 7.100):

Coronary Inflow:

i. Left Coronary Artery:

a. During isometric contraction phase, coronary inflow sharply falls and reaches minimum and even falls and reaches minimum and even falls below the zero level due to backflow. Because, the aortic pressure is at minimum and the compression on the coronary vessels is maximum.

b. During reduced ejection phase, the coronary inflow again falls, because, the aortic pressure is falling and the compression is continued.

c. During isometric relaxation phase, the coronary inflow sharply rises, because, the aortic pressure is fairly high and the compression is minimum. Maximum coronary filling takes place during this phase due to fall of coronary vascular resistance.

d. During rapid ventricular filling phase, the coronary inflow continues to rise but slowly, because, the relax­ation of the cardiac musculature continues and the vessels open up further.

e. In the later part of diastole, the coronary inflow slowly diminishes, because, the aortic pressure is falling and the coronary vessels are stretched due to filling of heart and the consequent elongation of cardiac muscle.

ii. Right Coronary Artery:

During isometric contraction phase, the coronary inflow sharply falls and rapidly rises again during the maximum ejection phase and falls during the reduced ejection phase.

iii. In the isometric relaxation phase the coronary inflow rises but not so steeply like the left coronary inflow. So greater coronary inflow takes place in diastole than systole due to less compression of the coronary vessels during relaxation of the cardiac muscle and diminution of intramural tension.

The left coronary inflow during systole is affected much as the pressure differential between aorta and left ventricle becomes -1mm of Hg. But the right coronary inflow during the systole is not so affected as such pressure differential is 95mm of Hg.

In the coronary sinus the outflow of blood gradually rises from the isometric contraction phase and reaches its peak during protodiastolic phase and then gradually falls.

Circulatory Status of the Cardiac Muscle under Certain Diseased Conditions:

i. Aortic Stenosis:

In aortic stenosis, there is initially increase of coronary flow along with increase of coronary perfusion. With the stenosis of the aorta, the intraventricular pressure of the left ventricle is increased and the left heart has to work against increased resistance. Consequently there is hypertrophy of the left ventricle with decrease of coronary flow if the stenosis is maintained for some time.

ii. Pulmonary Hypertension:

Pulmonary hypertension may be the cause of mitral stenosis, emphysema, atelectasis, pneumonia, etc. Under such state the right ventricular pressure is greatly increased and this increase of intraventricular pressure causes decrease of coronary flow of the right heart because the arteriovenous pressure difference is greatly decreased. Pulmonary hypertension may be associated with right ventricular hypertrophy and ultimately leading to right heart failure.

iii. Aortic Insufficiency:

Patients suffering with aortic insufficiency are always associated with anginal pain. This anginal pain is due to coronary insufficiency. This coronary insufficiency is mostly due to decrease of aortic pressure and also of central coronary diastolic pressure.

iv. Mitral Stenosis:

In mitral stenosis, an obstruction is exerted during flow of blood from left atrium to left ventricle. If this state is prolonged then pulmonary hypertension may happen and coronary flow of the right heart is greatly affected.

v. Aortic Coarctation:

It is the condition when a vessel remains constricted or narrowed and thereby the blood flow through the vessel is decreased. In coarctation of the thoracic aorta, work load of the heart is increased as the heart has to work against the resistance. The venous return by way of the inferior vena cava may be decreased but the total venous return may be unaffected only by opening up of other branches of the aorta.

Thus in case of mild form of coarctation, the cardiac output and at the same time coronary flow may be maintained but if the constriction is in severe form and the blood flow through the aorta is severely affected then the venous return, cardiac output and the coronary flow are greatly decreased. As the heart has to work against increased resistance, there is possibility of left ventricular hypertrophy along with decreased coronary flow. Ultimate fate of it is the congestive heart failure.

vi. Hypertensive Cardiovascular Disease:

In essential hypertension having no organic changes in the heart and blood vessels, the mean coronary flow remains unaltered although the systemic pressure remains elevated. But in hypertension having coronary atherosclerosis or arteriosclerosis, the elastic behaviour of the coronary vessels are altered, the flow may be affected greatly, although the systemic pressure remains at higher level.

vii. Ischaemic Heart Disease:

Ischaemic heart disease is the condition when cardiac muscle suffers from coronary insufficiency.

This coronary insufficiency is due to major cause of:

(a) Sclerosis of the coronary vessels, or

(b) Coronary occlusion by thrombosis.

In both the cases if these are not so severe than the mean coronary flow is maintained through the development of anastomosing channels in between the affected vessels and the unaffected vessels. In such case the affected area (ischaemic area) gets blood supply through-backflow.

If the subject maintains a normal well-adjusted life and the heart is not given any unusual work load then the management or rehabilitation of this patient is possible through the newly adjusted circulatory machineries. But further cardiac attack or any increased work load of the heart becomes an unmanageable episode of such patient because readjustment becomes impossible.

viii. Coronary Spasms and Intercoronary Reflexes:

Coronary spasms have been described to be the major cause of acute myocardial infarction. It is of general opinion that occlusion of one branch of coronary vessels by thrombus or an embolus may cause widespread spasm in the other arteries causing massive damage of the cardiac muscle and fatal ventricular fibrillation may occur.

Le Roy and Snider (1941) have claimed that the sudden death of a patient following myocardial infarction is due to widespread reflex vasoconstriction of the other coronary vessels, whose primary stimulus is the infarct; the afferent pathway is the cardiosensory nerves and the efferent pathway is the vagus.

Hall, Manning and others favour these concepts of intercoronary reflex because ventricular fibrillation and death due to acute coronary occlusion may be averted if the subjects are under deep anaesthesia or cholinergic blockade particularly of atropine. But the role of vagus in precipitating this reflex vasoconstriction is still under doubt because intercoronary administration of acetylcholine, the neurohumour of vagus, always causes vasodilatation. So this part should require further elucidation.

ix. Pathological Physiology of Angina Pectoris and Acute Myocardial Infarction:

Ischaemia is the cause of pain of angina pectoris and of acute myocardial infarction. Angina pectoris is thus a symptom of cardiac ischaemia but not a disease. The anginal pain is often associated with disproportionate blood supply according to myocardial requirement. In ischaemic heart disease the patient often complains this pain following a heavy meal or a physical exertion or an excitement.

The pain is due to accumulation of metabolites produced during coronary ischaemia. The metabolites stimulate the nerve endings. But the actual stimulus at the nerve endings that may cause the pain is not yet known. Sir Thomas Lewis has described it the P factor which has some characteristics with lactic acid.

Predisposing cause of myocardial infarction is the coronary obstruction due to atherosclerosis. The obstruction may be due to gradual shortening of the vessels itself by the deposition of lipid in the intima or by the locally formed thrombus. If the ischaemia is prolonged then it may lead to irreversible changes of necrosis.