بسم الله الرحمن الرحيم

والصالة والسـالم

على سيـد المرسلين

سيدنا وحبيبنا محـمد

صلى الله عليه وسلم

PHYSIOLOGY OF THE

CARDIOVASCULAR SYSTEM

LECTURE 17

By

Prof. Ahmed Emad Omar

CORONARY CIRCULATION

Functional Anatomy: The cardiac muscle is supplied by two coronary arteries, that arises from the sinuses behind the cusps of the aortic valves at the root of the aorta.

The left coronary artery supplies mainly the anterior and lateral portion of the left ventricle, and the anterior part of the interventricular septum,

whereas the right coronary artery

supplies mainly the right ventricle, as

well as the posterior part of the left

ventricle and the posterior part of the

intraventricular septum.

Venous blood, collected by the cardiac veins

(great, middle and small), is emptied into the

coronary sinus.

Coronary Circulation: Arterial Supply

Figure 18.7a

The coronary arterial tree is divided functionally into large coronary arteries, which lies on epicardial surface, that conduct blood with little resistance.

And small arteries descending into myocardium, where their arterioles are of two types:

a) subepicardial vessels and b) subendocardial vessels. As they are the principle resistance vessels of

the heart, change in their diameter regulate the coronary blood flow

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.

Factors Affecting Coronary Blood Flow

1- 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 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.

2- Mechanical factors:

The heart muscle compress on the coronary wall. Coronary flow in the atria and right ventricle is not reduced during systole.

C.B.F. during different phases of cardiac cycle:

• 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).

3- Chemical Factors • At rest, the heart extracts 70-80 % of the

O2 from blood delivered to it, and because no much O2 is left, only increasing coronary blood flow can increase O2 supply. Oxygen demand is major factor in local blood flow regulation.

• The blood flow increases when the metabolism of the myocardium is increased. Metabolic products such as adenosine, O2 lack, H+, lactate, K+, and prostaglandin produce coronary vasodilatation.

• A highly efficient mechanism regulating

coronary blood flow (CBF) depending on heart

activity and rate of cardiac muscle metabolism.

Mechanism:

• Increase heart activities (inc. HR & force of

contraction) causes inc. of the rate of cardiac

muscle metabolism and inc. metabolites in the

ISF around the cardiac muscle cells. Dec.

(hypoxia), inc. CO2 , inc. H+ and inc.

adenosine causes VD of coronaries inc. CBF.

4- 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:

a) Myogenic response: an increase in passive

stretch, caused by increased perfusion

pressure, causes active smooth muscle

contraction.

b) Chemical theory: Decrease perfusion pressure Increase

adenosine & Decreased oxygen Vasodilatation increase CBF

c) 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.

5- Neural controlA- 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.

B- 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.

6- Reflex control

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

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

Angina pectoris• Recurrent shot-lived attacks of inadequate CBF,

usually during exertion or emotional lesion, the pain associated with it is called angina pectoris.

• 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.

• The anginal pain is usually felt substernal and is often transferred to left arm and left shoulder and may also radiate to the neck.

Myocardial ischemia

Angina pectoris• Caused by partial

occlusion of coronary blood vessels.

• AtheroscleresisSymptoms:• Chest pain felt in the

chest, reffered to Lt shoulder and Lt little & ring fingers.This pain is felt during muscle exercise and emotions, and disappear by rest.

Myocardial infarction • Caused by complete

occlusion of one of the branches of coronary arteries.

• Thrombosis inside coronary

Symptoms:• Severe chest pain and

dyspnea. Occurs at any time and not disappear by rest.

NB: Pain is due to accumulation of metabolites in cardiac muscle causing stimulation of cardiac pain receptors.

Myocardial infarction

• When the blood supply of the myocardium is severely interrupted, irreversible changes and death of muscle cells (infarction) may occur.

• The first change, abnormal rapid repolarization of the infracted muscle (accelerated opening of K+ channels), it lasts for few minutes, then the resting membrane potential of infracted muscle decline because of the loss of intracellular K+, 30 minutes later the infracted fibers begin to depolarize more slowly than the surrounding normal fibers.

Myocardial infarction • If coronary thrombosis occurs, irreversible changes

occur in the myocardium leading to necrosis and death of the muscle fibers called infarction.

• Obstruction of a major coronary artery by thrombosis, is associated with bradycardia and hypotension by a vagal reflex initiated by some chemicals released from the damaged myocardium.

• It is usually complicated by fatal ventricular fibrillation.

• It is usually accompanied by ECG changes; raised S-T segment in lead II, deep Q in V5 & V6 and inverted T wave.

• It is accompanied by release of marker enzymes in the blood (CPK & LDH).

ECG CHANGES IN CORONARY ISCHEMIA

• Mild ischemia: increase the duration of depolarization.

• If the apex of the ventricles have abnormal long period of depolarization, repolarization of the ventricles would not begin at the apex as it normally does.

• The vector of repolarization would point to direction opposite to the usual vector, causing inverted T-wave.

Current of injury

• Damage of the heart muscle, often cause part of the heart to remain partially or totally depolarized all the time.

• Current flows between the pathologically depolarized and the normally polarized area.

• All of these changes causes current flow that produces elevation of the S-T segment in the ECG leads recorded with electrodes over the infracted area, leads on the opposite side of the heart shows ST segment depression.

• After some days or weeks, the ST segment abnormalities subsides. The dead muscles becomes electrically silent. The infracted area is negative relative to the normal myocardium during systole, leads to appearance of Q wave (of leads in which is was not present), and increase in the size of normal Q wave.

• Myocardial infarction are often complicated by serious ventricular arrhythmia

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