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Cardiovascular system

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How much is the resting coronary blood flow?

Resting coronary blood is 225 ml or 0.7 or 0.8 ml/g of heart muscle, i.e. 4-5% of the total cardiac output.

^ Describe the phasic changes in coronary blood flow.

During the phases of cardiac cycle there are changes in coronary blood flow. During systole, blood flow in the left ventricle falls to a low value. This is due to compression

of intramuscular vessels during systole. During diastole, the blood through coronary capillaries rapidly rises, because there is relaxation of ventricular muscle and therefore there is no longer obstruction to the blood flow.

Blood passing through coronary capillaries of right ventricle also show similar phasic changes. They are far less because force of contraction of the right ventricle is much less (Fig. 13.15).

Fig. 13.15 Phasic flow of blood through the coronary capillaries of left ventricle.

Describe the arrangement of coronary vessels in different layers of the heart.

On the surface of the cardiac muscle there are large epicardial arteries. From them smaller intramuscular arteries penetrate the muscle. They give rise to nutrient arteries in their way to supply muscle. Immediately beneath the endocardium, there is a plexus of subendocardial arteries. During systole when the left ventricle contracts forcefully, blood flow through subendocardial plexus almost falls to zero. To compensate for this, subendocardial arterial plexus is more extensive than the nutrient arteries in the middle and outer layers of the heart. Therefore, during diastole, flow through the subendocardial arteries is considerably greater.

^ How is the coronary blood flow controlled?

Coronary blood flow is controlled as follows:

1. Local blood flow regulation. It is most important factor which regulates coronary blood flow. Under the resting state, 70% of O2 is removed by the heart muscles as the blood passes through arteries. Therefore not much additional oxygen can be provided unless the blood flow increases. Increased oxygen consumption by the heart increases the blood flow proportionately. Yet exact mechanism by which this is done is not certain. Probably decreased oxygen consumption causes release of vasodilator substances such as adenosine (due to increased degradation of adenosine triphosphate) from the muscle cells. This adenosine causes vasodilatation and then reabsorbed back into the cardiac cells to be reused. Hydrogen ions, bradykinin, CO2, prostaglandins are the other suggested vasodilator substances.

According to other theory, O2 lack directly causes vasodilatation because muscles of the vessel wall itself get deficient oxygen. This causes muscle wall relaxation and vasodilatation.

2. Nervous control. Autonomic nerves control the blood flow directly as well as indirectly. Normally indirect effects are opposite to direct effect but play important role in control of blood flow.

(a) ^ Direct effect. Distribution of parasympathetic nerve fibres (through vagus) to coronary system is so less that parasympathetic stimulation has very slight direct effect, causing dilatation of coronary arteries.

Sympathetic nerve fibres extensively innervate the coronary vessels. The transmitters released at their endings are epinephrine and norepineph-rine. Norepinephrine acts on alpha receptors and causes vasoconstriction. Epicardial vessels have preponderance of alpha receptors. Epinephrine acts on beta receptors of coronary vessels causing vasodilatation. Intramuscular arteries have preponderance of beta receptors. But overall effect is vasocon­striction of the coronary vessels. Metabolic local factors are more important in controlling blood flow, therefore they over-ride the effect of nervous stimulation.

(b) Indirect effect. Indirect effect of nervous stimulation on coronary blood flow is through their action on the heart, e.g. sympathetic stimulation causes increase in heart rate and increase in force of contraction of the heart. This in turn increases the cardiac output and the coronary blood flow.

Parasympathetic stimulation causes decreased heart rate and decreased force of contraction of the heart. This in turn reduces the cardiac output and hence the coronary blood flow.

^ What does cardiac muscle use for its metabolism normally?

Under the resting condition, cardiac muscle uses mainly fatty acids for its energy, rather than carbohydrate. But under anaerobic or ischaemic conditions, glucose is utilized through anaerobic glycolysis.

^ How is coronary blood flow measured?

The most common method used for measuring coronary blood flow is nitrous oxide method. This is based on Fick principle. It gives almost accurate value.


Person inhales a mixture of 15% nitrous oxide and air for 10 minutes. The amount ot nitrous oxide taken in per minute is determined.

During inhalation of the gas several blood samples are taken from an artery and through a catheter introduced into the mouth of coronary sinus (collection of mixed venous blood) at intervals. The nitrous oxide content of each of the blood sample is determined. Arteriovenous difference in nitrous oxide is calculated. Then coronary blood flow is determined by following formula:

Quantity of nitrous oxide taken up per minute

Coronary blood flow = ---------------------------------------------------------

Difference of nitrous oxide content of arterial and venous blood

^ Enumerate the factors affecting coronary blood flow.

Factors affecting coronary blood flow are:

  1. Mean aortic pressure. This is the force for driving blood into the coronary arteries. Rise in mean aortic pressure increases the blood flow and vice versa. But if pressure remains high for a long time, because of increased work load on the heart, heart will go into congestive cardiac failure.

  1. Cardiac output. Greater the cardiac output, greater is the coronary blood flow.

  1. Metabolic factors. Increased metabolism of the heart increases O2 consumption leading to relative hypoxia. This hypoxia causes dilatation of vessels and increase in blood flow (blood flow also increases due to release of adenosine).

  2. Effect of ions. K+ions in low concentration causes dilatation of coronary vessels whereas high K+ ion concentration causes constriction of the coronary vessels.

  1. Nervous stimulation. Already explained.

  1. Hormones. Thyroid hormone increases coronary blood flow because of increase in metabolism.

Adrenaline and noradrenaline cause increase in blood flow as already explained (indirectly by increasing the cardiac output).

7. Exercise. During exercise, coronary blood flow increases because of sympathetic stimulation.

^ What is ischaemic heart disease?

Ischaemic heart disease is the disease resulting from insufficient coronary blood flow. The most common cause of decreased coronary blood flow is atherosclerosis. Coronary vessel occlusion may occur due to thrombus formation of the atherosclerotic plaque, embolus coming from other areas or coronary vessel spasm due to irritation of smooth muscle.

^ Describe the collateral circulation in the heart.

In the heart there is almost no communication existing among larger coronary arteries, but many anastomoses do exist among the smaller arteries (20-250 mm diameter). They open up within few seconds after the sudden occlusion of larger artery. The blood flowing through them is only one-half that needed to keep cardiac muscle alive. But collateral blood flow begins to increase and become double by the end of second or third day and reaches to normal by one month. When atherosclerosis causes constriction of coronary arteries slowly over a period of many years, collateral vessels develop at the same time and therefore patient never experiences acute episode of cardiac dysfunction.

^ What is myocardial infarction?

Immediately after an acute coronary occlusion, the area of muscle that has either zero flow or very little flow that cannot sustain the cardiac muscle function, is said to be infarcted. The overall process is known as myocardial infarction.

Subendocardial muscle normally has difficulty in obtaining adequate blood flow as blood vessels are intensely compressed during systole of the heart. Subendocardial muscle frequently becomes infarcted without any evidence of infarction in the outer portions.

^ What are the causes of death following acute coronary occlusion?

There are four major causes of death following acute myocardial infarction as follows:

1. Cardiac shock. The heart becomes incapable of contracting with sufficient force to pump enough blood in the arterial tree. This is called as coronary shock or cardiac shock or low cardiac output failure.

2. Damming of blood in venous system. When heart is not properly pumping the blood forward, it causes damming of blood in blood vessels of lungs or in the systemic circulation. This increases right and left atrial pressures, increased capillary pressure. The cause of death is acute pulmonary oedema.

3. Rupture of infarcted area. Few days after the infarction, dead cardiac muscle begins to degenerate, becomes thin and ruptures leading to loss of blood in pericardial cavity (cardiac tamponade), compression of heart from outside, blood cannot return to right atrium. This leads to sudden decreased cardiac output and death.

^ 4. Ventricular fibrillation. In this condition coordinated, effective contraction of ventricles is lost. At any given instant, many small portions of ventricular muscle will be contracting, at the same time, equally as many other portions are relaxing. Thus there is never a coordinate contraction of the entire ventricular muscle at once. This leads to failure of a ventricle as a pump leading to negligible amount of stroke volume. It is a very serious condition because if ventricular fibrillation begins within 4 to 5 seconds there is a lack of blood flow to the brain. Unless ventricular fibrillation is treated instantly it is almost invariably fatal. Main factors which can initiate ventricular fibrillation are sudden electric shock or ischaemia of the hart.

^ What is angina pectoris?

Development of cardiac pain whenever the load on the heart becomes too great in relation to coronary blood flow is called angina pectoris. Therefore, patient gets pain on exertion. Pain is hot, pressing and constricting type. It is treated by giving vasodilator drugs. Most commonly used vasodilators are nitroglycerin and other nitrate drugs.

^ What is the surgical treatment for coronary disease?

Following surgical procedures are done for treating coronary disease:

1. Aortic coronary bypass. Small vein grafts are anastomosed from the aorta to the side of the more peripheral coronary vessels. Each graft supplies a peripheral coronary artery beyond a block. The vein that is usually used is a long saphenous vein.

2. Coronary angioplasty. This is done to open partially blocked coronary vessel (before they become totally occluded) by passing small balloon-tipped catheter under radiographic guidance into the coronary system.

^ Describe anatomy of cerebral circulation.

Blood enters the cranium through two internal carotid and two vertebral arteries. Two vertebral arteries combine to form a basilar artery which in turn divides into two posterior cerebral arteries.

Each internal carotid artery divides into middle and anterior cerebral arteries. These six arteries (anterior, middle and posterior cerebral arteries on two sides) intercommunicate with the help of their branches forming circle of Willis. These three vessels supply different parts of brain.

Brain has a very rich blood supply. Grey matter has a greater supply than the white matter. Cerebral arteries are not end arteries. They freely anastomose especially at the circle of Willis. Because of this, blood flows adequately to different parts of brain, especially during the time of emergency. Venous blood drains into large cerebral sinuses (superior sagittal, inferior sagittal, cavernous). All sinuses ultimately form two transverse sinuses which become continuous with the two internal jugular veins.

^ How is cerebral blood flow measured?

Cerebral blood flow is measured by nitrous oxide method based on Fick principle.


Person inhales 15% nitrous oxide. Blood samples are collected from any peripheral artery and from the jugular vein at frequent intervals, while the subject is inhaling the mixture of nitrous oxide and air. Nitrous oxide content of each sample is determined. Cerebral blood flow per minute is determined from the arteriovenous difference of nitrous oxide and the partition co-efficient for N2O between the blood and the brain.

^ What is average blood flow to the brain?

Under resting state, 54 ml of blood is supplied per 100 g of brain tissue per minute or 770 ml/min. Total O2 consumption by brain is 50 ml/min.

How is cerebral circulation regulated?

Cerebral blood flow is autoregulated. Various factors help in this autoregulation as follows:

  1. Arterial CO2 tension — Increase in CO2 tension in the arterial blood increases the blood flow by causing dilatation of arterioles (Fig. 13.16).

  2. Hypoxia—Decreased O2 supply to the brain also causes vasodilatation. This is due to lack of O2 supply to smooth muscle of the vessel (causing smooth muscle to relax and cause vasodilatation). Lack of O2 also causes release of certain vasodilator substances which cause direct effect on the vessel wall causing vasodilatation. The most important of it is adenine.

Cerebral blood flow depends upon the difference between mean arterial pressure and internal jugular pressure because the difference between these two pressures is the driving force for cerebral circulation. Greater the driving force, greater is the blood flow. Cerebral blood flow is maintained therefore by maintaining general blood pressure through sino-aortic mechanism

Fig. 13.16 Relationship between PCO2and cerebral blood flow.

Cerebral blood flow is inversely related to cerebrovascular resistance which in turn depends on:

  1. Intracranial pressure — It has a negative correlation with blood flow.

  2. Viscosity of blood — Decreased viscosity increases the blood flow.

  3. Diameter of cerebral vessels — It is mainly controlled by CO2,O2 in blood and neurohormones as described above.

Adrenaline increases the cerebral blood flow.

^ What is the minute blood flow in pulmonary circulation?

The right ventricular output flows to pulmonary circulation. It is about 5 1/min.

What is the systolic and diastolic pressure in pulmonary circulation?

Pulmonary circulation is a low pressure circulation. Pressure in the pulmonary artery during systole is about 22 mm Hg and during diastole it is about 10 mm Hg. Pulmonary capillary pressure is about 8 mm Hg.

What are the functions of pulmonary circulation?

  1. Exchange of gases.

  2. Pulmonary blood vessels act as filters. They trap emboli which pass through pulmonary circulation.

  3. Pulmonary circulation maintains nutrition to the lung tissue.

  4. Left ventricular output is dependent on return of blood from pulmonary circulation to the left atrium.

  5. Conversion of angiotensin I to angiotensin II by angiotensin converting enzyme.

What are the peculiarities of pulmonary circulation?

  1. At the arterial end of capillaries, fluid filters out in tissues through the capillary endothelium. But from pulmonary capillaries no fluid passes into the tissues. This is because in pulmonary capillary blood colloidal osmotic pressure (25 mm Hg) is much higher than the hydrostatic pressure of blood in capillaries.

  2. Pulmonary capillaries filter emboli and prevent them reaching and blocking the blood vessels of important organs such as heart and brain.

  3. Pulmonary vascular bed is a low resistance circuit. Vessels are short and distensible and therefore can accommodate large quantity of blood.

  4. Local action of CO2 and low O2 on pulmonary vascular bed is opposite to that at systemic vessels. Excess CO2 and low O2 causes vasoconstriction.

What is circulatory shock?

Circulatory shock means generalized inadequacy of blood flow throughout the body to the extent that body tissues get damaged due to too little delivery of oxygen and nutrients.

Explain different types of shock and their causes. 1. Shock caused by reduced cardiac output

It is subdivided into

  1. Cardiogenic shock, due to decreased pumping ability of the heart because of cardiac abnormalities, e.g. myocardial infarction, toxic states of heart, severe heart valve dysfunction, heart arrhythmias.

  2. Shock caused by decreased venous return:

(i) Hypovolumic shock. There is decrease in blood volume due to any cause, e.g.

external or internal haemorrhage (injury, fracture), fluid loss (diarrhoea,

vomiting, excess sweating, burns), (ii) ^ Decrease in vascular tone, especially of venous reservoirs as in

  • Neurogenic shock, caused by general or spinal anaesthesia, brain damage, emotional fainting.

Anaphylactic shock, an allergic reaction which releases marked venous and arteriolar dilatation and increased capillary permeability due to release of histamine or histamine like substances.

^ Obstructive shock, caused by obstructive blood flow, e.g. tension pneumothorax, pulmonary embolism, cardiac tumour, etc.

2. Shock occurring without decrease in cardiac output It is subdivided into

(a) Excessive metabolism of the body due to which normal cardiac output is inadequate.

(b) Septic shock. Abnormal tissue perfusion patterns so that most of the cardiac output is passing through blood vessels besides those that are supplying the local tissues with nutrition. It occurs due to blood borne infection, e.g., peritonitis. Usually there is high fever, vasodilation, high cardiac output and sludging of blood in septic shock.

What are signs and symptoms of circulatory shock?

1. Decreased blood pressure.

2. Tachycardia and therefore reduced stroke volume.

3. Reduction in velocity of blood flow producing stagnant hypoxia and cyanosis.

4. Pale and cold skin due to vasoconstriction.

5. Decreased urine output due to reduced renal blood flow and GFR

6. Blood flow to vital organs is affected. Reduced blood flow to brain causes fainting.

7. Due to tachycardia there is increase in work of heart but its blood flow is reduced. This leads to excessiveproduction and collection of lactic acid.

8. Respiration becomes rapid.

9. If patient is conscious, there is intense thirst.

10. Agitation, restlessness.

Name different stages of circulatory shock. Stages of shock

(i) Non-progressive stage (compensated stages) Normal circulatory compensatory mechanisms eventually cause full recovery without help of outside therapy.

(ii) ^ Progressive stage— shock becomes steadily worse until death.

(iii) Irreversible stage— shock progresses to such an extent that all forms of known therapy are inadequate to save person's life.

Explain different compensatory mechanisms occurring in hypovolumic shock.

In hypovolumic shock there is reduction in blood volume most commonly due to haemorrhage. The degree of shock depends on the amount of blood loss. About 10% of total loss of blood has no effect either on blood pressure or cardiac output. If loss is more cardiac output is reduced and later on blood pressure decreases.

Circulatory system can recover if degree of loss is not greater than a certain critical

amount. Crossing this critical amount causes death as shock itself causes more shock resulting into progressive shock.

If shock is not severe enough to cause its own progression, person recovers. Shock of this lesser degree is non-progressive shock. Circulatory system recovers, due to various negative feedback control mechanisms set for maintaining cardiac output and blood pressure. They are termed as compensatory mechanisms. These are

(1) Rapid or short-term mechanisms.

(2) Long-term mechanisms. ^ Rapid compensatory mechanisms

(1) Baroreceptor reflex. Fall in blood pressure causes lesser degree of stretching of baroreceptors. Discharge from these receptors stimulates vasomotor centre and there is sympathetic stimulation leading to generalized vasoconstriction (sparing vessels of brain and heart). Vasoconstriction is most marked in skin, kidneys and viscera. This causes shifting of greater amount of blood in circulation. Constriction of veins on account of sympathetic stimulation also causes increased shifting of stored venous blood in circulation leading to increased venous return and cardiac output. In kidneys both afferent and afferent blood vessels constrict but afferent vessels constrict to a greater extent. This leads to reduction in GFR.

(2) Chemoreceptor reflex. Haemorrhage causes loss of red cells leading to reduced O2 carrying capacity. The resultant anaemia and stagnant hypoxia as well as acidosis stimulates chemoreceptors which also excite vasomotor centre to cause same effects as those caused by baroreceptor reflex. Fall in blood pressure below 80 mm Hg usually initiates chemoreceptor reflex.

(3) ^ CNS ischaemic response. When blood pressure falls below 50 mm Hg this response is initiated. It causes more powerful sympathetic stimulation.

(4) Reverse stress relaxation. This causes blood vessels to constrict down around the diminished blood volume so that available blood volume is adequately circulated.

(5) Release of epinephrine and norepinephrine. Haemorrhage is a potent stimulator of secretion of these hormones from adrenal medulla. The increase in blood levels of these hormones contribute relatively little to generalized vasoconstriction. They cause stimulation of reticular formation making patient restless and apprehensive.

(6) ^ Increase in circulating angiotensin II level. Due to ischaemia there is a secretion of renin from the kidneys which increases level of angiotensin II in blood. It causes thirst which makes person drink more fluid. This helps to restore extracellular fluid (ECF).

Increased angiotensin II causes vasoconstriction leading to rise in blood pressure. It also causes increased aldosterone secretion (after about 30 minutes) which in turn causes increased absorption of salt and water by kidneys which helps in restoring extracellular fluid volume. All these effects help in preventing progression of shock.

(7) ^ Release of excess vasopressin or ADH. Release of ADH causes retention of water by kidneys and helps in restoring ECF.

(8) Capillary fluid shift mechanism. Drop in capillary pressure causes fluid from interstitial space to move into the capillaries along most of their course helping to maintain circulatory volume.

From different mechanisms described above reflexes provide immediate help within 30 seconds of haemorrhage. Angiotensin, vasopressin, reverse stress relaxation require 10 minutes to an hour for complete response. Readjustment of blood volume by increased absorption of water from intestine and increased absorption of salt and water from kidneys require 1 to 48 hrs. Recovery takes place if shock does not become progressive. Long-term compensatory mechanisms

(1) Restoration of plasma volume and proteins. After a moderate haemorrhage plasma volume is restored to normal in 12 to 72 hrs. There is rapid entry of preformed albumin from extravascular stores. After this initial influx albumin and rest of the plasma protein losses are restored by hepatic synthesis over a period of 3 to 4 days.

(2) ^ Restoration of red cell mass. There is excess release of erythropoietin which leads to increased rate of ery thropoiesis within 10 days. Normal red cells mass is restored in 4 to 8 weeks.

What is progressive shock?

When shock becomes severe enough structures of circulatory system begin to deteriorate and various types of positive feedback mechanisms develop. These cause vicious cycle of progressively decreasing cardiac output. This is called progressive shock.

^ What is irreversible shock?

After shock has progressed to a certain stage, transfusion or any other therapy becomes incapable of saving the life of a person. This is irreversible shock.

What is the treatment of circulatory shock?

The treatment of shock is aimed at correcting the cause and helping physiological compensatory mechanisms. /. Fluid replacement therapy

(1) Blood or plasma transfusion. If the shock is due to haemorrhage transfusion of blood is the best therapy. If shock if due to plasma loss, plasma or appropriate electrolytic solution can correct the shock. Plasma substitute such as dextran can be used.

(2) Saline. Less effective. //. Sympathomimetic drugs

They mimic sympathetic stimulation. They are most useful in neurogenic and anaphylactic shock. They are not useful in haemorrhagic shock. ///. Other therapy

(a) Head low position,

(b) Oxygen.

(c) Glucocorticoids. They are useful because they increase the strength of heart in last stages of shock, by stabilizing lysosomal membranes they prevent release of enzymes of cells and help in metabolism of glucose by the severely damaged cells.


Long Questions

• Describe how normal arterial blood pressure is maintained.

• Describe the normal electrocardiogram. How is it recorded? What is the physiolog­ical significance of its reflections?

• Describe the pressure and volume changes occurring in the left ventricle during the cardiac cycle.

• Describe the sequence of events in a cardiac cycle.

• Define cardiac output. What are the factors affecting it? Describe any one method for its measurement in man.

• Describe in detail the production and propagation of cardiac impulse.

• Describe the regulation of heart rate.

• Describe the physiology of coronary circulation.

• What is shock? Explain different causes, symptoms, signs and treatment of shock.

Short Questions

• Peripheral resistance.

• Heart sounds.

• Coronary circulation.

• Pulmonary circulation.

• Capillary circulation.

• Jugular pulse tracing.

• Sino-aortic baroreceptor reflex.

• Baroreceptors.

• S.A. node as pacemaker.

• Electrocardiogram.

• P.R. interval.

• Carotid sinus.

• Cerebral circulation.
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