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Cardiovascular system

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What is the function of veins?

Sixty per cent of the circulating blood is present in the venous system. So it serves as a blood reservoir. Especially extensive and compliant areas which act as specific blood reservoirs are liver sinuses, large abdominal veins, venous plexus beneath the skin and spleen.

^ What is the structure of capillary system?

Capillaries are thin-walled vessels which lie between arterioles and venules and supply blood to the tissues. Blood from arterioles passes into metarterioles—> capillaries —> venules—> returns to the general circulation.

Arterioles are highly muscular and can change their diameter. The metarterioles (the terminal arterioles) do not have continuous muscle coat but at the point from where true capillaries originate smooth muscle fibres encircle the metarteriole forming precapillary sphincter. This sphincter can open or close the entrance to the capillaries. Total surface area of tissue capillaries is 500-700 sq.m.

Capillary is lined by unicellular layer of endothelial cells which is surrounded by basement membrane on the outside. The diameter of capillary is 4-9 mbarely large enough for the passage of red blood cells, other blood cells squeeze through it. Thin slit lying between two endothelial cells of the capillary wall is called as intercellular cleft. Each of this cleft is interrupted periodically by short ridges of protein attachments that hold the endothelial cells together but each ridge in turn is broken after a short distance, so that in between them fluid can percolate through the cleft. Cleft usually has a uniform spacing with a width of approximately 6- 7 nm. These are termed as 'slit pores'. In some tissues pores in the capillaries have special characteristics, e.g. (a) In the brain, junctions between capillary endothelial cells are tight junctions allowing only small molecules to pass into the brain tissue and therefore act as blood- brain barrier, (b) In the liver, clefts or pores are very wide so that even plasma proteins can pass from the blood into the liver tissues, (c) In kidney, number of small oval windows called fenestrae penetrate directly through the middle of endothelial cells in addition toclefts.

Blood flows into the capillaries intermittently, because of phenomenon of vasomotion, i.e. intermittent contraction of metarterioles and precapillary sphincters. This in turn is mainly controlled by concentration of oxygen in the tissues.

^ What is the function of capillary system?

Function of capillaries is to maintain average rate of blood flow through each tissue. Capillary bed maintains average capillary pressure and average rate of transfer of substances between blood of capillaries and the surrounding interstitial fluid.

Lipid soluble substances can directly diffuse through the cell membranes of the capillary. Water soluble substances cannot pass through lipid membranes of endothelial cells. Such substances pass through the pores.

^ What is interstitium? What is present in it?

Spaces between the cells are collectively known as interstitium. It contains fluid known as interstitial fluid and two major types of solid structures—collagen fibres and proteoglycan filaments. Collagen fibres are strong and therefore they provide most of the tensional strength to the tissue. Proteoglycan filaments form fine reticular filaments described as 'brush pile'.

Proteoglycan filaments and fluid entrapped in them has a characteristic of gel and is called tissue gel. Rest of the fluid (which is in very small quantity) forms the free fluid. This amount is very slight (less than 1%). When the free fluid in the tissue space increases, oedema results. Free fluid and gel are continuously interchanging with each other.

^ State the factors determining fluid movement from blood to interstitial fluid and in opposite direction.

Following factors affect the fluid movement between blood in capillaries and the interstitial fluid:

1. Capillary pressure. This tends to force the fluid out through the capillary membrane. At the arterial end of capillary, pressure is 30-40 mm Hg and at the venous end of capillary, pressure is 10-15 mm Hg and in the middle, pressure is about 25 mm Hg.

  1. Interstitial fluid pressure. This tends to force fluid inward through the capillary membrane. It is about -3 to -5 mm Hg.

  2. Plasma colloid osmotic pressure. This tends to cause inward movement of fluid through the capillary membrane. It is about 28 mm Hg.

  3. The interstitial fluid colloid osmotic pressure. This tends to cause the fluid movement outward through the capillary membrane and it is about 8 mm Hg.

All above forces are called Starling's forces.

What are the functions of tissue blood flow?

1. Delivery of oxygen to the tissues.

2. Delivery of other nutrients to the tissues.

3. Removal of CO2from the tissues.

4. Removal of hydrogen ions from the tissues.

5. Maintenance of proper concentration of other ions in the tissues.

6. Transport of various hormones and other specific substances to the different tissues.

Blood flow to the various tissues is usually regulated at the minimal level that will supply its requirements, neither more, nor less.

Name the local mechanisms controlling blood flow.

Local blood flow control occurs in two different phases:

1. Acute control occurs by rapid changes in local constriction of arterioles, metarterioles and precapillary sphincters. This occurs within seconds or minutes.

^ 2. Long-term control causes slow change in the flow over a period of days, weeks or even months. This is due to increase or decrease in physical sizes and the number of blood vessels supplying the tissue.

Describe acute control of local blood flow.

Local blood flow increases with increase in rate of tissue metabolism and vice versa. There are two basic theories for regulation of blood flow:

1. Vasodilator theory. Greater the rate of metabolism, lesser is the blood flow and lesser is the availability of oxygen and other nutrients to the tissues. This causes greater release of certain vasodilator substances from the tissues. These substances diffuse to precapillary sphincters, metarterioles and arterioles to cause their dilatation. Different vasodilator substances suggested are adenosine, CO2, lactic acid, adenosine phosphate compounds, histamine, potassium ions and hydrogen ions. Most of these substances are released in response to oxygen deficiency (especially adenosine and lactic acid). Adenosine plays important role in controlling coronary blood flow. But it is difficult to prove whether sufficient quantifies of any single vasodilator substance are formed in the tissues to cause measured increase in blood flow. Probably there is a combined effect of number of vasodilator substances.

2.O2demand theory (nutrient demand theory). O2 is required to maintain vascular muscle contraction. In absence of adequate blood flow, there is inadequate supply of oxygen and other nutrients. This causes vasodilatation because of opening of precapillary sphincters and metarterioles.

Normally precapillary sphincters and metarterioles, open and close cyclically (vasomotion). When there is a lack of oxygen, precapillary sphincters cannot contract properly. They open up and remain open for a long time. When O2 concentration is high, precapillary sphincters and metarterioles close and remain closed until tissue cells consume excess oxygen and oxygen concentration comes back to normal. Similarly,

lack of glucose, also has the same effect as lack of O2 on smooth muscle of precapillary sphincters and metarterioles.

^ What is the reactive hyperaemia?

When blood supply to a tissue is blocked for a few seconds to several hours and then is unblocked, the flow through the tissue usually increases to about five times normal and increased flow continues for few seconds to few hours (depending on how long the flow was blocked). This phenomenon is known as reactive hyperaemia. This is due to metabolic control of local blood flow and explains close relationship between local blood flow regulation and delivery of nutrients to. the tissues.

^ What is active hyperaemia?

When tissue becomes very active, such as during exercise, the rate of blood flow to the tissues increases. This is due to relative lack of nutrients and O2 leading to local vasodilatation. This is known as active hyperaemia.

What is the effect of arterial blood pressure on blood flow to the tissue?

Blood flow is maintained relatively normal despite of the arterial pressure variation between 70 mm Hg-175 mm Hg. This is called as autoregulation of blood flow, it is explained by two theories:

1. ^ Metabolic theory. When arterial blood pressure increases, the excess flow provides too many nutrients to the tissues and it also flushes the vasodilator substances. These two effects cause blood vessels to constrict and flow returns to almost normal despite of the increased pressure.

2. Myogenic theory. It is observed that sudden stretch on the small blood vessels causes smooth muscled of blood vessel wall to contract. Therefore when arterial blood pressure increases and stretches the vessel, it causes vascular contraction and reduces the blood flow nearly back to normal. Conversely at low blood pressures, the degree of stretch of the vessel is less, so that smooth muscle of the vessel relaxes and allows increased blood flow.

It is yet doubtful whether myogenic autoregulation is powerful mechanism.

^ Explain the long-term mechanism of blood flow regulation.

Long-term mechanism gives far more complete regulation than the acute mecha­nism. In this mechanism, degree of vascularity of the tissues changes. There is reconstruction of tissue vasculature to meet the needs of the tissue, e.g. arterial pressure falls to 60 mm Hg and remains at this level for a long time. The physical structural sizes of the vessels in the tissue increase and also the number of vessels increase.

Probable stimulus for increased or decreased vascularity in many instances is needed for tissue oxygen, e.g. increased vascularity occurs in tissues of many animals who live at high altitude.

Angiogenesis, i.e. growth of new blood vessels occurs mainly in response to angiogenic factors released from: (a) ischaemic tissues, (b) tissues that are growing rapidly, and (c) tissues having excessively high metabolic rate.

lower third of pons. It transmits impulses through the spinal cord and then through vasoconstrictor fibres to almost all the blood vessels. Following are certain important areas in the centre (Fig. 13.9):

  1. Vasoconstrictor area—It is also called area C-1. It is located bilaterally in the anterolateral portions of upper medulla.

  2. Vasodilator area — It is called area A-l. It is located bilaterally in anterolateral portions of lower half of medulla.

  3. Sensory area — It is called area A-2. It is located bilaterally in the tractus solitarius, in the posterolateral portions of the medulla and lower pons. Neurons in this area receive signals from glossopharyngeal and vagus

Fig. 13.9 Anatomy of sympathetic nervous control of the circulation.

What is vasomotor tone?

Vasoconstrictor area of vasomotor centre transmits signals continuously through the sympathetic vasoconstrictor fibres to the blood vessels. These impulses maintain partial state of contraction in the blood vessel which is called as vasomotor tone.

^ How does vasomotor centre control heart activity.

Lateral portions of vasomotor centre transmit excitatory signals through the sympathetic nerves to the heart. The medial portion of the vasomotor centre which lies near the dorsal motor nucleus of vagus nerve transmits inhibitory impulses to the heart through the vagus nerve.

Thus vasomotor centre can either increase or decrease the heart activity.

^ Describe the role of higher centres in controlling the vasomotor centre.

Higher centres control the vasomotor centre as follows:

  1. Reticular substance of pons, mesencephalon and diencephalon — Lateral and superior portions of reticular substance cause excitation of the vasomotor centre. Medial and inferior portions of reticular substance cause inhibition of the vasomotor centre.

  2. Hypothalamus — Posterolateral portions of hypothalamus cause excitation whereas the anterior part causes mild excitation or inhibition of vasomotor centre.

  3. Cerebral cortex — Stimulation of motor cortex excites the vasomotor center because of impulses transmitted to it via hypothalamus. Stimulation of anterior temporal lobe, orbital areas of frontal cortex, anterior part of cingulate gyrus, amygdala and septum can either excite or inhibit the vasomotor centre.

^ Explain the role of sympathetic vasodilator fibres.

Vasodilator sympathetic fibres mainly supply the skeletal muscles. Anterior hypothalamus mainly controls their activity. It plays role only during muscular exercise causing initial vasodilatation in the vessels of skeletal muscles to cause anticipatory rise in their blood flow.

^ What is vasovagal syncopy?

Fainting occurs when the person has intense emotional disturbances. This is due to intense stimulation of vasodilator fibres to skeletal muscle and at the same time transmission of strong inhibitory signals through the vagus nerve to the heart. There is fall in arterial pressure, decreased blood supply to the brain and person loses conscious­ness. This effect is known as vasovagal syncopy.

^ Explain the role of nervous system in controlling arterial pressure.

Nervous system is capable of controlling the circulation to cause rapid increase in jterial pressure. This is done by arteriolar constriction, constriction of veins and direct stimulation of the heart. The pressure rises within few seconds. Conversely sudden inhibition of nervous system can cause fall in arterial pressure within 10-40 s. Thus nervous control of arterial pressure is most rapid.

Name various reflex mechanisms which maintain normal arterial blood pres­sure.

  1. Baroreceptor reflex

  2. Chemoreceptor reflex

  3. Atrial reflex.

Describe the anatomy of baroreceptors.

Baroreceptors or pressoreceptors are the stretch receptors and are located in the walls of large systemic arteries. They are extremely abundant in two areas:

  1. Wall of internal carotid artery slightly above the carotid bifurcation. This area is known as carotid sinus.

  2. Wall of aortic arch. This area is known as aortic sinus. Baroreceptors are spray type nerve endings lying in the walls. They are stimulated when stretched.

Impulses from carotid sinus are carried by Hering's nerves to the glossopharyngeal nerve and then to tractus solitarius of medulla. Impulses from aortic sinus are carried through vagus nerve to the tractus solitarius (Fig. 13.10).

Fag. 13.10 The baroreceptor system.

Explain the response of baroreceptors to changes in arterial pressure.

Baroreceptors are stimulated on distension of the vessel wall. The carotid sinus represents the most distensible area of the arterial system. Carotid sinus baroreceptors are not stimulated at all when pressure is between 0 and 60 mm Hg. They respond progressively more and more rapidly and reach maximum at 180 mm Hg pressure.

Baroreceptors respond much more rapidly to changing pressures than to a stationary pressure. The normal operating range of baroreceptor varies from 60 - 180 mm Hg. The normal arterial pressure is around 100 mm Hg. A slight change in pressure causes strong autonomic reflexes to readjust the pressure.

Thus baroreceptor reflex mechanism functions most effectively in the pressure range where it is most needed.

^ Describe the baroreceptor reflex.

When the blood pressure increases above the normal level, it causes baroreceptor reflex as follows:

Explain buffer function of the baroreceptor reflex.

Baroreceptor system opposes either increase or decrease in arterial pressure and therefore it is called pressure buffer system and the nerves from the baroreceptors are called buffer nerves. This is possible because the baroreceptor system operates within 60-180 mm Hg pressure.

Baroreceptors therefore relatively maintain constant arterial pressure during various activities or changes in position, e.g. if the person who is lying down suddenly stands, this can cause arterial pressure in the head and upper part of the body to fall and marked reduction can cause unconsciousness. But this is not allowed to occur, because of falling pressure in the baroreceptors. When the person stands, he will elicit

baroreceptor reflex resulting into sympathetic discharge minimizing the decrease in pressure in the head and upper part of the body.

^ Why baroreceptor system is ineffective in causing long-term regulation of blood pressure?

When there is increase in blood pressure, baroreceptors send impulses but later on rate becomes slower and slower (adaptation).

Describe the role of chemoreceptors in control of blood pressure.

Carotid and aortic bodies contain chemoreceptors which are mainly stimulated by chemical stimuli such as oxygen lack, carbon dioxide excess and hydrogen ion excess. They are profusely supplied with blood and therefore when blood pressure falls below a critical level 80 mm Hg chemoreceptors are stimulated because of diminished blood flow resulting into diminished O2 supply and building up of CO2 and H+ ions. They send impulse through Hering's nerves (from carotid bodies) and vagi nerves (from aortic bodies) to the vasomotor centre. This elevates arterial pressure. Thus reflex is responsible for bringing arterial pressure back to normal. But this reflex is not very powerful controller of arterial blood pressure. Still it is important as it is stimulated at low pressure and helps in preventing further fall in blood pressure.

^ Describe atrial reflex.

Atria contain stretch receptors. These are also called low pressure receptors. They play role in minimizing the effect of decreased blood volume on arterial blood pressure. The reflex occurs as follows:

Increase in atrial pressure also causes an increase in the heart rate. This is partly due to direct effect of stretching the sinus node but is mostly due to Bainbridge reflex. Stimulation of stretch receptors in atria -» afferent signals through vagus to medulla of brain —> efferent signals are transmitted through vagus and sympathetic nerves to increase heart rate and probably also the strength of contraction of heart.

^ What is CNS ischaemic response?

When blood flow to the vasomotor centre in the brain stem is decreased enough to cause nutritional deficiency (i.e. cerebral ischaemia) the neurons in the vasomotor centre are strongly excited. This is due to accumulation of CO2 /lactic acid locally near the vasomotor centre. Excitation of vasomotor centre causes strong sympathetic stimulation leading to vasoconstriction leading to increase in blood pressure. Peripheral vessels become totally occluded at certain areas, e.g. kidneys. This most powerful response that activates sympathetic vasoconstrictor system strongly is called CNS ischaemic response. It is initiated when blood pressure falls below 60 mm Hg. This acts as an emergency arterial pressure control system. If rise of pressure does not relieve CNS ischaemia, neuronal cells begin to suffer and within 3-10 minutes become totally inactive.

^ What is Cushing reaction?

When CSF pressure rises and becomes equal to arterial pressure, it compresses the arteries in the brain and cuts off the blood supply to the brain. This initiates the CNS ischaemic response. This causes rise in blood pressure. When blood pressure becomes greater than CSF pressure, blood flows through the vessels of brain and ischaemia is relieved. Blood pressure comes to equilibrium at a new level. This effect is called Cushing reaction. It protects the vital centres in the brain.

^ What is the role of skeletal nerves and muscles in controlling blood pressure?

Though mostly autonomic nervous system controls circulation, the skeletal nerves and muscles play role as follows:

1. Abdominal compression reflex. Whenever vasomotor centre is stimulated (e.g. baroreceptor reflex, chemoreceptor reflex) other reticular areas of brain stem are also stimulated. They send simultaneous impulses through skeletal nerves to skeletal muscles of the body especially abdominal muscles. Contraction of abdominal muscles compresses the abdominal venous reservoirs. This causes increased venous return to the heart and therefore increased cardiac output. This overall response is called abdominal compression reflex.

2. During exercise. During exercise the skeletal muscles contract and compress the blood vessels. This causes translocation of large quantities of blood from the peripheral vessels into the heart and lungs. This increases the cardiac output.

^ What is the role of nervous reflexes described above in maintaining the blood pressure?

Nervous reflexes cause rapid, powerful but short-term regulation of the arterial blood pressure. They gradually lose their ability with time because of adaptation of receptors.

^ What is stress relaxation and reverse stress relaxation?

When blood pressure is high, after some time smooth muscleof blood vessel relaxes leading to vasodilation and fall in blood pressure this is termed stress relaxation.

When blood volume and pressure is low the vessel constricts over a small volume and pressure inside rises, this is termed reverse stress relaxation.

^ Explain role of capillary fluid shift mechanism in regulation of blood pressure.

When arterial blood pressure rises the pressure at arterial end of capillaries becomes higher than normal. This causes greater fluid to be shifted from capillaries to interstitial fluid. This in turn reduces the total circulating blood volume and venous return and thus reduces the blood pressure.

When arterial blood pressure falls, pressure at arterial end of capillaries and therefore at venous end of capillaries is reduced.

This causes greater absorption of fluid from interstitial space into the capillary. This increases blood volume and therefore the blood pressure.

Enumerate various short-term mechanisms regulating blood arterial pressure.

The various short-term mechanisms regulating blood pressure are—

1. Neural reflexes

  1. Baroreceptor reflex.

  2. Chemoreceptor reflex.

  3. CNS ischaemic response.

  4. Atrial reflex.

  5. Abdominal compression reflex.

  1. Stress relaxation and reverse stress relaxation.

  2. Capillary fluid shift mechanism.

What is the basis for long-term regulation of blood pressure?

Arterial pressure and blood volume affect each other, (i) Arterial pressure influences blood volume as follows:

Because blood volume also influences the arterial pressure, in long run, blood volume changes may be the single most important determinant of blood pressure.

Therefore, renal body fluid system is the most fundamental basis of long-term regulation of blood pressure.

^ What is the role of salt in renal body fluid mechanism for controlling blood pressure?

Accumulation of salt indirectly increases the extracellular fluid volume because of two reasons:

1. When there is excess salt in the body, there is increased osmolality of body fluids. This increased osmolality stimulates the thirst centre, making person drink large quantities of water to dilute the extracellular fluid. Thus there is increase in extracellular fluid volume.

2. Increased osmolality of body fluids also stimulates hypothalamic posterior pituitary gland system to secrete increased quantities of ADH (anti-diuretic hormone).

This causes increased reabsorption of fluid from the distal renal tubules. This causes increase in extracellular fluid volume.

^ What is renin? What is its role in long-term regulation of blood pressure?

Renin is aprotein synthesized by juxtaglomerular cells of the kidneys. It is secreted in inactive form called prorenin and is stored in the juxtaglomerular cells. Renin is an enzyme. It acts on the substrate, i.e. plasma globulin or renin substrate or angiotensinogen present in the blood to release angiotensin I. This angiotensin I is converted to angiotensin II by angiotensin converting enzyme present in small vessels mainly in the lungs. Angiotensin II has two principal effects by which it causes elevation of arterial pressure as follows:

(a) It is a powerful vasoconstrictor. Therefore causes powerful vasoconstriction of arterioles and to a lesser extent also of veins. Constriction of arterioles increases the peripheral resistance and thus also increases the blood pressure. Mild constriction of veins increases the venous return. This in turn increases the cardiac output. Increased cardiac output increases the blood pressure.

(b) It directly acts on renal tubules and causes decreased excretion of salt and water. This causes increase in extracellular fluid volume and therefore the blood pressure.

Angiotensin also increases salt and water retention by kidneys indirectly by stimulating release of aldosterone from the adrenal cortex.

Aldosterone in turn acts on distal renal tubules to cause increased absorption of salt and water.

^ What is one kidney Goldblatt's hypertension?

When one kidney is removed and a constrictor is placed on the renal artery of the remaining kidney, then within few minutes arterial pressure begins to rise and continues to rise for several days. The hypertension produced in this way is called one kidney Goldblatt's hypertension. The early rise in blood pressure is due to renin-angiotensin vasoconstrictor mechanism. The second rise is caused by fluid retention.

^ What is two kidney Goldblatt's hypertension?

Hypertension that develops when the artery to one kidney is constricted while artery to the other kidney is still normal, is called two kidney Goldblatt's hypertension.

What is essential hypertension?

Hypertension of unknown origin is known as essential hypertension. In most of the patients, there is a strong hereditary tendency. It is also called primary hypertension.

^ What is neurogenic hypertension?

Acute hypertension which is caused by strong stimulation of sympathetic nerves (due to excessive anxiety) is called as neurogenic hypertension. Repeated acute episodes

can lead to prolonged renal type of hypertension because of sympathetic neurotransmit-ter directly affecting renal arteries leading to their permanent damage.

^ What is cardiac output? How much is it normally?

Cardiac output is the quantity of blood pumped into the aorta each minute by the heart. It is 5 litres in normal adult person.

What is cardiac index? How much is it normally?

Cardiac index is the cardiac output per square metre of body surface area. It is 3 litres in normal adult person weighing 70 kg.

^ What is stroke volume?

Stroke volume is the volume of blood pumped by each ventricle per heart beat.

What is venous return?

The quantity of blood flowing from the veins into the right atrium each minute is known as venous return.

What is Frank-Starling law of the heart?

Frank-Starling's law refers to the relationship between venous return (venous pressure) and cardiac output. An increase in venous return causes greater filling of ventricle during diastole resulting in a greater stretch on the cardiac muscle fibres. This produces a stronger contraction and a greater ejection of blood during systole. Stretch on the S .A. node also increases the rate of the heart. Stretched right atrium also initiates Bainbridge reflex (passing to vasomotor centre) causing increased heart rate. Thus an increased venous return produces increased cardiac output (Frank-Starling law). Therefore venous return is the most important factor controlling cardiac output.

^ What is the effect of local blood flow regulation on cardiac output?

The venous return to the heart is the sum of all the local blood flows from individual segments of the peripheral circulation. Cardiac output regulation therefore is a sum of all the local blood flow regulations and is therefore determined by all the factors that control local blood flow throughout the body. Long time cardiac output varies reciprocally to the changes in total peripheral resistance, when arterial blood pressure is maintained normal, i.e.

Arterial pressure

Cardiac output = ---------------------------

Total peripheral resistance

^ How much amount of blood can normal heart pump without any excess nervous stimulation?

Normal heart can increase the cardiac output with increased venous return (Frank-Starling law) upto about two and half times its normal. Venous return is limiting factor. So normal heart without any excess nervous stimulation has the cardiac output upto 131/min.

What is hypoeffective heart? Enumerate the factors causing hypoeffective heart.

When the pumping ability of the heart is below the normal, the heart is said to be hypoeffective heart.

Factors causing hypoeffective heart:

  1. Inhibition of nervous excitation of the heart.

  2. Valvular heart disease.

  3. Pathological factors causing abnormal rate and rhythm of the heart beat.

  4. Increased arterial pressure.

  5. Congenital heart diseases.

  6. Myocarditis.

  7. Cardiac anoxia.

  8. Myocardial damage or toxicity.

What is hypereffective heart? Enumerate the factors that cause hypereffective heart.

When the pumping ability of the heart is greater than normal, the heart is said to be hypereffective heart (Fig. 13.11).

Fig. 13.11 Cardiac output curves.

Factors causing hypereffective heart:

1. Nervous stimulation—When there is sympathetic stimulation of the heart, there is greatly increased heart rate and also increase in the strength of contraction of the heart. Because of these two effects, cardiac output may be increased upto 25 l/min.

2. Hypertrophy of the heart — Increase in mass and contractility of cardiac muscle is termed hypertrophy of the heart, e.g. heavy exercise.

When above two effects are combined, cardiac output becomes as much as 30-35 1/min.

What is the effect of sympathetic stimulation on cardiac output?

Sympathetic stimulation increases the cardiac output as follows:

  1. Increase the strength of contraction of the heart and thus increases cardiac output.

  2. Causes peripheral vasoconstriction. Constriction of veins increases the venous return to the heart and thus increases the cardiac output.

Describe the methods for measuring cardiac output.

Cardiac output can be measured by following methods:

  1. With the help offlowmeter. In animals, aorta and pulmonary artery or a great vein entering the heart is cannulated and other end of cannula is connected to a flowmeter of any type to record the cardiac output. Electromagnetic or ultrasonic flowmeter can be placed on the aorta or pulmonary artery to measure the cardiac output.

  2. Fick method of measuring output. O2 consumption perminute is determined — say it is 200 ml. O2 concentration of blood entering the heart on right side collected from right ventricle by cardiac catheterization. O2 concentration of blood leaving the left side of the heart (blood collected from any peripheral artery) are determined. From the above data one can find the amount of O2 carried by 1 litre of blood. Since total quantity of O2 consumed is known, cardiac output can be calculated as follows:

Cone, of O2 in arterial blood = 200 ml/L

Cone, of O2 in venous blood = 160 ml/L

Therefore arteriovenous difference in O2 concentration is 40 ml. This means that one litre of blood picks up 40 ml of oxygen from the lungs. Therefore for picking up 200 ml of O2, 5 L of blood would be required. So 5 L is the cardiac output.

O2 absorbed per min by lungs

Cardiac output = -----------------------------------

(In L/min) Arteriovenous O2 difference in ml/L of blood

3. Indicator dilution method. Small amount of indicator dye is injected in the large vein (5 mg of cardio green dye is injected). Dye passes from veins to right side of the heart, then to lungs and back to the left side of the heart and then to the arterial system. Concentration of the dye is recorded as it passes through the arterial system. None of the dye passes to arterial system for first 3 s after the injection, but later the arterial concentration of the dye increases and reaches maximum at the end of 6-7 s. Then the concentration of the dye falls rapidly but before reaching a zero point, some dye gets recirculated through the heart and concentration starts rising. To calculate mean concentration of dye in the artery, the down stroke of the graph is extrapolated to zero point (Fig. 13.12). Then area under entire curve is measured and the average

concentration for the duration of time curve is determined. After this cardiac output is calculated as follows:

Fig. 13.12 Dilution method: Dye concentration curves used to calculate two separate cardiac output levels.

4. Thermal dilution method. Small quantity of cold saline is rapidly injected through a catheter inserted into a peripheral vein and advanced to the right atrium. The quantity of thermal indicator delivefed to the blood is derived from the volume of injectate and its temperature is recorded by a fast response thermistor placed in the lumen of the catheter near the injection orifice. The resultant change in blood temperature is measured by a second thermistor bead mounted in the end of a cardiac catheter advanced from peripheral vein through right heart into the pulmonary artery. The shape and time course of the change in pulmonary artery blood temperature is almost similar to that of the dye concentration curve, following dye injection. Cardiac output is determined by following formula :


  1. Withdrawal of blood for sampling is not required. Therefore method is suitable in infants and children.

  1. Cold saline is absolutely harmless.

  2. Measurements can be repeated in rapid succession.

How is the blood flow through the skeletal muscles regulated?

During the periods of rest, the rate of blood flow to skeletal muscles is 3-4 ml/100 g of muscle.

At this time only 20-25% of muscle capillaries have flowing blood. During exercise when there are rhythmic contractions of the muscles, all dormant capillaries open up, greatly increasing the surface area and the rate of blood flow to the skeletal muscles. There is rhythmic increase in blood flow between the contractions.

Strong tetanic contraction of the muscle causes compression of blood vessels and even total stoppage of blood supply. Increase in blood supply during activity (exercise) is due to local regulation and also due to nervous control.

Local regulation. Due to exercise, muscles use oxygen very rapidly. This in turn decreases local oxygen concentration leading to vasodilatation. Many vasodilator substances (e.g. adenosine ions, acetylcholine, lactic acid) are also released which cause vasodilatation.

^ Nervous control. Skeletal muscles are supplied by sympathetic vasoconstrictor fibres and sympathetic vasodilator fibres.

Sympathetic vasoconstrictor nerves. These nerves release noradrenaline on stimu­lation and cause vasoconstriction and reduced blood flow to muscles. In addition norepinephrine secreted by adrenal medulla also passes into circulating blood to cause vasoconstriction. Adrenaline secreted by adrenal medulla acts on beta receptors of the vessels and causes vasodilatation.

^ Sympathetic vasodilator fibres. In cat and other lower animals, there are sympa­thetic vasodilator fibres which secrete acetylcholine at their endings, which in turn causes vasodilatation. Such fibres are not yet been proved in human beings (but adrenaline acting on beta-receptors of the vessels causes vasodilatation).

^ Describe the circulatory adjustments during muscular exercise.

Effects of exercise on circulatory system:

1. Mass sympathetic discharge — While signals are transmitted from cerebral cortex to muscles, they are also transmitted to vasomotor centre causing following effects:

  1. Increase in the heart rate and strength of contraction of the heart.

Most of the peripheral vessels constrict except arterioles in the active muscles (by vasodilatation due to local effect and effect of adrenaline). Thus most of the non-muscular areas except coronary and cerebral arteries of the body temporarily lend their blood to muscles.

2. Muscular walls of the veins and other capacitative areas of the circulation are contracted powerfully. This promotes increased venous return which in turn increases the cardiac output.

What is cardiac failure? What are its causes?

Failure of the heart to pump enough blood to satisfy the needs of the body is called cardiac failure. It may be manifested in two ways:

(a) Decrease in cardiac output.

(b) By damming of blood in the veins behind the left or the right heart. ^ Causes of heart failure

(a) Acute or chronically progressive coronary artery disease.

(b) Malfunction of heart valves.

(c) Congenital abnormalities of the heart.

(d) Severe hypertension.

What are acute and chronic effects of moderate heart failure? ^ Acute effects

When there is sudden damage to the heart as in myocardial infarction, pumping ability of the heart is immediately depressed. This causes reduction in cardiac output to as low as 21/min. It also causes damming of blood in the veins resulting into increased systemic venous pressure so that right atrial pressure rises to 4 mm Hg. This low cardiac output still sustains life but is associated with fainting.

When cardiac output becomes low, different circulatory reflexes are activated within 30 s, e.g. baroreceptor reflex, hemoreceptor reflex, CNS ischaemia response, reflexes originating in heart. Due to these reflexes, there is strong sympathetic stimulation within few seconds which causes direct effect on the heart. If musculature of the heart is diffusely damaged but still functional, it strengthens the musculature. Or if the part of the muscle has become non-functional, normal muscle is stimulated and compensates for non-functional muscle. Thus heart becomes a stronger pump. Sympa­thetic stimulation also causes increased tone in the blood vessels, especially the veins. This results into increased venous return. This, in turn, increases the pumping ability of the heart increasing cardiac output to about 4.2 1/min adequate to sustain life. Chronic effects After the few minutes of acute attack, a prolonged secondary state begins which causes: (a) Retention of fluid by the kidneys, and (b) progressive recovery of the heart.

(a) Retention of fluid by the kidneys. Decreased cardiac output decreases the urine output and therefore causes retention of fluid and increase in blood volume. When it is moderate, it helps in compensating the diminished pumping ability of the heart. It increases mean systemic filling pressure causing flow of blood towards the heart. Secondly it distends the veins, reduces the venous resistance and increases the flow of blood towards the heart.

If cardiac pumping ability is greatly reduced (less than 25-50% of normal) then blood flow to kidneys is greatly reduced and there is low urinary output. Also there is retention of excess fluid but it has no beneficial effect on circulation as heart is already pumping at its maximal ability. This leads to development of oedema which is detrimental.

(b) ^ Progressive recovery of the heart. Heart gradually recovers because of new collateral blood supply and hypertrophy of undamaged musculature. This is achieved ordinarily within 5-7 weeks.

Thus there is compensation for the damage (compensated heart failure) and person has normal resting cardiac output but if he performs heavy exercise, pumping ability of the heart cannot be increased to a desired level and symptoms of acute failure may return, i.e. cardiac reserve is reduced in compensated heart failure.

What is the effect of severe heart damage?

If heart is severely damaged, sympathetic reflexes, fluid retention are not useful in causing weakened heart to pump a normal output. Therefore cardiac output can never rise enough. Fluid continues to be retained and person develops more and more oedema progressively eventually leading to death. This is called decompensated heart failure. This is treated by: (i) strengthening the heart by giving cardiotonic drugs, (ii) by administering diuretic drugs.

What is left heart failure? When does it occur?

In large number of patients with acute failure, left sided failure predominates over right sided failure leading to unilateral left sided failure. Very rarely there is unilateral right sided failure. When there is predominant left heart failure, right heart pumps normal quantity of blood to the lungs but blood is not pumped out of lungs into the systemic circulation because of left sided failure. This causes increased volume of blood to be retained in the lungs, increased pulmonary capillary pressure (pulmonary vascular congestion) and pulmonary oedema.

What is high output cardiac failure? When does it occur?

When person's cardiac output is much higher than normal, and he has signs of heart failure (high right and left atrial pressures, oedema), it is called 'high output failure'. This is due to over beating of heart with increased venous return and not due to decreased pumping ability of the heart.

This is caused due to circulatory abnormality that drastically decreases the total peripheral resistance.


(a) Arteriovenous fistula.

(b) Beriberi.

(c) Thyrotoxicosis.

What is low output cardiac failure?

  1. In many cases of acute heart attacks, there is slow progressive cardiac deterioration

and heart becomes incapable of pumping adequate blood flow to keep the body alive. All body tissues suffer and begin to deteriorate, ultimately leading to death, within few hours or few days. This type of circulatory shock is called cardiogenic shock or cardiac shock or power failure syndrome. Patient dies of cardiogenic shock before compensatory processes can return cardiac output to normal.

Give an account of the heart sounds.

Closure of the valves of the heart is associated with audible sounds. Normally the heart sounds are heard with a stethoscope which are described as first and second heart sounds. Occasionally third heart sound which is very weak is heard. But fourth heart is not heard by stethoscope because it has very low frequency. It can only be recorded in phonocardiogram (Fig. 13.13).

Fig. 13.13 Heart sounds.

Heart sounds are not directly heard over the valves themselves but they are better heard over four auscultatory areas.

  1. Mitral area — This area lies over the apex beat (normally in the fifth left intercostal space three and half inches lateral to the midsternal line).

  2. Tricuspid area — This lies at the lower end of sternum.

  3. Aortic area — This area lies in the right second intercostal space near the lateral border of the sternum.

  4. Pulmonary area—This area lies in the left second intercostal space near the lateral border of the sternum.

Both the heart sounds, first and second are heard in all four auscultatory areas, but at mitral and tricuspid areas first heart sound is better heard because sound caused by A-V valves are transmitted to the chest wall through the respective ventricles. Second heart sound is better heard over the aortic and pulmonary areas because sounds caused by closure of semilunar valves are transmitted to the aorta and pulmonary artery.

1. ^ First heart sound. This sound is produced due toclosure of A-V valves. Slapping together of valve leaflets sets up vibrations causing vibrations of the adjacent blood, walls of the heart and major vessels around the heart. Contraction of ventricles causes valves to bulge against atria until chordae tendineae abruptly stop the backbulging. The elastic tautness of the valves (tricuspid and mitral valves) then cause backsurging blood to bounce forward again into each respective ventricle. This sets blood, ventricular walls and valves into vibration. It causes vibrating turbulence in the blood. Vibrations travel to surrounding tissues and to the chest wall where sound can be heard with the help of the stethoscope. It is like a word LUBB. It is better heard over mitral and tricuspid areas. The duration of the first sound is 0.14 s, and is low pitched. Significance

  1. It indicates the onset of clinical systole of the ventricles.

  2. The duration and intensity of the first sound indicates the condition of myocardium. If myocardium is weak, first heart sound is short and low pitched. It is prominent when there is hypertrophy of myocardium.

  3. Normal first sound also indicates that A-V valves are properly closing (there is no incompetence).

2. Second heart sound. The second heart sound is due to closure of semilunar valves. It is of higher frequency than the first sound because of (i) tautness of the semilunar valves in comparison with A- V valves, and (ii) greater elastic co-efficient of the arteries (which provide the principal vibrating chambers) in comparison with the much looser ventricular chambers (which are vibrating chambers for the first heart sound).

Thus second heart sound is of higher frequency (high pitched), sharp and of short duration (0.11 sec). It is like a word DUP. The intensity of the sound depends on blood pressure. Sometimes two valves, aortic and pulmonary do not close simultaneously during inspiration. This causes splitting of second sound during inspiration.


  1. It indicates end of systole and beginning of diastole of the ventricles.

  2. Clear second sound indicates that the semilunar valves are closing properly, i.e. there is no incompetence.

  3. Interval between first and second sound is shorter and it indicates clinical systole. The interval between second heart sound and the next first heart sound is longer and it indicates clinical diastole of the heart.

  1. Third heart sound. Occasionally a very weak rumbling third heart sound is heard at the middle third of the diastole. It does not appear until middle third of diastole because in early part of the diastole the heart is not filled with blood sufficiently to create even small amount of elastic tension in the ventricles. The frequency of this sound is low and sometimes so low that it cannot be heard, yet it can be recorded in the phonocardiogram. Its duration is 0.04 second. It can be identified by its relation with the second sound and it coincides with descending limb of V wave of jugular venous pulse.

  2. ^ Fourth heart sound. It is also called atrial sound and is caused by in-rushing of blood into the ventricle when atria contract which initiates vibrations similar to those of the third heart sound. It has a very low frequency, i.e. below 20 cycles/second. Therefore it can never be heard with the help of stethoscope but it can only be recorded by phonocardiogram. It coincides with 'a' wave of jugular venous pulse.

^ What is phonocardiogram?

A specially designed microphone to detect low frequency. It is applied to the precordium. Heart sounds are amplified and recorded by a high speed recording apparatus (oscillograph). The recording is called a phonocardiogram. Machine is also connected with a mirror arrangement which reflects a beam of light on a moving photographic plate. Sounds thus can be graphically recorded.

^ How much is normal heart rate and how is it regulated?

Normal heart rate varies between 72 and 80 beats/min. Regulation of heart rate

Heart rate is adjusted according to the metabolic needs of the body, e.g. it increases during exercise and decreases during sleep so that optimum blood is supplied to the tissues.

Two factors mainly regulate the heart rate as follows:

1. ^ Local mechanism. Any factor which affects S.A. node orjunctional tissue affects the rhythmicity and also the heart rate.

2. Nervous mechanism. There is cardioinhibitory centre connected with vagus and cardioexcitatory centre connected with sympathetic nerves. Vagtos exerts a tonic inhibitory control over the heart which is referred to as vagal tone. In addition vagus is reflexly stimulated through the sino- aortic mechanism. Stimulation of vagus causes decrease in the heart rate, whereas stimulation of sympathetic causes increase in the heart rate.

Cardiac centres, i.e. cardioinhibitory and cardioacceleratory centres are in recip­rocal relation, i.e. stimulation of one depresses the other and vice versa. These cardiac centres are influenced either directly or reflexly.

1. Excitement quickens the heart rate and sudden shock lowers the heart rate. These changes are due to impulses coming to centres from the cerebral cortex and the hypothalamus.

2. Heart rate is also influenced reflexly by cardioinhibitory and cardiostimulatory reflexes and reflexes from other parts of the body.

(a) Sino-aortic reflex—When blood pressure rises, baroreceptors are stretched and sensory impulses from them increase the vagal tone, so that heart rate falls.

(b) Cardioacceleratory reflexes—Venous engorgement of the right atrium and the great veins reflexly increases the heart rate. This is known as Bainbridge reflex. Afferent impulses from engorged veins and right atrium pass via afferent nerves to cardiac centre to cause increase in the heart rate. This occurs during muscular exercise (due to increased venous return).

(c) Reflexes from other parts of the body

(i) Hypoxia — Hypoxia stimulates the respiratory centre reflexly through the chemoreceptors. It also stimulates cardiac centre to cause increase in heart rate. Therefore rapid pulse in heart failure, anaemia, haemorrhage, high altitude, CO poisoning is due to this mechanism.

(ii) CO2 excess—It has a direct as well as reflex effect in causing stimulation of the heart rate.

(iii) Body temperature — Increase in body temperature increases the heart rate by direct action on S.A. node as well as by stimulating cardioacceleratory centre.

(iv) Increased intracranial pressure — It directly stimulates the vagus and lowers the rate.

(v) Adrenaline — It directly stimulates the heart rate but reflexly inhibits it (adrenaline increases the blood pressure and therefore by sino-aortic reflex mechanism reduces the heart rate).

(vi) Thyroxine — Thyroxine increases the heart rate by stimulating meta­bolic rate of S.A. node, increasing BMR of the body and by stimulating the sympathetic.

(vii) Exercise—It increases the heart rate and causes increased venous return, Bainbridge reflex, sympathetic stimulation, CO2excess, etc.

^ What is circulation time? How is it determined?

Time taken for particle in the blood to flow from one point in circulation to the other is known as circulation time. It measures average linear velocity of blood.

Methods of determination

Some substance is injected intravenously and time taken for arrival of that substance at the point of question is determined. The substances used are histamine, fluorescein, potassium ferrocyanide, calcium chloride, radioactive substances, etc.

Circulation time depends on:

(a) Length of circuit.

(b) Method employed — Repeated estimation with same method should be done. Time is measured with the help of the stop watch. Each substance has a characteristic effect on arriving at a specific point, e.g. ether has smell, decholine causes bitter taste.

Factors affecting circulation time are:

(a) Increased cardiac output.

(b) Exercise.

(c) Excitement.

(d) Adrenaline.

(e) BMR — Increase in BMR increases the velocity of blood flow and reduces circulation time.

Normal values of some circulation times:

(a) Arm to tongue —5 ml of 2% decholine is injected into the cubital vein. As soon as drug reaches the tongue, patient feels a bitter taste. The total time taken from arm to tongue is 13 sec.

  1. Arm to lungs — Found with the help of ether. It is 6 seconds.

  2. Arm to face — Found with histamine which causes flushing of face. Time is 24 seconds.

  1. Arm to heart — 12-15 seconds.

  2. Total circulation time — 25 seconds. Clinical significance

Circulation time is reduced in the following conditions:

  1. Increased BMR, as in hyperthyroidism, fever.

  2. Anaemia.

Circulation time is increased in following conditions:

  1. Heart failure — Either right or left sided failure. In right sided failure ether time is lengthened (arm to lungs). In left sided failure decholine minus ether is lengthened.

  2. Hypertension.

  3. Myxoedema.

  4. Polycythaemia vera.

  5. Shock.

  6. Peripheral failure.

What is plathysmograph?

Plathysmograph is the instrument used to find out total volume of blood flowing through an organ or part.

Describe the anatomy of coronary blood supply.

The heart receives its nutrient supply through left and right coronary arteries. Only inner 75-100 (xm of endocardial surface can obtain significant amounts of nutrients from the blood present in heart chambers.

Left coronary artery mainly supplies the anterior and lateral portions of the left ventricle. Right coronary artery mainly supplies most of the right ventricle as well as posterior part of the left ventricle in most of the persons. In about 20% of people, left artery predominates and in 30% both arteries provide nutrients equally. In 50% of persons, right coronary artery predominates.

Most of the venous blood from the left ventricles is collected by way of coronary sinus (it is 75% of total coronary flow) and the venous blood from the right ventricle is collected through anterior cardiac veins directly into the right atrium. A small amount of blood is collected through Thebesian veins which directly open into all the chambers of the heart (Fig. 13.14).

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