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Cardiovascular system

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Enumerate the functions of cardiovascular system.

  1. Distribution of metabolites and oxygen to all the body cells.

  2. Collection of waste products and CO2 from different body cells and carry them to excretory organs.

  3. Thermoregulation — Carrying of heat from active metabolic sites (where heat is generated) to body surface where it is dissipated. Blood flow through skin varies to enhance or decrease the heat loss to the environment.

  4. Distribution of hormones to the target tissues.

Heart which is a muscle pump provides the driving force causing flow of blood for the system whereas arteries are the distributing channels. Veins act as reservoirs and also collect and return the blood back to the heart.

Between arteries and veins, there are capillaries which actually supply blood to tissue cells. They act as exchange vessels because they are thin walled.

^ Name various chambers of the heart.

Heart is divided into left and right heart. Each half is further divided into two parts—atrium and ventricle. Thus, there are four chambers of the heart: left and right auricles (atria) and left and right ventricles. Right side of the heart collects the deoxygenated blood from tissues and pumps it to the lungs for oxygenation, whereas left heart collects the oxygenated blood from lungs and pumps the oxygenated blood to different tissues. Thus, heart actually has two pumps—right and left.

^ How are the different chambers of the heart separated?

Left chambers of the heart are separated from the right chambers by a continuous partition. The atrial portion of this partition is known as interatrial septum while ventricular part is known as interventricular septum.

The right atrioventricular opening is guarded by a tricuspid valve so named because it has three cusps, viz. anterior, posterior and medial. Left atrioventricular opening is guarded by a bicuspid valve (mitral) which has two cusps, viz. anterior and posterior.

^ What are semilunar valves?

From left ventricle arises the aorta which carries blood to the tissues and from right ventricle arises the pulmonary artery (trunk) which carries deoxygenated blood to the lungs. The openings between aorta, pulmonary artery and respective ventricles are guarded by semilunar valves, having three cusps.

^ What is the function of valves in the heart?

Valves allow unidirectional flow of blood. Atrioventricular valves open towards the ventricles and close towards the atria. They allow blood to flow from atria to ventricles but when ventricles contract, they are closed and thus prevent back flow of blood from ventricles to atria.

Semilunar valves open away from ventricles and close towards the ventricles. These valves open when ventricles contract allowing the blood to flow from ventricles to aorta and pulmonary trunk. They close when ventricles relax thus preventing back flow of blood from aorta or pulmonary trunk into the ventricles.

^ Describe the course of systemic circulation.

Systemic or greater circulation is responsible for pumping oxygenated blood to different tissues and collecting deoxygenated blood from tissues back to the heart. In this circulation, blood is pumped by the left ventricle to all the tissues (except the lungs) and is returned back to the right atrium. Vessels carrying blood away from heart are termed arteries and those carrying blood from tissues to heart are called veins. In systemic circuit, blood leaves left ventricle via a single large artery, the aorta. The systemic arteries branch from aorta dividing into progressively smaller branches. The smallest arteries form arterioles which branch into very small, thin walled capillaries only lined by single layer of endothelial cells. Through these, exchange of materials between blood, tissues and cells occurs. Capillaries unite to form thicker vessels called venules (arterioles, capillaries and venules are collectively known as microcirculation).

Venules in systemic circulation unite to form larger vessels called veins. The veins from various peripheral organs unite to form two large veins: inferior vena cava which collects blood from lower portions of the body and superior vena cava collecting blood from the upper half of the body. Through these two veins, blood returns to the right atrium.

^ Describe the course of pulmonary circulation.

Pulmonary circulation is responsible for pumping the deoxygenated blood to the lungs and collecting oxygenated blood from lungs back to the heart as follows:

Blood leaves the right ventricle via a single large artery, the pulmonary trunk which divides into two pulmonary arteries, one supplying each lung. In the lungs, the arteries continue to branch ultimately forming capillaries that unite into the venules and veins. The blood leaves the lungs via pulmonary veins which empty into the left atrium.

^ Describe in short the structure of cardiac muscle.

Cardiac muscle (myocardium) consists of the separate cardiac muscle cells (striated) that are electrically connected to one another by tight junctions. These connections are low resistance patnways and are called intercalated disc. Though there is no anatomical connection between different cardiac muscle fibres from functional point of view, action potential passes from one cardiac muscle cell to the other through gap junctions and cardiac muscle acts as a syncytium of many cardiac muscle cells, i.e. excitation of one cardiac cell causes the action potential to spread to all the other cells. Heart is composed of two separate syncytiums—the atrial syncytium (walls of two atria) and ventricular syncytium (walls of two ventricles). Action potential is conducted from atrial syncytium to ventricular syncytium by way of specialized conducting system. Normally there is one functional electrical connection between atria and the ventricles. This is A. V. node and its extension 'bundle of His'. Because atria and ventricles are two separate syncytiums, atria contract a short time ahead of ventricular contraction (Fig. 13.1).

Fig. 13.1 The syncytial nature of cardiac muscle.

Describe the specialized excitatory conductive system of the heart.

There is a specialized excitatory system which generates rhythmic impulses to cause rhythmic contraction of the heart and special conductive system which conducts these impulses throughout the heart.

Excitatory and conductive system (Fig. 13.2)

  1. S. A. node (sino-atrial node). It is located near the junction of superior vena cava and the right atrium. It acts as a pacemaker because the rate of impulse generation is highest.

  2. Interatrial tract (Bachman 's bundle). It is a band of specialized muscle fibres that run from sinoatrial node to left atrium. It causes simultaneous depolarization of both the atria, since the velocity of conduction of impulse in this tract is faster than rest of the atrial muscles.

  3. Internodal tracts. Three pairs of specialized celts connect sinoatrial node to atrioventricular node. They are anterior, middle and posterior. Through them impulses from sinoatrial node reach atrioventricular node to initiate ventricular contraction. These are specialized conducting fibres mixed in the atrial muscle.

  4. A. V. node (atrio-ventricular node). It is located just beneath the endocardium on the right side of the interatrial septum, near the tricuspid valve. Normally it is the only path through which ventricles are activated.

  5. Bundle of His. It is the continuation of A.V. node and is located beneath the

endocardium on the right side of the interventricular septum. It divides into two branches known as right and left bundle branches. These proceed on each side of the interventricular septum to their respective ventricles.

6. Purkinjefibres. These fibres arise from both the bundle branches and branch out extensively just beneath the endocardium of both the ventricles.

Fig. 13.2 Special excitatory and conductive system of the heart.

What is the resting membrane potential of normal cardiac muscle?

Resting membrane potential of normal cardiac muscle is -85 to 95 mV

Describe the action potential of the cardiac muscle.

Fig. 13.3 An action potential from Purkinje fibre of the heart showing plateau.

Record of action potential in the ventricular muscle shows that there is an initial

spike, i.e. rising of resting membrane potential from -85 to 90 mV to a slightly positive value(up+20mV). The positive portion is called overshoot potential. After initial spike, membrane remains depolarized for 0.2 s in atrial and 0.3 s in ventricular muscle fibres. This sustained depolarization is seen as plateau. After plateau there is abrupt repolar­ization (Fig. 13.3).

What is the cause of plateau recorded in cardiac muscle action potential?

  1. Initial spike of action potential of cardiac muscle is due to opening of fast voltage- gated sodium channels causing diffusion of sodium ions into the fibres. Plateau is due to opening of slow voltage - gated calcium sodium channels through which calcium and sodium ions continue to diffuse into the fibre. This causes prolonged phase of depolarization, i.e. plateau.

  2. At the onset of action potential, permeability of membrane for potassium decreases about five fold. This greatly decreases potassium outflux during action potential plateau and thereby prevents repolarization. When slow calcium-sodium channels close at the end of 0.2- 0.3 s, then membrane permeability for potassium rapidly increases causing rapid outflux of potassium. This results into returning of membrane potential to resting level (repolarization).

What is the velocity of conduction of impulse in the cardiac muscle?

Velocity of conduction of impulse (action potential) in both atrial and ventricular muscle fibres is about 0.3-0.5 m/s.

How much is the refractory period of cardiac muscle?

Absolute refractory period of atrial muscle is 0.15 s and relative refractory period is 0.03 second. Ventricles have absolute refractory period much longer 0.25-0.30 s and relative refractory period for additional 0.05 second.

Explain phenomenon of excitation-contraction coupling in the cardiac muscle.

Sarcoplasmic reticulumin the cardiac muscle is less well developed than in skeletal muscle. It is present as a network of tubules surrounding the myofibrils. It has dilated terminals (cisternae) which are located next to the external cell- membrane and T tubules. Sarcoplasmic reticulum and cisternae contain high concentration of ionic calcium.

T tubules are continuations of cell membrane and they conduct action potential to the interior of the cell. They invaginate to the interior of the cell at the 'Z' line of sarcomere. Therefore there is only one T tubule present per sarcomere.

When action potential passes over the cardiac muscle membrane, it passes to the interior of the muscle cells through T tubules.

Action potential acts on the membranes of longitudinal sarcoplasmic tubules to cause instantaneous release of calcium. Calcium ions diffuse into the myofibrils and catalyze chemical reactions that promote sliding of actin and myosin filaments which in turn produce muscle contraction. In addition, in cardiac muscle (as against that in skeletal muscle) extra calcium ions diffuse into the sarcoplasm from T' tubules without which contraction strength would be considerably reduced.

'T' tubules of cardiac muscle contain mucopolysaccharides which are negatively charged and bind an abundant store of calcium ions. 'T' tubules open directly to the exterior and therefore calcium ions in them directly come from extracellular fluid. These calcium ions diffuse into the sarcoplasm when action potential propagates along the'T' tubules. Because of this, strength of cardiac muscle contraction depends to a great extent on calcium concentration in extracellular fluid. Whereas skeletal muscle contraction is hardly affected by calcium concentration in ECF.

^ What is the duration of contraction in cardiac muscle?

Duration of contraction for atrial muscle is 0.1 second and for ventricular muscle is 0.3 second.

What is autorhythmicity?

Cardiac fibres especially, specialized conducting system have the property of self-excitation because of which they can cause initiation of rhythmic impulses which in turn can cause automatic rhythmic contractions. This property is called autorhythmicity. Sinus node normally initiates the rhythmic impulse and controls the rate of beating of the heart. Thus] it is called as pacemaker of the heart.

^ Explain the mechanism responsible for sinus nodal rhythmicity.

Sino-atrial nodal fibres have a resting membrane potential which is not steady. It manifests a slow depolarization. This is because of leakage of the resting membrane for sodium. This causes slow diffusion of sodium ions into the S.A. nodal fibres under resting condition. The potential therefore, slowly rises from -55 mV due to entry of sodium ions. When potential rises to a threshold level, i.e. -40 mV, the slow voltage-gated sodium-calcium channels open and action potential is initiated. Entry of sodium and calcium through the opened channels causes a rapid depolarization (i.e. action potential). Then at the end of depolarization, potassium channels open and Na+-Ca++ channels close. This causes potassium ions to diffuse out of the fibres resulting into rapid repolarization to -55 to -60mV. Again because of leakage of membrane to sodium ions, there is slow diffusion of sodium ions causing slow depolarization. When potential reaches a threshold (-40 mV), another action potential is initiated because of opening of slow voltage-gated sodium-calcium channels. Thus there is initiation of impulses (action potentials) at regular intervals of time (autorhythmicity) (Fig. 13.4).

^ Describe the impulse conduction from S.A. node to Purkinje system.

Action potential is initiated in the S.A. nodal fibres. Ends of S.A. nodal fibres are fused with surrounding atrial muscle fibres. Therefore action potential originated in S.A. node travels outward in these fibres. This way impulse spreads over the atria. Conduction is more rapid in several small bundles of atrial fibres called interatrial tract or band. Conduction through these fibres causes simultaneous depolarization of both the atria. The rate of conduction in these fibres is 1 m/s.

Fig. 13.4 Rhythmic discharge of an S.A. nodal fibre.

There are three pairs of internodal tracts (anterior, middle, posterior) through which impulse passes from S.A. node to A.V. node fibres.

Impulse reaches A.V. node within 0.03 sec after its origin in S.A. node. At A.V. node, there is adelay of 0.09 s and further delay in 'bundle of His', for 0.04 s (total delay is 0.13 s) (Fig. 13.5).

Fig. 13.5 Transmission of the cardiac impulse through the heart showing the time of appearance (in fraction of a second) of the impulse in different parts of the heart.

Causes of A. V. nodal delay

(a) Fibres connecting internodal tract and A.V. node are called transitional fibres. These are very small fibres conducting the impulse at a very slow rate, i.e. 0.02 - 0.05 m/s.

  1. Velocity of impulse conduction in A.V. nodal fibres is also slow, i.e. 0.05 m/s.

  2. Resting membrane potentials of transitional fibres and A.V. nodal fibres are much less negative than rest of the cardiac muscle fibres.

  3. There are very few gap junctions connecting successive fibres in the pathway.

Bundle of His conducts impulse from A.V. node to its left and right branches. Except in certain abnormal states, fibres of A.V. bundle conduct the impulse from atria to ventricle and not in the reverse direction. This allows forward conduction of impulse. Atrial muscle is separated from ventricular muscle by a continuous fibrous barrier which acts as a barrier to passage of impulse through any other route from atria to ventricles except through A.V. bundle.

A.V. bundle passes downward in ventricular septum for 5-15 mm and then divides into left and right bundle branches. Through these branches, impulse passes to two ventricles. Branches divide into Purkinje fibres which become continuous with cardiac muscle fibres.

The time taken for impulse to travel from bundle branches to Purkinje fibres is 0.03 second. Through Purkinje fibres, impulse is spread rapidly to ventricular muscle fibres. The velocity of transmission of impulse in ventricular muscle fibres is 0.3-0.5 m/s. It first spreads oVer the endocardial surface and then the cardiac muscle fibres which are arranged indouble spirals. Therefore impulse does not necessarily travel outwards (towards the surface) but it angulates towards the surface along the directions of spirals. Therefore transmission from endocardial surface to epicardial surface takes about 0.03 second. Thus total time for transmission in normal heart from initial bundle branches to ventricles is 0.06 second.

Time required Pathway of impulse

S.A. node S.A. node

0.03 s

A.V. node Atria through interatrial band

0.13 s

Bundle branches A.V. node through three internodal bands

0.03 s

Purkinje fibres Transitional fibres

0.03 s

Endocardial to A.V. node

epicardial surface

Bundle of His

Bundle branches

Purkinje fibres

Endocardial and epicardial surfaces of ventricles

Total time required for conduction from S.A. node to endocardial surface is 0.22 second.

^ What is the importance of A.V. nodal delay?

Atria and ventricles are excited at different times and also contract at different times because of A.V. nodal delay.

Why does sinus node act as a pacemaker of the heart?

Other parts of the conductive system are also capable of generating their rhythm but still S.A. node acts as a pacemaker because rate of impulse generation by S.A. node is highest.

^ What is ectopic pacemaker?

When pacemaker is other than S.A. node it is called as ectopic pacemaker, e.g. A.V. node or Punkinje fibres may act as pacemakers. Ectopic pacemaker causes abnormal sequence of contraction of different parts of the heart.

What are the causes of shift of pacemaker?

Causes of shift of pacemaker from S.A. node to other sites are:

(a) Rate of discharge in other parts of the heart becomes higher than that of S.A. node.

(b) Blockage of transmission of impulse from S.A. node to A.V. node.

What is Stokes-Adams syndrome?

When there is A.V. block, atria continue to beat at the normal rhythm (i.e. of S.A. node) while new pacemaker develops in Purkinje system of ventricles with a rate of 15-40/min. But after a sudden block, Purkinje system does not begin its rhythm immedi­ately. It takes about 15-30 s. During this time, ventricles fail to contract. Thus the person faints because of lack of blood flow to the brain. This delayed pick-up of heart beat is called Stokes-Adams syndrome. If period is too long, death may occur.

^ Explain the role of autonomic nervous system in controlling heart rhythm.

Heart is supplied by parasympathetic and sympathetic nerves. Parasympathetic supply passes through vagus nerve. Sympathetic supply comes from 1 to 5 thoracic segments of spinal cord. Preganglionic fibres relay in superior, middle and inferior cervical ganglia. Postganglionic nerves supply the heart, Vagi nerves mainly innervate sinus and A.V. nodes, to a lesser extent the muscle of two atria and even to a lesser extent the ventricular muscle. Sympathetic nerves are distributed to all parts of the heart, especially to ventricular muscles as well as to other areas.

^ Effect of parasympathetic stimulation

Parasympathetic stimulation causes release of acetylcholine at vagal nerve end­ings. It causes: (a) decrease in the heart rate by decreasing the rate of sinus rhythm, (b) decreased excitation of A.V. node, A.V. junctional fibres, atrial musculature, thus

reducing the rate of transmission of impulse into ventricles. Strong stimulation may completely block the transmission and ventricles may stop beating for 4-10 s. If it happens, Purkinje system initiates the rhythm causing ventricular contraction at a rate of 15-40/min. This phenomenon is called vagal escape.

^ Mechanism of action. Acetylcholine released at the nerve endings increases the permeability of the fibre membrane for potassium ions. This causes rapid diffusion of potassium to the exterior of the fibre causing hyperpolarization, decreasing excitability of the tissue.

Effect of sympathetic stimulation

Sympathetic stimulation increases the rate of sinus rhythm, rate of conduction of impulse as well as increased excitability in all the portions of the heart. Force of contraction of atria and ventricles increases greatly.

^ Mechanism of action. Stimulation of sympathetic nerves causes release of norepi-nephrine at the nerve endings. Probably this increases permeability of cardiac muscle fibre to sodium and calcium. In A.V. node increased sodium permeability makes it easier for action potential to excite the surrounding portion, decreasing rate of conduction time from atria to ventricles. Increased permeability for calcium increases the contractile strength of the heart.

^ What is vagal tone?

Right vagus nerve innervates the S.A. node and liberates acetylcholine from its endings. Normally, vagal activity hyperpolarizes S.A. node fibres by increasing permeability of S.A. nodal fibres for potassium. This hyperpolarization slows the firing rate of S.A. node from its automatic rate of 90-120 beats/min to the actual heart rate of about 72 beats/min. This normal vagal activity is called vagal tone.

^ What is cardiac cycle?

The period of beginning of one heart beat to the beginning of the next is called cardiac cycle.

What is normocardia?

Normal resting heart rate of 60-100 beats/min is called normocardia.

What is tachycardia?

Heart rate more than 100 beats/min is termed as tachycardia.

^ What is bradycardia?

Heart rate below 60 beats/min is termed as bradycardia. It is commonly seen in well-trained athletes.

Name various cardiac cycle events.

Cardiac cycle includes both electrical (ECG) and mechanical events. Electrical events precede and initiate the corresponding mechanical events.

Name different mechanical events occurring during cardiac cycle.

Main events in cardiac cycle are: (a) atrial contraction (systole) and atrial relaxation (diastole) (b) ventricular contraction (systole) and (c) ventricular relaxation (diastole) The total period of one cycle is 0.8 sec. Atrial systole—0.1 sec and atrial diastole—0.7 sec. Ventricular systole—0.3 sec and ventricular diastole—0.5 sec. Other events are as follows:

  1. Atrial systole (0.1 sec).

  2. Ventricular systole consisting of:

(i) Isovolumic (isometric) contraction (0.5 sec), (ii) Rapid ejection (0.11 sec), (iii) Reduced ejection (0.14 sec).

(c) Ventricular diastole consisting of: (i) Protodiastole (0.04 sec).

(ii) Isovolumic (isometric) relaxation (0.06 sec), (iii) Rapid passive filling (0.11 sec), (iv) Reduced filling (diastasis) (0.19 sec).

Describe various events in the cardiac cycle.

1. Atrial systole (contraction). During the period of ventricular relaxation, blood flows from atria to ventricles. About 75% of the blood flows to ventricles before atria contract. Both atria contract almost simultaneously and pump the remaining 25% of blood into the respective ventricles (therefore even if atria fail to function it is unlikely to be noticed unless a person exercises). The contraction of atria increases, the pressure inside the atria to 4-6 mm Hg in the right atrium and about 7-8 mm Hg in the left atrium. The pressure rise in right atrium is reflected into the veins and this wave is recorded as 'a' wave (recorded from jugular vein with the help of a transducer).

Then there is a period of atrial diastole for rest of the cardiac cycle (0.7 second) during which various ventricular events occur in sequence as follows:

2. Ventricular systole (contraction). At the termination of atrial contraction, the pressure of blood in the ventricles rises (normally less than 12 mm Hg). Rising ventricular pressure now exceeds the atrial pressure.

This causes closure of A.V. valves which is a major component responsible for generating first heart sound. Then there are following phases of ventricular systole:

(a) ^ Isovolumic or isometric contraction. At the beginning of this phase A.V. valves are closed but semilunar valves are not yet opened. Thus ventricular chambers are sealed from both atria and the arteries. The ventricle starts contracting but volume of blood inside both the ventricles remains the same hence this phase is called as isovolumic phase of contraction. This phase lasts for about 0.05 second. During this phase ventricles contract as a closed chamber and pressure inside the ventricles rises rapidly to a high value.

When pressure in the left ventricle is slightly above 80 mm Hg and right ventricular pressure slightly above 8 mm Hg, then the ventricular pressures push the semilunar valves open. This causes ejection of blood from ventricles to the respective arteries in next phases.

  1. ^ Rapid ejection phase. As soon as the semilunar valves open, blood is rapidly ejected. About two-third of the stroke volumeis ejected in this rapid ejection phase. The duration of this phase is about 0.11 second. Pressure inside the left ventricle rises to 120 mm Hg during this phase. The end of rapid ejection phase occurs at about the peak of ventricular and atrial systolic pressure. The right ventricular ejection begins before that of left and continues even after left ventricular ejection is complete. As both the ventricles almost eject same volume of blood, the velocity of right ventricular ejection is less than that of the left ventricle.

  2. ^ Reduced ejection phase. During later two-third of systole rate of ejection declines. During this phase of reduced ejection, rest one-third stroke volume is ejected. This phase lasts for about 0.14 second. During the period of slow ejection ventricular pressure falls to a value slightly lower than that in aorta but still blood continues to empty into aorta because blood flowing out has built up momentum. As this momentum decreases, kinetic energy of

u; momentum is converted to pressure in the aorta. This causes aortic pressure

to rise slightly above that of the ventricle. 3. Ventricular diastole or relaxation. It occurs in following phases:

  1. Protodiastole—At the end of ventricular systole, ventricles start relaxing allowing rapid fall in the intraventricular pressures. This is the period of protodiastole which lasts for 0.04 seconds. At the end of this phase, elevated pressures in distended arteries (aorta and pulmonary artery) immediately pushes the blood back towards the ventricles which snaps the aortic and pulmonary semilunar valves closed. This is the major component in generating second sound (closure of semilunar valves). It also causes dicrotic notch in the down slope of aortic pressure called incisura. Incisura indicates end of systole and the onset of diastole.

  2. ^ Isovolumic or isometric relaxation — The ventricles continue to relax as closed chambers as semilunar valves are closed and A.V. valves are not yet open. This causes rapid fall of pressure inside the ventricles (from 80 mmHg to about 2 to 3 mm Hg in the left ventricle). This phase lasts for 0.06 seconds. Because the ventricular volume remains constant, this phase is called as isovolumic phase. When ventricular pressures fall below the atrial pressures the A.V. vajves open.

  3. ^ Rapid filling phase — During ventricular systole because A.V. valves are closed, large amount of blood accumulates in atria because veins continue to empty the blood into them and this causes increase in pressure inside atria. High atrial pressure causes the blood to flow rapidly into the ventricles. Then pressures in both the chambers fall as ventricular relaxation continues.

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