Cardiovascular System

Enumerate the functions of cardiovascular system

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 the path of blood through entire cardiovascular system

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 pathways 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 syncytium—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 AV node and its extension ‘bundle of His’. Because atria and ventricles are two separate syncytium, atria contract a short time ahead of ventricular contraction (Fig. 13.1).

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 pacemaker of the heart.

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.

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 SA node acts as a pacemaker because rate of impulse generation by SA node is highest.

Explain the mechanism responsible for sinus nodal rhythmicity

Sinoatrial 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 SA 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 −60 mV. 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. 13.3).

Describe the impulse conduction from SA node to Purkinje system

Action potential is initiated in the SA nodal fibres. Ends of SA nodal fibres are fused with surrounding atrial muscle fibres. Therefore, action potential originated in SA 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.

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

Impulse reaches AV node within 0.03 sec after its origin in SA node. At AV node, there is a delay of 0.09 second and further delay in ‘bundle of His, for 0.04 second (total delay is 0.13 second) (Fig. 13.4).

What is the importance of AV nodal delay?

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

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

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 to +20 mV). The positive portion is called overshoot potential. After initial spike, membrane remains depolarized for 0.2 second in atrial and 0.3 second in ventricular muscle fibres. This sustained depolarization is seen as plateau. After plateau there is abrupt repolarization (Fig. 13.5).

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

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 to 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 to 0.30 second and relative refractory period for additional 0.05 second.

Explain phenomenon of excitation-contraction coupling in the cardiac muscle

Sarcoplasmic reticulum in 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 ectopic pacemaker?

When pacemaker is other than SA node it is called ectopic pacemaker, e.g. AV 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 SA node to other sites are:

What is Stokes-Adams syndrome?

When there is AV block, atria continue to beat at the normal rhythm (i.e. of SA node) while new pacemaker develops in Purkinje system of ventricles with a rate of 15 to 40/min. But after a sudden block, Purkinje system does not begin its rhythm immediately. It takes about 15 to 30 seconds. 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 AV 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.

What is vagal tone?

Right vagus nerve innervates the SA node and liberates acetylcholine from its endings. Normally, vagal activity hyperpolarizes SA node fibres by increasing permeability of SA nodal fibres for potassium. This hyperpolarization slows the firing rate of SA node from its automatic rate of 90 to 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 to 100 beats/min is called normocardia.

What is tachycardia?

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

What is bradycardia?

Heart rate below 60 beats/min is termed 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).

Other events are as follows:

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 to 6 mmHg in the right atrium and about 7 to 8 mmHg 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 mmHg). Rising ventricular pressure now exceeds the atrial pressure.

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

3. Ventricular diastole or relaxation. It occurs in following phases:

During rapid filling and diastasis phase about 75% of blood passes from atria to ventricles. Then the next cycle begins with atrial contraction.

What is stroke volume?

Volume of blood that is ejected by each ventricle with each beat is stroke volume. It is 70 ml.

What is ventricular end diastolic volume?

Ventricular end diastolic volume is the volume of blood in the ventricle just prior to the onset of ventricular contraction. Normally left ventricular end diastolic volume is 110 to 120 ml. It is markedly reduced if the heart rate increases. When heart rate increases periods of systole and diastole become shorter. Decreased period of diastole decreases the filling of ventricle and therefore the end-diastolic volume.

What is ventricular end systolic volume?

Volume of blood remaining in the ventricle at the end of ejection is called end systolic volume. It is normally 40 to 50 ml.

What is ejection fraction?

The fraction of end-diastolic volume that is ejected is called the ejection fraction. Normally it is about 60%.

Describe the pressure changes in atria during cardiac cycle

Atrial pressure curves show three major pressure elevations which are called ‘a’, ‘c’ and ‘v’ waves.

Describe the pressure changes in the left ventricle during cardiac cycle

Before atrial systole, the pressure inside the left ventricle is almost zero. When left atrium contracts and forces blood into the left ventricle pressure rises to about 7 mmHg.

At the end of atrial systole, AV valve closes and semilunar valve is not yet open. Ventricle contracts as a closed chamber (isometric contraction) and therefore pressure inside the ventricle rapidly rises from 7 to 80 mmHg.

At the end of isometric contraction, semilunar valve opens and ventricle starts contracting isotonically. This causes pressure to rise to a peak level of 120 mmHg during rapid ejection phase. Then there is reduced ejection phase in which because of decreased volume of blood in the ventricle pressure decreases slightly to 100 mmHg. Then semilunar valve (aortic valve) is closed and ventricular diastole starts.

During isovolumic relaxation phase, ventricle relaxes as a closed chamber and therefore there is a great pressure fall in the left ventricle from 100 mmHg to about 2 to 3 mmHg. Then AV valve opens and ventricular filling begins.

During rapid filling and diastasis though the ventricle is getting filled and volume of blood is increasing because of relaxation of ventricle, pressure in the ventricle drops to almost zero (Fig. 13.6).

Describe the volume changes in the ventricles

During ventricular diastole, filling of ventricles increases the volume of blood in ventricle, to about 110 to 120 ml which is called end diastolic volume. During ventricular contraction, blood flows rapidly out in phase of rapid ejection and comparatively slowly in slow ejection phase leading to fall in volume to 40 to 50 ml (70 ml blood is pumped out). Thus end systolic blood volume is 40 to 50 ml (Fig. 13.6).

What is the function of papillary muscles?

Papillary muscles are attached to the veins of AV valves by the chordae tendineae. Papillary muscles contract when ventricular walls contract and pull veins of the valves towards the ventricle to prevent the excessive bulging of valves towards the atria during ventricular contraction.

Describe aortic pressure changes during cardiac cycle

Pressure in the aorta varies between 80 to 120 mmHg during cardiac cycle. During the period of rapid ventricular ejection, the pressure in the aorta is slightly less than that of the ventricle. The peak aortic pressure is arterial systolic pressure and occurs at the end of rapid ejection. It is 120 mmHg. Then pressure slightly falls during reduced ejection phase. At the end of reduced ejection phase aortic pressure becomes slightly more than that in the ventricles. This causes closure of semilunar valves, but also causes backward flow of blood. After the aortic valve has closed, pressure in the aorta falls slowly throughout the diastole because blood stored in distended elastic arteries continues to flow to the periphery. Before the ventricles contract again, aortic pressure falls to 80 mmHg (diastolic pressure). The incisura during the down slope of the aortic pressure indicates the end of ventricular systole (Fig. 13.6).

Describe pressure changes in the pulmonary artery during cardiac cycle

Pressure curve in the pulmonary artery is similar to that of aorta but pressures are low (about one-sixth of that in aorta). Pulmonary artery systolic pressure averages 15 to 18 mmHg and its pressure during diastole is 8 to 10 mmHg.

What is work output of heart?

Work output of the heart can be expressed as stroke work output or minute work output. Stroke work output of the heart is the amount of energy that the heart converts to work during each heart beat. Minute work output is the total amount of energy that is converted to work in a period of one minute.

∴ Minute work output = Stroke work output × Heart rate.

How does heart muscle derive energy for work?

The energy for work of the heart is derived from oxidative metabolism mainly of fatty acids and to a lesser extent of other nutrients. Therefore, rate of O₂ consumption by the heart is excellent measure of the chemical energy liberated while heart performs the work.

How much is mechanical efficiency of the heart muscle?

Ratio of work output to total chemical energy expenditures (amount of energy converted to work) is called efficiency of heart. Maximum efficiency of normal heart is 20 to 25%. In heart failure, it may reduce to 5 to 10%.

Describe regulation of heart pumping

Pumping of heart is regulated by two mechanisms: intrinsic cardiac regulation, and control by autonomic nervous system.

1. Intrinsic regulation. Heart adapts to changes in blood volume it receives. Rate of blood flowing into the heart through veins each minute is known as venous return. Greater the venous return, greater is the pumping ability to pump excess incoming blood into the arteries. This intrinsic ability to adapt to changing volume is called “Frank-Starling” mechanism of heart. This is because the force of contraction of heart is proportional to initial length of muscle fibre (Frank-Starling law). When there is increased venous return, there is stretch on the cardiac muscle wall which increases the initial length of muscle fibres which in turn increases the force of contraction. Stretch of muscle also increases the heart rate.

2. Control by autonomic nervous system.

What are the effects of ions on heart function?

What is the effect of temperature on heart?

Increase in temperature causes increased permeability of heart resulting into acceleration of self-excitation process. Contractile strength of heart is often enhanced temporarily with moderate increase in temperature. But prolonged elevation of temperature exhausts the metabolic system and causes weakness.

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. 13.7).

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

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 to closure 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 back bulging. The elastic tautness of the valves (tricuspid and mitral valves) then cause back surging 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 second, and is low pitched.

What is phonocardiogram?

A specially designed microphone to detect low frequency. It is applied to the precor-dium. 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.

What is an electrocardiogram?

Record of the electrical changes during the cardiac cycle is known as electrocardiogram.

Name the machine used for recording ECG

Electrocardiograph is the machine used to record ECG.

Describe the method of recording ECG

Action potentials generated in the muscle cells of heart can be recorded by placing recording electrodes on the surface of the skin.

The electrodes are connected to the machine (electrocardiograph). The tracings are usually made at a standard recording speed of 25 mm/sec and amplification (1 mV = 1 cm deflection). These tracings are made over the standard ECG paper. This paper is divided into small squares. Each small square on horizontal axis represents 0.04 sec and on vertical axis represents 0.1 mV.

Most modern electrocardiograph has a direct pen writing recorder that writes electrocardiogram with a pen directly on a moving sheet of paper. Pen is often a thin tube connected at one end to a ink well; and its recording end is connected to a electromagnet system capable of moving the pen back and forth at high speed. As the paper moves forward, the pen records the electrocardiogram. In other recorder instead of ink pen, special paper is used. The paper turns black on exposure to heat. The stylus (recording pen) is made hot by electrical current flowing through its tip. Another type of paper turns black when electric current flows from the tip of the stylus.

What is a lead?

Lead is the connection between two points on the body surface and the electrocardiograph. Hence a lead consists of:

What are bipolar leads?

Bipolar leads mean the ECG is recorded from two specific electrodes placed on the body.

Name different bipolar limb leads used

Different bipolar limb leads used for recording ECG are:

Describe bipolar limb leads

Three leads are formed by measuring the potential differences between any two of the limb electrodes. The leads are selected by a switch on standard ECG machine.

Lead I. For recording ECG in lead I, negative terminal of the electrocardiograph is connected to the right arm and positive terminal to the left arm. When right arm is negative with respect to left arm, the positive wave is recorded.

Lead II. For recording ECG in lead II, negative terminal of the electrocardiograph is connected to the right arm and positive terminal to the left leg. When right arm is negative with respect to left leg, the positive wave is recorded by electrocardiogram.

Lead III. For recording ECG in lead III, negative terminal of the electrocardiograph is connected to the left arm and the positive terminal to the left leg. If left arm is negative with respect to left leg, ECG records the positive wave.

What is Einthoven's triangle?

Einthoven's triangle is the diagrammatic way of illustrating that the two arms and left leg form apices of triangle surrounding the heart. It is the equilateral triangle with the right and left shoulders and left leg as the three apices. The right leg serves as a ground connector. All four electrodes must be attached to the extremities.

What is Einthoven's law?

Einthoven's law states that if electrical potentials of any two of the bipolar limb electro-cardiographic leads are known at any given instant, the third one can be determined mathematically by simply summing the first two (but positive and negative signs of different leads must be observed while making the summation) (Fig. 13.8).

What are unipolar leads? Describe unipolar chest leads

If the three limb leads are connected to a common terminal through electrical resistance the combined voltage from the three leads will be zero, theoretically. This common terminal can be attached to the negative pole of a galvanometer (indifferent electrode) and a fourth or exploring electrode can be attached to the positive pole. The galvanometer can still only read the potential difference between two points but because the common electrode is at zero volts, other electrode (exploring) will provide the actual or absolute voltage at the body surface. This arrangement of connections is termed a unipolar lead. They are used to record, from standardized sites on precordium. There are six such precordial leads called ‘V’ leads.

The placement of exploring electrode in leads V₁ to V₆ is as follows:

Describe augmented unipolar leads

There are three unipolar augmented leads: aVR, aVL and aVF. Any of the three limb electrodes can be used to record cardiac potential in comparison to the common terminal, e.g. voltage recorded in RA (right arm) can be determined by the equation.

RA − (RA + LA + LL) the resulting voltage is small because the potential difference is reduced by the RA potential in common terminal, i.e. (RA + LA + LL).

Disconnecting the RA lead from the common terminal increases the potential difference by 50% and results in augmented limb lead aVR.

In this type of recording two of the limbs are connected through electrical resistances to the negative terminal of the electrocardiograph while the third limb is connected to positive terminal.

Name different waves and intervals in normal ECG

Explain different abnormalities in ‘P’ wave

What does prominent ‘Q’ wave indicate?

Prominent ‘Q’ wave indicates old infarction.

What is P-R interval? When is it prolonged?

Interval from onset of P to the onset of QRS is called P-R interval. It measures conduction time from SA node to the ventricles. Normally it is 0.13 to 0.16 second. If it exceeds 0.2 second, it indicates impaired conduction through AV node. First degree block is produced when PR interval is between 0.2 to 0.3 second. Second degree block is produced when the PR interval is increased to 0.25 to 0.45 second.

What is the effect of complete atrioventricular block?

When there is complete atrioventricular block, impulses from atria cannot pass to the ventricles. Ventricles start beating at their own rhythm called idioventricular rhythm. ECG shows that there is complete dissociation between P waves and QRS complexes.

How much is normal QRS interval? When is it prolonged?

Normal QRS interval is 0.08 second. It should not exceed 0.1 second. It is measured from onset of ‘Q’ to the cessation of ‘S’ wave. It measures total ventricular depolarization time. If it is prolonged it indicates bundle branch block.

What is P-P interval?

P-P interval is the interval between two successive P waves. Equal P-P intervals indicate rhythmic depolarization of the atria.

What are the abnormalities in ‘T’ wave?

‘T’ wave is the repolarization wave of the ventricles. It is normally positive because apex of heart repolarizes earlier than the base of the heart. In old age it is flattened. Exercise increases its amplitude in healthy hearts. It is inverted when there is ischaemia (sometimes T wave is inverted in lead III without any apparent reason). Abnormalities of ‘T’ wave in shape, size, duration, direction in leads I and II are of diagnostic importance. These changes indicate myocardial damage associated with cardiac hypoxia (ischae-mia). When there is ischaemia of the cardiac muscle, ischaemic portion of the heart takes a longer time for depolarization.

What is Q-T interval? What does it indicate?

Q-T interval is measured from the onset of ‘Q’ wave to the end of ‘T’ wave. It is normally 0.36 second and it indicates total systolic time of ventricles.

What is T-P interval? What is its significance?

T-P interval is measured from the end of T wave to the beginning of P wave. It measures the diastolic period of the heart. Variable T-P intervals indicate atrioventricular dissociation.

Name the conditions which cause abnormal voltages of QRS complex

Voltage of QRS is measured from peak of R wave to the bottom of S wave. It varies between 0.5 and 2 mV (lead III recording lowest and lead II recording the highest voltage). When sum of voltages of QRS complex in three standard leads is greater than 4 mV, it is considered that the patient has a high voltage ECG.

The cause of this high voltage in most of the cases is increased muscular mass of the heart (hypertrophy).

There may be decreased voltage of ECG due to cardiac myopathies, pericardial effusion (due to short circuiting of electrical potentials generated by heart into pericardial fluid), pulmonary emphysema (due to decreased conduction of electric current through emphysematous lungs). Lungs thus prevent flow of electric current from heart to the surface electrodes.

When is prolonged and bizarre pattern QRS complex obtained?

When there is hypertrophy of the ventricle or ventricles, ventricle takes a longer time for depolarization and therefore QRS complex lasts for a longer time. It can also be prolonged if there is a block in either the bundle branches, or in Purkinje fibres. Bizarre QRS pattern is obtained when

What is ‘J’ point? What is its significance?

The exact point at which the wave of depolarization just completes its passage through the heart (occurs at the end of QRS complex), all parts of the ventricles are depolarized so that no current is flowing around the heart (even the current of injury disappears). Therefore, the potential of ECG at this instant is exactly zero voltage. This point is known as ‘J’ point. A horizontal line is drawn through all ‘J’ points is the zero potential line in ECG from which all potentials caused by current of injury must be measured. The potential of current of injury in each lead is the difference of the level of T-P segment of ECG and zero potential time. Potential of current of injury above the zero line is positive (lead I) and potential of current of injury below the zero line is negative (lead III).

What is ST segment shift?

Portion of ECG between end of QRS complex and the beginning of T wave is called ST segment. J point lies at the very beginning of this segment. Whenever there is current of injury, ST segment and T-P segment are not at the same potential level in the record. Actually T-P segment shifts away from zero potential and not the ST segment that is shifted away from the zero axis. Still mostly TP segment of ECG is considered as reference potential level rather than ‘J’ point. Therefore, when a current of injury is evident in ECG it is called ST segment shift.

What is mean electrical axis?

During most of the cycle of ventricular depolarization, the direction of electrical potential (negative to positive) is from the base of ventricles toward the apex. This preponderant direction of the potential during depolarization is called mean electrical axis of the ventricles or the mean QRS vector. The mean electrical axis of normal ventricles is 59 degrees but it can swing to left about 20 degrees or to the right about 100 degrees.

What is right axis deviation? When does it occur? How is it diagnosed?

When mean axis is deviated to right, i.e. MEA of about 170°, it is called right axis deviated. It is caused by right ventricular hypertrophy or right bundle branch block. This can be diagnosed by observing QRS complex in leads I and III. When there is right axis deviation, S wave is prominent in lead I and R wave is prominent in lead III (S₁ R₃ pattern).

What is left axis deviation? When does it occur? How is it diagnosed?

When mean electrical axis is deviated to left, it is called left axis deviation, i.e. mean axis is about −15°. This is associated with obesity, left ventricular hypertrophy or left bundle branch block. This can be diagnosed by observing QRS complex in leads I and III. When there is left axis deviation, R wave is prominent in lead I and S wave is prominent in lead III (R₁ S₃ pattern).

What is sinus rhythm?

Sinus rhythm is present when SA node is the pacemaker. It is assumed if each P wave is followed by a normal QRS complex. P-R and, Q-T intervals are normal and P-R interval is regular.

What is sinus arrhythmia?

In sinus arrhythmia, there is a sinus rhythm except that RR interval (cardiac rate) varies with respiration. Heart rate normally increases during inspiration and decreases during expiration.

What is AV nodal rhythm?

When AV node becomes the pacemaker, the rhythm recorded is AV nodal rhythm, i.e. there is ectopic pacing from AV node. It is also called junctional rhythm. It is characterized by inverted ‘P’ wave and normal QRS complex. The rate is slower than sinus.

What is atrial tachycardia?

Atrial tachycardia is the one which occurs when an atrial site (outside the SA node) becomes the dominant pacemaker.

What is a premature beat?

Premature beat (premature contraction or ectopic beat) is a contraction of the heart prior to the time that normal contraction would have been expected.

What is premature atrial beat?

When the ectopic focus of the premature beat is located in atrium, atrial premature beat or atrial beat is recorded. The ‘P’ wave of this beat occurs too soon in the heart cycle. P-R interval is shortened indicating that ectopic origin of the beat is near the AV node.

An interval between premature contraction and next succeeding contraction is slightly prolonged which is called compensatory pause. The reason for this is that the premature contraction originated in the atrium some distance from the sinus node and the impulse had to travel through a considerable amount of atrial muscle before it discharged the sinus node. Therefore, the sinus node discharged very late in premature cycle, and this made the succeeding heart beat also late in appearing. Premature atrial contractions may occur frequently in healthy persons.

What is pulse deficit?

During premature contraction, heart contracts ahead of time. The ventricles are sometimes not filled with blood normally and stroke volume output during the contraction is therefore decreased or sometimes even absent. Therefore, during such a contraction, pulse wave passing to periphery may be so weak that it is not felt at the radial artery. Thus a deficit in the number of pulses felt in the radial pulse in relation to number of contractions in the heart is called pulse deficit.

What is premature ventricular contraction?

When the ectopic focus of the premature beat is located in the Purkinje system or myocardium of the ventricle, ventricular ectopic beat is recorded. Here the QRS complex is usually considerably prolonged and it has a high voltage. T wave has got potential opposite to that of QRS complex.

What is paroxysmal tachycardia?

When there is increase in heart rate in paroxysms, it is called paroxysmal tachycardia. Paroxysms usually begin suddenly and last for few seconds. It is called atrial paroxysmal tachycardia or ventricular paroxysmal tachycardia depending upon the site of irritable focus.

What is atrial flutter?

When atrial rates are between 220 to 350/min, it is called atrial flutter. During atrial flutter AV node is unable to transmit all of the atrial impulses and therefore the ventricular rate is half, one-third or one-fourth of the atrial rate.

What is atrial fibrillation?

A totally irregular, rapid atrial rate in which there is contraction of only small portions of atrial musculature at any one time is called atrial fibrillation. ECG shows small irregular oscillations called F waves due to depolarization of small units of atrial musculature. There are no recognizable P waves. QRS and T waves are normal but RR interval is irregular.

What is ventricular fibrillation?

Rapid, irregular ineffective contractions of small segments of ventricular myocardium is termed ventricular fibrillation. In this, peripheral pulse is absent because cardiac output is zero. Condition can be distinguished from cardiac standstill only on ECG. ECG shows undulating waves of varying frequency and amplitude.

What is the function of arteries?

Arteries are the vessels which carry blood from heart to the periphery. They transport blood under high pressure to the tissues. For this reason, they have strong vascular walls. Blood flows rapidly in the arteries.

What are arterioles? What is their function?

Arterioles are small branches of arterial system. They act as control valves through which blood is released into the capillaries. They have strong muscular wall capable of contracting and completely closing and dilating, thereby controlling the blood flowing to the capillaries.

What is the function of capillaries?

Capillaries are thin-walled vessels. Their function is to exchange fluid, nutrients, electrolytes, hormones and other substances between the blood and the interstitial fluid.

What is the function of veins?

Veins are the vessels which carry the blood towards the heart. They are thin-walled and act as major reservoirs of blood. The walls are muscular and therefore veins can contract or expand and reserve small or large volume of blood depending on the needs of the body.

Explain the proportion of blood present in different parts of circulation

About 84% of the entire blood volume of the body is in the systemic circulation (64% in veins, 13% in arteries, 7% in systemic arterioles and capillaries). Heart contains 7% of blood volume and pulmonary vessels contain 9% of blood volume.

What is the relationship between velocity of blood flow and cross-sectional area of the vessels?

Cross-sectional area of veins is about four times larger than that of arteries. Therefore, there is large storage of blood in venous system as compared to in the arterial system, because velocity of blood flow is inversely proportional to the cross-sectional area.

Which vessels have largest cross-sectional area?

Capillaries have largest cross-sectional area, i.e. 2500 cm².

Describe how does pressure change in various portions of circulation

The pressure in aorta is highest because blood is pumped by heart continuously in aorta. As blood flows to systemic circulation, pressure falls progressively to approximately zero by the time it reaches the right atrium.

Pressure in aorta varies between 120 and 80 mmHg during systole and diastole of the heart respectively. Average pressure in aorta is about 100 mmHg.

In systemic capillaries pressure drops to 35 mmHg at the arterial ends and about 10 mmHg at the venous end with average functional pressure equal to 17 mmHg.

In pulmonary circulation pressure is much less. In pulmonary artery systolic pressure is 25 mmHg and diastolic pressure is of 8 mmHg. The average pulmonary capillary pressure is about 7 mmHg.

Explain the relationship between pressure, flow and resistance

Flow of blood through any vessel is determined by two factors:

Name the methods of measuring blood flow

Blood flow is expressed in ml/s or l/min. It is measured by:

What is streamline or laminar flow?

When each layer of blood remains the same distance from the wall while flowing through a long smooth vessel, it is called streamline or laminar flow. When the flow is streamline, blood flows at a steady rate.

What is turbulent flow?

When blood flows crosswise in the vessel as well as along the vessel usually forming whorls in the blood called eddy currents, the flow is said to be turbulent. When eddy currents are present blood flows with much greater resistance than when the flow is streamline because of increased friction of flow caused by eddy currents.

Explain factors causing tendency for turbulent flow

The tendency for turbulent flow is directly proportional to the velocity of blood flow, diameter of blood vessel and is inversely proportional to viscosity of the blood divided by its density.

Reynolds’ number is a measure of tendency to turbulence to occur. It is calculated as follows:

When Reynolds’ number rises above 200 to 400, turbulent flow will occur. When it is about 2000, turbulence will occur even in straight smooth vessel. In large arteries even normally Reynolds’ number rises to 200 to 2000. Therefore, there is always some turbulent flow.

What is resistance to blood flow?

Resistance is the impediment to blood flow.

What is the unit for resistance?

Unit for expressing resistance is the peripheral resistance unit (PRU). If pressure difference between two points in a vessel is 1 mmHg and the blood flow is 1 ml/sec, the resistance is said to be 1 PRU.

Occasionally resistance is expressed in CGS units as dyne sec/cm⁵ and is calculated by following formula:

How much is the total peripheral resistance normally?

At rest, rate of blood flow through circulatory system is 100 ml/s and the pressure difference from systemic arteries to systemic veins is 100 mmHg. Therefore, total peripheral resistance is 100/100, i.e. 1 PRU. It can increase to 4 PRU when vessels are strongly constricted. It can fall to low as 0.2 PRU when vessels become greatly dilated.

In pulmonary circulation, the net pressure difference (pulmonary arterial and left atrial pressure) is 14 mmHg whereas rate of blood flow is 100 ml/s. Therefore, total pulmonary resistance at rest is 0.14 PRU.

What is conductance of flow in a vessel?

Conductance is a blood flow through a vessel for a given pressure difference expressed as ml/s/mmHg. It is the reciprocal of resistance.

It changes directly with the diameter of vessel. The relationship is as follows:

Conductance thus increases in proportion to fourth power of the diameter.

What is Poiseuille's law?

Poiseuille's law is the formula which is useful in calculating the rate of blood flow in a vessel. According to it

Thus from the formula it is clear that the diameter of the vessel plays the greatest role in determining the rate of blood flow. This makes it possible for the arterioles, responding with small changes in diameter to nervous or local signals either to turn off completely the blood flow to the tissues or to cause a vast increase in blood flow.

Name major factors affecting resistance to blood flow

According to Poiseuille's law,

Where r = radius of vessel, η = viscosity of blood, and l = length of the vessel.

How does viscosity of blood affect the blood flow?

According to Poiseuille's law, greater the viscosity, lesser is the blood flow. Viscosity in turn depends upon the haematocrit, i.e. percentage of cells. Greater the haematocrit, greater is the viscosity. Blood flow in very minute tubes exhibits far less viscosity effect because in these tubes red cells instead of moving randomly line up and move through the vessel thus eliminating viscous resistance.

What is the effect of pressure on vascular resistance and tissue blood flow?

Increase in arterial pressure greatly increases the blood flow because of two factors:

What is the importance of vascular distensibility?

All the vessels are distensible. Distensible nature of the arteries allows them to accommodate the pulsatile output of the heart and to average out the pressure pulsation. This provides almost smooth, continuous blood flow through the tissues.

Veins are most distensible vessels, therefore they act as blood reservoirs and store large quantities of blood which can be called into use whenever required.

In pulmonary circulation, veins are similar to those of systemic veins. Pulmonary arteries normally operate under low pressure and have distensibilities about one-half those of veins.

What is the unit of vascular distensibility?

Vascular distensibility is expressed as the fractional increase in volume for each mmHg rise in pressure.

What is vascular compliance?

Vascular compliance is the total quantity of blood that can be stored in a given portion of circulation for each mmHg pressure rise

Compliance of vein is about 24 times that of corresponding artery because it is 8 times as distensible and has a volume 3 times as great. Therefore, compliance is equal to distensibility × volume.

What is the relationship between volume and pressure in arterial system and venous system? What is the effect of sympathetic stimulation?

With mean arterial pressure of 100 mmHg, arterial system (larger and smaller arteries, arterioles) have 750 ml of blood which reduces to 500 ml when pressure falls to zero.

Normally, venous system contains 2500 ml of blood and tremendous changes in the volume are required to change the pressure. Sympathetic stimulation increases the smooth muscle tone of the vessels. This in turn increases the pressure. This causes large volume of blood to shift into the heart.

What is stress relaxation?

When extra volume of blood is suddenly injected into a vessel, at first there will be a large pressure increase but because of stretching of the wall, smooth muscle fibres of the vessel will relax and this will allow pressure to return back towards the normal. This phenomenon is known as stress relaxation.

What is pulse?

It is the wave of expansion that passes along the arterial tree from aorta to the peripheral arteries during systole of the heart.

Normally which artery do you choose for feeling the pulse? Why?

Pulse is felt at the radial artery because the artery is superficial and it lies on the bone. On examination of pulse, one notes rate, rhythm, volume, tension, equality of both sides, etc.

What is pulsus paradoxus?

Pulsus paradoxus is the condition in which pulse becomes very strong (high volume) during inspiration and very weak (low volume) during expiration. Thus pulse becomes very strong and very weak alternately in relation to that of respiratory cycle. Normally also pulse volume increases during inspiration and decreases during expiration. But this change is so small that it is hardly noticed. When the change becomes very prominent, pulse is described as pulsus paradoxus. This type of pulse is noticed during deep breathing, cardiac tamponade (compression of heart from outside due to fluid in pericardial sac, constructive pericarditis, etc.). Under such conditions during inspiration there is increased (greater than normal) negative pressure in the thorax, venous return is increased, this in turn increases the stroke volume and pulse becomes stronger. Exactly opposite changes occur during expiration leading to reduced volume of pulse (weak pulse).

What is central venous pressure?

Pressure in the right atrium is known as central venous pressure because all the systemic veins open into the right atrium.

Name the factors determining right atrial pressure

Right atrial pressure depends on balance between ability of atrium to pump the blood into the ventricle and the tendency for blood to flow from the peripheral vessels into right atrium. If right atrium is pumping strongly, the right atrial pressure tends to decrease. Weakness of the atrial wall tends to increase the right atrial pressure. Increase in flow of blood into the right atrium through veins (venous return) increases the right atrial pressure and vice versa.

State the factors increasing the venous return

How much is normal right atrial pressure? When does it rise or fall?

Normal right atrial pressure is zero mmHg (i.e. equal to atmospheric pressure). The pressure in the right atrium can rise as high as 20 to 30 mmHg in following abnormal conditions:

Right atrial pressure can decrease to as low as −3 to −5 mmHg due to the following reasons:

How much is the pressure in the large veins?

Large veins do not offer any resistance when they are distended. But at the entry of thorax most of the large veins are compressed at many points by the surrounding tissues. This impedes the blood flow. Therefore, large veins do offer considerable resistance to blood flow and thus pressure in the peripheral veins is greater than that of the right atrial pressure. It is 4 to 7 mmHg. Venous pressure rises in heart failure.

What is hydrostatic pressure? How much is it in vascular system?

Pressure at the surface of water is equal to the atmospheric pressure, i.e. zero mmHg but the pressure rises by 1 mmHg for each 13.6 mm distance below the surface. This pressure results due to weight of water and therefore is called hydrostatic pressure.

How does hydrostatic factor affect the arterial pressure?

Hydrostatic factor also affects the peripheral pressures in the arteries, e.g. standing person has arterial pressure of 190 mmHg in the feet. Therefore, arterial pressure is stated as pressure at the hydrostatic level of heart.

What is the function of valves in the veins?

The venous pressure in feet is always +90 mmHg in a standing position because of hydrostatic pressure effect. Movement of legs and muscle contractions (muscle pump) squeeze the blood out of veins. The valves are arranged in the veins so that direction of blood can only be towards the heart. This lowers the pressure in the veins. Therefore, in walking adult, venous pressure remains less than 25 mmHg.

What are varicose veins?

The valves in the venous system become incompetent (when there is overstretching of veins by excess venous pressure as in pregnancy). Stretching of the veins increases their cross-sectional area and valves of the veins no longer remain functional because of which there is failure of muscle pump leading to further increase in size of the veins and destroys the function of valves entirely. Thus large, bulbous protrusions of the veins called varicose veins develop.

How is venous pressure assessed?

Clinically venous pressure is assessed by observing the degree of distension of neck veins. When right atrial pressure is increased up to 10 mmHg, the lower neck veins begin to protrude in sitting position (in normal person in this position neck veins are never distended).

Venous pressure can be measured directly by inserting needle into the vein and connecting it to a pressure recorder. Right atrial pressure can be measured by inserting a catheter through the veins into the right atrium.

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 to 700 sqm.

Capillary is lined by unicellular layer of endothelial cells which is surrounded by basement membrane on the outside. The diameter of capillary is 4 to 9 u. barely 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 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 to 7 nm. These are termed ‘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 to clefts.

Blood flows into the capillaries intermittently, because of phenomenon of vasomo-tion, 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 endothe-lial cells. Such substances pass through the pores.

Capillary dynamics are discussed in chapter on “Blood.”

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 to 40 mmHg and at the venous end of capillary, pressure is 10 to 15 mmHg and in the middle, pressure is about 25 mmHg.

2. Interstitial fluid pressure. This tends to force fluid inward through the capillary membrane. It is about −3 to −5 mmHg.

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

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

All above forces are called Starling's forces.

What are the functions of tissue blood flow?

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:

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. O₂ demand 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 precapil-lary sphincters and metarterioles.

Normally precapillary sphincters and metarterioles, open and close cyclically (vaso-motion). 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 to 175 mmHg. This is called 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 muscles 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 mmHg 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 ang-iogenic factors released from: (a) ischaemic tissues, (b) tissues that are growing rapidly, and (c) tissues having excessively high metabolic rate.

Many angiogenic factors are small peptides. Three of them are most important. They are endothelial cell growth factor (ECGF), fibroblast growth factor (FGF) and angiotensin. They are released either from the tumours or from other tissues that generally have inadequate blood supply. Deficiency of oxygen and other nutrients leads to formation of these factors. Essentially all the angiogenic factors promote new vessel growth in the same manner. They cause sprouting of new vessels from either venules or capillaries in following steps:

What is collateral circulation?

When either an artery or a vein is blocked, a new vascular channel usually develops around the blockage and allows at least partial resupply of blood to the affected tissue. The circulation through these new channels is called collateral circulation.

What is humoral regulation of circulation?

Humoral regulation of circulation is regulation by substances secreted into or absorbed into body fluids, e.g. hormones, ions, etc. Most important humoral factors affecting circulation are:

What is the effect of different ions on the vessels?

Describe sympathetic and parasympathetic nerve supply to heart and vessels

There is autonomic nerve supply to the heart and blood vessels, i.e. sympathetic and parasympathetic supply. The most important system which controls circulation is the sympathetic nervous system.

1. Sympathetic supply. All the blood vessels except capillaries, precapillary sphincters and metarterioles are innervated by sympathetic nerves.

Stimulation of sympathetic nerves to small arteries and arterioles causes vasocon-striction and therefore increased peripheral resistance, thus changing rate of blood flow to the tissues. There are very few vasodilator fibres supplying the vessels.

Stimulating sympathetic nerves to large vessels especially veins cause their constriction and therefore blood stored in them is translocated to the heart. This increases the venous return and therefore the cardiac output (plays a major role in regulation of cardiovascular function). Stimulation of sympathetic nerves to heart causes increase in the heart rate (positive chronotropic), increase in the force of contraction of the heart (positive inotropic), increased rate of conduction of impulse through the heart (positive dromotropic) and increased excitability (positive bathmotropic).

2. Parasympathetic supply. Parasympathetic fibres are carried to the heart through vagus nerve. The effect of parasympathetic stimulation is to decrease the heart rate, force of contraction, rate of conduction of impulse through the heart and decreased excitability (negative chronotropic, inotropic, dromotropic and bathmotropic effects). There is no parasympathetic supply to blood vessels.

What is blood pressure?

Blood pressure is the lateral pressure exerted by flowing blood on the walls of the vessels. Systolic pressure is the maximum pressure during systole and diastolic pressure is the minimum pressure in the arteries during diastole.

Name methods used for measuring blood pressure

How much is normal blood pressure?

Normal systolic pressure in adult is 120 ± 15 mmHg and diastolic pressure varies from 80 ± 10 mmHg.

What is mean arterial pressure?

Mean arterial pressure is the average of all the pressures measured millisecond by millisecond over a period of time. It is determined by adding 60% diastolic and 40% systolic pressure. It is about 100 mmHg.

When mean arterial pressure is chronically above 110 mmHg, person is labelled is hypertensive. Hypertension can be mild, moderate or severe.

What is pulse pressure? What is its significance?

Pulse pressure is the difference between systolic and diastolic pressure. Pulse pressure indicates stroke volume.

Describe the vasomotor centre

Vasomotor centre is situated bilaterally in the reticular substance of medulla and 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. 13.10):

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 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:

Explain the role of sympathetic vasodilator fibres

Vasodilator sympathetic fibres mainly supply the skeletal muscles. Anterior hypothala-mus 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 arterial 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 to 40 seconds. Thus nervous control of arterial pressure is most rapid.

Enumerate various short-term mechanisms regulating blood arterial pressure

The various short-term mechanisms regulating blood pressure are:

Name various reflex mechanisms which maintain normal arterial blood pressure

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:

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. 13.11).

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 mmHg. They respond progressively more and more rapidly and reach maximum at 180 mmHg pressure.

Baroreceptors respond much more rapidly to changing pressures than to a stationary pressure. The normal operating range of baroreceptor varies from 60 to 180 mmHg. The normal arterial pressure is around 100 mmHg. 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:

Thus blood pressure returns back to normal.

Exactly opposite sequence of events occur when blood pressure is lowered.

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 to 180 mmHg 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 mmHg 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:

This pressure is brought to normal 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 mmHg. This acts as an emergency arterial pressure control system. If rise of pressure does not relieve CNS ischae-mia, neuronal cells begin to suffer and within 3 to 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 muscle of 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.

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

When there is increase in extracellular fluid volume, it causes rise in blood volume and therefore rise in blood pressure. Rising pressure has a direct effect on kidneys to excrete excess of water (pressure diuresis) and also increase output of sodium (pressure natri-uresis). Pressure diuresis and pressure natriuresis bring blood volume back to normal and therefore returning blood pressure back to normal.

Thus pressure diuresis and natriuresis is the fundamental mechanism of long-term regulation of blood pressure. With evolution however multiple refinements have been added to make the fundamental system more exact in its control. Especially important refinement is renin-angiotensin mechanism.

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:

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

Renin is a protein 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 angiotensino-gen 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:

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 the importance of renin-angiotensin mechanism?

Despite variable salt intake, long-term level of arterial pressure is maintained normal because of renin-angiotensin system as follows:

Decrease in salt intake will have exactly opposite effects.

What is neurogenic hypertension?

Acute hypertension which is caused by strong stimulation of sympathetic nerves (due to excessive anxiety) is called neurogenic hypertension. Repeated acute episodes can lead to prolonged renal type of hypertension because of sympathetic neurotransmitter directly affecting renal arteries leading to their permanent damage.

What are the lethal effects of hypertension?

Hypertension if left untreated can cause following lethal effects:

What is the treatment of essential hypertension?

There are many antihypertensive drugs. The common drugs are:

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 SA 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 within physiological limits (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. Cardiac output varies reciprocally to the changes in total peripheral resistance, when arterial blood pressure is maintained normal, i.e.

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) up to about two and half times its normal. Venous return is limiting factor. So normal heart without any excess nervous stimulation has the cardiac output up to 13 l/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:

What is hypereffective heart? Enumerate the factors that cause hyper-effective heart

When the pumping ability of the heart is greater than normal, the heart is said to be hypereffective heart (Fig. 13.12).

Factors causing hypereffective heart:

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

What is the effect of sympathetic stimulation on cardiac output?

Sympathetic stimulation increases the cardiac output as follows:

Describe the methods for measuring cardiac output

Cardiac output can be measured by following methods:

1. With the help of flowmeter. 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 per minute 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:

Concentration of O₂ in arterial blood = 200 ml/L

Concentration 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.

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 seconds after the injection, but later the arterial concentration of the dye increases and reaches maximum at the end of 6 to 7 seconds. 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. 13.13). 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:

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 delivered 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 the following formula:

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

What are signs and symptoms of circulatory shock?

Name different stages of circulatory shock

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 compensatory mechanisms. These are:

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.

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 to 4 ml/100 g of muscle.

At this time only 20 to 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 nore-pinephrine 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).

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

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

What is circulation time? How is it determined?

What is plethysmograph?

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

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:

What are acute and chronic effects of moderate 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, and (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.

What is low output cardiac failure?

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.

Describe the anatomy of coronary blood supply

The heart receives its nutrient supply through left and right coronary arteries. Only inner 75 to 100 μm 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 people, 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).

How much is the resting coronary blood flow?

Resting coronary blood is 225 ml/min or 0.7 or 0.8 ml/g of heart muscle, i.e. 4 to 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).

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 subendo-cardial 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.

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.

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.

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

3. 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).

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

5. Nervous stimulation. Already explained.

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

Adrenaline and noradrenaline cause increase in blood flow as already explained.

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 to 250 u.m 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 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 heart.

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.

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:

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 sinoaortic mechanism.

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

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 l/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 25 mmHg and during diastole it is about 10 mmHg. Pulmonary capillary pressure is about 8 mmHg.

What are the functions of pulmonary circulation?

What are the peculiarities of pulmonary circulation?