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7. Cardiovascular system I. Circulation of blood. Physiologic properties of heart muscle.William Harvey discovered circulation of blood. Circulation of blood is caused by

movement of blood on circulation of the blood system ensuring metabolism

between tissues and environment, participating in a regulation of functions of an

organism and maintaining homeostatic conditions.

Basic functions of blood:- nutrients transport to the adoption areas;- metabolism products transport from a place of formation to a place of release;

- gases transport;

- hormones transport and others bioactive substances;

- heat transport (thermoregulation) from active metabolic sites, where it is

generated to the body surface, where it is dissipated;

- transport of protective factors.

The major functions of the cardiovascular system are to distribute metabolites and

oxygen to all body cells and to collect waste products and carbon dioxide for

excretion.

The circulation is divided into the lesser pulmonary circulation (from the right ventricle venous blood flows through the pulmonary artery, small arteries,

arterioles to the lungs, where in the alveolar capillaries oxygen and carbon dioxide

are exchanged between the blood and the tissues. Blood which has oxygen leaving

the lungs flows to the left auricle (atrium).

and the major systemic circulation(from the left ventricle arterial blood flowsthrough the aorta, which empties into smaller arteries, arterioles, and eventually

capillaries and transports nutrients and oxygen to the tissues and transports away

waste products and carbon dioxide. Blood leaving the tissues enters the venules

and then flows into the larger veins, which carry the blood to the right auricle

(atrium) through the superior and inferior vena veins cava.

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The heart is four-chamber. Main condition of normal work of a system of blood

circulation in that both ventricles of heart for want of contraction should reject an

identical amount of blood.

Bloods flows to the vessels during contraction of the ventricles ventricular

systole and during relaxed all four chambers (diastole) occur filling cavities of

heart by blood.

Morphofunctional characteristic of myocardium

The wall of heart consists of 3 layers: internal - endocardium, average (muscular) -

the myocardium and outside - epicardium - is covered with heart outside.

Structural basis of heart is myocardium, which consist of from the cardiacmyocytes. Distinguish two main kinds of cardiac myocytes:

1) Working cardiac myocytes (contractile, typical);

2) Cardiac myocytes of conducting system of heart (automatism cells, atypical

cardiac myocytes and cardiac pacemaker cells).

Working cardiac myocytesmake a main mass of myocardium cells. In their

structure are: a) myofibrils; b) sarcoplasmic reticulum; c) numerous mitochondria.There are numerous nexuses (intercalated disks) between separate cardiac

myocytes. They ensure electric conducting of excitation throughout the

myocardium and derivate uniform functional syncytium. Owing to myocardium is

subject to the All or none law. The excitation if only one cell is spread for the

whole myocardium.

Cardiac myocytes of conducting system of heart -these cells and their processesconstitute the conducting system of heart. Features of these cells that: a) they have

less myofibrils; b) they of a smaller size; c) they have greater excitability.

The parts of the conducting system are:

1) The sinus node (or sinoatrial) node2) The atrioventricular (A-V) node3) The internodal and interatrial pathways

4) The atrioventricular bundle of His5) The Purkinje fibers network

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Conducting system of the heart.

Typical transmembrane action potentials for the SA and AV nodes, other

parts of the conduction system, and the atrial and ventricular muscles are shown

along with the correlation to the extracellularly recorded electrical activity, i.e.,

the electrocardiogram (ECG).

The sinoatrial node is located in the right atrium near the entrance of the superior

vena cava. The initial depolarization normally arises in this node. The excitation

then spreads from the SA node throughout the Bachmans, Torel`s and

Venkenbach`s bundles in two direction: 1) to the AV node; 2) to the cardiac

myocytes of atriums.

The atrioventricular node is located at the base of the right atrium (at the border

between atrium and ventricle). It delays impulses from the atria to the ventricle.

The internodal and interatrial tracts transmit impulses in the atrium.

The interatrial tract (Bachmans bundle) is a band of specialized muscle fibbersthat run from the SA node to the left atrium. The interatrial tract causes almost

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simultaneous depolarization of both atria since the conduction velocity through this

tissue is faster than through the regular atrial muscle fibers.

The internodal tracts. The parts of the internodal pathway are the anterior, middle

and posterior internodal pathways. They connect the SA and AV nodes (carry

impulses from the SA node to the AV node).

The bundle of His is the continuation of the AV node. His length is 12-40 meters. It

divides into the right and left bundle branches to the right and left ventricles.

The Purkinje fibers arise from both bundle branches and contact with contractile

myocytes.

Physiological properties of the myocardium

Each of the cardiac cells contains many bundles of protein strands

called myofibrils, which, in cardiac muscle, are surrounded by an

extensive network of tubules known as the sarcoplasmic

reticulum. The sarcoplasmic reticulum in cardiac muscle is much

less developed than in skeletal muscle. It contains dilated

terminals (cysternae). The sarcoplasmic reticulum and the

cysternae contain high concentrations of ionized Ca 2+ . Myofibrils

are composed of thick (myosin) and thin (actin, troponin,

tropomyosin) filaments. Sarcomeres are the contractile unit of

myofibrils. Cardiac-muscle cells are considerably shorter than

skeletal-muscle fibers. Adjacent cells are joined end to end at

structures called intercalated disks (occur at z lines and maintain

cell-to-cell cohesion). Adjacent to the intercalated disks are gap

junctions, similar to those in many smooth muscles.

Cardiac muscle (myocardium) combines properties of both

skeletal and smooth muscle such as:

1. Excitability of myocardium.

-is the ability of the heart to initiate an action potential in response to an

inward, depolarizing current.

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-changes during the course of an action potential; these changes are described

by refractory periods.-reflects the recovery of the channels that carry the inward currents for the

upstroke of the action potential.

2. Nonexcited state of myocardium.The refractory periods are the same like inskeletal muscle but periods time ratio is changed.

3. onductivity is different from skeletal muscle because the excitation isconducted on the conducting system at first and then - on the contraction

myocardium. The second property what excitation is passed through the nexuses.

4. Automatism is typical property of smooth muscles. It is provided withparticular

mechanism of spontaneous excitation of conducting system cells.

5. Contractility itsmolecular mechanism not differ from skeletal muscle. Butthere are following characteristics of contractility in myocardium:

- is single but long-term contraction;

- is obediences to the All or none law during contraction;

- is impossible smooth-tetanic contractions in myocardium.

Excitability of cardiac muscle, action potential of typicalcardiac myocytes

Excitability of (contraction) cardiac myocytes is determinated by functioning of

the membrane ion channels (Na +, K +, Cl - and Ca 2+). Calcium ions have the most

functional value.The resting membrane potential of contraction cardiac myocytes is usually

about -80 to -90 millivolts, and the action potential is 120 millivolts. Action

potential can be initiated when the potential rises to critical level of depolarization

(threshold) which about -55 millivolts.

There are 5 basic phases of the action potential:

Phase 1 is the rapid depolarization phase fast potential inversion (reversion) from -90to+30 mV is combined with activation of Na + channels. Is the upstroke of the action

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potential. Is caused by a transient increase in Na + conductance. This increase results in an

inward Na + current that depolarizes the membrane.

Phase 2 - is the rapid early repolarization phase is a brief period of initial repolarization.Is caused by closed Na + channels and K+, Cl - ions moving into the cell.

Phase 3 - is the long-term repolarization phase (plateau) is the most prolonged andfunctional important. Is caused by a transient increase in Ca 2+ current (Ca 2+ ions are moving

into the cardiac myocytes). With a duration of 0.1 sec for atriums myocardium and 0.3 sec-

for ventricles.

Phase 4 - is the rapid end-repolarization phase during phase 4, Ca 2+ conductancedecreases, but K + conductance increases and therefore predominates. The high K +

conductance results in a large outward K + current.

Phase 5 - is the rest phase (resting membrane potential)is a period during which inwardand outward currents are equal. In other words the resting membrane potential is recovered.

Refractory periods of myocardium, their ratio with actionpotential phases of cardiac myocytes and cardiac cycle

1. Absolute refractory period (ARP) reflects the long-term repolarizationphase (plateau) or ventricular systole.

-begins with the upstroke of the action potential and ends after the plateau,

-reflects the time during which no action potential can be initiated (heart cannot be excite even by the most strong irritant)

- duration about 0,3 sec.

- Physiological meaning of this phase: a) nothing can hinder blood output in

systole; b) high duration allowed heart to work only in regimen of single

contractions; c) hinder the excitation circulation in myocardium.

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2. Relative refractory period (RRP) - reflects the rapid end-repolarizationphase or origin of diastole.

-is greatly shorter than the absolute refractory period,

- duration about 0,03 sec ,-is the period during which a myocardium can be excite, but the irritation force

must be higher threshold (sup threshold).

3. Supernormal excitability period (SEP) or exaltation phase.

-is the short-term period increased excitability which is corresponding to the rest

phase or diastole termination;

-is the period during which a myocardium can be excite even sub thresholdirritants,

- given phase very dangerous because can arise the arrhythmias and extrasystoles.

Extrasystole, forms of extrasystoleExtrasystole - is premature contraction of whole heart or it segments as a result of

supplementary myocardium excitation. The origin of extrasystole is possible at all

phases of cardiac cycle except for systole. The extrasystoles differ in the place of beginnings of supplementary irritation:

sinus extrasystoles in which the sinoatrial nodeas a supplementary irritation center.atrial extrasystoles in which the supplementary irritation center is found in myocardium of

auricles.

atrioventricular extrasystoles in which the center is found in atrioventricular node.

ventricular extrasystoles in which the center is found in myocardium of ventricles.

Ventricular extrasystoles are the most demonstrative in physiological sense. Theycan experimentally reproduced by electric irritation of heart during diastole. At the

same time the supplementary myocardium contraction is increase in comparison

with normal force. The heart stops work (compensatory pause) for a time during

two cardiac cycles and after that it works in normal regimen.

Heart automaticity,

Action potentials of typical cardiac myocytes of sinoatrial node

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The automaticity is the capacity of heart for spontaneous, rhythmical self-

excitation. It is connected with absent of membrane potential in cells of conducting

system. The slow spontaneous diastolic depolarization (SDD)begins at onceafter the recovery of membrane potential in conducting system cells. SDDis basedon Ca + ions moving into the automaticity cells. SDD is completes a new actionpotential and so on. There no Na + channels in that cell therefore the rapid earlyrepolarization phase is absentin action potential . In all the action potential of theconducting system cells (for ex. Sinoatrial node) is no different from the action

potential of the working cardiac myocytes (contractile myocytes).

The spontaneous accrued action potential then spreads round the conducting

system to the contractile cardiac myocytes. As a result the heart is contracts. Its

repeatable process and heart is rhythmically contracts without external action.

The automaticity is serves as a mean mechanism of reconstruction of heart activity

after it transplantation.

Automatism centres, their interrelation

Separate structures of conducting system have differential degree of automatism

(pacemaker activity) which depends on spontaneous permeability of membrane to

Ca + ions and, perhaps, to Na + ions.

There are 3 main centers of automatism:

The sinoatrial node . The spontaneous diastolic depolarization (SDD)is occursin it cells with maximum speed, therefore the spontaneous generation rate is

maximal is about 70 per minute. That is the reason why this node is the center of automatism in first order . So, Pacemaker of the heart is another name for S.A.

node. Since the S.A. node initiates the heart beat, it is called Pacemaker of the

heart. In normal conditions the S.A. node is overrides of underlying centers of

automatism and all influence on heart is occurs through the S.A. node.

The atrioventricular node ( center of automatism in second order) . In normal

conditions it doesnt function, but with the loss of sinoatrial node communicationthe A.V. node is reveals its automatism (after the defined delay - transautomatic

delay).Heart rate in this situation is about 40-50 beats per minute.

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The bundle of His ( center of automatism in third order). Heart rate in this situation

is about 20-30 beats per minutetherefore the people in that case have the faints,convulsions (spasms) owing to insufficiency of brain circulation.

The final bundle branches of His are the Purkinje fibers, which dont haveautomatism property.

Excitation conductance, speed, mechanism

Excitation conducting in heart is occurs from Pacemaker of the heart (S.A. node)

throughout the conducting system. The cells of conducting system are more steady

to hypoxia. After that the excitation is conducted on the cells of contractile

myocardium. The mechanism of conducting - owing to interaction of cardiac

myocytes through nexuses - intermembranous contacts.

The conduction velocity is disparate in different parts of myocardium:

in auricles 0,8-1,0 m/sec.in upper part of the atrioventricular node 0,02-0,05 m/sec.

The conduction velocity through the A.V. node is extremely slow. That delay iscalled AV nodal delay, which is conditioned the absence of fast ions currents in

cells of this node. This delay provides time for atrial contraction to occur, which

enhances ventricular filling. So, the systole of atriums is arises before the systole

of ventriculars.

in the bundle of His and Purkinje fibers 1,0-1,5 m/sec.

in ventriculars 0,3-0,9 m/sec.Contraction of separate cardiac myocytes, the characteristics of

mechanism in comparison with skeletal muscular fibers

Both cardiac and skeletal muscles are striated and have actin and myosin filaments

that interdigitate and slide along each other during contraction. But there are some

differences:

a) in physiological conditions the skeletal muscles are contract mainly in regimenof tetanus. But heart is contract by single and long-term contractions;

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b) the element of fibers can become excited in skeletal muscles as against in heart,where all cardiac myocytes are contracted at one time (owing toAll or none

law)

c) in skeletal muscle all Ca 2+ store are pumped out to the sarcoplasmic reticulum(SR); in cardiac myocytes part of Ca 2+ gets out from the fibers to the intercellular

fluid.

d) in skeletal muscle the Ca 2+ involving in contraction is going on through Na +

channels (it is power-consuming process); The energy consumption is less in

cardiac myocytes, where Ca 2+ at the same time is factor of depolarization and

electromechanical coupling.

e) in contrast to skeletal fiber, the Ca 2+ is provides to transmission amplification innexuses ( they have many slow Ca 2+ channels);

In that way the Ca 2+ is main ion, which is provides interaction between

depolarization of membrane and contraction (electromechanical coupling). That is

why the regulation of Ca 2+ channels state to come as a powerful medicinal

influence.

Valve apparatus of heart, the functions of separate valves

Hearts valves - are specialized formation, which regulating of blood moving in

one direction - throughout the lesser [pulmonary] and greater [systemic]

circulation.

Left atrioventricular valve (mitral valve, bicuspid(al) valve) is locatedbetween the left atrium and ventricle. Because of its two flaps it is named as

bicuspid valve. Left A-V valve is prevents from return of blood (regurgitation)

to the left atrium at the time of systole of left ventricle.

Right atrioventricular valve(tricuspid valve) is located between the rightatrium and ventricle. Its functions the same.

Aortic valve(semilunar valve) is located between the left ventricle and aorta. Itis prevents from return of blood (regurgitation) to the left atrium at the time of

diastole of left ventricle.

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Pulmonary artery valve (semilunar valve) is located between the rightventricle and pulmonary artery. It is prevents from return of blood

(regurgitation) to the right ventricle at the time of diastole.

Thus, the A-V valves (the tricuspid and mitral valves) prevent backflow of blood

from the ventricles to the atria during systole. In a similar fashion, the semilunar

valves (the aortic and pulmonary valves) prevent backflow of blood from the aorta

and pulmonary artery into the ventricle during diastole.

Phase (angle) analysis of cardiac cycle. Blood pressure in heart cavities.

Blood pressure is usually expressed in millimeters of mercury (mm Hg)The events that occur at the beginning of heartbeat and last until the beginning of

the next heartbeat are called the cardiac cycle. CC is includes systole(contraction) and diastole (relaxation) of heart parts. Its cycling work. The

ventricles fill with blood during diastole and contract during systole.

Each beat of the heart begins with a spontaneous action potential that is

initiated in the sinus node of the right atrium near the opening of the superior vena

cava. The action potential travels through both atria and the A-V node and bundle

and into the ventricles. A delay of more than 110 of a second occurs in the A-V

node and bundle, which allows the atria to contract before the ventricles contract.

With heart beat rate of 75/min, each cardiac cycle lasts for 0,8 seconds, i.e.Auricular systole 0,1 sec.Ventricular systole 0,3 sec.General diastole 0.4 sec.

Total 0.8 sec.

Separately time relation of auricular and ventricle in a cardiac cycle is:Auricular Ventricle

Systole 0,1 sec 0,3 sec

Diastole 0.7 sec 0,5 sec

About 75 per cent of ventricular filling occurs during diastole before the

contraction of the atria, which causes the remaining 25 per cent of ventricular

filling.

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The ventricles fill with blood during diastole.The following events occur justbefore and during diastole:

During systole, the A-V valves are closed, and the atria fill with blood.

At the beginning of diastole, when ventricular pressure decreases below that of theatria, the A-V valves open.

The higher pressure in the atria pushes blood into the ventricles during diastole.

The period of rapid filling of the ventricles occurs during the first third of diastole

and provides most of the ventricular filling.

Atrial contraction occurs during the last third of diastole and contributes about

25 per cent of the filling of the ventricle.

Outflow of blood from the ventricles occurs during systole.The followingevents occur during systole:

At the beginning of systole, ventricular contraction occurs, the A-V valves close,

and pressure begins to build up in the ventricle.

Ventricular systoleis consists of following periods and phases:

Tension period lasts until opening semilunar valves. Aorta pressure is about70-80 mm Hg. Its period consists of next phases:

phase of asynchronous contraction (0,05 sec)phase of isometric contraction (0,03 sec)Thus, all heart valves close atthis time.

Period of blood ejection begins from the aortic and pulmonary valves open.The left ventricular pressure of about 120-130 mmHg, and the right ventricular

pressure of about 20-25 mm Hg. Its period consists of next phases:

phase of rapid ejection (0,12sec) -most ejection occurs during this phasephase of slow ejection (0,15sec)

Thus, ventricular ejection increases pressure in the aorta to 120 mm Hg

(systolic pressure).

Ventricular diastole(relaxation)is consists of following periods and phases:Protodiastolic phase (0,04) -the semilunar valves are closing at this time withthe help of reverse current of blood.

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Phase of isometric relaxation (0,08) when ventricles begins to spreadthemselves

Period of fillingconsists of:Phase of rapid filling of ventricles (during atrial diastole) 0,08 secPhase of slow filling of ventricles (during atrial systole) 0,27 sec

Thus, during diastole, blood continues to flow into the peripheral circulation,

and arterial pressure decreases to 80 mm Hg( aortic diastolic pressure).

Phase (angle) analysis of cardiac cycle is occurs often with the help of

polycardiography method (simultaneous registration of electrocardiogram,

phonocardiogram and ballistocardiogram).

Blood volume,stroke volume and cardiac output.Additional volumes.

Systolic (stroke) volume (SV) is defined as the amount of blood output per ventricle per beat (amount of blood is ejected into the aorta by one of the ventricles

with each contraction (beat). It has a value of about 65-70 milliliters for men and

50-60 ml for women.

End-diastolic volume (EDV) -means ventricle blood number before the systole(130-140 ml)

End- systolic volume (ESV) -means ventricle blood number after the ventriclesystole (60-70 ml)

Systolic reserve volume (SRV) -means blood number, which add to SV under more strong myocardium contraction (30-40 ml)

Diastolic reserve volume (DRV) -means blood number, on which can beincreased of EDV(30-40 ml)Residual heart volume (RHV) -means blood number, which keeps in ventricleafter the strongest contraction (40 ml).

The most exact heart activity factor is the cardiac output (minute volume of heart or minute cardiac output).Minute cardiac output is defined as the amountof blood leaving the ventricle per minute ( 5 liters/min).Minute cardiac output iscalculated as follows:

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The cardiac output is determined by multiplying the heart rate (HR)the

number of beats per minuteand the stroke volume (SV)the blood volume

ejected by each ventricle with each beat:

CO = HR X SVThus, if each ventricle has a rate of 72 beats/min and ejects 70 ml of blood with

each beat, the cardiac output is:

CO = 72 beats/min X 0.07 L/beat = 5.0 L/min

These values are approximately normal for a resting adult. Since, by coincidence, total blood

volume is also approximately 5 L, this means that essentially all the blood is pumped around the

circuit once each minute. During periods of strenuous exercise in well-trained athletes, the

cardiac output may reach 35 L/min, that is, the entire blood volume is pumped around the circuit

seven times a minute. Even sedentary, untrained individuals can reach cardiac outputs of 20-25

L/min during exercise.

Minute cardiac output can increase due to increase SV or HP.

Electro stimulation and cardiac massageThere are two methods of electro stimulation in clinical practice:

Direct myocardium stimulationowing to the implantation of heart pacemaker. Inthat case the pacemaker impulse is transmitted to electrodes, which are placed to

myocardium. It can be used when the heart rate is decreased, for example, when

the conduction of excitement over the heart is blocked. In this situation the heart

works with a frequency of heart pacemaker (stimulator).

Indirect myocardium stimulationthrough the thorax with the help of defibrillator is arrangement, which to generate electric impulse with a few thousands voltage.

It can be used when the cardiac [heart] arrested as a result of ventricular fibrillation

(is absent contracted contraction) or when occur arrhythmias.

Cardiac massage is method of artificial regeneration of blood circulation inorganism by rhythmical pressing of heart. It leads to blood movement from the

heart cavities into the great vessels. It can be used when the heart has stopped andhasnt work as a pump. Forms of massage include:

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Direct (immediate, transthoracic approach ) - withthe help of one or two handson the open thorax.Indirect (closed, external). The person conducting external massage mustrhythmically to squeeze thorax and heart between the sternum and vertebralcolumn.

II. Dipolar theory of ECG origin. Electrocardiography

Electrocardiography -is a record of electric potentials variation of heart, whichhelps to receive information about excitability, conductivity and automatism of heart.

ECG is a record of tracings obtained by electrocardiograph during different periods of

cardiac cycle. As the depolarization wave passes through the heart, electrical currents

pass into surrounding tissue, and a small part of the current reaches the surface of the

body. The electrical potential generated by these currents can be recorded from

electrodes placed on the skin on the opposite sides of the heart. This recording is called

an electrocardiogram.

The science of electrocardiography is about 100 years old. The techniques of recording

electrical activity from the heart originally were developed by Dutch physiologist,

Willem Einthoven, who referred to the recording of this electrical activity as an

"Elektro Kardio Gramm" (thus the abbreviation EKG).The EKG provides a method of

evaluating excitation events, arrhythmias, and tissue damage, the presence of ischemiaor necrosis, and hypertrophy of the heart.

The body tissues function as an electrical conductor because they contain electrolytes.

The electrical activity of heart is conducted to the body surface through the body fluids.Attaching electrodes to the body surface allows voltage changes to be recorded within

the body after adequate amplification of the signal. A galvanometerwithin the EKGmachine is used as a recording device. Galvanometers record potential differences

(voltages) between two electrodes.

EKG recordings (electrocardiographs)are merely the differences in voltage between

two electrodes located on the body surface.

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The process of action potentials spread in heart can be explained as dipole movement,

which is located at the border of excited and unexcited myocardium parts. Dipole is a

double-charged system. Charges are equal in size and opposite in charge (positive and

negative). These dipoles are formed elementary electromotive force. The electromotive

force of dipole is vector quantity. Vector always directs from negative pole to positive.

There are many vectors arise in heart during excitation. They have different size and

direction. The EKG represents the sum vector - algebraic sum of allvectors.

The wave size (P, Q, R, S, T or U wave) of ECG will be depend upon

the following:

-Sum vector size-Specific resistance of tissue

-Vector orientation in respect of lead axis

Therefore the amplitude of ECG waves will be:

-Proportionate to axial angle of dipoles

-Maximum if axes were parallel

-Zero on conditions that they are perpendicular

The waves size is proportionate to the distance squared from electrodes to heart (this lowis not correct when electrode removal more than 12 centimeters).

ECG registration. The Electrocardiographic leads

The ECG vector is the changing electric field. (This includes magnetic component too,

which changes proportionate to electric field). Human body functions as a nonmoving

conductor because it contains electrolytes solution. According to laws of physics,

electromotive force is developed in nonmoving conductor, which placed in changing

magnetic field. That electromotive force is called electrocardiogram.

The standard EKG consists of recordings from 12 different leads ( 3 standard bipolarleads, 3 augmented unipolar leads, 6 unipolar (V) leads) EKG limb leads. A leadconsists of the recording from electrodes placed at specific sites on the body. Each lead

shows the same cardiac events as other leads but from a different view. Additional leads

are used in special circumstances.

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For recording of those leads the electrodes are collided on right arm (red color), on left

arm (yellow color) and on left leg(green color). All electrodes are connected up in pairs

to electrocardiograph . The fourth electrode is collided on right leg for ground (black color). The signs (+) and (-) are meaning adequate connection of electrodes to the

different galvanometers poles (positive and negative) in other words positive andnegative poles of each leads.

a) Standard bipolar leads (are offered in 1913) by Einthoven:

(1) Lead I left arm (-) and right-arm (+)

(2) Lead II -right-arm (-) and left leg (+)

(3) Lead III -left leg (+) and left arm (-)Three leads are formed by measuring the potential differences between any two of the limb electrodes.

Bipolar limb leads involve an electrocardiogram recorded from electrodes on two

different limbs. There are three bipolar limb leads:

To record from lead I, the negative terminal of the electrocardiogram is connected to

the right arm, and the positive terminal is connected to the left arm. During the

depolarization cycle, the point at which the right arm connects to the chest is

electronegative compared with the point at which the left arm connects, so that the elec-trocardiogram records positivelywhen this lead is used.To record from lead II, the negative terminal of the electrocardiogram is connected to

the right arm, and the positive terminal is connected to the left leg. During most of the

depolarization cycle, the left leg will be electropositive compared with the right arm, so

that the electrocardiogram records positivelywhen this lead is used.To record from lead III, the negative terminal is connected to the left arm, and the

positive terminal is connected to the left leg. During most of the depolarization cycle,

the left leg will be electropositive compared with the left arm, so that the

electrocardiogram records positivelywhen this lead is used.

Einthoven's law states that the electrical potential of any limb lead equals the sumof the potentials of the other two limb leads.The positive and negative signs of the

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different leads must be observed when using this law. The following example illustrates

Einthoven 's law. We first assume that the right arm is 0.2 millivolt negative with

respect to the average potential in the body, the left arm is 0.3 millivolt positive, and the

left leg is 1.0 millivolt positive. Therefore, lead I will a potential of 0.5 millivolt,

because this is the difference between 0.2 millivolt in the right arm and 0,3 millivolt

in the left arm. Similarly, lead II will have a potential of 1.2 millivolts, and lead III willhave a potential of 0,7 millivolt.

You can see three standard leads which are form equilateraltriangle (Einthovens triangle ) which apexes are :

right arm, left arm, left leg. In center of triangle is found of heart (or

punctate single heart dipole whichequally remote from all threestandard leads.

The line between two electrodes is called electric lead axis.

Axises of standard leads are sides of triangle. Einthoven`s triangle (equilateral triangle

with the right and left shoulders and left leg as the three apices. The right leg serves as a

ground connector. It lines are drawn perpendicularly from the center of each side of an

equilateral triangle. They will meet at the center of the triangle. These lines represent

the zero potential lines for the three sides of the triangle .

b) Augmented unipolar leads by Goldberger`sAny of the three limb electrodes can be used to record cardiac potentials in comparison

to the common terminal. So, records the difference in voltage between the extremity,

which is connected with positive electrocardiograph input and joint electrode (two other extremities).

aVR right arm is the active electrode (is the potential difference between RA and

(LA+LL)

aVL - left arm is the active electrode (is the potential difference between LA and

(RA+LL)

aVF - left leg (foot) is the active electrode (is the potential difference between LF and

(LA+RA)

c) Unipolar (V) chest leads by Wilsons

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The active electrode is located on standardized sites of thorax. Second electrode is

formed by conjoined leads from three extremities. There are six precordial leads, also

termed V leads in the standard ECG. These precordial leads measure electrical activity

in the horizontal plane of the body.

V1 is in the fourth intercostals space (ICS) just to the right of the sternum

V2 is in the fourth ICS just to the left of the sternum

V3 is halfway between V2 and V4

V4 is at the midclavicular line in the fifth ICS

V5 is an the anterior axillarys line at the same level as V4

V6 is in the midaxillary line at the same level as V4 and V5

Electrocardiogram

Except the positive [upward] waves P, R, Tand U, which are above the isoelectric line,may be the negative(Q and S), which areunder the isoelectric line.

Normal electrocardiogrammeasured from lead II1. P wave (duration - 0,11 sec;amplitude less or equal 0,2 mV) positive, represents the initiationand propagation(spread)excitation

in atriums.

- represents depolarization of atrial muscle (a P wave caused by the electrical potential

generated from depolarization of the atria before their contraction)-does not include atrial repolarization, which is "buried" in the QRS complex

2. PR interval (duration 0,12-0,20 and depend on heart rate : if HR - PR is shorter)

-is the interval from first atrial depolarization to the beginning of the Q wave (initial

depolarization of the ventricle).

-increases if conduction velocity through the atrioventricular (AV) node is slowed (as in

heart block)

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The P-R interval is a measure of the AV conduction time and it includes the delaythrough the AV node.

-varies with heart rate: When heart rate increases, the PR interval decreases.

3. Q wave (duration 0,04 sec, amplitude - one fourth of R wave) is usually negative.

- represents depolarization of the interventricular septum and conducting system4. QRS complex (its duration is normally less than 0,08 sec)represents

depolarization of the ventricles

A QRS complex caused by the electrical potential generated from the ventricles

before their contraction. QRST (Q-T) - ventricles complex because represents the

excitation spread (QRS) and excitation fading (segment RS-T and T wave)

5. QT interval (electric systole)is the interval from the beginning of the Q wave to the end

of the T wave

- represents the entire period of depolarization and repolarization of the ventricles

- has a normal value of 0,35 second (this approximates the time of ventricular contraction).

The normal duration of Q- T interval is determined by Bazette`s formula:Q- TK R-R ,

where K- coefficient is come to 0,37 for males, 0,38 for children and 0,40 forwomen; R-R is duration of one cardiac cycle.

6. ST segment

-is the segment from the end of the S wave to the beginning of the T wave.

-is isoelectric.

-represents the period when the entire ventricle is depolarized

7. T wave is positive (duration 0,16-0,24 sec, amplitude is about 0,5 mV)

- is caused by ventricular repolarization. A T wave caused by the potential generated

from repolarization of the ventricles ( 0.27 sec)

8. Sometimes after the T wave is recoded little positive U wave,which origin isunknown. It may be that U wave represents period of short-term increase ventricle

excitability of myocardium (phase of exaltation) after the ventricular systole ending .

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9. R-R interval (duration from 0,8 to 1,0 sec)

-is the time between successive QRS complexes . The heart rate is equal to 60 dividedby the R-R interval in seconds.

Heart rate60 R-R secAtrial and ventricular contractions are related to the electrocardiogram waves.

During the depolarization process, the average electrical current flows from thebase of the heart toward the apex.

10. R wave is usually positive (duration 0,04-0,06 sec, amplitude -1,0-1,5 mV)

- represents excitation spread in myocardium of right and left ventricles. In the end of this wave the excitation involves whole myocardium except for basal part.

11. S wave is usually negative (duration 0,06 sec, amplitude in wide-ranging)

- represents depolarization of basal ventricles parts

12. T-P interval (electric diastole)between T wave and a new P wave

- varies with heart rate

13. P-Q segment- represents atrium depolarizationThe principle of ECG analysis

During ECG analysis we must find location of its elements and isoelectric line-

deviation. The amplitude of ECG waves is determined by vector average and their

polarity vector direction. ECG intervals characterize of depolarization speed.

The main activities of ECG:

a) heart rateb) axis of heart positionc) amplitude of waves (mV)d) duration of waves and segments (sec)e) systolic index (per cent)

Dependence of ECGwaves amplitude from their projection ontoleadaxis

It was showed on Einthovens triangle, in which three standard leads are form

equilateral triangle. In the center of this triangle is found united cardiac dipole.

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With the help of dipole projection we can determine of R wave amplitude in standart

lead. So, if the intermediated arrangment of electric heart axis than the maximum

amplitude of R wave was in II lead, minimum in I and average amplitude in IIIlead. During analysis of R waves amplitude we must to use Einthoven 's law: theamplitude of R wave in every standard lead equals the sum of the potentials of theother two limb leads.Its low lies in base of axonometry calculation of axis deviationangle in I lead line.

Electric heart axis. Intermediate, vertical and horizontal position. Determination techniques

Line, which runs thruough the main vector QRS to the crossing with I lead line is calledelectrical heart axis. The position of electrical heart axis is showed by angle value,which arises by electrical axis and positive half-I-lead. It coincides with anatomical

axis of heart. It determines by two methods:

a) to the amplitude of R wave in standart leads;

b) with the help of method of axonometry (more exact)

Divides three variants of arrangment heart axis in thorax:1) Normal (intermediate) position, where angle is come to +30-+69 degree and

the R amplitude predominates in II lead.

2) Vertical (dextrogram)position, where angle is come from +70 to+90 degreeand the R amplitude predominates in III lead. Heart is called suspended (drop)heart. It is observed in physiological conditions, especially asthenics have it.

3) Horizontal position (levocardiogram), where angle is come from +0 to+29degree and the R amplitude predominates in I lead. Hypersthenes persons havereclining position of heart.

Sound phenomenon in heart. Origin of heart sounds.Method of phonocardiography.

Above projection of heart valves it is possible to listened heart sounds by means of aphonendoscope (a method of auscultation). It is possible not only to listen to heart

sounds, but also to register by means of phonocardiograph. A principle of a methodphonocardiography (FCG) following: in a place of a projection of valves of heart placea sensitive microphone, heart sounds to intensify and write down on the paper.

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FCG - an objective method of research of heart sounds. At auscultation usuallylisten to 2 heart sounds.

The first heart sound - systolic - coincides with the beginning of a systole. Threecomponents participate in its formation: valvular, muscular, vascular. They consist of following components:

1) Closing of atrioventricular valves;2) Their vibrations;3) Turbulent movement of the blood hitting about the valve;4) Vibrations of a ventricles wall;5) Fluctuations of aortas walls and a pulmonary trunk during ejection.

The basic component is valvular . Duration of the first tone - 0,10 - 0,14 seconds.The second heart sound - diastolic - coincides with the beginning of

ventricles diastole. Its components:1) beat of semilunar valves flappers each other at closing;

2) Turbulent movement of blood in an aorta;3) Vibration of an aorta and a pulmonary artery.The basic component is valvular . Duration of the second tone- 0,06 - 0,11 seconds.At FCG it is possible to register the third and fourth heart sounds.

The third heart sound arises owing to vibration of ventricles walls in a phaseof fast filling.

The fourth heart sound arises at a systole of auricles and return of a part of blood to auricles. Methods of auscultation and FCG are applied first of all tostudying job of valving system in heart.

IHeart sound II Figure 1: FCG

0,1-0,14 sec 0,06-0,1 sec

Figure 2: Simultaneous registration of ECG and FCG

Mechanical display of heart work

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Apex beat (bulging of thorax) comes to light by method of palpation or bymeans of the apparatus apexcardiographat each systole in left fifth intercostal onmediumclavicular line . It is investigation of moving of a top of heart aside aforward thorax at change of the form of heart during a systole.

Ballistocardiography - a method of registration pulse micromovings(microdisplacement) of a body caused of blood projection from ventricles in largevessels. Allows studying force of heart contractions, the phase analysis of ancardiac cycle (at polycardiography). Now it is applied seldom.

Dynamocardiography- analysis of position changes of the centre gravityof the thorax, caused by contractions of heart.

Researchof the size of chambers of heart, coronary vessels by means of Angioroentgentography

The principle of a method consists in probe introduction of contrast solution (opaque tox-ray substances) in chambers of heart, with the subsequent radiography of heart. It is

applied in cardiosurgery; in connection with opportunities of an echocardiography

application of a method is limited.

It is much more often applied coronography - a rontgenologic (al) method of permeability evaluation of large (up to 1 mm in diameter) coronary arteries. It is carried

out at introduction radiopaque substance through a probe in a mouth of one of coronary

arteries. Coronographyenables exactly to localize sites of constriction of the coronaryarteries amazed by an atherosclerosis, its degree.

THE ECHOCARDIOGRAPHY (EchoCG), principles, the technique,parameters of heart activity

Echocardiography ( EchoCG)is a noninvasive method of heart research, based on use

of ultrasound reflection from borders of two environments division with different

densities (a tissue - blood). Most a wide spread occurrence has received Doppler

Echocardiography . A principle of a method: registration of a frequencies difference of direct and reflected from a moving surface the ultrasound.

Technique: the Ultrasonic sensor is located on a thorax greased by a liquid, improvingconductivity of ultrasound; turning the sensor under a different corner, scan heart.

Method EchoCGallows to estimate:1) A status of heart valve apparatus;2) The sizes and the area of chambers of heart;

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3) speed of movement of blood through valves;4) end-diastolic volume;5) end-systolic volume;6) systolic volume;7) thickness of ventricles walls;8) a gradient of pressure between valves,

9) contractive ability of a myocardium and other parameters of heart work.III. Regulation of heart activity

Myogenous mechanisms of regulation of heart activitya) Franc-Starlings law (heart law). and Anrep`s effect.

The Frank-Starling mechanism intrinsically regulates cardiac pumping ability. When

venous return of blood increases (during diastole), the heart muscle stretches more,

which makes it pump with a greater force of contraction (during systole). The extra

stretch of the cardiac muscle during increased venous return, within limits, causes the

actin and myosin filaments to interdigitate at a more optimal length for force

generation. In addition, more stretch of the right atrial wall causes a reflex increase in

heart rate of 10 to 20 per cent, which helps the heart to pump more blood.

So, Frank-Starling mechanism describes the increase in cardiac output (or strike

volume) that occurs in response to an increase in venous pressure or end-diastolic

volume. Frank-Starling mechanism is based on the length-tension relationship;

increases in end-diastolic volume cause an increase in fiber length, which causes anincrease in developed tension (The force of heart contractions is increased duringmyocardium tension). But it law is not realize if end-diastolic volume is increased more

than 180 ml, because the actin and myosin filaments are strongly stretched.

b) Anrep`s effect.In contrast to Franc-Starlings law, the Anrep`s effect develops during increase diastolic

pressure in aorta. But it realizes through the Franc-Starlings law: increase coronary

blood flow is causes by increase of diastolic pressure in aorta. As a result cardiac

myocytes are stretched, that is the reason of force increase of myocardium contraction.

c) Chronoinotropy determines the force-rate relationship of heartcontractions. It myogenous mechanism is not connected with a change of cardiac

myocytes length. According to chronoinotropy, increase of heart rate lead to the

force of contraction increase too (and vice versa). The mechanism of this effect is

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connected with storage or decrease of Ca in cardiac myocytes and also with

increase or decrease of cross - bridges quantity.

Humoral mechanismsof heart activity regulation a) Influence of ions Ca2+, K +, Na+

During increase Ca 2+ in blood the excitability and contractility of cardiac muscle

increase and during decreases Ca 2+ in blood decreases . The mechanism of this effect isconnected with:

1) in the first place, increase Ca 2+ in conducting system cells (it leads to rate

increase)

2) in the second place, increase Ca 2+ in contractile cells (it leads to force

contraction increase)

In experiments with isolated heart, the cardiac arrest during systole is connected with

over concentration of Ca 2+.

At increase of K + (potassium) in blood the activity of pacemaker cells of

automatism and heart rate decrease. Besides that, increase the force of heart

contractions down to the cardiac arrest in diastole phase. The mechanism of this effect

is connected with increase membrane permeability to the K + ions and therefore

hyperpolarization of cardiac myocytes. Decreases of K + concentration cause the

opposed effects.

At some increase of Na + (sodium) the myocardium contractility to increase

because to increase activity of Na +, Ca 2+ exchange. Decreases of Na + concentration in

blood cause the cardiac arrest in result of electromechanical coupling mechanism

breach.

b) Influence of hormones on heart activity.Most of the hormones stimulate the heart activity (such as epinephrine, nor epinephrine,

glucagons, insulin.

Thyroxin stimulates of heart work with the help of increases -adrenoreceptors

quantity. The action of glucocorticoids is the similar, but they increase of -

adrenoreceptors sensitivity. Hormones, which amplify heart work (with the help of activation of Ca 2+ channels), are called:

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- Epinephrine (force on -adrenoreceptors)- Angiotensin II (force on angiotensin receptors in heart)- Histamine (force on H2 histamine receptors)- SerotoninBradykinin and acetylcholine are the examples of negative influence on heart.

They decrease of Ca2+

channels activity.c) Influence of metabolites.Because for normal heart function our body is needed in energy, therefore all

metabolites, which to increase energy production, stimulate of heart work. Among these

are: creatine phosphate, free fat acids, lactic acid and glucose.

The factors, which decrease heart work, are: hypoxia and intracellular acidosis.

Intracardiac reflexes, as kind of intracardiac regulation Intracardiac reflexes (cardio cardiac reflexes) lock on the level of intramural heart

ganglion. There are two types of receptors in atriums and left ventricle:

1) to response for the perception of active tension.

2) to response for the passive stretching of atrium and ventricular walls.

Afferent fibers move to the neurons of intramural ganglion. Myocardium is innervated

by the axons of these neurons.

Examples of cardio cardiac reflexes:

a) Contractions of left ventricle increase during increase of blood flow to the right

atrium. Physiological sense in: left ventricle clearing to following blood flow.

b) The heart contractility depresses, because chambers of heart, chambers of aorta

and coronary vessels are overflowing by blood. Physiological sense in: decrease of

pressure in aorta and coronary vessels.

At the same time with parasympathetic neurons, the sympathetic neurons take part in

intracardiac regulation. In physiological conditions the intracardiac and extracardiac

reflexes are interacted.

Intracardiac regulation ensures adequate work of heart after the transplantation.

Extracardiac regulation of heart work Extracardiac regulation is realized through parasympathetic and sympathetic nerve

centers. Centers of parasympathetic regulation are located in medulla oblongata (vagus

[X cranial] nerve nuclei). SA node is innervated by right nerve and AV node is

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innervated by left nerve. Centers of sympathetic innervation is located in lateral horns

of spinal cord (in thoracic segments), innervate both conducting system and contractile

myocardium.

Vagus irritation causes Ach excretion in postganglionic fibers. Vagus nerve

exerts influence on:

- heart rate ( negative chronotropic effect heart rate decreases),- force of heart contractions ( negative inotropic effect force of heartcontractions decreases),

- conduction velocity throughout the myocardium ( negative dromotropic effect- conduction velocity throughout the myocardium decreases)- myocardium excitability ( negative bathmotropic effect myocardiumexcitability decreases).

Parasympathetic stimulation ( Ach) via muscarinic receptorsdecreases the strength of contraction in atria by decreasing Ca 2+ entry into the cell during the plateau of the

cardiac action potential. The right vagus nerve influences on chronotropic and

bathmotropic functions, but the left vagus nerve influences on dromo and inotropic

functions.

The irritation of sympathetic nerves, which innervate the heart, causes to release

neurotransmitter epinephrine from the postganglionic fibers. Epinephrine via -

adrenoreceptors is believed to increase all functions of heart referred above: arise

positive chrono-, bathmo-, ino-and dromotropic effects.Besides it, sympatheticnerves (as in epinephrine) cause the reason of trophic action they increase of

contraction force without changes of heart rate.

The central mechanisms of heart activity regulation The main centers, which regulate heart and vessels work are located in medulla

oblongata:

a) Dorsolateral (pressor) center amplify heart activity through sympathetic nerves.

b) Ventromedial (depressor) center increase heart activity by reciprocal inhibition of neurons

activity of dorsolateral center and direct influence of vagus nerves on heart.

Others department of CNS influence on heart too:

a) neocortex amplify heart rate ( causes prelaunch tachycardia);

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b) paleocortex (anterior cingulate gyrus) - increase (brake) heart activity.

c) Different parts of hypothalamus can to amplify and brake of heart activity.

Reflex regulation of heart activity from different reflex zonesa) Bainbridge reflex(reflex from cava veins) - reflex increase of heart rate and force of heart contractions in response to increase pressure in cava veins and atriums. It begins

from mechanoreceptors of veins and atriums, after that tone of vagus nerve is

decreased, as a result increased activity of sympathetic nerves. So, increase heart rate

and myocardial contractility, as is allowed pumps additional amount of blood from

venous system.

b) Reflex from carotid sinus (Gering reflex) and aortic arch (Ceone reflex)begin onbaroreceptors of corresponding reflex zones. When pulsation from baroreceptors is

increased, the tone of vagus nerve and heart rate increase, but contraction force

decreases. Therefore in patient with increased arterial pressure observed slow heart rate,

which is called bradycardia.c) Dagnini-Aschner [oculocardiac] reflexbelongs to the group of clinically important

vegetative reactions and extensively used in clinic for definition of vagus nerve tone. Itshows in heart rate changes (usually decrease) after the press on eyeballs, during 3-4

minutes after the press. In this case the mechanoreceptors of trigeminus are irritated

through hypothalamus, which nuclei to increase tone of vagus nerve nuclei.

d) Holtz's reflex interoreceptors irritation of abdominal cavity.

Tone of the centers of cardiac nerves, its value Tone of heart nerves - constant excitation of neurons of centers these nerves. Adult

people have predominated tone of centers of vagus nerves. It forms by reflex impulses

from vascular receptors (particularly, from baroreceptors) arrive in medulla oblongata.

Therefore constant excitation is supported in vagus nerves nuclei. As a result, nervous

impulses are coming in vagus nerve to the heart. They inhibit of heart activity. On

vagus nerves transection, the heart rate increases more than in twice. Tone of

sympathetic centers, as a rule, increase during activation of sympathetic centers, for

example, during the stress and practically is absent in quiet state.

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Tone of vagus nerve can changes in following cases:

1) Newborn (baby) has not tone of vagus nerve, because adrenergic innervation of

SA node predominates. Tone of vagus nerve increases with age and finally is shaping to

the age of 20-25 years.

2) In one's sleep - tone of vagus nerve increases.

3) At operative intervention on abdominal cavity organs (impulses go from the

abdominal nerve and increase tone of vagus nerves centers.

4) In the increase of Ca 2+ ions concentration or epinephrine in blood.

Characteristics of nervous regulation of heart in age aspect Nervous regulation of heart has not material meaning during period of intrauterinedevelopment of fetus. Heart rate of fetus depends on pacemaker automatism. Newborn

innervation of SA node occurs by adrenergic structures; cholinergic heart innervation

forms in a few months after birth. Therefore heart rate is about (for newborn) 130

contractions per minute. Influence of vegetative nerves on heart activity decreases for

people of middle age, but the meaning of humoral regulation increases with the help of

circulating in blood substances.

Mechanisms of regulation of cardiac muscle activity after itstransplantation

After the heart transplantation, the Extracardiac level of regulation disappears.

Therefore after the heart transplantation, the reconstruction of heart activity occurs in

the following order:

a) Activity of transplanted heart recommences owing to automatism of cardiac

muscle (heart either begins to contract or starts by direct massage or defibrillation after

the decreasing of K + to normal level).

b) After that, the regulation of heart activity occurs owing to intracardiac

regulation. Intracardiac regulation ensures circulation of the blood, which is adequate to

the physical activity.

c) Humoral regulation has defined value in those cases (especially the

amplification of heart activity with the help of epinephrine and similar substances.

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IV. HemodynamicsHemodynamics - study of movement of blood through circulatory system.

The blood vessels carry blood from the heart to the tissues and back to the heart.The resistance to flowdepends to a minor degree upon the vis cosity of the blood butmostly upon the diameter of the vessels, principally the arterioles. The blood flow to

each tissue is regulated by local chemical and general neural and humoral mechanisms

that dilate or constrict the vessels of the tissue.

1. Basic principles of hemodynamicsHemodynamics - study of blood flow over the vessels. There are 3 main basic indexes

of hemodynamics:

a) P - Pressure in blood vessels;

b) Q - Volume velocity of blood flow;

c) R - Hydrodynamic resistance

The volume velocity of blood flow through a vessel can be calculated by the formula:

Q = P/ R (ml/min)You can find extreme importance of the relationship among pressure, flow and

resistance :R = P/Q

P = QXR

2. Linear and volume velocity of blood flow, blood circulation timeVolume velocity of blood connects with pressure at the entry and at the output of

circulatory system. Because blood pressure is more than 10 times below in venous

system, than in arterial system, P is the arterial pressure.Q is quantity of blood, which flows for unit time via the any department of vascular system (for example, via the aorta, capillaries). The term MCO is used in physiology.Minute cardiac output is defined as the amount of blood leaving the ventricle per

minute (4- 5 liters /min).

For Q definition is used method of integral or local rheography. Method principle: themore blood flows through the circulatory system, the smaller electric resistance of body

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or individual organs. At the same time resistance test (measurement) occurs with the

help of current with frequency about 30-300 kHz. Plethysmography is the old method

of Q measurement.The important index of hemodynamics is linear velocity of blood flow(V),

V = Q/ R 2 (cm/sec)We can see that V is inversely as the square of vessels radius. So, velocity is directly

proportional to blood flow and inversely proportional to the cross-sectional area at any

level of the cardiovascular system.

-For example, linear velocity of blood flowis higher in the aorta (small cross-sectionalarea) than in the sum of all the capillaries (large cross-sectional area).V in aorta is 20 cm/sec .

V in arteries is 10-15 cm/sec.

V in arterioles is 0,2-0,3 cm/sec .

V in capillaries is 0,02-0,03 cm/sec

Mean time of blood circulation is 20-30 sec under heart rate is about 70-80 beats per

minute, four fifth of all blood circulation time falls at greater [systemic] circulation and

one fifth falls at lesser [pulmonary] circulation.

3. Total peripheral resistance of vessels (TPRV)Resistance can be expressed by the following Poiseuille equation:

- Viscosity of blood1 Total length of blood vesselr4 - radius of blood vessel to fourth powerResistance is directly proportional to the viscosity of the blood. Blood cells, which

localized near the wall, offer more resistance than those, which in the center. Therefore

during considerable viscosity of the blood (for ex.- fluid loss at cholera), signs of heart

failure (cardiac insufficiency) are observed (blood pumps with difficulty).

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For example,increasing viscosity by increasing hematocrit will increase resistanceand decrease flow. Resistance is directly proportional to length of vessel. Maximal

resistance to blood current must be in the thinnest vessels, like arterioles and capillaries.

50 per cent of TPRV falls at arterioles (because they have small diameter and biglength).

TPRV of capillaries is 25 per cent, because total length of capillaries is less than inarterioles.

Resistance is inversely proportional to the fourth power of the vessel radius. This is a

powerful relationship. For example, if blood vessel radius decreases by a factor of 2,then resistance will increase by a factor of 16 (2 4), and flow will therefore decrease by a

factor of 16.

4. Types of blood flow: 1) Stream line or laminar flowis a silent flow, occurs only at velocities up to a criticallevel. Within the blood vessel, a very thin layer of blood is in contact with the vessel

wall. This does not move or moves very slowly. The next layer within the vessel has a

low momentum. The next layer has a higher momentum. So, momentum increases in

the inner layers so that, the momentum is maximum in the center of the stream. This

type of flow is known as stream line flow and it does not produce any sound within the

vessel.

2) Turbulent flowcreates sounds. When the velocity of blood flow increases criticallevel, the flow becomes turbulent.

Factors maintaining volume of blood flow

1. Pressure gradientThe volume of blood flow through any blood vessel is directly proportional to the

difference between the pressures at either end of the blood vessel. This difference in

pressure is known as pressure gradient (P 1-P2), where P 1 pressure at proximal end of

the vessel, P 2 - pressure at distal end of the vessel.For ex., the maximal gradient exists between the aorta (100 mmHg) and the inferior

vena cava (0 mmHg). So, the pressure gradient is 100-0=100 mmHg2. Resistance (R) to blood flow (peripheral resistance)

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The volume of blood flow is inversely proportional to the resistance. Resistance is the

tension against which the blood flows (resistance is maximal in the arterioles). Three

important factors, which determine the peripheral resistance, are:

- Radius of blood vessels

- Pressure gradient

- Viscosity of blood

Resistance is inversely proportional to the radius of the blood flow. So, the lesser the

radius, more will be R. r R The r of the arterioles is very less because of the sympathetic tone. So, the R is more

here. The arterioles are known as resistant vessels because of this reason.

3. Viscosity of bloodThe volume of blood flow is inversely proportional to the viscosity of blood. Viscosity

is the friction of blood against the wall of the blood vessel. The number of red blood

cells is the main factor, which determines the viscosity of the blood. Another factor

determines viscosity in plasma is mainly albumin.

4. Diameter of blood vesselsThe volume of blood flow is directly proportional to the diameter. The aorta has a

maximum diameter and capillary has got the minimum diameter. But in circulation, the

diameter of the vessel is considered in relation to the cross sectional area through which

the blood flows. The cross sectional area is progressively increased as the distance from

the heart is increased. So, the aorta has got less cross sectional area of 4sm compared

to that of capillaries, which is 2500 sm.

5. Velocity of blood flow is the rate of blood flow through a particular region. Themean volume of blood flow is directly proportional to the velocity of blood flow. It

mainly depends upon the:

- Diameter- Cross sectional area of blood vessel

Velocity of blood flow:

- is directly proportional to cardiac output- is decreased as the distance from the heart is increased

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- is inversely proportional to the viscosity of blood

Three factors are responsible for the maintenance of the velocity of blood flow.

1. Cardiac output (increases in cardiac output leads to increase in the velocity of blood

flow in all parts of the circulation)

2. Cross sectional area of the blood vessel

3. Viscosity of the blood (if viscosity is more, the velocity of blood flow is reduced)

The velocity of blood flow changes according to the phases of cardiac cycle. Blood

flows in the large arteries at a greater speed during systole than during diastole.

Normally, a sudden increase or decrease in the arterial blood pressure

momentarily increases or decreases the blood flow. Within short time, the local

mechanism (autoregulation) start functioning and the blood flow is brought to relatively

normal level. There are 2 theories, which to explain the autoregulation:

1) Myogenic TheorySmooth muscle fibers in the blood vessels are responsible for autoregulation. So,

sudden stretching of blood vessels causes contraction of smooth muscle fibers present

in the wall of vessels. So, when the arterial pressure increases suddenly, the stretching

of the blood vessels immediately causes vasoconstriction and thereby the blood flow is

controlled.

2) Metabolic TheoryWhen the blood flow is reduced, there is accumulation of metabolites. These

metabolites dilate the blood vessels and bring the blood flow back to normal. When

blood flow increases, the vasodilator metabolites (CO 2, H+ ions, adenosine, lactate) are

washed out of the tissues. This leads to vasoconstriction and the volume of blood flow

becomes normal.

5. Functional characteristics of vessels All vessels depending on function can be divided on:

1) Cushioning vessels are the elastic and big muscular arteries2) Resistive vessels are terminal arteries, arterioles and venules.

3) Exchange vessels are the capillaries.4) Capacitive vesselsare the veins.

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5) Shunting vessels are the arterio-venous anastomoses along which blood flowsfrom arterioles to venules by-passing (omitting) the capillaries.

The physiological role of vesselsThe walls of all arteries are made up of 3 layers: an outer layer of

connective tissue, the adventitia; a middle layerof smooth muscle, the media; and aninner layer, the intima, made up of the endothelium and underlying connective tissue.

The walls of the aorta and other arteries of large diameter contain arelatively large amount of elastic tissue, primarily located in the inner and externalelastic laminas. They are stretched during systole and recoil on the blood during

diastole. The arteries transport blood under high pressure to the tissues and have strong

vascular walls and rapid blood flow.

The walls of the arterioles contain less elastic tissuebut much more smoothmuscle. The muscle is innervated by noradrenergic nerve fibers, which are constrictor

in function and in some instances by cholinergic fibers, which dilate the vessels. The

arterioles are the major site of the resistance to blood flow, and small changes in their caliber cause large changes in the total peripheral resistance. The arterioles are the last

branches of the arterial system and act as control valves through which blood is released

into the capillaries; these vessels have strong muscular walls that can be constricted or

dilated, giving them the capability of markedly altering blood flow to the capillaries in

response to changing tissue needs.

The capillaries, which exchange fluids, nutrients, and other substancesbetween the blood and the interstitial fluid; they have thin walls and are highly

permeable to small molecules. The blood flow in capillaries has following

characteristics:

1) as the diameter of capillaries decreases , the volume of plasma decreases too.

2) as the diameter of capillaries decreases , the velocity of blood flow increases

Foreus-Lendkvest phenomenon: the red blood cells line up the vessels one after another. It causes reduction of friction between formed elements. So, owing to the

elasticity (flexibility) of membrane, the erythrocyte can go over the capillary, which is

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smaller to diameter. During the advance of erythrocyte over narrow capillary, the

capillary is maintained in expanded state.

There are two mechanisms of exchange in capillaries: 1) diffusion and 2) filtration and

reabsorption

Diffusionoccurs through pores of membranes and intercellular compounds. Thecapillary wall is very thin, consisting of a single layer of endothelial cells.Capillaries are very porous, with several million slits, or pores, between the cells that

make up their walls (the width of the pores are about 8 nanometers) to each square

centimeter of capillary surface. Because of the high permeability of the capillariesfor most solutes and the high surface area, as blood flows through the capillaries, large

amounts of dissolved substances diffuse in both directions through these pores. In this

way, almost all dissolved substances in the plasma, except the plasma proteins,continually mix with the interstitial fluid.

The three primary factors that affect the rate of diffusionacross the capillary walls are: 1. The pore size in the capillary ; in most capillaries, the pore size is 6 to 7 nanometers.

The pores of some capillary membranes, such as the liver capillary sinusoids, are much

larger and are therefore much more highly permeable to substances dissolved in plasma.

2. The molecular size of the diffusing substance : water and most electrolytes (Na and

Cl) have a molecular size that is smaller than the pore size, allowing rapid diffusion

across the capillary wall. Plasma proteins have a molecular size that is greater than the

width of the pores, restricting their diffusion.

3. The concentration difference of the substance between the two sides of the

membrane ; the greater the difference between the concentrations of a substance on the

two sides of the capillary membrane, the greater the rate of diffusionin one directionthough the membrane. The concentration of oxygen in the blood is normally greater

than in the interstitial fluid, allowing large quan tities of oxygen to move from the blood

toward the tis sues . Conversely, the concentrations of the waste products of metabolism

are greater in the tissues than in the blood, allowing them to move into the blood and to

be carried away from the tissues.

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The following mechanism after diffusion is a filtrationof fluid part of bloodcoupled with solutes and back reabsorption of fluid.

In the fingers, palms, and ear lobes of humans and the paws, ears, and other

tissues of some animals, there are short channels that connect arterioles to venules, by -

passing the capillaries. These arteriovenous (A-V) anastomoses,or shunts, havethick, muscular walls and are abundantly innervated, presumably by vasoconstrictor

nerve fibers.

The walls of the venulesare only slightly thicker than those of the capillaries.The walls of the veins are also thin and easily distended. They contain relatively little

smooth muscle, but considerable venoconstriction is produced by activity in the

noradrenergic nerves to the veins and by circulating vasoconstrictors such as

endothelins. Anyone who has had trouble making venipunctures has observed the

marked local venospasm produced in superficial forearm veins by injury. The venules

collect blood from the capillaries and gradually coalesce into progressively larger veins.

The veins, which function as conduits to transport blood from the tissuesback to the heart; veins also serve as reservoirs for blood and have thin walls, low

pressure, and rapid blood flow. The intima of the limb veins is folded at intervals to

form venous valvesthat prevent retrograde flow. The way these valves function wasfirst demonstrated by William Harvey in the 17th century. There are no valves in the

very small veins, the great veins, or the veins from the brain and viscera. Capacitivefunction of veinsis conditioned by big degree of stretching (it is connect withdepositing (pooling, storage) of blood especially in liver veins and big veins of

abdominal cavity.

Structure of the Microcirculation Blood enters the capillaries through an arteriole and leaves through a venule. Blood

from the arteriole passes into a series of metarterioles, which have structures midwaybetween those of arterioles and capillaries. Arterioles are highly muscular and play a

major role in controlling blood flow to the tissues. The metarterioles do not have a

continuous smooth muscle coat, but smooth muscle fibers encircle the vessel atintermittent points called precapillary sphincters. Contraction of the muscle in these

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sphincters can open and close the entrance to the capillary. This arrangement of the

microcirculation is not found in all parts of the body, but similar arrangements serve the

same purposes. Both the metarterioles and arterioles are in close contact with the tissues

that they serve, and local conditions, such as changes in the concentration of nutrients

or waste products of metabolism, can have direct effects on these vessels in controlling

the local blood flow.

LYMPHATIC SYSTEMLymphatic system is a closed system of lymph channels or lymph vessels through which

lymph flows. It is a one way system and allows the lymph flow from tissue spaces towards the blood.

The lymphatic system arises from tissue spaces as a meshwork of delicate vessels. These vessels are

called lymph capillaries. The lymph capillaries start from tissue spaces and ended terminals calledcapillary bulbs. These bulbs contain valves, which allow flow of lymph in one direction, i.e. towards

blood. There are some muscle fibers around these bulbs. These muscle fibers cause contraction of

bulbs so that, lymph can move through the vessels. The capillaries unite to form large lymphatic

vessels. The lymphatic vessels become larger and larger. The structure of lymph capillaries is slightly

different from that of blood capillaries. The lymph capillaries are more porous and the cells lie

overlapping on one another. This allows the fluid to move into the capillaries and not to outside.

LYMPH VESSELSare situated in the following regions: deeper layers of skin; subcutaneous tissues,wall of abdominal cavity, omentum, linings of respiratory tract except alveoli, linings of digestive

tract, linings of urinary tract, linings of genital tract, liver and heart.

The lymph vessels are not present in the following structures: superficial layers of skin, central

nervous system, cornea, bones and alveoli of lungs

LYMPH NODESare small glandular structures located in the course of lymph vessels. The lymphnodes are also called lymph glands or lymphatic nodes. Each lymph node constitutes masses of

lymphatic tissue covered by a dense connective tissue capsule. The structures are arranged in threelayers namely, cortex, paracortex and medulla.

Cortex of lymph node consists of primary and secondary follicles. The primary follicle

develops first. When some antigens enter the body and reach the lymph nodes, the cells of primary follicle proliferate. After the proliferation of cells, the primary follicles become thesecondary follicle. Cortex also contains some B lymphocytes, which are usually aggregated into the

primary follicles.

Paracortex: This is in between cortex and medulla. Paracortex contains T lymphocytes.

Medulla: Medulla contains both B and T lymphocytes. Blood vessels of lymph node pass through

medulla.

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The lymph node receives lymph by one or two lymphatic vessels called afferent vessels. After passing

through the small channels arising from the afferent vessels, lymph circulates through cortex,

paracortex and medulla of the node. From medulla, the lymph leaves the node via one or two efferent

vessels.

The lymph nodes are present along the course of lymphatic vessels in elbow, axilla, knee and groin.The lymph nodes are also present in certain points in abdomen, thorax and neck where many lymph

vessels join.

FORMATION OF LYMPHLymph is formed from interstitial fluid, due to the permeability of lymph capillaries. When blood passes via blood capillaries in the tissues, 9/10 of fluid passes into

venous end of capillaries from arterial end. And, the remaining 1/10 of the fluid passes into lymphcapillaries, which have more permeability than blood capillaries.

So, when lymph passes through lymph capillaries the composition of lymph is more or less similar to that of interstitial fluid including protein content. Proteins present in the interstitial fluid cannotenter the blood capillaries because of their larger size. So, these proteins enter lymph vessels,which are permeable to large particles also. The tissue fluid in liver and gastrointestinal tract contains

more protein and lipid substances. Thus, lymph in larger vessels has more proteins and lipids.

CONCENTRATION OF LYMPHWhen the lymph passes through the lymph nodes,the lymph becomes concentrated because of the absorption of water and the electrolytes

in the lymph node. The proteins and lipids, which are not absorbed, remain in the lymphitself. Many bacteria are removed from lymph and phagocytozed by themacrophages of lymph node.RATE OF LYMPH FLOWAbout 120 ml of lymph flows into blood per hour. Out of this, about 100ml/hour flows through thoracic duct and 20 ml/ hour flows through the right lymphatic duct.

The flow of lymph is promoted by the increase in:

1. Interstitial fluid pressure

2. Blood capillary pressure

3. Surface area of lymph capillary by means of dilatation

4. Permeability of lymph capillaries and

5. Functional activities of tissues

COMPOSITION OF LYMPHUsually, lymph is a clear and colourless fluid. Lymph contains 96%water and 4% solids. Some blood cells are also present in lymph.

SOLID SUBSTANCES OF LYMPH

1. Proteins: Proteins form 2 to 6% of solids in lymph. The proteins in lymph are albumin, globulin,fibrinogen, prothrombin, clotting factors, the antibodies and enzymes.

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2. Lipids: Lipids, which form 5 to 15% of solids, are present in the form of chylomicrons and

lipoproteins.

3. Carbohydrates: The carbohydrate present in lymph is mostly glucose. The glucose content in

lymph is about 120 mg%.

4. Amino acids: Almost all the amino acids present in plasma are present in lymph also.5. Nonprotein nitrogenous substances: Urea, and creatinine are the nonprotein nitrogenous

substances present in lymph.

6. Electrolytes: Sodium, calcium and potassium are present in low quantities in lymph than in

plasma, whereas, chlorides and bicarbonates are mo lymph than in plasma.

CELLULAR CONTENT OF LYMPHLymph contains mostly lymphocytes. The normal lymphocyte count in lymph is about 1,000 to 2,000

per cu mm. Monocytes, macrophages and plasma cells are present in lymph occasionally.FUNCTIONS OF LYMPH

1. The important function of lymph is to return the proteins from tissue spaces into

blood.

2. Lymph flow plays an important role in redistribution of fluid in the body.

3. Through the lymph, the bacteria, toxins and other foreign bodies are removed from

tissues.

4. Lymph flow is responsible for the maintenance structural and functional integrity of

tissue. Obstruction to lymph flow affects various tissues particularly myocardium,

nephrons and hepatic cells.

5. Lymph flow serves as an important route for intestinal fat absorption. This is the

reason for the milky appearance of lymph after fatty meal.

6. It also plays an important role in immunity transporting lymphocytes.

FUNCTIONS OF THE LYMPH NODESare:1. When lymph passes through the lymph nodes filtered, i.e. the water and electrolytes are removed.

But, the proteins and lipids are retained in the lymph.

2. The bacteria and other toxic substances are destroyed by macrophages of lymph nodes. Because of

lymph nodes are called defense barriers.

During infectionin a particular region of the body, the lymph nodes draining that regionbecome swollen due to excessive activities inside. Sometimes, the swollen Iymph nodes

cause pain.

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V. Regulation of (blood) circulation. Arterial blood pressure and arterial pulseVessels tone is a state of long- supported excitation of smooth muscles of vessels,

which is not accompanied by development of fatigue.

Basal tone is a continuous stress (tension) of smooth muscular system, which arises

because there are many pacemaker cells (cells of automatism) inside that muscular

system.

Regulable tone is a sum of following influences to the vessels:

a) Stretching response of smooth muscles ( )

b) Reaction for vasoactive substances (which are formed in vessels)

c) Reaction for humoral factors of blood

d) Reaction of smooth muscles for nerve influence

Influence of blood volume to the vessels toneThe blood volume can influence to the vessels tone:

1. Slowly increasing blood volume causes gradual dilation of vesselsbecause of plasticity of smooth muscular system.

2. Fast increasing blood volume causes vasoconstriction and increase of pressure.

Modulating function of vessel wall1. Reaction of vessel wall to the level of oxygen in blood

Deficiency of oxygen leads to vasodilatation, but abundance of oxygen during long time

leads to constriction of vessels (spasm).

2. Modulating influence of vessel endothelium: cells of endothelium produces of

vasoactive factors, from which are:

a) Prostacyclinand Prostaglandinsare vasodilatorsb) Thromboxaneis a vasoconstrictor

Humoral regulation of vessels toneVasoconstrictors:

1. Adrenaline (it influence can be both the vasoconstrictor and the vasodilator ). Inphysiological concentration it influence to adrenoreceptors and produces vasodilatation.

In increased concentration it stimulates adrenoreceptors and produces vasoconstriction.Therefore reaction depends on predomination of or adrenoreceptors in vessel. For ex.,

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adrenoreceptors predominate in skin vessels, but adrenoreceptors in heart and

kidneys.

2. Noradrenalinhas the affinity to adrenoreceptors (therefore vasoconstrictive action)3. Angiotensin IIcauses vasoconstriction of arterioles4. Vasopressin (antidiuretic hormone; ADH)is a potent vasoconstrictor 5. Serotonincauses arteriolar vasoconstriction and is released in response to blood vesseldamage to help prevent blood loss. Serotoninhas been implicated in the vascular spasmsof migraine headaches.

Vasodilators:

1. Acetylcholinethrough M-cholinoreceptors acts as vasodilator (especially in skeletalmuscles)

2. Histaminethrough H1-receptors acts as vasoconstrictor, but through H2-receptors actsas vasodilator (relaxes of smooth muscles of vessels). Histamine causes arteriolarvasodilation and venous vasoconstriction.Histamine is released in response to tissuetrauma.

3. Prostaglandins are the vasodilatators because they increase of membrane`spermeability for potassium ions (that leads to hyperpolariza-tion of muscle cell)

4. Metabolites,lake as lactate, adenosine, carbon dioxide, pyruvic acid, kininsare thevasodilatators.

5. Bradykinin-causes arteriolar vasodilation and venous vasoconstriction.Bradykinin produces, like histamine, increased filtration out of capillaries, and causeslocal edema.

Nervous regulation of vessels toneIncre

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