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МІНІСТЕРСТВО ОХОРОНИ ЗДОРОВ'Я УКРАЇНИ ВИЩИЙ ДЕРЖАВНИЙ НАВЧАЛЬНИЙ ЗАКЛАД УКРАЇНИ

“УКРАЇНСЬКА МЕДИЧНА СТОМАТОЛОГІЧНА АКАДЕМІЯ”

КАФЕДРА ФІЗІОЛОГІЇ

ЗАПОРОЖЕЦЬ Т.М., ТКАЧЕНКО О.В.

ФІЗІОЛОГІЯ

НАВЧАЛЬНИЙ ПОСІБНИК ДЛЯ СТУДЕНТІВ

МЕДИЧНОГО ТА СТОМАТОЛОГІЧНОГО ФАКУЛЬТЕТІВ

ЧАСТИНА 3. ФІЗІОЛОГІЯ ВІСЦЕРАЛЬНИХ СИСТЕМ:

«ФІЗІОЛОГІЯ СЕРЦЕВО-СУДИННОЇ

ТА ДИХАЛЬНОЇ СИСТЕМ»

ПОЛТАВА 2009

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Approved by the Central methodical commission the protocol N.4 from 19.02.2009

It has been composed by Zaporozhets T.N., d.med.sci., prof., Tkachenko E.V.,

cand.med.sci., assistant Reviewers: The doctor of medical sciences, professor Kostenko V.A., the head of

pathological physiology department of higher state educational institution of Ukraine “Ukrainian Medical Stomatological Academy”, Poltava.

Cand.Phil.Sci Znamenskaya I.V., the higher lecturer of foreign languages department of higher state educational institution of Ukraine “Ukrainian Medical Stomatological Academy”, Poltava.

The manual contains theoretical material and material for practical classes, questions for students' self-preparing as well as tests and tasks (with answers) for training to Krok-1. It is illustrated by figures and tables.

Затверджено Центральною методичною комісією Протокол № 4 від 19.02.2009 р.

Склали: Запорожець Т.М., д.мед.н., професор. Ткаченко О.В., к.мед.н.,

асистент Рецензенти: Доктор медичних наук, професор Костенко В.О., завідувач кафедри

патологічної фізіології Вищого державного навчального закладу України “Українська медична стоматологічна академія”, м.Полтава

Кандидат філологічних наук Знаменська І.В., старший викладач кафедри іноземних мов Вищого державного навчального закладу України “Українська медична стоматологічна академія”, м.Полтава

Посібник містить теоретичний матеріал та практичні завдання, питання до самопідготовки студентів, а також навчальні тести та задачі (із відповідями) для підготовки до ліцензійного іспиту з “Крок-1”. Посібник вдало ілюстрований тематичними малюнками і таблицями.

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CONTENT

CONTENT MODULE 12: “BLOOD CIRCULATION SYSTEM” .................................. 4 LESSON 41 ................................................................................................................ 4 HEART MUSCLE PHYSIOLOGICAL PECULIARITIES INVESTIGATION ................ 4 LESSON 42 .............................................................................................................. 16 HEART EXCITEMENT DYNAMICS INVESTIGATION. ECG REGISTRATION ...... 16 LESSON 43 .............................................................................................................. 29 HEART EXCITEMENT DYNAMICS INVESTIGATION. ECG ANALYSIS ................ 29 LESSON 44 .............................................................................................................. 34 HEART PHYSIOLOGICAL PECULIARITIES DETERMINING ON ECG .................. 34 LESSON 45 .............................................................................................................. 39 HEART PUMP FUNCTION AND HEART TONES INVESTIGATION. PHONOCARDIOGRAPHY (PhCG) .......................................................................... 39 LESSON 46 .............................................................................................................. 51 ARTERIAL PRESSURE AND PULSE DETERMINING IN HUMANS. SPHYGMOGRAPHY (SPhG) ................................................................................... 51 LESSON 47 .............................................................................................................. 59 VESSELS ROLE IN BLOOD CIRCULATION. HAEMODYNAMICS LAWS. RHEOENCEPHALOGRAPHY .................................................................................. 59 LESSON 48 .............................................................................................................. 81 HEART ACTIVITY AND BLOOD CIRCULATION REGULATION INVESTIGATION ...................................................................................................... 81 LESSON 49 .............................................................................................................. 93 SITUATIONAL TASKS ON CREDIT MODULE:”BLOOD CIRCULATION SYSTEM” .................................................................................................................. 93 LESSON 50 .............................................................................................................. 93 PRACTICAL EXPERIENCES MANAGEMENT ON CONTENT MODULE 12 “CIRCULATION SYSTEM PHYSIOLOGY” .............................................................. 93 CONTENT MODULE 13: “RESPIRATION SYSTEM” .............................................. 93 LESSON 51 .............................................................................................................. 93 EXTERNAL RESPIRATION INVESTIGATION ........................................................ 93 LESSON 52 ............................................................................................................ 102 LUNG VENTILATION. GAS EXCHANGE. GASES TRANSPORT WITH BLOOD ................................................................................................................... 102 LESSON 53 ............................................................................................................ 108 RESPIRATION REGULATION ............................................................................... 108 LESSON 54 ............................................................................................................ 115 SITUATIONAL TASKS AND PRACTICAL EXPERIENCE ON CONTENT CREDIT 13: “RESPIRATION SYSTEM” ................................................................. 115 TESTS ON HEART-VASCULAR AND RESPIRATION SYSTEMS PHYSIOLOGY ........................................................................................................ 115 GLOSSARY ............................................................................................................ 119

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CONTENT MODULE 12: “BLOOD CIRCULATION SYSTEM” LESSON 41

HEART MUSCLE PHYSIOLOGICAL PECULIARITIES INVESTIGATION 1. The topic studied actuality: Organism requirements to blood circulation system

vary greatly. That is why heart activity must be changed in big ranges. So, human heart minute volume (blood amount pumping with ventricle for 1 min) comprises 5 l under resting conditions while 30 l at hard physical trainings. Heart optimal adaptation is possible only in the case when all its functions (excitement distribution, contraction, valves activity, coronary circulation et al.) are changed in significant correspondence one to another. The least inclinations from norm can lead to heart activity serious disorders.

Valves activity disturbances are so widely spread in babies and can be lethal very often. They can be opened uncompletely (stenosis) or be closed uncompletely (insufficiency). It hardens heart activity significantly. The results are as following as: heart cavities must develop increased pressures or pump more blood. Then their volume becomes bigger and it leads, in turn, to their hypertrophy or dilation. Valves vices can be compensated for many years due to these adaptive mechanisms. One can tell about two types of such adaptive changes. If one can see only loading with pressure than first heart hypertrophy is not accompanied by its cavities significant widening (left ventricle hypertrophy at aortal stenosis can be as an example). But if heart has to perform additional work for increased volume pumping than cavities widening is observed together with hypertrophy (for example, left ventricle hypertrophy and dilation at aortal valve insufficiency). Myocardium adaptive structural changes directed to these vices compensation are limited. While cardiac fibers radius increasing also diffusion distance between these fibers cytoplasm and capillaries grow. It is dangerous with heart oxygenation disorder. If hard pathology is present during some time, than heart insufficiency can appear.

2. Study aims: To know: circulation system structure and functions, heart muscle physiological

peculiarities providing heart functions. To be able to: establish whether normal are cardiac muscle physiological

features determining frequency, rhythm, velocity and force of heart contraction; to draw schematically heart conductive system.

3.Pre-auditory self-work materials. 3.1.Basic knowledge, skills, experiences, necessary for study the topic:

Subject To know To be able to Anatomy Heart morphology Show main heart elements on

special tables or alive preparations

Histology, cytology and embryology

Heart histological peculiarities: layers (epicardium, myocardium, endocardium), valves, main cells; heart embryogenesis

Draw heart conductive system and designate its main elements with telling about their histological structures to recognize heart histological preparations

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Pathological anatomy

Patho-morphological changings at heart diseases

Recognize special macropreparations

Pathophysiology Main pathophysiological mechanisms lying on the base of heart pathology in part heart insufficiency; adaptive mechanisms (hypertrophy in part) realizing under physiological overloadings and pathological conditions

Pediatry and Neonatology

Myocardium physiological peculiarities in children; myocardium pathology (in part, myocarditis) ethiology, pathogenesis, clinics, therapy and prevention principles

To treat and to prevent named pathological states

Internal Diseases Myocardium physiological peculiarities; myocardium pathology (in part, myocarditis) ethiology, pathogenesis, clinics, therapy and prevention principles


3.2. Topic content

Main heart functions: 1. Generating blood pressure. Heart contractions generate blood pressure, which is responsible for blood movement through blood movement through blood. 2. Routing blood. The heart separates the pulmonary and systemic circulations and ensures better oxygenation of blood flowing to the tissues. 3. Ensuring one-way blood flow. The valves of the heart ensure a one-way flow of blood through the heart and blood vessels. 4. Regulating blood supply. Changes in the rate and force of contraction match blood delivery to the changing metabolic needs of the tissues, such as during rest, exercise, and changes in body position.

HEART MUSCLE BIOPHYSIC FEATURES. CONDUCTIVITY, CONTRACTIVITY, AUTOMATISM, EXCITABILITY

Main cardiac muscle peculiarities: · automatism; · excitability; · conductance; · contractility.

Automatism – is ability to self-excitation under impulses occurring in myocardium itself. Its nature is not yet clear but there are some data about its connection with cells-pacemakers activity located in heart nodes. Systolic node is the first order pacemaker. Sinus node biopotentials distinguishing features: repolarization phase doesn’t result in membrane potential restoration but transforms into secondary (diastolic) depolarization which after threshold potential

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reaching causes new action potential occurrence. Automatism is possessed by all heart conductive system elements (atrio-ventricular node, Purkin’e fibers). It is decreased with impulse passage from heart base to its apex (from heart venous end to its arterial end). This regularity is known as Gaskell’s law (rule, gradient).

Excitability also has its peculiarities in cardiac muscle. Myocardium is contracted with maximal force to threshold stimuli i.e. heart contraction force doesn’t depend on irritation force (law “everything or nothing”). One can differentiate contractive (working, typical) myocardiocytes and conductive (atypical). Contractive myocardium possesses excitability but doesn’t possess automatism. During diastole resting potential of these cells is stable and its level is higher than in pacemakers (80-90 mV). Action potential in these cells occurs under pace-makers excitement. It reaches cardiomyocytes and causes depolarization of their membranes.

Working myocardium action potential consists of following phases: · fast depolarization; · initial fast repolarization; · slow repolarization (plateau phase); · fast ending repolarization. Important myocardium activity peculiarity is the following: cardiomyocytes action

potential duration is about 300-400 msec that corresponds to myocardium contraction duration.

ELECTRICAL POTENTIALS IN CARDIAC MUSCLE Resting Membrane Potential in individual cardiac muscle fiber, the resting membrane potential is about -85 to -

95 mV. In SA node it is -55 mV. In Purkinje fibers, it is about -90 to -100 mV. Action Potential The electrical activity that takes place in the cardiac muscle is known as action

potential. Action potential in a single cardiac muscle fiber occurs in 4 phases (Fig.14 ).

1. A rapid depolarization 2. Initial repolarization 3. A plateau 4. Final repolarization The approximate duration of the action potential in cardiac muscle is 250 to 350

m sec (0.25 to 0.35 sec). 1. Depolarization The depolarization is very rapid and this lasts for about 2 m seconds. The

amplitude of the depolarization reaches + 20mV. 2. Initial Repolarization Immediately after depolarization, there is an initial rapid repolarization for a short

period and it is represented by a notch. 3. Plateau Afterwards, the muscle fiber remains in the depolarized state for sometime

before further repolarization. This forms the plateau in the action potential curve. The plateau lasts for about 0.2 sec in atrial muscle fibers and for about 0.3 sec in ventricular muscle fibers. Due to this long plateau in action potential, the contraction time is longer in cardiac muscle by about 5 to 15 times than in skeletal muscle.

4. Final Repolarization

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The repolarization occurs after the plateau. It is a slow process and it lasts for about 0.05 to 0.08 sec before the reestablishment of resting membrane potential.

FIGURE: 14 Action potential in ventricular muscle. 1 = Depolarization, 2 = Initial

rapid repolarization, 3 = Plateau, 4 = Final repolarization

IONIC BASIS OF ACTION POTENTIAL 1. Depolarization In cardiac muscle fiber, depolarization occurs in two phases. a) First phase is an abrupt upward deflection, which represents rapid

depolarization and b) Second phase occurs after initial repolarization. lt is a period of prolonged depolarization, which appears as a plateau in the graph. It represents the continuation of depolarization for many milliseconds (refer below). The rapid depolarization (first phase) is because of rapid opening of fast sodium channels and the rapid influx of sodium ions as in the case of skeletal muscle fiber.

2. Initial Repolarization The initial rapid repolarization just before plateau is due to the transient opening

of potassium channels and efflux of a small quantity of potassium ions from the muscle fiber. Simultaneously, the fast sodium channels close suddenly and slow sodium channels open causing slow influx of a low quantity of sodium ions.

3. Plateau During the plateau (second phase of depolarization), the slow calcium channels

open. These channels are kept opened for a longer period causing influx of large number of calcium ions. Already the slow sodium channels are opened through which the slow influx of sodium ions continues. The entry of both calcium and sodium ions into the muscle fiber greatly balances the potassium efflux. Thus, the positivity is maintained inside the muscle cell causing prolonged depolarization, i.e. plateau. The calcium ions entering the muscle fiber play an important role in the contractile process.

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4. Final Repolarization Final repolarization starts at the end of plateau. Now, the efflux of potassium ions

increases resulting in movement of large number of potassium ions out of the muscle fiber. This exceeds the number of calcium ions moving in. This is the cause for final repolarization. The efflux of potassium ions continues until the end of repolarization.

Restoration of Resting Membrane Potential At the end of final repolarization, all the sodium ions, which entered the cell

throughout the process of action potential move out of the cell by the activation of sodium-potassium pump. Three sodium ions move out for every two potassium ions moving in. Simultaneously, the excess of calcium ions, which entered the muscle fiber also move out through sodium-calcium pump. Thus, the resting membrane potential is restored.

There is correlation between cardiac muscle excitement and contraction. Myocardial contraction trigger is action potential like in skeletal muscle. Depolarization phase coincides absolute refractiveness phase. But as absolute refractiveness is very long in cardiac muscle (up to 0,3 sec) than cardiac muscle excitability is absent in course of all contraction (shortening) period. That’s why cardiac muscle doesn’t give smooth tetanus. Relaxation period corresponds to fast repolarization period and relative refractiveness period. That’s why it also doesn’t give infused tetanus. During relative refractiveness phase superliminal stimuli can cause myocardium excitement and its contraction out of turn – extrasystole – appears as answer reaction.

PACEMAKER POTENTIAL - ELECTRICAL POTENTIAL IN SA NODE

The electrical potential in SA node is different from that of other cardiac muscle fibers. In the SA node each impulse triggers the next impulse. This is mainly due to the unstable resting membrane potential.

The resting membrane potential in SA node has a negativity of only -55 to -60 mV. This is different from the negativity of-85 to -95 mV in other cardiac muscle fibers.

The depolarization starts very slowly and the threshold level of—40 mV is reached very slowly. After the threshold level, rapid depolarization occurs up to +5 mV. This is followed by rapid repolarization. Once again, the resting membrane potential becomes unstable and reaches the threshold level slowly. This type of resting membrane potential is called prepotential or pacemaker potential.

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Figure: 15. Pace-maker potential.

Ionic Basis of Electrical Activity in Pacemaker

The resting membrane potential is not stable in the SA node. To start with, the sodium ions leak into the pacemaker fibers and cause slow depolarization. This slow depolarization forms the initial part of pacemaker potential. Then, the calcium channels start opening. At the beginning, there is a slow influx of calcium ions causing further depolarization in the same slower rate. This forms the later part of the pacemaker potential. Thus, the initial part of pacemaker potential is due to slow influx of sodium ions and the later part is due to the slow influx of calcium ions.

When the negativity is reduced to —40 mV, which is the threshold level, the action potential starts with rapid depolarization. The depolarization is because of influx of more calcium ions. Unlike in other tissues, the depolarization in SA node is mainly due to the influx of calcium ions rather than sodium ions.

After the rapid depolarization, the repolarization occurs. Repolarization is due to the efflux of potassium ions from the pacemaker fibers. The potassium channels remain open for a longer time, causing efflux of more potassium ions. This leads to the development of more negativity beyond the level of resting membrane potential. This exists only for a short while. Then, the slow depolarization starts again, leading to the development of pacemaker potential which triggers the next action potential.

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Contractiveness peculiarity is also cardiac muscle subjugation Frank-Starling’s law: the more heart is stretched in course of diastole, the stronger its contraction is in course of systole. Besides, as it was explained above, the second law of heart muscle activity is law “everything or nothing”.

Various factors affect the contractile properties of the cardiac muscle. The different contractile properties are as follows.

ALL OR NONE LAW If a stimulus is applied, whatever may be the strength, the muscle responds to

the maximum or it does not give response at all. This is called all or none law. Below the threshold level, i.e. if the strength of stimulus is not adequate, the muscle does not give response.

This can be demonstrated in the quiescent (quiet, not beating) heart of frog. To make the heart quiescent, the first Stannius ligature is applied between the sinus venosus and right auricle. First, one stimulus is applied with a minimum strength of 1 volt at the base of ventricle and the contraction is recorded. Then, the strength of stimulus is increased to 2 volts and the stimulus is applied after 20 seconds. The curve is recorded. The procedure is repeated by increasing the strength every time and applying the stimulus with an interval of 20 seconds (Fig. 15).

The amplitude of all the contractions remains the same irrespective of increasing the strength of stimulus. This shows that cardiac muscle obeys all or none law.

All or none law is applicable to whole of cardiac muscle. This is because of syncitial arrangement of cardiac muscle. In the case of skeletal muscle, it is applicable only to a single muscle fiber.

STAIRCASE PHENOMENON

The stimuli are applied at the base of ventricle of a quiescent heart of frog at an interval of two seconds without changing the strength. For the first few contractions, the force is gradually increased and then the force of contraction remains same.

The staircase phenomenon occurs because of time interval of two seconds in between the stimuli. During this period, the beneficial effect is produced which may facilitate the force of successive contraction. So, there is a gradual rise in force of contraction

FIGURE: 16. All or none law and staircase phenomenon in cardiac muscle

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SUMMATION OF SUBLIMINAL STIMULI When a stimulus with a subliminal strength is applied the quiescent heart does

not show any response. When few stimuli with same subliminal strength are applied in succession, the heart shows response by contraction. This is due to the summation of the stimuli.

REFRACTORY PERIOD

This is the period in which the muscle does not show any response to a stimulus. Refractory period is of two types.

1. Absolute refractory period. 2. Relative refractory period. Absolute Refractory Period. Absolute refractory period is the period during which the muscle does not show

any response at all, whatever may be the strength of the stimulus. Relative Refractory Period The relative refractory period is the period during which the muscle shows

response if the strength of stimulus is increased to maximum. Refractory Period in Cardiac Muscle Cardiac muscle has a long refractory period. The absolute refractory period

extends throughout contraction period. It is for 0.27 sec and relative refractory period extends curing first half of relaxation period with a measurement of about 0.26 sec. So, the total refractory period is 0.53 sec.

Demonstration of Refractory Period in Heart Refractory period is demonstrated in the heart of a pithed frog. Refractory period

can be recorded in beating heart as well as the quiescent heart. Refractory Period in Beating Heart First, normal cardiogram is recorded with the heart of a pithed frog. The impulses

for the heartbeat arise from the sinus venosus. An artificial stimulus (electrical stimulus) is applied by keeping the electrode at the base of the ventricle. When the stimulus is applied during systole, the heart does not show any response. This is because the absolute refractory period extends throughout the systole.

When a stimulus is applied during diastole, the heart contracts since, the diastole is the relative refractory period. This type of contraction of the heart is called extra-systole or premature contraction. The extrasystole is followed by the stoppage of the heart for a while. The temporary stoppage of the heart before the heart restores the normal beat is called compensatory pause. The duration of the extrasystole and the compensatory pause is equivalent to the duration of two cardiac cycles.

Cause for Compensatory Pause A natural impulse from the sinus venosus arrives at the time of contraction period

of the extra-systole. As this period is absolute refractory period, this natural impulse cannot cause contraction of the heart, and the heart has to wait for the arrival of next natural impulse from sinus venosus. Till the arrival of the next impulse, the heart stops in relaxation.

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FIGURE: 17. Refractory period in beating heart of frog

Conductance – is cardiac muscle ability to conduct excitement both through

working myocardium fibers and conductive system. Excitement wave conductance velocity through heart different parts:

· muscular contractive atrial fibers – up to 0,8-1,0 m/sec; · in atrio-ventricular node – 0,02-0,05 m/sec; · in His’s fascicle – 1,0-1,5 m/sec; · in Purkinj’e fibres – 3,0-4,0 m/sec.

Slow excitement conductance in atrio-ventricular node is called atrio-ventricular lack. It is equal to 0,04-0,06 sec.

CONDUCTIVE SYSTEM IN HUMAN HEART The conductive system in human heart comprises: 1. AV node 2. Bundle of His 3. Right and left bundle branches 4. Purkinje fibers SA node is situated in right atrium just below the opening of superior vena cava.

AV node is situated in the right posterior portion of intraatrial septum. The impulses from SA node are conducted to AV node by three types of intenodal fibers.

1. Anterior internodal fibers of Bachman 2. Middle internodal fibers of Wenckebach and 3. Posterior internodal fibers of Thorel. All these fibers converge towards the AV node and interdigitate with fibers of AV

node. From AV node, the bundle of His arises and this divides into right and left branches. These branches run on either side of the interventricular septum and give off Purkinje fibers which spread all over the ventricular myocardium.

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FIGURE: 18. Sinoatrial node and conductive system of the heart

4. Materials for auditory self-work. 4.1. List of study practical tasks necessary to perform at the practical class. Materials and methods: kymograph, universal strand, Engelman’s cardiograph

with light two-armed lever, fuze plate, instruments set, cotton wool, Ringer’s physiological solution, thread.

Investigation object: frog.

Task 1. Frog’s heart activity observation and registration Frog must be motionless without decapitating. To dissect carefully

thoracoabdominal cavity, pericardium, to denude heart and to observe his work. To pay the attention to the order of different heart parts contractions.

You can see venous sinus contractions better if heart is raised by its apex and its dorsal surface is observed. Venous sinus is separated from atriums by white stripes.

To count heart beating frequency for 1 min, then to register electrocardiogram. To gain this it’s necessary to catch heart apex by serfin.

Using received heart beating frequency for 1 min they count the frog’s heart cycle duration.

Task 2. To draw in increased habitus the scheme of 2-3 cardiac contractions and mark on it:

1. Atriums systole. 2. Atriums diastole. 3. Ventricles systole. 4. Ventricles diastole. 5. Total heart pause.

Task 3. Stannius experiment (frog’s heart different regions automatism degree study)

Having caught heart apex by serfin, to register cardiac contractions. To count their amount for 1 min.

To put the first (isolating) ligature between venous sinus and atrium. To register heart work having counted cardiac contractions number for 1 min. To stretch the

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thread under aortas and to put the second ligature (irritating) on the border between atriums and ventricle. To register heart work having counted cardiac contractions number for 1 min. To put third ligature to lower ventricle third and to mark heart apex state. Then it’s necessary to cut heart apex and to put it on the subject table with Ringer’s solution drop. To irritate heart apex with needle puncture and to note it’s reaction.

To draw the experiment scheme in copy-books, making the conclusion about pacemakers.

Pacemaker in Amphibian Heart Sinus venosus is the pacemaker in amphibian heart. This can be proved

experimentally by applying Stannius ligatures, and by other methods. Stannius Ligature Experiment This is an experiment in a pithed frog demonstrated by a German biologist

Stannius; ligature means tying. (Pithing is a process in which the brain and spinal cord are severed by using a needle to restrict the movements of the frog during the experiment. The pithed frog is technically dead. But some of its organs continue to function for some time).

Heart of the pithed frog is exposed and the tip of the ventricle is pinned and connected to a recording device by means of a thread. After recording the normal heartbeats (normal cardiogram or sinus rhythm), a ligature is applied between the sinus venosus and right auricle. This is called first Stannius ligature. When the ligature is applied, the heart stops beating immediately. This is because, the impulses produced by sinus venosus cannot be conducted to the other chambers of the heart. However, the sinus contractions are continued. After some time, the auricular muscle becomes the pacemaker and starts producing the impulses for heartbeat but at a slower rate. During this, the auricles contract first followed by ventricular contraction. This rhythm of the heart is called auriculoventricular rhythm.

When a second ligature is applied between auricles and ventricle, the heart stops beating again, because the impulses from auricles cannot reach the ventricle. After few minutes, the ventricle starts beating but, at a much slower rate. These contractions are known as the idioventricular rhythm. Thus, all the three parts of the heart—sinus venosus, auricular musculature and ventricular musculature have the property of rhythmicity. However, sinus venosus is the pacemaker because it produces the impulses at a faster rate.

FIGURE:19. Effect of Stannius ligatures on frog's heart

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Task 4. To draw human conducting heart system scheme And to indicate excitement conductance velocity through atriums and ventricles

typical and atypical fibers. Task 5. Refracterity and ventricle extrasystole receiving Frog must be motionless without decapitating. To dissect carefully thoraco-

abdominal cavity, pericardium, to denude heart and to observe his work. To fix heart apex with serfin and to register electrocardiogram. One of irritating electrodes is attaching to the serfin. The second electrode must be located on heart base. They have to select such a voltage that the frog’s heart reacts but the animal doesn’t shudder. Short-termed irritation must be realized during ventricles systole. To repeat it some time.

Then to irritate the ventricles in course of diastole. After 3-4 normal contractions one should repeat the irritation. Mark the extrasystole and compensatory pause. Draw the scheme in your copy-book.

Task 6. To compare myocardium answer to the irritation force increasing To put the first ligature by Stannius (see above). The registration must be done

on stopped drum (it’s necessary to turn it by hand). The heart contraction is registered as vertical line. To mark irritation threshold. To register cardiac muscle answer to the increasing stimulus force (one should use constant current). The investigator must use 4-6 stimuli including threshold level.

To analyze the character of cardiac muscle answer according to the irritation force. It’s very important to use equal time spaces between irritations (approximately 30 sec).

Task 7. To draw the curve of cardiac muscle excitability change in course of single excitement cycle

One should indicate on the figure: 1) myocardium length change; 2) membrane potential change; 3) cardiac muscle excaltation change.

5. Literature recommended: 1. Lecture course. 2. Mistchenko V.P., Tkachenko E.V. Methodical instructions for dental students (short lecture course).-Poltava, 2005.-P.28-30, 7-11. 3. Mistchenko V.P., Tkachenko E.V. Methodical instructions for medical students (short lecture course).-Polatava, 2005.-P.55-56. 4. Methodical instructions on chapter “Cardiac-vascular system physiology” on practical classes for dental and medical students. 5. Concise Physiology /Guyton-Ganong-Chatterjee. Ed. By Dr Gull R.Sh.-Lahore: K.E.Medical College.-1998.-P.19-51, 94-97. 6. Kapit W., Macey R.I., Meisami E. The Physiology Colouring Book: Harpers Collins Publishers, 1987.-P.26-27, 29, 31. 7. Bullock J., Boyle III J., Wang M.B. Physiology.-1991.-P.99-106, 118-124, 127-130. 8. Stuart Ira Fox. Human Physiology.-8-th Ed.-Mc Graw Hill, 2004.-P. 378-383. 9. Seeley R.R., Stephens T.D., Tate P. Essentials of Anatomy and Physiology.-The 3rd Ed.-McGraw Hill, 1999.-P.306, 314-317.

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6. Materials for self-control: Control questions:

1. What fibers in myocardium do you know? 2. What subcellular structures do cardiac muscular fibers consist of? 3. Tell about cardiomyocytes contraction mechanism. 4. What are differences between skeletal, smooth and cardiac muscles? 5. What is heart cycle? Call its duration and main phases. 6. What do you know about membrane resting and action potential ion bases in

myocardium? 7. What’s the nature of repolarization phase? 8. Myocardiocytes action potential phases. 9. Cardiac automatism, its biological role. 10. Diastolic depolarization and threshold potential significance in heart automatism

supporting. 11. Cardiac conduction system main elements. What peculiarities of excitement

transmittance in atriums and ventricles do you know? 12. What are the main peculiarities of excitement transmittance through atrial-

ventricular node? 13. Relative and absolute heart refractiveness. 14. What is the refracterity period significance for heart activity? 15. Extrasystole and compensatory pause as they are. 16. Cardiac muscle contraction laws. 17. Law “everything or nothing” limitation for cardiac muscle. 18. Primary myocardium fibres length influence on contraction force. 19. Physical-chemical processes in myocardium in course of its contraction and

relaxing.

LESSON 42 HEART EXCITEMENT DYNAMICS INVESTIGATION. ECG REGISTRATION

(DEMONSTRATION IN LABORATORY) 1. The topic studied actuality. ECG formation mechanisms knowledge as well as

ability to perform this curve analysis is essential because it allows determine what is pacemaker, to assess sequence, velocity of excitement distribution in heart, excitement impulses rhythmicity and generation rate with pace-maker.

2. Study aim. To know: ECG electrophysiological bases, electrocardiographic leads, normal

ECG characteristics, its interpretating vector theory. To be able to: find main elements on ECG. 3.Pre-auditory self-work materials. 3.1.Basic knowledge, skills, experiences, necessary for study the topic:

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Patho-morphological changings at heart diseases


Pathophysiology Representation about normal ECG, its analysis; arrhythmias pathophysiological bases

To interpretate ECG with arrhythmias different types


Myocardium physiological peculiarities in children; arrhythmias ethiology, pathogenesis, clinics, therapy and prevention principles

To interpretate ECG in children under physiological and pathological conditions; to treat and to prevent named pathological states

Internal Diseases Myocardium physiological peculiarities in different-aged adults; arrhythmias ethiology, pathogenesis, clinics, therapy and prevention principles

To interpretate ECG in the adult under physiological and pathological conditions; to treat and to prevent named pathological states

3.2. Topic content

EXCITEMENT WAVE DISTRIBUTION THROUGH HEART Through atria

Under normal conditions excitement wave generated in sino-atrial node cells is generated through short conductive tract to right atrium, through 3 interventricular tracts -of Bahman, Torel and Venkebach - to atrio-ventricular node and through interventricular Bahman’s bundle – to left atrium. One must remember that sino-atrial (sinus) node is pace-maker of the first order or potential pace-maker. It means that other pacemakers of 2nd, 3rd, 4th orders (atrio-ventricular node, His’ bundle with his arms and Purkinj’e fibers correspondingly) are the latent ones and they don’t determine contraction rhythm. They are also called as ectopic ones. These latent pace-makers can be as pace-makers of the 1st order only at different blockades.

Remember! Total direction of heart excitement through atria is the following: from up to down

and a bit on the left from sino-atrial node to atrio-ventricular node superior part. Right atrium is in excitement process first (because of sinus node location), then

left atrium is added and finally only left atrium is excited. Heart excitement total time through atria is not more than 0,1 sec.

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Figure 20 . Excitement distribution through atria contractile myocardium

a – right atrium initial excitement; b – right and left atria excitement; c – left atrium ending excitement.

Black color is used for excited (hatched) locuses designation the ones that are under excitement at the moment (continuous locuses). PI, PII, PIII mean atria depolarization moment vectors.

Through ventricles Remember!

1. There exist so-called atrio-ventricular lack. As it is known, atria are contracted consequently while ventricles are contracted simultaneously. So, this lack time is essential for all blood passage to ventricles and ventricles effective, powerful and adequate contraction.

2. At heart impulses acceleration more than 180-200 beating per 1 min even healthy person can have partial (atrio-ventricular) blockade of impulses distribution from atria to ventricles.

3. Heart excitement total time through ventricles is 0,08-1,0 sec. 4. Depolarization wave direction in ventricular wall is from endocardium to

epicardium. 5. Normal sequence of ventricles excitement events: · interventricular septum; · dominant part of right and left ventricles (ventricular apex, posterior and

lateral walls). Ventricles basal or posterior-inferior parts are excited the latest.

Figure 21. Excitement distribution through ventricles contractile myocardium a – interventricular septum excitement (depolarization ) - 0,02 sec; b – depolarization of apexes, ventricles anterior, posterior and lateral walls (0,04-

0,05 sec); c – depolarization in left and ventricles basal parts as well as in interventricular

septum (0,06-0,08 sec). Color designations – see the previous figure.

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DEPOLARIZATION AND REPOLARIZATION WAVE DIPOLE FEATURES AT SINGLE MUSCULAR FIBER SURFACE.

REPRESENTATION ABOUT VECTOR. Electrical phenomena occurring at excitive environment surface (heart fiber) are

described by means of so-called excitement distribution dipole conception. De- and repolarization process through single muscular fiber is double charges layer transfer. These charges are located on the boarder between excited (-) and non-excited (+) fiber locuses. These charges equal by level and opposite by charge are located on very little distance one from another and are designated as elementary cardiac dipoles. Dipole positive pole (+) is always directed to non-excited while negative pole (-) – to excited locus of myocardial fiber. Dipole creates elementary electro-moving force (EMF).

Elementary electro-moving force (EMF) is a vector numeral characterized not only by potential qualitative meaning but also by direction – space orientation from (-) to (+).

Thus, vector of any dipole is directed from its negative pole to its positive one. Remember!

1. If dipole vector is directed to positive lead electrode than positive electrogram dense or inclination up from isoline will be registered. 2. If dipole vector is directed to negative lead electrode than negative electrogram dense or inclination down from isoline will be registered. 3. If dipole vector is located perpendicularly to the lead axe than isoline is registered on ECG. It means that both positive and negative inclinations are absent on ECG. Summary moment heart vector determined as algebraic sum of all vectors which

are their compounds at one or other moment of excitement distribution through the heart.

Middle resulting vector is a sum of all separate moment vectors. It reflects middle direction and EMF direction during all ventricles depolarization period.

Thus, heart is considered to be one point current source (origin) – whole cardiac dipole.

Figure 22. Different variants of summary resulting vector (electrical moving force

EMF) formation.

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VECTORAL ANALYSIS; The mean QRS vector (cardiac axis) in normal conditions is at about + 59°. It

varies between - 30° and + 110°. When the axis deviates towards the left, i.e. in anti clockwise direction, away

from - 30° it is called left axis deviation. When the axis deviates towards the right (clockwise direction), away from + 110°, it is known as right axis deviation.

The left axis deviation occurs in left ventricular hypertrophy and left bundle branch block. The right axis deviation occurs due to right ventricular hypertrophy and right bundle branch block.

EKG REGISTRATION

EKG leads systems Potentials difference changings at body surface occurring during heart activity

are recorded by means of ECG different leads systems. Each lead registers potentials difference existing between heart electrical field two definite points where electrodes are located. Thus, different electrocardiographic leads are different one from another first of all by body parts from which potentials difference is registered.

Electrodes putted in every one from chosen points at body surface are switched to electrocardiograph galvanometer. One electrode is linked with galvanometer positive pole (it is lead positive or active electrode), second electrode – to its negative pole (lead negative or non-active electrode).

Nowadays 12 leads are obligatory in clinical practice: 1) 3 standard; 2) 3 augmented (or enforced) one-poled leads from extremities; 3) 6 thoracic leads.

Standard leads

Standard two-poled leads proposed by Einthoven in 1913 fixate potentials difference between electrical field two points located far from heart and situated in frontal plane – on extremities.

Electrodes marking: - red – right arm; - yellow – left arm; - green – left leg; - black – right leg -landing electrode.

Remember! Standard leads from extremities are registered at following switching

electrodes by pairs: 1) Ist lead – left arm (+) and right arm (-); 2) IInd lead – left arm (+) and right arm (-); 3) IIIrd lead – left leg (+) and left arm (-).

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Figure 23. Position of electrodes for standard limb leads

RA = Right arm. LA = Left arm. LL=Left leg

Figure 24. Standard leads from extremities formation.

Below – Einthoven’s triangle every side of which is the axe of one or other standard lead.

CALCULATION OF MEAN QRS VECTOR The amplitude of QRS complex is determined from ECG recorded at 2 of the 3

standard limb leads. The amplitude of QRS complex in the remaining lead will be known from the calculation.

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The amplitude is measured in mm. For determining the amplitude of QRS complex, first the height of R wave is measured. From this the height of the negative wave Q or S (whichever is more) is deducted.

An equilateral triangle is drawn. This equilateral triangle represents Einthoven's triangle. The heart is said to lie in the center of Einthoven's triangle. The electrical potential generated from the heart appears simultaneously on the roots of the three limbs namely the left arm, right arm and the left leg. Each side of this triangle represents one standard limb lead. From the midpoint of each side. a perpendicular line is drawn towards the center. The meeting point of the perpendicular lines represents the center of electrical activity in the heart.

On each side of the triangle, the amplitude of QRS complex is plotted from mid point towards the positive point of the lead. For example, the amplitude of QRS complex in lead I is 10 mm and in lead II, it is 16 mm.

In the triangle, upper side represents lead I and in lead I, the left is positive. So, a 10 mm line is drawn on upper side from the midpoint towards left (positive). This 10 mm distance along the axis of lead I is called the projected vector for lead I (Fig. 24). In the same way, the projected vector for Lead II is drawn on the right side of the triangle.

From the positive end of each projected vector another perpendicular line is drawn towards the interior of the triangle. Now an arrow is drawn between the center of potential in lead III is 6 mV. This also can be measured from the triangle drawn to calculate the vector.

Enforced (augmented) leads from extremities Augmented leads from extremities were proposed by Goldberger in 1942. They

register potentials difference between one extremity with given lead positive electrode on it (right arm, left arm or left leg) and two other extremities middle potential. Thus, negative electrode in these leads is so-called united electrode of Goldberger. This electrode is formed while connection through two other extremities additional resistance.

Remember!

Three augmented one-poled leads from extremities are designated so: *aVR – augmented voltage right – enforced lead from right arm; *avL – augmented voltage left – enforced lead from left arm; *aVF – augmented voltage foot – enforced lead from left leg.

Thoracic leads

They were proposed by Wilson in 1934. These one-poled leads register potentials difference between active positive electrode putted in definite points at thorax surface and negative Wilson’s united electrode. The latest one is formed while three extremities (right arm, left arm and left leg) connection through additional resistances. These extremities united potential is near to zero (it is about 0,2 mV).

V1 is in the fourth intercostal place (ICS) just to the right of the sternum. V2 is in the fourth intercostal place (ICS) just to the left of the sternum.

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Figure 25.

V3 is halfway between V2 and V4. V4 is at midclavicular line (MCL) in the fifth ICS. V5 is in the anterior auxillary line at the same level as V4. V6 is in the midauxillary line at the same level as V4 and V5.

Figure 26. Thoracic leads location at thorax surface.

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Thoracical leads register potentials (heart electro-moving force) changings in horizontal plane comparatively to standard leads and augmented leads from extremities which register them in frontal plane.

FIGURE 27: Degree of instantaneous vector at different leads

ECG registration

It is performed while quiet breathing. First one should make ECG record in standard leads (I, II, III), then in augmented leads from extremities (aVR, aVL and aVF) and thoracical leads. One should record not less than 4 heart cycles QRST in each lead. As a rule, ECG is made while paper movement velocity equal to 50 mm/sec. But one should use 25 mm/sec in teaching ECG and when prolonged record is necessary (for instance, at arhythmias differentiated diagnostics). Modern clinics now in USA or Canada can use devices with speed equal to 100 mm/sec. It is important to take into account because 1 little cage horizontally is equal to 0,04 sec at 25 mm/sec (you will use this data at your lessons, 0,02 – at 50 and 0,01 – at 100.

NORMAL ECG Main elements or waves: · denses – P, QRS, T – inclination up (positive dense) or down (negative

dense) from isoline; · segments – distance from the end of previous dense to the beginning of next

dense lying on isoline – segments PQ, ST, TP; · interval – distance from the beginning of previous dense to the beginning of

next dense lying on isoline or, with other words, it is sum of dense and segment– PQ, RR, QT.

On must determine 2 parameters (duration in seconds horizontally and altitude in millivolts vertically) for dense and only one parameter – duration – for segments and intervals.

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TABLE 11. Waves of normal ECG Elements From - To Cause Duration

( d) Amplitude (mV)

Pwave — Atrial depolarization 0.1 0.1 to 0.12 ORS complex

Ventricular depolarization

0.08 to 0.10 Q = 0.1 to 0.2 R = l S = 0.4

'wave — Ventricular

0.2 0.3 P-R interval Onset of P

wave to onset

Atrial depolarization and conduction

0.18 (0.12 to 0.2)

—

Q-T interval Onset of Q wave and end

Electrical activity in ventricles

0.4 to 0.42 —

ST segment End of S wave and onset of T

— 0.08 —

FIGURE 28: Waves of normal ECG

P dense It reflects right and left atria depolarization process. Right atrium depolarization is

described as P-dense ascendant part; left atrium depolarization – as P-dense descendant part.

Remember! Ø Under physiological conditions P is always positive in I, II, aVF, V2-V6. If it is

negative here, it indicates to retrograde (from ventricles to atria) excitement course.

Ø P-dense can be positive or two-phased in III, aVL and V1 and it can be even negative in III and aVL.

Ø P-dense is always negative in aVR. Ø P-dense duration is not more than 0,1 sec and its altitude – 1,5-2,5 mm. Atrial

hypertrophy causes P-dense altitude increasing.

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Segment P-Q It reflects atrial-ventricular lack or delay. Impulses do not spread neither to atria

nor to ventricles. That is why potentials difference is equal to zero and isoline is recorded. Its duration is fluctuated from 0,06 to 0,1 sec.

Interval P-Q It reflects atrial-ventricular conductance or excitement conductance through

atrial-ventricular node, His’ bundle and its branches. Its duration is from 0,12 to 0,20 sec. Its increasing indicates to atrial-ventricular conductance. It can be shortened at tachycardy.

Q dense It reflects interventricular septum depolarization. It is little by its altitude because

interventricular septum contains muscular fibers little amount. Q-dense is negative because its moment vector is directed oppositely to excitement wave total course. Normal parameters: altitude – 0-0,1 mV (0 – dense absence), duration time is 0,02-0,04 sec.

Remember! · Q-dense under physiological conditions can be recorded in all standard and

augmented one-poled leads as well as in V4-V6. · Q altitude in all leads except aVR is not more than h of R-dense altitude and its

duration is 0,03 sec. · In aVR healthy person can have deep and wide Q or even QRS.

R-dense It reflects left and right ventricles depolarization. It is the biggest ECG dense.

Remember! · Under normal conditions R-dense can be recorded in all standard and

augmented leads from extremities. It is sometimes practically non-expressed or even absent in aVR.

· Its altitude is gradually increased from V1 to V4, and then reduced a little in V5 and V6. Sometimes it can be absent in V1.

· R in V1 and V2 reflects excitement distribution through interventricular septum and in V4-V6 – through left and right ventricles muscle.

· Its altitude in I, II, III is 0,5-2,0 mV, in V1-V6 – 0,8-2,5 mV (up to 3,0 mV). Its duration is from 0,02 to 0,04 sec.

· Its altitude increasing can indicate to ventricles hypertrophy while its configuration (shape) changing (dilated, densed, deformed) – to ventricles myocardium scar changings (after myocardial infarction for instance).

Dense S It is determined by ventricles basal (posterior-inferior) parts depolarization.

Remember! · In a healthy person S - dense altitude in different ECG leads is fluctuated in wide

ranger (limits) being not more than 20 mm. In I-III its altitude (h) is 0-0,1 mV and its duration (t) is 0,02-0,04 sec.

· S-altitude is little in leads from extremities except aVR at heart normal location in thorax.

· S-dense is gradually decreased in thoracical leads from V1 to V4, it has little altitude or even absent in V5 and V6.

· R- and S-denses equality in thoracical leads (so-called transitional zone) usually takes place in V3 or (more seldom) between V3 and V4. This zone can be located in right or left thoracical leads. This position depends greatly on heart location in thorax. We will tell about this below during ECG analysis discussing.

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QRS complex or ventricular complex It is Q, R and S-denses uniting (integrity). Its total duration must not be less than 0,12 sec. Its altitude corresponds to R-

dense altitude. Segment S-T

It corresponds to both ventricles complete excitement period. It is located on isoline (potentials difference between ventricles is equal to zero). Its deviation up/down must not be more than 0,5 mm; in thoracical leads such deviation must not be more than 2 mm. Such deviation increasing can indicate to myocardial hypoxy or ishemy.

Dense T It reflects fast ending ventricles repolarization. Under normal conditions it must

have the same direction like R-dense. Remember! · Its duration is 0,2-0,3 sec, its altitude is 0,2-0,4 mV. · T-dense always is positive in I, II, aVF, V2-V6, moreover TI>TIII and TV6>TV1. · T-dense can be positive, two-phased or negative in III, aVL and V1. · T-dense is always negative in aVR.

Interval Q-T It is called as ventricles electrical systole. All ventricles parts are excited.

Interval R-R It corresponds to heart cycle and thus equal to 0,80 sec. This interval is less than

norm at bradycardy and more than norm at tachycardy. Interval Q-T (QRST)

It is measured from QRS (dense Q or R) beginning till T-dense end. This interval is named as ventricles electrical systole. All ventricles are excited during it. Its duration is opposite to heart rate.

Normal value is measured by Bazett’s formule:

Q-T = K√(R-R) where: · K=0,37 for women; · K=0,40 for men; · R-R – one cardiac cycle duration.

U-dense It is registered more often in children, adolescents and sportsmen. It corresponds

to exhaltation period after left ventricle electrical systole ending. This dense appearance means predisposition to extrasystole.

4. Materials for auditory self-work. 4.1. List of study practical tasks necessary to perform at the practical class. Materials and methods: electrocardiograph (device for electrocardiogram

registration), bed, gauze, physiological solution, electrode paste. Investigation object: human being.

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Task 1. To register ECG in 3 standard leads.

The investigated person is lied on the bed near the device. He must be relaxed in maximal extent. The investigator should prepare the investigated person’s skin to the electrodes putting (according to the scheme on the device lateral wall). Skin in the locuses of contact with electrodes must be washed by tampones with alcohol, then hydrophilic packing should be putted and electrodes are fixed. Then the investigator registers EKG in 3 standard leads.

Task 2.

To register ECG in 3 unipolar leads from extremities (by Goldberger). One-poled leads from extremities are designated also as usual one-poled leads,

with addition letter “a” at the beginning (first letter of Latin word “augmented” – enforced). Leads aVR, aVL and aVF are differed one from another by denses direction and their size (altitude).

AVR lead is unique in which positive electrode is connected with body locus, almost always charged negatively (right hand), that’s why P, T denses and QRS complex main dense (R) are negative.

In aVL lead P dense has small altitude, often it can be two-phased with first negative phase, sometimes all dens is negative.

P dense is positive in aVF lead; QRS complex may consist of main positive dense R which can be preceeded by Q dense and S dense can follow after R.

In healthy people QRS in one-poled augmented leads is changed according to heart localization in thorax: at horizontal localization for example in aVL R dense becomes higher, in AVF S dense becomes deeper, usually positive in this lead T dense can be negative or flatted (softened).

Task 3.

To register ECG in unipolar thoracic leads (by Wilson). This ECG is an essential addition to the ECG registered in usual leads. It allows

evaluating myocardium state more properily at different disorders. For instance, in course of heart attack (myocardium infarctum) on ECG registered in thoracic leads the changings can occur before the same in usual leads. It has, of course, great diagnostic importance.

One should put thoracic electrode very distinctly in course of thoracic leads registration. Because electrode is near the electrical field origin, that’s why any even very little displacement leads to significant change of registered potential.

P dens in V1 and V2 leads can be positive, two-phased, negative; in V3-V6 – positive.

QRS complex in V1-V2 consists of small initial dense r and main negative dense S. Size of these denses in V2 lead is usually bigger than in V1 lead. Thoracic lead in which QRS complex consists of denses R, S with equal altitude, is known as transition zone. Its borders – V2, V3, between them, more seldom in V4.

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5. Literature recommended 1. Lecture course. 2. Mistchenko V.P., Tkachenko E.V. Methodical instructions for medical students (short lecture course).-Polatava, 2005.-P.56-57. 3. Methodical instructions on chapter “Cardiac-vascular system physiology” on practical classes for dental and medical students. 4. Concise Physiology /Guyton-Ganong-Chatterjee. Ed. By Dr Gull R.Sh.-Lahore: K.E.Medical College.-1998.-P.54-58, 94. 5. Kapit W., Macey R.I., Meisami E. The Physiology Colouring Book: Harpers Collins Publishers, 1987.-P. 28. 6. Bullock J., Boyle III J., Wang M.B. Physiology.-1991.-P.107-112. 7. Stuart Ira Fox. Human Physiology.-8-th Ed.-Mc Graw Hill, 2004.-P.387-390. 8. Seeley R.R., Stephens T.D., Tate P. Essentials of Anatomy and Physiology.-The 3rd Ed.-McGraw Hill, 1999.-P.318-319.

6. Materials for self-control:

Control questions: 1. Electrocardiography (ECG) physiological bases. 2. Depolarization and repolarization dynamics in heart. 3. Electrocardiographical leads (abductions). 4. Normal electrocardiogram characteristics. 5. ECG registration in human being. 6. Which processes in myocardium can be reflected on ECG? 7. Give the characteristics of ECG denses. 8. Give the characteristics of ECG segments and intervals.

LESSON 43 HEART EXCITEMENT DYNAMICS INVESTIGATION. ECG ANALYSIS

1. Topic studied actuality. Rhythm and conductivity disorders in heart are

rather spread pathological conditions of different-aged people. ECG belongs to such standard methods and widely-used diagnostic methods like total blood, urine analysis and is prescribed to every person at preventive and medical examination. That is why ECG physiological and pathophysiological bases must be managed by doctor of any speciality.


ECG characteristics, its interpretating vector theory, ECG deshiphrating algorhythm.

To be able to: establish pace-maker by ECG, whether it generates rhythmical impulses; to assess excitement distribution velocity through heart, heart electrical axe position.


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special tables or alive preparations Histology, cytology and embryology


Draw heart conductive system and designate its main elements with telling about their histological structures to recognize heart histological preparations.


Pathomorphological changings at heart diseases









3.2. Topic content.

EKG analysis performance You must follow next algorhythm. Cardiac rhythm and conductivity analysis. Heart contraction regularity assessment. It is assessed at intervals R-R duration comparison between cardiac cycles

registered consequently. Interval R-R is usually measured between R denses apexes.

Heart regular or correct rhythm is diagnosed when measured R-R intervals duration is equal or difference is ±10% from R-R average duration.

Cardiac contractions number (heart contraction rate – HCR) counting. It is assessed at correct rhythm by formule:

HCR=60: (R-R)

where: 60 is seconds number in 1 minute; R-R – interval duration expressed in seconds.

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Excitement source determining. Sinus rhythm is characterized by:

· positive P-denses in II standard lead and these P-denses come before every complex QRS;

· all P-denses constant equal shape in one and the same lead. Atrial rhythms (from atria inferior parts) are characterized by negative denses P

in II and III and non-changed QRS complexes following after them. Rhythms from AV-binding are characterized by:

· P-dense absence – this dense coincides to usual non-changed QRS-dense or · negative P-denses located after usual non-changed QRS complexes.

Ventricular (idio-ventricular) rhythm is characterized by: · slow ventricular rhythm (less than 40 beatings per 1 min); · presence of dilated and deformed QRS complexes; · absence of usual connection between QRS complex and P-denses.

Figure 29.

Conductivity function assessment. P-dense duration should be assessed for approximate assessment of

conductivity function. P duration characterizes electrical impulse coming velocity through atria.

Then interval P-Q (R) duration should be assessed. It describes conductance speed through atria, AV-node and His’ system.

Ventricular complex QRS duration tells about excitement conductance through ventricles.

ECG registration speed must be taken into account during all these measurements.

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These denses and intervals duration increasing indicates to conductance retardation in heart conductive system corresponding part.

Then, after this, internal inclination interval is essential to be measured in thoracic leads V1 and V6.

Determining heart turnings round antero-posterior, longitudinal and transversal axes.

Heart turnings: · round anterior-posterior axe; · round longitudinal axe; · round transversal axe.

Heart electrical axe location determining in frontal plane. It is performed in

standard and enforced leads. Remember!

One can differentiate heart electrical axe position following variants: · normal position when angle α is from +30° till +69°; · vertical position when angle α is from +70° till +90°; · horizontal position when angle α is from 0° till +29°; · axe inclination to the right when angle α is from +91° till ±180°; · axe inclination to the left when angle α is from 0° till -90°.

Normal, horizontal and vertical position of heart electrical axe (from 0° till +90°)

can be resent both in healthy people and in patients with ventricular hyperthrophy or intraventricular conductivity disorder.

Electrical axe inclination to the right (more than +90°) or to the left (less than 0°) as a rule testifies to pathological changings presence in heart muscle.

Angle alpha visual detection (is performed in standard and augmented leads). Method is based on 2 principles: 1. Maximal positive value of QRS-complex denses algebraic sum is observed in

such an electrographic lead the axe of which approximately coincides to heart electrical axe position and parallel to it.

2. Complex like RS where denses algebraic sum is equal to zero (R=S or R=Q+S) is recorded in the lead the axe of which is perpendicular to heart electrical axe.

Remember! 1. Heart electrical axe normal position is characterized by angle α from +30° till

+69° and: RII≥RI≥RIII; R is approximately equal to S in III and aVL. 2. Horizontal position or heart or heart electrical axe inclination to the left is

characterized by angle α from +30° till -90° and: high R-denses in I and aVL, moreover RI≥RII≥RIII; deep S in III. 3. Vertical position or heart or heart electrical axe inclination to the right is

characterized by angle α from +70° till +180° and: high R-denses in III and aVF, moreover RIII≥RII≥RI; deep S in I and aVL.

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Heart turnings determining round longitudinal axe. Heart turnings round longitudinal axe pointed conditionally through heart apex

and base are determined by QRS-complex configuration in thoracic leads the axes of which are located in horizontal plane.

Remember! ECG sign of heart turning round longitudinal axe clockwise is the following: transitional zone (denses S and R equality) possible replacement to the left into

V4-V5. Remember!

ECG sign of heart turning round longitudinal axe counter clockwise the following: transitional zone possible replacement to the right in V2. Heart turnings determining round transversal axe. Heart electrical axe position in 6-axed system of Beyle is expressed

quantitatively by angle α that is formed by heart electrical axe and the I-st standard lead positive half

Atrial P-dense analysis. Ventricular QRST-complex analysis:

· QRS-complex analysis; · RS-T segment analysis; · T-dense analysis; · interval Q-T analysis.

To establish denses voltage (for excitability function assessment). Voltage can be assessed on R dense altitude (measured in mV) in standard and

thoracic leads. Also R dense altitude can be measured in mm. In standard leads R dens altitude must be not less than 5 and not more than 22

mm; in thoracic leads – not less than 8 and not more than 25 mm. If these limits are counted than one can tell about preserved voltage. If any dense voltage is less than norm than one can think about cardiosclerosis or cardiac insufficiency. If denses voltage is upperthan norm than it can testify to hypertrophy of heart corresponding part (if P – atria, R – ventricles).

Electrocardiographic conclusion. Rule!

· If dipole vector is directed to the positive pole of lead than there will be positive element on ECG – positive dense.

· If dipole vector is directed to the negative pole of lead than there will be negative element on ECG – negative dense.

· If dipole vector is directed perpendicular to the lead axe than there is isoline (baseline) on ECG.

· Any dipole vector is directed from its negative (excited) to positive (non-excited) pole. 4. Materials for auditory self-work. 4.1. List of study practical tasks necessary to perform at the practical class. Materials and methods: ECG sets. Investigation object: human being.

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Task 1. To perform ECG analysis when proper algorhythm usage.

5. Literature recommended: 1. Lecture course. 2. Mistchenko V.P., Tkachenko E.V. Methodical instructions for medical students (short lecture course).-Polatava, 2005.-P.56-57. 3. Methodical instructions on chapter “Cardiac-vascular system physiology” on practical classes for dental and medical students. 4. Concise Physiology /Guyton-Ganong-Chatterjee. Ed. By Dr Gull R.Sh.-Lahore: K.E.Medical College.-1998.-P.54-58, 94. 5. Kapit W., Macey R.I., Meisami E. The Physiology Colouring Book: Harpers Collins Publishers, 1987.-P. 28. 6. Bullock J., Boyle III J., Wang M.B. Physiology.-1991.-P.107-112. 7. Stuart Ira Fox. Human Physiology.-8-th Ed.-Mc Graw Hill, 2004.-P.387-390. 8. Seeley R.R., Stephens T.D., Tate P. Essentials of Anatomy and Physiology.-The 3rd Ed.-McGraw Hill, 1999.-P.318-319. 6. Materials for self-control: Control questions: 1. Electrocardiography (ECG) physiological bases. 2. Depolarization and repolarization dynamics in heart. 3. Electrocardiographical leads (abductions). 4. Normal electrocardiogram characteristics. 5. Heart electrical axis, its localization determining. 6. ECG registration and analysis in human being. Which processes in myocardium can be reflected on ECG? 7. Give the characteristics of ECG denses. 8. Give the characteristics of ECG segments and intervals. 9. Which myocardium functions can be reflected on ECG? 10. Term “heart electrical axis”. 11. Heart electrical axis localization under normal conditions. 12. Term “transitional zone”. 13. Rhythm and frequency determining on ECG.

LESSON 44 HEART PHYSIOLOGICAL PECULIARITIES DETERMINING ON ECG

1. Topic studied actuality. Rhythm and conductivity disorders in heart are

rather spread pathological conditions of different-aged people. ECG belongs to such standard methods and widely-used diagnostic methods like total blood, urine analysis and is prescribed to every person at preventive and medical examination. That is why ECG physiological and pathophysiological bases must be managed by doctor of any speciality.

35

FIGURE 30. Classification of arrhythmia


ECG characteristics, its interpretating vector theory, ECG deshiphrating algorhythm.

To be able to: establish pace-maker by ECG, whether it generates rhythmical impulses; to assess excitement distribution velocity through heart, heart electrical axe position.


36







Pathomorphological changings at heart diseases









3.2.Topic content. Sinus node function state is determined on heart frequency and cardiac

contractions rhythm. At sinus node disorders arhythmias are occurred. One can differentiate:

Sinus tachycardia – sinus node is a pace-maker, rhythm is regular, cardiac contractions frequency is more than 80 per minute. EKG denses are usually normal, R-R-distance is equal, shortened, T-P-interval is also shortened.

The principal current responsible for each part of the potential is shown under or beside the component. L, long-lasting; T, transient.

Other ion channels contribute to the electrical response. Note that the resting membrane potential of pacemaker tissue is somewhat lower than that of atrial and ventricular muscle. Arhythmia main reasons are: hypersympathicotony, hypovagotony, sinus node injure due to its ishemia, infection, toxins.

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Figure 31

Sinus bradycardia - is characterized by sinus rhythm inhibition, when heart contractions rate is from 40 to 60 per 1 minute. Rhythm is regular, pace-maker is sinus node, the automatism of which is reduced. ECG denses are usually unchanged, R-R-intervals are equal and prolonged. It cat be dealt with hypervagotony, hyposympathicotony, local influence on sinus node (infarction, hypoxy), infectious-toxic affections.

Sinus arhythmia – is a result of sinus node irregular activity that leads to unequal excitement impulses formation in it. It causes alternating periods of rhythm quickening and retardation. R-R-distance between different QRS-complexes is unequal and the difference between maximal and minimal R-R is more than 10 per cent comparatively to average R-R. One can differentiate respiratory and non-respiratory sinus arhythmia (respiratory form is more frequent). Heart contractions rate changings in course of respiratory cycle can be connected with sympathetic and parasympathetic nerves tone fluctuation due to respiration phases.

Comparative sinus rhythm inhibition with extraregular impulse formation and consequent heart contraction occurrence (extrasystole) takes place at additional excitement focus existence in a heart. Extrasystole is a premature excitement and contraction of all heart or its parts, the impulse for which is usually origined from heart conductive system different locuses. It is observed frequently in practically healthy people in course of physical or nervous loading, strong emotions, stressful situations and also at diseases of heart, lungs, alimentary tract, kidneys et al. One can differentiate following extrasystoles types:

Atrial – are characterized by P dens deformation on ECG; QRS complex is unchanged, compensatory pause follows after atrial extrasystole;

38

Ventricular – are characterized by QRS complex enlarging and deformation, connection with P dens is absent, complete compensatory pause is observed; left-ventricular extrasystole has high P dens in V1-V2 and deep S in V5-V6; right-ventricular one has high R dens in V5-V6 and deep S in V1-V2.

Under normal conditions impulse from sinus node is spread through myocardium in a definite sequence.

Conductive function disorders can be localized at different levels. One can differentiate:

1.Sino-atrial block – impulse from the sinus node is blocked before it enters the atrial muscle. There is complete cessation of “P” waves with resultant stand still of atrium. Later ventricle picks up a new rhythm, usually a/v node acting as new pace-maker, so that the ventricular QRS and T complex is not altered. There are 3 degrees of such block:

· of the 1st degree – impulses formation retardation in sinuse node or its conduction retardation (it is not detected on ECG);

· of the 2nd degree – part of impulses don’t reach atria, atrial and ventricular contractions are failed; one can see P-P-interval shortening on ECG, then – very prolonged pause;

· of the 3rd degree – is so-called complete blockade; on ECG one can mention P dens, QRS complex and T dens failing and isoline is registered; it can be obsereved at myocarditis, heart vices, atherosclerotic processes, hyperpotassiumaemia and so on.

Atrioventricular block – takes place when the impulse transmission from atria into ventricles is blocked either at a/v node. Main reasons: ishemia or inflammation of a/v node, excessive vagal stimulation. One can differentiate 3 degrees of atrio-ventricular block.

The subjects breathes five times per minute, and with each inspiration the RR interval (the interval between R waves) declined, indicating an increase in heart rate. Note the marked reduction in the magnitude of the arrhythmia in the older man. These records were obtained after β-adrenergic blockade but would have been generally similar in its absence:

· 1st degree or incomplete heart block – when PR-interval is increased above 0,02 sec in a heart beating at normal rate;

· 2nd degree – when PR-interval is increased more than 0,25 to 0,45 second, cardiac impulse passes into ventricles after one atrial contraction and fails to pass in next; the patient is said to have “second degree heart block”;

· 3rd degree – complete block of impulse transmission from atria into ventricle is present that’s why ventricles after escaping from atrial control start their own natural rate of beat; P-denses are unconnected from QRS complex and are deposited on ventricles systole and diastole different moments; P-P-distance is less than R-R-distance because atria are contracted more frequently than ventricles.

His’ fiber bundles block - is a disorder or complete excitement conductance stoppage through His’ fiber right or left bundles. Block through right bandle is registered on thoracic leads, there are also some changings in standard leads; though left one – is diagnosted on thoracic and standard leads.

4. Materials for auditory self-work.

39

4.1. List of study practical tasks necessary to perform at the practical class. Materials and methods: ECG sets. Investigation object: human being.

Task 1. To determine sinus node automatism – sinus tachycardia, bradycardia and

arhythmia

Task 2. To determine extrasystoles occurrence – atrial and ventricular ones

Task 3. To determine myocardium conductive function – sino-atrial, atrio-

ventricular and His’ fiber bundles block

5. Literature recommended 1. Lecture course. 2. Mistchenko V.P., Tkachenko E.V. Methodical instructions for medical students (short lecture course).-Polatava, 2005.-P.52-53. 3. Methodical instructions on chapter “Cardiac-vascular system physiology” on practical classes for dental and medical students. 4. Concise Physiology /Guyton-Ganong-Chatterjee. Ed. By Dr Gull R.Sh.-Lahore: K.E.Medical College.-1998.-P.54-58, 94. 5. Kapit W., Macey R.I., Meisami E. The Physiology Colouring Book: Harpers Collins Publishers, 1987.-P. 28. 6. Bullock J., Boyle III J., Wang M.B. Physiology.-1991.-P.107-112. 7. Stuart Ira Fox. Human Physiology.-8-th Ed.-Mc Graw Hill, 2004.-P.387-390. 8. Seeley R.R., Stephens T.D., Tate P. Essentials of Anatomy and Physiology.-The 3rd Ed.-McGraw Hill, 1999.-P.318-319.

6. Materials for self-control: Control questions: 1. Which myocardium features can be assessed on ECG? 2. Arhythmias main types. 3. Excitability changings and extrasystoles occurrence. 4. Conductivity disorders while impulse coming through conductive system.

LESSON 45 HEART PUMP FUNCTION AND HEART TONES INVESTIGATION.

PHONOCARDIOGRAPHY (PhCG) 1. The topic studied actuality. Heart activity is accompanied by row of physical

phenomena. While their investigation one can receive definite information about heart state and its definite functional properties. Heart tones and bioelectrical phenomena occurrence in heart give necessary information for heart functional state assessment. These indexes give both quantitative and qualitative information of heart activity and are widely used both in physiology and clinics.

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Heart vices are always accompanied by heart sounds disorders. These vices have both innate and acquired nature and rather spread in a human population especially in babies.

2. Study aims: To know: heart structure and function, places for tones auscultation. To be able to: auscultate heart tones, to determines the tones on

phonocardiogram. 3.Pre-auditory self-work materials. 3.1.Basic knowledge, skills, experiences, necessary for study the topic:







Patho-morphological changings of myocardium and valves in part at heart diseases


Pathophysiology Heart vices pathophysiological mechanisms


Myocardium physiological peculiarities in children; heart vices ethiology, pathogenesis, clinics, therapy and prevention principles


Internal Diseases Myocardium physiological peculiarities in different-aged adults; rheumatism and heart vices ethiology, pathogenesis, clinics, therapy and prevention principles


3.2. Topic content.

VALVES OF THE HEART The valves of the heart permit the flow of blood through the heart in only one

direction. There are four valves in human heart. Two of the valves are in between the atria and the ventricles called atrioventricular valves. The other two are the semilunar valves, placed at the opening of the blood vessels arising from the ventricles, i.e. systemic aorta and pulmonary artery.

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FIGURE 32: Valves of the heart

Atrioventricular Valves The left atrioventricular valve is otherwise known as mitral valve or bicuspid

valve. It is formed by two valvular cusps or flaps. The right atrioventricular valve is known as tricuspid valve and it is formed by three cusps. The brim of the atrioventricular valves is attached to the atrioventricular ring, which is the fibrous connection between the atria and ventricles. The cusps of the valves are attached to the papillary muscles by means of chordae tendinae. The papillary muscles arise from the inner surface of the ventricles. The papillary muscles play an important role in closure of the cusps and in preventing the back flow of blood from ventricle to atria during ventricular contraction.

Semilunar Valves The semilunar valves are present at the openings of systemic aorta and

pulmonary artery and are known as aortic valve and pulmonary valve respectively. Because of the half moon shape, these two valves are called semilunar valves. Both the semilunar valves are similar in structure and each one has three flaps. These valves open towards the aorta and pulmonary artery and prevent the back flow of blood into the ventricles.

CARDIAC CYCLE

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Table 12. Cardiac cycle phases

Ventrcicular systole – 0,33 sec

1) Tension phase – 0,08 sec: 2) Ejection phase – 0,25 sec:

a) Asynchronic contraction phase – 0,05 sec b) Isometric contraction phase – 0,03 sec – a/v and semilunar valves are closed a) rapid ejection phase - 0,12 sec – semilunar valves opening; pressure in right ventricle is 15-25 mm Hg, left ventricle – 70-80 mm Hg; b) slow ejection phase – 0,13 sec – pressure in right ventricle is 25-30 mm Hg, left ventricle – 120-130 mm Hg

Ventricular diastole

protodiastolic period – 0,04 sec – from ventricles diastole beginning till semilunar valves closage; isomtric relaxation period- 0,08 sec – all valves are closed; ventricles filling with blood – 0,25 sec: ventricles filling phase due to atria systole – 0,1 sec

a) rapid filling – 0,09 sec; b) slow filling – 0,16 sec

Atraial systole occurs on the background of ventricular diastole. Than ventricular

systole occurs while atria are relaxed. Atrial systole – 0,1 sec. Atrial diastole – 0,7 sec: · 0,3 sec – coincides to ventricular systole; · 0,4 sec coincides to ventricular diastole and heart general pause occurs.

Table 13

Pressure in heart chambers in heart cycle different phases Phase Right half Left half Atrial systole Atria – 4-5 mm Hg

Ventricles – near 0 Atria – 5-7 mm Hg Ventricles – near 0

Ventricular systole Atria – near 0 Ventrciels – 30 mm Hg

Atria – near 0 Ventricles – 120 mm Hg

Total pause Atria – near 0 Ventricles – near 0

Atria – near 0 Ventricles – near 0

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Every heartbeat consists of two major periods called systole and diastole. During systole, there is contraction the cardiac muscle and pumping of blood from the heart. During diastole, there is relaxation of cardiac muscle and filling of blood. Various changes occur in different chambers of the heart during each heartbeat. These changes are repeated during every heartbeat in a cyclic manner.Thus, the cardiac cycle is defined as the succession of co-ordinated activities, which take place during every heart beat.

DIVISIONS OF CARDIAC CYCLE The contraction and relaxation of both the atria of heart are called atrial systole

and atrial diastole respectively. The contraction and relaxation of both the ventricles are called ventricular systole and ventricular diastole respectively.

However, in clinical practice, systole means ventricular systole and diastole means ventricular diastole. Thus, the events of cardiac cycle are classified into two divisions.

1. Systole 2. Diastole. Atrial events are not described separately since these events merge with the

ventricular events. SUBDIVISIONS AND DURATION OF CARDIAC CYCLE

When heartbeats at the normal rate of 72/minute, the duration of each cardiac cycle is about 0.8 second. The duration of systole is 0.27 second and that of diastole is 0.53 second. Generally, systole is divided into two subdivisions and diastole is divided into five subdivisions. The subdivisions and the duration systole and diastole are as follows:

The total duration of cardiac cycle is 0.27 + 0.53 = 0.8 second. Among the atrial events, atrial systole occurs during the last phase of ventricular

diastole. Atrial diastole is not considered as a separate phase, since it coincides with the ventricular systole and earlier part of ventricular diastole. The atrial systole extends for about 0.1 second and the duration of atrial diastole is about 0.7 second.

DESCRIPTION OF EVENTS OF CARDIAC CYCLE For the sake of better understanding, the description of events of cardiac cycle is

commenced with atrial systole. ATRIAL SYSTOLE

Duration of atrial systole is 0.11 second. This is also called second or last rapid filling phase or pre-systole. It is considered as the last phase of ventricular diastole.

During this period, only a small amount, i.e. blood is forced into ventricles from atria. Atrial systole is not essential for the maintenance of circulation. Many persons with atrial fibrillation survive for years, without suffering from circulatory insufficiency. However such persons feel difficult to cope up with physical stress like exercise. During this period, the intraatrial pressure is increased. There is slight increase in intraventricular pressure and ventricular volume.

ISOMETRIC CONTRACTION PERIOD This is the first phase of ventricular systole. Isometric contraction or isovolumetric

contraction lasts for 005 second. Immediately after atrial systole, the atrioventricular valves are closed due to increase in ventricular pressure. The semilunar valves are already closed. Now the ventricles contract as closed cavities in such a way that, there is no change in the volume of ventricular chambers or in the length of muscle fibers. Only, the tension is increased in ventricular musculature. This type of contraction is called isometric contraction or isovolumetric contraction. Thus, during isometric contraction, the pressure is increased sharply inside the ventricles.

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Significance of Isometric Contraction During isometric contraction period, the ventricular pressure is greatly increased.

When pressure in the ventricles increases above the pressure in the aorta and pulmonary artery, the semilunar valves open. Thus, the pressure rise in the ventricle caused by isometric contraction is responsible for opening of semilunar valves leading to ejection of blood from the ventricles.

EJECTION PERIOD The duration of ejection period is 0.22 second. Due to the opening of semilunar

valves and the contraction of ventricles, the blood is ejected out of both the ventricles. This period is of 2 stages. First stage is called the rapid ejection period and lasts for 0.13 second. Immediately after the opening of semilunar valves, a large amount of blood is rapidly ejected from both the ventricles. Second stage is called the slow ejection period. The duration of this period is 0.09 second. In this stage, the blood is ejected out with much less force.

PROTO-DIASTOLE Since this is the first stage of ventricular diastole, this is called proto-diastole.

Duration of this period is 0.04 second. Due to the ejection of blood, the pressure in aorta and pulmonary artery increases and pressure in ventricles drops. When the intraventricular pressure becomes less than the pressure in aorta and pulmonary artery, the semilunar valves close. During this period, practically no other change occurs. Thus, proto-diastole indicates only the end of systole and beginning of diastole. pulmonary artery increases and pressure in ventricles drops. When the intraventricular pressure becomes less than the pressure in aorta and pulmonary artery, the semilunar valves close. During this period, practically no other change occurs. Thus, protodiastole indicates only the end of systole and beginning of diastole.muscle fiber. So, this is called the isometric or isovolumetric relaxation period. There is fall in intraventricular pressure.

Significance of Isometric Relaxation During isometric relaxation period, the ventricular pressure is greatly reduced.

When the pressure in the ventricles becomes less than the pressure in the atria, the atrioventricular valves open. Thus, the fall in pressure in the ventricles, caused by isometric relaxation is responsible for the opening of atrioventricular valves leading to filling of ventricles.

RAPID FILLING PHASE Duration of this period is 0.11 second. When the pressure in ventricles becomes

less than that in atria the AV valves open. Blood accumulates in both atria during atrial diastole. When AV valves are opened, there is a sudden rush of blood into ventricles, so, this period is called the first rapid filling period. About 70% of filling takes place during this phase.

SLOW FILLING PHASE

Duration of slow filling phase is 0.19 second. After the sudden rush of blood, the ventricular filling becomes slow. Now, it is called the slow filling. This is also called diastasis. About 20% of filling occurs in this phase.

ATRIAL SYSTOLE After slow filling period, the atria contract, a small amount of blood enters the

ventricle from the atria and, the cycle is repeated. The atrial systole is also called the last rapid filling phase and, about 10% of ventricular filling takes place during this period.

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FIGURE 33. Events of cardiac cycle

INTRAATRIAL PRESSURE CHANGES DURING CARDIAC CYCLE

SIGNIFICANCE The pressure in the atria is called the intraatrial pressure. The intraatrial pressure

is essential to open the atrioventricular valves and ventricular filling. It is also the main factor causing the development of venous pulse.

METHODS OF STUDY Intraatrial pressure can be recorded by cardiac catheterization. The left atrial

pressure can also be determined indirectly by measuring pulmonary capillary wedge pressure.

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Pulmonary Capillary Wedge Pressure The pulmonary capillary wedge pressure accurate reflects the left atrial pressure.

So, the left atrial pressure can be determined indirectly by measuring the pulmonary capillary wedge pressure.

The pulmonary capillary wedge pressure is measured by using cardiac catheter with a balloon at its tip. By means of venous puncture, the catheter is guided into right ventricle through right atrium. From the right ventricle, it is advanced towards the proximal portion of pulmonary artery and the balloon is inflated. Then, the catheter alone is advanced further into the distal portion of pulmonary artery leaving the inflated balloon at the proximal portion. This allows the catheter to float in a wedge position. In this position, the pressure in the right ventricle is obstructed by the inflated balloon. The pressure transducer attached to the catheter detects only the wedge pressure ahead of catheter, i.e. the pressure in the pulmonary capillary bed (the word wedge refers to being obstructed). Because of the absence of any valve between pulmonary capillary bed and left atrium, the measurement of this pulmonary capillary wedge pressure reflects the left atrial pressure.

MAXIMUM AND MINIMUM PRESSURE IN ATRIA The maximum pressure obtained in the left atrium is 7to I 8 mm Hg and, the

maximum pressure obtained in the right atrium is 5 to 6 mm Hg. The minimum pressure obtained in the atria is 0 to 2 mm Hg.

HEART TONES Heart sounds are actually the sounds produced by the heart during a cardiac

cycle. They are detected by direct or immediate auscultation and by means of phonocardiogram.

Heart sounds mechanism Heart sounds are produced by the closure of valves, due to which vibration starts

in the valves, walls of the heart and adjacent blood. This vibration is heard in the form of heart sounds from the chest wall.

Types of heart sounds There are 4 heart sounds which are:

· The first heart tone. · The second heart tone. · The third heart tone. · The fourth heart tone.

The first heart tone Nature Dull and prolonged-often described as “LUB”. Occurrence Occurs at the beginning of ventricular systole. Causes Produced due to the closure of a/v valves. Area of Auscultation For mitral valve is apex of heart at 5th intercostal space. For tricuspid valve is left

sternal border in 4th intercostal space. Mechanism of Production Sudden changings in the pressure of ventricles cause vibration of the walls and

vessels. This causes vibration in the aorta wall and in blood itself.

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Significance 1. Indicates ventricular systole. 2. Its duration and loudness indicate myocardium condition. 3. Indicates compliance of a/v valve.

The second heart tone

Nature Sharp and short usually described as “DUB”. Occurence At the end of ventricular systole. Causes It is produced due to closure of semilunar valves (i.e. aortic and pulmonary). Area of Auscultation

For pulmonary valve is parasternal line in the 2nd left intercostal space. For aortic valve is parasternal line in the 2nd

right intercostal space. Mechanism of Production closure of semilunar valves and the vibration of valves; vibration of blood and the walls of pulmonary artery, aorta and to lesser extent the ventricles. Significance

· Indicates systole end and diastole beginning. · Indicates semilunar valves compliance.

The third heart tone

Nature Occasionally heard. It is weak and rumbling in nature. Occurrence At the beginning of middle third of the diastole. Causes and Mechanism It is produced due to the oscillation of blood back and forth between the walls of

the ventricles and is initiated by inrushing blood from the atria. Significance Indicates beginning of the ventricular filling.

The fourth heart sound

Nature Weak and rumbling. It is never heard with stethoscope but can be recorded on

phonocardiogram. Occurrence This sound occurs when atria contract. Causes and Mechanism It is caused by inrushing of blood into ventricles, which initiates vibrations similar

to those of 3rd heart tone. Significance Indicates the end of ventricular filling and occurs just before the 1st heart sound.

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Table 14 Heart sounds

Heart sounds

Occurs during

Cause Characteristics

Duration , sec

(second)

Frequency (cycles

per second)

Relation with ECG

Vibrations in phono-

cardiogram

First Isometric contraction and ejection period

Closure of atrioventri--cular valves

Long, soft and low pitched Resembles the word 'LUBB'

0.10 to 0.17

25 to 45

Coincides with 'Rr

wave

9 to 13

Second Protodiastole and part of isometric relaxation

Closure of semilunar valves

Short, sharp and high pitched Resembles the word 'DUBB'

0.10 to 0.14

50 Precedes or appears 0.09 second after summit of T wave

4 to 6

Third Rapid filling

Rushing of blood into ventricle

Low pitched

0.07 to 0.1

1 to 6 Between T wave and 'P' wave

1 to 4

Fourth Atrial systole

Contraction of atrial musculature

Inaudible sound

0.02 to 0.04

0.02 to 0.04

Between 'P' wave and 'Q' wave

1 to 2

Abnormal or ectopic heart sounds are known as murmurs. They occur when

there is some valvular or any other abnormality causing turbulence of blood flow either due to great velocity of ejection or its regurgitation. They are the study subject of pathological physiology, pediatry and other clinical subjects.

Main of them are: · murmur of aortic stenosis; · murmur of aortic regurgitation; · murmur of mitral regurgitation; · murmur of mitral stenosis et al.

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 action potentials and ECG are plotted on the same time axis but with different zero points on the vertical scale. LAF, left anterior

49

fascicle. The portions of the heart contracting in each phase are indicated in color. RA and LA, right and left atria; RV and LV, right and left ventricles.

PHONOCARDIOGRAPHY

Phonocardiography (PCG) – is an instrumental method of graphical registration of sounds occuring in course of heart activity. As an order, one should record ECG in and usual volume or at least in the II standard lead.

The investigation must be performed in a warm, isolated from noises room, under quiet patient’s state, while his lying.

Heart sounds – tones and murmurs are represent as oscillattions on PCG. Cardiac cycle intervals free from tones and murmurs, look like zero line (isoline).

Under normal conditions one can determine oscillations corresponding to the I and the II heart tones, seldom – III and IV tones, functional (accidental) murmur and low-frequented oscillations of ballistic nature.

The I tone origin coincides QRS complex (on ECG) second half, II tone origin – coincides approximately T-dens end (usually being late on 0,02-0,04 sec).

One can differentiate several I tone components on PCG. Initial low-sized and frequented oscillations connect with ventricular muscles contraction; main or central segment of the I tone consisting of relatively highly-frequented oscillations occurs due to mitral and tricuspidal valves closure.

One can differentiate II tone aortal and pulmonal components on PCG. Aortal component occurs a little before, its altitude is bigger in 1,5-2,0 times comparatively to the second one. Interval between aortal and pulmonal components of II tone can reach 0,06 sec. Sometimes, especially during childhood, one can register the II tone splitting.

III tone graphically looks like 1-2 low-sized, low-frequented oscillations. Usually III tone is registrated in children.

IV tone is registered on PCG as 1-2 low-frequented, low-sized oscillations. 4. Materials for auditory self-work. 4.1. List of study practical tasks necessary to perform at the practical class. Materials and methods: tonometer, phonendoscope, phonocardiograms set. The investigated object: human being.

Task 1.

To auscultate heart tones under resting state. Auscultation places (proections) of heart tones components:

· the 5th intercostal space on 1 cm on the left inside to linea medio-clavicular – mitral valve;

· the 2nd intercostal space on the right from sternum end – aorta valve; · the 2nd intercostal space on the left from sternum end – pulmonary artery valve; · ensiform (xiphoid) process basis – tricuspid valve.

Task 2.

To auscultate heart tones after physical loading. To auscultate heart tones in one examined person before and after physical

loading (20 sitting down for 30 seconds).

50

Task 3. To perform phonocardiogram analysis.

To register phonocardiogram on 2-3 investigated people, then to perform its analysis. To use standard phono- and polycardiograms.

To draw phonocardiogram fragment, to designate the 1st and the 2nd tones on it.

FIGURE 34: Comprehensive diagram showing ECG, phonocardiogram, pressure changes and volume changes during cardiac cycle

51

5. Literature recommended 1. Lecture course. 2. Mistchenko V.P., Tkachenko E.V. Methodical instructions for dental students (short lecture course).-Poltava, 2005.-P.28-30, 7-11. 3. Mistchenko V.P., Tkachenko E.V. Methodical instructions for medical students (short lecture course).-Polatava, 2005.-P.55-56. 4. Methodical instructions on chapter “Cardiac-vascular system physiology” on practical classes for dental and medical students. 5. Concise Physiology /Guyton-Ganong-Chatterjee. Ed. By Dr Gull R.Sh.-Lahore: K.E.Medical College.-1998.-P.19-51, 94-97. 6. Kapit W., Macey R.I., Meisami E. The Physiology Colouring Book: Harpers Collins Publishers, 1987.-P.26-27, 29, 31. 7. Bullock J., Boyle III J., Wang M.B. Physiology.-1991.-P.99-106, 118-124, 127-130. 8. Stuart Ira Fox. Human Physiology.-8-th Ed.-Mc Graw Hill, 2004.-P. 378-383. 9.Seeley R.R., Stephens T.D., Tate P. Essentials of Anatomy and Physiology.-The 3rd Ed.-McGraw Hill, 1999.-P.311-314, 317-321.

6. Materials for self-control: Control questions: 1. Heart role in hemodynamics. 2. Pressure and blood volume changings in heart chambers in course of cardiac cycle. 3. Heart valves role in hemodynamics. 4. Heart tones, their genesis. 5. Heart tones registration methods. 6. Heart tones auscultation best locuses. 7. Phonocardiogram analysis.

LESSON 46 ARTERIAL PRESSURE AND PULSE DETERMINING IN HUMANS.

SPHYGMOGRAPHY (SPhG) 1. The topic studied actuality. Hemodynamics is the regularities according to which blood movement through

vessels is performed. Factors providing blood circulation are as follows as: – pressure gradient; – vessels transversal section; – this section square et all. There are different physiological methods widely used in clinics for their

assessment: – pulse investigation; – blood pressure measurement; – circulation volumary velocity estimation. Getting knowledge about these methods is essential for dentists because oral

mucosa is a powerful reflexogenic zone, the influence on which causes circulation

52

system organs activity changings particularly cardiac contractions frequency (pulse changes) and arterial pressure level. This circumstance should be taken into account in course of treaty measurements performance in oral cavity.

Hypertension can be both primary and secondary or essential (it means that it can accompany different diseases). Hypertensive disease places one of the first places among adult people death reasons (together with myocardium infarction, stroke et al.). Taking blood pressure belongs to urgent manipulations all over the world.

Eastern Medicine with its paying much attention to diagnostics can tell about more than 100 pathological conditions on the base of the human pulse.

2. Study aims: To know: arterial pressure and pulse origin mechanisms, factors determining

their changings. To be able to: perform pulse assessment by palpation, make analysis of

sphygmogram; measure arterial pressure in a human being by Korotkov. 3.Pre-auditory self-work materials. 3.1.Basic knowledge, skills, experiences, necessary for study the topic:

Subject To know To be able to Anatomy Vessels anatomy Show main vessels on special

tables or alive preparations Histology, cytology and embryology

Vessels histological peculiarities: layers

To know main vessels types on the preparations


Patho-morphological changings of vessels


Pathophysiology Hypertonic disease pathophysiological mechanisms

Internal Diseases

Vessels physiological peculiarities in different-aged adults; hypertonic disease ethiology, pathogenesis, clinics, therapy and prevention principles

To treat and to prevent hypertonic disease

3.2. Topic content. Blood pressure – force whith which blood presses onto vessel walls. It depends on: a) heart activity; b) vessels resistance; c) their diameter; d) their length; e) blood viscosity. Maximal (systolic) pressure is registered during heart systole. Its size is equal

to 100-130 mm merc col (on brachial artery). There is a tendency to this pressure

53

increasing during last years of practically healthy children even of school age. Its level depends mainly on heart activity.

Minimal (diastolic) pressure is characterized by size registered during diastole. Norma: 65-90 mm merc col. Vascular wall tone is a dominant factor determining this pressure.

Pulse pressure – mathematic difference between systolic and diastolic pressure level. Its maximal size is in arteries near heart. The farther from heart the pressure pulse difference is decreased and beginning from arterioles it disappears.

Middle-dynamic pressure – expresses energy with which blood is moved, it provides blood movement through vessels and it is the average resulting size for all pressure fluctuations (oscillations) alongside all vascular system. Its level is less than systolic but more than diastolic. Norma: 90-100 mm merc col.

Venous pressure - Venous pressure also affects the venous return. The pressure in the venules is 12-18 mm Hg. In the smallerand larger veins, the pressure gradually decreases. In the great veins, i.e. inferior vena cava and superior vena cava, the pressure falls to about 5.5 mm Hg. At the junction of vena cavae and right atrium, it is about 4.6 mm Hg. The pressure in the right atrium is still low and it alters during cardiac action. It falls to zero during atrial diastole. This pressure gradient at every part of venous tree helps as a driving force for venous return.

FIGURE 35. Mechanism of muscle pump A. During contraction of the muscle B. During relaxation of the muscle

54

Pressure changings in course of transport through all vessels: – aorta – 120-130 mm merc col.; – arteries – 100-120 mm merc col.; – arterioles- 40-80 mm merc col.; – capillaries – 20-40 mm merc col.; – veins – 5-10 mm merc col.; – vena cava - up to 0 mm merc col.

Figure 36

Arterial pulse – or push, arterial wall fluctuation caused by systolic pressure increasing in arteries. Pulse wave appears in aorta when pressure is sharply increased in it and its wall is stretched. This wave is spread with velocity 3-15 m per second from aorta to arterioles. It may be registered on large, superficially located arteries, by palpation or graphically (sphygmogram). At palpation its necessary to perform on both hands simultaneousely (hands must be at heart level) in one and the same patient location from initial investigation. If one can not determine any difference further pulse investigation should be performed on one hand (at pulse difference on both hands pulse is called different). Different pulse may be diagnostic sign of mitral valve stenosis, aortal aneurisme.

One can differentiate on sphygmogram: anacrote (it corresponds to ventricles systole) – curve ascent (rising); catacrote (it corresponds to blood slow exile from ventricles in its beginning, rest

part – ventricules dyastole) – curve descent (falling down, drop);

55

dycrote – there is dycrotic ascent on catacrote, it corresponds to blood return to heart during dyastole and its shock to semicircular valves.

Pulse clinical characteristics main indexes: Frequency – shocks (beats) amount per minute. Norma: 60-80 per minute

(sometimes it is considered to 90). It may be estimated both on sphygmogram and by palpation.

Frequent pulse (tachycardy, trachysphygmy) – it takes place at hyperthermia, in course of physical loading. At body temperature increasing on 1°C in adults pulse frequency increases on 8-10 beats, in children – on 15-20 beats per 1 min.

Seldom pulse (bradycardy, bradysphygmy) – in sportsmen, in well-trained people.

Pulse frequency is changing in course of aging:

· newborns – 130-140 beats per min; · 1 year – 120-130; · 7 years – 90-100.

Rhythm – is determined both on sphygmogram and by palpation. Rhythmical (regular) pulse – it is observed at equal spaces between pulse

waves. Arythmical (irregular) - it is observed at unequal spaces between pulse waves.

Physiological arhythmias may be at intensive muscular loading, thermal procedures.

Pulse velocity – intensivity with which pressure in artery is increased during pulse

wave arising and is reduced in course of its drop (it is determined the best on sphygmogram).

Rapid pulse - it may be in course of physical activity, aortal valve insufficiency. Slow pulse – at faint, aortal ostium constriction. Pulse altitude – is determined on sphygmogram. High pulse -it is rapid or fast at the same time. Low pulse – it is slow at the same time. Pulse tension – vascular wall force or resistance degree to its pressure with

fingers. Solid pulse – pulse is accelerated and becomes stronger after vessel wall

pressure. As a rule, it is observed at elderness due to vascular elasticity reducing; at hypertonic disease.

Soft pulse – pulse becomes slower and low-expressed after vessel wall palpation. It is under norma.

Diagnostic value: on tension degree one can tell about maximal blood pressure level. There is direct correlation between these 2 indexes.

Pulse filling – consists of pulse altitude and its tension. The higher systolic pressure plus blood volume and pulse altitude, the filling is stronger.

Full pulse. Empty pulse – if pulse is small by its size, it is empty, as a rule. Filliformis pulse – it is practically unexpressed - it is observed at strong bleeding,

collapse and so on.

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Venous pulse – pressure and volume fluctuations in veins in course of one cardiac cycle delt with blood outflow dynamics into right atrium in systole and diastole different phases. These fluctuations are transmitted in retrograde direction (ahead); one can find them out in large veins located near heart – usually cava or jugular. Pulse wave distribution velocity is 1-3 m/sec. This pulse wave reason differs from that for arterial pulse. Vein pulse reason is blood outflow stoppage from veins to heart in course of atrial and ventricular systole. In this moment blood stream is lacked in large veins that results in pressure rising up in them. This pulse is registered graphically and this curve is named as phlebogram.

3 phlebogram waves: wave “a” - occurs in course of right atrium systole: blood outflow from veins to

heart is stopped and pressure in rised up in them; when atrium is relaxed blood begins to pass in its cavity, pressure in vein is reduced and curve reaches its initial level;

wave “c” – new wave after drop which corresponds to pulse of neighbouring carotid artery and reflects fluctuation of its wall. Carotid artery push is communicated to vein and causes occurrence of increased pressure rapid wave in it. After such short-termed rising pressure is falling down because blood outflows in atrium constantly and atrium is in diastole;

wave “v” - after atriums filling pressure in vein is increased again, blood stagnation and venous wall stretching take place; all this causes third wave appearance.

Venous pulse can be investigated both graphically and by palpation. 4. Materials for auditory self-work. 4.1. List of study practical tasks necessary to perform at the practical class. Materials and methods: pulsotachometer, tonometer, phonendoscope,

stopwatch, sphygmograms sets. The investigated object: human being.

Task 1.

To investigate pulse by means of palpation method. Radial artery should be insignificantly pressed by index, middle and ring-finger to

the underlied bone in fore-arm (antebrachium) distal end. Pulse should be counted in course of 1 min. The investigator should determine pulse frequency, rhythm, filling, tension under resting state and after physical loading (15-20 sitting down).

Task 2.

To register and to analyze sphygmogram. To determine such pulse features as frequency, rhythm, altitude, velocity. Sphygmography (SPG) is arterial wall movement registration. Such movement

occurs under blood pressure wave influence in course of each heart contraction. Arterial wall deformation degree in course of pulse wave passage depends on vessel features and blood pressure level.

Sphygmography allows to count: · pulse wave distribution velocity; · SPG can be used at heart cycle phasic analysis (polycardiography method);

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· blood circulation system state assessment; · heart vices diagnostics.

2 SPG types (according to registration methodics):

· contact (direct); · contact-free (distanced): by means of distance devices.

Contact-free SPG registration methodics. It is quite simple: on the locus of vessel pulsation, for instance, radial artery, the

investigator must put device (piezocristallic, tensometric or cavital ones), the signal from which reaches registrative device (for example, electrocardiograph).

One register at SPG direct oscillations of arterial wall caused by pulse way passage through the vessel.

2 SPG types (according to localization):

1) of central pulse – reflects pressure fluctuations in aorta and is registered in: · carotid artery; · subclavial artery; 2) of peripheral pulse – on arteries: · femoral; · brachial; · radial; · of foot (dorsal et al.).

Central and peripheral pulse is differed by major wave shape. It connects with oscillations weakening through the vascular bed length.

SPG main phases: 1. Anacrote - corresponds to heart systole fast blood expulsion phase – curve

ascendant part. 2. Systolic plataux – is formed by shock and residual wave and corresponds to

heart systole slow blood expulsion wave. 3. Catacrote – corresponds to heart diastole – curve descendant part. 4. Incisura – sudden pressure decreasing in aorta at the moment of semilunar

valves closage. 5. Dicrotic dense – corresponds to semilunar valves closage and pressure

increasing secondary wave occurrence.

The curve of central arterial pulse is origined from little perisystolic wave, caused by isometric contraction phase. Rapid sleep ascendant follows it. Such ascendant is named anacrote. This ascendant reflects blood passage form left ventricle to central arteries. Under normal conditions anacrote duration is 0,08-0,1 sec. Then descendant part – catacrote – takes place. Catacrote end (up to incisura) means left ventricle systole end. Incisura is located in catacrote. The lowest incisura point reflects the moment of semilunar valves complete closage. Under normal conditions incisura is located on the altitude of 2/3 of all pulse wave general altitude. Dicrote, or secondary ascendance, comes after incisura. It is the reflection of isometric relaxation phase initial period. The wave itself is caused by blood portion reflection at the moment of semilunar valves closage.

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The curve of peripheral arterial pulse differs from central one with expressed incisura absence. Main wave is expressed good on it (anacrote-catacrote) and secondary dicrotic wave represents separate wave as it is.

For pulse wave distribution velocity registration in elastic arteries type one should perform synchronic registration of pulse on carotid artery and femoral artery (in inguinal area). On difference between SPG beginning (time) and on the basis of vessels longitude one can count distribution velocity (under norm it is equal to 4-8 m/sec). For pulse wave distribution velocity registration in muscular arteries type one should register synchronically carotid pulse and radial pulse (on radial artery). The counting is the same. The velocity under norm is 6-12 m/sec, thus, more significant comparatively to the same for elastic arteries.

By means of mechanocardiograph one can register simultaneously pulse on carotid, femoral and radial arteries with following indexes estimation.

Diagnostical importance: For vascular wall pathology diagnosis. Treatment effectiveness evaluation (applied at this pathology). For example, at vessels sclerosis pulse wave velocity is increased due to

increased rigidity of vascular wall. In course of physical training sclerosis intensiveness is decreased and it is reflected on pulse wave distribution velocity diminishing.

SPG analysis principles: 1. SPG shape assessment: apex shape, incisura depth, dicrote altitude. At low

peripheral contraction SPG has sleeply arising anacrote, acute apex and deep incisura. High periperal pulse is an opposite phenomenon.

2. SPG altitude assessment. It doesn’t have its absolute value. It is conducted according to its main components correlation with main wave size.

3. Time correlations (in per cent) – from systolic wave general duration. 4. Pulse velocity investigation. Central and peripheral pulse SPG synchronic

record, distance determining from one measure point to another: V=l : (t of central pulse – t of peripheral pulse), where: l – distance from measure point of central and peripheral pulse; t – central and peripheral pulse origin. Pulse velocity in children – 4 m/sec; elder people – 10 m/sec (because of vessels

elasticity decreasing).

Task 3. To determine arterial pressure under rest and after physical loading. Arterial pressure is determined by auscultative method on Korotkov. To measure pressure right after physical loading (20 sitting down for 30 sec) and

then in 5 min. To determine heart-vascular system reaction type according to the observed reaction on physical activity.

Type I – normotonic – systolic pressure insignificant increasing and unchanged or a little increased diastolic pressure.

Type II – hypertonic – both systolic and diastolic pressure is increased significantly.

Type III – hyposthenic – insignificant decreasing (up to 10 mm merc col) both of systolic and diastolic pressure.

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Type IV – asthenic – heart activity frequening at systolic arterial pressure insignificant changings.

If restoration period is prolonged at II, III and IV reaction types more than onto 5 min, than such reactions are considered to be inadequate, they testify to heart-vascular system low functional ability.

5. Literature recommended: 1.Lecture course. 2.Mistchenko V.P., Tkachenko E.V. Methodical instructions for dental students (short lecture course).-Poltava, 2005.-P.35-36. 3. Mistchenko V.P., Tkachenko E.V. Methodical instructions for medical students (short lecture course).-Polatava, 2005.-P.57-64 4. Methodical instructions on chapter “Cardiac-vascular system physiology” on practical classes for dental and medical students. 5. Concise Physiology /Guyton-Ganong-Chatterjee. Ed. By Dr Gull R.Sh.-Lahore: K.E.Medical College.-1998.-P.61-65, 92-94, 102-104. 6. Kapit W., Macey R.I., Meisami E. The Physiology Colouring Book: Harpers Collins Publishers, 1987.-P.32, 33, 38, 40, 42. 7. Bullock J., Boyle III J., Wang M.B. Physiology.-1991.-P.124-127. 8. Stuart Ira Fox. Human Physiology.-8-th Ed.-Mc Graw Hill, 2004.-P.429-439. 9. Seeley R.R., Stephens T.D., Tate P. Essentials of Anatomy and Physiology.-he 3rd Ed.-McGraw Hill, 1999.-P. 350-353. 6. Materials for self-control: Control questions: 1. Hemodynamics laws. 2. Arterial pulse, pulse wave velocity. 3. Pulse clinical characteristics. 4.Sphygmogram analysis. 5. Blood pressure determining methods. 6. Factors influencing on blood pressure level. 7. Terms “pulse pressure”, “hemodynamic pressure”. 8. Pressure changes in course of physical activity.

LESSON 47 VESSELS ROLE IN BLOOD CIRCULATION. HAEMODYNAMICS LAWS.

RHEOENCEPHALOGRAPHY 1. The topic studied actuality. Rheography is widely used in dentistry for

maxillar-dental system vessels assessment. It is bloodless method. It allows to investigate tissues, organs or body separate parts blood supply. This method is based on tissues resistance graphical registration in course of electrical current transmission through them.

Pulp hemodynamics assessment method is called rheodentography while parodont tissue – rheoparodontography. One can also to register oral mucosa

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rheogram. These investigative methods are performed in therapeutic (operative and restorative) dentistry.

Rheography application in surgical dentistry for circulation and vessels state determining is of essential importance because these factors determine tissular trophycs and regenerative possibilities. All this influence greatly on surgical treatment effectiveness of many diseases of maxillar-facial region.

In orthopedic (prosthetic) dentistry rheography is used for pulp and parodont functional state assessment in course of denturing (particularly with removable dentures), traumatic overloading degree determining and also for parodontosis orthopedic treatment effectiveness control.

Pediatric dentistry has great possibilities and prospects for parodontal tissues reactivity investigation, superior lip and palate circulation assessment in course of cheilo- and uraniscoplasty (uranoplasty), in course of dentition anomalies orthodontic treatment.

Rheography changes can be observed at hypotonic, hypertonic disease as well as vegetative-vascular dystony. The latest state is observed in every second person nowadays. Sometimes the diagnosis can be proven only on the basis of this valuable diagnostic method data.

2. The study aims: To know: main hydrodynamics laws and their possibility to be used in

hemodynamics; vascular bed functional differentiation and its role in hemodynamics.

To be able to: measure arterial pressure, analyze rheogram. 3.Pre-auditory self-work materials. 3.1.Basic knowledge, skills, experiences, necessary for study the topic:

Subject To know To be able to Anatomy Vessels anatomy Show main vessels on



Vessels histological peculiarities: layers, cells and fibers

To know main vessels types on the preparations


Patho-morphological changings of vessels


Pathophysiology

Hypertonic, hypotonic disease and vegetative-vascular dystony forms and pathophysiological mechanisms

Internal Diseases

Vessels physiological peculiarities in different-aged adults; hypertonic and hypotonic disease as well as vegetative-vascular dystony ethiology, pathogenesis, clinics, therapy and prevention principles

To treat and to prevent hypertonic and hypotonic disease as well as vegetative-vascular dystony

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3.2.Topic content. Functional vessels classification:

1. Elastic: · aorta; · pulmonary artery; · other large vessels.

2. Muscular: · middle arteries; · shallow arteries.

3. Resistive (vessels of resistance): · ending arteries; · arterioles.

4. Of exchange (exchangeable): · capillaries.

5. Cavitary: · veins; · venules.

HEMODYNAMICS is circulation physiology chapter using hydrodynamics laws

for investigating blood movement through vessels. Hemodynamics main indexes:

– volumary velocity; – linear velocity; – velocity of blood circle (14-20 sec under physiological conditions); – pressure in different areas. Systemic hemodynamics represents blood movement in heart and magistral

vessels. Regional (organic) hemodynamics is organs blood supply. Tissular hemodynamics or microcirculation – tissues blood supply, blood

movement in the shinest vessels. Blood movements through the vessels obey to some regularities known as

hydrodynamics laws. But they are named as hemodynamics laws according to blood vessels.

Hemodynamics laws. The I-st law. Q=ΔP:R, where Q – blood supply volumary velocity, ΔP – pressure

difference in vascular bed beginning and end (pressure gradient). Blood stream volumary velocity is rised at pressure difference increasing in blood vessels arterial and venous parts and hydrodynamic resistance lowering.

The II-nd law. Q=рr4 : 8ηl x ΔP, where Q – blood supply volumary velocity, ΔP –

pressure difference in vascular bed beginning and end (pressure gradient), r – the vessel radius, l – the vessel length, з – blood viscosity. Blood stream volumary velocity is directly proportional to the vessel radius change and oppositely proportional to blood viscosity as well as the vessel length.

Taking into account that radius is in the fourth power it becomes clear that radius change plays major role in vascular bed adaptive reactions.

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The III-rd law. Laplas' law. The less is the vessel radius and the thinner is blood vessel wall, the less is its tension at equal pressure.

Capillaries wall tension is less in 10 thousands times than in aorta and in 1300 times than in cavitary vein. That is why capillary the wall of which consists of 1 layer is not ruptured under stretching power action.

Factors determining hemodynamics peculiarities (3 first are the main, rest

are additional ones): – pressure; – resistance; – velocity; – vessel diameter and length; – blood content; – pressure gradient; – blood flow type (see below); – blood viscosity et al. Vessel radius depends on vascular wall smooth myocytes tone. Smooth

myocytes contraction leads to radius lowering, resistance increasing as a result of which volumary velocity is decreased. The bigger is viscosity, the bigger is radius and less is volumary velocity. The bigger is the vessel length, the higher is resistance and the less is volumary velocity. Vessels length is constant in the biggest areas, that is why it is paid less attention but there are organs performing periodical or rhythmical activity:

– lungs – length is increased at inspiration; lungs volume increasing during inspiration increases vessels resistance due to their constriction and prolonging; – heart – coronary vessels length is changed dependently on cardiac cycle stage; – alimentary tract – overstretching with food increases length. Circulation peculiarities: – one-sided blood traffic through vessels; – its continuosity; – laminarity; – turbulent character. One-sided movement - is provided by pressure gradient (difference) at the

beginning and at the end of vascular system. It is 120-150 mm merc col. in initial circulation part and 5-0 mm merc col - in ending part (veins inflowing into heart).

Circulation continuosity – is linked with vessels elasticity, when blood is pumped in aorta by heart (it possesses elasticity) then all its volume can not come through the vessels at once. More blood part is remained temporarily in dilated (due to elasticity) aorta region and then (in course of diastole) leaves it due to aorta walls muscular contraction. The more elastic is aorta and other large arteries, the better circulation continuosity is realized. And on the contrary, at elasticity loss (with ageing, at sclerosis and other vessels injuries) circulation continuosity is disturbed.

Laminar or streamline and turbulent character of blood circulation movement character through vessels. Laminar circulation - is blood movement by separate layers in parallel to vessel axis (it is realized practically in all vessels). Erythrocytes move in the vessel center because they are the hardest, then leucocytes and platelets while plasma layer is attached directly to the vessel wall. Red blood cells

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increase blood viscosity and that is why they are in the vessel center for correct, undisturbed circulation. Turbulent circulation – with blood turbulence – occurs in the places of dilations, constrictions, flexures and pressures on them. Turbulent flow increase liquid internal friction that lowers volumary velocity.

Blood movements velocity types: 1. Volumetric velocity – blood amount flowing through transversal vessel section

in time unit. It is expressed in ml/min and depends on pressure gradient at vessel beginning and end as well as on resistance to blood stream. Its size depends on organ state (for instance, in course of muscular activity this velocity increases in them in tens times). This velocity is determined by rheography method.

2. Linear velocity – distance which blood particle passes through time unit. It is determined in m/sec and is under norma:

– in aorta – 0,5-1,0 m/sec, – large arteries – up to 0,5 m/sec, – in veins – 0,25 m/sec, – in capillaries – 0,05 m/sec. Investigation methods: direct – stains and different substances introduction;

indirect – ultrasound. 3. Circulation velocity – blood transport time on circulation circle. Norma: 14-20

sec. Investigative methods: radioactive.

Capillary circulation and its peculiarities Circulation in this part provides its main function – exchange between blood and

tissues. That’s why main link in this system – capillaries – they are called exchangeable vessels. Their function is tightly linked with vessels they are originated from - arterioles and vessels they come into (inflow) – venules. There exist direct arterio-venous anastomoses, connecting them out off capillaries. Mentioned vessels plus lymphatic capillaries are microcirculation system. This is main link of blood circulation system. Main reasons of diseases biggest part are in this region. Capillaries are the base of this system. Under rest state in norma only 25-35 per cent of them are opened, i.e. in working state; if more – one can see haemorrhagias and even organism death from internal bleeding, because blood is accumulated in capillaries and doesn’t reach heart.

Capillaries are located in intercellular spaces and that’s why metabolism occurs between blood and intercellular fluid.

Capillary exchange factors: 1. Hydrostatic pressure difference between capillary origin and its end (30-40 mm

and 10 mm merc col correspondingly). 2. Low blood movement velocity (0,05 m/sec). 3. Filtration pressure (difference between oncotic pressure in intersticium and

hydrostatic pressure in arterial capillary end – 15 mm merc col.). At its increasing – liquid comes into vessels and cellular dehydratation is developed.

4. Reabsorbtion pressure (difference between hydrostatic pressure in venous capillary end and oncotic pressure in intersticium – 15 mm merc col.). At its increasing – liquid (fluid) maily comes into tissues and oedemas are developed (for example, at proteins deficiency).

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Capillary pulse (or Kwinke pulse) – pseudopulse, linked with rhythmical oscillations at small arteries dilation in course of ventricules systole. It is easily observed at thermal procedures: if one attaches mirror to lips small vessels pulsation is seen. But more often such pulse is pathology sign: aortal insufficiency, thyreotoxicosis.

Figure 37. Microcirculative bed.

Venous circulation Veins are cavitary vessels, approximately 70-80 per cent of blood are located in

them; they possess large ability to stretching and comparatively low elasticity. Their internal surface has valves (with exception of shallow veins, portal veins and cava veins) which:

– encourage blood stream to the heart; – prevent its regurgitation (movement ahead); – protect heart from excessive energy consumption to blood oscillative movements overcoming. Blood in veins come rapidly despite low pressure in them. Why? – Pressure gradient in blood circulation arterial and venous ends; – heart residual force; – thorax suckering action (respiratory pump); – sceletal muscles contractions (muscular pump); – diaphragm activity.

Lymphatic circulation It’s necessary for fluid and substance (proteins) excessive amount, particles

(microbes and others) removal; it serves as messengers between blood and cells. Blood comes into lymph, lymph – in tissues, from tissues in blood and on the contrary.

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Lymphatic system: · lymphatic capillaries; · lymphatic vessels; · lymphatic nodes.

Lymphatic capillaries - capillaries beginning blindly, which consist of endothelial tubules systems penetrating tissues. Their cavity is wider comparatively to blood capillary, endotheliocytes are larger, fissures between them are bigger, basal membrane is absent. Some organs don’t have any lymphatic capillaries such as cutaneous (skin) epithelium, mucosae, placenta, brain.

Lymphatic vessels look like blood vessels, but they are thinner, muscular layer is less developed and there are many constrictions (valves) in them. Valves are pair intime plicas directed one opposite other and creating activity like in locks (sluices).

Lymphatic nodes perform very significant role in organism. One can tell about following main functions: 1) haemopoiesis (lymphopoiesis); 2) filtration – lack of:

· side bodies; · bacterias; · tumor (particularly malignant) cells; · toxins; · side proteins.

3) immunity: · plasmocytes production; · antibodies production; · T- and B-lymphocytes differentiation.

4) participating in metabolism of: · proteins; · fats; · vitamins.

Lymph This is product of blood, cells, intersticial fluid. That’ s why its content is similar to

all these compounds. Its reaction is alkaline, it has proteins (fibrinogen and other coagulation factors), lymphocytes, salts, fats and other substances. Daily production is up to 2,0 l of lymph.

Lymph types (according to lymphocytes number): · peripheral (0,5 x 109/l); · central (passing through lymphatic nodes where lymphocytes amount is from 2,0

to 20,0 x 109/l). Lymph formation stages:

· tissular liquid formation; · proper lymph formation; · lymph movement through vessels.

Tissular fluid formation occurs in capillaries. Tissues and blood osmotic pressure difference is essential for this. Under physiological conditions lymph formation from tissular fluid is insignificant (because filtration and reabsorbtion pressures are equal - see above). At oncotic pressure reducing (at protein deficiency in fasting) filtration pressure is rised up and reabsorbtion pressure is decreased. Fluid in such a case

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will come in tissues that leads to swelling (oedema) development. But such a phenomenon will be in course of physical training too: filtration pressure increases due to capillary presure increasing (the result of hydrostatic pressure increasing in magistral vessels). Fluid amount in tissues will grow too (muscles increase their weight to 20 per cent). Lymphatic vessels begin their active functionning and take fluid excessment off.

But tissular liquid is not yet a lymph. It becomes itself when fluid passes into lymphatic vessels. Lymph formation is a rather complicated process. One can differentiate both physico-chemical reactions (diffusion, permeability, osmotic pressure) and secretory process (cellular secretion) in it. There are some substances increasing lymph formation. They are known as lymphogonic: peptones, hystamine et al. Some food products also possess lymphogonic features: crabs, squids, strawberry et al. Leeches action is based on this.

Lymph movement is realized due to: · lymphatic vessels walls contraction (8-20 times per 1 minute); · negative pressure in thorax; · muscular contractions (intramuscular lymphatic heart). This mechanism lymph

movement through vessels is essential for massage performance. At hypodynamy when this mechanism is disturbed, lower extremities oedemas are developed.

Lymph while proteins return from intercellular fluid to blood participates in fluid balance (equillibrium) support into tissues.

CARDIAC OUTPUT

Cardiac output is the amount of blood pumped from each ventricle. Usually, it means the left ventricular output rough aorta into various organs of the body. Cardiac output is the most important factor in cardiovascular system, because, the rate of blood flow through different parts of the body depends upon the cardiac output.

DEFINITIONS AND NORMAL VALUES Cardiac output is expressed in three ways, stroke volume, minute volume and

cardiac index. However, in routine clinical practice cardiac output refers to minute volume.

1. STROKE VOLUME The stroke volume is defined as the amount of blood pumped out by each

ventricle during each beat. Normal value is 70 ml (60 to 80 ml) when the heart rate is normal (72/minute).

2. MINUTE VOLUME This is the amount of blood pumped out by each ventricle in one minute. This is

the product of stroke volume and heart rate. Minute Volume = Stroke volume x Heart rate. Normal value is 5 liters/per ventricle/minute.

CARDIAC INDEX The minute volume from ventricle expressed in relation to square meter of body

surface area is called cardiac index. It is defined as the amount of blood pumped out of ventricle per minute per square meter of the body surface area. Normal value is 2.8 ± 0.3 liters/one square meter of body surface area/ minute. The body surface area of a normal adult is 1.734 square meter.

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EJECTION FRACTION The fraction of end diastolic volume that is ejected out by each ventricle is called

ejection fraction. Normally, it is 60-65%. CARDIAC RESERVE

The maximum amount of blood that can be pumped out by the heart above normal value is called cardiac reserve. Cardiac reserve plays important role in increasing the cardiac output during the conditions like exercise. This is essential to withstand the stress of exercise.

Cardiac reserve is usually expressed in percentage. In normal young healthy adult, the cardiac reserve is 300 to 400%. In old age it is about 200 to 250%. It is increased to 500 to 600% in athletes. In cardiac diseases, the cardiac reserve is minimum or nil.

VARIATIONS IN CARDIAC OUTPUT PHYSIOLOGICAL VARIATIONS

1. Age: In children, cardiac output is less because of less blood volume. The cardiac index is more than in adults because of less body surface area. 2. Sex: In females, cardiac output is less cardiac index is more than in males, because of less body surface area. 3. Body build: Greater the body build, more is the cardiac output. 4. Diurnal variation: Cardiac output is low in early morning and increased in day time. It depends upon the basal conditions of the individuals. 5. Environmental temperature: Moderate change in temperature does not affect cardiac output. Increase in temperature above 30°C raises cardiac output. 6. Emotional conditions: Anxiety, apprehension and excitement increase cardiac output about 50 to 100% through the release of catecholamines which increase the heart rate and force of contraction. 7. After meals: During the first one hour after taking meals, cardiac output is increased. 8. Exercise: Cardiac output is increased depending upon severity of exercise because of increase in heart rate and force of contraction. 9. High altitude: In high altitude, the cardiac outputs increased because of the secretion of adrenaline due to lack of oxygen. 10. Posture. While changing from recumbent to upright: position, the cardiac output is decreased because of pooling of blood in lower limb. 11. Pregnancy: During the later months of pregnancy cardiac output is increased by 45 to 60%. 12. Sleep: Cardiac output is slightly reduced unaltered during sleep.

PATHOLOGICAL VARIATIONS Increase in Cardiac Output Cardiac output is increased in the following conditions: 1.Fever: Cardiac output is increased due to increased oxidative processes at

fever. 2.Anemia: Cardiac output is increased due to hypoxia. 3.Hyperthyroidism: Due to increased basal metabolism, cardiac output is

increased. Decrease in Cardiac Output Cardiac output is decreased in the following conditions:

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1.Hypothyroidism: Due to the decreased basal metabolism, cardiac output is decreased. 2.Atrial fibrillation: Because of incomplete filling, cardiac output is decreased. 3.Incomplete heart block with coronary sclerosis or myocardial degeneration: Cardiac output is decreased because of defective pumping action of the heart. 4.Congestive cardiac failure: Cardiac output is less because of weak contractions of heart. 5.Shock: Cardiac output is reduced because of poor pumping and circulation. 6.Hemorrhage: Because of decreased blood volume, cardiac output is less.

DISTRIBUTION OF CARDIAC OUTPUT The whole amount of blood pumped out by right ventricle to lungs. And, the blood

pumped by left ventricle is distributed to different parts of the body. The distribution of cardiac output is according to the metabolic activities of various regions of the body.

The heart, which pumps the blood to all the other organs receives least amount of blood.

FACTORS MAINTAINING CARDIAC OUTPUT 1. Venous return 2. Force of contraction 3. Heart rate 4. Peripheral resistance.

VENOUS RETURN This is the amount of blood, which is returned to the heart different parts of the

body. When it is increased, the ventricular filling is increased and cardiac output is increased. Therefore, the cardiac output is directly proportional to venous return provided the other factors remain constant. If venous return increases and heart rate decreases, the cardiac output cannot increase. Venous return in turn depends upon five factors:

1. Respiratory pump. 2. Muscle pump. 3. Gravity. 4. Venous pressure. 5. Vasomotor tone. 6. Respiratory pump. 1. Respiratory pump During inspiration, the intrapleural pressure (intrathoracic pressure) becomes

more negative. At the same time, descent of diaphragm increases the intraabdominal pressure. This compresses abdominal veins and pushes the blood upward towards the heart. Because of negative pressure in thorax, the diameter of inferior vena cava is increased with reduction in pressure inside. And, due to increased intraabdominal pressure, the flow of blood into right atrium is increased. This action of respiration is called respiratory pump. Respiratory pump is much stronger in forced respiration and in severe muscular exercise.

2. Muscle Pump During muscular activities, the veins are compressed or squeezed. Due to the

presence of valves in veins, during compression the blood is moved towards the

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heart. This is called the muscle pump. When muscular activity increases the venous return is more.

When the skeletal muscles contract, the vein located in between the muscles is compressed. The valve of the vein proximal to the contracting muscles is opened and the blood is propelled towards the heart. The valve of the vein distal to the muscles is closed by the back flow of blood.

During the relaxation of the muscles, the valve proximal to the muscles closes and prevents the back flow of the blood. And the valve distal to the muscles opens and allows the blood to flow upwards.

3. Gravity Gravitational force reduces the venous return. When a person stands for a long

period, gravity causes pooling of blood in the legs, which is called venous pooling. Because of venous pooling, the amount of blood returning to heart decreases.

4. Venous Pressure and larger veins, the pressure gradually decreases. In the great veins, i.e. inferior vena cava and superior vena cava, the pressure falls to about 5.5 mm Hg. At the junction of vena cavae and right atrium, it is about 4.6 mm Hg. The pressure in the right atrium is still low and it alters during cardiac action. It falls to zero during atrial diastole. This pressure gradient at every part of venous tree helps as a driving force for venous return.

5. Sympathetic Tone The venous return is aided by sympathetic or vasomotor tone also. The

sympathetic tone causes constriction of venules. This venoconstriction pushes the blood towards heart.

2. FORCE OF CONTRACTION The cardiac output is directly proportional to the force of contraction provided the

other three factors remain constant. Force of contraction depends upon diastolic period and ventricular filling. Frank Starling's law of heart is applicable to this.

According to Frank Starling's law, the energy liberated by the heart when it contracts is a function of length of its muscle fibers at the end of diastole, i.e. the force of contraction of heart is directly proportional to the initial length of muscle fibers before the onset of contraction.

During diastolic period due to the ventricular filling, the muscle fibers are stretched resulting in increase in the length of muscle fibers. This increases the end diastolic pressure in the ventricle, which is called pre-load. This determines the force of contraction.

At the end of isometric contraction period, the semilunar valves are opened and blood is ejected into the aorta and pulmonary artery. This increases the pressure in these vessels. Now, the ventricles have to work against this pressure for further ejection. This pressure in aorta and pulmonary artery is called after-load.

3. HEART RATE Cardiac output is directly proportional to heart rate provided the other three

factors remain constant. Moderate change in heart rate does not alter the cardiac output. If there is a marked increase in heart rate, the diastolic period is shortened and ventricular filling reduces. This results decrease in cardiac output.

During marked decrease in heart rate, the diastolic period is prolonged while other factors remain constant. Hence, the ventricular filling is more and cardiac output is more.

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4. PERIPHERAL RESISTANCE This is the resistance or load against which the heart has to pump the blood. So,

the cardiac output is inversed, proportional to peripheral resistance. Peripheral resistance is the resistance offered to bloc: flow at the peripheral

blood vessels. The resistance; offered at arterioles. So, the arterioles are called resistor; vessels. In the body, the maximum peripheral resistance is offered at the splanchnic region.

MEASUREMENT OF CARDIAC OUTPUT Cardiac output can be measured by direct methods or indirect methods. A. Direct methods (in animals only) 1. By using cardiometer 2. By using flowmeter B. Indirect methods (in animals and humans) 1. By using Fick's principle 2. By using indicator dilution technique or dye dilution technique. 3. By thermodilution technique 4. By using ballistocardiography By Using Fick's Principle According to Fick's principle, the amount of a substance taken up by an organ (or

by the whole body) or given out in a given unit of time is the product of amount of blood flowing through the organ and the arterial-venous difference of the substance across the organ.

Amount of Amount of Arterio – substance = blood * venous taken or given flow/minute difference

Modification of Fick's Principle to Measure Cardiac Output The Fick's principle can be modified to measure the cardiac output or a part of

cardiac output (amount of blood to an organ). Thus, cardiac output or the amount of blood flowing through an organ in a given unit of time can be determined by the formula given below.

Amount of substance taken or given by the organ/minute Cardiac output = Arterio-venous difference of the substance across the organ By modifying Fick's principle, cardiac output is measured in two ways:

– By using oxygen consumption – By using carbon dioxide evolved.

Measurement of Cardiac Output by Using Oxygen Consumption Fick's principle can be used to measure cardiac output by determining the

amount of oxygen consumed in the body in a given period of time and dividing this value by the arterio-venous difference across the lungs.

O2 consumed (in ml/minute) Cardiac output = Arterio-venous O2 difference Oxygen consumption: To measure the amount of oxygen consumed, a

respirometer or BMR apparatus (Benedit Roth apparatus) is used. Oxygen content in arterial blood: For determining the oxygen content in arterial

blood, blood is collected from any artery.

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Oxygen content in venous blood: For determining the oxygen content of venous blood, only mixed venous blood is used, since oxygen content is different in different veins. The mixed venous blood is collected from right atrium or pulmonary artery. This is done by introducing a catheter through basilar vein of forearm.

4. Materials for auditory self-work. 4.1. List of study practical tasks necessary to perform at the practical class. Materials and methods: rheopletysmograph, particles flow indicator for relative

circulation velocity determining, rheograph, rheograms. Investigated object: human being.

Task 1.

Systolic and minute circulation volume determining under rest and after physical loading.

Under resting condition the investigated person is investigated systolic and diastolic pressure on Korotkov. One should estimate pulse pressure (PP), ask age (A), determine pulse rate (PR). The data received must be putted in Starr’s formula for circulation systolic and minute volume estimation:

SV=1001+0,5PP-0,6DP-0,6A; DV=SV x PR. The similar estimation should be performed with the data received after physical

loading (20 sitting down for 30 sec).

Task 2. To determine relative circulation velocity by means of particles flow

indicator (demonstration). One division of such device is equal to 5 units. It can determine relative linear

velocity (divisions amount x 5 x 10 sm/sec, putted on the device). One can compare sounds in veins like wind, rain or storm noise, the sound is coarse, low, it doesn’t pulsate and is not diminished. Sounds over the arteries have another characteristics: they pulsate, can be reduced; the deeper vessel is located, the better sound can be heard because of lower density.

Device significance:

Atherosclerotic process localization determining. Plaque at blood shock change arterial pressure, pulse velocity, linear velocity.

Treatment effectiveness assessment on collateral circulation repair degree. Surgeon in course of operation can determine, vein or artery is near him. Such determining helps to give medical care faster and more effective (because

one drugs surve for intravenous injection, others – for intraarterial application). At shock, collapse, sudden children’s death syndrome all drugs must be injected

intraarterially. Congenital heart and vessels vice – aorta coarctation – can be diagnosed only by

means of such device usage (and, less exact, by means of palpation): pulse is more expressed on upper extremities than on lower extremities; linear velocity is more expressed on upper extremities too. As it is known, under physiological conditions both pulse and linear velocity are larger on lower extremities comparatively to upper ones.

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Task 3. To perform extremities rheogram record and to get acquanted to main

rheographic indexes. Rheography is a powerful, diagnostically available investigative method for

general and organ circulation assessment. It is based on organism alive tissues electrical resistance fluctuations registration in course of electrical current passage through them. Neutral for organism and non-sensitive high-frequented (from 100 to 500 kHz) and small force (up to 10 mA) uncostant current is used.

Alive tissues are good conductors. Maximal conductiveness is the characteristics of blood, minimal one – bones and skin. There exists reverse dependence between electroconductiveness and resistance: the more electroconductiveness is, the less resistance is. There is important rule: the more significant tissular circulation and blood-filling in tissues are, the more electroconductiveness and less resistance are.

Tissue electroconductiveness degree depends on tissular circulation and blood-filling. At the moment of increased circulation appearance in interelectrode space in course of systole the electrical conductiveness is increased which is accompanied by rheographic wave resistance decreasing and its altitude increasing. In course of diastole blood outflows from the tissues electrical conductiveness is reduced, resistance is increased and rheographic wave altitude is decreased.

There are 2 main rheography types: bipolar (usual, two-electrodic) and tetrapolar. Electrodes are plate-like and ring produced by: lead, copper, brass and

aluminum foil. For extremities rheogram registration one should use electrode, which must be

putted longitudinally on arm and fore-arm or on femur and tibia. The more distance between two electrodes is, the more significant resistance fluctuation is between them and thus the higher rheographic waves are.

The investigation should be performed: · in patient’s horizontal state; · on an empty stomach or in 2 hours after eating; · after 10 min of resting; · at air temperature equal to 20-22°C.

The investigated person must be lied down before 15 min comparatively to investigation beginning. After the device adjusting and electrodes putting the rheogram is registered and after this – caliber signal in 0,1 Om, while pressing calibrator button. Paper movement velocity should be 50 mm/sec. Rheogram is registered at patient’s usual (shallow) expiration. One should register and record 4-5 rheogram cycles for rheographic waves clinical assessment.

For resistance diminishing skin of investigated area is processed with alcohol, two-layed flannel paddings washed in 5-10% sodium chloride or 2% sodium hydrocarbonate must be putted between skin and electrodes. In other cases electrodes are lubricated with thin layer of current-conducting paste. Electrodes should be fixed strongly with rubber belt. It is so-called bipolar rheography (current electrodes are measured at the same time).

Now several words about tetrapolar rheography. The investigative zone is limited by 2 measure electrodes out of which 2 current electrodes should be placed. At such method paddings and paste are excessive and are not used. Electrodes are fixed on the body investigated area after its fats deprivation with alcohol.

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There can be several reasons of rheogram results perversion: -electrodes incomplete attachment; -electrodes non-correct fixation; -skin dryedness; -muscular trembling; -patient’s movements; -external electrical obstacles; -bad rheograph earth (ground); -bad patient’s earth. One can differentiate 2 main rheogram parts:

· systolic (main); · diastolic.

Systolic wave, occurring rhythmically after each heart systole, reflects arterial blood inflow to the investigated area (blood-filling intensiveness).

Diastolic part depends significantly on venous blood outflow. Systolic wave consists of:

· anacrote (ascendant part) (norm: 0,1±0,01 sec); · apex; · catacrote (descendant part) – up to incisura; · dicrote (secondary diastolic wave);

sometimes systolic wave is preceded by presystolic wave the genesis of which is considered to be delt with atria contractions.

Main wave is origined from the point which corresponds to blood rapid inflow beginning to the investigated area. One can differentiate also curve maximal peak which characterizes fast filling maximal velocity. Further, curve ascendance is retarded (slow filling phase) with next transformation to rounded apex, which corresponds to the moment when blood inflow is equal to blood outflow and blood-filling velocity is equal to zero. Gently sloping descendance follows apex and indicates to blood outflow predominance over blood inflow. Descendance is ended with incisura after which rheogram curve diastolic wave is origined. Incisura corresponds to semilunar valve closage. Dicrotic dense is the sign of secondary or diastolic wave beginning.

Differentiated rheogram - i.e. main rheogram first derivate, characterizes blood inflow and outflow in the investigated area. It characterizes investigated area blood filling velocity changings and allows to receive data about vascular tone.

Differentiated rheogram allows: · to amplify volumary rheogram distinctive points localization; · to determine blood filling velocity at any time moment.

Rheogram qualitative analyzis: · pulse waves regularity; · ascendance and descendance steepness; · apex character; · incisura expression; · dicrote expression.

Healthy people rheogram: · systolic wave steep ascendance; · gently sloping descendance;

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· sharpened apex; · good expressed incisura.

Hypertonics rheogram (arteries elasticity decreasing): · altitude reducing; · apex rounding; · curve gently sloping due to dyastolic waves disappearance.

Hypotonics rheogram (arteries elasticity increasing, veins elasticity decreasing): · altitude rising up; · incisura increasing (deepening); · apex sharpening; · high dicrote.

Rheogram at dystonia:

· the worst; · it is diagnostically with the biggest difficulties: for example, there can be altitude

increasing and incisura decreasing. Arrhythmias:

· curves irregularity. Left ventricle systolic overloading:

· slow ascendance. All this is the expression of rheogram qualitative analysis.

Figure 38. ECG – electrocardiogram. T- pulse wave distribution wave; A-D – distance from curve ascendance beginning to dicrotic wave origin; H1 – main wave altitude; H2 – dicrotic (reflected) wave altitude. RG – rheogram;

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Figure 39. Rheogram of brain vessels (rheoencephalogram) REG – rheoencephalogram; ECG – electrocardiogram; Diff. – differentiated rheogram; PhCG – phonocardiogram. Rheogram quantitative analysis means such indexes determining as: Rheographic index (RI) – rheographic wave altitude (h2, in mm) relation to

calibre impulse size (K, mm): RI=h2 (mm):K (mm). Norm: 1,5±0,01 cm. It characterizes pulse blood-filling level on investigated area. II. Altitude (h2, Om) – It characterizes pulse blood-filling level and is counted by

means of division of altitude measured from its apex to maximal (the highest) point (h1, mm), in calibre signal size (in mm) and multiplication the ciphra received on calibre signal (in Om):

h2=h1 (mm) : K (mm) x K (Om). Norm: 0,12-0,13 mm. III. Altitude-rate index (ARI) – rheographic indcx (RI) relation to cardiac cycle

duration (R-R, sec): ARI=RI : R-R (on ECG, registered in parallel). It characterizes volumary circulation level (through vessel transversal section in

course of 1 sec) in the investigated region. IV. Diastolic index (systolic-diastolic index)characterizes arterial and venous

circulation correlation and is estimated by formula:

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RDI=h2 : h4 x 100%, where RDI – rheographic diastolic index. Norma: 75%. It is used for venous outflow indirect assessment. V. Dicrotic index (tone index)characterizes arterioles tone (peripheral

resistance level) and is estimated by formula: DI=h3 (Om) : h2 (Om) x 100%. Norm : 40-70%. VI. Rheographic wave distribution time on area “heart – investigated area”

(Q-A). Synonym: rigidity index. Norm: on the right – 0,192, on the left – 0,183. It is defined from ECG dense Q beginning to rheogram wave beginning. It is

reduced at: - hypertony; - magistral vessels sclerosis. VII. Vessels systolic filling time (a) – It is and interval from systolic wave

ascendance beginning till perpendicular turned down from its apex (bc). It reflects arterioles tone and elasticity mainly average and large ones. VIII. Rapid blood-filling time (a1) – It is an interval from systolic wave

ascendance beginning to its sleepest ascendance in the point, projected from differentiated curve peak.

It characterizes large vessels walls rigidity and myocardium contractive function. IX. Slow blood-filling time

Is estimated on formula:

It depends on vascular wall rigid-viscous features. X. Rheographic co-efficient:

RC=a : R-R x 100% It reflects arterial tone state and excepts heart contraction rate influence on

systolic blood-filling time. XI. в : (R-R, sec) – catacrote duration relation to the cardiac cycle duration. It

depends on heart contraction rate and it becomes increased at venous outflow retardation.

The most important indexes in clinical practice are the following: · rheographic index; · diastolic index · dycrotic index.

Task 4. To get acquanted to rheography application in dentistry.

Rheodentogram – reflects circulation state in pulp under physiological and pathological conditions.

Rheoparodontogram – demonstrates parodont vessels structural changings and functional state in course of parodontitis, gingivites, treatment ways and methods assessment. Its configuration is changed in course of these diseases,

Oral mucosa rheogram – under norm very weak low-frequented oscillations are registered. In course of chronic recidivating aphthosis rheogram altitude isn’t changed but rheogram configuration character is changed.

For rheoparodontogram registration dental devices are putted on corresponding areas of alveolar process.

a2=a-a1 (sec).

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In healthy people one can see non-similarity of rheoparodontogram shape at different parodontal areas.

Incisors characteristics: - steep ascendant; - sharp apex; - steep descendant; - expressed incisura. Molars characteristics: - gently sloping ascendance; - apex like plataux or blunt angle; - non-distinct incisura expressiveness; - descendance gently sloping. Canines and premolars features: - rheogram has intermediate character between mentioned above. Rheographic index: -for incisors – 5,3-6,3; -canines – 6,3-7,0; -premolars – 5,6-6,4; -molars – 6,3-8,0. Parodontogram ascendance average duration: -for incisors – 0,13-0,15; -canines - 0,15-0,19; -premolars – 0,14-0,18; -molars – 0,17-0,20 sec. Descendance duration: -incisors – 0,72 sec; -0,80 sec – molars. In course of pathological conditions in parodont rheoparodontogram can be

changed: - curve apex is like blunt angle; - incisura and dicrote are expressed non-distictly and are replaced to its apex; - descendance duration is increased; - rheographic index is reduced; - ascendance duration is increased; - two latest features testify local blood circulation disorders. For rheodentogram registration electrodes are fixed on mucosa from vestibular

side (active) and from palatal side alongside root of the examined tooth (passive electrode). Rheodentogram reflects objectively blood stream state in pulpal area under physiological and pathological conditions.

In course of pulpitis rheodentogram altitude is increased.

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Figure 40. Intact tooth rheodentogram.The first wave – ECG. The second wave – RDG.

Figure 41. Rheoparodontogram of person with intact parodont.

Figure 42. Rheoparodontogram of sick person with parodontitis of heavy degree.

Figure 43. Rheoparodontogram at isolated (a) and generalized (b)

atherosclerosis of parodontal vessels.

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The first wave – ECG. The second wave – RPG. b) Calibrating signal – 0,1 Om.

Task 5. To get acquainted to pletysmography method

Pletysmography (from Greek “pletysmos” – increasing + “grapho” – to write, to descript) – body volume or its parts volume changings registration method. It is the method of understanding separate body parts volume fluctuations graphical method connected with vessels blood-filling in course of and under influence of functional loadings for blood circulation and vessels in a given area functional state investigation. In experimental investigation one can use visceral organs pletysmography (of liver, kidney et al.). Such a type is known as oncography. Special place has general pletysmography (or body pletysmography), which is clinically used for external respiration functions assessment and circulation minute volume investigation.

Pletysmography is based on liquids and gases feature to save constant volume at unchanged temperature and pressure that allows to transmit volume fluctuation of any body part putted in hermetic vessel (pletysmographic receptor), filled with air or water, to the registrating device.

Main elements Waves of the 1st order – or volumary pulse – reflect blood-filling fluctuations in

course of cardiac cycle. Each wave looks like sphygmographic wave. It has sleep ascendance, apex and descendance with additional “dicrotic” waves on it, the expression of which is rather different. Volumary pulse altitude id est wave expression from its base to its apex, characterizes maximal systolic growth of arteries blood-filling in course of blood pressure increasing in them on pulse pressure (difference between systolic and diastolic one).

Waves of the 2nd order - have respiratory waves period, are registered unconstantly; in course of usual breathing their altitude is usually lower than altitude of volumary pulse but in some cases, especially at dyspnoe and in obese people with highly-situated diaphragm it can be significantly more expressed.

Waves of the 3rd order – are all registered blood-filling oscillations with the period more expressed than respiratory waves period; sometimes they are relatively rhythmic and are considered as vascular-respiratory center periodics and activity. But more often these waves are aperiodic. Investigated person psychological training to the investigation influences greatly on their expression and existence. Under emotional quiet in a waking state one can usually register so-called zero pletysmogram (which include only waves of the 1st and the 2nd orders, moreover the waves of the 2nd order have minimal expression).

Pletysmogram application for vascular tone assessment is based on representation about tone as vascular wall myocytes tension that defines wall’s ability to be resilient to the tension, i.e. to express rigid features.

Clinical application As a diagnostic method pletysmography is mainly used at vascular diseases for

regional circulation state and disorders degree, arterial and venous tone objective assessment, for vessels functional and organic diseases differential diagnosis and also for treatment effectiveness definition. Interpretation of the data received is given taking into account special normal values. But more available diagnostically

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are symmetrical investigations of injured and uninjured vessels in one and the same patient and also pletysmograms dynamics under functional loadings and pharmacological probes influence.

At peripheral arteries obliterating diseases and Raynod disease there are several diagnostic signs: circulation significant decreasing, volumary pulse altitude reducing, dicrotic waves low expression or even absence.

For organic and functional arterial flow disorders nature differentiation one can use next probes:

– with physical loading; – with warmth; – with passive hyperemia; – pharmacological probes. For varicous dilation and prophound veins thrombosis diagnostics one can study

different parameters of venous filling and circulation by their changing by means of veins occlusion or investigated person body status changing. For example, one can see occlusional veins blood-filling increasing and significant venous reflux at patient’s transition from his lying pose to his staying at varicous disease; venous thrombosis is characterized by decreasing of their blood-filling volume and venous drenaige velocity.

So, this method is widely used in angiosurgery for vasculopathies diagnosis and differential diagnosis.

5. Literature recommended 1. Lecture course. 2.Mistchenko V.P., Tkachenko E.V. Methodical instructions for dental students (short lecture course).-Poltava, 2005.-P.30. 3.Mistchenko V.P., Tkachenko E.V. Methodical instructions for medical students (short lecture course).-Polatava, 2005.-P.56-59. 4. Methodical instructions on chapter “Cardiac-vascular system physiology” on practical classes for dental and medical students. 5. Concise Physiology /Guyton-Ganong-Chatterjee. Ed. By Dr Gull R.Sh.-Lahore: K.E.Medical College.-1998.-P.61-63, 65-68, 72-83, 104-111. 6. Kapit W., Macey R.I., Meisami E. The Physiology Colouring Book: Harpers Collins Publishers, 1987.-P.34-36, 38. 7. Bullock J., Boyle III J., Wang M.B. Physiology.-1991.-P.133-135, 121-124. 8. Stuart Ira Fox. Human Physiology.-8-th Ed.-Mc Graw Hill, 2004.-P. 419-422. 9. Seeley R.R., Stephens T.D., Tate P. Essentials of Anatomy and Physiology.-The 3rd Ed.-McGraw Hill, 1999.-P. 336-339. 6. Materials for self-control: Control questions: 1. Blood stream minute and systolic volumes (discharges). 2. Pletysmography and its importance in medicine. 3. Linear and volumetric blood stream velocities. 4. Rheography main principles. 5. Rheogram and its indexes. 6. Rheography peculiarities in dentistry (only for dental department students). 7. Rheography in therapeutic, surgical, orthopedic dentistry and dentistry of

childhood (only for dental department students).

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LESSON 48 HEART ACTIVITY AND BLOOD CIRCULATION REGULATION

INVESTIGATION 1. The topic studied actuality. Circulation adaptation to organism needs is

performed by means of central and peripheral mechanisms close interconnections. Regulatory mechanisms of heart-vascular system provides definite correlation between heart activity, vascular bed cavity and transversal square and also circulating blood amount. Tissues and organs blood supply optimal conditions are supported due to these indexes taking into account these organs and tissues functional state.

Circulation regulation is a providing blood minute volume level corresponding to organism needs due to heart ventricles systolic volume and its contraction rate change, resistive vessels (first of all arteries) diameter change or blood volume changing deponated in cavital vessels (veins).

Heart-vascular activity nervous regulation is determined both by influence of autonomic nervous system sympathetic and parasympathetic parts and brain central structures. There exists also local influence to heart. Significant role in such regulation has humoral mechanisms (hormones, metabolites, cellular metabolism products).

Circulation regulation in maxillary-facial area and oral cavity is performed by neuro- and myogenic mechanisms.

Resistive vessels constrictory reactions in this area on sympathetic fibres impulses are realized by means of noradrenaline releasing in their endings and by alpha-adrenoreceptors excitement. There are also beta-adrenoreceptors and cholinoreceptors in jaws vessels. Axon-reflectory mechanism is a very essential for parodont and dental pulp. Also blood vessels myogenic regulative mechanism is these regions characteristics. Arterioles and precapillary sphincters myogenic tone increasing leads to strong constriction or even to partial closure of microcirculative bed and limits significantly nutritive vessels (providing transcapillary exchange) square. It prevents enforced liquid filtration to tissues and blood intravascular pressure, i.e. it serves tissue physiological protection from oedema development. Circulation myogenic regulative mechanism has special role for dental pulp availability providing. For pulp, located in a closed space, limited by tooth walls, this mechanism is of essential importance for microcirculation regulation under physiological and pathological conditions, for instance, at inflammation. Vessels myogenic tone regulative mechanisms weakening is one of powerful factors for pulpar, parodontal oedema development and oral cavity other tissues in course of inflammation.

Resistive vessels myogenic tone is reduced significantly at functional loadings on tissues that leads to regional blood supply increasing and “working hyperaemia development”.

At parodontosis, when parodontal tissues blood supply is disturbed, functional loadings action (for example, in course of mastication), decreasing microvessels myogenic tone, can be used for treaty-preventive aims to parodont trophycs and blood supply improvement.

Oral cavity mucosa is a large reflexogenic zone, afferent impulsation from which can change heart activity and blood vessels tone. So, at gustatory receptors

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irritation with sweat substances extremities vessels dilation occurs, bitter substances cause their constriction.

Noceoceptive stimuli cause significant changings in blood circulation system. Such disorders can be changed dependently on irritation intensivity and organism reactivity. Cardiac activity changings way depends on heart beating initial velocity: it can be accelerated (tachycardia) or inhibited (bradycardia) after nociceptive irritation. Tachycardia is observed more freaquently in people with hypersympathicotony, bradycardia – at hypervagotony.

Any dental operation is a complicated emotional-painful factor which can change cardiac-vascular system state. Tooth preparation even in healthy people can cause changings in blood circulation system, the expression of which depends on organism individual features. Psycho-emotional tension can be even more expressed than the treatment itself. Complications from the side of circulation system are seldom in out-patient dental practice. For possible complications prediction and their liquidation dentist should pay special attention to patients with cardiac-vascular system pathology.

Any dental interfearence is a powerful stressogenic factor especially for the patients with down-regulation and heart-vascular system compensatory possibilities inhibiting. Complications prevention requires measurement performance directed first of all to emotional tension and pain diminishing and liquidation. Negative emotions cause arterial pressure significant rising up especially stongly in hypertonic disease patients. Such patients have expressed hemodynamic changings not only as an answer reactions to the dental operation but also to its waiting the reason of which is enforced psycho-emotional excitability and lability of nervous centres regulating arterial pressure. Though dental pathology character very often needs oral cavity sanation for heavy complications prevention by the side of main cardiac-vascular pathology.

Very often psycho-emotional tension occurring in patients in course of dental manipulations is so strong that can lead to short-termed arterial pressure increasing – crisis (unconscious state, fainting-fit) occurring as the result of brain circulation disturbances which acquire urgent aid from the doctor’s side.

Heart activity regulation is in providing of blood minute volume size proper to organism needs due to heart ventricles systolic volume and its contraction rate. Heart activity nervous regulation is determined by autonomic nervous system sympathetic and parasympathetic parts influence and also brain central structures. Under resting state sympathetic heart nerves possess moderate tonic activity. Vaguses more expressed impulsation opposes to it. Many hormones and other biologically active substances circulating into blood cause heart activity changings. Knowledge mechanisms providing changings in heart activity is necessary for doctors for proper diagnostics, correction under pathological conditions in cardiac-vascular system and also possible disorders prevention.

2. Study aims: To know: mechanisms of myogenic, humoral and nervous regulation of

heart activity and vascular tone To be able to: explain regulative mechanisms while physiological probes

performance 3. Pre-auditory self-work materials. 3.1.Basic knowledge, skills, experiences, necessary for study the topic:

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Subject To know To be able to Anatomy Vessels and heart anatomy Show main vessels on special

tables or alive preparations Histology, cytology and embryology

Vessels and heart histological peculiarities: layers, cells and fibers

To know main vessels types and heart layers on the preparations


Patho-morphological changings of vessels and heart


Pathophysiology Hypertonic, hypotonic disease, vegetative-vascular dystony and arhythmias forms and patho-physiological mechanisms

Internal Diseases Vessels physiological peculiarities in different-aged adults; hypertonic and hypotonic disease vegetative-vascular dystony ethiology, pathogenesis, clinics, therapy and prevention principles

To liquidate hypertonic and hypotonic crisis and arrhythmias without medicines while only physiological probes usage

3.2.Topic content. Heart and vessels work in complicated functional interrelations. Besides, heart

has its own (myogenic) regulative mechanisms. One of them – heterometric – is performed as answer to myocardium fibres length change (Starling’s law). Such cardiac regulative mechanism can provide circulatory insufficiency compensation and its anomalies. It is characterized by very high sensitivity. It may be observed at introduction of 1-2 % of all circulating blood mass in magistral veins.

Second myogenic regulative mechanism type is homeometric. Myocardial fibres ending dyastolic stretching degree is not important for its realizing. The most important is correlation between cardiac contractions and aortal pressure (Anrep’s effect): aortal pressure increasing causes initial heart systolic volume decreasing and then – heart contractions force increasing and cardiac discharge stabilizing at new contractions level.

Thus, heart activity myogenic regulational mechanisms may permit its contraction significant changes.

Besides, heart has sympathetic and parasympathetic innervation like vessels. At tone dominance of one of them heart and vessels activity will be different.

Efferent nerves tone support is provided by cardiac-vascular regulation center. Heart-vascular regulative center – is a rather complicated structure in which dominant importance has its “working” part, located in medulla oblongata. It was there where neurons are located from which excitement are transmitted on effector ways (parasympathetic and sympathetic) while reaching heart and vessels. That’s why their reflectory regulation is always performed simultaneousely. When sympathetic nervous system tone is dominant (hypersympaticotony) than heart activity is increased:

• its contraction frequency is rised up – positive chronotropic effect; • contraction force is increased – positive inotropic effect; • excitability is increased – positive bathmotropic effect;

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• conductance is rised up - positive dromotropic effect; • tone is increased – positive tonotropic effect. At hyperparasympatheticotony – on the contrary, all mentioned effects will be

negative. Vascular tone will be changed too: in the first case – to increase, in the second –

to decrease. It will influence on size of their filling with blood and arterial pressure. “Working” part of heart-vascular regulation center consists of 2 parts: • pressor – its irritation causes vasoconstriction; • depressor – its irritation causes vasodilatation. These parts of “working” center receives the information from different receptor

groups located in heart, vessels and out of blood circulation system. That’s why while characterizing blood circulation system reflectory regulative

mechanism one can differentiate 2 reflexes types: proper and conjugated. Proper reflexes – are such acts occuring in the structures of a given system and

realizing in it. Such receptive zones in blood circulation system are vascular presso- and chemoreceptive zones. Special place in this reflectory group has sino-carotid zone. Reflectory act from carotid zone pressoreceptors is called as sino-carotid reflex (Chermak’s reflex). This reflectory act is performed at blood pressure increasing in a given zone. Pressoreceptors irritation leads to nervous impulse occurrence, further coming through sino-carotid nerve in medulla oblongata where it passes on vessel-motor depressor part. From depressor part information is switched to sympathetic nervous system through inhibiting reticular neurons and through exciting reticular neuron – to parasympathetic part of this system and through efferent fibres - to heart and vessels smooth muscles. As the result of parasympathetic nervous system tone predominance both heart and vessels work is decreased (heart contractions freaquency and force, systolic volume size, blood pressure are decreased).

Another blood circulation system proper reflex type are chemoreflexes from same vessels zones. They answer to blood chemical content change, for example, CO2 excess in blood. Reflectory arch of such reflex is a very similar to sino-carotid reflex reflectory arch but information comes to pressor part of heart-vascular regulation center. Then information through exciting reticular neurons come to synaptic, through inhibiting – to parasympathetic part of autonomic nervous system. Result: hypersympatheticotony and further heart activity enforcement and vascular tone increasing (heart contractions freaquency and force, systolic volume size, blood pressure are increased). CO2 is more effectively removed from organism due to such mechanism.

Conjugated reflexes – reflectory acts that are originated from different receptive groups located out of blood system boundaries. As it is known, there are many such zones in organism but according to receptors classification one can differentiate 3 types of such reflexes:

1) Proprioreceptive – are originated from supporting-moving apparatus receptors for instance in course of physical activity. From these receptors (they are localized in muscles, tendons, ligaments) the information occurring in them comes to heart-vascular regulation center pressor part that leads to heart and vessels activity enforcement (see above the mechanism). Pulse frequency and blood pressure increasing in course of physical training is explained by this (probe with physical activity).

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Reflexes of localization are too closely to these reflexes. One of them is known as orthostatic probe: one determine pulse freaquency and blood pressure in investigated person while his lying on the bed. Then the investigated person must be gradually putted into vertical state and the measurements are repeated. Under norma these indexes are increased in course of orthostatic probe. The explanation: information flow from proprioreceptors (while someone’s staying muscles, joints, ligaments are tensed) is increased in spine. Then information goes to medulla oblongata, to pressor part of heart-vascular regulation center. Clinosthatic probe is the directly opposing to the previous probe: the investigated person is gradually putted from vertical to horizontal status. The information from proprioreceptors is significantly decreased and depressor part of regulative center became dominant that leads to pulse and pressure reducing.

2) Interoreceptive – are connected with different inner organs activity. Everyone knows very well that heart and vessels activity is always changed in course of respiration, digestion, excretion changings. For example, if one presses on epigastrial region (epigastrial reflex) it’s accompanied by vessels hypotony, blood pressure and heart frequency reducing. Mechanism: at peritoneum receptors irritation (that occurs at pressure to epigastral region) information finally reaches depressor center and then to heart, vessels leading to their function decreasing or even stoppage. That’s why fights are so dangerous because they may be accompanied by shocks to epigastrial region and in the most horrible cases even to instant (moment) death.

3) Extero-receptive conjugated reflexes are multiple nervous acts group occurring at the irritation of body surface and mucosae separate receptive fields. Example: ocular-heart reflex (Danini-Ashner’s reflex): at pressure to eyeballs information comes to depressor centre. Result: heart contraction frequency and blood pressure decreasing.

4) One knows very well vascular reactions to warmth (dilatation), coldness (constriction), pain (moderate pain leads to vasodilatation, strong – to constriction), touching (especially of lovely person). Due to separate points irritation (acupuncture points) on skin surface one can achieve definite success in heart activity and vessels tone regulation that is widely used in clinical practice particularly in facial-maxillary region (at neurites, myosites, myalgias et al.).

Humoral-chemical regulation of heart and vessels activity is determined by hormones, mediators and different chemical substances (metabolites) action.

Substances increasing heart and vessels activity: 1. Hormones: · adrenaline; · noradrenaline; · vasopressin; · thyroxine; · insulin; · renin et all. 2. Mediators: · noradrenaline; · serotonin and others. 3. Metabolites: · calcium excess;

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· oxygen excess. 4. Substances decreasing heart and vessels activity: · acethylcholine; · hystamine; · many prostaglandines (f.ex. prostacycline); · acids (lactic et al.); · CO2 surplus (excess). Acid products (lactic acid, CO2) accumulating in course of physical activity

decrease tone of working muscles blood vessels increasing blood supply to them. At this time magistral vessels are in increased tone due to adrenaline and noradrenaline concentration increasing in answer to load. Such tone redistribution in different vessels of blood circulation system provides high reliability of a given system functionning.

Thus, we see that heart-vascular activity regulation is a complicated process in what both reflectory (conditioned and unconditioned) and humoral-chemical mechanisms take part.

Table 15. Summary of factors affecting the caliber of the arterioles.

Constriction Dilation Local factors Decreased local temperature Autoregulation

Increased CO2 and decreased O2 Increased K+, adenosine, lactate, etc. Decreased local pH Increased local temperature

Endothelial products Endothelin-1 Locally released platelet serotonin Thromboxane A2

NO Kinins Prostacyclin

Circulating hormones Epinephrine (except in skeletal muscle and liver) Norepinephrine AVP Angiotensin II Circulating Na+-K+ ATPase inhibitor Neuropeptide Y

Epinephrine in skeletal muscle and liver CGRPα Substance P Histamine ANP VIP

Neural factors Increased discharge of noradrenergic vasomotor nerves

Decreased discharge of noradrenergic vasomotor nerves Activation of cholinergic dilator fibers to skeletal muscle

Effect of Changes in Electrolyte Concentration on Heart The distribution of electrolytes in extracellular fluid and intracellular fluid is

responsible for the electrical activity rite tissues including myocardium. Thus, any change of concentration of any of the electrolytes will definitely influence on the electrical activity of the cardiac muscle.

EFFECT OF CHANGES IN SODIUM CONCENTRATION Normal sodium concentration in serum is 135 to 145 mEq/L.The change in the

concentration of sodium does not change the electrical activity of heart severely.

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Only the low reduce of sodium in the body fluids reduces the electrical activity of cardiac muscle and the ECG shows low Mage waves. But, the changes in the concentration of potassium and calcium ions have significant effects on the heart.

EFFECT OF CHANGES IN POTASSIUM CONCENTRATION The normal potassium concentration in serum is about ito5 mEq/L. The changes

in ECG are developed when potassium level is increased to 6 mEq/L or when it is reduced to 2 mEq/L.

EFFECT OF HYPERKALEMIA Increase in potassium concentration decreases the resting membrane potential

leading to hyperpolarization. It also reduces the excitability of cardiac muscle. When the potassium concentration increases slightly to 6 or 7 mEq/L, the ECG

shows a tall T wave. P-R interval and QRS complex are normal. With further increase in potassium level, i.e. to about 8 mEq/L, the P-R interval and the duration of QRS complex are prolonged. This is because of the effect of hyperkalemia on the conductive system of the heart. Hyperkalemia decreases the rate of conduction. The severe hyperkalemia beyond 9 mEq/L makes the atrial muscle unexcitable. So, in ECG the P wave is absent. The QRS complex merges with T wave. This condition is fatal because, it can lead to ventricular fibrillation or stoppage of heart in diastole due to the lack of excitability.

EFFECT OF HYPOKALEMIA Decrease in potassium concentration is known as hypokalemia. It reduces the

sensitivity of heart muscle. When the potassium level falls to 2 mEq/L, the S-T segment in ECG is depressed. The amplitude of T wave is reduced with the appearance of U wave. Sometimes, the U wave merges with T wave. Because of this, the Q-T interval is mistaken for being prolonged.

Further reduction in potassium level, i.e. below 2mEq/ L, depresses the S-T segment greatly below the isoelectric baseline. It also causes inversion of T wave. The U wave becomes more prominent. The P-R interval also is prolonged.

EFFECT OF CHANGES IN CALCIUM CONCENTRATION Normal concentration of calcium in serum is 9 to 11 mg/ dl (4.5 to 5.5 mEq/L).

Mostly, the hypocalcemia affects the heart rather than hypercalcemia. EFFECTS OF HYPERCALCEMIA Elevated calcium level in extracellular fluid is known as hypercalcemia and it

increases the excitability and contractility of heart muscle. In animals, under experimental conditions, the heart stops in systole when a large quantity of calcium ion is infused. The stoppage of the heart in systole is called the calcium rigor. The calcium rigor is a reversible phenomenon and the heart starts functioning normally when the calcium ions are washed. In clinical conditions, the effect of hypercalcemia is very rare. It reduces the duration of S-T segment and QI interval.

EFFECTS OF HYPOCALCEMIA Reduction in calcium concentration is called hypocalcemia. It reduces the

excitability of the cardiac muscle. So, in ECG, the duration of S-T segment and Q-T interval is prolonged.

How and in what sequence these mechanisms are switched on under physiological conditions for instance in course of physical work? At this activity type increased oxygen consumption and enforced carbon dioxide releasing occurs. It may be achieved due to increased activity not only of respiration system but also blood circulation apparatus. Describe the consequence of switching of all

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these regulatory mechanisms on. At the early beginning, in the period of preparation to work the blood circulation system activity is increased by means of 2 mechanisms: conditioned-reflectory and humoral. Conditioned-reflectory – the situation itself before physical activity (sportsmen before running) is conditioned stimuli complex (in example with sportsman these are running way, stadium, spectators, referees and so on) which will cause the changes from the side of heart and vessels. Emotional load at this is a reason of enforced adrenaline releasing from suprarenal glands. The result of this is more expressed increasing of heart and vessels activity. Organism prepares given (cardiac-vascular) system to future wok in such a way.

Humoral: in course of performing of physical activity itself conjugated reflexes from proprioreceptors, proper reflexes from chemoreceptors (metabolism products accumulation and first of all CO2) are involved into regulation and hormones (adrenaline, vasopressin et al.) continue to be released. All these factors encourage further heart and vessels activity increasing. At the same time in working organs (muscles) acid products are accumulated, decreasing vessels tone in these organs and blood fills them in more extent providing feeding and removal of metabolism exchange.

After physical activity performing everything came into its initial level due to involvement ito the work proper receptors from pressoreceptors directed to heart and vessels activity restriction (restoration).

Factors affecting heart rate.1 Heart rate accelerated by: – Decreased activity of baroreceptors in the arteries, left ventricle, and

pulmonary circulation – Increased activity of atrial stretch receptors – Inspiration – Excitement – Anger – Most painful stimuli – Hypoxia – Exercise – Epinephrine – Thyroid hormones – Fever – Bainbridge reflex Heart rate slowed by: – Norepinephrine1 – Increased activity of baroreceptors in the arteries, left ventricle, and

pulmonary circulation – Expiration – Fear – Grief – Stimulation of pain fibers in trigeminal nerve – Increased intracranial pressure 1 Norepinephrine has a direct chronotropic effect on the heart, but in the intact

animal, its pressor action stimulates the baroreceptors, leading to enough reflex increase in vagal tone to overcome the direct effect and produce bradycardia.

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CIRCULATION REGULATION PECULIARITIES IN SEPRATE ORGANS There are both blood circulation and its regulation several distinguishing features

in different organs. It is connected with different organs innervation and their various sensitivity to hormones, mediators and different chemicals which can influence on vascular vessels activity.

Circulation in heart It is performed by coronary arteries, big capillaries amount. Circulative conditions

in coronary arteries differ greatly from circulation in other organs. In course of ventricles systole myocardium presses vessels in it. That’s why blood circulation is weakened, oxygen supply is decreased to the tissues. Right after systole heart blood circulation is increased. Main regulative role of sympathetic and parasympathetic influencings interrelations is in rapid and adequate coronary circulation adaptation to current organism organism needs. Vagus excitement leads to coronars dilation. Cardiac sympathetic rami (branches) excitement results in coronarodilation and blood stream activation in them. Oxygen myocardial consumption sufficiency is important for coronary circulation regulation. Cardiac muscle hypoxy results in myocardial chemoreceptors excitement which leads to reflectory arterioles dilations and blood stream activation. Carbonic dioxide accumulation in blood causes the same effect (that’s why coronary circulation is increased at respiration lack).

Circulation in brain It is more intensive in this region comparatively to all others. About 15 per cent of

blood from every cardiac discharge in large circle comes into brain vessels. Brain vessels are muscular, with excessive adrenergic innervation that allows them to change their cavity in wide limits. Circulation distribution in brain is rather unequal: its maximal level is in hypothalamus and cortex.

Brain circulation independence from general (systemic) circulation is its important feature. It is explained by skull rigidity and brain disability to be pressed. That’s why all liquids volume in intracranial vessels is practically constant. Even small increasing of this volume caused by significant arterioles dilation that leads to circulation increasing is compensed easily with insufficient veins constriction the volume of which is rather more.

Under norma, vasonstricting nervous fibres influence on brain blood stream insignificantly. Such weak brain innervation with vasoconstricting nerves is favourable for it. When blood pressure decreases for instance after strong bleeding (at which peripheral vessels are constricted), brain vessels are dilated. Brain circulation remains constant even under such conditions due to autoregulation (but only if blood pressure is not less as 50-60 mm merc col.) At further blood pressure decreasing blood circulation will be reduced in brain too that may leads to unconscious state.

In brain vessels tone regulation local factors are of great importance too. Merabolism intensivity activation in brain, blood content change (CO2 level increasing) causes brain vessels dilation. H+-ions role, oxygen tension are very important in these reactions too (at oxygen low tension – brain vessels are dilated, at high tension – are constricted, on the contrary). At oxygen content increasing in air brain vessels are constricted.

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Blood circulation in lungs Lung circulation peculiarity: circulation small circle vessels are relatively short,

resistance in them is less; that’s why pressure in them is in 5-6 times lower comparatively to aortal. Lung vessels capacity may be increased or decreased. Thus, due to this mechanism, lung filling with blood may varies in the limits of 10-25 per cent from common blood amount in organism. It provides blood depot creation. Lung net vessels big ability to stretching creates favourable conditions for easy blood stream and volume change. Inspiration leads to blood regional content increasing and to regional resistance decreasing to blood in course of usual breathing or even in course of hyperventillation.

At hypertony in reflexogenic zones vessels with parallel reflectory heart activity weakening and large circle vessels dilation lung circle reflectory filling takes place. Due to this blood pressure is leveled and blood distribution between circulation big and small circles occurs. At pulmonal arteries pressure increasing, when small circle is overfilled with blood, reflexes from pulmonal artery receptors occurs on large circle vessels. As the result of this blood amount is increased in large and is decreased - in small circle. It prevents blood stagnation in lungs and provides heart activity and blood circulation as a whole.

SYSTEMIC CIRCULATION This is otherwise known as greater circulation. The blood, which is pumped from

left ventricle passes through a series of blood vessels of arterial tree or arterial system and reaches the tissues. The blood vessels of the arterial system are the aorta, larger arteries, smaller arteries and arterioles. The arterioles branch into the capillaries. The capillaries are responsible for exchange of various substances between blood and the tissues. This is because, the wall of the capillaries is permeable to various substances.

After exchange of materials at the capillaries, the blood enters the venous system and returns to right atrium of the heart. The blood vessels of the venous tree or venous system are the venules, smaller veins, larger veins and vena cava. From right atrium, blood enters the right ventricle. Thus, through the systemic circulation, the oxygenated blood or arterial blood is supplied from heart to the tissues and the venous blood returns to the heart from the tissues.

PULMONARY CIRCULATION This is otherwise called lesser circulation. Blood is pumped from right ventricle to

lungs through pulmonary artery. The exchange of gases occurs between blood and alveoli of the lungs through pulmonary capillary membrane. The oxygenated blood returns to left atrium through the pulmonary veins.

Thus, the left side of the heart contains oxygenated or arterial blood and the right side of the heart contains the venous blood.

4. Materials for auditory self-work. 4.1. List of study practical tasks necessary to perform at the practical class. Materials and methods: kymograph, universal stand, Engelman’s cardiograph,

cork plate, instruments set, cotton-wool, gauze, Ringer’s physiological solution, ligature, current source, electrodes, calcium chloride and adrenaline solutions (1 x 10-5 – 1 x 10-6 g/ml) as well as acetylcholine solution (1 x 10-7 – 1 x 10-8 g/ml), bed, tonometer, phonendoscope.

The investigation object: human being.

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Task 1. To investigate Golts’ reflex on frog’s heart.

In decapitated, but not unmoved frog one should dissect heart without abdominal cavity dissection. To count contractions number per minute, to register cardiogram. Then to make disjointed seizures on frog’s abdomen with tweezers handle. To observe heart activity. To determine heart stoppage time in seconds. To repeat observations. To register cardiogram. To repeat the experiment after spine destruction.

To write data received in table. To draw reflectory arc scheme, to indicate all its links.

Task 2. To investigate vagal-sympathetic stem irritation influence on frog’s heart

activity. To find vagal-sympathetic stem in the same decapitated frog. To register

cardiogram and to count contractions amount for 1 min. To inflict short-termed irritation by means of electrodes, to register cardiogram. To find irritation and sympathetic action result on record. To iflict long-termed irritation in 2-3 minutes. To determine, whether heart stoppage time corresponds to irritation time.

Cardiograms must be drawn or sticked into students’ copy-books. Irritation origin and end should be designated by arrow. To indicate on cardiogram changes caused by sympathetic and parasympathetic nerves. In conclusions to mark sympathetic and parasympathetic nerves influence on frog’s heart contraction rate and force.

Task 3. To investigate calcium, potassium ions excess, adrenaline and

acetylcholine solutions on heart activity. To raise a little and carefully naked frog’s heart with tweezers and to separate

with small scissors out of the body while all heart parts preservation and especially pace-maker (venous sinus).

To put isolated heart in box with Ringer’s solution. To count contraction amount per 1 min. To one more drop of chloric calcium solution, to determine contraction force and altitude changes. To wash heart from the solution and to reach contraction previous parameters. Then to add one drop of potassium chloride. To wash heart again after contractions amount counting and to add one drop of adrenaline solution of concentration mentioned above. To repair heart activity previous parameters and to add acetylcholine solution. To make a conclusion.

Cardiograms must be drawn or sticked into students’ copy-books. To indicate solutions introduction time on it. To explain registered changings reasons. In conclusions students should mark investigated substances influence character on heart activity.

Task 4. To investigate Chermak’s reflex from carotid sinuses

To determine heart contractions amount. To press onto carotid sinuses area (at a level of mandibles angles) in course of 10 sec from the both sides simultaneously. To determine cardiac contractions changings.

To write heart contractions rate before and after pressure onto carotid sinuses area in copy-book. To compare the results of your investigated person with the results of other investigations. To draw reflectory arc scheme, to mark all links on it.

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Task 5 To investigate ocular-cardiac reflex (Danini-Ashner’s).

To determine pulse rate. To press on to eyelids area in course of 10 sec and to count pulse again. Weak or zero expression of this reflex indicates to inhibitory state of corresponding formations in parasympathetic nervous system central parts.

To write heart contractions rate before and after pressure onto eyelids. To compare the results of your investigated person with the results of other investigations. To draw reflectory arc scheme, to mark all links on it.

Task 6.

To perform clino-stathic probe. The investigated person stands in a free posture in course of 10 min near the

bed. The investigator must determine the investigated person’s pulse and arterial pressure on the 1st and 5th minutes. Then the investigated person should lie down onto bed and his pulse and arterial pressure should be measured also on the 1st and 5th minutes.

The results should be written into copy-books, to be analyzed. Students must draw reflectory arcs of reflexes participating into hemodynamics regulation. In conclusions to explain circulation changings way in course of this probe performance.

Task 7. To perform ortho-stathic probe.

In clinosthatism the investigated person’s pulse and arterial pressure should be estimated on the 1st and 5th minutes. On the 11th minute the investigated person should change his posture from lying into standing and his pulse and arterial pressure should be measured also on the 1st and 5th minutes.

The results should be written into copy-books, to be analyzed. Students must draw reflectory arcs of reflexes participating into hemodynamics regulation. In conclusions to explain circulation changings way in course of this probe performance.

5. Literature recommended 1. Lecture course. Mistchenko V.P., Tkachenko E.V. Methodical instructions for dental students (short lecture course).-Poltava, 2005.-P.30. 3. Mistchenko V.P., Tkachenko E.V. Methodical instructions for medical students (short lecture course).-Polatava, 2005.-P.56-59. 4. Methodical instructions on chapter “Cardiac-vascular system physiology” on practical classes for dental and medical students. 5. Concise Physiology /Guyton-Ganong-Chatterjee. Ed. By Dr Gull R.Sh.-Lahore: K.E.Medical College.-1998.-P.61-63, 65-68, 72-83, 104-111. Kapit W., Macey R.I., Meisami E. The Physiology Colouring Book: Harpers Collins Publishers, 1987.-P.34-36, 38. Bullock J., Boyle III J., Wang M.B. Physiology.-1991.-P.133-135, 121-124. Stuart Ira Fox. Human Physiology.-8-th Ed.-Mc Graw Hill, 2004.-P.390-394, 399-400, 408-412, 416-418, 423-428. 9. Seeley R.R., Stephens T.D., Tate P. Essentials of Anatomy and Physiology.-The 3rd Ed.-McGraw Hill, 1999.-P.337, 355-370.

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6. Materials for self-control: Control questions: 1. Heart activity regulation. 2. Hemodynamical center, its structure. Pressor and depressor reflexes (proper and conjugated). 3. Blood pressure self-regulative system peripheral and central components. 4. Blood circulation regulation in course of organism adaptive reactions. 5. Microcirculation, lymph and lymphocirculation.

LESSON 49

SITUATIONAL TASKS ON CREDIT MODULE:”BLOOD CIRCULATION SYSTEM”

See p. 115 test control

LESSON 50 PRACTICAL EXPERIENCES MANAGEMENT ON CONTENT MODULE 12

“CIRCULATION SYSTEM PHYSIOLOGY”

PRACTICAL SKILLS ECG registration methodics.

1. To draw ECG, to mark its elements, to explain their origin. 2. Heart automatism indexes analysis on ECG. 3. Heart conductivity indexes analysis on ECG. 4. Heart tones, their determining on phonocardiogram (to draw, to describe). 5. Pulse characteristics that can be determined by palpation. 6. To draw sphygmogram (SPG), to mark its elements. Pulse characteristics that can be determined on SPG. 7. Rheography principle. To draw rheogram, to mark its main elements. 8. Arterial pressure measurement: to describe methodics and AP normal values. 9. Danini-Ashner's reflex: mechanism, practical usage. 10. Chermak's reflex: mechanism, practical usage.

CONTENT MODULE 13: “RESPIRATION SYSTEM”

LESSON 51 EXTERNAL RESPIRATION INVESTIGATION

1. The topic studied actuality. This topic is essential for dentists from their

professional positions because it deals with mastication, alimentary piece formation, subsequent swallowing as well as speech formation.

Oral respiration (air movement over the food) in course of mastication determines hot food cooling. In course of mastication and swallowing respiration changings occur. Such changings belong to respiratory system protective reflexes. They are

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expressed in respiration stoppage. Jaws are closed, soft palate is rised closing entrance into choanes. Simultaneousely with this palato-pharyngeal muscles are contracted. Septum is formed which closes passage between oral and nasal cavity in the result of these processes. Tongue moving ahead presses onto palate and pushes food piece into pharynx. Because of this food piece is pushed down into pharynx. Entrance into larynx is closed by epiglottis, vocal cord is closed to prevent food coming into trachea. As the result of all this food can pass only to oesophagus but not to respiratory tract.

Human respiratory system also participates in speech sounds formation. Oral cavity organs, for example, lips, tongue and teeth take part in acoustic effect providing, because expiration in course of conversation takes place through mouth. Normal prononciation with proper correct sound articulation is delt with dental row integrity. Teeth loss especially anterior determines speech disorders, separate sounds clarity deterioration and even leads to loss the possibility of separate sounds pronunciation. In parallel, one can see salivation and saliva throw through fissures forming at the place of teeth absence.

Dental rows integrity injury (especially incisives) leads to dental sounds forming changing and inhibiting (whistle, lisping). Pathological structures on tongue back leads to sounds reproducing inhibiting and disorders in labial (of lips) region. Changed occlusion influences greatly onto phonation result. It is especially expressed at opened, crossed occlusions, prognathy and progeny.

Phonation disorders at different changings in oral cavity receive corresponding names. Disorder delt with cleft palate (hard palate fissure) is called palatolaly. At anomalies in tongue structure and function occuring articulational disorders receive the name glossolaly. Uncorrect teeth structure and their localization in alveolar archs especially of anterior group (incisives and canines) are often reason of dyslalies. All mentioned dentist must take into account while treaty influencing in oral cavity performance.

Surgeon-dentist must forecast the possibility of speech-forming function in course of operations in oral cavity organs. Articulation mechanism knowledge is of essential importance for orthopedic dentist. Removable dentures production, especially at wide adenthias or complete teeth absence leads to articulational correlations changing in oral cavity. Naturally, it influences on vocal apparatus resonator function. Occlusion overstating at denturing, artificial teeth uncorrect installation and even well-done denture always at first stages of adaptation lead to speech-forming retardation. Patients with removable dentures often complaint on this or that dyslalies signs: sound-production inhibiting, additional whispering, whistle and lisping. All this is necessary to take into account at dentures constructing and creation, especially for people which use speech actively in their working activity (artists, singers, lecturers, dictors, teachers). Famous statement “to train somebody’s voice” to singer, artist, dictor or teacher means to tune respiration and articulation by definite behavioural measures usage.

2. Study aims: To know: respiration system structure and system, its role in organism, external

respiration mechanism and its investigative methods. To be able to: to assess external respiration indexes by spirogram.

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Subject To know To be able to Anatomy Respiratory ways anatomy Show main morphological

elements on tables and special models and to describe them


Respiratory system embryology, main histological elements; representations about alveolocytes (in part the ones producing surphactant)

Recognize micropreparations and describe main structural elements


Patho-morphological changes at main diseases of respiratory system


Pathophysiology Developmental mechanisms of main pathological processes in respiratory system

Interpretate spirogram

Internal Diseases Ethiology, pathogenesis, clinics, diagnostics, therapy and prevention principles of respiratory system pathological conditions

Treat and prevent respiratory system diseases


Mechanism of new-born first respiration; respiratory system peculiarities in different-aged children; representation about mucoviscidosis and hyalinic membranes syndrome

Treat and prevent respiratory system diseases in children

Dentistry Oral cavity role in respiration, phonation disorders ethiology, pathogenesis, clinics, diagnostics, therapy and prevention principles

Treat and prevent dysphonation

3.2. Topic content. Respiration organs begin their formation at the fetus intraembryonic development

4th week. Surphactant starts its producing at intraembryonal development end. Respiratory movements of embryo are periodic. They occur at closed vocal fissure that is why amnyoitic liquid does not pass into lungs; respiratory movements appear from the 12th week. Respiration rate is very high – 40-70 per 1 min.

Embryo respiratory movements do not provide gas exchange but they encourage lungs and respiratory musculature development as well as embryo circulation when

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increased blood inflow to heart due to negative pressure periodic appearance in thoracic cavity.

New-born first respiration is determined by following factors: 1) Blood gas content changing (carbonic dioxide accumulation and oxygen

diminishing) and acidosis – factors acting directly to new-born respiratory center because arterial chemoreceptors are still non-matured.

2) Afferent impulses from skin cold and tactile receptors, proprioreceptors and vestibular receptors enforcement during labors and right after them. These impulses activate CNS and respiratory center. CNS tone and the one of skeletal musculature (in part, respiratory one) is enforced.

3) When the baby head appears from maternal labor ways than sinner reflex is canceled. Sinner reflex represents respiratory center inhibiting at receptors irritation in external nasal meatuses area with liquid; if liquid is present than it is removed.

4) After the baby passage through labor ways pressed thorax is dilated significantly that also encourages the first respiration.

5) Delivery represents huge stress both for mother and for baby. Cortisol and epinephrine cause significant bronchodilation and air passage into embryo respiratory ways.

6) The first inspiration requires 10-15 times more energy than all next respiratory movements, it is longer like the first expiration. This energy is consumped to overcoming attachment forces between alveoles and liquid filling newborn airways and lungs. Respiration is vitally essential for human beings and animals life. Respiration is

gas exchange between organism external and internal environment. This process is performed in several stages: 1) External or lung respiration – performs gas exchange between organism

external and internal environment (between air and blood). 2) Gas transition and transfer – is performed due to alveoles permeability and

blood transport function. 3) Internal or tissular respiration – performs directly cellular oxidation process.

External respiration – is performed with cycles change, one respiratory act consists of inspiration and expiration phases. As a rule, inspiration is shorter than expiration. Inspiration act: thorax volume increases in 3 directions – vertical, sagittal and frontal. Why? There are some reasons: · Diaphragm contraction (if diaphragm in rest state is shifted on 1 cm it leads to

thorax increasing on 200-300 ml of air). Result of diaphragm contraction: decreasing (flattening) of its cupula; visceral organs (in abdominal cavity) pushing down, throrax increasing in vertical direction.

· Contraction of external oblique intercostal and intercartillaginous muscles: they are fixed to above-lied rib near spinal cord, to below-lied rib – near sternum. Result: throrax volume increasing in sagittal and frontal directions. Ribs are putted forward, up and towards. And it supports such lungs localization change.

· As lungs are connected with thorax through pleura visceral and parietal layers then lungs volume increasing occurs after thorax volume rising up. It leads to pressure decreasing in them. Pressure becomes lower than atmospheric one, air comes into lungs. Thus, negative pressure is third reason (factor).

· This negative pressure increases in course of inspiration because at lungs stretching their elastic draft - force with which lung strives for compression - is

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increased. Elastic draft is explained by 2 factors: there are many elastic fibres in alveoles walls - the first one – and the existance of surface tension of liquid tunic containing surfactants and covering alveole wall internal surface – the second one. Elastic draft (the 4-th factor of inspiration) is increased in course of inspiration, negative pressure is rised up in pleural cavity that encourages inspiration act.

Thus, inspiration is rather active process. Expiration act – under usual conditions is performed passively by means of

following factors: · thorax gravity force; · elastic graft of rib cartillages overwinded in course of inspiration; · abdominal cavity organs pressure.

But expiration as inspiration may be also active (for instance, at hyperventillation, cough, someone’s straining and so on), when internal intercostal muscles contraction occurs. These muscles are fixed near spinal cord to below-lied rib and near sternum to above-lied rib and their contraction cause pushing ribs down, ahead and inside.

Respiratory muscles in course of their activity pass through some resistance, 2/3 of which is elastic, defined by lungs and thorax tissues as well as surfactant action; 1/3 – non-elastic caused by gas stream friction with air ways.

Negative pressure appearance in pleural fissure is explained by following fact: new-born thorax grows faster than lungs that’s why lung tissue is undergone to constant tension. Pleural layers possess large absorbtive ability that encourages negative pressure creation. That’s why gas introducing in pleural cavity is absorbed after some time and negative pressure is restored in pleural cavity. Thus, negative pressure is constantly supported in pleural cavity. At inspiration – 4-5 mm Hg; deep (maximal) inspiration – up to 15, expiration – 2-3 mm Hg. Pressure isles than atmospheric one, but not less than 0 that is why it is relatively negative.

Pleuritis is accompanied by soldered joints formation between visceral and parietal pleura preventing thorax and lungs free movements.

If thorax is wounded than pressure in pleural fissure becomes equal to atmospheric one and lung is falling down, pneumothorax occurs. If we have liquid, blood and pus – the names will be correspondingly hydrothorax, hemathorax and pyothorax. Negative pressure in newborn pleural fissure is only at inspiration.

One can differentiate 2 main respiration types: 1) Thoracic (rib) – thorax dilation is connected mainly with ribs rising; respiration is

mainly performed by means of intercostal muscles activity, diaphragm is moved passively according to interthoracic pressure change. This respiration type is a female.

2) Abdominal (phrenic or diaphragmal) – diaphragm contraction (flattening) is main respiration factor as the result of which interpleural pressure is decreased and simultaneousely interabdominal pressure is increased. This respiration type is more effective because lungs are ventillated in more extent and stronger in course of it and blood venous return is released from abdominal cavity organs to heart. Diaphragmal respiration is more physiological! It is called male respiration. There exists one important rule for women: they must breath with thorax mainly only when their pregnancy!

Air amount in lungs after maximal inspiration is known as common lungs capacity (CLC). It is 4200-6000 ml in adults. Its compounds are: vital lung capacity (VLC) and residual volume (RV). VLC – air amount which leaves lungs

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in course of maximally deep expiration after maximally deep inspiration. It is equal to 3300-4800 ml under norma (in males 4000-4800 ml, in females – 3300-4000 ml). VLC consists of 3 lung volumes: 1) respirational volume (RV) of air inspirated and expirated in course of each

respiratory cycle under rest state – 400-500 ml; 2) reserve inspiration volume – additional air that one can inspirate in course of

maximal inspiration after usual inspiration – 1900-3300 ml; 3) reserve expiration volume – additional air that one can expirate in course of

maximal expiration after usual expiration – 700-1000 ml. At usual respiration we have reserve expiration volume and respirational volume

in our lungs. Residual volume – everything that is in lungs after deep inspiration - it is equal

to 1200-2000 ml. It is in our lungs even after death! Total lung capacity (TLC) is a sum of residual volume and vital lung capacity.

There exists one more volume – harmful space volume – air part that is remained in air ways (nasal ducts, oral cavity, nasopharynx, nasal additional sinuses, trachea, bronchi) and doesn’t reach lungs (this air doesn’t participate in gas exchange). Such an anatomical space is about 140-200 ml. It very useful despite its name “harmful” because air passing through them (especially when its passage through nasal ducts) becomes warm, humid, protected from side particles, bacterias. Physiological dead space (200 ml) is alveoles that are perfused but gas exchange is absent in them (ventilation is present, but gas exchange is absent). Respiration through nose is more physiological!

For 1 minute, at respiration frequency equal to 16-20, one inspirates volume that has name of minute volume (MV). Its size depends on 2 compounds: respiration volume and respiration frequency. Respiration frequency 16-20 (norma indicated in all textbooks and manuals) per 1 minute is not ideally physiological. Less respiration frequency which may be reached by corresponding training (the most often – physical training) - is more physiologic from the point of view delt with diseases prevention not only in respiratory appatarus but also in other organs and systems. Why less respiration frequency is more physiological? Describe these advantages on concrete example of trained person respiration. Imagine, please, 2 people before us, of equal constitution, but one of them is regularly done some kind of physical activity (regular morning exercise, running and so on). Respiration volume is always higher in trained person in comparison with untrained. Example. Respiration volume in trained person – 800 ml; in untrained - 400 ml. After small physical loading their respiration frequency is getting increased: in trained person – to 20 respiratory acts per minute, in untrained – rather higher (for example, 40). At such ziphras minute volume in both people will be equal to 16000 ml of air (400 ml x 40 and 800 ml x 20). In what are the advantages of one of them before other? In the first human being (trained) from 800 ml of respiratory volume 600 ml will come to alveoles with every inspiration (if both subjects have harmful space volume equal to 200 ml). In the second (untrained) person only 200 ml of air will come to alveoles. At respiration frequency 20 in first person 12000 ml of air reach alveoles for 1 minute (20 x 600 ml). At a frequency 40 in second person this air amount will be only 8000 ml of air (40 x 200 ml). Thus, in untrained person air amount reaching lungs is lower on 4000 ml. That’s why less respiration frequency is more physiological! It is reached by training (the best – by physical one). As it is known nowadays, civilized person is healthy, active, energetic and it may be so tens of years if his minute volume is not more than 4-5 l. The more minute volume

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predominates over this level, the more symptoms are of different organs pathologies occur. In people who have such problems (these are the civilization problems!!!) minute volume is equal to 8-12 litres in resting state. One can’t call such respiration healthy. Remember!!! External respiration normalization – reaching minute volume level 3-4 litres per minute! High frequency of our breathing is delt with its uncorrect character. In the most people amount time for inspiration is approximately equal to time for expiration. Besides, the most people performs their expiration right after their inspiration – it is also out of physiology. It’s necessary to lack someone’s breathing after inspiration and then slower then inspiration expiration comes, after which – new lack. Such respiration type reminds respiration on Buteyko, Frolov et al. But, unfortunately, people become follow this respiration “culture” only when they fell ill. Really it’s necessary to breath in such a way always! This is a Real Way to health and prevention of a great number of diseases!

Table 16 Main respiratory indexes

Age Respiration rate, per 1 min

Respiration (tidal) volume, ml

Air minute volume, ml

Air minute volume, ml/kg

Age Vital lung capacity, ml

1 month

40 30 1000 190 1 month 130

1 year 25 90 2400 220 6 years 1200 16 years 3400 The adults, men

16 500 6000-8000 The adults 3500-4500

The adults, women

16 500 5000-6000 2000-3000

4. Materials for auditory self-work. 4.1. List of study practical tasks necessary to perform at the practical class. Materials and methods: stop-watch, medical bed, cotton wool, spirograms,

spirometer, alcohol. The investigated object: human being.

Task 1. To determine respiration type, frequency and rhythm

To determine external respiration major parameters (according to thoracic or abdominal wall movement) under resting state and after 20 sitting down for 30 sec.

The results should be formulated as a table in which students have to include all indexes investigated before and after physical loading.

In conclusions: to compare received external respiration parameters before and after physical loading and make the conclusions about external factors influence on external respiration indexes in men and women.

Task 2.

To determine external respiration indexes on spirogram under resting state and after physical loading

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To determine correlation of residual volume (RV) and vital lung capacity (VLC) expressed in per cent. This index is fluctuated from 20 to 50 per cent under physiological conditions. Residual volume is not determined directly in clinics. It is 25-30% of VLC.

Students should draw spirograms in their copy-books and mark all investigated indexes. Then to write all results received in protocols.

To determine alveolar lung ventilation (ALV) by formule: ALV= (respiration volume – 150) x respiration rate, where 150 ml is dead space volume.

In conclusions: to notice investigated person external respiration functional state and to answer the question whether results received correspond to physiological constants.

Figure 44. ДО - respiration volume (RV) РО вд- inspiration reserve volume (IRV)

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РО выд- expiration reserve volume (ERV) ЖЕЛ- vital lung capacity (VLC) МВЛ- maximal lung ventilation (MLV)

Task 3. To determine VLC and NVLC (necessary VLC)

To process spirometer end with alcohol, to put spirometer arrow on “0” of scale. To perform deep inspiration than complete expiration in spirometer while standing.

To count NVLC on formula: NVLC (men) = [27,63-(0,112 x age)] x height (in cm). Under norm: 4,886±0,123 (l) NVLC (women) = [21,73 – (0,101 x age)] x height (in cm). Under norm: 3,234±0,097 (l)

It’s necessary to write ciphras received and to compare VLC and NVLC in investigated people.

In conclusions: to evaluate VLC of investigated person taking into account that VLC can differ from NVLC on ±20%. VLC is lungs function clinical index giving the information both about respiratory muscles force and about respiration other aspects. VLC depends on age, sex, height, body position: in vertical position (orthostatism) it is bigger than in horizontal one (clinostatism). Also VLC depends greatly on organism training degree.

VLC decreasing more than on 20% can indicate to pulmonal tissue absolute functioning reducing both at lung disease (bronchioles occlusion, tumor, pneumonia et al.) and at heart-vascular diseases. Inspiration and expiration reserve volume is reduced at this which indicates to the system thorax-lung reducing. Residual volume level is increased causing lung residual capacity increasing which indicates to bronchi destructive changings and pulmonal tissue elasticity reducing.

5. Literature recommended 1. Lecture course. 2. Mistchenko V.P., Tkachenko E.V. Methodical instructions for dental students (short

lecture course).-Poltava, 2005.-P.47-50, 58-60. 3. Mistchenko V.P., Tkachenko E.V. Methodical instructions for medical students

(short lecture course).-Poltava, 2005.-P.82-84. 4. Methodical instructions on chapter “Respiration system” on practical classes for

dental and medical students. 5. Kapit W., Macey R.I., Meisami E. The Physiology Colouring Book: Harpers Collins

Publishers, 1987.-P.43-46. 6. Stuart Ira Fox. Human Physiology.-8-th Ed.-Mc Graw Hill, 2004.-P.480-493. 7. Seeley R.R., Stephens T.D., Tate P. Essentials of Anatomy and Physiology.-The

3rd Ed.-McGraw Hill, 1999.-P. 394-406. 6. Materials for self-control:

Control questions:

1. Respiration and its main stages. 2. External respiration mechanism. 3. Main and additional respiratory muscles. 4. Pressure in pleural cavity, its origin and role in external respiration origin. 5. External respiration role in food piece formation, mastication and swallowing. 6. External respiration role for speech sounds formation. 7. Dental diseases influence on oral cavity speech function.

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LESSON 52

LUNG VENTILATION. GAS EXCHANGE. GASES TRANSPORT WITH BLOOD 1. The topic studied actuality: Lungs ventilation is disturbed due to respiratory

apparatus pathological changings. It is useful to differentiate 2 ventilation disturbances types: restrictive and obstructive.

Restrictive type: all pathological states at which lungs respiratory excursions are decreased.

Obstructive: it is determined by air ways constriction and thus aerodynamic resistance increasing.

Probes which allow to determine one or another disorders type: 1) lungs vital capacity (its decreasing is a restrictive type feature; very seldom –

obstructive one – only at bronchial conductivity diffused disorders); 2) prolonged expiration volume and duration on Wotchall-Tiffno method (obstructive

disorders index); 3) respiration reserve (restrictive disorders index); 4) maximal lung ventilation (it is reduced both in course of restrictive and

obstructive ventilation disorders). For differential diagnostics one should determine vital lung capacity and

prolonged expiration volume. All these indexes determining is performed on spirogram.

2. Study aim: To know: gases diffusion laws from one environment to other; morphology and

peculiarities of pulmonary and vascular membranes blood gases pass through (by diffusion); gases transport forms with blood hemoglobin physical-chemical features and its chemicals.

To be able: to explain gases diffusion mechanisms on the boarder “lungs-blood” and “blood-tissues” as well as gases transport ways; to be able to determine respiration lack maximal duration as well as lungs expiratory functional vital capacity, lungs maximal ventilation and respiration reserve.


Subject To know To be able to Anatomy Respiratory ways anatomy Show main morphological

elements on tables and special models and to describe them





Patho-morphological changes at main diseases of respiratory system


Pathophysiology Developmental mechanisms of restrictive and obstructive


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respiratory insufficiency Internal Diseases Ethiology, pathogenesis,

clinics, diagnostics, therapy and prevention principles of respiratory system pathological conditions accompanied by obstructive and restrictive respiratory insufficiency

Treat and prevent respiratory system diseases


Mechanism of new-born first respiration; respiratory system peculiarities in different-aged children; representation about mucoviscidosis and hyalinic membranes syndrome

Treat and prevent respiratory system diseases in children

3.2. Topic content. Exchange of gases:

1. External respiration: exchange of O2 & CO2 between external environment & the cells of the body efficient because alveoli and capillaries have very thin walls & are very abundant (your lungs have about 300 million alveoli with a total surface area of about 75 square meters)

2. Internal respiration - intracellular use of O2 to make ATP 3. Occurs by simple diffusion along partial pressure gradients

What is Partial Pressure?: 1. It's the individual pressure exerted independently by a particular gas within a

mixture of gasses. The air we breath is a mixture of gasses: primarily nitrogen, oxygen, & carbon dioxide. So, the air you blow into a balloon creates pressure that causes the balloon to expand (& this pressure is generated as all the molecules of nitrogen, oxygen, & carbon dioxide move about & collide with the walls of the balloon). However, the total pressure generated by the air is due in part to nitrogen, in part to oxygen, & in part to carbon dioxide. That part of the total pressure generated by oxygen is the 'partial pressure' of oxygen, while that generated by carbon dioxide is the 'partial pressure' of carbon dioxide. A gas's partial pressure, therefore, is a measure of how much of that gas is present (e.g., in the blood or alveoli).

2. The partial pressure exerted by each gas in a mixture equals the total pressure times the fractional composition of the gas in the mixture. So, given that total atmospheric pressure (at sea level) is about 760 mm Hg and, further, that air is about 21% oxygen, then the partial pressure of oxygen in the air is 0.21 times 760 mm Hg or 160 mm Hg.

Partial Pressures of O2 and CO2 in the body (normal, resting conditions): 1) Alveoli:

a. PO2 = 100 mm Hg b. PCO2 = 40 mm Hg

2) Alveolar capillaries: a. Entering the alveolar capillaries:

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Ø PO2 = 40 mm Hg (relatively low because this blood has just returned from the systemic circulation & has lost much of its oxygen) Ø PCO2 = 45 mm Hg (relatively high because the blood returning from the systemic circulation has picked up carbon dioxide)

While in the alveolar capillaries, the diffusion of gasses occurs: oxygen diffuses from the alveoli into the blood & carbon dioxide from the blood into the alveoli.

Leaving the alveolar capillaries · PO2 = 100 mm Hg · PCO2 = 40 mm Hg

Blood leaving the alveolar capillaries returns to the left atrium & is pumped by the left ventricle into the systemic circulation. This blood travels through arteries & arterioles and into the systemic, or body, capillaries. As blood travels through arteries & arterioles, no gas exchange occurs.

Entering the systemic capillaries PO2 = 100 mm Hg PCO2 = 40 mm Hg

Body cells (resting conditions) PO2 = 40 mm Hg PCO2 = 45 mm Hg

Because of the differences in partial pressures of oxygen & carbon dioxide in the systemic capillaries & the body cells, oxygen diffuses from the blood & into the cells, while carbon dioxide diffuses from the cells into the blood.

Leaving the systemic capillaries PO2 = 40 mm Hg PCO2 = 45 mm Hg

Blood leaving the systemic capillaries returns to the heart (right atrium) via venules & veins (and no gas exchange occurs while blood is in venules & veins). This blood is then pumped to the lungs (and the alveolar capillaries) by the right ventricle.

How are oxygen & carbon dioxide transported in the blood? Oxygen is carried in blood: 1 - bound to hemoglobin (98.5% of all oxygen in the blood) 2 - dissolved in the plasma (1.5%) Because almost all oxygen in the blood is transported by hemoglobin, the

relationship between the concentration (partial pressure) of oxygen and hemoglobin saturation (the % of hemoglobin molecules carrying oxygen) is an important one.

Hemoglobin saturation: Ø extent to which the hemoglobin in blood is combined with O2 Ø depends on PO2 of the blood:

Ошибка! Неизвестный аргумент ключа. Figure. Oxyhemogflobin dissociation curve. The relationship between oxygen levels and hemoglobin saturation is indicated

by the oxygen-hemoglobin dissociation (saturation) curve (in the graph above). You can see that at high partial pressures of O2 (above about 40 mm Hg), hemoglobin saturation remains rather high (typically about 75 - 80%). This rather flat section of the oxygen-hemoglobin dissociation curve is called the 'plateau.'

Recall that 40 mm Hg is the typical partial pressure of oxygen in the cells of the body. Examination of the oxygen-hemoglobin dissociation curve reveals that, under

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resting conditions, only about 20 - 25% of hemoglobin molecules give up oxygen in the systemic capillaries. This is significant (in other words, the 'plateau' is significant) because it means that you have a substantial reserve of oxygen. In other words, if you become more active, and your cells need more oxygen, the blood (hemoglobin molecules) has lots of oxygen to provide. When you do become more active, partial pressures of oxygen in your (active) cells may drop well below 40 mm Hg. A look at the oxygen-hemoglobin dissociation curve reveals that as oxygen levels decline, hemoglobin saturation also declines - and declines precipitously. This means that the blood (hemoglobin) 'unloads' lots of oxygen to active cells - cells that, of course, need more oxygen.

The oxygen-hemoglobin dissociation curve 'shifts' under certain conditions. These factors can cause such a shift: Ø lower pH Ø increased temperature Ø more 2,3-diphosphoglycerate Ø increased levels of CO2

These factors change when tissues become more active. For example, when a skeletal muscle starts contracting, the cells in that muscle use more oxygen, make more ATP, & produce more waste products (CO2). Making more ATP means releasing more heat; so the temperature in active tissues increases. More CO2 translates into a lower pH. That is so because this reaction occurs when CO2 is released:

CO2 + H20 H2CO3 HCO3- + H+ & more hydrogen ions = a lower (more acidic) pH. So, in active tissues, there are

higher levels of CO2, a lower pH, and higher temperatures. In addition, at lower PO2 levels, red blood cells increase production of a substance called 2,3-diphosphoglycerate. These changing conditions (more CO2, lower pH, higher temperature, and more 2,3-diphosphoglycerate) in active tissues cause an alteration in the structure of hemoglobin, which, in turn, causes hemoglobin to give up its oxygen. In other words, in active tissues, more hemoglobin molecules give up their oxygen. Another way of saying this is that the oxygen-hemoglobin dissociation curve 'shifts to the right' (as shown with the light blue curve in the graph below). This means that at a given partial pressure of oxygen, the percent saturation for hemoglobin with be lower. For example, in the graph below, extrapolate up to the 'normal' curve (green curve) from a PO2 of 40, then over, & the hemoglobin saturation is about 75%. Then, extrapolate up to the 'right-shifted' (light blue) curve from a PO2 of 40, then over, & the hemoglobin saturation is about 60%. So, a 'shift to the right' in the oxygen-hemoglobin dissociation curve (shown above) means that more oxygen is being released by hemoglobin - just what's needed by the cells in an active tissue!

Carbon dioxide - transported from the body cells back to the lungs as: 1 - bicarbonate (HCO3) - 60% formed when CO2 (released by cells making ATP) combines with H2O (due to

the enzyme in red blood cells called carbonic anhydrase) as shown in the diagram below

2 - carbaminohemoglobin - 30% formed when CO2 combines with hemoglobin (hemoglobin molecules that have

given up their oxygen)

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3 - dissolved in the plasma - 10% Figure. Carbon dioxide transport. 4. Materials for auditory self-work. 4.1. List of study practical tasks necessary to perform at the practical class. Materials and methods: spirograph, oxygen, clamps for lips and nose, paper for

registration, cotton wool, alcohol. The investigated object: human being.

Task 1.

To investigate respiratory ways conductance by forced (prolonged) expiration duration and volume measurement by Wotchall-Tiffno method. To determine expiratory forced expiration volume for 1 sec (expiratory functional

vital lung capacity EFVLC) and forced expiration duration up to the moment of its sharp inhibiting on forced expiration spirogram. For this it’s necessary to postpone 2 cm (it corresponds to 1 sec at strip movement 1200 mm/min; if v=600 mm/min, 1 sec is equal to 1 cm) from the moment of forced expiration beginning and to lower the perpendicular up to the crossing with expiration curve. To determine air volume expirated for 1 sec and to estimate its correlation to VLC according to following formula:

EFVLC (for 1 sec) x 100% : VLC

In healthy people this ciphra must be not less than 70%. Forced expiration under norm is 2-4 sec.

Normal values: – men - 3800±124 ml; – women - 2628±100 ml. To make the conclusion about respiratory ways conductance in an investigated

person (according to the data received). Respiratory resistance increasing indicates to mucosa oedema, hyperemia, as well as respiratory ways smooth myocytes spasmatic phenomena and pus secrete conglomeration.

Qualitative assessment of forced expiration volume curve gives the representation about breathing mechanics state. Gently sloping form of the curve superior 1/3 reflects large bronchi resistance, stretching ending part reflects to weakening conductivity in shine respiratory ways as well as lungs elasticity lowering. Stepped course of the curve reflects valvular mechanism of bronchial conductivity disorder. Functional vital lung capacity and Tiffno index are lowered significantly at diseases accompanied by obstructive disorders of ventilation (bronchial asthma). Tiffno index decreasing at non-significant change in FVLC are observed at ventilation restrictive disorders (chronic pneumonia).

Table 17 Tiffno index dependence on age

Age, years Average value Norm limits, % 4-6 94,0 85 7-11 89,0 75 12-16 84,0 70

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Task 2. To determine respiration reserve.

Respiration reserve (RR) is determined by formula: RR=MLV-MRV

where MLV – maximal lung ventilation; MRV – minute respiratory volume. RR is more than RMV not less than in 15-20 times (under physiological

conditions). It’s necessary to write in all estimation results in the copy-books. Students have to assess received indexes of respiration reserve taking into

account that RR in healthy people is not less than 85% of MLV. It reduces at respiratory insufficiency up to 50-60% or even more.

Given volumes determine ability to ventilated air amount rising and are decreased at different pathological conditions. Inspiration reserve volume decreasing is observed at restrictive processes, at pulmonary tissue elasticity lowering. Expiration reserve volume decreasing takes part more often at obstructive injuries especially accompanied by emphysema.

Task 3.

To determine maximal lung ventilation (MLV) Students must choose the mostly characteristic (distinctive) locus with the

duration in 10 sec (20 cm) on spirogram of maximally frequent and deep respiration movements. Then it's necessary to determine respiratory movements amount and multiply them on 6. This size corresponds to respiration frequency for 1 min. Then students should count average respiratory volume and multiply it on the received respiration rate. The size received corresponds to maximal lung ventilation. Under normal conditions it is equal to 80-200 l/min. Individual maximal lung ventilation should be counted on spirometric ruler. According to A.G.Dembo, necessary MLV (NMLV) is equal to VLC x 35. While making comparison between MLV and NMLV one can assess the investigated person respiratory system functional state.

MVL undergoes to significant individual fluctuiations and depends on different pulmonary and extrapulmonary factors. MVL like Tiffno index allows testify to summary changings in respiration mechanics. It reflects muscular power, thorax and lungs stretching as well as resistance to air flow. It characterizes respiration reserve abilities.

MVL decreasing can be observed both as a result of pulmonary volumes decreasing because of restrictive disorders accompanied by lungs stretching lowering and at bronchial resistance increasing as a result of organic (functional) obstructive changins. If MVL is normal but VLC is significantly lowered one can tell about restrictive disorders. MVL significant lowering at practically normal VLC is characteristic for obstructive injuries.

5. Literature recommended: 1. Lecture course. 2. Mistchenko V.P., Tkachenko E.V. Methodical instructions for dental students (short lecture course).-Poltava, 2005.-P.50-53.

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3. Mistchenko V.P., Tkachenko E.V. Methodical instructions for medical students (short lecture course).-Polatava, 2005.-P.84-86. 4. Methodical instructions on chapter “Respiration system” on practical classes for dental and medical students. 5. Kapit W., Macey R.I., Meisami E. The Physiology Colouring Book: Harpers Collins Publishers, 1987.-P.47-50. 6. Stuart Ira Fox. Human Physiology.-8-th Ed.-Mc Graw Hill, 2004.-P.493-499. 7. Seeley R.R., Stephens T.D., Tate P. Essentials of Anatomy and Physiology.-The 3rd Ed.-McGraw Hill, 1999.-P. 406-410.

LESSON 53 RESPIRATION REGULATION

1. The topic studied actuality: Doctor very often deals with situation when it is

essential to help the patient with respiration disorder rapidly, effectively, qualified. For instance – during labors taking, to drowned man, at intoxication with CO (carbonic monoxide).

2. Study aim: To know: respiration regulation main processes; to know about respiratory center

structure and activity. To be able: to determine respiration lack maximal duration in human being during

inspiration, expiration, inspiration after hyprventilation and to perform the analysis of mechanisms influencing on respiration lack duration.


Subject To know To be able to Anatomy

Respiratory ways anatomy Show main morphological elements on tables and special models and to describe them





Patho-morphological changes at main diseases of respiratory system as well as hypertony and hypotony


Pathophysiology Developmental mechanisms of main pathological processes in respiratory system


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Internal Diseases

Ethiology, pathogenesis, clinics, diagnostics, therapy and prevention principles of respiratory system pathological conditions as well as hypertonic and hypotonic states

Make correction in respiratory and heart-vascular systems without medicines application


Respiratory system and heart-vascular system peculiarities in different-aged children

Make correction in respiratory and heart-vascular systems without medicines application

3.2. Topic content. Respiration regulation is performed by means of reflectory reactions occurring as

a result of excitement of specific receptors located in lung tissue, vascular reflexogenic zones and other regions. Respiration regulation central apparatus are the structures of:

– spine; – medulla oblongata; – hypothalamus; – brain hemispheres. Main function of respiration management is performed by stem repiratory

neurons which transmit rhythmic sygnals into spine to respiratory muscles motoneurons.

Respiratory nervous center – is central nervous system neurons integrity providing respiratory muscles co-ordinated rhythmical activity and external respiration constant adaptation to changing conditions inside organism and in environment. Main (working) part of respiratory nervous center is located in medulla oblongata. One can differentiate 2 parts in it: inspiratory (inspiration center) and expiratory (expiration center). Medulla oblongata respiratory neurons dorsal group primarily consists of inspiratory neurons. They give particularly the stream of descendant ways getting the contact with diaphragmal nerve motoneurons. Respiratory neurons ventral group sends primarily descendant fibres to intercostal muscles motoneurons. One can see region in pons anterior part called as pneumotaxic center. This center deals with activity both of inspiratory and expiratory center parts providing the change of inspiration and expiration. Respiratory center important part is neurons group of spine cervical part (III-IV cervical segments), where diaphragmal nerves nuclei are situated.

Apneustic center (located in the pons) - stimulate I neurons (to promote inspiration).

Pneumotaxic center (also located in the pons) - inhibits apneustic center and inhibits inspiration.

Respiratory center excitement mechanisms are the following. 1. One of the most important ways of its excitement is automatism. There is not

one point of view to automatism nature but there exist data about secondary depolarization occurrence in respiratory neurons (like diastolic depolarization in myocardium) which reaching its critical level gives new impulse.

2. But one of main ways of respiratory center excitement is its irritation by carbonic acid. As it was mentioned above, there remains much carbonic acid in

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blood leaving lungs. It performs the function of medulla oblongata neurons main irritator. It is mediated through special structures – chemoreceptors, located directly in medulla oblongata structures (“central chemoreceptors”). Thus, the second way – through blood.

3. They are very sensitive to carbonic dioxide tension and acid-alkaline state of intercellular liquor washing them.

4. Carbonic acid can easily diffund from brain vessels in liquor and stimulates medulla oblongata chemoreceptors.

5. Reflectory way - there are 2 reflexes groups (like for cardio-vascular system): proper and conjugated.

I. Proper reflexes – the reflexes originated from respiratory system organs and finished in it.

1) Reflex from lung mechanoreceptors. According to localization and type of percepted irritations, reflectory answer to irritation one can differentiate 3 types of such receptors: receptors of stretching, irritant receptors and lung juxtacapillary receptors. 2) Lung stretching receptors – are primarily located in air ways (trachea, bronchi)

smooth muscles. There are approximately 1000 receptors in every lung and they are connected with respiratory center by large mielinized afferent fibres of vagus with very high conductance velocity. Direct irritator – internal tension in air ways walls tissues. Such impulses frequency is increased at lung stretching in course of inspiration. Lung swelling causes inspiration reflectory inhibition and transition to expiration. These reactions are stopped at vagus cutting and respiration becomes retarded and deep. Mentioned reactions are called Gering-Breyer’s reflex. This reflex is reproduced in adult person when his respiratory volume is more than 1 l (at physical training for instance). It is of essential importance in new-borns. Their adaptation is slow.

Ø Irritant receptors or slowly adaptating air ways mechanoreceptors, trachea and bronchi mucosa receptors. They answer to lung volume significant changes, chemical or mechanical irritators (mucus, tobacco, dust particles and so on) action to mucosa. Their adaptation is fast. At side bodies coming into respiratory ways there occurs cough reflex after irritant receptors activation. Reflectory arch of cough reflex – receptors – superio-laryngeal, glosso-pharyngeal, trygeminal nerves – expiratory part of respiratory center. Result - strong expiration – cough. At isolated irritation of nasal respiratory ways receptors second immediate expiration occurs – sneezing.

Ø Juxtacapillary receptors are located near alveolar and respiratory bronchi capillaries. Irritators: pressure increasing in circulation small circle and intersticial liquid volume increasing in lungs. Such situation is observed at blood stagnation in small circulation circle, lung oedema, lung tissue injury (at pneumonia et al.). Impulses from these receptors are directed to respiratory center through vagus causing frequent surface breathing occurrence. There may be not only freaquent breathing (tachypnoe) but also reflectory bronchoconstriction.

5) Reflexes from respiratory musculature proprioreceptors: 1.Reflex from intercostal muscles proprioreceptors is realized in course of

inspiration when these muscles while their contraction send information through intercostal nerves to respiratory center expiratory part and as a result expiration occurs.

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2.Reflex from diaphragm proprioreceptors – is performed as an answer to its contraction in course of inspiration. Result: information comes through diaphragmal nerves first in spine, than in medulla oblongata in its expiratory part and expiration occurs.

Thus, all respiratory system proper (own) reflexes are realized in course of inspiration and are resulted in expiration.

II. Conjugated reflexes – reflexes originated out of respiratory system. 1. Reflex onto conjugation of blood circulation and respiration systems – is

originated from perypheral chemoreceptors of vascular reflexogenic zones. The most sensitive of them are located in sino-carotid zone region. 2. Sino-carotid chemoreceptive conjugated reflex – is performed at carbonic

dioxide accumulation in blood. If its tension increases than the irritation of the most sensitive chemoreceptors (they are in this zone in sino-carotid body) occurs, excitement wave comes from them through IX pair of cranio-cerebral nerves and reaches respiratory center expiratory part. Expiration occurs which enforces releasing of excessive carbonic acid in surrounding space. Thus, blood circulation system (while this reflectory act performance it works more intensively: heart contractioin frequency and blood stream velocity increase) influences on respiration system.

3. Exteroreceptive reflexes are originated from tactile (remember your breathing reaction on touching of lovely person), temperature (warmth – increases, coldness – decreases respiratory function), noceoceptive (weak stimuli and of a middle force - increase, strong – suppress breathing) receptors.

4. Proprioreceptive reflexes – are performed due to irritation of receptors of skeletal muscles, joints, ligaments. It is observed in course of physical training doing. Why? If under rest state it’s necessary 200-300 ml oxygen per minute for human than at physical loading given volume must be significantly increased. Under these conditions both minute volume and arterio-venous difference on oxygen are increased. These indexes increasing is accompanied by oxygen consumption rising up. At work duration of only 2-3 minutes and its significant power oxygen consumption grows uninterruptedly from the very beginning of work and is decreased only after its stoppage. At work duration more, oxygen consumption, while increasing in course of first minutes, is supported all the time on its constant level. Oxygen consumption increases the more the harder physical work it is. Maximal oxygen amount that organism can use per 1 minute at the hardest work for it is called oxygen maximal consumption (OMC). Work at which person reaches his OMC level must have duration not less then 3 minutes. There exists many ways of OMC determining. It doesn’t predominate 2,0-2,5 l/min in untrained people. It can be twice large in sportsmen and even more. OMC is an index of organism aerobic productivity. This human ability to perform very hard physical work, providing his energetic consumption due to oxygen used directly in course of work. It is known that even well-trained person can work at oxygen consumption 90-95% from his OMC level not more than 10-15 min. One having more aerobic productivity reaches better results in work (sport) at practically equal technic and tactic preparation. Why oxygen consumption is increased in course of physical activity? One can differentiate several reasons:

-additional capillaries opening and blood increasing in them;

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-oxyhemoglobin dissotiation curve movement to the right and below; -temperature increasing in muscles. For performing their work, muscles need in energy, the accumulations of which

are restored while oxygen transport. Thus, there exists definite dependence between work power and oxygen amount necessary for work. That blood amount necessary for work is called oxygen asking. Oxygen asking can reach up to 15-20 liters per minute and even more in course of hard work. But maximum of oxygen consumption is less in 2-3 times. Does it possible to perform the work if minute oxygen accumulation predominates OMC? For correct answer this question one should remember for what oxygen is used in course of muscular activity. It is essential for macroergic substances restoration providing muscular contraction. Usually oxygen interacts with glucose and it releases the energy while its oxidation. But also glucose can be destructed without oxygen, i.e. by anaerobic way as a result of which energy releases too. These are also other substances possessing the ability to be destructed without oxygen. Thus, muscular activity can be provided at insufficient oxygen coming into organism too. But in this case many acid products are formed and it’s necessary oxygen for their destruction because they are destructed by oxidation. Oxygen amount necessary for metabolism products oxidation that were formed in course of physical activity is called oxygen debt. It appears in course of work and is liquidated in restoration period after work end. Usually this disappearing takes from several minutes to 1 hour and a half. Everything depends on work duration and intensivity. Lactic acid plays the most important role in oxygen debt forming. To continue his work at lactate presence in blood in great amounts organism must have powerful buffer systems and his tissues are to be adapted to work under hypoxy conditions. Such organism adaptation serves as one of factors providing high aerobic productivity. All the mentioned above complicate respiration regulation at physical activity because oxygen taking in organism is increased and its blood hypoxy leads to chemoreceptors irritation. Signals from them come in respiratory center as the result of which respiration becomes more frequent. A great number of carbonic acid is formed in course of muscular activity that comes into blood and it can acts to respiratory center directly through central chemoreceptors. If blood hypoxy leads primarily to breathing quickening than carbonic acid surplus causes its deepening. Both these factors act simultaneously in course of physical activity and that’s why respiration quickening and deepening takes place. Finally, impulses coming from working muscles, reach respiratory center and enforces its activity. At respiratory center functionning all its parts are functionally interconnected by means of following mechanism: at carbonic acid accumulation respiratory center inspiratory part is excited from information comes in pneumotaxic part, then to its expiratory part. The latest, besides, is excited by means of a whole group of reflectory acts – from receptors of lungs, diaphragm, intercostal muscles, respiratory ways, vessels chemoreceptors. Inspiration center activity is inhibited due to its excitement through special inhibitory reticular neuron and inspiration is changed by expiration. As expiration center is inhibited it doesn’t send impulses far into pneumotaxic center and information flow is stopped from it to expiration center. Carbonic acid is accumulated in blood by this time and inhibitory influencings on expiratory part are inhibited. Inspiration center is excited due to such information flow redisposition and expiration is changed by inspiration. And everything is repeated again.

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Vagus is an essential link in respiration regulation. Main influencings to expiration center come through it. That’s why at its injury (like at pneumotaxic center injury) respiration is changed so that inspiration remains normal and expiration is sharply prolonged – vagus-dyspnoe.

As it was mentionned above in course of coming to the highlands lung ventillation increasing occurs based on vascular zones chemoreceptors stimulation.

Heart contraction freaquency and minute volume are increased simultaneously with this. These reactions improve oxygen transport in organism a little but not not for long. That’s why at durable staying into mountains with adaptation to chronic hypoxy initial (urgent) respiration reactions gradually leave their place to more economic adaptation of gas-transport organism system. In constant residents of highlands respiration reaction to hypoxy is too weak (hypoxic deafness) and lung ventillation is supported practically on the same level like in plane residents. At the same time at durable staying under conditions of highlands vital lung capacity, caloric oxygen equivalent, myoglobine content in muscles, mitochondrial enzymes activity (providing biological oxidation and glycolysis) are increased; organism tissues (particularly central nervous system) sensitivity to insufficient oxygen supply is decreased. At high more than 12000 m air pressure is very small and under these conditions even breathing by pure oxygen doesn’t solve the problem. That’s why at flyings at this high one need hermetic cockpits (planes, cosmic ship).

Sometimes human being has to work under increasing pressure conditions (divering). In the depth nitrogen becomes its dissolving in blood and in course of fast rising out off the depth it doesn’t manage to release from blood, gas vesicles cause vessel emboly. Occuring condition is called kessonic disease. It is accompanied by pain in joints, giddiness, dyspnoe, unconsciousness. That’s why nitrogen in air mixtures is changed on insoluble gases (for instance, helium).

Human being can delay free his breath not more than on 1-2 minutes. After preliminary lung hyperventillation this respiration delay is rised up to 3-4 minutes. But durable, for example, diving after hyperventillation is very dangerous. Blood oxygenation sharp decreasing can cause sudden unconsciousness. Under this state swimmer (even experienced one) under stimulus action caused by carbonic acid partial tension increasing in blood can inspirate water and choke (drown).

Thus, at the end of our lecture we must to remember you that healthy breathing – is nasal, as slow and seldom as possible, with its lack in course of inspiration and, especially, after it. While prolonging the inspiration, we stimulate vegetative nervous system sympathetic part work with all following consequences. While prolonging the expiration, we carry carbonic acid in blood more and longer that positively influences on blood vessels tone (decreases it) will all following consequences. Due to this oxygen under such situation can come in the farthest microcirculative vessels preventing disorders of their function and development of many diseases. Correct breathing – is a prevention and treatment of big group of diseases not only of respiratory system but also of other organs and tissues! Breath for enjoy!

4. Materials for auditory self-work.

4.1. List of study practical tasks necessary to perform at the practical class. Materials and methods: spirograms, stop-watches. The investigated object: human being.

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Task 1. To perform probes with respiration delay on inspiration (Shtange probe)

and on expiration (Genche probe) under resting state. The investigated person must sit. He must inspirate deeply and in the highland of

a very deep (but not maximal) inspiration he must delay his respiration while pressing his nose. Delay time must be registrated on stop-watch. Then he can delay his respiration after deep expiration (but rest in 5-7 min of usual, not deep respiration).

Probes results assessment: delay on inspiration under norm is 55-60 sec (minimally 30-40 sec); in expiration – 30-40 sec (minimally 20 sec). In young trained people delay time is increased.

Task 2. To perform probes with respiration delay on inspiration and expiration after

20 sitting down for 30 sec (probe with physical loading). The investigated person performs 20 sitting down for 30 sec, then right after this

he delays his respiration on inspiration clamping his nostrils. After respiration restoration the physical loading is repeated and respiration is retarded (delayed) on expiration.

To perform spirogram analysis with respiration delay on inspiration and expiration under resting conditions and after physical loading.

Task 3. Muller's probe.

To count the investigated person pulse initial rate. To try to perform inspiration at closed mouth and clamped nose, to do corresponding musculature strong contraction. To count pulse in course of probe paying the attention to it's rhythmicity and filling.

Task 4. Walsava probe.

To count the investigated person pulse initial rate. To try to perform expiration after deep inspiration at closed mouth and clamped nose. To count pulse in course of probe paying the attention to it's rhythmicity and filling.

5. Literature recommended: 1. Lecture course. 2. Mistchenko V.P., Tkachenko E.V. Methodical instructions for dental students (short lecture course).-Poltava, 2005.-P.53-58. 3. Mistchenko V.P., Tkachenko E.V. Methodical instructions for medical students (short lecture course).-Polatava, 2005.-P.87-90. 4. Methodical instructions on chapter “Respiration system” on practical classes for dental and medical students. 5. Kapit W., Macey R.I., Meisami E. The Physiology Colouring Book: Harpers Collins Publishers, 1987.-P.51-52. 6. Stuart Ira Fox. Human Physiology.-8-th Ed.-Mc Graw Hill, 2004.-P.499-515.410-419. 7. Seeley R.R., Stephens T.D., Tate P. Essentials of Anatomy and Physiology.-The 3rd Ed.-McGraw Hill, 1999.-P. 410-419.

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LESSON 54 SITUATIONAL TASKS AND PRACTICAL EXPERIENCE ON CONTENT

CREDIT 13: “RESPIRATION SYSTEM”

PRACTICAL SKILLS 1. To draw spirogram, to mark main respiratory volumes that can be determined

on it, their normal values.

TESTS ON HEART-VASCULAR AND RESPIRATION SYSTEMS PHYSIOLOGY

HEART-VASCULAR SYSTEM PHYSIOLOGY TESTS

1. Vessels constriction and dilation regulation processes are very important for organism proper functionning. Call hormone causing vasoconstriction:

a)* noradrenaline; b) aldosterone; c) thyroxine; d) glucagone; e) parathormone.

2. One can see significant hypersympathicotony in course of emotional stress. Indicate the most possible heart activity changings:

a) arhythmias; b) heart stoppage due to tetanic heart muscle contraction; c) heart contraction frequency and force decreasing; d) heart activity remains unchangeable; e) *heart contraction frequency and force increasing.

3. Patient takes drugs blocking calcium channels. Indicate processes in myocardium they influence on:

a) excitability; b) *electro-mechanical conjugation; c) conductiveness; d) automatism;

e) rhythm assimilation. 4. Patient has impulse conductance velocity decreasing while its passage

through atrio-ventricular node.It will lead to: a) dense P altitude increasing; b) cardiac contractions rate diminishing; c) *interval P-Q prolongation; d) QRS complex enlarging; e) segment S-T duration increasing.

5. In course of cardiomiocytes action potential registration one can see plateau phase duration increasing. It is connected with:

a) sodium channels activation; b) rapid calcium channels activation; c) potassium channels inactivation; d) *slow calcium channels activation;

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e) slow calcium channels inactivation. 6. In course of neck muscles massage in patient his arterial pressure is sharply

decreased. Indicate main reason: a) *carotid sinus baroreceptors irritation; b) skin vessels dilation; c) muscles vessels dilation; d) reflectory muscular relaxation; e) inner (visceral) organs vessels dilation.

7. In which cardiac cycle period all heart valves are closed: a) rapid expulsion; b) asynchronic contraction; c) *isometric contraction; d) slow expulsion; e) active (fast) filling.

8. Which muscular contraction type is cardiac muscle distinguishing characteristic:

a) smooth (complete) tetanus; b) *single contraction;

c) incomplete tetanus; d) tonic contraction; e) isometric contraction.

9. Patient was injected by noradrenaline. Through which receptors it caused vasoconstriction?

a) *alpa-adrenoreceptors; b) beta-adrenoreceptors; c) N-cholinoreceptors; d) M-cholinoreceptors; e) H1-hystaminic receptors.

10. Indicate QRS complex normal duration: a) 0,04-0,12 sec; b) 0,02-0,05 sec; c) *0,08-0,1 sec; d) 0,06-0,15 sec; e) all answers are uncorrect.

11. Indicate possible reason of such EKG disorder at which one can see unequal interval R-R (with their duration 0,6-1,0 sec):

a) heart attack (myocardial ishemia); b) myocardial infarctum; c) left ventricle hypertrophy; d) arhythmia;

e) all answers are uncorrect. 12. It was established under experimental conditions that at trophyc Pavlov’s

nerve irritation cardiac contractions enforcement is observed. Indicate acting mediator:

a) *adrenaline; b) acetylcholine; c) serotonin; d) dophamine;

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e) GAOA (gamma-amino-oleic acid). 13. It is known that pulse wave distribution velocity in elder people is higher than

in young. Age changings of which cardiac-vascular system features do influence on investigations results?

a) Blood circulation velocity. b) *Vascular wall elasticity. c) Heart throw level. d) Heart contractions rate. e) Arterial pressure.

14. In course of EKG-investigation of patient suffering from thyroid hyperfunction it was made the conclusion about tachycardia. On the basis of which EKG elements analysis it has been done?

a) Interval P-T. b) Segment P-Q. c) Interval P-Q. d) *Interval R-R. e) Complex QRS.

15. There are next changings on patient’s EKG: segment S-T transposition and dens T prolongation (up to 0,25 sec). Indicate heart function with the disorders of which such changings are delt with?

a) Ventricles depolarization. b) Atria depolarization. c) Atria repolarization. d) *Ventricles repolarization. e) Excitement transmission through a/v node.

16. Cardiomyocytes calcium channels were partially blocked on isolated rabbit’s heart. Indicate heart activity changings due to this operation:

a) contractions rate decreasing; b) *contractions rate and force diminishing; c) contractions force decreasing; d) heart stoppage in dyastole; e) heart stoppage in systole.

17. EKG-investigation of 45-yeared man demonstrated P dens absence in all leads. Block of which conductance system part can be predicted?

a) Gis’ fascicle left bundle. b) Gis’ fascicle right bundle. c) Purkin’e fibers. d) Atrio-ventricular node. e) *Sino-atrial node.

18. Which effects can be observed in emotionally excited person as the result of hypersympathicotony?

a) Positive inothropic, bathmothropic, tonothropic and negative chronothropic and dromothropic effects. b) Negative bathmothropic and dromothropic, positive chronothropic and inothropic effects. c) *Positive chronothropic, inothropic, bathmothropic and dromothropic effects.

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d) Positive chronothropic without any expressions of dromothropic, bathmothropic, inothropic and tonothropic effects. e) Positive bathmothropic, inothropic, chronothropic and negative dromothropic effect.

19. Prove that vagus irritation causes conductive heart function inhibition: a) *interval P-Q prolongation on EKG more than 0, 20 sec; b) QRST complex prolongation on EKG more than 0,45 sec; c) anacrote prolongation on sphygmogram; d) catacrote prolongation on sphygmogram; e) it’s necessary to determine heart throw level and to mark its diminishing.

20. In rabbit in 1 month after surgical kidney artery constriction significant systemic arterial pressure increasing was registrated. Indicate main acting substance under such conditions:

a) *angiotensin-II; b) vasopressin (antidiuretic hormone); c) adrenaline; d) noradrenaline; e) serotonin.

21. Which myocardium physiological peculiarities can be assessed on EKG? a) Excitability, automatism, contractiveness. b) *Excitability, conductiveness, automatism. c) Excitability, contractiveness, refractiveness. d) Contractiveness, automatism, conductiveness. e) Contractiveness, refractiveness, automatism.

22. Atypical cardiomyocytes were processed by pharmacological agent under experimental conditions as the result of which their membrane potential increasing (hyperpolarization) was observed. Indicate this substance:

a) tyroxine; b) adrenaline; c) noradrenaline; d) *acetylcholine; e) atriopeptide.

23. Patient has significant blood volume decreasing as the result of bleeding. Which homeostatic index will be restored first of all?

a) Calcium content in blood. b) Osmotic pressure. c) Oncotic pressure. d) Sodium ions content in blood. e) *Circulating blood volume.

RESPIRATION SYSTEM PHYSIOLOGY

1. Brain stem cutting between pons cerebri and medulla oblongata under experimental conditions in animal causes expiration phase duration increasing. Respiratory center connection with which brain structure is injured at this case?

a) *Pneumotaxic center. b) Reticular formation. c) Cerebellum.

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d) Brain cortex. e) Red nuclei.

2. Human being presence under decreased atmospheric pressure conditions leads to hypoxy development. Indicate kidney reaction under such conditions:

a) erythropoietines secretion diminishing; b) filtration decreasing; c) filtration increasing; d) *erythropoietines secretion increasing; e) reabsorbtion disorder.

3. Under experimental conditions in course of experiment on dog examinator was deteremining blood gas content influence on respiration process. Maximal influence on carotid zone chemoreceptors with the following respiration enforcement has:

a) *hypoxy; b) hyperoxy; c) hypocapnia; d) lactate increasing; e) pH changing.

4. Injuries of which medulla oblongata centers first of all lead to death? a) alimentary, of muscular tone; b) *respiratory, heart-vascular; c) of protective reflexes, alimentary; d) motoric reflexes, alimentary; e) of musclular tone, protective reflexes.

GLOSSARY

ON CONTENT MODULE 12: BLOO CIRCULATION SYSTEM

A Acute myocardial infarction (AMI or MI) commonly known as a heart attack, is a disease state that occurs when the blood supply to a part of the heart is interrupted. The resulting ischemia or oxygen shortage causes damage and potential death of heart tissue. Aorta: the largest of the arteries in the systemic circuit. Aortic Valve: lies between the left ventricle and the aorta. Antidiuretic hormone: Produced in the posterior pituitary ADH (vasopressin), major function is to regulate blood pressure by water retention by the kidneys. Arteriole: a small diameter blood vessel that extends and branches out from an artery and leads to capillaries. Atrial natriuretic peptide: Produced in the atria of the heart, it increases urinary excretion of sodium which causes water loss which in turn the viscosity of the blood is lowered and in turn lowers the blood pressure. Atrioventricular Node (abbreviated AV node): the tissue between the atria and the ventricles of the heart, which conducts the normal electrical impulse from the atria to the ventricles. Atrioventricular valves: large, multi-cusped valves that prevent backflow from the ventricles into the atria during systole.

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AV Bundle: collection of heart muscle cells specialized for electrical conduction that transmits the electrical impulses from the AV node.

B Barbiturates: CNS depressants, sedative-hypnotics. Blood Pressure: the pressure exerted by the blood on the walls of the blood vessels.

C Capillaries: the smallest of a body’s vessels, they connect arteries and veins. Cardiac Cycle: term used to describe the sequence of events that occur as a heart works to pump blood through the body. Cerebral Vascular Accident (CVA): Also known as a stroke, is a rapidly developing loss of a part of brain function or loss of conciousness due to an interruption in the blood supply to all or part of the brain. That is, a stroke involves the sudden loss of neuronal function due to a disturbance in cerebral perfusion. There are many different causes for the interruption of blood supply, and different parts of the brain can be affected. Because of this, a stroke can be quite heterogeneous. Patients with the same cause of stroke can have widely differing handicaps. Similarly, patients with the same clinical handicap can in fact have different causes of their stroke. Chordae Tendinae: cord-like tendons that connect the papillary muscles to the tricuspid valve and the mitral valve in the heart. Coronary Arteries: blood vessels that supply blood to, and remove blood from, the heart muscle itself. Continuous Capillaries: have a sealed epithelium and only allow small molecules, water and ions to diffuse.

D Deep-vein thrombosis (DVT): is the formation of a blood clot ("thrombus") in a deep vein. It commonly affects the leg veins, such as the femoral vein or the popliteal vein or the deep veins of the pelvis. Occasionally the veins of the arm are affected. Diastole: period of time when the heart relaxes after contraction in preparation for refilling with circulating blood. Diastolic Pressure: lowest point in blood pressure where the heart relaxes.

E Edema: The swelling that forms when too much tissue fluid forms or not enough taken away. Electrocardiogram: the recording of the heart's electrical activity as a graph. Epinephrine: Produced in the adrenal medulla of the adrenal glands, major function is vasoconstriction that will in turn increase respiratory rate and increase cardiac out put.

F Fenestrated Capillaries: have openings that allow larger molecules to diffuse. Fibrous Pericardium: a dense connective tissue that protects the heart, anchoring it to the surrounding walls, and preventing it from overfilling with blood.

H Heart Rate: term used to describe the frequency of the cardiac cycle.

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Hepatic Veins: blood vessels that drain de-oxygenated blood from the liver and blood cleaned by the liver (from the stomach, pancreas, small intestine and colon) into the inferior vena cava. Hypertension or High Blood Pressure: medical condition wherein the blood pressure is chronically elevated.

I Inferior Vena Cava (or IVC): a large vein that carries de-oxygenated blood from the lower half of the body into the heart. Intraventricular Septum: the stout wall separating the lower chambers (the ventricles) of the heart from one another.

L Left Atrium:receives oxygenated blood from the left and right pulmonary veins. Lub-Dub: first heart tone, or S1; caused by the closure of the atrioventricular valves, mitral and tricuspid, at the beginning of ventricular contraction, or systole. Lumen: hollow internal cavity in which the blood flows. Lymph: originates as blood plasma that leaks from the capillaries of the circulatory system, becoming interstitial fluid, filling the space between individual cells of tissue.

M Mitral valve: also known as the bicuspid valve; prevents blood flowing from the left ventricle into the left atrium. Myocardium: the muscular tissue of the heart.

N Norepinephrine: Produced in the adrenal medulla of the adrenal glands, major function is a strong vasoconstrictor that will in turn increase respiratory rate.

P Pacemaker Cells: cells that create these rhythmical impulses of the heart. Plaque: an abnormal inflammatory accumulation of macrophage white blood cells within the walls of arteries. Pulmonary Valve: lies between the right ventricle and the pulmonary artery; prevents back-flow of blood into the ventricle. Pulse: the number of heartbeats per minute. Purkinje Fibers (or Purkinje tissue): located in the inner ventricular walls of the heart, just beneath the endocardium; specialized myocardial fibers that conduct an electrical stimulus or impulse that enables the heart to contract in a coordinated fashion.

R Right Atrium: receives de-oxygenated blood from the superior vena cava and inferior vena cava.

S Serous Pericardium: functions in lubricating the heart to prevent friction from occurring during heart activity. Semilunar Valves: positioned on the pulmonary artery and the aorta. Sinoatrial Node: (abbreviated SA node or SAN, also called the sinus node): the impulse generating (pacemaker) tissue located in the right atrium of the heart. Sinusoidal Capillaries: special forms of fenestrated capillaries that have larger opening allowing RBCs and serum proteins to enter. Systole: contraction of the heart.

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Systolic Pressure: the highest point in blood pressure when the blood is being pumped out of the left ventricle into the aorta during ventricular systole. Superior Vena Cava (SVC): a large but short vein that carries de-oxygenated blood from the upper half of the body to the heart's right atrium.

T Thrombus: a blood clot in an intact blood vessel. Tricuspid Valve: on the right side of the heart, between the right atrium and the right ventricle; allows blood to flow from the right atrium into the right ventricle when the heart is relaxed during diastole.

V Vasoconstriction: the constriction of blood vessels. Vasodilation: the dilation of blood vessels. Veins: carry de-oxygenated blood from the capillary blood vessels to the right part of the heart. Ventricle: a heart chamber which collects blood from an atrium. Venule: a small blood vessel that allows deoxygenated blood to return from the capillary beds to the larger blood vessels.

GLOSSARY ON CONTENT MODULE 13: RESPIRATION SYSTEM

A Aerobic capacity – the ability of an organ to utilize oxygen and respire aerobically to meet its energy needs Alveoli – small, sac-like dilations Apnea – the temporary cessation of breathing Apneustic center – a collection of neurons in the brain stem that participates in the rhythmic control of breathing

B Bohr effect – the effect of blood pH on the dissociation of oxyhemoglobin. Dissociation is promoted by a decrease in the pH Bronchiole – the smallest of the air passages in the lungs containing smooth muscle and cuboidal epithelial cells

C Carbonic anhydrase – an enzyme that catalyzes the formation or breakdown of carbonic acid. When carbon dioxide concentrations are relatively high, this enzyme catalyzes the formation of carbonic acid from carbonic dioxide and water. When carbon dioxide concentrations are low, the breakdown of carbonic acid to carbon dioxide and water is catalyzed. These reactions aid the transport of carbon dioxide from tissues to alveolar air. Cellular respiration – the energy-releasing metabolic pathways in a cell that oxidize organic molecules such as glucose and fatty acids Chemoreceptor - a neural receptor that is sensitive to chemical changes in blood and other body fluids Cheyne-Stokes respiration – breathing characterized by rhythmic waxing and waning the depth of respiration, with regularly occurring periods of apnea (failure to breathe)

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D Dyspnea – subjective difficulty in breathing

E Emphysema – a lung disease in which alveoli are destroyed and the remaining alveoli become larger. It results in decreased vital capacity and increased airway resistance

G Gas exchange – the diffusion of oxygen and carbon dioxide down their concentration gradients that occurs between pulmonary capillaries and alveoli, and between systemic capillaries and the surrounding tissue cells

H Hering-Breuer reflex – named for Austrian internist, Josef Breuer (1842-1914), and the German physiologist Heinrich E.H (1866-1948). Process in which action potentials from stretch receptors in the lungs arrest inspiration, expiration then occurs Hyaline membrane disease – a disease affecting premature infants who lack pulmonary surfactant. It is characterized by collapse of the alveoli (atelectasis) and pulmonary edema; also called respiratory distress syndrome Hyperbaric oxygen - oxygen gas present at greater than atmospheric pressure Hypercapnia – excessive concentration of carbon dioxide in the blood Hyperpnea – increased total minute volume in part during exercise. Unlike hyperventilation, the arterial blood carbon dioxide values are not changed during hyperpnea because the increased ventilation is matched to an increased metabolic rate Hyperventilation – a high rate and depth of breathing that results in a decrease in the blood carbon dioxide concentration to below normal Hypoxemia – a low oxygen concentration of the arterial blood

I Intrapleural space – an actual or potential space between the visceral pleura covering the lungs and the parietal pleura lining the thoracic wall. Normally, this is a potential space; it can become real only in abnormal situations Intrapulmonary space – the space within the air sacs and airways of the lungs

L Lung surfactant – a mixture of lipoproteins (containing phospholipids) secreted by type II alveolar cells into the alveoli of the lungs. It lowers surface tension and prevents collapse of the lungs, as occurs at hyaline membrane disease when surfactant is absent

M Maximal oxygen uptake – the maximal rate of oxygen consumption by the body per time unit during heavy exercise. Also is called the aerobic capacity.

O Oxygen debt – the extra amount of oxygen required by the body after exercise to metabolize lactic acid and to supply the higher metabolic rate of muscles warned during exercises Oxyhemoglobin saturation – the ratio, expressed as a percentage, of the amount of oxyhemoglobin compared to the total amount of hemoglobin in blood

P Phonocardiogram – a visual display of heart sounds

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Pneumotaxic center – a neural center in the pons that rhythmically inhibits inspiration in a manner independent on sensory input Pneumothorax – an abnormal condition in which air enters the intrapleural space, either through an open chest wound or from a tear in the lungs. This can lead to the collapse of lungs (atelectasis)

R Respiratory acidosis – a lowering of the blood pH to below 7,35 as a result of the carbon dioxide accumulation caused by hypoventilation Respiratory alkalosis – a rise in blood pH to above 7,45 as a result of the excessive elimination of carbonic dioxide caused by hyperventilation Respiratory distress syndrome – a lung disease of the newborn most frequently occurring in premature infants, that is caused by abnormally high alveolar surface tension as a result of deficiency in lung surfactant; also called hyaline membrane syndrome Respiratory zone - the region of the lungs in which gas exchange between the inspired air and pulmonary blood occurs. It includes the respiratory bronchioles, in which individual alveoli are found, and the terminal alveoli.

S

Sleep apnea – a temporary cessation of breathing during sleep, usually lasting for several seconds

T Total minute volume – the product of tidal volume (ml per breath) and ventilation rate (breaths per minute) Transpulmonary pressure – the pressure difference cross the wall of the lung; equal to the difference between intrapulmonary pressure and intrapleural pressure

V Valsavaґs maneuver – exhalation against a closed glottis so that intrathoracic pressure rises to the point that the veins returning blood to the heart are partially constricted. This produces circulatory and blood pressure changes that could be dangerous. Vital capacity – the maximum amount of air that can be forcibly expired after a maximal inspiration

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