Pediatric Physical Examination / Клінічне обстеження дитини / Катілов О. В. та ін. by Nova Knyha

Pediatrics

Pediatric Physical Examination

Katilov O. V., Dmytriiev D. V., Dmytriieva K. Yu., Makarov S. Yu.

pediatric physical examination

Vinnytsia Nova Knyha 2018

УДК 616-053.2-07 ББК 57.3 К49

Рекомендовано Державною установою “Центральний методичний кабінет з вищої медичної освіти МОЗ України” як навчальний посібник для іноземних студентів вищих навчальних закладів МОЗ України, які навчаються російською мовою (протокол засідання Комісії від 27.10.2016 р. № 3)

Authors: Katilov O. V. — MD, PhD, Associate Professor of National Pirogov Memorial Medical University, Vinnytsya. Dmytriiev D. V — MD, PhD, Associate Professor of National Pirogov Memorial Medical University, Vinnytsya. Dmytriieva K. Yu. — MD, PhD, Associate Professor of National Pirogov Memorial Medical University, Vinnytsya. Makarov S. Yu. — MD, General Practitioner. Reviewers: M. D., professor Bulat L. M. M. D., professor Nedelska S. N. M. D., professor Bolbot Yu. K. M. D., professor Kablukova O. K.

К49

Клінічне обстеження дитини : навчальний посібник для студ. вищих навч. закладів = Pediatric physical examination : textbook for students of higher educational institutions : переклад з укр. мови / O. V. Katilov, D. V. Dmytriiev, K. Yu. Dmytriieva, S. Yu. Makarov – Vinnytsia : Nova Knyha, 2018. – 504 p. : il. ISBN 978-966-382-685-1 Taking into account the analysis of the concepts of domestic and foreign scientific schools, the textbook contains the fundamentals and principles of pediatric clinical examination. The book is intended for students of medical universities, interns and pediatric residents, as well as general practitioners. УДК 616-053.2-07 ББК 57.3 У представленому навчальному посібнику, з урахуванням аналізу концепцій вітчизняних і зарубіжних наукових шкіл, викладено основи і принципи клінічного обстеження дитини. Книга призначена для студентів медичних університетів, лікарів інтернів та початківців лікарів-педіатрів, а також лікарів загальної практики.

ISBN 978-966-382-685-1

ontents FOREWORD............................................................................................................................7 LIST OF ABBREVIATIONS.....................................................................................................8 CHAPTER 1. General examinationof a child...................................................................... 10 Assessment of general condition...................................................................................................................10 Main principles of physical development evaluation of a child older than 1 month.............................12 Patterns of physical development of a child.................................................................................................17 Assessment of physical development of a newborn....................................................................................22 Rules of anthropometric indicators measuring...........................................................................................24 Semiotics of disorders of physical development.........................................................................................25 CHAPTER 2. Diagnostics and semiotics of skin diseases............................................... 30 Clinical anatomy and physiology of the skin.............................................................................................. 30 Anatomical and physiological features of the skin in children.................................................................32 Skin characteristics in the neonatal period..............................................................................................34 Clinical examination.......................................................................................................................................36 Main (physical) methods of examination....................................................................................................36 Survey and examination.........................................................................................................................36 Palpation...................................................................................................................................................43 Additional methods of examination........................................................................................................44 General semiotics and differential diagnosis of skin diseases...................................................................45 Skin dysplasia and dystrophy...................................................................................................................45 Infectious diseases of the skin...................................................................................................................46 Allergic and toxicoallergic diseases..........................................................................................................57 Skin changes in non-infectious diseases...................................................................................................58 Principles of differential diagnosis of infectious and allergic rashes.......................................................64 Hemorrhagic rash syndrome....................................................................................................................65 Skin vascular formations..........................................................................................................................67 Skin pigmentation disorders.....................................................................................................................68

CHAPTER 3. Diagnostics and semiotics of peripheral lymph nodes lesions................ 72 Clinical anatomy and physiology of lymph nodes......................................................................................72 Clinical examination of lymph nodes ..........................................................................................................76 Main (physical) methods of examination................................................................................................76 Examination.............................................................................................................................................76 Palpation...................................................................................................................................................76 General semiotics of lymph nodes lesions...................................................................................................78

CHAPTER 4. Diagnostics and semiotics of skeletal system diseases........................... 81 Anatomical and physiological features of the skeletal system...................................................................81 Clinical examination of the skeletal system.................................................................................................87 Main (physical) methods of examination................................................................................................87 Palpation of the skeletal system.............................................................................................................96 General semiotics of skeletal system disorders...........................................................................................97 Dental pathology......................................................................................................................................98 Microcephaly.............................................................................................................................................98 Craniosynostosis (craniostenosis) ...........................................................................................................99 Macrocephaly..........................................................................................................................................100 Rickets.....................................................................................................................................................101 Hip dysplasia..........................................................................................................................................102 CHAPTER 5. Diagnostics and semiotics of muscular system diseases....................... 105 Anatomical and physiological features of the muscular system.............................................................105 Clinical examination and semiotics of the muscular system disorders.................................................107 CHAPTER 6. Diagnostics and semiotics of respiratory system diseases.................... 113 Clinical anatomy and physiology of the respiratory system....................................................................113 Clinical examination of the respiratory system.........................................................................................120 Main (physical) methods of examination..............................................................................................120 Survey......................................................................................................................................................120 Examination...........................................................................................................................................123 Palpation.................................................................................................................................................135 Percussion...............................................................................................................................................137 Auscultation...........................................................................................................................................141 Additional methods of investigation......................................................................................................154 X-ray diagnostics...................................................................................................................................154 Spirometry..............................................................................................................................................159 Peak flow metry.....................................................................................................................................163 General semiotics of respiratory diseases in children..............................................................................165 ARVI.......................................................................................................................................................165 Acute laryngotracheitis...........................................................................................................................169 Acute tonsillitis. Tonsillopharyngitis......................................................................................................170 Acute bronchitis......................................................................................................................................172 Bronchial asthma....................................................................................................................................173 Pneumonia..............................................................................................................................................176 Pleurisy...................................................................................................................................................179 Respiratory failure..................................................................................................................................181 Chapter 7. Diagnostics and semiotics of cardiovascular system diseases................. 183 Clinical physiology of cardiac work............................................................................................................183 Anatomical and physiological features of the cardiovascular system in children................................188 Antenatal fetal circulation......................................................................................................................189 Clinical examination of the cardiovascular system..................................................................................191 Main (physical) methods of examination..............................................................................................191 Survey......................................................................................................................................................191 Examination...........................................................................................................................................194

Palpation.................................................................................................................................................196 Heart auscultation.................................................................................................................................206 Additional methods of examination......................................................................................................219 Electrocardiography..............................................................................................................................219 Heart X-ray.............................................................................................................................................239 General semiotics of the cardiovascular system diseases in children....................................................240

CHAPTER 8. Diagnostics and semiotics of the urinary system diseases.................... 249 Clinical physiology of the renal function...................................................................................................249 Anatomical and physiological features of the urinary system in children............................................255 Clinical examination of the urinary system...............................................................................................256 Main (physical) methods of examination..............................................................................................256 Survey......................................................................................................................................................256 Examination...........................................................................................................................................257 Palpation and percussion......................................................................................................................259 Additional methods of examination......................................................................................................261 Laboratory methods..............................................................................................................................261 Instrumental methods ..........................................................................................................................275 Additional methods of the kidneys investigation include the following:.......................................275 General semiotics of the urinary system diseases.....................................................................................279 CHAPTER 9. Diagnostics and semiotics of gastrointestinal diseases......................... 286 Clinical physiology of the gastrointestinal tract........................................................................................286 Anatomical and physiological features of the gastrointestinal tract in children...................................291 Clinical examination of the gastrointestiwnal tract..................................................................................293 Main (physical) methods of examination..............................................................................................294 Survey......................................................................................................................................................294 Examination...........................................................................................................................................302 Auscultation of the abdominal area....................................................................................................310 Percussion...............................................................................................................................................312 Palpation.................................................................................................................................................315 Additional methods of examination......................................................................................................320 Laboratory methods..............................................................................................................................320 Instrumental methods...........................................................................................................................324 General semiotics of GIT organs diseases in children.............................................................................327 CHAPTER 10. Diagnostics and semiotics of ENT-organs diseases.............................. 336 Clinical anatomy of ENT-organs and hearing physiology.......................................................................336 Main methods of ENT-organs examination..............................................................................................344 Additional methods of ENT-organs examination....................................................................................355

CHAPTER 11. Diagnostics and semiotics of the nervous system diseases................ 358 Clinical physiology of the nervous system.................................................................................................358 Clinical assessment of the neurological status and semiotics of disorders in newborns and infants...............................................................................................................................360 Approximate dynamics of the psychomotor development of a child during the first years of life.......372 Clinical assessment of the neurological status and semiotics of disorders in older children and adolescents....................................................................................................................373

Stigmas of dysembryogenesis......................................................................................................................379 Meningitis...............................................................................................................................................380 Encephalitis.............................................................................................................................................383 Hydrocephaly..........................................................................................................................................383 Cerebral palsy.........................................................................................................................................385

CHAPTER 12. Diagnostics and semiotics of the endocrine system diseases............. 387 Clinical physiology of the endocrine system.............................................................................................387 Clinical examination of the endocrine system..........................................................................................404 Semiotics of main endocrine glands diseases............................................................................................407 Growth disorders in children.................................................................................................................407 Diseases of the hypothalamic-hypophyseal system...............................................................................414 Thyroid diseases......................................................................................................................................416 Adrenal gland diseases...........................................................................................................................418 Pancreatic diseases.................................................................................................................................421 Diseases of gonads..................................................................................................................................423 CHAPTER 13. Diagnostics and semiotics of the blood system diseases.................... 425 Clinical physiology of the blood system.....................................................................................................425 Clinical examination of the blood system..................................................................................................429 Additional methods of examination......................................................................................................431 Laboratory methods..............................................................................................................................431 Semiotics of blood diseases..........................................................................................................................447 Syndrome of anemia...............................................................................................................................447 Iron-deficiency anemia.........................................................................................................................448 Đ&#x2019;12- and folate-deficiency anemia........................................................................................................450 Hemolytic anemias................................................................................................................................450 Iron overload syndrome.........................................................................................................................451 Hemorrhagic syndrome..........................................................................................................................451 Myelodysplastic syndrome......................................................................................................................456 CHAPTER 14. Possibilities of ultrasound investigation in clinical examination......... 458 Main principles of ultrasound investigation..............................................................................................458 Ultrasound investigation of the skin......................................................................................................460 Ultrasound investigation of lymph nodes..............................................................................................464 Ultrasound investigation of the musculoskeletal system.......................................................................466 Ultrasound diagnostics of respiratory system diseases..........................................................................472 Ultrasound diagnostics of heart diseases (echocardiography)..............................................................475 Ultrasound diagnostics of urinary system diseases...............................................................................476 Ultrasound diagnostics ofÂ gastrointestinal diseases..............................................................................479 Ultrasound diagnostics of brain diseases (neurosonography)..............................................................480 Ultrasound diagnostics of endocrine system diseases...........................................................................483 CHAPTER 15. Clinical examination of a child in the critical condition......................... 489 BIBLIOGRAPHY.................................................................................................................. 496

CHAPTER Diagnostics and semiotics of cardiovascular system diseases

Clinical physiology of cardiac work Heart function consists in blood pumping from veins into arteries, i.e. generation of the pressure gradient, as the result of this blood constant movement occur. This means, that the main heart function is blood movement (“pump” function). For supporting of the normal organism being in different conditions, the heart can work in a wide range of frequency due to physiological function. Main functions of the cardiovascular system: 1. Maintenance of constant organism homeostasis. 2. Oxygen and nutrients delivery in all organs and tissues. 3. Excretion of metabolism products from the organism.

Physiological functions of the heart: 1. Automatism. 2. Conduction. 3. Excitability. 4. Contractility. 5. Refractoriness. Heart automatism is ability to contract under the influence of generated stimulation. Cardiac performance occurs due to the presence in the area of the right atrial appendage of automatism driving center (center of the first order) – sinoatrial node. Excitation from sinoatrial node along fibers reaches atrioventricular node (center of the second order), that is located in the wall of right atrium between the atria and ventricles. Then excitation pass to the myocardium of ventricles along the fibers of the bundle of His (center of

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Bachmann's (interatrial) bundle SA-node

АВ-junction Bundle of His Left bundle branch

AV-node

Purkinje fibers Internodal conduction (Bachmann's, Wenkebach's and Thorel's) Right bundle Left posterior Left anterior fascicle branch tracts fascicle

Fig. 7.1. Scheme of the center of cardiac automatism and conduction system of the heart

the third order) and reaches cardiomyocytes (Fig. 7.1). The sinoatrial node is the normal pacemaker. It has increased sensitivity compared to other parts of the heart to humoral and nervous regulation and spontaneous impulse generation. In the impairment of automatism in the pacemaker of the first order, heart contractions will continue due to impulses that occur in the center of the second order (AVnode). In this rate, the contraction frequency will be approximately two times lower, than before the impairment in the area of the sinoatrial node. All parts of the non-specific conductive system of the heart are capable of automatism, but practically that does not happen because the upper parts have more frequent rhythm of spontaneous activity. During upper center work, function of lower one is suppressed. The law of gradient heart automatism (Gaskell's law) indicates, that capability of automatism is as lower, as far the certain part of the heart is located from the heart basis and closer to the apex.

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The lower is automatism center is located anatomically, the lower is the heart rate. All of the centers are capable of impulse generating with the certain frequency. Then for general conception, the work of these centers in adults is shown, i.e. HR in children varies with age. Automatism centers and heart rate: 1. The automatism center of the first order – cells of SA-node, that generate electric impulses with the frequency of approximately 60–80 per minute in adults. 2. The automatism center of the second order – cells of AB-junction (zones of the AV-node transition into His bundle and lower part of atria), and also some cells of the initial part of His bundle, that produce impulses with the frequency of 40–60 per minute in adults. 3. The automatism center of the third degree – final part of the His bundle, branches of His bundle. They have the lowest automatism function, generating approximately 25–45 impulses per minute in adults. Conduction – tissue capability of excitation impulses conduction. This function is typical for conductive system and contractile myocardium. The speed of impulse conduction is different in different heart parts. Maximal speed is observed at the level of Purkinje fibers cells (4000 mm/s), minimal (50–200 mm/s) – in AVnode. Heart conductive system provides impulse conduction, that occurs in the pacemaker, and physiological consequence of heart chambers excitation (Fig. 7.2). Heart excitability – this is a capability of the myocardium to excite under influence of chemical and physical stimuli. Cells of the conductive system and contractile myocardium are capable of excitation. Heart excitation follows the law “all-ornone”. This means, that before-threshold

Сhapter 7

C Р3

Р2 Р1

0.02 s

0.04–0.05 s

0.05–0.08 s

Fig. 7.2. Scheme of excitation sequence of different parts of the heart: А–C – sequence of atrial excitation; D – excitation of the ventricular septum; E, F – excitation of ventricles

stimuli do not cause the respond, while stimuli, that reach threshold, cause maximum strong respond. Heart muscle does not perceive other stimuli. This feature is called refractoriness. The duration of refractoriness phase of ventricles is equal to systole duration. Refractoriness protects myocardium from the overload. The electric current is formed at contractile myocardium excitation, that spread through the human body and can be registered at any point – inside, as well as on the body surface (principle of ECG work). Contractility – a capability of the heart muscle to contract under stimuli influence. The force of myocardium contraction is directly proportional to the initial length of muscle fibers. Blood pumping by the heart is carried out by alternating contraction (systole) and relaxation (diastole) of the myocardium. Muscle contraction in the heart is a well-organized periodical process, that is controlled by conductive system and refractoriness. Refractoriness of the myocardium is a temporary state of the myocardium unexcitability. Refractoriness phase is a time interval, during which new cardiac impulse can

not cause repeated generation of action potential in still excited muscles. Periodic blood ejection in the vascular system occurs due to rhythmic myocardium contraction. Periods of heart contraction and relaxation forms the cardiac cycle (Fig. 7.3). It consists from atrial systole, ventricular systole and overall pause. Ventricles are filling with blood during diastole due to a passive passage of blood from atria. Atrial systole is observed at the end of diastole (P-wave on ECG), when the remaining blood pass from atria to ventricles; following which the ventricular systole starts (Fig. 7.4). The heart is under the constant influence of nervous system and humoral factors. Sympathic regulation increases heart general activity, that is followed by increased rate and strength of heart contraction. The parasympathic regulation is acting inversely – decreasing rate and strength of heart contractions (Fig. 7.5). So, sympathic regulation increased heart efficiency as a pump, while parasympathic decrease the pumping function of the heart, which allow the heart to rest between the periods of high activity.

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Isovolumic relaxation

Pressure (mmHg) Volume (ml)

100

Diastasis

Ejection

Isovolumic contraction 120

Rapid inflow Atrial systole

Aortic valve opens

Aortic valve closes Aortic pressure

80 60 40

A-V valve opens

A-V valve closes

Atrial pressure

0 130

v Ventricular pressure Ventricular volume

P T

Q 1

Systole

Electrocardiogram

S Phonocardiogram

Dyastole

Systole

Fig. 7.3. Scheme of cardiac cycle (Arthur Guyton, 2008)

Head and neck Aorta Pulmonary artery Lungs

Right atrium

Pulmonary valve

Pulmonary veins Left atrium

Tricuspid valve

Mitral valve Aortal valves

Right ventricle

Left ventricle Inferior vena cava

Body and lower limbs

Fig. 7.4. Blood flow direction in the heart

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ะกhapter 7

Autonomic regulation of heart

Parasympathetic

Sympathetic

Vagus nerve

(slows heartbeat)

Т1

(accelerates heartbeat)

Chain of sympathetic ganglia

Fig. 7.5. Schematic view of autonomic regulation of heart

Blood pressure is determined by three factors: stroke volume, circulating blood volume and resistance to blood flow in peripheral vessels. Sympathetic stimulation increases simultaneously the heart contraction strength and resitance to blood flow due to vessels contraction. These lead to an expressive but not durable increase of blood pressure, if the sympathetic system does not stimulate kidneys at the same time, keeping saline and water. Moderate parasymathietc stimulation through the vagus nerve, decreases pumping function of the heart and almost does not influence the peripheral vessels resistance, that leads to a slight decrease of blood pressure. But intensive vagal stimulation can sharply slow down and sometimes even stop the heart contractions for several seconds, that leads to short-term blood pressure drop practically to the zero level.

Parasympathetic nervous system effects on the heart work: 1. Chronotropic influence (on the heart rate). 2. Inotropic (on the contraction force). 3. Bathmotropic influence (on the excitability). 4. Dromotropic (on the conductivity). Main functional indicators of the heart performance: 1. Stroke volume (SV) – amount of blood, that is expulsed at every contraction into the aorta: • newborn – 2.5–3.5 ml; • 1 year – 10 ml; • 16 years – 60 ml. 2. Minute volume MV – the amount of blood expulsed by the left ventricle into the aorta in 1 minute (MV = SV × HR).

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Anatomical and physiological features of the cardiovascular system in children 1. The heart in newborns is relatively big in size. 2. In early age, heart occupies bigger volume in the chest. 3. Right and left ventricle is almost equal in size in the newborn. 4. Atria in newborns are relatively bigger in relation to ventricles. 5. The axis of the heart in the newborn lies almost horizontally. 6. Complete heart differentiation ends at 10–14 years. Continuous growth and functional development of the cardiovascular system occur in children. The most intensive heart growth is observed in children in two periods of life: from 2 till 6 years and in the pubertal period. The heart has an oval or spheric shape in the newborn, which is due insufficient ventricles development and relatively big atria. Up to 10–14 years in average heart obtains the form as in adults.

Due to the high diaphragm position and almost horizontal body position in children of the first year of life, the heart is located more horizontally. The heart takes an oblique position at the end of the first year of life. The heart in children is located higher than in adults. Heart volume in children is bigger in relation to the chest volume than in adults. Features of the anterior heart surface projection on the chest wall (Fig. 7.6): • anterior heart surface in newborns is formed by the right atrium, right ventricle and the part of the left ventricle; • at 1 year and later anterior heart surface is represented by right ventricle. Features of cardiac apex projection on the chest wall: • Cardiac apex in newborns consists of two ventricles, from 6 months – only of the left ventricle. • Cardiac apex projection in the newborn is in the 4th intercostal space, from 1.5 years – in the 5th intercostal space.

Aortal arch Superior vena cava I II III

Right atrium Right ventricle

I II

Pulmonary trunk

III IV

Left atrium auricle

Left ventricle Inferior vena cava Anterior median line Right sternal line

Left medio-clavicular line

Fig. 7.6. Projection of the heart on the anterior chest wall in children older than 1 year

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Сhapter 7

Pressure (mmHg) 120 90 60 30 0 Capacity, %

Large arteries

14 % 5 % 64 % Arterioles Capillaries Venules Veins and of the systemic terminal (greater) arteries circulation

Fig. 7.7. Blood pressure and spreadness in vessels

Heart mass in the newborn constitute 0.8 % of body weight and is relatively bigger than in adults. Right and left ventricles are similar by their thickness (approximately 5 mm). Atria and great vessels are relatively bigger. To the end of the first year of life heart size doubles, and to 3 years – triples. To 17 years heart usually increases in 10 times. In the preschool and junior school age, the heart growth slows down and accelerates in the pubertal period. Different parts of the heart grow unevenly. Left ventricle significantly increases its volume and to the end of first half-year exceed the right ventricle by mass in two times. Cardiac volume at birth is approximately 22 cm3, in one year it increases to 40 cm3 and then for 6–10 cm3 each year. Histological differentiation of the myocardium in child ends at 2–3 years and conductive system – at 3–4. Vessels lumen in infants is wide. Arteries are equal to veins by width, and their lumen relation is 1 : 1. Then veins become wider and by 16 years this relation reaches 1 : 2.

The growth of arteries and veins does not often correspond to the velocity of heart growth (one of the reasons of functional murmurs presence). Arterial walls are more elastic than venous, with this lower peripheral resistance is connected comparatively to adults (Fig. 7.7). The blood volume in the newborn is around 0.5 l, in adults – 4–6 l, but the blood volume in relation to body weight is higher in newborn, than in adults. Blood volume to body weight in newborns is 15 % in average, in infants – 11 %, in adults – 7–8 %. In boys blood volume is relatively higher than in girls. Approximate volume of circulating blood in newborns is 100 ml/kg, in children older than 1 months – 80/ml/kg, in adults – 65 ml/kg (Fig. 7.8).

Antenatal fetal circulation Up to two months of pregnancy fetal nutrition is carried out by vitelline sac (embryonal period). From the end of the 2nd month of preg-

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160

12–13 years 10–11 years

140

6–9 years

Height (cm)

120

3–5 years 2–3 years

100 80

1 year 6–10 months

60 40 20 0

Fig. 7.8. Comparison of blood volume in children of different age (scheme). Each bottle is 500 ml

nancy, placental circulation is settled, and it is preserved till the child's birth (placental or fetal period). Gas and nutrients exchange between fetal and maternal blood is carried out in the placenta. The heart anlage starts on the second week of antenatal development. In first 6 weeks heart consists of 3 chambers, then the four are formed due to the atria division. At the same time, the heart division into right and left halves and cardiac valves formation are taking place. Formation of great arterial trunks starts from the 2nd week of life. Enriched blood with oxygen and other nutrients in the placenta (1), by unpaired umbilical vein (3) in the umbilical cord reaches the fetus (Fig. 7.9). All blood in the fetus is mixed and has maximal oxygenation (80 %) in the umbilical vein (Fig. 7.10). Umbilical vein delivers blood to the hepatic portal and flow into portal vein (4). Due to this liver receive the most reach with oxygen blood. Some of the blood before flowing into the portal vein is discharged trough the Arantius' duct (5, ductus venous) into inferior vena cava (6) and is mixed with venous blood, that flow off the lower part of the body, liver (first mixing).

190

Umbilical arteries

Umbilical vein

Fig. 7.9. Scheme of umbilical cord vessels. Vein is bigger in diameter and unpaired

When mainly arterial blood is mixed with venous, the oxygen saturation percent decreases. Then by inferior vena cava the blood flow into the right atrium (7), where also superior vena cava flow into, that carry blood from the upper part of the body (second mixing). But in the right atrium this both flows do not com-

Сhapter 7

6 5 4 3 2

the last fourth blood mixing happens (10). The most oxygenated blood goes for nutrition of the brain, heart and upper part of the body. At the end venous blood through two umbilical arteries (11) flows back into the placenta, where it is enriched with the oxygen and nutrients and goes back to the fetus through the umbilical vein (see Fig. 7.10). Fetal and maternal blood do not mix. Anatomical formations, that are typical only for antenatal circulation: 1. Arantius' duct. 2. Botallo's duct. 3. Open oval window. 4. Umbilical arteries and vein.

Clinical examination of the cardiovascular system 1 11

Fig. 7.10. Scheme of fetal circulation (explanations in text)

pletely mix, because blood from inferior vena cava passes through the oval window (8) into the left atrium, while blood from the superior vena cava passes from the right atrium into the right ventricle. The small amount of blood from pulmonary veins also flows into the left atrium (third mixing). This mixing does not significantly influence on the gas content in blood, that flow into the left ventricle. Highly oxygenated blood in systole passes through the aorta into greater systemic circulation. Blood, that is expulsed into the pulmonary trunk, is divided into two directions. Only 10 % of blood is going for oxygenation of nonfunctioning lungs and through the pulmonary veins returns into the left atrium. The other biggest part flows into the aorta through the Botallo's duct (9, ductus arteriosus), where

Main (physical) methods of examination Clinical examination of the cardiovascular system includes following consequent stages: survey → examination → palpation → auscultation.The main feature of clinical heart diagnostics in world medicine nowadays is an absolute denial of the heart percussion use in children and in adults. This is due to the generally accessible accurate methods of heart investigation (for example, ultrasound) and late correlation of heart sizes change detected in percussion and clinical manifestations.

Survey Complaints, that are typical for CVS diseases in children: 1. Dyspnea. 2. Bad tolerability of physical activity. 3. Sudden changes of skin color (paleness, cyanosis). 4. Edema. 5. Syncope.

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Dyspnea in children with cardiac pathology is one of the early and most common signs. at the onset of cardiac failure, dyspnea occurs only with heavy physical activities, and with heart failure progressing occurs even at rest. There are two main mechanisms of the dyspnea development in cardiovascular diseases: blood congestion in lungs and impaired carbonic acid excretion. Increased excitability of the respiratory center due to oxygen starvation and accumulation of gas in intestines or fluid in the abdominal cavity, that lead to diaphragm raising, also plays some role. Dyspnea occurs at blood congestion in lungs and slowed blood flow in the greater circulation, which indicates the weakness of the left ventricle. Special dyspnea type is observed in cardiac asthma, that is rarely diagnosed in children. In the basis of the cardiac asthma episode lies acutely developed left ventricle failure at preserved strength of the right ventricle (left ventricular failure). Bad tolerability of physical activity – low tolerance to physical activity – is observed in children with impaired cardiac output and hemodynamics in heart defects, myocardites. Preschool children does not participate in outdoor games (aerobic), often instinctively make pauses during the game for rest. In combined defects (for example, Fallot's tetrad), the child can suddenly take forced position during walk, squatting down for rest. Edema in patients occurs due to chronic right ventricular failure. The main cause os edema occurrence is an increased pressure in venous capillary endings, when the fluid passes into tissues. Edema is firstly formed at limbs, then with heart failure progressing fluid can accumulate into serous cavities (pleural, pericardium), and ascites develops. Massive spreaded edema is called anasarca. Edema in children is observed significantly rarer in general, than in adults. Differential diagnosis of cardiac and renal edema is rep-

192

resented in chapter № 8 “Diagnostics and semiotics of urinary system diseases”. Clinical features of cardiac edema: 1. Occur to the end of the day, decrease in the morning. 2. Occur on the legs at the beginning. 3. Are often connected with cyanosis. 4. Increase during the physical activity. 5. “Dense” in palpation (pit after pressure disappears slowly). 6. Spread downside-up with progressing. In literature it is often described such a symptom, that is typical for heart failure, as “cold in palpation”. This criterion of edema describing is subjective and not correct. Firstly, we assess edema typical on the symmetric parts of the body (limbs, sacrum) in every patient individually; secondly, we could not know, what was their temperature before our examination. Moreover, the peripheral temperature of wrists and feet is an individual feature in different persons. Syncope – short-term loss of consciousness, which course with loss of postural tone and falling. Syncope in cardiovascular diseases occurs due to a decrease in cardiac output or the heart rhythm impairment. To diseases, that lead to the cardiac output decrease, refer aortic stenosis, pulmonary stennosis, hypertrophic cardiomyopathy, Fallot's tetralogy, atrium myxoma, cardiac tamponade. Expressed bradycardia and tachycardia can decrease cardiac output up to the development of arterial hypotension and syncope,, particularly heart rhythm impairment such as paroxysmal tachycardia and Morgagni – Adams – Stokes attacks, conduction abnormalities with prolonged Q–Т interval. Causes of syncope can be cardiac, as well as not connected with cardiovascular diseases. Syncope refers to reasonably spread symptoms, and around 30 % of healthy children report at least one or more espisodes of consciousness loss during life.

Сhapter 7

Syncope should be differentiated from other conditions, that course with consciousness impairment: epilepsy, vestibular vertigo. The main complaints in children are: episodes of dyspnea, cyanosis, sudden weakness during physical activity. The physical activity equivalents in this group of children are crying and feeding. Complaints, that allow to suspect the cardiac pathology in infants: 1. Sudden cry and anxiety, that changes with long-lasting weakness and paleness. 2. Sucking interruption, that is accompanied by dyspnea and intensive sweating occurrence. 3. Paroxysmal hypercyanotic attacks – sudden paleness with dyspnea, that change into cyanosis with consciousness loss, seizures or apnea. Main pathogenetic mechanisms of the cardialgies development: 1. Myocardial ischemia. 2. Pericardium inflammation. Cardialgies are nor typical symptom of the cardiovascular pathology in children, on the opposite to adults. It is necessary to understand, that not every pain in the area of heart projection is connected with cardiac pathology. It is necessary to understand under cardialgy the pain in the aree of the heart due to just the cardiac pathology. The next clinical tendency is noted: at complaints of the pain in the areae of the heart in adults of older age, the doctor should in the first to exclude the cardiac pathology, and at complaints of the chest pain in children, doctolast of all. According to data of foreign guidelines, cardialgies consist only 1 % of all chest pain causes in children. The structure of CVS diseases changes with age, and the percenatge of cardialgies as the cause of chest pain increase and reach 40–60 % in elderly patients.

This is caused by the low frequency of occurrence of the main mechanism of the cardiac pain in children. The leading pathogenetic mechanism of the cardiac pain is a myocardial ischemia. Diseases, that have in their pathogenesis the myocardial ischemia, are more spreaded in elderly patients (ischemic heart disease, ie myocardial infarction, non-specific arteritis and other), but almost never occur in children. Cardialgies connected with heart affection can be observed in children in abnormal coronary circulation, pericardites, in sharply dilation of the heart and greater vessels. For example, cardialgies can be observed in an abnormal origin of left coronary artery from pulmonary artery (Bland – White – Garland syndrome). Cardialgies are rarely observed in myocardites in children. The second reason of cardiac pain is inflammation of the pericardial pleurae; it is observed in fibrinous pericarditis. The pain intensity varies from mild to severe. In this case, pain is short-term and disappears with fluid accumulation in the pericardial cavity. In cardialgies presence in adults, their character should be necessarily assessed: pain character (acute, dull, burning, stabbing), time of occurrence (nocturnal, diurnal, constant), irradiation, pain connection with physical activity and body position. It is not correct to ask such questions to a child up to adolescence, ie it is impossible to get an adequate answer. Complaints on the sudden palpitations is rarely observed in children, due to the rarity of paroxysmal tachycardias and features of the psychoemotional development in childhood. Complaints on the palpitation in children have mainly psychogenic character. It is conventional to describe joint pain in the group of symptoms that are typical for CVS diseases. But it is not indeed because the joint syndrome is currently observed rarely in cardiac diseases in children. Joint syndrome in heart pathology is traditionally

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connected with rheumatic fever, which is currently a rare disease in children, and if it is observed, then it usually has a course like a chorea minor, without joint affection. To general complaints in cardiovascular diseases refer: headache, nausea, vomiting, appetite loss.

Examination Examination of a child for the assessment of cardiovascular system consists of a general examination, examination of the heart area and peripheral vessels. Features, that should be assessed at the examination of the cardiovascular system: 1. Cervicl vessels pulsation. 2. Skin color. 3. Edema presence. 4. Cardiac hump presence. 5. Apical beat localization. 6. Pulsation in the epigastric area. 7. Child's physical development. The examination is started from patient's face and neck. At cervical examination, attention is paid to the presence or absence of carotid arteries pulsation – “carotid shudder” (in aortic regurgitation), pulsation and swelling of jugular veins (congestion in the smaller circulation, tricuspid regurgitation) (Fig. 7.11). Insignificant swelling of jugular veins can be observed in a horizontal position in healthy children, it disappears with the transition into the vertical position. Causes of the visible pulsation: 1. “Carotid shudder” – aortic regurgitation. 2. Jugular veins pulsation (positive venous pulse) – tricuspid regurgitation. 3. Epigastric pulsation – right ventricular hypertrophy, aortic pulsation. Mechanism of the “carotid shudder” occurrence is connected with an abrupt and

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External jugular vein

Sternocleidomastoid muscle

Carotid artery

Fig. 7.11. Antomical localization of jugular veins and carotid arteries

rapid increase of pressure in carotid arteries during systole and rapid blood flow return in the diastole due to aortic regurgitation. “Carotid shudder” is observed at the neck in front of m. sternocleidomastoideus (Fig. 7.11). It is necessary to distinguish cervical veins swelling and positive venous pulse. Cervical veins swelling is typical for congestion in the smaller circulation, and positive venous pulse is typical for tricuspid regurgitation. Venous pulse is normally absent. In tricuspid regurgitation, during systole the reverse blood flow occurs into the right atrium and then superior vena cava. The blood is actually regurgitated into both venae cavae, but inferior vena cava is hidden under the chest carcass and is not accessible for visualization. For detection of positive venous pulse, it is necessary to compare at the same time the pulsation of the right jugular vein and apical beat – they coincide. In the case of difficulties, it is necessary to compress the right jugular vein with two fingers (see Fig. 7.12), the vein between fingers collapses due to absent blood flow, then with lower finger eleva-

Сhapter 7

Paplation of external jugular vein

Palpation of radial artery

Fig. 7.12. Mechanism of positive venous pulse verification

tion, we can see the downside-up blood flow during systole, that indicates positive venous pulse (Fig. 7.13). Epigastral pulsation can be due to two causes: significant right ventricular hypertrophy and abdominal aorta pulsation. The pulsation in the epigastrium in both cases coincide with the pulse (apical beat). At significant right ventricular hypertrophy, the right ventricle during systole strikes the left liver lobe, which in turn transfer the knock wave to the epigastral area (Fig. 7.16). Aortic pulsation in the epigastrium can be physiological and pathological. Pathological

pulsation is observed in children with abdominal aorta coarctation, and physiological can be observed in patients with the asthenic constitution in the horizontal position, especially at expiration. Types of skin color changes in the cardiac pathology: â&#x20AC;˘ paleness; â&#x20AC;˘ cyanosis. It is accepted to differentiate by origin and manifestations: central (diffuse) and peripheral (acrocyanosis). By origin central cyanosis can be of cardiac, respiratory, cerebral, metabolic, hemolytic nature. Diffuse cyanosis in cardiac pathology is observed at the impaired blood oxygenation in lungs (in pulmonary stenosis, pulmonary embolism), in some congenital heart defects (Fallot's tetralogy, transposition of the great vessels). Expressiveness of the diffuse cyanosis varies from slightly cyanotic lips tone to the violet blue coloration of the whole skin. It is more observable on the mucous membranes and body parts with thin skin (tongue, lips, face, under nails). In patients with dark skin color, cyanosis is less visible but is observed finely on the tongue. Acrocyanosis manifests with skin cyanosis of the most remote from the heart parts of the body. Acrocyanosis is finely expressed in the feet, hands, lips, tip of the nose and ears (see Fig. 2.5). In central cyanosis, skin is usually warm by touch, and in acrocyanosis â&#x20AC;&#x201C; cold.

Fig. 7.13. Technique of positive venous pulse determining

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Skin paleness in children with cardiovascular pathology is observed in congenital defects with arteriovenous shunt: atrial septal defect, patent arterial duct, aortic stenosis and others. The chest protrusion at the heart area can be observed during examination – “cardiac hump”, that can be accompanied with visible pulsation in some cases. Such protrusion can be observed in children with congenital heart defects and is due to the significant hypertrophy of the right ventricle (Fig. 7.14). Cardiac hump is usually formed in childhood due to the presence of cartilaginous tissue in the chest wall skeleton. Even in significant right ventricular hypertrophy due to acquired defect in adults, cardiac hump can not form because of the rigid osseous carcass. The localization of the apical beat can be determined during the examination in athenic patients, but the main method of its examination is a palpation. The level of the physical development, especially in congenital heart defects, objectively reflects the degree of hemodynamic impairment. Defects with slight hemodynamic impairments in the compensation period are not accompanied by physical development disorders. In hemodynamics decompensa-

Fig. 7.14. Cardiac hump in 3-years old child (after operation)

196

tion and in combined heart defects, children are usually backward from the average values in weight and height.

Palpation Indicators, that are determined during palpation: 1. Cardiac impulse. 2. Apex beat. 3. “Purring thrill”. 4. Retrosternal pulsation. 5. Epigastric pulsation. 6. Pulse and its characteristics. 7. Capillary test. The cardiac impulse is a beat of the anterior heart wall (right ventricle) at the chest wall (Fig. 7.15). It is normally absent. Can be palpated in patients with the asthenic constitution after the physical activity. The positive cardiac impulse in the patient at rest indicates the significant right ventricular hypertrophy (Fig. 7.16). The bigger its area, the bigger is right ventricular hypertrophy, ie the bigger part of the right heart is adjacent to the anterior chest wall. Characteristics of the apical beat: 1. Absence or presence. 2. Spreadness. 3. Force.

Fig. 7.15. Technique of cardiac impulse assessment

Сhapter 7

Cardiac impulse

Epigastral pulsation

Fig. 7.16. Localization of cardiac impulse and epigastral pulsation in case of right ventricular hypertrophy

The character of epigastral pulsation can be verified by palpation. Diffuse epigastral pulsation with the upside-down direction is a sign of the right ventricular hypertrophy (Fig. 7.16), and in the posteroanterior direction – aortic pulsation. Aortic pulsation is detected below the xiphoid process and slightly laterally from the midline, is located longitudinally and percepted as a powerful pulsating elevations, that became weaker at deep inspiration. Apex beat is a beat of the cardiac apex (left ventricle) at the chest anterior wall

(Fig. 7.17). At the apex beat palpation, doctors lay his hand in the transverse direction in such manner, that the plan basis is placed on the sternum and second, third and fourth fingers are correspondingly located in the IV, V and VI intercostal spaces. Then for determining the characteristics of the apex beat, tips of slightly bent second, third and fourth fingers are stated in the intercostal space, where the apical beat was found (Fig. 7.18). Normal characteristics of the apex beat: 1. At horizontal line – under 1.5 years in the 4th, and then in the 5th intercostal space. 2. At vertical line: • under 2 years – in 1–2 cm laterally to midclavicular line; • 2–7 years – in 1 cm laterally; • 7–12 years – in the line; • older than 12 years – in 0.5 cm medially. 3. Area – 1 × 1, in older age – 2 × 2 cm. The apex beat can also be negative, when during systole the part of the chest retracts, but not bulge (McKenzie symptom). Negative apex beat is pathognomic for adhesive pericarditis, in which pericardium is acreted together with the chest wall.

Fig. 7.17. Mechanisms of formation of apex beat and cardiac impulse: А – apex beat; B – cardiac impulse

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Fig. 7.18. Stages of apex beat palpation

Features of the apex beat assessment in children: 1. Localization. 2. Area. 3. Force. In left ventricular hypertrophy, the bigger part of the heart is adjacent to the anterior chest wall, so surface and force of the apex beat increases. The lateral displacement of apical beat has special value in diagnostics. For example, in aortic defects, apical beat shifts not only laterally but also downside (Fig. 7.19). Double apex beat is observed in hypertrophic cardiomyopathy.

Fig. 7.19. Scheme of apex beat displacement in case of left ventricular hypertrophy

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If the apex beat area is above 2 cm2 in adolescents and adults it is considered as diffuse, if below 1 cm2 – limited. In children up to adolescence we should not focus on this numbers but on the changes of the area in dynamics. The force of the apex beat is determined by the pressure, that the heart apex exerts on the palpate fingers. There is apex beat of a moderate (normal) force, forceful and weakened. The apex beat magnitude is determined by the amplitude of the intercostal spaces variations (high and low), but this feature is too subjective, and due to narrow intercostal space in children does not have diagnostic value. The direction of apex beat displacement has an important value. Apex is the most movable part of the heart, that is projected on the chest wall and is easily accessible for the visual examination and palpation. Apex beat displacement to the right is observed in pulmonary fibrosis, to the left – in the large rightsided exudative pleurisy or pneumothorax (Fig. 7.20). In left-sided exudative pleurisy (or pneumothorax) apex beat can be not detectable (Fig. 7.21). Apex beat displacement in left and right ventricular hypertrophy is represented on the Fig. 7.22. For convenience of the causes of apex beat absence memorization in palpation

Сhapter 7

Median line

Pneumothorax

Effusion fluid Apex beat

Fig. 7.20. Scheme of apex beat displacement

Рис. 7.21. Scheme of apex beat disappear-

in case of massive right-sided pneumothorax

ance in case of left-sided pleurisy (or pneumothorax)

Point of maximal pulsation

Right ventricular hypertrophy

Left ventricular hypertrophy

Left ventricular hypertrophy with dilation

Fig. 7.22. Schematic representation of right and left ventricular hypertrophy

the mnemonic scheme, Dr. РОРЕ is used (Table 7.1). Apex beat can be not detectable in the norm, as well as in pathology (Table 7.1). The phenomenon of so-called “purring thrill” (thrembling) can be detected at palpa-

tion as the local vibration of the chest wall like a thrembling of the purring cat's body, which a palpable equivalent of the low-frequency component of the cardiac murmur, that occur when blood pass through the narrowed openings. This pnemonenon is observed in sev-

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Table 7.1. Causes of apex beat absence on the left (DR POPE)

Normal Dextrocardia Apex behind a Rib (turn pa ent to le lateral posi on)

Pathology Pericardial eﬀusion Obesity and thick chest wall Pleural eﬀusion (le sided) Emphysema

eral heart defects and can be detected in systole as well as diastole, so “purring thrill” can be systolic and diastolic. For “purring thrill” symptom determining, it is necessary to put the palm on the whole heart area (Fig. 7.23). To determine if the vibration is systolic or diastolic it is necessary to palpate carotid artery or auscultate the first tone at the same time. In children with mitral stenosis “purring thrill” is determined in the area of heart apex and coincide with diastole (diastolic vibration), and in aortic stenosis – in the right second intercostal space (systolic vibration), in the patent ductus arteriosus and pulmonary stenosis – in the left second or third intercostal space. Along with this phenomena in the right II intercostal space the pulsation of ascending aorta can be found, and at the presternum – palpable equivalent of the pericardial rub. For palpable determining of the retrosternal pulsation the palm of the right hand is settled along the sternum, the distal phalanx of the middle finger is established in the jugular fossa and palpate it (Fig. 7.24). Pulsation in the jugular fossa is normally not observed. It can occur during the periods of stress and physical activity and is due to the increased aortal arch beat at increased systolic volume. Constant expressed retrosternal pulsation is observed in the aortic arch aneurysm and aortic regurgitation. Pulse is a balloting motion of arterial walls caused by blood flow due to cardiac contractions.

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Fig. 7.23. Tecnhique of “purring thrill” determining

Fig. 7.24. Technique of retrosternal pulsation determining

Pulse in school age children and older is usually assessed on a. radialis, a. femoralis, a. dorsalis pedis (Fig. 7.25). Firstly, the pulse synchronism is assessed on a. radialis on both hands simultaneously, if the difference in pulse characteristics is absent, fur-

Сhapter 7

Temporal Carotid

Apical Brachial Radial Femoral

Popliteal Posterior tibial Dorsalis pedis

Fig. 7.25. Places of pulse determining

ther investigation is carried out on one hand. Child's hand in relaxed condition is settled at the level of the heart, the doctor with the right hands wraps around the area of the wrist joint in such manner, that the thumb is located on the back surface of the examined forearm, and with middle and index fingers carries out the palpation of the radial artery. Pulse on a. femoralis is examined in the vertical and horizontal position of the child, palpation is carried out by index and middle fingers of the right hand in the inguinal fold in the place of artery outlet from under the Poupart's ligament. Pulse in infants can also be determined on the a. temporalis. In newborns and infants it is more correctly to determine heart rate, but no the pulse, by auscultation or palpation at the heart apex. It is connected with technical difficulties of palpation in younger children, as well as with weak pulse wave.

Indicators, that should be assessed: 1. Heart rate (HR). 2. Rhythmicity. Only pulse frequency, rhythmicity and symmetricity are determined on the a. radialis due to the accessibility of this artery for palpation in the dressed person, but conducting the assessment of pulse wave on the radial artery is wrong. The great artery is necessary for this (carotic or femoral), that maximally reproduce the starting features of the pulse wave. Mean normal values of heart rate in children: • newborn – 140–160; • 1 year – 120–130; • 5 years – 100; • 10 years – 85; • 12 years – 80; • 15 years – 70–75. Relation of breathing and heart rates in children: • newborn – 1 : 2–2.5; • infant – 1 : 3; • preschool age – 1 : 3.5–4; • school age – 1 : 4–5. For heart rate determining, the count should be conducted for one minute. The phenomenon, when there is the difference between heart contractions, counted on the apex, and pulse is called pulse deficit (pulsus deficiens). Pulse rhythmicity is assessed by the regularity of the intervals between the pulse beats (rhythmic and arrhythmic pulses are defined). Respiratory arrhythmyia is a variant of the norm in children: pulse become more frequent during inspiration, and slows down during expiration. Pulse tension is determined by the force, that is required to compress the artery, so the pulse beats will disappear. There are normal

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tension pulse, high-tension pulse – pulsus durus and low-tension pulse – pulsus mollis, that indicates the decreased vessels tone. The examination of pulse filling is carried out with two fingers. Proximaly located finger compresses the artery till pulse disappears, then the pressure ends and distally located finger percepts the filling of artery with blood. The following pulses are defined by filling: pulse of normal filling; full pulse – p. plenus (filling is more than normal) and empty pulse – p. vacuus (filling is less than normal). By the velocity of the pulse wave elevation and descent, the pulse forms are defined (by the moderate compressing of the artery with both fingers. If during pulse palpation we get the feeling of fast elevation and fast descent of the pulse wave, than this pulse is called abrupt, pulsus celer. If the pulse wave slowly elevates and descends, then this pulse is called slow. High pulse is also defined – p. аltus (characterized with fast good filling and descent of the pulse wave), and small pulse – p. рarvus, for which slow and small feeling and descent of the pulse wave is typical. They are usually observed with other pulse forms. For example: celer et parvus (pulse quickly become of a good filling and then fast descent of the pulse wave is observed), tardus et parvus (pulse wave elevates slowly, reaches small filling and then descend slowly). Normally pulse is equal on both hands, with the frequency appropriate to age, rhythmic, of moderate tension, full. Pulse characteristics described above have an academic character in pediatrics exclusively. Different cardiovascular morbidity structure in children and adults, the variability of normal values in different age periods, uneven growth and maturing of different systems and organs, plenty of functional disorders and many other do not allow to use in practice this pulse characteristics. In children up to preschool age, it is in general more rational to assess the charac-

202

ter of heart contractions during auscultation, than pulse using palpation. Alternating pulse is characterized by changes of high and low pulse waves. This pulse is a symptom of the weakness of the left ventricle myocardium. due to this the big variation of blood volume, that is pumped out into the aorta during different systole. Paradoxical pulse – when pulse waves become lower during inspiration, and higher during expiration. This is explained by the fact that in patients with several diseases the decrease of stroke volume and systolic blood pressure during inspiration. If the decrease is above 20 mmHg, it can be detected during pulse palpation. Dicrotic pulse – two pulse waves are detected, and second with lower amplitude occurs after the closing of aortic valves at that, ie in diastole. More often this pulse type is determined in severe heart failure or hypovolemic shock. Capillary pulse is observed in aortic regurgitation. The rhythmic redness and paleness of nail bed is observed, when applying pressure on the nails edge. Capillary test is used fo assessment of peripheral perfusion – time of capillaries filling. Patient's hand is settled at the level of the heart, distal phalanx is compressed for 5 seconds till fading and then released. The time till the nail bed color returns to normal is measured. Normally it is not above 2 seconds – for children and men, 3 seconds – for women and 4.5 sec – for elderly patients. Increased test duration indicates the tissues hypoperfusion, dehydration till the hypovolemic shock development and toxic shock. This also is used as a method for diagnosis of severe degree fo dehydration. The most common pulse disorders in children: 1. Tachycardia. 2. Bradycardia. 3. Rhythm disorders.

Сhapter 7

Normal variation of the heart rate in adults and adolescents is considered 60–90 per minute. Heart rate below 60 per minute is considered as bradycardia, above 90 – tachycardia. Pulse variations of ± 10 % from average age norm is considered normal in younger children, decrease for more than 10 % – bradycardia, and increase correspondingly – tachycardia. Blood pressure (BP) is the lower, the younger child is. Arterial blood pressure is divided into maximal (systolic), minimal (diastolic) and pulse. Systolic pressure – is the maximal blood pressure in the artery, that is reached during left ventricle contraction. Diastolic pressure – is the minimum, to which the blood pressure decrease before the next systole. Pulse pressure is the difference between systolic and diastolic pressures. For example, blood pressure above 80 mmHg is a highly specific sign of aortic regurgitation, anomalously low pulse pressure (below 25 % of systolic) indicates the decreased stroke volume of the left ventricle (pericarditis, cardiac tamponade). Pulse pressure also decreases in expressed tachycardia. Systolic pressure in the newborn is 70 mmHg in average, to the age of one year it increases to 90 mmHg. The growth of the blood pressure is more intensive during first 2–3 years of life and during pubertal period. Diastolic arterial blood pressure composes 1/2–2/3 of systolic. Pressure increase with age occurs simultaneously with the growth of the pulse wave velocity through the muscular vessels and is connected with their tone increase. Specific peripheral resistance increases with age due to: • increase of the resistant vessels length and capillaries convolution; • decreased expansibility of resistants vessels walls; • increased tone of vascular smooth vessels.

The sum of the heart rate and systolic blood pressure in all childhood period is approximately 200. Blood pressure in children is measured with a tonometer, the cuff size depends on child's age (the cuff width should be around 2/3 of the shoulder circle. Insufficient cuff length increases the numbers of pressure, too long cuff – decreases. It is better to conduct Korotkoff's sounds auscultation with stethoscope without membrane, but not with the phonendoscope, ie this tone has low frequency. For the blood pressure measurements on the legs, the cuff is placed on the lower one-third of the hip and stethoscope is placed in the popliteal fossa. Blood pressure in healthy children is for 5–15 mmHg higher on the lower limbs, than on the upper. If auscultated tones are preserved during BP measurement till the pressure decrease almost to zero (“endless tone” phenomenon), than diastolic BP is defined at the moment of abrupt Korotkoff's tones muting. It is accepted to make the blood pressure count from the closest even number. Approximate blood pressure in children can be counted according to the following formulas: systolic pressure is equal to 90 + 2n, diastolic – 60 + n (n – child's age in years). Systolic pressure in children of the first year of life is equal 75 + n, where n is child's age in months. This formulas determines an average pressure in children and can vary in a wide range. Therefore it is important to measure blood pressure in children in dynamics for determining the individual norm. Conditions, that are necessary for the correct BP measurement: • food, coffee and strong tea intake is excluded during 1 hour before the measurement; • it is recommended not to smoke during 30 minutes before BP measurement; • sympathomimetics intake is excluded, including nasal and eye drops;

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•

• •

BP is measured after 5-minutes rest; if there was significant physical or emotional loads previous to BP measurement, the period of rest should be prolonged to 15–30 minutes; the cuff size should correspond to hand size; Hg column or tonometer pointer should be at zero point before the measurement beginning.

Central venous pressure (CVP) – pressure in the right atrium and system of superior vena cava. Central venous pressure characterizes the filling of the right ventricle with blood, ie represents the end-diastolic pressure (at tricuspid stenosis absence). For CVP determining, it is initially necessary to measure pressure in the jugular vein. For CVP measurement patient should be in the horizontal position, the head is turned to the left side under 45 ° angle; jugular vein is visualized in such position. The centimetre rule is settled at the place of presternum and sternum connection (angle of Louis), the point of maximal pulsation on the jugular vein is determined with the help of another rule. To obtain CVP pressure, it is necessary to add 5 cm to obtained result (Fig. 7.26). add-

10 9 8 7 6 5 4 3 2 1

Jugular vein

Fig. 7.26. Technique of central venous pressure (CVP) measurement

204

ing of this number is connected with the fact, that the center of the right atrium (pressure in it – 0) is approximately for 5 cm below the sternum. This relation is typical for people with the normal constitution and does not depend on the body position. These methods can be used in children of older school age and adolescents. For screening CVP assessment the Lewes method can be sued, which is based on the fact, that the jugular vein pulsation is normally observed at 2–3 cm above the Louis' angle. If in patients in sitting position cervical veins are visible, then CVP exceeds 7–8 cmH2O. Normal CVP in children is considered between 4–8 cmH2O. CVP allows to confirm or exclude cardiogenic or pulmonary causes of edema at legs. If the CVP is not increased, than the cause of edema is rather renal or hepatic. Any heart (or lung) disease, that leads to the right ventricle failure, will be accompanied by increased CVP. Absolute and relative cardiac dullness was traditionally defined. Theoretically, absolute cardiac dullness is determined as the part of the heart, that is directly adjacent to the chest wall, but indeed only the left ventricle is adjacent normally (heart apex). Beyond the absolute dullness area, is an area of relative cardiac dullness, that approximately outlines the edges of the heart. As at the area of relative dullness borders, its anterior surface is located deep under the lungs, and it is detected with relatively loud percussion by the transition of reduction sound (Fig. 7.27). Obviously, it is very subjective even if the doctor has wide experience. The right border of the relative cardiac dullness is formed by the right atrium and is normally located by the right sternal edge or in 0.5–1 cm to the right. If the heart is not enlarged, this border is determined inaccurately due to the remoteness of the heart right border from the anterior chest wall. The upper

Сhapter 7

Mechanism of heart borders displacement

LA RA LV RV

Absolute cardiac dullness Relative cardiac dullness

Flat waist of heart

Fig. 7.27. Absolute and relative cardiac dullness during percussion

border is formed by the pulmonary trunk and auricle of the right atrium. Due to an oblique location of the upper border, it's determining is rather relative. The left border of the relative cardiac dullness is formed by the narrow strip of the left ventricle, that come to the anterior heart surface. It corresponds to the apex beat and is accurately determined during palpation, so there is no importance in the percussion conduction. Physiological changes of relative cardiac dullness borders occur in deep breathing. It is possible to rather relatively determine, which of the heart chambers is dilated. In isolated dilation of the left ventricle, the cardiac dullness spread mainly to the right and downwards, in significant right ventricle dilation â&#x20AC;&#x201C; only to the left or to the right and upwards. Determining of the cardiac dullness to the right from sternum is in most cases connected with an increase of the right atrium (Fig. 7.28). The dullness area is always smaller than the heart actual sizes, due to its round contours (Fig. 7.28). A significant enlargement of the heart size always causes the enlargement of the dullness area, but the slighter

Left border of relative cardiac dullness Flat waist of heart

Right border of relative cardiac dullness

Absolute cardiac dullness is extended

Fig. 7.28. Mechanism of heart borders displacement

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А. Frontal plane Aorta SVC

Pulmonary artery

RA LV RV IVC

B. Cross section

Right lung

Left lung LA

Aorta

PA LV

Fig. 7.29. Heart orientation in the chest: А – heart projection on the anterior chest wall; B – heart localization in transverse plane

increase is impossible to detect, while the purpose of the modern medicine is early diagnostics. If we also want to use certain daignostic method, the range of its variability should be assessed. The area of relative dullness is determined indistinctly. Rounded heart surfaces do not correspond to the chest wall and cardiac edges outlined at percussion are usually for 1–1.5 cm or smaller than it's silhouette observed at radiographs (Fig. 7.29).

Heart auscultation The purpose of the heart auscultation is auscultation and assessment of sound phenom-

206

ena, that occur during heart work. The leading position in the clinical heart examination is given to auscultation, but it is necessary to realize possibilities of this examination method. The human ear is able to recognize sounds in the range between 20–20,000 Hz, but not lower or higher. Optimal range for an average doctor is 1000–5000 Hz, that corresponds to the range of human voice, but in the same time the frequency of the majority of heart tones does not exceed the threshold of 500 Hz; so III and IV tones (around 100 Hz) are not audible for the majority of doctors. Heart cycle normally begins with the atria contraction (IV tone), that ends the diasyolic filling of ventricles with blood. Due to this systole begins and atrioventricular valves close (I tone). The closing of semilunar valves of the aorta and pulmonary trunk (II tone) indicates the beginning of new systole and new heart cycle (Fig. 7.30). If the heart rate does not exceed 120 beats per minute, than diastole is always longer than systole. General rules of auscultation: 1. Auscultation is carried out in the horizontal and vertical position according to purposes. 2. It is better to conduct auscultation on the height of expiration (while breathholding if necessary). 3. Auscultation is initially held at rest. 4. Auscultation is conducted after the physical activity if necessary. 5. Valves are aucsultated in the certain order. 6. Doctor position is slightly to the patients right side (the doctor is righthanded) or left side (the doctor is lefthanded). Logical order of the heart auscultation consists in two stepwise actions. The consequence of the heart auscultation as an organ

Сhapter 7

Diastole

Systole

Systolic pressure (mmHg)

120

Aortic pressure

100 80

Aortic valve opens

Left ventricular pressure

60 40

Aortic valve closes (dicrotic notch)

Left atrial pressure

AV valve closes

AV valve opens

Ventricular volume (ml)

0 End-diastolic volume

120 90

End-systolic volume

60 R

R T

ECG Q S Heart sounds PCG

Phase of cardiac cycle

S3 1а

Q S

S1 1b 0.2

1c 0.4

1c Atrial systole

1а

0.8 0.6 Time (sec)

Ventricular filling 1a Rapid filling 1b Diastasis

Isovolumetric contraction

S1 1b

0.2

Ventricular ejection

Isovolumetric relaxation

Fig. 7.30. Interrelation of cardiac cycle and electrocardiogram (ECG) and phonocardiogram (PCG). All sounds that occur during heart work are divided into main (obligatory) and additional. Main sounds are called heart tones, additional – murmurs. Heart tones are abrubt and short, murmurs are prolonged

and the consequence of valves auscultation (5 points) is often confused in the clinical practice. The consequence of the heart auscultation: 1. Heart tones assessment (I and II tones). 2. Heart murmurs assessment if they are present (5 points).

Heart tones must be auscultated and assessed in the first place. It is always necessary to assess 1st tone, and then 2nd. 1st tone assessment should be conducted only on the heart apex, so auscultation should always begin from the apex (localization of the apex beat). 2nd tone assessment is conducted at the heart basis over the aorta and pulmonary artery. For an understanding of

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Closing and opening of valves during systole happens not simultaneously, but pause between them is so minimal, that the human ear can not auscultate it. The consequence of valves closing and openings during 1st tone: 1. Mitral valve closing. 2. Tricuspid valve closing. 3. Pulmonary artery valve opening. 4. Aortic valve opening.

Tricuspid and mitral valves close

Aortic and pulmonary valves close

“LUB”

“DUB”

Beginning of systole

End of systole/ Beginning of diastole

Fig. 7.31. Main components of heart tone formation

heart tones changes, it is necessary to know mechanisms of their formation (Fig. 7.31). Components, that forms 1st tone: 1. Valvular (vibration of pleurae of atrioventricular valves at the phase of isometric contraction of the ventricle). 2. Muscular (caused by the vibration of the ventricles myocardium at the period of isometric contraction). 3. Vascular (caused by the vibration of the initial portion of the aorta and pulmonary tract during the ejection period and opening of semilunar valves). 4. Atrial (caused by the vibration of atria during contraction).

Systole

Diastole

The second tone is assessed on the heart basis, in the second or third intercostal space to the left or right to the sternum. As the second tone has medium- and high-frequent B

Systole

А “Lub” “Dub”

The 1st tone is formed only by the closing of AV-valves if pathology is absent. The closing of the mitral valve is louder, so it plays the main role in the formation of the 1st tone. Semilunar valves during ventricles systole usually open noiseless. The main characteristics of the first tone are its intensity (loudness), the second important feature is splitting. Splitting occurs due to uneven closing and opening of heart valves. The 1st tone is usually more intensive on the apex than the 2nd (Fig. 7.32). Components, that form 2nd tone: 1. Valvular (due to vibration of semilunar leaflets of aortic and pulmonary artery valves during their closing at the beginning of diastole). 2. Vascular (vibration of aortic and pulmonary artery walls due to return blood flow) (Table 7.2).

Diastole

“Dub” “Lub”

Diastole

Systole

Heart tones

Diastole

Fig. 7.32. Diagrammatic representation of heart tones: А – on the apex; B – on the base. Difference in tones intensity: tone I prevales over the apex (S1), tone II – over the base (S2)

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Сhapter 7

Навчальне видання

Катілов Олександр Васильович Дмитрієв Дмитро Валерійович Дмитрієва Катерина Юріївна Макаров Сергій Юрійович

Клінічне обстеження дитини Навчальний посібник (англійською мовою)

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