COMPLETE EXAMINATION OF RESPIRATORY SYSTEM IN PEDIATRICS. IT HAS BEEN SUMMARIZED FROM ALL WELL KNOWN 32 BOOKS UNDER GUIDANCE OF ONE OF THE BEST PEDIATRIC DOCTORS AND PROFESSORS .
BY DR. SURAJ R. DHANKIKAR.
COMPLETE EXAMINATION OF RESPIRATORY SYSTEM IN PEDIATRICS. IT HAS BEEN SUMMARIZED FROM ALL WELL KNOWN 32 BOOKS UNDER GUIDANCE OF ONE OF THE BEST PEDIATRIC DOCTORS AND PROFESSORS .
BY DR. SURAJ R. DHANKIKAR.
Congenital heart disease is one or more problems with the heart's structure that exist since birth. Congenital means that you're born with the defect. Congenital heart disease, also called congenital heart defect, can change the way blood flows through your heart. IF YOU LIKE GIVE YOUR LIKES AND FOLLOW THIS LINK
A congenital heart defect is a problem with the structure of the heart. It is present at birth. Congenital heart defects are the most common type of birth defect. The defects can involve the walls of the heart, the valves of the heart, and the arteries and veins near the heart. They can disrupt the normal flow of blood through the heart. The blood flow can slow down, go in the wrong direction or to the wrong place, or be blocked completely.
Doctors use a physical exam and special heart tests to diagnose congenital heart defects. They often find severe defects during pregnancy or soon after birth. Signs and symptoms of severe defects in newborns include
Rapid breathing
Cyanosis - a bluish tint to the skin, lips, and fingernails
Fatigue
Poor blood circulation
Many congenital heart defects cause few or no signs and symptoms. They are often not diagnosed until children are older.
Many children with congenital heart defects don't need treatment, but others do. Treatment can include medicines, catheter procedures, surgery, and heart transplants. The treatment depends on the type of the defect, how severe it is, and a child's age, size, and general health.
Methods of measurement of blood pressure in children.
Steps for accurate measurement and how to plot the measurement on charts and compare it with the normal blood pressure percentile with example.
A cyanotic heart defect is a group-type of congenital heart defects (CHDs). The patient appears blue (cyanotic), due to deoxygenated blood bypassing the lungs and entering the systemic circulation. This can be caused by right-to-left or bidirectional shunting, or malposition of the great arteries.
Cyanotic heart defects, which account for approximately 25% of all CHDs, include:
Tetralogy of Fallot (ToF)
Total anomalous pulmonary venous connection
Hypoplastic left heart syndrome (HLHS)
Transposition of the great arteries (d-TGA)
Truncus arteriosus (Persistent)
Tricuspid atresia
Interrupted aortic arch
Pulmonary atresia (PA)
Pulmonary stenosis (critical)
Eisenmenger syndrome(Reversal of Shunt due to Pulmonary Hypertension) .
Patent ductus arteriosus may cause cyanosis in late stage.
Rheumatic heart disease is a condition in which the heart valves have been permanently damaged by rheumatic fever. The heart valve damage may start shortly after untreated or under-treated streptococcal infection such as strep throat or scarlet fever.
Bronchiectasis
A condition characterized by chronic permanent dilation & destruction of bronchi due to destructive changes in the elastic and muscular layers of bronchial walls.
The common thread in the pathogenesis of bronchiectasis consists of difficulty clearing secretions & recurrent infections with a “vicious circle” of infection and inflammation resulting in airway injury and remodelling.
PLEASE REFER TO REFERENCE TEXTBOOKS FOR CLARITY.
Congenital heart disease is one or more problems with the heart's structure that exist since birth. Congenital means that you're born with the defect. Congenital heart disease, also called congenital heart defect, can change the way blood flows through your heart. IF YOU LIKE GIVE YOUR LIKES AND FOLLOW THIS LINK
A congenital heart defect is a problem with the structure of the heart. It is present at birth. Congenital heart defects are the most common type of birth defect. The defects can involve the walls of the heart, the valves of the heart, and the arteries and veins near the heart. They can disrupt the normal flow of blood through the heart. The blood flow can slow down, go in the wrong direction or to the wrong place, or be blocked completely.
Doctors use a physical exam and special heart tests to diagnose congenital heart defects. They often find severe defects during pregnancy or soon after birth. Signs and symptoms of severe defects in newborns include
Rapid breathing
Cyanosis - a bluish tint to the skin, lips, and fingernails
Fatigue
Poor blood circulation
Many congenital heart defects cause few or no signs and symptoms. They are often not diagnosed until children are older.
Many children with congenital heart defects don't need treatment, but others do. Treatment can include medicines, catheter procedures, surgery, and heart transplants. The treatment depends on the type of the defect, how severe it is, and a child's age, size, and general health.
Methods of measurement of blood pressure in children.
Steps for accurate measurement and how to plot the measurement on charts and compare it with the normal blood pressure percentile with example.
A cyanotic heart defect is a group-type of congenital heart defects (CHDs). The patient appears blue (cyanotic), due to deoxygenated blood bypassing the lungs and entering the systemic circulation. This can be caused by right-to-left or bidirectional shunting, or malposition of the great arteries.
Cyanotic heart defects, which account for approximately 25% of all CHDs, include:
Tetralogy of Fallot (ToF)
Total anomalous pulmonary venous connection
Hypoplastic left heart syndrome (HLHS)
Transposition of the great arteries (d-TGA)
Truncus arteriosus (Persistent)
Tricuspid atresia
Interrupted aortic arch
Pulmonary atresia (PA)
Pulmonary stenosis (critical)
Eisenmenger syndrome(Reversal of Shunt due to Pulmonary Hypertension) .
Patent ductus arteriosus may cause cyanosis in late stage.
Rheumatic heart disease is a condition in which the heart valves have been permanently damaged by rheumatic fever. The heart valve damage may start shortly after untreated or under-treated streptococcal infection such as strep throat or scarlet fever.
Bronchiectasis
A condition characterized by chronic permanent dilation & destruction of bronchi due to destructive changes in the elastic and muscular layers of bronchial walls.
The common thread in the pathogenesis of bronchiectasis consists of difficulty clearing secretions & recurrent infections with a “vicious circle” of infection and inflammation resulting in airway injury and remodelling.
PLEASE REFER TO REFERENCE TEXTBOOKS FOR CLARITY.
Transposition of the great arteries is a serious but rare heart defect present at birth (congenital), in which the two main arteries leaving the heart are reversed (transposed). The condition is also called dextro-transposition of the great arteries.
A brief description about the fetal circulation for BSc Nursing students. This PPT includes the slides aboute fetal circulation from the basic Anatomy and Physiology of Heart and Circulatory system till the Applied aspects of it.
USMLE CVS 008 Fetal and regional circulation anatomy .pdfAHMED ASHOUR
Fetal circulation and regional circulation refer to the distinct patterns of blood flow in the developing fetus and the circulatory pathways within different regions of the body.
Understanding these circulation patterns is crucial for comprehending the physiological adaptations that occur during fetal development and in the various regions of the body after birth.
After birth, the circulatory system undergoes significant changes, such as closure of the foramen ovale and ductus arteriosus, leading to the establishment of the adult circulatory pattern.
Blood from the placenta is carried to the fetus by the umbilical vein. In humans, less than a third of this enters the fetal ductus venosus and is carried to the inferior vena cava, while the rest enters the liver proper from the inferior border of the liver. The branch of the umbilical vein that supplies the right lobe of the liver first joins with the portal vein. The blood then moves to the right atrium of the heart. In the fetus, there is an opening between the right and left atrium (the foramen ovale), and most of the blood flows through this hole directly into the left atrium from the right atrium, thus bypassing pulmonary circulation. The continuation of this blood flow is into the left ventricle, and from there it is pumped through the aorta into the body. Some of the blood moves from the aorta through the internal iliac arteries to the umbilical arteries, and re-enters the placenta, where carbon dioxide and other waste products from the fetus are taken up and enter the maternal circulation.
Fetal Circulation by Barkha Devi,Lecturer,Sikkim Manipal College of NursingBarkha Devi
This PowerPoint will provide you a short a sweet lecture about fetal circulation. Please give me your feed back .
-Discuss anatomy and physiology of fetal circulation
-Compare and contrast fetal circulation to infant circulation
-Define specialized structures of fetal circulation
This system has three main components: the heart, the blood vessel and the blood itself. The heart is the system's pump and the blood vessels are like the delivery routes. Blood can be thought of as a fluid which contains the oxygen and nutrients the body needs and carries the wastes which need to be removed
Model Attribute Check Company Auto PropertyCeline George
In Odoo, the multi-company feature allows you to manage multiple companies within a single Odoo database instance. Each company can have its own configurations while still sharing common resources such as products, customers, and suppliers.
Welcome to TechSoup New Member Orientation and Q&A (May 2024).pdfTechSoup
In this webinar you will learn how your organization can access TechSoup's wide variety of product discount and donation programs. From hardware to software, we'll give you a tour of the tools available to help your nonprofit with productivity, collaboration, financial management, donor tracking, security, and more.
June 3, 2024 Anti-Semitism Letter Sent to MIT President Kornbluth and MIT Cor...Levi Shapiro
Letter from the Congress of the United States regarding Anti-Semitism sent June 3rd to MIT President Sally Kornbluth, MIT Corp Chair, Mark Gorenberg
Dear Dr. Kornbluth and Mr. Gorenberg,
The US House of Representatives is deeply concerned by ongoing and pervasive acts of antisemitic
harassment and intimidation at the Massachusetts Institute of Technology (MIT). Failing to act decisively to ensure a safe learning environment for all students would be a grave dereliction of your responsibilities as President of MIT and Chair of the MIT Corporation.
This Congress will not stand idly by and allow an environment hostile to Jewish students to persist. The House believes that your institution is in violation of Title VI of the Civil Rights Act, and the inability or
unwillingness to rectify this violation through action requires accountability.
Postsecondary education is a unique opportunity for students to learn and have their ideas and beliefs challenged. However, universities receiving hundreds of millions of federal funds annually have denied
students that opportunity and have been hijacked to become venues for the promotion of terrorism, antisemitic harassment and intimidation, unlawful encampments, and in some cases, assaults and riots.
The House of Representatives will not countenance the use of federal funds to indoctrinate students into hateful, antisemitic, anti-American supporters of terrorism. Investigations into campus antisemitism by the Committee on Education and the Workforce and the Committee on Ways and Means have been expanded into a Congress-wide probe across all relevant jurisdictions to address this national crisis. The undersigned Committees will conduct oversight into the use of federal funds at MIT and its learning environment under authorities granted to each Committee.
• The Committee on Education and the Workforce has been investigating your institution since December 7, 2023. The Committee has broad jurisdiction over postsecondary education, including its compliance with Title VI of the Civil Rights Act, campus safety concerns over disruptions to the learning environment, and the awarding of federal student aid under the Higher Education Act.
• The Committee on Oversight and Accountability is investigating the sources of funding and other support flowing to groups espousing pro-Hamas propaganda and engaged in antisemitic harassment and intimidation of students. The Committee on Oversight and Accountability is the principal oversight committee of the US House of Representatives and has broad authority to investigate “any matter” at “any time” under House Rule X.
• The Committee on Ways and Means has been investigating several universities since November 15, 2023, when the Committee held a hearing entitled From Ivory Towers to Dark Corners: Investigating the Nexus Between Antisemitism, Tax-Exempt Universities, and Terror Financing. The Committee followed the hearing with letters to those institutions on January 10, 202
The Roman Empire A Historical Colossus.pdfkaushalkr1407
The Roman Empire, a vast and enduring power, stands as one of history's most remarkable civilizations, leaving an indelible imprint on the world. It emerged from the Roman Republic, transitioning into an imperial powerhouse under the leadership of Augustus Caesar in 27 BCE. This transformation marked the beginning of an era defined by unprecedented territorial expansion, architectural marvels, and profound cultural influence.
The empire's roots lie in the city of Rome, founded, according to legend, by Romulus in 753 BCE. Over centuries, Rome evolved from a small settlement to a formidable republic, characterized by a complex political system with elected officials and checks on power. However, internal strife, class conflicts, and military ambitions paved the way for the end of the Republic. Julius Caesar’s dictatorship and subsequent assassination in 44 BCE created a power vacuum, leading to a civil war. Octavian, later Augustus, emerged victorious, heralding the Roman Empire’s birth.
Under Augustus, the empire experienced the Pax Romana, a 200-year period of relative peace and stability. Augustus reformed the military, established efficient administrative systems, and initiated grand construction projects. The empire's borders expanded, encompassing territories from Britain to Egypt and from Spain to the Euphrates. Roman legions, renowned for their discipline and engineering prowess, secured and maintained these vast territories, building roads, fortifications, and cities that facilitated control and integration.
The Roman Empire’s society was hierarchical, with a rigid class system. At the top were the patricians, wealthy elites who held significant political power. Below them were the plebeians, free citizens with limited political influence, and the vast numbers of slaves who formed the backbone of the economy. The family unit was central, governed by the paterfamilias, the male head who held absolute authority.
Culturally, the Romans were eclectic, absorbing and adapting elements from the civilizations they encountered, particularly the Greeks. Roman art, literature, and philosophy reflected this synthesis, creating a rich cultural tapestry. Latin, the Roman language, became the lingua franca of the Western world, influencing numerous modern languages.
Roman architecture and engineering achievements were monumental. They perfected the arch, vault, and dome, constructing enduring structures like the Colosseum, Pantheon, and aqueducts. These engineering marvels not only showcased Roman ingenuity but also served practical purposes, from public entertainment to water supply.
Instructions for Submissions thorugh G- Classroom.pptxJheel Barad
This presentation provides a briefing on how to upload submissions and documents in Google Classroom. It was prepared as part of an orientation for new Sainik School in-service teacher trainees. As a training officer, my goal is to ensure that you are comfortable and proficient with this essential tool for managing assignments and fostering student engagement.
Introduction to AI for Nonprofits with Tapp NetworkTechSoup
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2024.06.01 Introducing a competency framework for languag learning materials ...Sandy Millin
http://sandymillin.wordpress.com/iateflwebinar2024
Published classroom materials form the basis of syllabuses, drive teacher professional development, and have a potentially huge influence on learners, teachers and education systems. All teachers also create their own materials, whether a few sentences on a blackboard, a highly-structured fully-realised online course, or anything in between. Despite this, the knowledge and skills needed to create effective language learning materials are rarely part of teacher training, and are mostly learnt by trial and error.
Knowledge and skills frameworks, generally called competency frameworks, for ELT teachers, trainers and managers have existed for a few years now. However, until I created one for my MA dissertation, there wasn’t one drawing together what we need to know and do to be able to effectively produce language learning materials.
This webinar will introduce you to my framework, highlighting the key competencies I identified from my research. It will also show how anybody involved in language teaching (any language, not just English!), teacher training, managing schools or developing language learning materials can benefit from using the framework.
2. 1. Stages of the formation of the heart and
blood vessels in the prenatal period.
The heart is laid in the second week of the embryo’s
intrauterine development as a form of two heart germs -
primary endocardial tubes. In the future, they two germs
merge into one two-layer primary heart tube (scheme 1).
The primary heart tube is located in the pericardial cavity
vertically ahead of the intestinal tube. The endocardium
develops from its inner layer, and the myocardium and
epicardium from the outer layer.
3.
4. The mechanism and timing of the closure of the
main fetal circulatory system after the birth of a
child.
At the end of 3rd week there is simultaneous growth of 2
partitions - one from the atrium, and the other - from apex of
the ventricle. They grow in the direction of the primary
atrioventricular aperture.
During this time, the heart, which is initially formed in the
cervical region, descends into the chest cavity and
simultaneously rotates. If this process is disturbed, will be
appeared so named anomalies of the heart localization:
cervical position, cervicothoracic and abdominal position.
5. The mechanism and timing of the closure of the
main fetal circulatory system after the birth of a
child.
Sometimes changes during cornering of heart lead to the reverse
location of the heart, i.e. the ventricles are located on the right, the
atriums on the left. This anomaly is accompanied by reverse
arrangement of pectoral and abdominal organs. It is named “situs
viscerus inversus”
By the end of 7th-8th week, the heart turns from two-chamber into
a four-chamber.
Valve apparatus occurs after formation of partitions and valves
will be formed due to development of endocardial protrusions (pads)
.
The main elements of the conducting system - the sinus node
(Kiss-Flyaka), the AV node (Ashoff-Tavara) and the His bundle and
Purkinje fibers are laid in the heart muscle during the first weeks
(before the S-shaped bend of the heart tube).
6. Fetal circulation
The fetus receives the necessary for the development
nutrients and oxygen from the mother through the vessels of
placenta.
The placenta is connected with the fetus by theumbilical
cord, which includestwo umbilical arteries (branches of
internal iliac arteries) and theumbilical vein . These vessels
pass from the cord into the fetus through the umbilical ring
(scheme 2).
7.
8. Fetal circulation
Through the arteries, venous blood delivers from fetus to placenta, where will be
enriched with nutrients, oxygen and becomes arterial.
Than, the blood returns to the fetus through the umbilical vein, which approaches
the liver and be divided into two branches.
One of branches directly flows into the inferior vena cava (venous ductus). Another
branch passes into the portal vein for blood supply of the liver (scheme 3).
From here, blood poures out through the hepatic veins into the inferior vena cava,
where it is mixed with venous blood from the lower body and enters the RA.
The opening of the inferior vena cava is located opposite the oval opening in the
IAS. Therefore, most of blood from the inferior vena cava falls into the LA, and then
into the LV.
9.
10. 1.
2.
3.
4.
Closing dates:
The venous duct closes in the first months after birth, complete obliteration
begins at week 8 and ends at 10-11 weeks of age. The umbilical vein with
the venous duct turns into a round ligament of the liver.
Shunt through OH ceases to function in the next 3-5 hours after birth,
because with the beginning of pulmonary respiration, the blood flow through
the lungs increases almost 5 times.
Anatomic closure of OH occurs at the age of 5-7 months. But, in 50% of
children up to 1 year old, the OH anotomically are existed, and in 30% of
people - throughout their lives. However, it does not have any significance
for hemodynamics.
The arterial (Botallov) duct in healthy full-term newborns closes by the end
of the first or second day of life, but in some cases it may function for
several days. PDA to 2 months of life is a heart defect.
11. 2. Anatomical and physiological features of the heart and blood
vessels in different age periods. Critical periods of cardiovascular
system development.
The mass of the heart in newborn is about 0.8% of body weight (in adults
0.45%). The right and left ventricles are approximately equal. The thickness of
their walls is about 5 mm.
In children, LV grows more intensively due to the increasing vascular
resistance and blood pressure. In parallel, increase also the size of main
vessels.
Pulse in newborns is arrhythmic, the duration of pulse waves and the
intervals between them is uneven.
Blood pressure in children increases more rapidly in the first 2–3 years and
in puberty period.
With age, stroke volume of heart and minute volume of heart increase, the
total peripheral resistance decreases.
12. 3. Methods of objective investigation of the cardiovascular
system in children.
Inspection. Color of skin;
Palpation. apical impulse. palpation of pulse in arteries;
Percussion. Borders of heart;
Auscultation. Listening to the heart sounds (tones, murmurs).
13.
14. Borders of the heart in children
Child
age
Borders of heart relative dullness Heart
diameterLeft edge Top edge Right edge
0-2 yrs 1-2 sм
outwards
from left
MCL
II rib Right
parasternal
line
6-9 sм
2-7 yrs 0,5-1,0 sм
outwards
from left
MCL
II intercostal
space
Inwards
from right
parasternal
line
8-12 sм
15. Methods of instrumental research
1.
2.
3.
4.
5.
6.
ECG study. The electrical activity of various parts of the heart, rhythm and
conduction disturbances, and myocardial ischemia are assessed. In children, the
interpretation of ECG is very difficult due to the age differences of indicators.
Phonocardiogram allows to evaluate heart sounds and identify additional noises..
Chest X-ray allows to assess the size and shape of the heart. Will be calculated
necessary indicators (KTI).
Echocardiography - an ultrasound of the heart. Allows to obtain data on the size of
the cavities of the heart, the thickness of its walls and partitions, the size of Ao, PA.
EchoCG allows to evaluate the movement of the valves, their shape, see the slack
of the valves (prol, etc.
5. Angiocardiography - a method of X-ray examination of the cavities of the heart
and large vessels with the introduction of contrast agent.
6. Functional tests of cardiovascular system.
16. 1.
2.
3.
4.
4. Age features of the functional indicators of
cardiovascular system in children and adolescents
Heart rate
Blood pressure
Stroke volume of the heart (SVH)
Minute heart volume (MVH)
17. Heart rate in children
Age HR
(min)
Age HR
(min)
Age HR
(min)
Newborn 135-140 5 year 93-100 11 year 78-84
6 months 130-135 6 year 90-95 12 year 75-82
1 year 120125 7 year 85-90 13 year 72-80
2 year 110-115 8 year 80-85 14 year 72-78
3 year 105-110 9 year 80-85 15 year 70-76
4 year 100-105 10 year 78-85 16 year 68-72
18. Blood pressure in children
Normal values of BP in children (Hg mm)
Age Systolic Diastolic
Newborns 60-80 40-50
1-6 months 90 40-50
2-12 months 100 50-60
2 – 6 year 100-110 60-70
7-10 year 100-120 60-80
11-14 year 110-120 70-80
19. Indices of heart volumes
Blood circulation indices in children
Age Stroke heart volume
(ml)
Minute heart volume
(l/min)
Newborns 2,5-4,6 0,36-0,56
1 year 10,2-11,0 1,33-1,37
3-6 years 3133 2,83-2,91
7– 9 years 38-40 2,93-3,01
10-12 years 49-50 3,47-3,55
13-15 years 55-57 3,69-3,77
20. 5. Characteristics of cardiac noise in children, the differences
between functional noise from organic, the noise of "small" anomalies
of the heart and blood vessels.
-
-
-
-
-
Important characteristics of cardiac murmures:
location in the cardiac cycle (systolic, diastolic);
intensity, volume;
localization, place of the highest listening, irradiation;
character (blowing, scraping, crunching of snow, machine, rough, soft,
gentle);
duration and configuration (for all systole, meso-, proto and others).
Systolic murmurs
1. Functional (physiological)
2. Organic (pathological)
Diastolic murmurs
22. Questions
1.
A.
B.
C.
2.
3.
Congenital heart diseases (CHD)
Classification of
Semiotics of the
Hemodynamics of CHD
Hemodynamics of the most common acquired heart defects
Signs of lesions of myo-, endo-, pericarditis in children
23. Classification
•
•
CHD of "white" type are characterized by normal or reduced
contents of hemoglobin due to increase of pulmonary blood
volume and increase of arterial blood inflow from the left parts
of heart to right.
CHD of "cyanotic" type are characterized by increase of quantity
of restored hemoglobin of erythrocytes due to decrease of its
use by blood in lungs, increase of quantity of venous blood
inflowing into systemic circulation
24. Terminology
•
•
•
•
•
•
•
•
CHD - Congenital Heart Disease
PC – Pulmonary Circulation
SBC – Systemic Blood
Circulation
PDA – Patent Ductus Arteriosus
ASD – Atrial Septal Defect
VSD – Ventricular Septal Defect
AVC – Atrioventricular Canal
TGV – Transposition Of Great
Vessels
•
•
•
•
•
PAIS, ISPA – Pulmonary
Artery Isolated Stenosis
CA – Coarctation of Aorta
PA – Pulmonary Artery
LA – Left Atrium
RA – Right Atrium
25. Classification
Hemodynamic changes Nosology forms
CHD with enrichment of PC PDA, ASD, VSD, AVC, TGV
CHD with decreasing of PC ISPA, Fallot diseases
CHD with decreasing of SBC CA, SAo
CHD unchanged BC Dextracardia, anomalies of aortic
position
26. Hemodynamic changes in CHD.
1.
2.
3.
For all CHD with enrichment of PC, hypervolemia occurs in the
pulmonary vessels due to coming of additional blood volume from the
left side of heart through the defects (ASD, VSD), or persistent duct
(PDA). In AVC and TGV additional inflow of blood to the right
chambers of heart is caused by retrograde enrichment of blood
circulation.
Hemodynamics in ISPA and Fallot diseases is caused by narrowing of
the outfall of PA, i.e. the mechanical obstacle leads to hypovolemia of
PC. Less blood flows into LA due to stenosis (narrowing).
In CA and SAo, decrease of blood volume in the vessels of systemic
circulation occurs also due to mechanical obstacle in different parts
of aorta.
27. Semiotics frequent CHD
•
•
•
•
•
The main general clinical manifestations of CHD are:
chest deformity (cardiac hump);
discoloration of the skin cover;
displacement of heart dullness (enlargement of sizes);
reduced sonority of tones;
appearance of pathological noises (murmurs).
28. Ventricular Septum Defect
is oval, round or cone-shaped aperture in
membranous (upper) or muscular (lower)
part of interventricular septum
•
•
•
•
Coarse (rough) systolic murmur
along the left edge of sternum,
maximum in 4th intercostal space, wide
irradiation zone in heart area.
Enlargement of heart size to the
right and left.
X-ray – enlarging of RV and LV,
increased pulmonary pattern due to the
overflow of pulmonary circulation.
ECG - hypertrophy of both ventricles.
29. Patent Ductus Arteriosus
shunt of blood from aorta to PA
•
•
•
•
Continuous systolic and
diastolic murmurs in II-III intercostal
space at the left edge of sternum.
In newborns, only systolic
component of murmur and
amplified II tone in the PA are heard.
X-ray - increase of heart size
mainly due to left sections, bulging
of PA arc and the overflow of the
vasculars of the PC.
ECG - hypertrophy of left parts or
both ventricles.
30. Atrial Septum Defect
result of abnormal development of
primary and secondary interatrial
septums and endocardial rollers
•
•
•
•
Moderate systolic murmur in the
2nd intercostal space to the left of
the sternum, accent II tone on the
PA,
Expansion of RA and RV borders
Overflow of the PC vessels.
ECG - deviation of electrical
activity to the right, RV hypertrophy.
31. Tetralogy of FALLOT
•
•
•
•
Components:
pulmonary artery stenosis
high ventricular septal defect
transposition of aorta to the
right (location "astride" on
interventricular septum or
dextraposition of aorta)
right ventricle hypertrophy
●
●
●
32. Tetralogy of Fallot
•
•
•
•
Cyanosis, dyspnea-cyanosis
attacks,
Systolic murmur along the
left edge of the sternum. II tone
on PA is weakened.
X-ray - the impoverishment
of pulmonary pattern, the heart
is small and in the shape of
“boot ”, the arc of PA sinks.
ECG - hypertrophy of RV.
33. Transposition of Great Vessels
severe CHD, when aorta
departs from right ventricle and
carries nonoxygenated blood,
and pulmonary artery – from
left ventricle and carries
oxygenated blood,
atrioventricular valves and
ventricles of heart are
generated correctly
34. Transposition of Great Vessels
•
•
•
•
General cyanosis from birth.
Murmur may not be, or
systolic concomitant septum
defect or PA stenosis.
X-ray – enlargement of right
sides of heart, the “form of
egg, lying on its side ”.
ECG - RV hypertrophy.
35. Pulmonary Artery stenosis
•
•
•
•
Coarse systolic murmur,
maximum II-III intercostal space,
left sternum edge, sharp
weakening or absence of II tone on
the PA
May be attack of cyanosis due
to dropping of blood from the RA
through oval opening.
X-ray - significant enlargement
of right parts of heart.
ECG - hypertrophy of RV and RA.
36. is represented with congenital
narrowing or full break of aorta
in the place of its arch isthmus
(sometimes in chest or
abdominal part).
Coarctation of Aorta
37. Coarctation of Aorta
•
•
•
•
•
•
Severe breathing shortness,
Mass of moist rales in the lungs in early age children.
Systolic murmur in 2nd intercostal space to the left or right of the
sternum, sometimes only on the back.
Sharp weakening of pulse and decrease of BP in the legs. On
hands the pulse full and high, BP is normal or increased.
X-ray – enlargement of heart sizes due to left or right parts,
increased pulmonary pattern.
ECG - hypertrophy of ventricles.
39. Mitral valvular insufficiency
•
•
•
The failure of bicuspid valve of heart is characterized by
expansion of left atrio-ventricular orifice (hole). It’s most often
cause is rheumatic lesion, it develops as a result of folding of
sashes (wrinkling) of MV leaflets.
Hemodynamics is characterized by dropping of blood from the
LV into the cavity of the LA during systole, increase of blood
volume in LA, then in the vessels of the lungs by retrograde
mechanism. It will lead to increase BP in PA.
Auscultation: amplification of II tone on PA, systolic murmur at
heart apex or at the V point
40. Mitral stenosis
•
•
•
This is a narrowing of the left atrio-ventricular orifice. The
main reason is rheumatic fever.
Hemodynamics: through the narrowed a-v orifice during
diastole from the LA into LV blood flows with difficulties. This will
lead to the expansion of LA due to increased pressure in it, then
increase of blood volume and blood pressure in the vessels of the
lungs.
Auscultation: there is heard loud and short (clapping) I tone
and diastolic murmur at the apex of heart. Accent II tone on PA.
Apical impulse is weakened, palpable "cat's purr."
41. •
•
A result of wrinkling of the AC leaflets in infective endocarditis.
Hemodynamics: part of the blood through insufficiently closed
aortic valves during diastole returns to the LV. Hypertrophy and
dilatation of LV, increase of blood volume, then expansion of the left
a-v orifices, increase of blood volume in LA and further in vessels of
lungs by retrograde machanism.
Auscultation: at the apex, the weakening of the I tone is heard, on
the heart basis, or in III – IV intercostal space to the left of sternum -
proto-diastolic murmur. The murmur is quiet, gentle, flowing, better
heard in standing position with tilts the body forward.
Aortic valvular insufficiency
43. Myocarditis
•
•
•
•
•
is inflammation of the heart muscle.
most often develops in rheumatic fever, viral and other
infections, and with other diseases (allergies, toxicosis, etc.).
is characterized by significant expansion of boundaries of
relatively dullness of heart, muffling and deafness of tones,
especially I tone, increase of HR (tachycardia).
At the apex of heart, systolic murmur is heard.
ECG: decrease of voltage of T wave and shortening of S-T
interval, are characteristic conduction system disturbances (s-a, a-
v, intraventricular blockade, extrasystoles).
44. Endocarditis
•
•
•
is an inflammation of the inner lining of the heart.
The most common causes are rheumatic fever and other
infectious (bacterial, septic) diseases. Rheumatic endocarditis
occurs after acute streptococcal infection (sore throat) or
chronic tonsillitis exacerbation.
In children, valvular endocarditis is often meet in patients
with CHD as a complication
45. Pericarditis
•
•
•
•
•
is relatively rare as a isolated inflammatory process.
More often, pericarditis is associated with other inflammatory
lesions of heart - myocarditis or endomyocarditis. Pericarditis
may be dry or exudative.
Exudative pericarditis in dependence on the nature of effusion
may be serous, hemorrhagic and purulent.
Pericarditis is characterized by sharp weakening of heart
tones and with appearance of pericardial friction noise.
ECG, sharp decrease of the voltage and S-T shift upward from
the isoline are determined
47. Definition:
CONGENITAL HEART DISEASE (CHD) means
congenital defect of heart structure, tissue and
great vessels with pathologic changes of
intracardiac haemodynamics developed in the
intrauterine period of fetus
48. Epidemiology:
● The prevalence of CHD among newborn
children is approximately 8 per 1000 cases.
● Congenital heart diseases are one of the
most widespread congenital anomalies in
children.
The chd are frequent anomalies after
congenital pathology of the locomotorium and
the central nervous system.
51. Ethiology:
Significant constitutional factors of CHD formation:
● chromosomal disorders (5%)
● mutations of one gene (2-3%)
● damaging factors of an environment (1-2 %)
● polygenic-multifactorial inheritance (90%)
52. Ethiology:
The significant environment factors of CHD formation:
● influence of X-ray on organism of the woman during
first trimester of pregnancy;
● influence of ionizing radiation, chemicals;
● influence of some medicines, drugs etc.;
● influence of infectious and viral agents (rubella,
cytomegaly, flu, Coxsackie viruses);
● influence of ethanol (mothers with alcoholism in 30%
of cases have damaged children);
● high mountain lands (PDA is often registered).
53. Classification:
CHD of "white" type are characterized by normal or
reduced contents of hemoglobin due to increase of
pulmonary blood volume and increase of arterial blood
inflow from the left parts of heart to right.
CHD of "cyanotic" type are characterized by increase
of quantity of restored hemoglobin of erythrocytes due
to decrease of its use by blood in lungs, increase of
quantity of venous blood inflowing into systemic
circulation
54. Classification:
FAILURE OF
HEMODYNAMICS
WITHOUT
CYANOSIS
WITH
CYANOSIS
WITH INCREASE OF
PULMONARY
CIRCULATION
PATENT DUCTUS ARTERIOUS,
ATRIAL SEPTAL DEFECT,
VENTRICAL SEPTAL DEFECT
TRANSPOSITION OF
GREAT VESSELS
WITH DECREASE OF
PULMONARY
CIRCULATION
PULMONARY ARTERY ISOLATED
STENOSIS (CYANOSIS IN A LATE
STAGE)
FALLOT’S DISEASE
WITH DECREASE OF
SYSTEMIC CIRCULATION
COARCTATION OF AORTA, AORTIC
STENOSIS
WITHOUT DISORDERS TOLOCHINOV-ROGE’S DISEASE
55. Classification
I SIGNS OF HEART FAILURE AT REST ARE ABSENT, ONLY AFTER A PHYSICAL PRESSURE (LONG
SHOUT, ANXIETY, AT FEEDING) THE CHILD HAS DYSPNEA, PALLOR, REFUSAL OF BREAST OR
FREQUENT BREAKS IN SUCKING.
IIA Signs of heart failure at rest, small dyspnea (respiratory rate exceeds normal not more than
50%), moderate tachycardia (heart rate exceeds normal to 10-15%), Hepatomegaly (liver
increases not more than 3 cm), on X-ray the moderate expansion of heart shadow.
IIB Significant dyspnea (RR is 50-70% more than norm), Tachycardia (HR 15-25% more than norms)
, Liver increased more than 3-4 cm, Ascites is possible, on X-ray expressive growth of heart
sizes, child is restless, appetite is lowered, possible vomiting.
III SHARP DYSPNEA (RR IS ON 70-100% MORE THAN NORM), TACHYCARDIA (HR IS ON 30-40%
MORE THAN NORM), BIG DENSE LIVER, HEART BORDERS ARE SHARPLY EXPANDED,
STAGNANT MOIST RALES IN LUNGS ARE LISTENED, PULSE OF THE LOWERED FILLING, THERE
ARE ASCITES, EDEMAS, ANASARCA. THE CHILD IS LANGUID, PALE, APPETITE IS ABSENT.
DEGREE OF CIRULATION FAILURE
56. PDA
Patent ductus arterious
(PDA) concerns to CHD of "
white" type with increase of
PC, with shunt of blood
from aorta to PA that leads
to overflow of PC and an
overload of the left parts of
heart.
The prognosis at PDA is
adverse – 20% of children
dies without surgical
procedures in I phase, age
of life is reduced up to 35-39
years
57. PDA clinical manifestations
● Palpation: the apical impulse is strengthened,
displaced to the left and downwards. Pulse at the big
shunt - high, frequent.
● Percussion: borders are expanded to the left and
upwards.
● Auscultation: in ІІ-ІІІ i/c space to the left of sternum -
systolic, and then systolic-diastolic ("machine")
murmur, spent on apex of heart, cervical vessels, aorta,
to interscapular space. II tone on PA is strengthened.
● Systolic BP is normal, diastolic BP is sharply lowered
(up to 30-40 mmHg).
59. PDA medicamentous
Medicamentous treatment is used only in
maternity hospital in newborns within the
two first weeks of a life, later it becomes
inefficient
Indometacin - 0,1 mg/kg 3-4 times a day
intravenously. The effect is the better,
than age of the child is less (treatment is
desirable for spending during the first 8-14
days of a life)
60. PDA surgery
Planned operation in the age more than 3-5 years improves the
prognosis
Bandaging of PDA after thoracotomy PDA endovascular occlusion
61. ASD
Atrial septal defect (ASD) is
CHD of "white" type with
increase of PC, result of
abnormal development of
primary and secondary
interatrial septums and
endocardial rollers.
The prognosis in ASD is
defined by size of defect and
severity of hemodynamic
disorders (it is adverse at early
developed heart failure),
average age of life is 35-40
years.
62. ASD clinical manifestations
● At palpation: the apical impulse is weakened, sometimes
systolic trembling.
● At percussion: heart borders are expanded, expansion of
vascular bandle borders to the left due to increase in the
basic trunk and left pulmonary artery branch
● At auscultation: not rough systolic murmur in II-III
intercostal space to the left of a sternum. In big left to right
blood shunt and development of pulmonary hypertension
diastoilic murmur of Grechem-Still can be listened. II tone on
PA is strengthened and split.
● Systolic BP is lowered (less blood acts in aorta), diastolic BP
is not changed
63. ASD diagnostics
It is possible to visualize
ASD by means of a two-
dimensional
echocardiography
64. ASD surgery
ASD it can be closed
spontaneously in the first 5
years of a life in connection with
relative reduction of the sizes of
defect with the years on a
background of increase in heart
(initially functional, and then its
anatomic closing), if to age of
5-6 years spontaneous ASD
closing does not happen,
planned operation is indicated
65. VSD
Ventricular septal defect (VSD) is
CHD of "white" type with PC
increase, it is oval, round or cone-
shaped aperture in membranous
(upper) or muscular (lower) part of
interventricular septum, with
diameter from 1 up to 20 mm
The prognosis at muscular defect
is favorable (age of a life is more
than 40 years), at membranous
defect it is depended by timely
operative intervention
66. VSD
Defects of muscular (lower)
part of septum (Tolochinov-
Roge disease ) have the cone-
shaped form and decrease in
size in time of ventricle systole.
Disease often proceeds
without hemodynamic
disorders, development and
behavior of these children
does not differ from those in
healthy children
67. VSD
Defect of membranous (upper)
part of septum is shown by
complaints to pallor, dyspnea,
cough, cyanosis at shout (venous-
arterial shunt arises), weakness,
fatigue, frequent pulmonary
infections. Physical development
retardation already is
characteristic.
Early developing parasternal
cardiac hump, sometimes of the
significant sizes («Devis chest»).
68. VSD, clinical manifestations
● At palpation: the apical impulse is displaced to the left and
downwards – strengthened, rising, diffuse.
In III-IV intercostal space to the left of sternum systolic trembling is
caught (the evidence of blood shunt in RV).
● At percussion: borders initially are expanded to the left and
moderately upwards, in increase of pulmonary hypertension degree
– to the right, due to right heart chambers.
● At auscultation: in III-IV intercostal space connected with I tone
rough long systolic murmur conducted on all heart and on a back is
defined.
Simultaneously on apex mesodiastolic murmur is defined
II tone on PA is strengthened and split
● Systolic BP is lowered at normal diastolic
69. CHD: VSD
VSD DIAGNOSTICS
Doppler
echocardiography and
colour dopplergraphy
are capable to reveal
localization of very
small defects which are
not found out by means
of a two-dimensional
echocardiography
70. CHD: VSD
Opened cardio-surgical operation Endovascular interventions with use of various
catheters, cylinders, occluders and other adaptations
Emergency operation is indicated at increased blood
circulation failure, planned - at the age of 3-6 years
71. CHD: TGV
Transposition of great
vessels (TGV) is severa CHD
(of "cyanotic" type) with PC
increase, when aorta departs
from right ventricle and
carries nonoxygenated blood,
and pulmonary artery – from
left ventricle and carries
oxygenated blood,
atrioventricular valves and
ventricles of heart are
generated correctly
72. CHD: TGV
Without compensating
communications (ASD, VSD, PDA) TGV
is incompatible with a life
The prognosis at TGV is adverse: 28,
7% of children with TGV die in the first
week of life, 51,6% – in the first month,
89,3% – by the end of the first year, 7%
– in the age till 5 years, 2% – in the age
up to 10 years
It is diagnosed already just after
delivery (total cyanosis and dyspnea),
more often meets in boys
73. TGV clinical manifestations
Since 2-4 weeks of a life the basic
manifestation of TGV biventricular,
refractored to treatment, heart failure
(dyspnea, tachycardia, hepatomegaly,
pulmonary rales), repeated ARVI,
pneumonias are characteristic. The heart
sizes on the first week are normal or
slightly increased, in the further
cardiomegaly quickly develops (in
diameter and upwards) with early
appearance of cardiac hump.
On X-ray the cardiac shadow has typical
ovoid configuration («egg laying on one
side»)
74. TGV diagnostics
Echocardiographic diagnostics is
based on identification of
ventricules and main vessels,
definition of their spatial mutual
relation and the relation to
ventricules
Treatment is only surgical and whenever possible it should be early. In early
children's age palliative operation (creation or expansion of ASD for
improvement of blood exchange between PC and SC) is spent, corrective
operation (intraheart moving of arterial and venous blood streams by
means of patch – atrioseptoplastica) is spent in the age of 6-12 months
75. CHD with PC decrease
Common anatomic sign - increase of quantity of venous blood
inflowing into systemic circulation due to pulmonary artery
stenosis
CHD with
PC decrease
PAIS Fallot’s disease
76. IPAS
Pulmonary artery isolated
stenosis (IPAS) is CHD of "white"
type with increase of PC, is
widespread diseases (6,8-9,0% of
all CHD).
The prognosis at PAIS is defined
by a degree of a stenosis and
severity of hemodynamic
disorders. Average age of life is 24,
5 years.
77. IPAS clinical manifestations
● At small stenosis degrees ("white" variant) children well develop,
complaints are insignificant (appearance of dyspnea at loading),
frequently fingertips, nose, cheeks have a crimson shade. Unique
manifestations of defect are systolic trembling and rough systolic
murmur in II intercostals space at the left from sternum in a
combination to weakening of II tone on PA (valvular component is
not present).
I tone on apex is strengthened. BP is not changed.
Signs of HF are absent or do not exceed IIB degree on right-
ventricular type.
● Expressed stenosis – the size of shunt defines by presence of
cyanosis from crimson up to dark blue ("cyanotic" variant). Intensity
of cyanosis increases with the years, symptoms of «watch glasses»
and «drum-type sticks» are characteristic.
78. IPAS
On X-ray at average and big
defects lung marking is
strengthened on arterial channel,
a trunk and branches of
pulmonary artery are expanded,
protrusion of arch is defined
TREATMENT in sharp stenosis
is planned operation at the age
of 3 years (transcutaneous
balloon valvulotomy or opened
valvulotomy)
79. Tetrology of FALLOT
Fallot’s disease is the most frequent
CHD of "cyanotic" type, with decrease
of PC.
The most frequent is Fallot’s tetralogy.
Frequency of the TF in newborns is
5-8%, and in older age – 12-14% of all
CHD and 50-75% of all "cyanotic"
defects.
The prognosis in TF is adverse: 75% of
not operated patients die in the age up
to 2 years, average age of life of not
operated patients is 12 years
80. Tetrology of FALLOT
Components:
● pulmonary artery stenosis
● high ventricular septal
defect
● transposition of aorta to
the right (location "astride"
on interventricular septum
or dextraposition of aorta)
● right ventricle hypertrophy●
●
●
81. Clinical manifestations
● Since a birth cyanosis is observed in 40% of cases, more often it become by
manifest to 6-12 months, symptoms of «watch glasses» and «drum-type
sticks» are characteristic.
● For children of 1-2 years the motor development retardation is characteristic.
● Children with TF badly transmit physical activity, often squat or lay in bed with
legs led to abdomen, facilitating a state because of reduction of venous
inflow to the heart.
82. Clinical manifestations
● At auscultation: loud I tone, rough systolic murmur of ejection
along the left edge of sternum with maximum in III and IV or
in II intercostal space (at combination with valvular stenosis)
is defined. II tone on PA is weakened.
● Maximal BP is lowered.
● In peripheral blood: hemoglobin and erythrocytes are
increased (compensation of hypoxemia), that promotes
increase of blood viscosity with danger of thromboses and
embolisms
83. Tetralogy of FALLOT
On X-ray heart is defined in the
form of «clog» or «little boot» due
to the rounded and raised above a
diaphragm apex and falling back
of PA arch ("waist" of heart is
underlined).
84. CHD: FALLOT’S TETRALOGY
TREATMENT. Planned
operations are carried out
after age of 5-6 years. The
remote results of operative
treatment of not complicated
forms of Fallot’s tetralogy are
good (95% of patients are
practically healthy).
85. CHD with SC decrease
Common anatomic sign – decrease of arterial blood quantity
entered to SC due to one of part aorta narrowing
CHD
with SC decrease
Coarctation
of aorta
86. COARCTATION OF AORTA
COARCTATION OF AORTA (CA) is CHD
of "white" type with SC increase, it is
represented with congenital narrowing
or full break of aorta in the place of its
arch isthmus (sometimes in chest or
abdominal part).
Frequency of CA makes 6,3-15% of all
CHD. CA meets in 3-5 times more
often in boys, than in girls.
The prognosis in CA severe forms is
adverse, surgical intervention is
necessary at early children's age
87. CA clinical manifestation
● In children of early age CA is accompanied by repeated
pneumonias, the phenomena of pulmonary-heart failure
from first days of life, sharp skin pallor, the expressed
dyspnea are objectively marked, stagnant rales in lungs
(imitation of pneumonia) are possible
● Children are retarded in physical development
● The apical impulse is strengthened, rising
● The intense pulse on cubital arteries (in elbow bends),
sharply weakened or absent pulse on femoral arteries are
defined
● Borders of deep cardiac dullness are expanded to the left
due to left ventricle hypertrophy
88. CA clinical manifestation
● On the heart basis or behind in interscapular area at the
left (the projection of aorta isthmus) the rough systolic
murmur of ejection is listened. On apex systolic murmur of
mitral valve insufficiency due to left ventricle overflow in a
systole can be listened
● At accompanying with PDA in II intercostal space at the
left systolic-diastolic murmur is listened
● II tone on aorta and pulmonary artery is strengthened
● BP on hands in children with isolated CA amount to high
figures – 190-200/90-100 mmHg, at combination with PDA
BP is 130-170/80-90 mmHg.
On legs BP is not defined or sharply lowered.
89. CA diagnostics
On X-ray in children of early
age lung marking is normal or
is strengthened on arterial
bloodstream, heart has the
spherical form with the raised
apex and the expanded
ascending aorta
90. CHD: COARCTATION OF AORTA
COARCTATION OF AORTA DIAGNOSTICS
By means of
angiocardiography is
possible to visualize defect
and to estimate a state of
collateral bloodstream
91. CHD: COARCTATION OF AORTA
COARCTATION OF AORTA TREATMENT
At severe forms of CA
surgical intervention is
necessary at early children's
age.
If course of defect is not
severe in order to prevent of
recoarctation in a place of
correction operation is
postponed up to 6-11 years
ANASTOMOSIS «END-TO-END»
ISTHMOPLASTY
92. CHD: conservative treatment
1.
2.
Conservative treatment of CHD
pursues the NEXT TASKS:
Administration of the urgent aid at
catastrophic states
Treatment of complications and
accompanying diseases
93. CHD: conservative treatment
CATASTROPHIC STATES
requiring carrying out of urgent actions
at CHD:
1. Acute left-ventricular failure in
children with CHD of "white" type
2. Attacks of cyanosis and dyspnea in
children with CHD of "cyanotic" type
94. CHD: conservative treatment
ACUTE LEFT-VENTRICULAR FAILURE
develops at joining of acute intercurrent
diseases in children with CHD of "white"
type (with increase of PC) when dyspnea
increases, tachycardia, cyanosis,
plentiful moist rales in lungs with threat
of their edema appears
95. CHD: conservative treatment
Left acute left-ventricular treatment:
● Raised position of the patient
● Oxygen therapy with constant positive pressure (the
oxygen humidified by 20% spirit or solution of foam-
extinguisher antifomsylan)
● Nasotracheal suction
● Lasix 2% 2-5 mg/kg day parenterally, at once is possible to
enter 1/2 doze
● Euphullin 2,4% 1 ml/year of a life intravenously, but no
more than 5 ml
● «Sedative mix» – aminazine 2,5%, pipolphen 2,5% and
promedol 1% on 0,1 ml/years of a life everyone on
pheopolyglycin intravenously in drops
96. CHD: conservative treatment
Left acute left-ventricular treatment:
● Cardiac glycosides:
STROPHANTHIN 0,05% intravenously in single dozes for
children of 1-12 months 0,05-0,1 ml, 1-3 years 0,1-0,2 ml,
4-7 years 0,2-0,3 ml, more older than 7 years 0,3-0,4 ml
CORGLYCON 0,06% intravenously in single dozes for
children of 1-12 months 0,1 ml, 1-3 years 0,1-0,2 ml, 4-7
years 0,3-0,4 ml, more older than 7 years 0,5-0,8 ml
● Glucocorticoids for decrease in permeability of alveolar-
capillary membranes and for struggle against hypotonia
(predhisolon 3-5 mg/kg in day)
97. CHD: conservative treatment
HYPOXEMIC ATTACKS OF CYANOSIS
AND DYSPNEA
develop at CHD of "cyanotic" type
(with decrease of PC) when due to
spasm of exit part of RV and PA
stenosis there is a full shunting of
bloodstream to aorta at sharp
decrease of bloodfilling of PC
On a background usual for such children acrocyanosis the
attack of dyspnea, tachycardia and strengthening of
cyanosis develops, the child initially is excited, further he
can run into state of hypoxemic coma with spasms
98. CHD: conservative treatment
TREATMENT OF HYPOXEMIC ATTACKS OF CYANOSIS AND
DYSPNEA:
● Obsidan (β-adrenergic blocker, removing spasm of PA
entrance) 0,1% 0,1-0,2 mg/kg intravenously slowly (1 ml/
minute) in 10 ml of 20% glucose, further obsidan or its
analogues inderal, anaprilin are given orally in a daily doze of
0,25-0,5 mg/kg
● Oxygen therapy with constant positive pressure on inspiration
● Cordiamin as stimulator of CNS (the respiratory and
vasculomotor centers) hypodermically or intramuscularly in
single dozes to children till 6 months 0,1-0,2 ml, 7-12 months 0,
25-0,3 ml, 1-3 years 0,3-0,4 ml, 4-6 years 0,4-0,6 ml, 7-14 years
0,7-1,0 ml
99. CHD: conservative treatment
TREATMENT OF HYPOXEMIC ATTACKS OF CYANOSIS AND
DYSPNEA:
● Narcotic analgetic (promedol 1% 1 mg/kg)
● Anticonvulsant means (sodium oxybutyrat 20% 0,5 ml/kg
intramuscularly, simultaneously it takes antihypoxic effect)
● Cardiac glycosides (increasing heart ejection, increase the
shunt from right to left and provoke an attack) and diuretics
(on a background of characteristic for "cyanotic" defects
polycythemia increase condensation of blood even more)
ARE CONTRA-INDICATIVE
● At decrease in a color index less than 0,8 preparations of iron
orally are administered
100. CHD: conservative treatment
CHRONIC HEART FAILURE – main manifestation and
complication of CHD. CHD TREATMENT includes:
● Cardiac glycosides – digoxin. The doze of saturation 0,03-0,075
mg/kg is administered into 2-3 days, in case of effect they pass to
supporting doze (1/4-1/6 from doze of saturation)
● Diuretics are selected individually, since smaller dozes, at
stabilization of state they pass to intermittent courses of treatment
(intake 2-3 times a week)
● Vasodilatators. For patients with low heart ejection (left-to-right
shunt) hydralasin, minoxidil are administered (post-loading
decreases and shunt of blood in PA decreases). For patients with
combination of stagnation of venous blood circulation in lungs and
low heart ejection the preparations captopril, prasosin are
administered (with reducing pre- and post-loading )
101. CHD: conservative treatment
СHF treatment includes also:
● Anabolic steroids (retabolil, nerobol), non steroid anabolics (inosin,
riboxin, potassium orotat, carnitin)
● Cardiotrophic preparations: cocarboxilase (5-7 mg/kg day № 15),
panangin, vitamin В12 with folic acid, vitamin В15 (calcium
pangamat), vitamin В5 (calcium panteonat), vitamin В6 (pyridoxal-
phosphate), vitamin E (solcoseril)
Conservative therapy is carried out with the purpose of
preparation for a unique way of treatment of the child
with CHD - OPERATION
Optimum term for operative treatment of CHD is the
second phase of course (relative compensation) in the
age of 3-12 years
102. CHD: out-patient supervision
At identification of CHD the child to be reported
is taken on the account by the children's
cardiologist with obligatory examination 1 times
in 3-4 months in the first 2 years of a life (in the
first phase of course), and in the subsequent –
1-2 times a year with regular X-ray and ECG
investigations and blood pressure measurement