Cardiovascular System (pediatrics)

Anatomical and physiological features
of the cardiovascular system in children
Lecture 1

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.

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.

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).

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).

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.

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.

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.

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).

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

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.

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)

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

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

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

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

Semiotics of congenital and acquired
heart diseases in children
Lecture 2

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

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

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

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

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.

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).

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.

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.

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.

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
●
●
●

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.

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

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.

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.

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

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.

Hemodynamics of the most common
acquired heart defects in children

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

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."

•
•
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

Signs of lesions of myo-, endo-,
pericarditis in children

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).

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

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

CONGENITAL HEART DISEASE
IN CHILDREN

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

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.

Embriology:
CHD are formed as a result of embryogenesis disorder
during 2-8 weeks of gestation.

Ethiology:
ENVIRONMENT
FACTORS
X-RAY IRRADIATION ACTION
SOME DRUGS ACTION
INFECTION AGENTS ACTION
BAD HABITS
GENETICAL
FACTORS
ANOMAL STRUCTURE OF
CHROMOSOMES
GENETICAL MUTATIONS
POLYGENIC-MULTIFACTORIAL
INHERITANCE

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%)

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).

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

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

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

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

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).

PDA diagnostics
THE SPIRAL COMPUTER TOMOGRAPHY
WITH THREE-DIMENSIONAL
RECONSTRUCTION
AORTOGRAPHY

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)

PDA surgery
Planned operation in the age more than 3-5 years improves the
prognosis
Bandaging of PDA after thoracotomy PDA endovascular occlusion

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.

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

ASD diagnostics
It is possible to visualize
ASD by means of a two-
dimensional
echocardiography

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

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

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

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»).

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

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

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

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

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

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»)

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

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

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.

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.

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)

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

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●
●
●

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.

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

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).

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).

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

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

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

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.

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

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

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

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

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

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

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

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)

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

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

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

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 )

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

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

Cardiovascular System (pediatrics)

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