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UDK 616.124.6-053.2-07-08-036
ARTERIAL HYPOXIA AS A FACTOR AFFECTING THE COURSE OF CONGENITAL
HEART DEFECTS IN CHILDREN
Khaydarova L.R.
Andijan State Medical Institute
Republic of Uzbekistan
Abstract:
The most common forms of congenital heart defects (CHDs) in children include
ventricular septal defect (VSD), atrial septal defect (ASD), and Tetralogy of Fallot. The natural
course of these defects is often complicated by the development of severe complications caused
by arterial hypoxia. The high mortality rate associated with septal heart defects in children is
primarily due to progressive congestive heart failure and pulmonary hypertension. In patients
with cyanotic CHDs, the leading pathogenetic factor is diffuse hypoxemia. Insufficient arterial
blood oxygenation exacerbates the clinical manifestations of the defect and contributes to the
development of cardiac arrhythmias, which may be regarded as an additional adverse prognostic
factor in congenital heart disease.
Keywords:
congenital heart defects, arterial hypoxemia, VSD, ASD, Tetralogy of Fallot, ECG,
cardiac arrhythmias.
Relevance:
Congenital heart defects (CHDs) represent the most prevalent group of
developmental anomalies in children and remain a leading cause of disability and mortality in the
pediatric population [3,4,9]. Moreover, a further increase in the incidence of CHDs is projected.
This trend may be partly attributed to advancements in diagnostic techniques, including
improved training of ultrasound specialists and enhanced imaging technologies [6,7,10].
The prognosis of children with congenital heart defects (CHDs) depends on the type of defect,
the degree of arterial hypoxia, the timeliness of diagnosis, and the presence of comorbid
conditions [3,8].
The most prevalent defects belong to the so-called “big six,” including ventricular septal defect
(VSD), atrial septal defect (ASD), and Tetralogy of Fallot [1,2,7]. The natural progression of
these defects is often associated with the development of severe complications. In children with
acyanotic CHDs, the primary causes of death are congestive heart failure and the development of
pulmonary hypertension. In contrast, children with cyanotic CHDs have a high mortality rate due
to profound hypoxemia and thromboembolic complications [1,3,5].
The key mechanisms underlying impaired cardiac hemodynamics in these defects include
volume or pressure overload of cardiac chambers. Prolonged exposure to these conditions
depletes compensatory mechanisms, leading to chamber dilation and hypertrophy, which
subsequently results in heart failure. Heart failure, in turn, causes systemic hemodynamic
disturbances, contributing to either pulmonary hyperemia or hipoemia. This leads to the clinical
manifestations of circulatory hypoxia—regional in VSD and ASD, and diffuse in Tetralogy of
Fallot [1,5,9,10].
Pulmonary hyperemia (pulmonary hypertension) in VSD and ASD is a significant risk factor for
recurrent pneumonia, while diffuse hypoxia can lead to multiple organ dysfunction. Structural
remodeling of the heart due to dilation and hypertrophy, along with hypoxic, ischemic, and
metabolic disturbances in the myocardium, may contribute to conduction system disorders and
be accompanied by various arrhythmias, which further aggravate the clinical course of CHDs
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[1,4,5].
In this regard, our objective was to study the impact of arterial hypoxia on the course of
congenital heart defects (CHDs) in young children.
Results
: The study and data collection were conducted at the Andijan Regional Multidisciplinary
Children's Center. To address the objectives of this research, we examined children who received
treatment in the Cardiorheumatology Department during the year 2024, along with a
retrospective review of medical records.
The study included 71 children aged from 6 months to 3 years, of whom 72% were between 1
and 3 years old. In terms of gender distribution, boys predominated (55% compared to 45%),
both in the group under 1 year of age and in the older age group.
Based on the hemodynamic patterns of the circulatory system, we selected patients with septal
defects and pulmonary hypertension: specifically, ventricular septal defect (VSD) and atrial
septal defect (ASD). The cyanotic defect included in our study was the complex,
multicomponent Tetralogy of Fallot.
Upon hospital admission, 81,7% of the children were assessed as being in severe condition,
primarily due to symptoms of grade II heart failure. Capillary blood oxygen saturation levels
were measured in all children at the time of admission. The lowest oxygen saturation levels—
ranging from 91% to 84%—were observed in children with Tetralogy of Fallot. In children with
septal defects, the saturation levels were as follows: 94–88% in cases of ventricular septal defect
(VSD) and 93–91% in atrial septal defect (ASD).
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Frequent respiratory infections and repeated hospitalizations were observed in all of the children
included in our study. The results we obtained are consistent with data reported in the literature.
The nature of complaints in all examined children with congenital heart defects (CHDs) was
dependent on the degree of hypoxia. The most common and universal symptom, regardless of the
type of hemodynamic disturbance, was dyspnea, which was recorded in 88,6% of children with
ventricular septal defect (VSD), 77,8% of those with atrial septal defect (ASD), and in all
children with Tetralogy of Fallot. In children with septal defects, the incidence of dyspnea was
associated with excessive pulmonary blood flow, whereas in Tetralogy of Fallot, it was caused
by arterial hypoxemia due to right-to-left shunting.
Hemodynamic disturbances in these heart defects were also reflected in the results of
electrocardiographic (ECG) examinations. Regardless of the degree of arterial hypoxemia,
abnormalities in cardiac automatism were represented by sinus tachycardia and sinus
tachyarrhythmia. Increased electrical activity of the right ventricle was recorded in children with
both ventricular and atrial septal defects.
Conduction disorders of varying frequency were observed in all examined children. Incomplete
right bundle branch block (RBBB) was detected in 80% of children with VSD, 33.3% with ASD,
and 50% with Tetralogy of Fallot. Complete RBBB was found exclusively in children with
Tetralogy of Fallot (5,6%). First-degree atrioventricular (AV) block was registered in three
children (8,6%) with large ventricular septal defects and in one child with Tetralogy of Fallot.
ECG changes in children with VSD (n=35).
ECG sign
Аbs.
%
Sinus tachycardia
26
74,3%
Sinus arrhythmia
9
25,7%
Incomplete right bundle branch block (RBBB)
28
80%
AV block 1 degree
3
8,6%
High electrical activity of the right ventricle
7
20%
Left ventricular hypertrophy
18
51,5%
Right ventricular hypertrophy
17
48,5%
Таbl. 1
ECG changes in children with ASD (n=18).
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ECG sign
Аbs.
%
Sinus tachycardia
18
100%
Incomplete right bundle branch block (RBBB)
6
33,3%
High electrical activity of the right ventricle
9
50%
Right ventricular hypertrophy
11
61,1%
Таbl.2
ECG changes in children with tetralogy of Fallot (n=18).
ECG sign
Аbs.
%
Sinus tachycardia
3
16,7%
Sinus tachyarrhythmia
8
44,4%
Incomplete right bundle branch block
9
50%
Complete right bundle branch block
1
5,6%
AV block 1 degree
1
5,6%
Right ventricular hypertrophy
18
100%
Таbl. 3
Electrocardiographic signs of right ventricular hypertrophy were observed in 48,5% of children
with ventricular septal defect (VSD), 61,1% of those with atrial septal defect (ASD), and in all
children with Tetralogy of Fallot. Signs of left ventricular hypertrophy were noted in 51,5% of
children with VSD.
Structural changes in heart chambers and the dimensions of congenital defects were assessed
based on echocardiography findings. Among children with VSD (35 cases), the largest
proportion had defects measuring 4–8 mm (48,6%), followed by those with defects ≤4 mm
(34,3%), and defects >8 mm in 17,1% of cases. For ASD (18 children), the distribution by defect
size was as follows: up to 5 mm – 61,1% of cases, and 6–10 mm – 38,9%.
Among children with Tetralogy of Fallot, 66,7% had a ventricular septal defect measuring 6–10
mm, while the remaining children had defects larger than 10 mm. Regarding the localization of
right ventricular outflow tract obstruction, 72,2% had narrowing in the infundibular region, while
in 27,8% the stenosis was located at the level of the pulmonary valve.
Pulmonary hypertension in children with septal defects manifested on chest radiography as an
enhanced pulmonary vascular pattern along the arterial branches. In contrast, in Tetralogy of
Fallot, increased pulmonary translucency was due to a reduced vascular pattern. Cardiomegaly
was identified in all examined children—74,6% due to right ventricular enlargement, and 25,4%
due to left ventricular enlargement, the latter observed exclusively in children with VSD.
Thus, we established a correlation between arterial hypoxia and both the course and severity of
clinical manifestations of CHDs. The lower the oxygen saturation in arterial blood, the more
severe the clinical symptoms and the more pronounced the cardiac rhythm disturbances, which
may serve as an additional prognostic risk factor in congenital heart defects.
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