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UNIVERSIDAD TECNICA DE MACHALA
ACADEMIC UNIT OF CHEMICAL
SCIENCES AND HEALTH
MEDICINE SCHOOL
ENGLISH
CONGENITAL
CARDIOPATHY
STUDENTS
William Cruz
Kevin Herrera
TEACHER:
Mgs. Barreto Huilcapi Lina Maribel
CLASS:
EIGHTH SEMESTER ‘’A’’
Machala, El Oro
2018
CONGENITAL CARDIOPATHY
 Introduction.- Congenital heart diseases are structural defects of the
heart and of the great vessels resulting from an altered embryonic
development.
 Etiology.- The majority of congenital heart diseases have a
multifactorial etiology, with a complex interaction between genetic and
environmental factors.
1. Genetic syndromes and inheritance.- Mutations of isolated genes (2%)
or chromosomal anomalies (8%) have been found in less than 10% of
congenital heart diseases.
2. Maternal and environmental factors - fetuses exposed to alcohol,
cocaine and other drugs, as well as drugs such as thalidomine, lithium,
glucocorticoids, antiepileptics, warfarin, etc., have a higher incidence of
congenital heart disease. So also viral diseases that affect the mother such
as toxoplasmosis, rubella, etc.
3. Fetal circulation and transition to postnatal circulation. - The
persistence of short circuits such as atrioventricular communication.
ANOMALIES IN EMBIROLOGICAL DEVELOPMENT
 Cardiac malpositions
 Abnormalities of the primitive tube torsion (atrioventricular inversion)
 Defects of cardiac septation
 Obstructive lesions and short circuits
 Classification of congenital heart diseases. - Congenital acianotic heart
disease-Cyanotic congenital cardiopathies.
 Congenital acyanotic heart disease
 Cardiopathy with left to right shunt. - It is the largest group of
congenital heart diseases and accounts for about 50% of them; a) atria:
(CIA), b) ventricles (CIV), c) atria and ventricles (A-V)
 Pathophysiology.- The blood recirculates through the lungs without
entering the peripheral systemic arterial circulation. The
physiopathological and clinical consequences of short circuit I-D, which
depend on the magnitude of this and the anatomical place where they
occur are: pulmonary hyperflow, volume overload and cardiac cavities
dilation. In general, cardiopathies with short circuit I-D are symptomatic
when 50% or more of the flow that reaches the left side of the heart
deviates to the right.
 Interauricular communication.- corresponds to 10% of congenital heart
diseases and predominates in women. The most common anatomical form
is the ostium secundum type (70%), located in the oval fossa. Less
frequent are the ostium primum or partial AV canal (20%), and venous
sinus (10%). Clinical picture.- Large or medium defects may occur in the
first years of life with retarded growth and repeated respiratory infections,
which are due to lobar or segmental atelectasis and bronchial
hypersecretion secondary to extrinsic compression of the bronchus by
dilated pulmonary vessels .
 Treatment.- surgical closure.
 Interventricular communication.- is the most frequent congenital heart
defect (25% to 30% of congenital heart diseases as an isolated defect).
These defects can be of different sizes and be located in any area of the
interventricular septum; Perimembranous communications are more
frequent.
 Clinical picture.- The restrictive VSD is asymptomatic. Non-restrictive
VSD can cause severe heart failure, especially during the second or third
month of life. In large VSD, there is biventricular cardiomegaly and
pulmonary plethora on chest radiography.
 Treatment.- Surgical intervention is indicated in older children and adults
with symptoms attributable to the short circuit of I-D.
 Complete atrioventricular canal.- is characterized by the presence of a
ring and a common AV valve. In the complete form there is a septal defect
in the cruxcordis, which extends to the inter-ventricular and
interventricular septums; In the partial form, the two AV holes, right and
left, are separated and the septal defect can affect only the interventricular
septum of entry or the interatrial septum.
 Ductus arteriosus persistent - is an arteriovenous fistula that sends blood
to the lungs throughout the cardiac cycle.
 Congenital obstruction of the left heart.- These are lesions that extend
from the left ventricular-anatomic tract to the descending portion of the
aortic arch and prevent the normal dynamics of left ventricular ejection.
They can be located at the valvular, subvalvular or supravalvular level and
the obstruction can be total (atresia) or partial (stenosis). In cases of very
severe atresia or stenosis, aberrant flow patterns that occur during
intrauterine life influence the normal structural and functional
development of the left heart (hypoplastic left heart syndrome, SCIH). In
cases of stenosis, the cavities that precede the obstruction raise its pressure
to maintain cardiac output.
TYPES:
 Coarctation of the aorta.- Constriction of the light of the aorta, it is a
relatively frequent congenital malformation and constitutes 7-9% of them;
more in males; this defect is almost always located at the junction of the
distal aortic arch and the thoracic aorta.
 Treatment.- All patients must undergo surgical resection or percutaneous
angioplasty.
 Subaortic stenosis. - It is a fixed character lesion and congenital etiology,
which can be localized (fibrous membrane or fibromuscular impeller) or
tunneling; It is usually associated with other congenital malformations
such as IVC (35%). Surgical repair is indicated with gradients greater than
30-50 mm Hg, depending on the age of the patient.
CYANOTIC CONGENITAL HEART DISEASE
 Congenital cyanotic cardiopathies with increased pulmonary flow
(plethora) .- Transposition of the great vessels: the desaturated blood that
returns through the venae cava to the right atrium, returns to the aorta,
which originates in the right ventricle, without having passed through the
pulmonary circulation. Oxygenated blood that returns through the
pulmonary veins to the left atrium, returns to the lungs through the
pulmonary artery, which originates in the left ventricle.
 Congenital cyanotic cardiopathies with reduced pulmonary flow
(ischemia) .- in this group are all simple or complex cardiac defects
associated with obstruction to pulmonary flow and with a septal defect that
allows the short circuit D-I.
TYPES:
 Tetralogy of Fallot.-most frequent after 1 year of life; characterized by:
obstruction to the exit of the right ventricle, VSD, overlapping of the aorta
and hypertrophy of the RV.
 Sx. From Eisenmenger.- systemic-pulmonary communication, with bi-
directional or predominantly D-I short circuit, with Qp / Qs less than 1,
secondary to pulmonary hypertension.
 Cyanotic congenital cardiopathies with total mixture. - Single
ventricle. Fontan Circulation: single double-ventricle ventricular, tricuspid
atresia, stenosis or mitral atresia and heterotaxis.There are several possible
situations: Non-restrictive pulmonary output tract; Moderately restrictive
pulmonary outflow tract and balanced circulation; Very restrictive exit
tract and palliative surgical intervention in childhood.
BIBLIOGRAPHY REFERENCE
Gallego García de Vinuesa, P. "Cardiopathies Congenital", Farreras, V.
Rozman, C. Internal Medicine, Barcelona-Spain, Elsevier, 2016, Vol.1, pg. 542-
553.

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Congenital cardiopathies (12)

  • 1. UNIVERSIDAD TECNICA DE MACHALA ACADEMIC UNIT OF CHEMICAL SCIENCES AND HEALTH MEDICINE SCHOOL ENGLISH CONGENITAL CARDIOPATHY STUDENTS William Cruz Kevin Herrera TEACHER: Mgs. Barreto Huilcapi Lina Maribel CLASS: EIGHTH SEMESTER ‘’A’’ Machala, El Oro 2018
  • 2. CONGENITAL CARDIOPATHY  Introduction.- Congenital heart diseases are structural defects of the heart and of the great vessels resulting from an altered embryonic development.  Etiology.- The majority of congenital heart diseases have a multifactorial etiology, with a complex interaction between genetic and environmental factors. 1. Genetic syndromes and inheritance.- Mutations of isolated genes (2%) or chromosomal anomalies (8%) have been found in less than 10% of congenital heart diseases. 2. Maternal and environmental factors - fetuses exposed to alcohol, cocaine and other drugs, as well as drugs such as thalidomine, lithium, glucocorticoids, antiepileptics, warfarin, etc., have a higher incidence of congenital heart disease. So also viral diseases that affect the mother such as toxoplasmosis, rubella, etc. 3. Fetal circulation and transition to postnatal circulation. - The persistence of short circuits such as atrioventricular communication. ANOMALIES IN EMBIROLOGICAL DEVELOPMENT
  • 3.  Cardiac malpositions  Abnormalities of the primitive tube torsion (atrioventricular inversion)  Defects of cardiac septation  Obstructive lesions and short circuits  Classification of congenital heart diseases. - Congenital acianotic heart disease-Cyanotic congenital cardiopathies.  Congenital acyanotic heart disease  Cardiopathy with left to right shunt. - It is the largest group of congenital heart diseases and accounts for about 50% of them; a) atria: (CIA), b) ventricles (CIV), c) atria and ventricles (A-V)  Pathophysiology.- The blood recirculates through the lungs without entering the peripheral systemic arterial circulation. The physiopathological and clinical consequences of short circuit I-D, which depend on the magnitude of this and the anatomical place where they occur are: pulmonary hyperflow, volume overload and cardiac cavities dilation. In general, cardiopathies with short circuit I-D are symptomatic when 50% or more of the flow that reaches the left side of the heart deviates to the right.  Interauricular communication.- corresponds to 10% of congenital heart diseases and predominates in women. The most common anatomical form is the ostium secundum type (70%), located in the oval fossa. Less frequent are the ostium primum or partial AV canal (20%), and venous sinus (10%). Clinical picture.- Large or medium defects may occur in the first years of life with retarded growth and repeated respiratory infections, which are due to lobar or segmental atelectasis and bronchial hypersecretion secondary to extrinsic compression of the bronchus by dilated pulmonary vessels .  Treatment.- surgical closure.  Interventricular communication.- is the most frequent congenital heart defect (25% to 30% of congenital heart diseases as an isolated defect). These defects can be of different sizes and be located in any area of the
  • 4. interventricular septum; Perimembranous communications are more frequent.  Clinical picture.- The restrictive VSD is asymptomatic. Non-restrictive VSD can cause severe heart failure, especially during the second or third month of life. In large VSD, there is biventricular cardiomegaly and pulmonary plethora on chest radiography.  Treatment.- Surgical intervention is indicated in older children and adults with symptoms attributable to the short circuit of I-D.  Complete atrioventricular canal.- is characterized by the presence of a ring and a common AV valve. In the complete form there is a septal defect in the cruxcordis, which extends to the inter-ventricular and interventricular septums; In the partial form, the two AV holes, right and left, are separated and the septal defect can affect only the interventricular septum of entry or the interatrial septum.  Ductus arteriosus persistent - is an arteriovenous fistula that sends blood to the lungs throughout the cardiac cycle.  Congenital obstruction of the left heart.- These are lesions that extend from the left ventricular-anatomic tract to the descending portion of the aortic arch and prevent the normal dynamics of left ventricular ejection. They can be located at the valvular, subvalvular or supravalvular level and the obstruction can be total (atresia) or partial (stenosis). In cases of very severe atresia or stenosis, aberrant flow patterns that occur during intrauterine life influence the normal structural and functional development of the left heart (hypoplastic left heart syndrome, SCIH). In cases of stenosis, the cavities that precede the obstruction raise its pressure to maintain cardiac output. TYPES:  Coarctation of the aorta.- Constriction of the light of the aorta, it is a relatively frequent congenital malformation and constitutes 7-9% of them; more in males; this defect is almost always located at the junction of the distal aortic arch and the thoracic aorta.
  • 5.  Treatment.- All patients must undergo surgical resection or percutaneous angioplasty.  Subaortic stenosis. - It is a fixed character lesion and congenital etiology, which can be localized (fibrous membrane or fibromuscular impeller) or tunneling; It is usually associated with other congenital malformations such as IVC (35%). Surgical repair is indicated with gradients greater than 30-50 mm Hg, depending on the age of the patient. CYANOTIC CONGENITAL HEART DISEASE  Congenital cyanotic cardiopathies with increased pulmonary flow (plethora) .- Transposition of the great vessels: the desaturated blood that returns through the venae cava to the right atrium, returns to the aorta, which originates in the right ventricle, without having passed through the pulmonary circulation. Oxygenated blood that returns through the pulmonary veins to the left atrium, returns to the lungs through the pulmonary artery, which originates in the left ventricle.  Congenital cyanotic cardiopathies with reduced pulmonary flow (ischemia) .- in this group are all simple or complex cardiac defects associated with obstruction to pulmonary flow and with a septal defect that allows the short circuit D-I. TYPES:  Tetralogy of Fallot.-most frequent after 1 year of life; characterized by: obstruction to the exit of the right ventricle, VSD, overlapping of the aorta and hypertrophy of the RV.  Sx. From Eisenmenger.- systemic-pulmonary communication, with bi- directional or predominantly D-I short circuit, with Qp / Qs less than 1, secondary to pulmonary hypertension.  Cyanotic congenital cardiopathies with total mixture. - Single ventricle. Fontan Circulation: single double-ventricle ventricular, tricuspid atresia, stenosis or mitral atresia and heterotaxis.There are several possible situations: Non-restrictive pulmonary output tract; Moderately restrictive
  • 6. pulmonary outflow tract and balanced circulation; Very restrictive exit tract and palliative surgical intervention in childhood. BIBLIOGRAPHY REFERENCE Gallego García de Vinuesa, P. "Cardiopathies Congenital", Farreras, V. Rozman, C. Internal Medicine, Barcelona-Spain, Elsevier, 2016, Vol.1, pg. 542- 553.