Cardiac Buffs
The auscultation of a heart blow during the physical examination of a child is a frequent fact, which is why it constitutes the main reason for consultation in pediatric cardiology. This is how preschooling, even in one of four children, it is possible to auscultate a heart blow. Although much of these puffs occur in children with healthy heart: functional blow, frequently the finding of these is a topic of concern in families, since a heart blow can be a semiological sign of heart disease, organic signs, sign that is especially Frequent in congenital cardiopathies.
First of all, we will describe the characteristics of the cardiac puffs that are always organic, to subsequently describe the different types of functional puffs that can be found in the pediatric age. This is just a guide to orient yourself in the auscultation of cardiac puffs, since, although there are some who are clearly organic, and others that are clearly functional, there is an important group of them in which attention should be paid in other elements of auscultation to determine his " organicity " As the splitting and the intensity of the second noise, or the presence of third noise or clicks.
Organic heart murmurs
It should always be considered as organic heart blow:
All cardiac breath that is associated with a fricely palpable in the precordial area, or whose intensity is greater than III / VI.
All diastolic heart blowing. They may correspond to character soples " aspiration " From the beginning of the diadostle of sigmoid valve insufficiency, or to puffs from the medium of the lowest tonality diastole, " rolled ", them of absolute or relative stenosis of air-ventricular valves.
All continuous heart blowing that does not disappear with rotation movements of the neck. These puffs are often secondary to the persistence of the arteriosus ductus, being able also to be secondary to coronary fistulas or a aorto-pulmonary window.
All holosystolic breath, that is, it begins confused with the first cardiac noise, maintaining its intensity until the auscultation of the second cardiac noise. These puffs that can be plotted as rectangular, are generally secondary to interventricular communication or regurgitation of air-ventricular valves.
Functional cardiac puffs
In general terms we can say that functional heart blows are always asistolic, and ejective; That is, they begin after the first cardiac noise progressively increasing from intensity to the meso-systole and then decrease progressively of intensity, leaving the second cardiac noise free.
L Graph it, the shape of a diamond corresponds. Its intensity is always less than or equal to III / VI, and its tonality is never very serious. Functional cardiac puffs are characterized by important variations of the auscultatory characteristics with the patient's position changes. It should be considered that in children who are in a hyperdinnamic state, secondary to a febrile, anemia, or another, it is very frequent of auscultating cardiac puffs, usually systolic ejective blows from the base of the neck, those who disappear when this state returns. Within the functional heart murmurs it is possible to clearly identify the following:
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Soplo of Still. is characterized by being a systeric ejective swel of intensity less than or equal to III / VI, whose focus of better auscultation is low left parasternal. His tonality " vibratory " O " musical ", it is characteristic. It is usually irradiated to the neighboring areas of the precordium, and occasionally towards the neck, this breath characteristic appears towards the end of the first year of life or of preschool, and adolescence can be ausculted until the end.
Physiological stenosis of pulmonary branches. It is characterized by being a low intensity ejective swaying puff, whose focus of better auscultation is high left parasternal, also auscolting in armpits and back. This breath is typical of the newborns from the second week of life, particularly from the preterm and low birth weight, and is generally auscull until six months of age. This breath is secondary to the relative stenosis of the branches of pulmonary artery, after produced the change of fetal circulation to neonatal, stenosis that is overcome in the first semester of life. The presence of a cardiac breath of these characteristics after 8 months of age may have a pathological character.
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Venous Hum. Corresponds to a continuous breath, that is, it compromises systole and diastole, low intensity, which varies significantly until disappearing with the movements of rotation and bending of the head.Its focus of better auscultation is the base of the neck and the supraclavicular areas, ausulating better when the patient is sitting.More frequent at preschool, its differential diagnosis must be made with persistent arterious ductus.
Pulmonary breath.It corresponds to an ejective, low-intensity systolic blow, generally II / VI, whose focus of better auscultation is high left parasternal (pulmonary focus).Its differential diagnosis is with minimal pulmonary stenosis.It can be ausculted throughout the pediatric age.
Congenital cardiopathies
Congenital heart disease is defined as an abnormality in the structure and / or function of the heart in the newborn, established during pregnancy. In general, congenital heart disease correspond to heart malformations resulting from an altered embryonic development.
Congenital heart disease occur in 1% of live newborns. This figure does not include the small muscular interventricular communication of the newborn, the bicuspid aortic valve without functional alteration, the prolapse of the mitral valve, the persistent ductus of the preterm newborn, nor the heart rate disorders of anomalous electrical beams such as the Wolff Parkinson White syndrome, diagnostics that in some series exceed the aforementioned incidence for congenital heart disease in general. These cardiopathies are somewhat more frequent in men, although there are some specific malformations such as interrauricular communication or persistent arterious ductus that are more frequent in women. Of the total number of children who present a congenital heart disease, about half will be symptomatic during the first year of life, and most of these will require a corrective or palliative surgical procedure during this period.
Most congenital heart disease have a multifactorial etiology, with a complex interaction between genetic and environmental factors. Approximately 5% of children who present congenital heart disease, are carriers of a chromosomal anomaly, there are also numerous genetic syndromes, with autosomal recessive or dominant heritage, which are associated with congenital heart disease. 25% of carriers of congenital heart disease present some other malformation in some other system. A marriage that has a first child with congenital heart disease, has an approximate probability of 3% than a second child is born with heart disease; A father or mother carrier of a congenital heart disease has a probability between 2 and 10% than her son is born with a heart disease.
On the other hand, there are known environmental noxas that are associated with a greater incidence of congenital cardiopathies. It is as well as fetuses exposed to alcohol and other drugs, such as thalidomide, diphenylhydantoin, lithium, have a greater incidence of congenital heart disease. Fetal exposure to some viral infections, particularly during the first trimester of pregnancy, is also associated with a greater incidence of congenital heart disease, as it is clearly demonstrated for the rubella virus. Finally, fetal exposure to some maternal diseases such as diabetes, lupus erythematosus, is also associated with a higher incidence of heart disease.
There are numerous congenital cardiopathies and also various ways to classify them both according to their pathophysiology and their clinical presentation. The most basic classification is to divide them into cyanotics and acianotics. Cycanotic heart disease correspond to all those in which their dominant pathophysiological condition is the presence of intracardiac short circuit from right to left, and therefore its most important clinical characteristic is the presence of cyanosis. Acianotic heart disease is the most frequent, and also the most diverse, since its only common characteristic is the one that defines them: the absence of cyanosis in its clinical presentation. Within acianotic heart diseases are short circuit from left to right, which constitute something more than 50% of the total congenital heart disease, obstructive heart disease, and others less frequent such as valvular insufficiencies and right obstructive heart disease do not cyanotics.
CARDIOPATIES WITH SHORT OF LEFT TO RIGHT
It is the largest group of congenital cardiopathies, reaching around 50% of them (Table No. 1). Short from left to right can occur: at a headphone level, as in interrauricular communication (CIA) and partial anomalous venous drainage; At the ventricular level, as in interventricular communication (CIV); At the auricular and ventricular level, as in the septal defect ventricular auricle or auricle-ventricular channel (A-V); or at the top arteries, as in the persistent arterious ductus (DAP) and in the aorto-pulmonary window.
La alteración fisiopatológica que define a este grupo de cardiopatías es el paso de sangre oxigenada desde el lado izquierdo del corazón (aurícula izquierda, ventrículo izquierdo, o aorta) hacia el lado derecho de éste (aurícula derecha, ventrículo derecho, o arteria pulmonar), sangre que recircula por los pulmones sin entrar a la circulación arterial sistémica periférica. Las consecuencias fisiopatológicas y clínicas del cortocircuito van a depender de la magnitud de este y del nivel anatómico en que ocurre.
La magnitud de un cortocircuito de I-D a nivel ventricular o de grandes arterias depende fundamentalmente del tamaño del defecto que comunica las dos circulaciones y de la relación entre las resistencias vasculares pulmonar y sistémica. A menor resistencia pulmonar y a mayor resistencia sistémica, mayor el cortocircuito de izquierda a derecha. Dado que la resistencia vascular sistémica es normalmente alta y varía poco, la resistencia vascular pulmonar es generalmente el regulador más importante de un cortocircuito a nivel ventricular o arterial. Si el defecto que comunica ambas circulaciones es amplio no sólo se transmite flujo, sino que también presión sistólica; es así como en una CIV amplía la presión sistólica ventricular izquierda se transmite totalmente al ventrículo derecho ( CIV "no restrictiva"); por el contrario en una CIV pequeña se transmite muy poca o nada de la presión sistólica ventricular izquierda al ventrículo derecho, por lo que existe una importante gradiente sistólica de presión interventricular (CIV "restrictiva"). Dado que la resistencia pulmonar se encuentra elevada en las primeras semanas de vida, esto impide que ocurra un cortocircuito de izquierda derecha masivo en ese período. Por otra parte, la viscosidad sanguínea, determinada fundamentalmente por los glóbulos rojos, y su efecto en la resistencia vascular, puede también influir en la magnitud del cortocircuito de izquierda a derecha: mayor cortocircuito a menor concentración de hemoglobina.
In the situation of a short circuit of I-D at a headphone level, the magnitude of this will depend on the size of the defect and the relationship between the left and right ventricular distensibility. At greater right ventricular distention and at lower left ventricular distensibility, the greater is short from left to right. At birth, the difference in distensibility between the ventricles are minimal, so the short circuit is minimal independently of the size of the defect. To the extent that the patient grows the ventricles acquire their own characteristics (distensible, complacent, and thin walls the right; rigid and thick walls the left), the i-d short is increasing. That is why short circuits at the atrial level are no manifest in the first months of life.
The main and first physiopathological consequence of the I-D short is pulmonary hyperflow, whose amount is to be directly proportional to the magnitude of the short circuit. The second consequence of the shorter from left to right is the overload of volume and dilation of cardiac cavities: this is how the right-haired cavities and pulmonary artery are dilated in the short circuits; and in the short circuits at the ventricular and large arteries the pulmonary artery and the left headset and ventricular cavities are dilated. When the short circuit occurs through a broad defect at ventricular or large arteries, the left or aortic ventricular systolic pressure is also transmitted to the right ventricular and pulmonary artery, so that pulmonary hyperflow is associated with pulmonary arterial systolic hypertension. Ventricular volume overload leads to an increase in contractility and ventricular ejective volume according to the Frank-Starling mechanism, so that in these heartiopathies the ventricular contractility is normal or increased.
The overload of cardiac volume results in an increase in diastolic pressures and retrograde transmission of these pressures to pulmonary veins and pulmonary capillary. The increase in pulmonary capillary hydrostatic pressure results in extravasation of liquid to the interstitium and consequently in alveolar edema and pulmonary bronchiolar, and consequently a decrease in the " compliance " Pulmonary, an increase in the alveolo-arterial oxygen gradient, and an increase in the resistance of the fine airway, alterations that from the clinical point of view are manifested as obstructive bronchial tables and pulmonary edema (Table No. 4). On the other hand, patients with I-D short can also also have the thick airway by bronchial extrinsic compression; For example, the left lower source and lower lobar bronchus can be compressed by the left atrium below and the left pulmonary artery above, both dilated and hypertensive, compression that results in bronchial collapse in infants that do not have full the cartilaginous development of its track Aerial, producing lobar or segmental atelectasias, and rarely can result in emphysema lobar. All these consequences at a pulmonary level of heart-circuit hearts from left to right, which are also associated with greater bronchial hypersecretion, give them a greater propensity to these patients to present respiratory infections.
The pulmonary hypertension that accompanies these heart diseases leads indirectly to increase the right diastolic pressures, resulting in systemic venous congestion and hepatomegaly, signs of right heart failure that are generally associated with the signs of left heart failure described above. < / p >.
In general, hearts with short circuit ID are symptomatic when 50% or more of the flow that reaches the left side is diverted to the right side, that is when the pulmonary flow is 2 or more times the systemic flow (QP / Qs equal to or greater than 2/1).
El hiperflujo pulmonar, y en particular cuando se asocia a hipertensión sistólica pulmonar transmitida, llevan a un engrosamiento de la túnica media arteriolar y de la íntima arteriolar que provoca un aumento de la resistencia vascular pulmonar afectando también a la presión diastólica pulmonar (Tabla N°5). Este proceso intimal puede progresar a hialinización y fibrosis y eventualmente trombosis arteriolar llegando a constituir un daño irreversible y progresivo denominado enfermedad vascular pulmonar obstructiva, situación en que la resistencia vascular pulmonar alcanza a valores tan elevados que minimiza el cortocircuito de izquierda a derecha, para posteriormente revertirlo a de derecha a izquierda produciendo cianosis, lo que constituye el síndrome de Eisenmenger. Cuando el hiperflujo pulmonar se asocia a hipertensión, el compromiso arteriolar puede alcanzar la irreversibilidad tan precozmente como a los seis meses de edad (Canal A-V); cuando el hiperflujo no se asocia a hipertensión (CIA) el daño vascular se hace irreversible a partir de la tercera década.
The CIV is the most frequent congenital cardiac defect: it corresponds to 25 to 30% of congenital heart disease as an isolated defect. These defects can be of different sizes and locate in any area of the septum, the perimembranous being more frequent. Its clinical manifestations depend on the magnitude of the short circuit; When this is important, patients present respiratory paintings to repetition, feeding disorders, and bad weight increase. The management of symptomatic patients includes drugs such as digital, diuretics, and vasodilators, and in those who do not compensate properly or with very wide surgical closure defects.
The arterious ductus must be closed functionally by constricting its average tunic within the first 24 hours of life; Produceting the anatomical and definitive closure of the ductus within the first three weeks of life. The DAP also corresponds to about 10% of congenital heart disease, being particularly frequent in preterm newborns; 30 to 40% of those of less than 1750 grams of weight clinically have ductus. In the preterm the treatment is pharmacological with indomethacin in the first weeks; If this failure is indicated surgical ligation. In the infant and the child older the treatment is surgical.
The CIA corresponds to about 10% of congenital heart disease, more frequently on girls. The most common is the US ostium type, less frequent is the Primum Ostium or partial AV channel, secondary to the abnormal development of endocardial bearings, and venous type. In general, they are very little symptomatic in the pediatric age. The treatment is the closure, generally surgical, between 2 and 4 years of age.
Left obstructive cardiopathies
Left obstructive cardiopathies are all those that prevent or hinder normal blood flow through the left side of the heart, from pulmonary veins to thoracic aorta. The obstruction to the blood flow on the left side of the heart occurs more frequently at the level of ventricular output, obstruction that can be total, as in aortic atresia, or partial, which is called stenosis.
In those heart disease with stenosis, the cavities that precede the obstruction raise their pressures to maintain cardiac debit; Thus in a aortic stenosis, the systolic pressure of left ventricle rises, leading to hypertrophy and a decrease in ventricular distensibility, which causes an increase in ventricular diastolic pressure, pressure that is transmitted in retrograde shape to the left atrium, Pulmonary veins and capillaries, and finally pulmonary artery and right ventricle. The increase in pulmonary capillary pressure favors the translation of liquid to bronchiolar interstitium and alveoli, liquid that interferes with gaseous exchange and ventilation, and clinically leads to tachypnea and progressive respiratory commitment, including pulmonary edema and pleural effort, pulmonary commitment that It can lead to pulmonary arterial hypertension and right ventricular overload.
When the obstruction is totally or very severe, the blood flow is diverted in order to maintain the systemic and pulmonary debit, so most of these heart disease have a short circuit from left to right. In these severe obstructions the permeability of the arterial ductus and / or a large ovale (CIA) foramen (CIA) is absolutely necessary to maintain the cardiac debit and life of the patient, constituting dependent Ductus cardiopathies and / or CIA. Thus in an aortic atresia the ductus is fundamental so that the pulmonary artery divert part of its flow to the aorta and allows an acceptable cardiac debit, and in a mitral atresia the presence of a CIA is absolutely necessary for a cardiac debit. The progressive closure of the ductus in these patients leads to hypodébito signs, such as pallor, weak pulses and fills slow capillary, signs that many times suggest a septic picture.
heart disease with valvular insufficiency
correspond to cardiac lesions in which the blood ejected by one of the four cavities of the heart, partially returns to that cavity through a surplus-ventricular valve or incompetent Sigmoide (table). Regurgitation can occur in more than one valve. Although valvular regurgitation occurs in congenitally anomalous valves, more frequently occurs in valvular lesions acquired as rheumatic disease.
El efecto de una regurgitación valvular es el de una sobrecarga de volumen de las cavidades cardíacas involucradas: aurícula y ventrículo izquierdos en la insuficiencia o regurgitación mitral; aurícula y ventrículo derechos en la insuficiencia tricuspídea; ventrículo izquierdo en la insuficiencia aórtica, y; ventrículo derecho en la insuficiencia pulmonar. Esta sobrecarga de volumen se asocia a una hiperdinamia cardíaca y a contractilidad normal o aumentada, salvo en etapas tardías de la enfermedad. La regurgitación valvular puede asociarse a una estenosis relativa de esa válvula, dado al aumento del flujo anterógrado que significa la suma del volumen regurgitado más el volumen de eyección habitual.
Insufficiency or mitral regurgitation Although it may be congenital, is more frequently an injury acquired, particularly in relation to rheumatic fever. It is also observed in myocardiopathies of various etiologies, by dilation of the valvular ring; In severe aortic stenesis, at anomalous origin of left coronary artery, or in coronary anomalies due to Kawasaki disease. Also in diseases such as Marfan and Hurler syndromes with myxomatous mitral valve. The Fissure O " Cleft " Of mitral is generally part of a septal defect auricle-ventricular or defect of endocardial bearings.
Aortic valvular insufficiency of diverse magnitude is observed in patients with bicuspid aorta, with subaortic stenosis, with Subpulmonary CIV, or in patients postvalvaloplasty by aortic stenosis. In all these situations Valvular insufficiency tends to be progressive unless the underlying cause is corrected, such as CIV or subainstic stenosis.
Transient tricuspide regurgitation is frequently observed in the newborn, generally in relation to perinatal asphyxia. Tricuspidea regurgitation is also observed in relation to right ventricular dilation, or to malformations such as Ebstein's disease and pulmonary atresia with septum intact.
Non-cyanotic obstructive cardiopathies
This group of cardiopathies is generally diagnosed by cardiac puff finding in asymptomatic patient. The most frequent corresponds to pulmonary valvular stenosis. They are usually bicuspid valves with thick veils forming dome, some with hypoplastic ring, which in moderate and severe shapes is associated with right ventricular hypertrophy. In some forms of pulmonary valvular stenosis, as in the associated Noonan syndrome, the veils are thick and myxomatous.
stenosis " physiological " of pulmonary branches is frequent presentation from the second to third week of life and up to 6 to 8 months of age, being one of the most important causes of innocent blow at that age; It is more frequent in preterm and low weight newborns in general.
Congenital Congenital Cardiopathies
Estas cardiopatías constituyen un grupo heterogéneo, siendo su característica común la presencia de cortocircuito de derecha a izquierda a nivel cardíaco, con la consiguiente hipoxemia, manifestada clínicamente por cianosis marcada de piel y mucosas. Cianosis es la coloración azul de piel y mucosas como resultado de la desaturación de más de 3 g/dL de hemoglobina en la sangre arterial, por lo tanto, la intensidad de este signo depende no solo de la oxemia sino también de la concentración de hemoglobina; a mayor anemia menor cianosis para un mismo nivel de oxigenación. La cianosis puede ser central o periférica, dependiendo si la desaturación ocurre por cortocircuito a nivel cardíaco o pulmonar como ocurre en la cianosis central, o si esta ocurre por un aumento de la extracción de oxígeno tisular en relación a flujos lentos en circulación periférica como en la cianosis periférica producida por vasoconstricción secundaria al frío.
From the physiopathological point of view CARDIOPATIES CIRT-RIGHT TO THE LEFF ARE DIVERS FROM THREE GROUPS
- Obstructive cardiopathies on the right side with communication on the left side of the heart , as it happens with severe pulmonary stenosis associated with CIV
- CARDIOPATÍAS WITH TOTAL MIXED , in which systemic and pulmonary venous returns are mixed in a common cavity as occurs in a single ventricle
- CARDIOPATÍAS due to lack of mixing, with pulmonary and systemic circuits in parallel, as occurs in the transposition of large arteries.
In the first group, the most numerous, all simple or complex heart defects are found associated with pulmonary flow obstruction and with a septal defect that allows right to left short circuit which leads to hypoxemia. This obstruction to pulmonary flow does not necessarily occur at the pulmonary valvular level, being able to occur at the level of a CIV in a patient with tricuspine atresia, or at the subprily level by tissue with a single ventricle or double right ventricle ventricle. Thus this pathophysiology is common for a simple defect as a CIA with severe pulmonary valvular stenosis, as for a unique ventricle complex with poorly large arteries and lung atresia, constituting Fallot's tetralogy. These heart disease usually have decreased pulmonary flow, and in their most severe forms they require ductus permeability with short-left to right to maintain a lifetime lung flow (dependent ductus). Occasionally the ductus when remaining widely permeable allows a good pulmonary flow, and mild cyanosis in the newborn; As the ductus tends to close the pulmonary flow decreases and the cyanosis increases.
In the second group, all complex heart diseases are found without obstruction to pulmonary flow such as tricuspine atresia, unique ventricle, double ventricular output, arteriosus truncus, unobaled venous drainage. In this group, at the existence of total mixture between pulmonary and systemic venous returns without obstruction to pulmonary flow, there is a marked pulmonary hyperflow that results in greater pulmonary return than systemic, so that the mixture between venous returns results in systemic saturation over 80% E even around 90%. Thus the clinical manifestations, in addition to mild cyanosis, are similar to those of hearthopathies with short to right.
The third group corresponds to the physiology of transposition of large arteries, in which the lack of mixture between the pulmonary and systemic circulations occurs because the desaturated blood that returns through the veins cavas to the right atrium returns to the aorta and systemic circulation Without having gone through the pulmonary circulation, and the oxygenated blood that returns through the pulmonary veins to the left atrium, it returns to the lungs through the pulmonary artery without reaching systemic circulation. Thus, two independent circuits are produced; A systemic one with desaturated blood leading to severe hypoxemia, and a pulmonary with oxygenated blood that is not used. Obviously this situation is incompatible with life, unless there is some level of mixture between the two circulations, such as oval foramen and the arteriosus ductus, where there is a bidirectional short circuit that allows a mixture between the two circulations and the survival of the neonate by at least some hours. Unfortunately, the mixture at these levels is frequently insufficient, and transient, since the ductus tends to close in the first hours of life and the Foramen oval does the same in the course of days to weeks. In these heart disease, pulmonary flow is normal or increased, being able to develop pulmonary congestion and even pulmonary edema.
The main clinical characteristic of cyanosis by congenital cardiopathy unlike that of respiratory origin, is that it is not associated with respiratory distress, but only to deep breathing (hyperpine). The use of hyperoxia test has been classically provided to differentiate pulmonary cianosis of cardiac; This consists of measuring oxygen saturation of hemoglobin breathing air and then breathing oxygen at a concentration close to 100%. Because there is a fixed short circuit in heart disease, saturation does not rise more than 10%, reaching increases over 15% when the short circuit is intrapulmonary. In its physical examination these patients may not present another evident alteration outside of cianosis, a second single noise and cardiac puffs can be found in cardiac auscultation. Patients with long-standing cianosis have drum stick fingers (hypocratism) and cutaneous alterations such as erythematous ¨packs on the cheekbones and lobes of the ears.
El manejo general de estos pacientes va a depender del grado de cianosis; si ésta es marcada y se trata de un neonato con cardiopatía ductus dependiente, debe iniciarse infusión continua de Prostaglandinas E1. Si la cianosis es leve a moderada, solo se debe monitorizar estrictamente, hasta que se decida la necesidad de un procedimiento quirúrgico corrector o paliativo. La cirugía paliativa generalmente consiste en conectar una rama arterial sistémica a una de las ramas arteriales pulmonares para asegurar un flujo sanguíneo pulmonar adecuado, generalmente a través de un tubo de Goretex (shunt de Blalock Taussig modificado).
Fallot's tetralogy is the most frequent cyanotic heart disease, corresponding to right obstructive heart disease. It consists of a cardiac malformation secondary to a hypoplasia of the infundibular portion (output tract) of the interventricular septum, resulting in a wide civ, a dextrop aorta that rides over the VIV, and a subvalvular obstruction and / or variable grade pulmonary valvular In addition to right ventricular hypertrophy.
The transposition of large arteries is one of the two most frequent of the group, the pulmonary artery emerges from the left ventricle and the aortic artery of the right ventricle, in a heart whose internal anatomy is usually normal. It can be associated with other defects, with the CIV with the most frequent (30%). It is more frequent in males (2: 1).
As mentioned above, in this cardiopathy, pulmonary and systemic circulations are in parallel and not in series; In such a way that the desaturated blood is maintained in the systemic circulation and oxygen, it is maintained in pulmonary circulation (lack of mixing). The survival of these patients depends on the possibility of mixing between the two circulations through the Oval Foramen, the arterious ductus, or another defect.
