J. Boatman

Abbreviations

QP/QS - ratio of pulmonary to systemic blood flow

PLA - pressure in the pulmonary artery

VSD - ventricular septal defect

ASD - atrial septal defect

PH - pulmonary hypertension

PDA - open ductus arteriosus

Open ductus arteriosus

General information

In the fetus, the ductus arteriosus is a functioning vessel that connects the pulmonary

artery with the descending aorta, most often - just below the place of origin of the left

subclavian artery. High PVR, characteristic of the fetal circulation,

causes blood to flow from right to left (from the pulmonary artery to the aorta) through

arterial duct, as a result of which oxygen-poor blood from the pancreas bypasses

unexpanded lungs of the fetus, enters the descending aorta and goes to

placenta, where it is saturated with oxygen. After the birth of LSS, abruptly

decreases, resulting in a change in the direction of blood flow through

ductus arteriosus (from the aorta to the pulmonary artery).

The ductus arteriosus may remain open after birth, especially in preterm infants, with persistent hypoxemia, or with fetal rubella syndrome Clinical presentation Narrow PDA in infancy often goes unrecognized; may manifest in childhood or in adults with fatigue and shortness of breath.

A wide PDA often presents with symptoms of congestive heart failure (orthopnea, dyspnea on exertion, nocturnal attacks of cardiac asthma) that results from left-to-right shunting and chronic left-sided volume overload. Possible PH with the development of right ventricular failure (swelling of the cervical veins, ascites, enlarged liver, swelling of the legs). As PH progresses, a change in the direction of shunting is possible, which is manifested by isolated cyanosis of the legs, rapid fatigue of the legs during exercise, and paradoxical embolism Course and prognosis in the absence of treatment Narrow PDA generally does not affect life expectancy, although the risk of infective endocarditis increases.

Medium or wide PDA: Usually spontaneous closure does not occur. Over time, PH develops, congestive heart failure occurs, and the risk of infective endocarditis is high.

Life expectancy is reduced and averages 40 years. Infective endocarditis almost always occurs in a left-to-right shunt; the site of infection is the site of the pulmonary artery, located opposite the mouth of the duct and subjected to mechanical action of the blood stream. One of the manifestations of infective endocarditis is multiple embolism of the branches of the pulmonary artery.

Rare complication - dissection and rupture of PDA aneurysms Physical examination Appearance pulse palpation auscultation When shunted from right to left (as a result of severe PH) - cyanosis of the legs and thickening of the distal phalanges of the toes ("drumsticks"), since from the pulmonary artery enters the descending aorta oxygen-poor blood. If the PDA connects to the aorta proximal to the origin of the left subclavian artery, cyanosis of the left arm is possible.

Peripheral vasodilatation that occurs during exercise leads to an increase in right-to-left shunt, and therefore these symptoms become more distinct. With a large left-to-right shunt, there is a jumping pulse and high pulse pressure.

In the absence of HF, the pulsation of the jugular veins is normal. The apex beat is increased.

Constant trembling in the I or II intercostal space on the left, increasing in systole Normal I and II heart sounds are often lost in constant "machine" noise.

Noise usually begins after tone I, reaches a maximum intensity to tone II and weakens during diastole. Best of all, the noise is heard in the II intercostal space on the left; the noise is high-frequency, widely radiating, including in the back.

As PH progresses, the murmur disappears (first diastolic and then systolic components) as TPVR and PVR equalize.

With a large reset from left to right - signs of overload of the left ventricle and the left atrium.

Overload of the right ventricle and the right atrium indicates a pronounced PH. With a large reset - an increase in the LV and the left atrium, increased pulmonary vascular pattern, bulging of the ascending aorta and expansion of the proximal branches of the pulmonary artery. In PH, the RV increases. In a two-dimensional study, it is occasionally possible to visualize an enlarged ductus arteriosus.

Doppler studies (including color mapping) reveal a constant, occupying the entire systole and diastole, flow in the pulmonary artery trunk. Other signs include an increase in oxygen saturation (from the pancreas to the pulmonary artery) and a decrease in peripheral blood oxygen saturation (when shunting in both directions or from right to left). It is possible to identify other congenital malformations.

Sometimes it is possible to pass a catheter through the PDA (from the pulmonary artery to the descending aorta) Treatment medical surgical Prevention of infective endocarditis before and within 6 months after surgical correction (see p. 465).

HF is treated by conventional methods (see Chapter 9).

In infants, PDA closure is facilitated by prostaglandin synthesis inhibitors (particularly indomethacin) Elective surgical repair by duct ligation is safe (mortality

Preliminary results with endovascular methods for closing the PDA (double umbrella) are promising, although these methods are still considered experimental Ventricular septal defects Background VSD is the most common congenital heart disease. VSDs occur with equal frequency in both sexes. In most cases, they are diagnosed in infancy due to a rough heart murmur.

In 25-40%, spontaneous closure of the VSD occurs, of which 90% - before the age of years.

The degree of functional impairment depends on the magnitude of the reset and the LSS. If there is left-to-right shunt, but QP/QS 2:1), pulmonary blood flow and PVR increase significantly; RV and LV pressures equalize. As the PVR increases, it is possible to change the direction of the discharge (from right to left), which is manifested by cyanosis, a symptom of "drumsticks";

the risk of paradoxical embolisms increases. If untreated, right and left ventricular failure and irreversible changes in the pulmonary vessels (Eisenmenger's syndrome) develop. Types Membraneous (75%): located in the upper part of the interventricular septum immediately below the aortic valve and septal cusp of the tricuspid valve.

They often close spontaneously.

Muscular (10%): located in the muscular part of the septum, at a considerable distance from the valves and the conduction system. Muscular VSDs are multiple, fenestrated, and often close spontaneously.

Supracrestal (VSD of the outflow tract of the pancreas, 5%): located above the supraventricular crest (the muscle bundle that separates the cavity of the pancreas from its outflow tract). Often accompanied by aortic insufficiency.

The AV canal does not spontaneously close (AV septal defect, VSD of the RV inflow tract, 10%):

found in the posterior part of the interventricular septum near the site of attachment of the rings of the mitral and tricuspid valves. Often seen in Down's syndrome. VSD is combined with ASD of the ostium primum type and malformations of the leaflets and chords of the mitral and tricuspid valves.

Does not spontaneously close Clinical picture The first manifestation is usually a rough heart murmur. Small VSDs are often asymptomatic and may go unrecognized. With large VSD, there is often a lag in physical development and frequent respiratory infections.

In those rare cases, when a patient with a large VSD survives to adolescence and adulthood, there are symptoms of right and left ventricular failure (shortness of breath, swelling of the legs, orthopnea).

Eisenmenger's syndrome (irreversible PH due to left-to-right shunt) may present with dizziness, syncope, hemoptysis, brain abscesses, and chest pain Course and prognosis if untreated Small VSD: life expectancy does not change significantly, but risk of infective endocarditis increases.

Medium-sized VSD: HF usually develops in childhood; with spontaneous closure or reduction in size, improvement occurs. Severe PH is rare.

Large (no pressure gradient between the ventricles, or non-restrictive) VSDs:

in most cases are diagnosed at an early age, in 10% they lead to Eisenmenger's syndrome; most patients die in childhood or adolescence.

Maternal mortality during pregnancy and childbirth with Eisenmenger syndrome exceeds 50%; in 3.3% of cases, direct relatives of patients with VSD also have this defect. Physical examination appearance pulse palpation auscultation In HF, weakness, cachexia are observed; often find depressions in the lower part of the anterior chest wall, the so-called Harrison's furrows (arise due to chronic shortness of breath).

When resetting from right to left - cyanosis and "drumsticks" With small VSD, the pulse on the peripheral arteries is normal, the pulsation of the jugular veins is also not changed. In PH, there is swelling of the jugular veins, high-amplitude A waves (atrial contraction in a rigid RV) and, sometimes, a V wave (tricuspid regurgitation) on the jugular phlebogram Amplified apex beat. Trembling at the left lower edge of the sternum Rough holosystolic murmur at the left lower edge of the sternum. Pathological splitting of the II tone as a result of prolongation of the period of expulsion of the pancreas.

With supracrestal VSD, there is a diastolic murmur of aortic insufficiency Non-invasive ECG studies chest x-ray EchoCG With a large reset from left to right: overload of the left atrium and LV, deviation of the electrical axis to the left.

With PH: RV overload, deviation of the electrical axis to the right. With small VSD: normal.

With a large reset from left to right: an increase in the left ventricle, an increase in the pulmonary vascular pattern due to an increase in pulmonary blood flow.

With PH: a pronounced increase in the trunk and proximal parts of the pulmonary artery with a sharp narrowing of the distal branches, depletion of the pulmonary vascular pattern.

Doppler studies (including color mapping) evaluate the magnitude and direction of the shunt, calculate PAP. Invasive studies Cardiac catheterization and coronary angiography are performed to confirm the diagnosis, measure PAP and rule out CAD (with appropriate symptoms and before surgery).

The magnitude of the discharge can be assessed qualitatively using left ventriculography and quantitatively by blood oxygen saturation in the pancreas (see p. 516; unlike ASD, instead of oxygen saturation of mixed venous blood, the value of the average saturation in the right atrium is used) PAP (even with large VSD) can be treated conservatively. If spontaneous closure does not occur by 3-5 years of age, surgical correction is indicated.

In pulmonary congestion, hydralazine (or sodium nitroprusside for emergency therapy) is used, which reduces TPVR to a greater extent than PVR, resulting in a decrease in left-to-right shunt and improvement. With right ventricular failure, diuretics are prescribed.

ASD is a non-closure of the foramen
in the interatrial septum, due to which
communication between the atria is preserved.

Classification

Primary ASD (in 10%)
Occurs due to
non-closure of the primary
messages between
atrial and anomalies
development of primary MPP
The defect is located in
the lower part of the MPP
directly above
atrioventricular
holes

Classification

Secondary ASD (in 90%)
Occurs due to
developmental anomalies
secondary WFP
The defect is always
the lower edge of the MPP,
separating it from the level
atrioventricular
valves

Violation of hemodynamics

The main mechanism of hemodynamic disturbances in
ASD is the shunting of blood from the left atrium into
right
First of all, the volume load on the right
ventricle
With a large discharge of blood through the defect, often
there is a pressure difference between the right
ventricle and pulmonary artery
Prolonged supply of large amounts of blood
pulmonary vessels affects the dynamics of blood circulation
small circle and gradually leads to the development
pulmonary hypertension
Pulmonary hypertension usually occurs
after 16-20 years, and its frequency increases as
increasing the age of patients.
hemodynamically long-term compensated and
low-manifest vice

Clinic

up to 2-5 years, clinical symptoms are poor
Complaints: increased fatigue, shortness of breath,
heart rate during exercise
compared with peers
Almost 2/3 of patients have a history of
recurrent bronchitis and pneumonia
With a small defect (up to 10-15 mm)
the first symptoms of a defect may appear in them in
over 10 years of age

Objective examination

there is a lag in physical development, pallor
skin, "heart hump" in older children
age
the presence of cyanosis is not characteristic, since the pulmonary
hypertension and heart failure are more common
formed only by the age of 20
On palpation, an increased epigastric
push (with primary ASD also reinforced apical
push)
Auscultatory in the second intercostal space to the left of the sternum (in
projection of the pulmonary artery) is auscultated moderate
intensity systolic murmur, splitting 2 tones. At
primary ASD at the apex of the heart is also auscultated
systolic murmur of mitral insufficiency. At
during physical exertion, the noise during ASD increases, in contrast to
from physiological noise, which disappears under load.

Diagnostics

Chest x-ray - waist flattening
heart or protrusion of the "second arc", the shadow of the heart
expanded
ECG - signs of overload of the right heart,
hypertrophy of the right atrium and right ventricle,
rhythm disturbances.
echocardiography
MRI and CT

Wood units

calculated by dividing the pressure in
pulmonary artery per minute volume
blood flow in the small circle
(1 Wood unit = 1mm Hg×min -1 = 80 dyn×s×cm
-5) according to the formula: LSS \u003d (DLAsred - DZLA) / SV.
At the same time, the severity of PH is distinguished
in the following way:
light - LSS = 2-5 units,
moderate - LSS = 5-10 units,
severe - PSS > 10 units

Surgical correction

The optimal age for the operation is 5-12 years
Absolutely indicated for early surgical treatment "primary"
ASD and extensive "secondary" atrial septal defects
Patients with a significant shedding of blood (there are signs of overload
right ventricular volume) and pulmonary vascular resistance< 5
Wood units (WU), the defect is closed regardless of
severity of clinical symptoms
If a paradoxical embolism due to an ASD is suspected (provided that
that all other causes of embolism are excluded), regardless
size of the defect, the defect should be closed
Patients with pulmonary vascular resistance ≥ 5 U but less than 2/3
systemic vascular resistance, or with pulmonary arterial
pressure< 2/3 системного давления
With early surgical correction of the defect and in the absence of pulmonary
arterial hypertension has a good long-term prognosis

Operations

“open” (suturing of a defect or plastic with a patch under conditions
cardiopulmonary bypass)
Endovascular (implantation of an occluder in an ASD, their
application is limited by anatomical features
some defects, only if the patient does not have
concomitant heart disease)
absolutely contraindicated in pulmonary vascular
resistance greater than seven Wood units or bleeding on the right
to the left at the level of ASD (when peripheral blood is saturated
less than 94% oxygen.)
Other contraindications: endocarditis, recent
systemic infections, peptic ulcer and
duodenal ulcer, clotting disorders and
other contraindications to aspirin therapy, allergy to
nickel, recent myocardial infarction, unstable
angina, left ventricular ejection fraction less than 30%

Ventricular septal defect (VSD)

- a congenital heart disease in which
there is communication between right and left
ventricle.

Classification

S.Milio et al. (1980) distinguish the following
VSD localization:
1) perimembranous defect - inflow,
trabecular, infundibular;
2) infundibular defect (muscular,
subarterial);
3) muscle defect (inlet, trabecular)
VSDs vary in size and range from 1 mm to
30 or more mm.
Therefore, defects of large sizes are isolated, and
also medium and small sizes - diameter
0.5-1.0 cm.

Violation of hemodynamics

shunting of blood from the left ventricle to the right ventricle
from left to right)
The increase in pressure in the small circle is due to
significantly more blood flow and
increasing peripheral vascular resistance
lungs. This contributes to the development of pulmonary hypertension.
If pulmonary hypertension is due to a large shunt,
hemodynamics is stabilized by large overloads
both right and left sides of the heart.
Increased pressure in the right ventricle decreases
discharge value from left to right, pressure in the right and left
ventricles is equalized, volumetric
overload. Gradually increasing pressure in the right
ventricle causes blood to flow from right to left
arterial hypoxemia develops at first during exercise,
and then at rest. The patient develops cyanosis.

Qp - Qs

The ratio of total pulmonary blood flow to
systemic blood flow (Qp / Qs) can serve
blood shunt intensity criterion
through an intracardiac defect.
The normal Qp/Qs ratio is 1:1
shunt volume from left to right = Qp - Qs;
shunt volume from right to left = Qs - Qp.
If there is a reset from left to right, but QP/QS< 1,5:1,
then pulmonary blood flow increases slightly, and
there is no increase in LSS.
With large VSD (QP/QS > 2:1) significantly
increases pulmonary blood flow and PVR, pressure in
RV and LV are aligned.

SMALL DEFECTS

less than 1 cm in diameter and located in the muscle
partition parts
The amount of blood shed is small. Because of
low blood resistance in a small circle
circulatory pressure in the right ventricle and
pulmonary vessels increases slightly or
remains normal. However, excessive
the amount of blood entering through the VSD
small circle, returns to the left side of the heart,
causing the so-called volume overload
left atrium and ventricle. Therefore, when
small VSD for a long time
recorded moderate changes in
heart activity - overload of the left departments

Diagnostics

Complaints. Patients practically do not show complaints, and only in a part
Children experience mild fatigue and shortness of breath.
Inspection. The development of the child is normal, there is no cyanosis. Sometimes you can
note the slightly pronounced "heart hump".
Percussion. The borders of the heart are not changed.
Auscultation. Heart sounds are normal. Over the region of the heart
a coarse systolic murmur is heard with a maximum sound in
third - fourth intercostal space at the left edge of the sternum, intensifying towards
xiphoid process. The noise is not carried out on the vessels of the neck and on the back. II tone
often "covered" by systolic murmur.
ECG. Usually within the physiological norm. Sometimes in the left chest
assignments note signs of an overload of the left and right ventricles.
Radiography. There is a slight increase in both ventricles and
left atrium.
ECHOCG

LARGE VENTRICULAR SEPTAL DEFECTS

BIG DEFECTS
INTERVENTRICULAR SEPTAL
These are defects with a diameter greater than 1 cm or more
1/2 diameter of the aortic orifice.
appear in the first weeks and months
life.
pronounced and significant violations
blood circulation

Diagnostics

Complaints. difficulty feeding due to shortness of breath, frequent respiratory illnesses
(pneumonia, recurrent pneumonia).
Inspection. A significant lag in physical development, the presence of a "heart hump", shortness of breath with
light exertion and at rest.
Palpation. Systolic trembling is felt to the left of the sternum and in the region of the xiphoid process.
Systolic trembling is less, the larger the defect. With the same pressure in the left and right
there is no tremor in the ventricles. The liver is enlarged.
Auscultation. The I tone is strengthened over a top, the II tone is accentuated or split over a pulmonary artery.
Above the region of the heart, a systolic murmur of varying intensity is heard with a maximum
sounding at 4 m / r to the left of the sternum, when the pressures in the ventricles equalize, the noise disappears.
In the lungs - congestive moist rales in the lower sections.
ECG. Signs of hypertrophy of both ventricles and atria.
Radiography. The pulmonary pattern is enhanced due to the overflow of the pulmonary artery system. At
in severe sclerosis of the vessels of the small circle, the peripheral parts of the lungs look "transparent".
The heart is significantly enlarged due to both ventricles and the left atrium. Arch of the pulmonary artery
bulges along the left contour, and fluoroscopy shows its pulsation. The aorta is not dilated, sometimes
hypoplastic.
ECHOCG

Tetralogy of Fallot

VSD
pancreatic outlet stenosis and/or hypoplasia
pulmonary artery
large VSD, equal in diameter to the orifice
aortic root
dextroposition of the aortic root (actually
coming from both ventricles)
congenital hypertrophy of the pancreas

indications for surgery. Small ventricular septal defects do not require
surgical treatment, since there are no gross violations of the intracardiac
hemodynamics. Patients lead an active lifestyle for a long time.
Absolute indications for surgery
1. Critical condition.
2. Circulatory insufficiency, not amenable to drug therapy.
3. Suspicion of the development of irreversible changes in the lungs.
Relative indications for surgery
1. A large defect with a significant discharge of blood.
2. Frequent respiratory diseases, lag in physical development.
Surgical intervention is performed under conditions of cardiopulmonary bypass. It
consists either in suturing the defect on the gaskets, or in sewing in a patch.
Endovascular closure of the VSD with an occluder. As a rule, the catheterization method
used to close muscle defects in the trabecular part of the interventricular
partitions. Occluders can close muscular membranous VSDs
sizes up to 11 - 14 mm.

Open ductus arteriosus(PDA) - a vessel connecting the thoracic aorta and the pulmonary artery. Normally, it is necessarily present in the fetus and closes shortly after birth, turning into a bunch (ligamentum arteriosum). If the PDA does not close within 2 weeks, then they speak of the presence of a defect.

Anatomy. Most often, the PDA departs 5-10 mm below the mouth of the left subclavian artery and flows into the left pulmonary artery. With anomalies in the development of the aorta (right-sided aortic arch), there may be a right-sided discharge of the PDA, or a bilateral variant. The PDA is usually conical in shape, tapering towards the pulmonary end, but there are also variants of a tortuous, wide, or thin vessel.

Self-closing of the OAP. Normally, the closure of the PDA occurs in 2 stages: 1 - functional closure (contraction of the smooth muscles of its wall); 2 - anatomical closure (endothelial destruction and formation of connective tissue). In the case of non-closure of the PDA in the neonatal period, independent closure of the PDA in the future is practically impossible.

Hemodynamics and natural course of the disease. In the prenatal period, the PDA is a normal physiological communication between the aorta and the pulmonary artery, which ensures normal fetal hemodynamics. In the postnatal period, as the general pulmonary resistance falls, first a bidirectional, and then a left-right shunt occurs through the PDA. Due to the pressure difference between the aorta and the pulmonary artery, discharge into the pulmonary artery occurs both in systole and diastole. With small sizes of PDA, up to 3 mm. the discharge is not large, the course of the disease is favorable, for many years heart failure and pulmonary hypertension may not develop. With a large-diameter PDA (more than 5-6 mm), a serious condition may develop in the first months of life. In premature babies, the PDA must be closed almost immediately after birth, because. their PDA leads to the development of critical conditions in 1/3 of cases.

Diagnostics. PDA of a small size PDA (up to 3 mm) usually remains undiagnosed for a long time until echocardiography is performed during a routine examination or for other reasons. If a child has a large diameter PDA, then this is accompanied by frequent pulmonary diseases (up to severe, non-stoppable pneumonia), children are lagging behind in physical development, accompanied by the development of heart failure. PDA can be suspected on physical examination at any age. On palpation of the chest, it is not uncommon to detect systolic trembling. During auscultation in the 2nd intercostal space on the left, a systolic-diastolic murmur will be heard, usually quite loud (3/6 and above points), called "machine" noise. When measuring blood pressure, in children with a large PDA, a decrease in diastolic pressure can be noted. All this will be an indication for the appointment of three standard studies - chest x-ray, electrocardiography (ECG), echocardiography of the heart (EchoCG). On the radiograph, it is important to note the pulmonary pattern (normal or enriched), the size of the heart (cardiopulmonary ratio - CPR), the presence or absence of concomitant pulmonary pathology.

According to the ECG, the deviation of the electrical axis of the heart to the left is detected,
overload (hypertrophy) of the left heart; in advanced cases (with the development of true pulmonary hypertension), hypertrophy of the right heart. EchoCG allows you to visualize the PDA, measure the size; also assess the function of the ventricles of the heart, to identify the degree of pulmonary hypertension (SPPA); an important indicator in echocardiography is Qp/Qs ( ratio of pulmonary to systemic blood flow. Normally it is 0.9-1.2:1.0. Most modern EchoCG devices independently calculate this indicator after entering the relevant data. There are several Qp/Qs calculators on the Internet.), which allows you to assess the degree of pulmonary hypervolemia and set indications for surgical treatment. It is also important to diagnose other congenital heart diseases, since PDA is often combined with other heart defects. In all cases of detection of PDA, the child should be sent to a specialized institution (FTSSSh, Krasnoyarsk).

Treatment. In premature infants, conservative therapy of PDA is possible in the form of parenteral administration of inhibitors of prostaglandin synthesis (indomethacin), usually 2-3 courses are carried out. In other cases, surgical treatment is required. The indication for surgery will be pulmonary hypervolemia (Qp/Qs more than 1.5:1.0), the presence of signs of heart failure. In children with a large PDA (more than 5-6 mm.) Older than 1 year with clinical heart failure, it is also necessary to assess the degree of pulmonary hypertension (PSAP) and decide on the need for heart sounding to assess the resistance of the pulmonary circulation. In the presence of a PDA of small size (less than 3 mm), the absence of pulmonary hypervolemia (Qp / Qs less than 1.5: 1.0), expansion of the heart cavities (according to EchoCG), changes in the chest radiograph and ECG and the absence of a heart failure clinic, dynamic observation is possible 1 time in year.

Types of surgical treatment. In premature babies and children under 1 year of age, open surgical treatment is performed. Access by posterolateral left-sided thoracotomy, for the purpose of minimal surgical trauma, access is made no more than 4-5 cm, this is quite enough to perform the operation. In our center, the PDA is usually clipped with vascular clips. In older children, endovascular closure of the PDA is performed, with access through the femoral artery; exceptions are children with a large PDA and in the presence of concomitant pathology in need of correction. As a standard, in all children under 1 year of age, during surgery for other CHD, the PDA ligament or the PDA itself is isolated and clipped.

From the beginning of 2011 to November 2011, 38 children diagnosed with PDA passed through the FCSSH in Krasnoyarsk, which accounted for approximately 10% of all CHD treated in our center during this period. In 50% of children, endovascular closure of the PDA was performed. The average length of stay in our hospital with a diagnosis of PDA is 3 days for endovascular treatment and 4-5 days for open surgical correction. To date, almost all children older than 1 year old PDA is closed endovascularly.

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Simple shunts are pathological messages between the right and left halves of the heart, not combined with other defects. Normally, pressure is higher in the left side of the heart, so most often the discharge occurs from left to right, so that blood flow increases through the right side of the heart and pulmonary vessels. With a certain size and localization of the pathological message, the high pressure of the left heart can be transmitted to the pancreas, which leads to its pressure and volume overload. Normal RV afterload is y w from LV afterload, so the presence of even a small pressure gradient between the left and right ventricles can cause a significant increase in pulmonary blood flow. The ratio of pulmonary to systemic blood flow (Qp/QO can be calculated from SO-2 values ​​(obtained during cardiac catheterization) using the equation:

Q P /O S = (WITH a O 2 – CvO 2 )/(CpvO 2 - CraO 2 ).

where C aO2 is the oxygen content in arterial blood; С VO2 - oxygen content in mixed venous blood; C pvO2 - oxygen content in the blood of the pulmonary veins; C paO2 - oxygen content in the blood of the pulmonary artery.

If Q P /Qs > 1, then the direction of the reset- from left to right if Q P /Q S < 1,- справа налево. At Q P /Qs= 1, two options are possible: either there is no reset, or there is a bidirectional reset of equal flows.

A significant increase in pulmonary blood flow leads to stagnation in the pulmonary vessels and increases the content of extravascular fluid in the lungs, which causes a violation of gas exchange, a decrease in lung compliance and an increase in the work of breathing. With dilatation of the left atrium, the main left bronchus is compressed, and the dilated pulmonary vessels compress the small bronchi.

Constantly increased pulmonary blood flow after a few years leads to irreversible changes in pulmonary vessels, resulting in a steady increase in PVR. An increase in RV afterload is accompanied by hypertrophy and a progressive increase in right heart pressure. As the PVR increases, the pressure in the right parts of the heart begins to exceed the pressure in the left parts, as a result of which the reset changes direction from left to right to the opposite - from right to left (Eisenmenger's syndrome).

When there is little pathological communication between the chambers of the heart, shunt blood flow depends mainly on the size of the defect (limited shunt). With a large defect (unlimited shunt), the magnitude of shunt blood flow depends on the ratio between PVR and TPVR. When resetting from left to right, shunt blood flow increases if OPVR increases relative to PVR. On the contrary, with a right-to-left shunt, the shunt blood flow increases if the PVR increases relative to the OPVR. Common chamber malformations (eg, single atrium, single ventricle, common truncus arteriosus) represent an extreme form of unrestricted shunt; in these situations, shunt blood flow is bidirectional and completely depends on the ratio of OPSS/PVR.

At In patients with an intracardiac shunt, regardless of the direction of the discharge, it is necessary to completely exclude the possibility of air bubbles and clots from solutions entering the IV infusion system in order to prevent the development of paradoxical embolism of the cerebral or coronary arteries.

Atrial septal defect

The most common type of isolated atrial septal defect is ostium secundum. More rare type defects ostium primum and sinus venosus often associated with other heart defects. In children, most cases are asymptomatic, sometimes there are recurrent pulmonary infections. Congestive heart failure and pulmonary hypertension are more common in adult patients. In the absence of heart failure, the hemodynamic response to inhaled and non-inhaled anesthetics almost does not differ from the norm. It is impossible to allow an increase in the OPSS, because it is fraught with an increase in the discharge from left to right.

Ventricular septal defect

Ventricular septal defect is the most common congenital heart defect. The degree of functional impairment depends on the area of ​​the defect and the magnitude of the LSS. With a small defect, the reset from left to right is limited (the ratio Qp/Q s< 1,5-2,0: 1). Дефекты большего размера характеризуются значительным сбросом слева направо, величина которого прямо зависит от ОПСС и опосредованно - от ЛСС. Если Qp/Qs >3-5:1, patients often experience recurrent lung infections and congestive heart failure. As with atrial septal defect, in the absence of heart failure, the hemodynamic response to inhaled and non-inhaled anesthetics does not differ significantly from the norm. An increase in OPSS contributes to an increase in discharge from left to right. If, as the disease progresses, a right-to-left shunt occurs, then patients do not tolerate a sudden increase in PVR or a decrease in OPSS.

Open ductus arteriosus

Constant communication between the pulmonary artery trunk and the aorta can lead to a left-to-right shunt. Patent ductus arteriosus is the most common cause of cardiopulmonary disorders in preterm infants. Sometimes the defect does not manifest itself in infancy, but in childhood or in adults. Features of anesthesia are the same as for defects of the interatrial and interventricular septum.