Qp qs calculation. Congenital heart defects

Simple shunts are pathological communications 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 shunting occurs from left to right, so that blood flow through the right side of the heart and pulmonary vessels increases. With a certain size and localization of the pathological message, high pressure in the left chambers of the heart can be transmitted to the RV, which leads to its overload with pressure and volume. Normally, the afterload of the pancreas 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 by cardiac catheterization) using the equation:

Q P /O S = (WITH A O 2 – CvO 2 )/(CpvO 2 - SraO 2 ).

where C aO2 is the oxygen content in arterial blood; C 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 reset direction- 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 flows of equal magnitude.

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 disruption of gas exchange, decreased compliance of the lungs and increased work of breathing. When the left atrium dilates, the left main bronchus is compressed, and the dilated pulmonary vessels compress the small bronchi.

Permanently increased pulmonary blood flow leads to irreversible changes in the pulmonary vasculature over several years, resulting in a sustained increase in PVR. An increase in RV afterload is accompanied by hypertrophy and a progressive increase in pressure in the right heart. As PVR increases, the pressure in the right side of the heart begins to exceed the pressure in the left side, causing the discharge to change direction from left to right to the opposite direction - from right to left (Eisenmenger 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 size (unlimited shunt), the amount of shunt blood flow depends on the ratio between PVR and TPVR. During left-to-right shunting, shunt blood flow increases if TPVR increases relative to PVR. On the contrary, with right-to-left shunting, shunt blood flow increases if PVR increases relative to TPR. Common chamber defects (eg, single atrium, single ventricle, truncus arteriosus) represent an extreme form of unrestricted shunting; in these situations, shunt blood flow is bidirectional and completely depends on the TPVR/PVR ratio.

U In patients with an intracardiac shunt, regardless of the direction of 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 combined with other heart defects. In children, in most cases, the course is asymptomatic, sometimes recurrent pulmonary infections are observed. Congestive heart failure and pulmonary hypertension are more common in adult patients. In the absence of heart failure, the hemodynamic response to inhalational and non-inhalational anesthetics is almost no different from the norm. An increase in OPSS should not be allowed, because it is fraught with an increase in 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 PVR. For a small defect, the discharge from left to right is limited (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, then patients often experience recurrent pulmonary infections and congestive heart failure. As with an atrial septal defect, in the absence of heart failure, the hemodynamic response to inhalational and non-inhalational 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 shift occurs, then patients do not tolerate a sudden increase in PVR or a decrease in TPR.

Patent ductus arteriosus

Continuous communication between the trunk pulmonary artery and the aorta can result in left-to-right shunting. Patent ductus arteriosus is the most common cause of cardiopulmonary dysfunction in preterm infants. Sometimes the defect manifests itself not in infancy, but in childhood or in adults. The features of anesthesia are the same as for defects of the interatrial and interventricular septum.

Ventricular septal defect(VSD) - congenital heart disease with communication between the right and left ventricles.

Code according to the international classification of diseases ICD-10:

• Q21.0

Reasons

Etiology. Congenital defects (isolated VSD, part of a combined congenital heart disease, for example, tetralogy of Fallot, transposition of the great vessels, common truncus arteriosus, tricuspid valve atresia, etc.). There is evidence of autosomal dominant and recessive types of inheritance. In 3.3% of cases, this defect is also found in direct relatives of patients with VSD. Rupture of the interventricular septum in trauma and MI.

Statistics. VSD accounts for 9-25% of all congenital heart defects. It is detected in 15.7% of live-born children with congenital heart disease. As a complication of transmural MI - 1-3%. 6% of all VSDs and 25% of VSDs in infants are accompanied by a patent ductus arteriosus, 5% of all VSDs are accompanied by aortic coarctation, 2% of congenital VSDs are accompanied by aortic valve stenosis. In 1.7% of cases, the interventricular septum is absent, and this condition is characterized as a single ventricle of the heart. The male to female ratio is 1:1.

Pathogenesis. The degree of functional impairment depends on the amount of blood discharge and total pulmonary vascular resistance (TPVR). When shunting from left to right and the ratio of pulmonary minute volume to systemic blood flow (Qp/Qs) is less than 1.5:1, pulmonary blood flow increases slightly, and no increase in PVVR occurs. With large VSDs (Qp/Qs more than 2:1), pulmonary blood flow and pulmonary blood flow significantly increase, and pressures in the right and left ventricles are equalized. As the blood volume increases, the direction of blood discharge may change - it begins to occur from right to left. Without treatment, right and left ventricular failure and irreversible changes in the pulmonary vessels (Eisenmenger syndrome) develop.

Variants of VSD. Membranous VSDs (75%) are located in the upper part of the interventricular septum, under the aortic valve and the septal cusp of the tricuspid valve, and often close spontaneously. Muscular VSDs (10%) are located in the muscular part of the interventricular septum, at a considerable distance from the valves and conduction system, are multiple, fenestrated and often close spontaneously. Supracrestal (VSD of the outflow tract of the right ventricle, 5%) are located above the supraventricular crest, often accompanied by aortic insufficiency of the aortic valve, and do not close spontaneously. An open AV canal (10%) is found in the posterior part of the interventricular septum, near the site of attachment of the rings of the mitral and tricuspid valves, often found in Down syndrome, combined with ASD of the ostium primum type and malformations of the leaflets and chords of the mitral and tricuspid valves, does not close spontaneously . Depending on the size of the VSD, small (Tolochinov-Roger disease) and large (more than 1 cm or half the diameter of the aortic orifice) defects are distinguished.

Symptoms (signs)

Clinical picture

. Complaints:

. Objectively. Paleness of the skin. Harrison's furrows. Increased apical impulse, trembling in the area of ​​the left lower edge of the sternum. Pathological splitting of the second tone as a result of prolongation of the ejection period of the right ventricle. Rough pansystolic murmur at the left lower sternal border. With supracrestal VSD - diastolic murmur of aortic insufficiency.

Diagnostics

Instrumental diagnostics

. ECG: signs of hypertrophy and overload of the left sections, and with pulmonary hypertension - also of the right.

. Jugular phlebography: high-amplitude A waves (atrial contraction with a rigid right ventricle) and, sometimes, V wave (tricuspid regurgitation).

. EchoCG.. Hypertrophy and dilatation of the left parts, and in case of pulmonary hypertension - of the right ones.. Visualization of VSD in Doppler and B-mode.. Diagnosis of associated anomalies (valvular defects, coarctation of the aorta, etc.).. Determine systolic pressure in the right ventricle, the degree of blood discharge and Qp/Qs .. Adults undergo transesophageal echocardiography.

. X-ray of the chest organs... With small VSDs - a normal x-ray picture.. Bulging of the left ventricular arch, increased pulmonary vascular pattern.. With pulmonary hypertension - bulging of the pulmonary artery arch, expansion and lack of structure of the roots of the lungs with a sharp narrowing of the distal branches and depletion of the pulmonary vascular pattern.

. Radionuclide ventriculography: see Atrial septal defect.

. Catheterization of the heart chambers.. Indicated in cases of suspected pulmonary hypertension, before open heart surgery and in case of conflicting clinical data.. Calculate Qp/Qs.. Carry out tests with aminophylline and oxygen inhalation to determine the prognosis regarding the reversibility of pulmonary hypertension.

. Left ventriculography, coronary angiography: visualization and quantification of discharge, diagnosis of CAD in the presence of symptoms or before surgery.

Drug treatment. With an asymptomatic course and normal pressure in the pulmonary artery (even with large defects), conservative treatment is possible for up to 3-5 years of life. If there is stagnation in the pulmonary circulation, use peripheral vasodilators (hydralazine or sodium nitroprusside), which reduce the discharge from left to right. For right ventricular failure - diuretics. Before and for 6 months after uncomplicated surgical correction of VSD - prevention of infective endocarditis.

Treatment

Surgical treatment

Indications. Asymptomatic - if spontaneous closure of the defect does not occur by the age of 3-5 years, although better results are achieved with surgical treatment before the age of 1 year. Heart failure or pulmonary hypertension in young children. In adults, the Qp/Qs ratio is 1.5 or more.

Contraindications: see Atrial septal defect.

Methods of surgical treatment. Palliative intervention - narrowing of the pulmonary trunk with a cuff, is performed when emergency surgery is necessary for children weighing less than 3 kg, with concomitant heart defects and little clinical experience in radical correction of the defect at an early age. In case of a traumatic defect in the area of ​​the membranous part of the interatrial septum, suturing of the defect is possible. In other cases, the defect is repaired with a patch made of autopericardium or synthetic materials. In case of post-infarction VSD, plastic surgery of the defect is performed with simultaneous coronary bypass surgery.

Specific postoperative complications: infective endocarditis, AV block, ventricular arrhythmias, recanalization of VSD, tricuspid valve insufficiency.

Forecast. In 80% of patients with large VSDs, spontaneous closure of the defect occurs within 1 month, in 90% - before the age of 8 years, there are isolated cases of spontaneous closure of VSDs between the ages of 21 and 31 years. With small defects, life expectancy does not change significantly, but the risk of infective endocarditis increases (4%). With a medium-sized VSD, heart failure usually develops in childhood; severe pulmonary hypertension is rare. Large VSDs without a pressure gradient between the ventricles lead to the development of Eisenmenger syndrome in 10% of cases; most of these patients die in childhood or adolescence. Emergency surgical intervention is required in 35% of children within 3 months after birth, 45% within 1 year. Maternal mortality during pregnancy and childbirth with Eisenmenger syndrome exceeds 50%. With post-infarction VSD, 7% of patients survive 1 year in the absence of surgical treatment. Hospital mortality after narrowing of the pulmonary artery is 7-9%, 5-year survival rate is 80.7%, 10-year survival rate is 70.6%. Mortality during surgical treatment of post-infarction VSD is 15-50%. In-hospital mortality during closure of isolated congenital VSD with low LVVR is 2.5%, with high LVVR - less than 5.6%.

Abbreviations. Qp/Qs is the ratio of the pulmonary minute volume of blood flow to the systemic one. TPVR - total pulmonary vascular resistance.

ICD-10. Q21.0 VSD

When analyzing heart pathology Various special concepts are used, the most important of which are discussed in this section.
Atresia and hypoplasia. The term "atresia" is used in cases where any structure is not formed. Most often applied to valves or vessels, which may be completely absent or replaced by a membrane (valve) or fibrous tissue (vessel). The term "hypoplasia" reflects a decrease in the diameter, length or volume of the cardiac structure.

Distensibility, dilatation, ventricular hypertrophy. Distensibility determines the degree of resistance to blood flow in the ventricular cavities. In newborns, the right ventricle is less pliable, which determines greater resistance to the flow of blood into it from the right atrium and relatively high diastolic pressure in it.

Dilatation represents an enlargement of the cavity greater than two standard deviations for a given body surface area of ​​the child and occurs in response to acute or chronic volume overload. Hypertrophy characterizes the degree of increase in the total mass of the myocardium or intracellular structures compared to the norm. Externally, it manifests itself as a thickening of the wall of the heart chamber, sometimes to the detriment of its volume.

Dilatation and hypertrophy can be combined in various combinations and constantly accompany congenital heart defects.

Circulating blood volume.

This concept is used in relation to both large (BCC) and small (MCC) circles blood circulation. The condition of a healthy child is characterized by normovolemia - a normal volume of circulating blood. In cases of excessive blood flow from the placenta during umbilical cord clamping, systemic hypervolemia may occur. With congenital heart defects, changes most often affect pulmonary blood flow. Excessive blood flow into the pulmonary artery system is accompanied by hypervolemia of the ICC, and reduced blood flow is accompanied by hypovolemia. Normal inflow in combination with obstructed outflow leads to hypervolemia of the ICC of a stagnant nature.

Increased pressure in pulmonary artery system referred to as ICC hypertension. It can be of arterial origin (excess blood flow), a consequence of venous stasis (outflow obstruction) or damage to the wall of the pulmonary vessels by an obstructive process.

Even significant hypervolemia MCC may not lead to high pulmonary hypertension (for example, with an atrial septal defect), and hypertension, in turn, may not be combined with hypervolemia, and even vice versa, accompanied by hypovolemia (in cases where high pulmonary vascular resistance limits volumetric blood flow through the lungs ). A clear distinction between these concepts is important for analyzing the processes occurring during the development of pathological conditions in newborns and infants.

Blood flow volume and shunt size.

These parameters are used to characterize the UPS and small and large basins. circulation. The volume of blood flow is determined in milliliters or liters per minute and in most cases is calculated per square meter of body surface. In healthy newborns, normalized systemic blood flow is 3.1+0.4 l/min/m2.

If there is a blood discharge from the systemic circulation to the pulmonary circulation or vice versa, the volume of this discharge is calculated using the formulas:
Shunt from left to right = Qp - Qs; Shunt from right to left = Qs - Qp,
where Qp is the volume of blood flow in the pulmonary circulation, Qs is the volume of blood flow in the systemic circulation.

Since in practice the exact volumetric blood flow measurement associated with the analysis of oxygen consumption is difficult; the ratio of pulmonary and systemic blood flow (Qp/Qs) is more often used. When their ratio is 1:1, there is no shunt or it is the same in both directions. With cyanotic defects, pulmonary blood flow decreases and Qp/Qs can be, for example, 0.8:1. With left-to-right discharges, Qp/Qs increases and can reach 2:1 or more, determining the indications for surgery. Calculation of these parameters is possible using echocardiographic research.

J. Boatman

Abbreviations

QP/QS - ratio of pulmonary blood flow to systemic blood flow

PPA - pulmonary artery pressure

VSD - ventricular septal defect

ASD - atrial septal defect

PH - pulmonary hypertension

PDA - patent ductus arteriosus

Patent ductus arteriosus

General information

In the fetus, the ductus arteriosus is a functioning vessel connecting the pulmonary

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

subclavian artery. High PVR, characteristic of fetal circulation,

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

ductus arteriosus, causing oxygen-poor blood to bypass the pancreas

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

placenta, where it is saturated with oxygen. After birth, PVR sharply

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 patent after birth, especially in preterm infants, with persistent hypoxemia, or with fetal rubella syndrome Clinical presentation A narrow PDA in infancy often goes unrecognized; may manifest itself in childhood or in adults with fatigue and shortness of breath.

Wide PDA often manifests itself with symptoms of congestive heart failure (orthopnea, dyspnea on exertion, nocturnal attacks of cardiac asthma), which occurs as a result of left-to-right shunting and chronic volume overload of the left side of the heart. Possible PH with the development of right ventricular failure (swelling of the neck veins, ascites, enlarged liver, swelling of the legs). As PH progresses, a change in the direction of discharge is possible, which is manifested by isolated cyanosis of the legs, rapid fatigue of the legs during exercise and paradoxical emboli. Course and prognosis in the absence of treatment A narrow PDA generally does not affect life expectancy, although the risk of infective endocarditis increases.

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

Life expectancy is reduced and averages 40 years. Infective endocarditis almost always occurs with left-to-right shunting; The site of infection development is the section of the pulmonary artery located opposite the mouth of the duct and exposed to the mechanical action of the blood stream. One of the manifestations of infective endocarditis is multiple embolisms of the branches of the pulmonary artery.

A rare complication - dissection and rupture of PDA aneurysms Physical examination appearance pulse palpation auscultation When shunting from right to left (as a result of severe PH) - cyanosis of the legs and thickening of the distal phalanges of the toes (“clubs”), as 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 may occur.

Peripheral vasodilation, which occurs during physical activity, leads to an increase in the discharge from right to left, and therefore these symptoms become more pronounced. With a large discharge from left to right, a jumping pulse and a high pulse pressure are observed.

In the absence of HF, the pulsation of the jugular veins is normal. The apical impulse is increased.

Constant trembling in the 1st or 2nd intercostal space on the left, increasing in systole. Normal 1st and 2nd heart sounds are often lost in the constant “machine” noise.

The murmur usually begins after the first sound, reaches maximum intensity by the second sound and weakens during diastole. The murmur is best heard in the second intercostal space on the left; The noise is high-frequency and radiates widely, including to the back.

As PH develops, the noise disappears (first the diastolic and then the systolic components), as the peripheral vascular resistance and heart rate level become equal Non-invasive studies ECG chest radiography EchoCG Normal position of the electrical axis, sometimes - prolongation of the PQ interval.

With a large discharge from left to right - signs of overload of the LV and left atrium.

Overload of the RV and right atrium indicates severe PH. With a large discharge, there is an increase in the LV and left atrium, increased pulmonary vascular pattern, bulging of the ascending aorta and expansion of the proximal branches of the pulmonary artery. With PH, the pancreas enlarges. Two-dimensional examination occasionally allows visualization of a dilated ductus arteriosus.

Using a Doppler study (including color mapping), a constant flow in the trunk of the pulmonary artery, occupying the entire systole and diastole, is detected. Invasive studies, cardiac catheterization and aortography Aortography with the introduction of contrast near the junction of the ductus arteriosus with the aorta is a highly sensitive method for diagnosing PDA. Other signs include an increase in blood 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 defects.

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

HF is treated with generally accepted methods (see Chapter 9).

In infants, closure of the PDA is facilitated by inhibitors of prostaglandin synthesis (in particular, indomethacin). Planned surgical correction by ligation of the duct is safe (mortality

Preliminary results with endovascular methods of PDA closure (using the “double umbrella”) are encouraging, although these methods are still considered experimental. Ventricular Septal Defects Background VSD is the most common congenital heart defect. 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% occur before the age of one year.

The degree of functional impairment depends on the magnitude of the discharge and PVR. If there is a left to right shunt but QP/QS is 2:1) pulmonary blood flow and PVR are significantly increased; pressures in the RV and LV are equalized. As PVR increases, the direction of discharge may change (from right to left), which is manifested by cyanosis, a symptom of “drumsticks”;

the risk of paradoxical embolism increases. Without treatment, right and left ventricular failure and irreversible changes in the pulmonary vessels develop (Eisenmenger syndrome) Types Membranous (75%): located in the upper part of the interventricular septum immediately below the aortic valve and the 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 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 (muscle bundle separating the cavity of the pancreas from its outflow tract). Often accompanied by aortic insufficiency.

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

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

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

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

Eisenmenger syndrome (irreversible PH due to left-to-right shunting) may present with dizziness, syncope, hemoptysis, brain abscesses and chest pain. Course and prognosis in the absence of treatment Small VSD: life expectancy does not change significantly, but the 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 (without pressure gradient between the ventricles, or non-restrictive) VSD:

in most cases they are diagnosed at an early age, in 10% they lead to Eisenmenger 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 and cachexia are observed; depressions are often found in the lower part of the anterior chest wall, the so-called Harrison's grooves (arising due to chronic shortness of breath).

When dumping from right to left - cyanosis and “drumsticks” With small VSDs, the pulse in the peripheral arteries is normal, the pulsation of the jugular veins is also not changed. In PH, distension of the jugular veins, high-amplitude A waves (atrial contraction with a rigid RV) and, sometimes, wave V (tricuspid regurgitation) are observed on the jugular venogram. Increased apical impulse. Trembling at the left lower edge of the sternum. Rough holosystolic murmur at the left lower edge of the sternum. Pathological splitting of the second 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 studies ECG chest radiography EchoCG With a large discharge from left to right: overload of the left atrium and LV, deviation of the electrical axis to the left.

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

With a large left-to-right shunt: LV enlargement, increased pulmonary vascular pattern due to increased pulmonary blood flow.

In PH: pronounced enlargement of the trunk and proximal parts of the pulmonary artery with a sharp narrowing of the distal branches, depletion of the pulmonary vascular pattern. Two-dimensional echocardiography is carried out for the purpose of direct visualization of VSD, detection of pathology of the mitral and aortic valves, enlargement of the heart chambers, and concomitant congenital defects.

Using a Doppler study (including color mapping), the magnitude and direction of the discharge are assessed, and the PAP is calculated. Invasive studies Cardiac catheterization and coronary angiography are performed to confirm the diagnosis, measure the PAP, and exclude coronary artery disease (with appropriate symptoms and before surgery).

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

For pulmonary congestion, hydralazine (or sodium nitroprusside for emergency treatment) is used, which reduces peripheral vascular resistance to a greater extent than PVR, which leads to a decrease in left-to-right shunt and improvement of the condition. For right ventricular failure, diuretics are prescribed.