An 8-month-old has a ventricular septal defect. which nursing diagnosis below would best apply?

A ventricular septal defect [VSD] is an opening in the interventricular septum, causing a shunt between ventricles. Large defects result in a significant left-to-right shunt and cause dyspnea with feeding and poor growth during infancy. A loud, harsh, holosystolic murmur at the lower left sternal border is common. Recurrent respiratory infections and heart failure may develop. Diagnosis is by echocardiography. Defects may close spontaneously during infancy or require surgical repair.

Ventricular septal defect

Pulmonary blood flow and LA and LV volumes are increased. Atrial pressures are mean pressures. RV pressure and O2 saturation are variably elevated, positively related to defect size.

AO = aorta; IVC = inferior vena cava; LA = left atrium; LV = left ventricle; PA = pulmonary artery; PV = pulmonary veins; RA = right atrium; RV = right ventricle; SVC = superior vena cava.

Most ventricular septal defects are classified by location:

• Perimembranous [also called conoventricular]

• Trabecular muscular

• Subpulmonary outlet [supracristal, conoseptal, doubly committed subarterial]

• Inlet [atrioventricular septal type, atrioventricular canal type]

Perimembranous defects [70 to 80%] are defects in the membranous septum adjacent to the tricuspid valve and they extend into a variable amount of surrounding muscular tissue; the most common type of this defect occurs immediately below the aortic valve.

Trabecular muscular defects [5 to 20%] are completely surrounded by muscular tissue and may occur anywhere in the septum.

Subpulmonary outlet defects [5 to 7% in the US; about 30% in Far Eastern countries] occur in the ventricular septum immediately under the pulmonary valve. These defects are often referred to as supracristal, conoseptal, or doubly committed subarterial defects and are frequently associated with aortic leaflet prolapse into the defect, causing aortic regurgitation.

Inlet defects [5 to 8%] are bordered superiorly by the tricuspid annulus and are located posterior to the membranous septum. These defects are sometimes referred to as atrioventricular septal-type defects.

The magnitude of the shunt depends on defect size and downstream resistance [ie, pulmonary outflow tract obstruction and pulmonary vascular resistance].

In nonrestrictive ventricular septal defects, blood flows easily across larger defects; pressure equalizes between the right and left ventricles and there is a large left-to-right shunt. Assuming there is no pulmonic stenosis, over time, a large shunt causes pulmonary artery hypertension Pulmonary Hypertension Pulmonary hypertension is increased pressure in the pulmonary circulation. It has many secondary causes; some cases are idiopathic. In pulmonary hypertension, pulmonary vessels may become constricted... read more , elevated pulmonary artery vascular resistance, right ventricular pressure overload, and right ventricular hypertrophy. Ultimately, the increased pulmonary vascular resistance causes shunt direction to reverse [from the right to the left ventricle], leading to Eisenmenger syndrome Eisenmenger Syndrome Eisenmenger syndrome is a complication of uncorrected large intracardiac or aortic to pulmonary artery left-to-right shunts. Increased pulmonary resistance may develop over time, eventually... read more .

Restrictive ventricular septal defects, which are smaller defects, limit the flow of blood and the transmission of high pressure to the right heart. Small VSDs result in a relatively small left-to-right shunt, and pulmonary artery pressure is normal or minimally elevated. Heart failure, pulmonary hypertension, and Eisenmenger syndrome do not develop.

Moderate VSDs result in intermediate manifestations.

Symptoms and Signs of VSD

Auscultatory findings vary with the size of the defect. Small VSDs typically produce murmurs ranging from a grade 1 to 2/6 high-pitched, short systolic murmur [due to tiny defects that actually close during late systole] to a grade 3 to 4/6 holosystolic murmur [with or without thrill] at the lower left sternal border; this murmur is usually audible within the first few days of life [see table Heart Murmur Intensity Heart Murmur Intensity

]. The precordium is not hyperactive, and the 2nd heart sound [S2] is normally split and has normal intensity.

Moderate to large VSDs produce a holosystolic murmur that is present by age 2 to 3 weeks; S2 is usually narrowly split with an accentuated pulmonary component. An apical diastolic rumble [due to increased flow through the mitral valve] and findings of heart failure [eg, tachypnea, dyspnea with feeding, failure to thrive, gallop, crackles, hepatomegaly] may be present. In moderate, high-flow VSDs, the murmur is often very loud and accompanied by a thrill [grade 4 or 5 murmur]. With large defects allowing equalization of left ventricular and right ventricular pressures, the systolic murmur is often attenuated.

• Chest x-ray and ECG

• Echocardiography

Diagnosis of ventricular septal defect is suggested by clinical examination, supported by chest x-ray and ECG, and established by echocardiography.

If the VSD is large, chest x-ray shows cardiomegaly and increased pulmonary vascular markings. ECG shows right ventricular hypertrophy or combined ventricular hypertrophy and, occasionally, left atrial enlargement. ECG and chest x-ray are typically normal if the VSD is small.

Two-dimensional echocardiography with color flow and Doppler studies establishes the diagnosis and can provide important anatomic and hemodynamic information, including the defect’s location and size and right ventricular pressure. Cardiac catheterization is rarely necessary for diagnosis.

• For heart failure, medical therapy [eg, diuretics, digoxin, angiotensin-converting enzyme [ACE] inhibitors]

• Sometimes surgical repair

Small ventricular septal defects, particularly muscular septal defects, often close spontaneously during the first few years of life. A small defect that remains open does not require medical or surgical therapy. Larger defects are less likely to close spontaneously.

Diuretics, digoxin, and ACE inhibitors may be useful to control symptoms of heart failure Heart failure Congenital heart disease is the most common congenital anomaly, occurring in almost 1% of live births [ 1]. Among birth defects, congenital heart disease is the leading cause of infant mortality... read more

before cardiac surgery or to temporize in infants with moderate VSDs that seem likely to close spontaneously over time. If infants do not respond to medical treatment or have poor growth, surgical repair is often recommended during the first few months of life. Even in asymptomatic children, large VSDs should be repaired, usually within the first year of life, to prevent later complications, particularly persistent pulmonary hypertension and pulmonary vascular disease leading to Eisenmenger syndrome Eisenmenger Syndrome Eisenmenger syndrome is a complication of uncorrected large intracardiac or aortic to pulmonary artery left-to-right shunts. Increased pulmonary resistance may develop over time, eventually... read more . Current surgical mortality rate is