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Ventricular septal defect

Introduction
Cause
Examine
Diagnosis

Introduction

Introduction Ventricular septal defect refers to ventricular septal dysplasia during the embryonic period, which forms abnormal traffic and produces a left-to-right shunt at the ventricular level, which may exist alone or as part of a complex cardiac malformation. Ventricular deficiencies are the most common congenital heart disease. The ventricular septal defect is about 20% of the total number of congenital heart disease, which can exist alone or coexist with other malformations. The defect is between 0.1-3cm, which is larger in the membranous part and smaller in the muscle part, which is also called Roger's disease. If the defect is <0.5cm, the flow rate is small and there are no clinical symptoms. The small defect was mainly due to the enlargement of the right ventricle, and the left ventricle of the larger defect was more obvious than the right ventricle.

Cause

Cause

A left-to-right shunt is generated at the ventricular level, depending on the size of the defect. In patients with large defects, the blood flow in the pulmonary circulation increased significantly, flowing into the left atrium, after the chamber, and flowing into the right ventricle through the defect at the ventricular level, entering the pulmonary circulation, thus increasing left and right ventricular load, increasing left and right ventricles, and increasing pulmonary circulation blood flow. This leads to an increase in pulmonary arterial pressure and an increase in right ventricular systolic load, which eventually leads to an obstructive pulmonary hypertension, with bidirectional or right to left shunting.

Examine

an examination

Related inspection

Doppler echocardiography, cardiovascular diagnosis, echocardiography, electrocardiogram

X-ray examination

Moderately above the defect, the heart shadow is mild to moderately enlarged, the left heart edge is extended to the left, the pulmonary artery is conical, the aortic node is small, and the hilar is congested. Cardiac enlargement of severe obstructive pulmonary hypertension is not significant, the right pulmonary artery is large, the distal mutation is small, the branch is rat tail, and the peripheral texture of the lung field is sparse.

Cardiac examination

There is often a slight uplift in the precordial area. The third and fourth intercostal spaces of the sternal border were systolic and systolic tremors, and the III-IV full-systolic murmur was heard. The high-level funnel defect was tremor and murmur located in the second intercostal space. The second sound of the pulmonary valve area is hyperthyroidism. For those with large flow rates, soft functional diastolic mid-range murmurs can still be heard at the apex. In cases where pulmonary hypertension causes a decrease in partial flow, the systolic murmur gradually decreases or even disappears, while the second sound of the pulmonary valve area is significantly hyperactive and dilated, and may be associated with diastolic murmur of pulmonary valve insufficiency.

Electrocardiogram

The defect is small or normal. The defect is large, and the left ventricle is high voltage, hypertrophy or left and right ventricular hypertrophy with the increase of the flow rate and pulmonary artery pressure. In patients with severe pulmonary hypertension, right heart hypertrophy or strain.

X-ray: There is no change in the heart of the defect. When the defect is moderately large, the heart shadow increases to varying degrees, mainly to the right ventricle. In the case of large defect, the left and right ventricles are enlarged, the pulmonary artery is bulged, and the pulmonary vascular image is enhanced. When the pulmonary hypertension is severe, the lateral field of the lung field is clear.

Echocardiography

The left atrium, left and right ventricular internal diameters increased, and the interventricular septal echoes were continuously interrupted. Doppler ultrasound: The maximal turbulence was deeply measured by the defect of the right ventricle facing the defect and left ventricular surface tracking.

Cardiac catheterization

The level of blood oxygen in the right ventricle is higher than 0.9% of the volume in the right atrium, and occasionally the catheter can reach the left ventricle through the defect. According to the amount of flow, the pulmonary artery or right ventricular pressure increased to varying degrees.

Diagnosis

Differential diagnosis

Aortic insufficiency

1. Cardiac auscultation Aortic valve area diastolic murmur, a high-profile descending type of gas-like murmur, sitting position before the end of the end of expiration. The most loud area depends on whether there is significant ascending aortic dilatation, rheumatic aortic dilatation is lighter, the third rib in the left sternal border is the loudest, can be transmitted along the sternal border to the apical region; Marfan syndrome or syphilis In the case of a sexual heart, the murmur is most loud in the second rib on the right edge of the sternum because the ascending aorta or aortic annulus can be highly dilated. Generally, the more severe the aortic valve insufficiency, the longer the noise is, and the louder the louder. Mildly closed, this murmur is soft, only occurs in the early stage of diastole, only in the patient's sitting position forward, exhaled to hear; when heavier closure, the murmur can be full diastolic and rough, in severe or acute When the aortic valve is incomplete, the left ventricular end-diastolic pressure is increased to be equal to the aortic diastolic pressure, so the duration of the noise is shortened. Such as murmur with musical properties, often suggest that a part of the valve is turned, torn or perforated. Aortic dissection sometimes also has musical tones, probably due to diastolic proximal aortic intima through the aortic valve to ventricular prolapse or blood flow in the middle aortic lumen.

When the aortic valve regurgitation is obvious, the mid-systolic jetting is often heard in the aortic valve area at the base of the heart. The softer, shorter high-pitched murmur is transmitted to the neck and sternum, which is a great stroke volume. Caused by the aortic valve, not caused by organic aortic stenosis. The apical area is often audible with a soft, low-key rumbling-like diastolic or pre-systolic murmur, the Austin-Flint murmur. This is due to the massive aortic valve regurgitation, impacting the anterior leaf of the mitral valve, hindering its opening and shaking, causing relative mitral stenosis; at the same time, the aortic regurgitation and left atrial return blood impact, mixing, resulting Caused by eddy currents. This murmur is enhanced when the palm is firmly gripped, and is weakened when inhaling isoamyl nitrite. When the left ventricle is significantly enlarged, due to the functional mitral regurgitation caused by the extrapneumatic movement of the papillary muscle, it can be heard in the apical region and the systolic murmur during the full systole, and transmitted to the left iliac crest.

When the valve activity is poor or the reflux is severe, the second heart sound of the aortic valve is weakened or disappeared, and the third heart sound is often heard, suggesting left heart dysfunction; the fourth atrial sound is heard when the left atrial compensatory contraction is enhanced. Due to the large increase in systolic stroke volume, the aorta suddenly expands, causing a loud contraction early jet sound.

In acute severe aortic regurgitation, the diastolic murmur is soft and short; the first heart sound is weakened or disappeared, and the third heart sound can be heard, and the pulse pressure can be close to normal.

2. Other signs are paler, the apex beats to the left and down, the range is wider, and the powerful lifting pulsation can be seen. The heart of the voiced voice expands to the lower left. The aortic valve area can reach systolic tremor and conduct to the neck; the left lower edge of the sternum can reach diastolic tremor. The carotid pulsation was significantly enhanced and doubled. The systolic blood pressure is normal or slightly higher, the diastolic blood pressure is significantly reduced, and the pulse pressure difference is significantly increased. Peripheral vascular signs can occur: Corrigan's pulse, Quincke's sign, Traube's sign, femoral systolic and diastolic double murmur (Duroziez'ssign), And the head swings up and down with the heart rate (de-Musset'ssign). In pulmonary hypertension and right heart failure, jugular vein engorgement, enlarged liver, and lower extremity edema can be seen.