Acquired tricuspid regurgitation

Introduction to acquired tricuspid regurgitation Tricuspid regurgitation may be relative and organic. In the opposite case, the valve itself has no lesions, but the right ventricular hypertrophy, the atrioventricular ring corresponding expansion, causing poor tricuspid valve leaflets, resulting in closure Incomplete, severe rheumatic heart disease patients with mitral stenosis or regurgitation are often associated with relative tricuspid regurgitation. Organic tricuspid regurgitation is a sequela of rheumatic fever, clinically rare, mostly accompanied by mitral and aortic valve lesions. The pathological changes are thickening of the valve fibers, crimping, shortening of the chordae, enlargement of the annulus, and inability of the valve to completely align when the heart contracts, often with a fusion of the valve junction and thus a narrowing. basic knowledge The proportion of illness: 0.002%-0.005% Susceptible people: no specific population Mode of infection: non-infectious Complications: atrial fibrillation, pulmonary embolism

Acquired tricuspid regurgitation

Acquired simple tricuspid regurgitation can occur in carcinoid syndrome, because carcinoid plaque often sinks on the ventricular surface of the tricuspid valve and causes the tip of the valve to adhere to the right ventricular wall, causing tricuspid regurgitation. Most of these patients have pulmonary valve disease at the same time, and the right heart is obviously enlarged when the tricuspid regurgitation is incomplete.

The pathophysiology of tricuspid regurgitation is the result of tricuspid regurgitation, that is, systolic blood flow from the right ventricle back into the right atrium, resulting in enlarged right atrium, increased pressure, venous return, due to increased right ventricular load , compensatory and hypertrophic, prone to right heart failure.

Acquired tricuspid regurgitation prevention

For certain diseases such as primary pulmonary hypertension, mitral valve disease, pulmonary valve or funnel stenosis, right ventricular myocardial infarction, etc. or should always be alert and prevent functional tricuspid regurgitation; and in other diseases such as Ebstein malformations and common atrioventricular pathways in congenital anomalies, and some acquired lesions such as rheumatic inflammation, tricuspid papillary muscle dysfunction caused by coronary lesions, trauma and infective endocarditis, etc. The appearance of tricuspid regurgitation occurs.

Acquired tricuspid regurgitation complications Complications, atrial fibrillation, pulmonary embolism

Acquired tricuspid regurgitation can be complicated by atrial fibrillation, pulmonary embolism and right heart failure.

1, atrial fibrillation

Atrial fibrillation (AF) is one of the most common arrhythmias in adults, and its clinical manifestations are mainly as follows:

1. A few no obvious symptoms, or only palpitations, chest tightness and palpitation; 2. Individual severe cases of dizziness, syncope, angina pectoris, acute heart failure, and even acute pulmonary edema, 3. Part of the systemic arterial embolism may occur, with cerebral embolism most common 4, ventricular rate is fast and irregular, mostly in 120-180 beats / min, rhythm is absolutely not neat, heart sounds vary, pulse shortness (pulse rate is less than heart rate), when the ventricular rate is less than 90 beats / min Or above 150 beats / min, irregular rhythm may not be obvious.

2, pulmonary embolism

Pulmonary embolism is a serious complication caused by a blockage of the pulmonary artery. The most common embolus is a thrombus from the venous system. The clinical manifestations of pulmonary embolism can range from asymptomatic to sudden death. The common symptoms are Dyspnea and chest pain, the incidence rate is more than 80%, pleural pain is caused by inflammation of the adjacent pleural cellulose. Sudden occurrence often indicates pulmonary infarction. The pleural involvement can be radiated to the shoulder or abdomen. If there is post-sternal pain, Similar to myocardial infarction, chronic pulmonary infarction may have hemoptysis, other symptoms are anxiety, may be caused by pain or hypoxemia, syncope is often a sign of pulmonary infarction.

3, right heart failure

Right heart failure: may be caused by left heart failure, pulmonary congestion due to left heart failure, increased pulmonary pressure, increased right ventricular systolic load; congenital cardiovascular malformation with pulmonary hypertension often occurs right heart failure, right heart failure The symptoms are mainly caused by systemic hyperemia, and the clinical manifestations are:

1 edema: began to appear in the body of the pituitary body, the main cause of serious cases are two: one is the increase in sodium and no absorption of the kidney, so that the extracellular fluid increases; one is the increase in systemic venous pressure, capillary infiltration into the tissue More water is refluxed than in capillaries and lymphatic vessels.

2 liver enlargement often accompanied by pain: acute heart failure, abdominal pain and liver tenderness, liver blunt, liver can occur before edema, it is one of the early symptoms of right heart failure, chronic heart failure, long-term Hepatic blood stasis can occur jaundice.

3 jugular vein engorgement: jugular vein engorgement when sitting, more obvious when the liver is pressed by hand (hepatic neck reflux sign).

4 loss of appetite, nausea, vomiting, due to gastrointestinal bleeding.

5 less urine, and mild proteinuria and a small number of red blood cells, due to kidney blood stasis.

Acquired tricuspid regurgitation symptoms Common symptoms Fatigue hepatomegaly Right heart failure Lower abdominal pain Mitochondrial lower pacing frequency Increased jugular vein systolic murmur

Symptoms and signs of tricuspid regurgitation are related to the degree of valvular insufficiency. Mild regurgitation is not clinically detectable. In severe cases, fatigue may be present, poor appetite, pain in the liver area, abdominal distension, and lower extremity edema.

Typical signs are: jugular vein engorgement with pulsation; hepatomegaly and squeaking and pulsation; and systolic murmur in the fourth rib of the left sternal border, murmur at deep inspiratory enhancement (Carvallo sign), typical signs In patients with severe tricuspid regurgitation, it can be absent, such as long-term stagnation of the liver and hardening, but no more pulsation; after the right heart volume load reaches the extreme, the murmur is no longer enhanced with inhalation, so the Carvallo sign can negative.

Acquired tricuspid regurgitation

The disease can have the following inspection methods:

(1) X-ray photograph shows the right atrium and right ventricular hypertrophy, the right edge of the heart is convex, and at the same time there are changes caused by other valvular lesions.

(2) ECG shows atrial hypertrophy, P wave height and width; and right bundle branch block or right ventricular hypertrophy, and even myocardial strain, often atrial fibrillation.

(3) Echocardiography and Doppler examination: Facet ultrasound can detect the size of the tricuspid annulus, understand the thickening of the valve, help to distinguish between relative and organic lesions, tricuspid regurgitation Ultrasound angiography showed microbubbles to and from the tricuspid valve; Doppler can directly detect abnormal signals from the right ventricle to the right atrium, and can estimate the degree of reflux.

(4) Cardiac catheterization showed V-wave protrusion of right atrial pressure waveform, y descending branch became steeper, more obvious when inhaling, right atrial pressure waveform is similar to right ventricular pressure waveform, only amplitude is small, called right The ventricularized right atrial pressure is a manifestation of severe tricuspid regurgitation.

(5) Cardioangiography: Right ventricular angiography, right anterior oblique film photography can show tricuspid regurgitation and its extent, but there is a potential false positive due to the cardiac catheter crossing the tricuspid valve.

Diagnosis and diagnosis of acquired tricuspid regurgitation

The diagnosis of tricuspid regurgitation should include an understanding of the degree of incomplete closure. Typical clinical signs have a value in the diagnosis of severe tricuspid regurgitation. In the past, right ventricular angiography was used as a means of diagnosing suspicious cases and estimating the degree of reflux. In recent years, ultrasound and Doppler examinations have gradually replaced traumatic examinations.

It should be differentiated from mitral regurgitation with low ventricular septal defect.

Mitral regurgitation: typical ventricular systolic murmur in the apical region and enlargement of the left atrium and left ventricle.

Tricuspid regurgitation: the lower end of the left sternal border and the limited contraction of the localized squeaky squeak. When inhaling, the murmur is enhanced by the increase of blood volume, and the exhalation is weakened. When the pulmonary hypertension is high, the second heart sound of the pulmonary valve is hyperthyroidism. The v-wave of the jugular vein is enlarged, there may be liver pulsation, swelling, right ventricular hypertrophy can be seen by electrocardiogram and X-ray examination, and echocardiography can confirm the diagnosis.

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