Aortic valve insufficiency

Introduction

Introduction to aortic insufficiency Aortic insufficiency refers to the flow of blood in the diastolic aorta through the diseased aortic valve into the left ventricle, and the left ventricular preload increases, leading to enlargement of the left ventricle and hypertrophy. Aortic insufficiency is a common valvular heart disease. basic knowledge The proportion of sickness: 0.004% - 0.005% Susceptible people: no specific population Mode of infection: non-infectious Complications: heart failure, infective endocarditis, arrhythmia

Cause

Aortic valve insufficiency etiology

(1) Causes of the disease

Rheumatic heart disease Aortic valve insufficiency is caused by recurrent rheumatic inflammation, causing inflammation, fibrosis, contracture and deformation of the aortic valve margin, causing aortic valve insufficiency, thickening, fibrosis, calcification, neoplasms, etc. The leaf is closed poorly.

(two) pathogenesis

Hemodynamics produced by aortic regurgitation can be divided into two phases:

1. Left ventricular compensation period: Aortic valve insufficiency causes the left ventricle to receive left atrial blood return on the one hand during diastole; on the other hand, it needs to receive blood from the aorta, causing excessive left ventricular volume overload and early diastolic The final volume can be normal or slightly increased, but then progressive reflux can cause increased end-diastolic pressure and dilatation of the heart chamber through the sliding of myocardial fibers, sarcomere and myocardial hypertrophy, and the above-mentioned compensation mechanism promotes increased cardiac output and The left ventricular ejection fraction exceeds 50%. A large amount of cardiac output during systole can be injected into the systemic circulation, which can cause an increase in systolic blood pressure. The hypertrophic myocardium can maintain the compliance of the ventricular wall during systole and maintain the post-load in the normal range, but myocardial oxygen demand. Increased, aortic regurgitation of blood into the left ventricle can reduce the aortic diastolic blood pressure progressively, resulting in reduced coronary blood flow, so severe chronic aortic regurgitation can produce subendocardial ischemia.

2, decompensation period: Chronic aortic regurgitation of progressive capacity overload can continue for several years, only after the myocardial contraction function (variable force) damage, so that the final ejection fraction and variable force decline, with the heart Cavity expansion, the limit of myocardial hypertrophy mechanism, the left ventricular filling pressure is significantly increased, further increasing left atrial pressure and pulmonary venous pressure, leading to pulmonary congestion.

Prevention

Aortic valve insufficiency prevention

Rheumatic heart disease can be prevented. If it can effectively control the infection of a chain pharyngitis, it will not get rheumatic fever, and rheumatic heart disease will not occur. The main preventive measures are:

1, primary prevention

Refers to the prevention of the first episode of rheumatic fever, the key is early diagnosis and treatment of methyl chain tonsillitis, where fever, sore throat or discomfort, headache, abdominal pain, pharyngeal congestion and sputum tonsils have secretions should be swallowed swab culture before treatment To determine if there is a chain growth, if it is positive, start antibiotics immediately.

In addition to penicillin allergy, penicillin should be the drug of choice for all patients, for the following reasons:

1 All strains of Streptococcus hemolyticus are equally sensitive to penicillin;

2 After applying for more than 40 years, the average bacteriostatic and bactericidal concentration of penicillin against this bacteria did not change, still around 0.005g/ml;

3 There is no sign of resistance to penicillin;

4 so far no other antibiotics against streptococcal infection activity and clinical effect than penicillin G;

5 penicillin is relatively inexpensive, the antibacterial spectrum is narrow, so it will not inhibit the normal flora, can avoid double infection, and has fewer side effects than other effective antibiotics. Beta-penicillin is suitable for patients who can not complete oral penicillin treatment for 10 days; Personal history or family history; or geographical, socio-economic environment in patients with high RF area, intramuscular injection of benzathine alone is more painful, injection with benzathine penicillin plus procaine penicillin injection is not painful, mixed injection The dose of benzathine penicillin should be: 600,000 U for patients <27 kg and 1.2 million U for patients with >27 kg. For most small patients, a mixture of benzathine penicillin 900,000 U and procaine penicillin 300,000 U Good results can be obtained, but this preparation is not suitable for adolescent or adult patients. For areas with low RF incidence, penicillin V can be treated orally. Penicillin V has acid stability and absorption, and the concentration of penicillin produced is higher. High, for children and adults, the dose is 250mg, 3 times / d, a total of 10 days, must emphasize the importance of continuous medication for 10 days, even if the symptoms disappear after a few days of medication, should be served for 10 days, less than 10 Day effect The reduction is low, but it can not increase the curative effect for more than 10 days. The curative effect of treating streptococcal pharyngitis is the same or almost the same as that of oral penicillin. For adults, the effect of 2/d administration is unreliable, 3~4 times/d is better. , but the maximum dose does not exceed 1g / d, followed by cephalosporin IV, VI 0.25g, 4 times / d, a total of 10 days, but can not be used for patients with penicillin anaphylactic shock, tetracycline has not been produced domestically, sulfadiazine can not eliminate the chain Cocci, therefore not used to treat streptococcal angina, but continuous use of sulfadiazine is effective in preventing RF recurrence.

2, secondary prevention (prevention of recurrence of rheumatic fever) For patients with a clear history of rheumatic fever or existing rheumatic heart disease, continuous antibiotic treatment is needed to prevent recurrence of rheumatic fever.

(1) Precautionary period: Depending on the risk of recurrence, in general, people with upper respiratory tract infections, crowded living, poor medical conditions, and multiple episodes of history have a high risk of recurrence and a long time to prevent medication. On the contrary, it can be shortened appropriately. Patients with rheumatoid carditis have a relatively high risk of recurrence of carditis. They should receive long-term antibiotic prophylaxis until adult or lifelong prevention. On the contrary, patients who have not had rheumatic carditis have recurrence. The risk of involvement is low and antibiotic prophylaxis can be stopped in a few years. In general, prevention should last until at least 5 years after the patient reaches the twenties or the last rheumatic fever.

(2) Prevention program:

1 intramuscular injection of benzathine penicillin G: a common solution is long-acting penicillin preparation benzathine penicillin G 1.2 million U, intramuscular injection, once every 4 weeks, in acute RF high-risk countries and regions, and high-risk patients, preferably every 3 weeks Intramuscular injection 1 time.

2 oral antibiotics: patients with low risk of RF recurrence, such as those who have reached the end of puberty or adolescence or at least 5 years without recurrent rheumatic fever, can be changed to oral antibiotic prophylaxis, according to the recommended doses:

A. Sulfadiazine: body weight > 27kg, dose 1.0g, 1 time / d, weight 27kg, 0.5g per day, side effects are light and rare, occasionally can cause leukopenia, should check blood cell count every 2 weeks, pregnancy Advanced patients are banned because sulfadiazine can cross the placental barrier and compete with the bilirubin in the fetus for albumin binding sites.

B. Penicillin V: The dose is 250mg, 2 times / d, the allergic reaction is the same as the intramuscular injection of penicillin, and the penicillin skin test should be used before use.

C. Erythromycin: 250mg, 2 times / d, suitable for allergic to penicillin and sulfa drugs.

D. Chinese medicine such as honeysuckle, berberine, astragalus, cork, dandelion, radix isatidis, and andrographis paniculata; Chinese patent medicines such as silver yellow tablets, Yinqiao tablets, anti-inflammatory tablets, silver yellow needles, etc. have good effects on hemolytic streptococcal infection, choose application.

According to a recent WHO report, 33,651 RF or RHD patients were enrolled in secondary prevention for treatment in 1986-1990, but only about 63.2% of patients completed secondary prevention, 95.7% of whom used long-acting penicillin. Intramuscular injection once, 2.1% oral penicillin, 0.1% sulfadiazine, 2.1% erythromycin, 0.3% of patients had adverse reactions to penicillin, 53 cases of RF recurrence, accounting for 0.4% of patients/year, if not prevented The recurrence rate of rheumatic fever is as high as 60% of patients per year.

Complication

Aortic valve insufficiency complications Complications, heart failure, infective endocarditis, arrhythmia

1, heart failure: aortic valve insufficiency in the late stage of the disease can occur left heart failure, a small number of patients may also have right heart failure, and most patients with chronic aortic regurgitation may have died before right heart failure, left The occurrence of heart failure may be related to left ventricular overload, myocardial ischemia and myocardial fibrosis.

2, infective endocarditis: is the most important complication of chronic aortic regurgitation, infective endocarditis is an important factor leading to the deterioration of patients with aortic regurgitation, those originally only a mild master Patients with aortic regurgitation, once complicated by infective endocarditis, cause valve damage and cause extremely serious hemodynamic disturbances, threatening the lives of patients, and the consequences of severe aortic regurgitation are more serious .

3, arrhythmia: aortic valve insufficiency may occur in a variety of arrhythmias, such as early room, ventricular tachycardia, etc., often predicting left ventricular dysfunction, severe aortic regurgitation with obvious left ventricular hypertrophy and dilatation, There is a left bundle branch block and varying degrees of atrioventricular block.

Symptom

Symptoms of aortic insufficiency common symptoms Myocardial foramen ovale closed insufficiency dyspnea Lifting ventricular fibrillation water rushing labor dyspnea end sitting breathing nod sign

Generally, the aortic valve insufficiency gradually increased in 7 to 10 years. The initial left atrial and left ventricle did not increase the diastolic blood pressure. The clinical dysfunction after dysfunction or dyspnea, apical pulsation and carotid pulsation increased. Most patients found heart murmurs and were asymptomatic during physical examination. If there were significant symptoms after general activities, the condition has deteriorated further. Later in the course of the disease, angina and left heart failure often occur due to hypertrophic myocardial ischemia. Patients with advanced disease often have restless sleep, paroxysmal dyspnea at night, multiple nightmares, increased heart rate, flushing, chest pain or headache with paroxysmal hypertension. People with severe heart failure and angina often die at night. In addition, the patient is sweaty and cannot be heat resistant.

1, symptoms

(1) Left ventricular compensation period: excessive volume overload caused by chronic aortic regurgitation, due to normal cardiac output during the compensation period, left ventricular end-diastolic pressure is not high or slightly elevated, so it can maintain normal The circulatory function, without obvious symptoms, even if the left ventricular end-diastolic pressure has increased significantly, because the diastolic mitral valve can be closed early, so that the left atrial pressure and pulmonary venous pressure are not significantly increased for a considerable period of time, the compensation period can be For 20 to 30 years, due to increased left ventricular ejection volume and increased cardiac contractility, patients may have palpitations, apical pulsation and discomfort in the precordial area.

(2) Left ventricular decompensation period: Once the left heart function is decompensated, congestive heart failure occurs, and the condition often deteriorates rapidly. If not treated in time, it usually dies in left heart failure, angina or sudden death within 2 to 3 years.

1 angina pectoris: more than 50% of severe aortic regurgitation can occur angina pectoris, mostly in the supine position, seen in young patients with severe aortic regurgitation, in bed rest or wake up at night, with blood pressure Significantly increased, heart rate increased and mild breathing difficulties, not good for nitroglycerin.

The mechanism:

A. The amount of blood returning during sleep increases, and the capacity of the diastolic period is excessive, which causes the heart chamber to expand and the oxygen consumption to increase, causing myocardial ischemia.

B. Severe aortic regurgitation can reduce aortic diastolic blood pressure, resulting in reduced coronary blood flow.

C. Some elderly patients may have coronary heart disease, and frequent angina pectoris may indicate poor prognosis.

2 left ventricular dysfunction: due to impaired left ventricular systolic function, after long-term decompensation, once the pulmonary venous hypertension occurs, there may be labor dyspnea, night paroxysmal dyspnea, sitting breathing, and even pulmonary edema Late stage can cause signs of right heart failure.

3 sudden death: about 10% of aortic regurgitation can occur sudden death, the incidence is less than aortic stenosis, may be related to sudden fatal ventricular tachycardia (sustained ventricular tachycardia, ventricular fibrillation).

4 Others: Many patients have a lot of sweating, mainly in the upper body. Some patients complain of sweating. The cause of excessive sweat is unknown. It may be related to autonomic dysfunction. Occasionally, the patient complains of periodic carotid pain and tenderness. ~ 7 days to relieve themselves, the reason is unknown.

2, signs

Chronic aortic regurgitation:

(1) Left ventricular compensation period:

1 The apex beats and increases to the left.

2 The apex is a lifting pulsation.

3 The heart of the voiced voice expands to the lower left.

4 auscultation features:

A. Aortic valve area diastolic murmur: usually in the third and fourth intercostal space of the left sternal border (ie, the second auscultation area of the aortic valve area) can hear high-pitched, loudness-decreasing air-like diastolic early murmurs, usually the nature of the noise Splashing water or haqi; often passed to the apical region, caused by ascending aortic lesions caused by the obvious expansion of the ascending aorta caused by aortic annulus enlargement caused by relative aortic regurgitation or aortic valve prolapse, flip caused by the main Arterial insufficiency can be most loud in the second intercostal space on the right sternal border, and is transmitted along the right edge of the sternum. It is a musical or seagull-like early murmur, and the murmur and the second heart sound (S2) aortic valve components appear simultaneously. Therefore, the noise often covers the S2. When the noise is light, let the patient take the seat and lean forward slightly. At the same time, the breathing is paused after deep exhalation and the chest piece is easy to hear with the diaphragm type, the intensity of the noise and the size of the reflux port, pressure The step, the direction of the reflux beam and the heart function are related. The intensity does not fully represent the degree of reflux. It is more important to judge the severity of reflux and the duration of noise (reverse time). Mild reflux only occurs in diastolic early Severe reflux can be heard in full diastolic murmur; when severe reflux is associated with cardiac insufficiency, the left ventricular residual blood increases due to increased early left ventricular diastolic blood pressure; a large number of aortic regurgitation can rapidly increase left ventricular diastolic pressure. And the aortic diastolic pressure is balanced, the reflux time is shortened and (or) the reverse flow is reduced, the noise is shortened and lightened; and when the left heart function is improved, the noise becomes louder.

B.Austin-Flint murmur: severe aortic regurgitation can be heard in the apical region, a relatively low-key, short diastolic mid-stage rumbling murmur, often anterior systolic, called Austin-Flint murmur, aortic regurgitation The bundle impacts the anterior lobe of the mitral valve to cause it to rise and cause vibration; it is also possible that the left ventricular diastolic pressure is rapidly increased, forcing the mitral valve leaf to be not fully open, resulting in blood vortex.

C. Aortic valve area systolic murmur: When severe aortic regurgitation is incomplete, a 2 to 3/VI grade, high-pitched, short-duration, short-lived, jet-like systolic murmur can be heard in the aortic valve area. The murmur is rhomboid, appearing after S1, extending to early contraction, mid-term, late systolic disappearance, usually no systolic tremor, even audible early contraction, and mechanism of severe aortic regurgitation, left ventricular pacing Significant increase in blood volume and accelerated blood flow, resulting in relative aortic stenosis, compared with systolic murmurs of organic aortic stenosis, the latter usually loud, rough, high pitch, long time hair dryer A jet-like full systolic murmur, often accompanied by fine tremor during systole.

D. Mitral valve area systolic murmur: moderate to severe aortic regurgitation, due to the obvious enlargement of the left ventricle, the position of the papillary muscles moving down and the mitral annulus dilatation, can produce relative mitral regurgitation, can be The apical area hears a regurgitation systolic murmur, which is enhanced when the heart function is reduced, while the heart function is improved, while the organic mitral regurgitation is reversed.

E. The apical area S1 is often weakened: when the aortic valve regurgitation causes a rapid increase in left ventricular diastolic volume and pressure, especially when there is left ventricular dysfunction, the mitral valve can be closed early, so S1 is often weakened, when concurrent relative When the mitral regurgitation is incomplete, the apical systolic murmur in the apical region can conceal S1. Severe aortic regurgitation can often be heard in the apical region, due to the increased left ventricular ventricular filling during the early filling of the diastolic period. Caused by vibration of the chamber wall.

5 peripheral vascular signs:

A. water hammer pulse: for the systolic peripheral arteries rapidly filling, and part of the blood in the diastolic phase reflux to the left ventricle, so that the intravascular pressure drops rapidly, when the radial artery is pressed, it suddenly rises, This is more pronounced due to gravity when the patient's arm is raised too far.

B. Pistol shotsound: Place the chest piece on the patient's radial or femoral artery. You can hear the loud "beep-beep" sound when the artery beats, such as the sound of a gunshot. Caused by peripheral arteries.

C. Duroziez sign: When the abdominal aorta is lightly compressed with a stethoscope, the systolic and diastolic murmurs can be heard, reflecting the presence of severe aortic regurgitation.

D. Capillary pulsation (Qumcke sign): slightly pressurize the nail, observe the nail bed, or use the slide to gently press the mucous membrane of the lips and lips, all of which can see alternating capillary pulsation of redness and paleness, and around the systolic period during severe aortic regurgitation Capillaries are filled, while diastolic blood flows back, causing capillary ischemia.

E. Nod sign (DeMusset sign): Regular nodular movement consistent with heartbeat can be seen in severe aortic regurgitation.

F. Increased pulse pressure difference: systolic blood pressure increases when aortic valve is insufficiency, diastolic blood pressure decreases, and pulse pressure difference increases. When severe aortic valve insufficiency with left heart failure, LVEDP is significant due to decreased systolic blood pressure Increased arterial diastolic blood pressure, pulse pressure difference can be close to normal, it must be combined with clinical analysis, blood pressure is measured by a mercury column sphygmomanometer when severe aortic regurgitation, and the gunshot sound can still be heard when the diastolic pressure is zero. In the same situation, the intra-arterial pressure measurement method is found to have a diastolic blood pressure of > 3.9 kPa (30 mmHg) or more.

(2) Left ventricular decompensation period: In addition to the above signs, left heart failure can produce S3 galloping in the apex region.

According to the medical history, the aortic valve area and the aortic valve second auscultation area diastolic murmur and peripheral vascular signs, can make a diagnosis of aortic regurgitation, further according to echocardiography and cardiac catheterization, can be aortic valve Semi-quantitative diagnosis of the degree of flow and judgment of common causes.

Examine

Aortic valve insufficiency examination

1, X-ray examination: typical chronic aortic valve insufficiency has the following performance:

(1) Left ventricular enlargement: the apex is shifted to the left and the apex is enhanced, and the ratio of heart to chest is >0.50.

(2) The ascending aorta is significantly widened: the aortic arch is prominent, with significant pulsation, and the enlarged left ventricle constitutes the "shoe heart".

(3) There may be calcification of the aortic valve or annulus.

(4) Left heart failure often accompanied by enlargement of the left atrium and pulmonary congestion.

2, ECG: typical manifestations of left ventricular hypertrophy, strain, acute aortic regurgitation without left ventricular hypertrophy, may have ST-T changes in myocardial ischemia.

3. Echocardiography (UCG)

(1) M-type and two-dimensional UCG: aortic valve leaf thickening, echo enhancement, active stiffness, poor closure of diastolic valve leaflets, visible closure of the fissure, more than 2 ~ 3mm; aortic short axis section can be clearly displayed The structure and movement of the three flaps can show the specific position of the incomplete closure and the shape and size of the fissure when closed; the two-dimensional UCG is easier to display when there is prolapse or prolapse of the valve leaflet, and the anterior mitral valve can be observed in the M-type Rapid tremor during diastole.

The transesophageal UCG (TEE) shows the position and shape of the fissure more clearly, and more sensitively displays the color reflux bundle.

Indirect signs: left ventricular enlargement, ventricular septum, increased amplitude of posterior wall of left ventricle, widening of aortic root.

(2) Doppler UCG: sampling under the aortic valve, measurable and diastolic turbulent spectrum, color Doppler showing a colorful mosaic retrograde beam on a two-dimensional plane, observing the origin and origin of the retrograde bundle The width of the part, and can be semi-quantitative according to the area of the reflux beam.

M-type and two-dimensional UCG are not easy to detect when the incomplete crack is less than 2 mm, and the extremely small backflow beam can be detected very sensitively by spectral Doppler and color Doppler.

(3) Quantitative diagnosis of aortic regurgitation: Estimate the severity of aortic regurgitation according to the size of the Doppler signal distribution in the left ventricle or the reflux fraction (RF), according to the reflux fraction Can be divided into: mild RF <20%; moderate RF 20% ~ 40%; moderate to severe RF 40% ~ 60%; severe RF > 60%.

4, cardiac catheterization: left ventricular angiography can determine left ventricular end-diastolic volume, left ventricular end-systolic volume, left ventricular ejection fraction (EF), left ventricular end-diastolic pressure and left ventricular wall (ventricular septum, posterior wall) thickness.

5, ascending aorta angiography: can show the shape and size of the reflux, is valuable for estimating the degree of aortic regurgitation and understanding the various pathological processes of the aortic root, according to the contrast agent in the left ventricular reflux, the aortic valve The closure is not divided into 4 degrees:

(1) 1 degree: The contrast agent only reaches below the aortic valve and is removed by the contraction of the next ventricle.

(2) 2 degrees: The left ventricular contrast agent concentration gradually increased, but still lower than the gray level in the aorta.

(3) 3 degrees: The left ventricular contrast agent gradually increased in gray level to be the same as in the aorta.

(4) 4 degrees: The contrast of the contrast agent in the first diastolic phase is the same as that in the aorta.

Diagnosis

Diagnosis and diagnosis of aortic insufficiency

Differential diagnosis

Regarding the diagnosis of aortic regurgitation, the following points should be noted.

1. The diastolic murmur between the left and third ribs of the sternum is aortic regurgitation or pulmonary regurgitation.

2, the identification of structural aortic regurgitation and relative aortic regurgitation, clinical rheumatic aortic regurgitation and syphilitic aortic regurgitation and hypertension, relative aortic atherosclerosis Differential diagnosis of aortic regurgitation.

3. Identification of acute and chronic aortic regurgitation.

4, rheumatic aortic regurgitation and stenosis clinically how to judge the closure of the main or stenosis, can be identified from the following points.

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