Right ventricular myocardial infarction
Introduction to right ventricular myocardial infarction
Right ventricular myocardial infarction (RVMI) is usually caused by occlusion of the right coronary artery, often with clinical infarction of the inferior or posterior inferior myocardial infarction. The right ventricular anterior wall (1/4 to 1/3) is connected to the ventricular septum by the right ventricular branch of the left anterior descending coronary artery and the conical branch opening at the beginning of the right coronary artery. The rest of the right ventricular wall The right ventricle of the right coronary artery is supplied with blood. Due to the anatomical relationship, the RVMI has a left inferior wall and a posterior segment of the ventricular septal infarction. The affected vessel in the anterior wall infarction is the left anterior descending artery, and the range of the right ventricle is small. Therefore, even if the anterior wall infarction is complicated by RVMI, the lesions are small and the clinical symptoms of RVMI are rare.basic knowledge
The proportion of illness: 0.003%
Susceptible people: no special people
Mode of infection: non-infectious
Complications: cardiogenic shock, high atrioventricular block
Causes of right ventricular myocardial infarction
(1) Causes of the disease
Studies have shown that acute thromboangiography of the coronary arteries is the main cause of transmural myocardial infarction. Acute ischemic changes in right ventricular myocardial infarction are usually the result of acute occlusion of the right coronary artery, although coronary circumflex occlusion can also produce right ventricular infarction. , but the proportion is much lower than the right coronary artery.
The right ventricular anterior wall (1/4 to 1/3) is connected to the ventricular septum by the right ventricular branch of the left anterior descending coronary artery and the conical branch opening at the beginning of the right coronary artery. The rest of the right ventricular wall The right ventricle of the right coronary artery is supplied with blood. Due to the anatomical relationship, the RVMI has a left inferior wall and a posterior segment of the ventricular septal infarction. The affected vessel in the anterior wall infarction is the left anterior descending artery, and the range of the right ventricle is small. Therefore, even if the anterior wall infarction is complicated by RVMI, the lesions are small and the clinical symptoms of RVMI are rare.
According to the right ventricular involvement, RVMI can be divided into 4 grades: grade I, right ventricular inferior wall infarction range <50%; grade II, entire right ventricular inferior wall infarction; grade III, except the right ventricular inferior wall, affecting part of the anterior wall and Right ventricular free wall; grade IV, extensive infarction of the inferior and anterior wall of the right ventricle, at grades I and II, distal or middle occlusion of the right coronary artery is often found, while at grades III and IV, there is often a right coronary artery and Occlusion of the left anterior descending coronary artery, clinically low sputum syndrome and shock often occur.
Right ventricular infarction is almost always accompanied by low cardiac output, which may be due to dilatation of the right ventricle due to infarction, lack of left ventricular filling, pericardium has a limiting effect on total cardiac capacity, so in RVMI, right The diastolic pressure of the ventricle and the left ventricle are nearly equal, clinically similar to cardiac tamponade or pericardial constriction. According to the size of the left and right ventricular infarction, the clinical manifestations are: no heart failure type, right heart failure dominant type, left heart failure dominant type, Heart failure type.
Right ventricular myocardial infarction prevention
Because epidemiological data show that coronary heart disease is one of the most important diseases causing human death, and there is still no radical measures in clinical practice, it is of great significance for the active prevention of coronary heart disease. The prevention of coronary heart disease involves In the primary prevention and secondary prevention, primary prevention refers to taking measures to control or reduce the risk factors of coronary heart disease in people who have not suffered from coronary heart disease to prevent disease and reduce the incidence rate. Secondary prevention means Patients with coronary heart disease take medicinal or non-pharmacological measures to prevent recurrence or prevent exacerbations.
1. Primary prevention measures
Primary prevention measures for coronary heart disease include two situations:
(1) Health education: educate the whole population on health knowledge, improve citizens' self-care awareness, avoid or change bad habits, such as quitting smoking, paying attention to reasonable diet, exercising properly, maintaining psychological balance, etc., thereby reducing the incidence of coronary heart disease.
(2) Control high-risk factors: for high-risk groups of coronary heart disease, such as hypertension, diabetes, hyperlipidemia, obesity, smoking, and family history, etc., positive treatment, of course, some of these risk factors can be controlled Such as high blood pressure, hyperlipidemia, diabetes, obesity, smoking, less active lifestyle, etc.; and some can not be changed, such as family history of coronary heart disease, age, gender, etc., including the use of appropriate drugs for continuous control Blood pressure, correct abnormal blood lipid metabolism, limit smoking, limit physical activity, control physical activity, control weight, control diabetes, etc.
2. Secondary preventive measures
The secondary prevention content of patients with coronary heart disease also includes two aspects. The first aspect includes the content of primary prevention, that is, the risk factors of various coronary heart diseases should be controlled. The second aspect is to use drugs that have been proven effective. To prevent the recurrence of coronary heart disease and the exacerbation of the disease, the drugs that have been confirmed to have preventive effects are:
(1) Antiplatelet drugs: A number of clinical trials have confirmed that aspirin can reduce the incidence of myocardial infarction and reinfarction rate. The use of aspirin after acute myocardial infarction can reduce the reinfarction rate by about 25%; if aspirin can not tolerate Or allergic, clopidogrel can be used.
(2) -blockers: as long as there are no contraindications (such as severe heart failure, severe bradycardia or respiratory diseases, etc.), patients with coronary heart disease should use beta blockers, especially in the occurrence of acute coronary After the arterial event; there are data showing that the use of beta blockers in patients with acute myocardial infarction can reduce the mortality and reinfarction rate by 20% to 25%. The drugs available are metoprolol, propranolol, Thiolol and so on.
(3) ACEI: used in patients with severe impairment of left ventricular function or heart failure, many clinical trials (such as SAVE, AIRE, SMILE and TRACE, etc.) have confirmed that ACEI reduces mortality after acute myocardial infarction; Therefore, after acute myocardial infarction, patients with ejection fraction <40% or wall motion index 1.2, and no contraindications should use ACEI, commonly used captopril, enalapril, benazepril and blessing Simplice and so on.
(4) statin lipid-lowering drugs: the results of studies from 4S, CARE and recent HPS show that long-term lipid-lowering therapy for patients with coronary heart disease not only reduces the overall mortality rate, but also improves the survival rate; and requires coronary intervention The number of patients with CABG is reduced, which is due to the improvement of endothelial function, anti-inflammatory effects, effects on smooth muscle cell proliferation and interference with platelet aggregation, blood coagulation, fibrinolysis and other functions, simvastatin, and deforestation. Statins, fluvastatin, and atorvastatin all have this effect.
In addition, coronary angiography has coronary atherosclerotic mild stenotic lesions and clinically no ischemic symptoms, although it is not clearly diagnosed as coronary heart disease, it should be regarded as a high-risk group of coronary heart disease, giving active prevention, Long-dose aspirin can also be given for a long time, and risk factors such as dyslipidemia and hypertension can be eliminated.
Right ventricular myocardial infarction complications Complications, cardiogenic shock, high atrioventricular block
Acute right ventricular infarction may be complicated by cardiogenic shock, high atrioventricular block, supraventricular arrhythmia and mechanical complications.
About 10% of patients with acute right ventricular infarction will have clinical signs of severe low cardiac output and cardiogenic shock. The average interval from onset to shock is 44 h. Shock is common in patients with inferior wall infarction. The rate is related, indicating that right ventricular dysfunction plays a decisive role.
2. High atrioventricular block
High-grade atrioventricular block is one of the most common early complications of acute right ventricular and left ventricular infarction, and its incidence is much higher than that of simple left ventricular infarction (12%), which can be as high as 48% to 58%. In patients with right ventricular infarction, bradycardia due to high cardiac conduction block and loss of atrioventricular coherence contraction, which worsens hemodynamics, is an independent predictor of high mortality during hospitalization.
3. supraventricular arrhythmia
Patients with inferior wall infarction with right ventricular dysfunction are more likely to develop atrial arrhythmias and atrial fibrillation than those with normal right ventricular function.
4. Mechanical complications during right ventricular infarction
(1) ventricular free wall rupture: right ventricular free wall rupture is much less than left ventricular rupture, the incidence is only about 1 / 7, the right ventricular free wall rupture, can be manifested as a sudden deterioration of the condition after myocardial infarction, moderate Right ventricular heart failure and mild left ventricular heart failure, or even severe heart failure, may have no typical signs of pericardial tamponade.
(2) Interventricular septal perforation: After ventricular septal perforation, left ventricular anterior cardiac output rapidly decreases, pressure from the left side acts on the right ventricle, and right ventricular myocardium itself also has infarction, which quickly leads to right heart failure; infarction The right ventricle can not maintain the level of pulmonary blood flow necessary for cardiac circulation, and immediately falls into cardiogenic shock.
(3) papillary muscle rupture: occlusion of the right coronary artery can lead to dysfunction or rupture of the right ventricular posterior papillary muscle, causing severe tricuspid regurgitation, usually with severe chest pain in the 2nd to 7th day after acute infarction Full systolic murmur in the apical region, conduction to the ankle and back, accompanied by right heart failure or cardiogenic shock must consider the fracture of the papillary muscle.
(4) Right ventricular aneurysm: patients usually have no specific signs, and 1/3 to 1/2 of patients have apex pulsation or apex pulsation, which is caused by abnormal expansion of ventricular endometrial expansion. .
Right ventricular myocardial infarction symptoms common symptoms myocardial necrosis extensive hypotension Qimai bradycardia jugular vein engorgement atrioventricular block
Acute right ventricular infarction may have different clinical manifestations due to the severity of the lesion, alone or in combination with other parts of the myocardial infarction, time of visit and other factors.
Right heart function insufficiency
(1) Kussmaul sign positive (jugular jugular engorgement during deep inhalation): due to right ventricular infarction, right ventricular end-diastolic pressure caused by decreased right ventricular compliance and systolic function, increased right atrial pressure and venous pressure, normal When the person inhales, the intrathoracic pressure decreases, the venous pressure decreases, and the amount of blood returning increases. However, such patients suffer from venous return due to right ventricular diastolic dysfunction, resulting in a further increase in venous pressure.
(2) jugular vein engorgement, liver enlargement: This is caused by venous system congestion.
(3) S3 or S4 galloping occurs in the tricuspid valve region of the heart: the right ventricular compliance decline and the right atrial blood flow resistance increase.
(4) Relative to the tricuspid regurgitation due to enlargement of the right ventricle.
(5) In severe cases, hypotension and shock may occur.
Various types of arrhythmia can occur, but bradycardia arrhythmia is common, which is due to sinus node dysfunction and atrioventricular block, the incidence of atrioventricular block is 48%, its resistance Most of the stagnation sites are above the His bundle, which may be related to the majority of atrioventricular nodules originating from the right coronary artery branch.
Right ventricular myocardial infarction
1. Increased serum myocardial enzymology
Foreign statistics of acute inferior wall infarction serum CK>2000U / L for the diagnosis of right ventricular infarction can be up to 94%, while abnormally significantly increased CK-MB, aspartate aminotransferase, lactate dehydrogenase also predict the function of right ventricular infarction .
2. Atrial natriuretic factor secretion increased
Serum atrial natriuretic factor >100Pg/ml in acute inferior myocardial infarction is an early diagnostic indicator of right ventricular involvement.
V3R ~ V7R ST segment elevation 1.0mm, especially V4R, V5R changes more meaningful, abnormal Q wave or QS wave after 2-3 days of onset of disease, its HC lead diagnosis of right ventricular infarction has the following advantages:
1 normal human HC lead, V3R ~ V7R no pathological Q liquid.
2 The acute ST-segment elevation of HC lead was more obvious in acute right ventricular infarction.
3 old right ventricular infarction, HC lead in the right chest can detect pathological Q fluid.
1 The right ventricular internal diameter dilatation 23mm, the right ventricular end diastolic diameter / left ventricular end diastolic diameter 0.63, the ventricular septum and the left ventricular posterior wall in the same direction.
2 right ventricular segmental dyskinesia.
3 lack of right ventricular wall motion or contradictory movement.
4 There may be a wall thrombus in the right ventricular cavity.
5. Hemodynamic characteristics
1 Right atrial pressure and right ventricular filling pressure (RVFP) have a disproportionate increase compared with left ventricular diastolic pressure, PVFP/LVFP 0.65, right atrial pressure 10 mmHg (1.33 kPa) after resting or volume load The ratio of right atrial pressure to PCWP is 1.0.
2 pulmonary artery diastolic blood pressure and PCWP normal or slightly higher.
3 cardiac output and peripheral arterial pressure decreased, when the inferior wall, posterior wall and / or anterior wall infarction showed obvious right heart failure or hypotension without signs of left heart failure, more suggestive of right ventricular infarction.
6. Chest X-ray The right ventricle is enlarged without pulmonary congestion.
Diagnosis and diagnosis of right ventricular myocardial infarction
In summary, the clinical signs of right ventricular infarction depend on the degree of right ventricular necrosis, the main signs are: hypotension; increased jugular venous pressure; Kussmaul's sign; abnormal jugular pulsation (Y drop X drop); tricuspid valve Reflux; right heart sound and fourth heart sound; odd pulse; high atrioventricular block, of which jugular venous pressure and Kussmaul's sign are the most accurate clinical indicators of right ventricular ischemia or necrosis.
1. There is acute myocardial infarction in the inferior, posterior and/or anterior wall.
2. Clinical manifestations and signs of right heart dysfunction such as jugular vein engorgement, hepatomegaly, positive Kussmaul sign, severe hypotension, shock, but clear auscultation of the lungs.
3. Conventional electrocardiogram and HC lead indicate that V3RV7R ST segment elevation is 1.0mm, and ST segment elevation of any one or several leads in V4RV6R is >1.0mm or more. The diagnosis of right ventricular myocardial infarction is Highly sensitive and specific.
4. Hemodynamics due to the right ventricular infarction atrial loss of blood transfer function, resulting in significant reduction in stroke volume and arterial blood pressure, central venous pressure increased, right atrial pressure > 9.35mmHg (0.98kPa) (10cmH2O); RVEDP PCWP (pulmonary wedge pressure 2mmHg (0.27kPa) or more; PAP (right atrial pressure) / PCWP> 0.65.
5. Two-dimensional echocardiography suggests abnormal right ventricular wall motion, right ventricular enlargement and right ventricular ejection fraction decreased.
6. Radionuclide cardiac and blood angiography, which is helpful for the diagnosis of right ventricular infarction.
7. The right ventricle of the chest radiograph is enlarged without obvious congestion.
8. Coronary angiography can be confirmed.
1. Acute pulmonary embolism can increase right heart pressure, PCWP is not high, which is similar to right ventricular infarction, but the pulmonary artery pressure of acute pulmonary embolism is significantly increased, which can be distinguished from the latter.
2. Pericarditis and pericardial effusion two-dimensional echocardiography can confirm the diagnosis of pericardial effusion, constrictive pericarditis, although the right heart pressure is increased, but the ultrasound can show a small right ventricular cavity, pericardial thickening, thus Easy to differentiate from right ventricular infarction.
3. Inferior wall myocardial infarction MI often causes hypotension due to vasovagal reflex. The main difference between hypoxia and right hypotension in right ventricular infarction is that the former has a lower right heart pressure, while the latter increases, and the left ventricular infarction causes a cardiac source. In sexual shock, hypotension and pulmonary congestion exist simultaneously, and PCWP is significantly elevated, which is different from right ventricular myocardial infarction.