constrictive pericarditis
Introduction
Introduction to constrictive pericarditis Constrictive pericarditis is caused by various causes of pericardial edema, parietal inflammation, fibrinous exudate deposition, and gradually thickening, contracture and even calcification, oppression of the heart and large blood vessels, resulting in limited diastolic filling. This leads to a series of circulatory dysfunctions such as right atrium, increased vena cava pressure and decreased cardiac output. The most common cause of inflammation in China is tuberculosis and suppurative infection, followed by mold or viral infection. basic knowledge The proportion of illness: 0.01% - 0.05% Susceptible people: no special people Mode of infection: non-infectious Complications: cirrhosis, arrhythmia, myocardial ischemia, thrombosis
Cause
Cause of constrictive pericarditis
Causes:
Clinically, constrictive pericarditis can sometimes be seen from the development of acute pericarditis, but in most cases, the onset of the acute stage is concealed and difficult to find, so it has become constrictive pericarditis at the time of treatment and lost its original pathological features. It is often difficult to determine the cause. In the affirmative cause, idiopathic pericarditis is the main cause of constrictive pericarditis in Europe, America and Japan, but tuberculosis is the first in China, followed by suppurative and traumatic; In recent years, it is considered non-specific, uremic, lupus erythematosus can also cause constrictive pericarditis, tumor, radiotherapy and open heart surgery caused by constrictive pericarditis increased year by year, occasionally schistosomiasis, amoeba Reports of constrictive pericarditis caused by pericardial hemorrhage after parasitic infection, pericardial foreign body, chyle pericarditis, cholesterol pericarditis, dialysis treatment, kidney transplantation and anticoagulant therapy.
(two) pathogenesis
1. Pathological anatomy
The shape of the heart of constrictive pericarditis is generally in the normal range or occasionally reduced. Pericardial lesions often involve the subepicardial myocardium. In severe cases, myocardial atrophy, fibrosis, fatty infiltration and calcification, pericardial visceral and wall layers are widely adhered. Pericardial thickening is generally 0.3 ~ 0.5cm, or even 1cm or more, often accompanied by calcification, the pericardial cavity is sometimes completely filled with fibrous tissue into a fibrous scar tissue shell, tightly wrapped and oppressed the entire heart and large blood vessel roots, can also It is limited to certain parts of the surface of the heart. In most patients, the scar tissue is mainly composed of dense fibrous tissue, which is spotted or flaky glassy, and there is no characteristic pathological change of the primary lesion. Some patients have pericardium. The tuberculous or suppurative granulation tissue can be found to provide a basis for the diagnosis of the cause. If the outer fibrous layer is wrapped and the concentrated blood components and liquids are present, it indicates that the pericardial hemorrhage is an important factor for the formation of pericardial constriction.
2. Pathophysiology
The typical constrictive pericarditis, which is replaced by hard fibrous tissue due to the loss of elasticity of the pericardium, forms a fixed-sized heart shell that compresses the heart, limiting the diastolic filling of all heart chambers and increasing the venous pressure due to the pericardium. It is evenly narrowed, and the diastolic blood pressure of the four heart chambers is equally increased, which is equivalent to the emffusion of the pulmonary arterioles, and the venous pressure is increased. In the early stage of ventricular diastolic, the blood flows into the ventricle abnormally rapidly, but in the middle and late stages of ventricular diastolic Ventricular dilatation is suddenly limited by the loss of elastic pericardium, filling is blocked, the pressure in the ventricular chamber rises rapidly, and the blood impacts the ventricular wall and forms a vortex to generate vibration, so that the early extra audible sound during the auscultation can be heard. The full filling of the constrictive pericardial ventricle is completed early in diastole. This abnormality of left and right ventricular diastolic filling is characterized by a characteristic left and right ventricular pressure curve on the pressure curve confirmed by the cardiac catheter. Root pressure curve.
Another significant abnormality of constrictive pericarditis is that during breathing, changes in chest pressure cannot be transmitted to the pericardial cavity and the heart chamber. Therefore, when inhaling, the peripheral vein and right atrial pressure do not fall, and the vein enters the right atrium. The blood does not increase, which is the opposite of normal people and heart tamponade.
Due to abnormal ventricular filling, increased venous pressure, decreased cardiac output, and accelerated compensatory heart rate, but when physical activity is increased, heart rate cannot be further accelerated, cardiac output cannot meet the needs of the body, and clinical difficulty in breathing and blood pressure drop; At the same time, the kidney water and sodium retention, further increase the venous pressure, clinically there are large liver, lower extremity edema, ascites and pleural effusion.
In constrictive pericarditis, myocardial contractile function is generally normal or close to normal, but in severe cases or in advanced disease, myocardial ischemia, myocardial fibrosis, myocardial atrophy may cause hypofunction of contraction due to superficial coronary artery pressure in the pericardium. At this time, the pericardial resection is not effective.
Prevention
Constrictive pericarditis prevention
prevention:
Pericardial stripping surgery should be performed early, and most patients can achieve satisfactory results. The longer course of the disease may be due to myocardial atrophy and cardiogenic cirrhosis, and the prognosis is poor. If left untreated, the condition deteriorates, and a small number of cases are chronically ill, and life and work are severely restricted. For patients with tuberculosis, anti-tuberculosis treatment is also needed.
1. Prepare the work according to the patient's condition before surgery. Such as limiting sodium salt, appropriate application of diuretics (furosemide, hydrochlorothiazide), maintaining water and electrolyte balance, strengthening nutrition, supplementing protein, vitamins, small amount of blood transfusion or plasma, anti-tuberculosis treatment for tuberculosis patients, and appropriate removal of pleural effusion.
2, the surgical path is often used for mediastinal sternal approach or left anterior thoracotomy. In severe cases, the operative mortality rate is high, and about 75% of deaths die from acute or subacute heart failure. Therefore, strict root volume after surgery, proper cardiac support is still an important part of the success of the operation.
3, the generally thickened pericardium binds the heart, the whole body is bruised, and there are signs of jugular vein engorgement, hepatomegaly, ascites, pleural effusion and so on. Tuberculous pericarditis can develop symptoms 3 to 6 months after the acute phase. Common fatigue, shortness of breath, oliguria, bloating, loss of appetite, ascites, liver enlargement, systemic edema, increased breathing difficulties.
Complication
Constrictive pericarditis complications Complications cirrhosis arrhythmia myocardial ischemia thrombosis
Chronic cardiac tamponade, cardiogenic cirrhosis, pulmonary stenosis, arrhythmia, myocardial ischemia, atrial thrombosis and protein-losing enteropathy can be seen.
1, chronic cardiac tamponade
The pericardium of constrictive pericarditis increases stiffness due to chronic inflammation, and the pericardium can not expand, so that the pericardial pressure and intracardiac pressure are significantly increased. Once the pressure in the pericardium reaches the right atrial and right ventricular diastolic blood pressure level, the heart crosses. The wall pressure drops close to zero and a pericardial tamponade occurs.
2, cardiogenic cirrhosis
Accounted for 16.6% of all cardiac sclerosis; due to chronic constrictive pericarditis, hypertrophy, stiff pericardium limits cardiac filling, elevated right ventricular diastolic pressure and right atrial pressure, blocked by hepatic venous return, blood flow in the hepatic vein The sinus stay time is delayed, and the cardiac output is reduced, the blood oxygen saturation is reduced, and the oxygen content in the central area of the hepatic lobules is further reduced. The hepatocytes in this area are atrophied and disappear, and the collapse of the intrahepatic reticular scaffold and fibrous tissue hyperplasia are slowly formed. With the prolongation of time, fibrosis develops to adjacent leaflets and connects with adjacent fibrous tissue around the central vein, surrounding the original portal vein region, forming an abnormal lobule, which is considered to be cardiogenic cirrhosis. Pathological features, hepatic hypoxia during constrictive pericarditis is slow and incomplete, so no acute extensive necrosis or massive necrosis occurs, the inflammatory response is light, no obvious hepatocyte proliferation.
3, pulmonary artery stenosis
Chronic constrictive pericarditis, because the site of the four aneurysms of the heart (the atrioventricular sulcus) is the site with the greatest degree of cardiac motility. At the pericarditis, the pericardial wall and the visceral layer have the largest friction, so the inflammatory response is strong. Fibrosis, calcification, and even the banding of the heart reduce the systolic and diastolic function of the heart. Therefore, chronic constrictive pericarditis can have clinical manifestations and hemodynamic changes similar to pulmonary stenosis.
4, arrhythmia
Sympathetic nerve excitation, atrial enlargement, epicardial inflammation, myocardial ischemia and mechanical compression, etc., mostly atrial arrhythmia, sinus tachycardia, early ventricular, can also be complicated by bundle branch block.
5, myocardial ischemia
Pericarditis can be complicated by myocardial ischemia, which is due to:
1 Coronary artery spasm: may be related to the decrease in the concentration of prostacyclin with dilated vasodilation in the pericardial cavity during pericardial coronary artery and pericardial effusion.
2 thickening, calcified pericardium compression of the coronary artery.
3 coronary blood flow decreased during cardiac tamponade.
4 toxic effects of drugs on the myocardium.
6, atrial thrombosis
Chronic constrictive pericarditis, due to a significant enlargement of the atrium, limited ventricular filling, slow atrial blood flow, plus easy to atrial fibrillation caused by blood siltation in the atria, easy to form thrombotic complications, thrombosis can almost fill the entire atrium To the extent that the patient can present with symptoms of pulmonary or systemic embolism, multiple episodes can be repeated.
7, protein loss enteropathy
In chronic constrictive pericarditis , systemic venous pressure increases, intestinal lymphatic vessels expand due to reflux obstruction, lymph fluid leaks into the intestinal lumen, protein or chylomicrons in the lymph fluid are lost, resulting in the loss of a large amount of protein, patient performance For severe edema, bloating, diarrhea and other gastrointestinal symptoms as well as general malaise, anemia, convulsions and other systemic manifestations.
Symptom
Constrictive pericarditis symptoms common symptoms squatting jugular venous dyspnea dyspnea cardiogenic respiratory distress calcification angiography see double ball scutellaria ascites spleen function hyperthyroid edema
1, symptoms
The main symptoms of constrictive pericarditis are abdominal distension and lower extremity edema, which is related to increased venous pressure. Although there is difficulty in breathing or sitting breathing, it is not caused by cardiac dysfunction, but is caused by ascites or pleural fluid pressure. In addition, patients often complain of fatigue, loss of appetite, upper abdominal fullness and so on.
2, signs
1 low blood pressure, fast pulse, 1/3 occurrence of odd pulse, 30% and atrial fibrillation.
2 venous pressure increased significantly, even after diuretic venous pressure remained high, jugular vein engorgement, more obvious when inhaling (Kussmaul sign), early collapse of jugular jugular vein collapse (Freidreich sign), Kussmaul sign and Freidreich Signs are non-specific signs, cardiac tamponade and severe right heart failure for any reason, can be seen.
3 visual examination of the heart see systolic apical retraction, early diastolic apex beat, palpation with diastolic pulsation impact, percussion heart rhythm sound normal or enlarged, sternal left margin 3 ~ 4 intercostal hearing pericardial slap sound, no noise .
4 other signs: such as jaundice, lung bottom wet voice, liver, ascites more obvious than lower extremity edema, similar to cirrhosis.
Type
The length of time that the pericardial stenosis is different is different. Usually, the acute pericarditis develops into a pericardial constriction within one year after the occurrence of acute pericarditis, and the acute constriction is called chronic constriction. The evolution process has three forms:
1 continuous type, acute pericarditis after a few days of systemic reaction and symptoms, such as fever, chest pain, etc. can be gradually relieved, or even completely disappeared, but the liver venous, jugular vein engorgement and other venous congestion signs are not reduced, but In such patients, it is difficult to determine the boundaries between the acute phase and the constricted phase. This is related to the fact that the exudate is absorbed, and the pericardial thickening and narrowing are almost simultaneously related, so it is difficult to distinguish the boundaries of the two phases.
2 intermittent type, the symptoms and signs of the acute phase of pericarditis can completely disappear in a certain period of time, the patient thinks that the lesion has healed, but after a few months, the symptoms and signs of pericardial constriction reappear, which is slower than the pericardium, in the longer time It is related to the formation of narrowing inside.
3 slow-up type, the clinical manifestations of acute pericarditis in this type of patients are mild or even no history, but there are progressive fatigue, weakness, abdominal distension, lower extremity edema and other symptoms, pericardial constriction within 1 to 2 years.
Examine
Constrictive pericarditis
Laboratory inspection
There may be mild anemia, long-term disease due to liver congestion often liver function damage, plasma protein, especially albumin decreased, ascites and pleural effusion are often leakage, venous pressure is significantly increased.
Film degree exam
1, ECG examination
QRS wave low voltage, T wave flat or inverted, both of which are strong evidence for the diagnosis of constrictive pericarditis, ECG changes often indicate the extent and extent of myocardial involvement, 50% of P wave widening has a notch Less than half of the patients have atrial fibrillation, and atrioventricular block and indoor bundle branch block are less common. Wide Q-waves are seen in extensive pericardial calcification, and about 5% of patients have right ventricular outflow tract due to pericardial scar. Room hypertrophy with right axis deviation.
2, X-ray inspection
Pericardial calcification is the most reliable X-ray sign of acute pericarditis. It is seen in most patients with constrictive pericarditis. It is often incompletely ring-shaped, and the size of the heart is normal. Some patients are slightly increased. It may be related to pericardial effusion or pericardial thickening. Some patients have a triangular or spherical shape, and the heart shadow becomes straight or forms an abnormal heart arch. If the aortic node is narrowed or concealed, the left and right atrium, right ventricle or pulmonary artery conus is enlarged. The superior vena cava dilatation, etc., X-ray fluoroscopy see the heart beat weakened or disappeared, the thickest part of the pericardium is obvious, also visible widening of the hilar, pulmonary edema, pleural thickening or pleural effusion.
3, ultrasound examination
Although echocardiography can be seen in pericardial thickening, there is no specific index for the diagnosis of constrictive pericarditis. M-mode echocardiography can show that the thickened pericardium consists of two parallel lines, at least between the visceral and parietal pericardium. 1mm clear clearance, it can be seen that during the early diastolic atrial contraction, the ventricular septum suddenly moves backwards, which overlaps with the pericardial slamming sound. The two-dimensional echocardiogram shows that the ventricular cavity is limited, the atrium is normal or slightly larger, and the pericardium Echo enhancement, inferior vena cava dilatation, fixed heart shape, and atrioventricular valve activity; when the rapid to slow filling transition period, see ventricular filling suddenly stopped, increased blood flow during inhalation, due to right ventricular diastolic restriction The interventricular septum is pushed to the left.
4, CT and MRI examination
CT examination has a high specificity and resolution for pericardial thickening. It can evaluate the shape of the pericardium and the shape of the great vessels of the heart, such as vena cava dilatation, left ventricular posterior wall fibrosis and hypertrophy, etc., which is suspicious narrowing. The valuable detection method of pericarditis, MRI can clearly show that the characteristic change of constrictive pericarditis is pericardial thickening, can accurately measure its thickness, determine its involvement range, and can show the heart caused by restricted diastolic function. Abnormal changes in vascular morphology and internal diameter, such as right ventricular outflow tract stenosis and hepatic vein, inferior vena cava dilation.
5, cardiac catheterization
For suspected constrictive pericarditis, cardiac catheterization helps:
1 proves that the diastolic filling pressure is increased;
2 understand the impact of narrowing the pericardium on stroke volume and cardiac output;
3 evaluation of myocardial contractile function;
4 Identification of constrictive pericarditis and restrictive cardiomyopathy;
5 Excluding the pericardial fibrosis caused by coronary artery compression, patients with constrictive pericarditis, the left and right heart pressure curves can be recorded simultaneously by left and right cardiac catheters, right heart catheterization shows pulmonary arterial pressure, pulmonary artery diastolic pressure, right Ventricular end-diastolic pressure, right atrial mean pressure and vena cava pressure were significantly increased and tend to be equal, cardiac output decreased, right atrial pressure curve showed M or W waveform, increased and almost equal a wave, V wave and deepened The Y-wave and normal X-wave formation; the right ventricular pressure curve shows the plateau wave at the early stage of diastolic sag and late diastole, ie the root square curve (Fig. 3).
Cardiac catheterization can also carefully record the increase in right atrial pressure curve after breath holding, and also help to identify the difference in hemodynamics between constrictive pericarditis and restrictive cardiomyopathy and cardiac tamponade, constriction Pericarditis and cardiac tamponade, both have increased right and left ventricular diastolic blood pressure, decreased cardiac output and stroke volume, normal or decreased left ventricular end-diastolic volume, and limited diastolic filling, but both have Significantly different hemodynamic characteristics, prominent manifestations of cardiac tamponade are:
1 obvious odd pulse.
2 When the inhalation, the right atrial pressure drops significantly.
3 The pressure in the pericardial cavity is increased.
4 The right atrial pressure curve shows the advantage of X drop, and the Y drop is absent or smaller.
5 The right and left ventricular pressure curve showed early diastolic decline, and the diastolic stage showed plateau waveform. If the right ventricular systolic pressure increased significantly >60 mmHg, or the left ventricular diastolic pressure was more than 5 mmHg at rest or exercise, more Supporting restrictive cardiomyopathy, however, in some restrictive cardiomyopathy, left and right ventricular diastolic blood pressure is in equilibrium, and hemodynamics during rest or exercise are difficult to differentiate from constrictive pericarditis.
Diagnosis
Diagnosis and differentiation of constrictive pericarditis
Diagnosis of constrictive pericarditis
History of pericardial disease, combined with jugular vein bulging, hepatomegaly, ascites, but the heart is not big, the heart sound is far away with pericardial squeaking sound, can initially establish the diagnosis of pericardial constriction, and then chest X-ray examination found pericardial calcification, ECG A low-voltage and T-wave change can be used to determine the diagnosis. For atypical cases, cardiac catheterization can be performed to obtain an intracardiac pressure curve to aid diagnosis.
Differential diagnosis
1, cirrhosis, portal hypertension, ascites
Although the patient had hepatomegaly, ascites and edema, similar to constrictive pericarditis, but no jugular vein engorgement and peripheral venous pressure increased, no odd pulse, normal apex beat; esophageal stenosis showed esophageal varices; liver Functional impairment and hypoproteinemia.
2, pulmonary heart disease
Jugular vein engorgement during right heart failure, hepatomegaly, ascites, edema, need to be differentiated from constrictive pericarditis, pulmonary heart disease has a history of chronic respiratory disease; breathing difficulties at rest; two lungs wet voice; inhalation Jugular vein subsidence, Kussmaul sign negative; blood gas analysis hypoxemia and compensated or non-compensatory respiratory acidosis; ECG right ventricular hypertrophy; chest X-ray film see coarse lung texture or pulmonary congestion, right lower pulmonary artery segment widened, Heart shadows tend to expand, etc., and can be differentiated from constrictive pericarditis.
3, heart valve disease
Localized pericardial constriction due to the constriction limited to the atrioventricular sulcus and large vessel entrance and exit can produce signs similar to valvular disease and vena cava obstruction, such as narrowing confined to the left atrioventricular sulcus, forming an external pressure atrioventricular access Stenosis, signs and hemodynamic changes resemble mitral stenosis. Rheumatic heart disease mitral stenosis may have a history of rheumatic fever without a history of pericarditis. Heart murmurs exist for a long time. Echocardiographic mitral thickening Or wall-like changes, limited valve activity and the left ventricular posterior wall in the same direction, chest X-ray examination, normal heart beat without pericardial calcification, cardiac catheterization, constrictive pericarditis has a characteristic pressure curve, combined with the heart Angiography facilitates the identification of congenital or acquired acquired valvular disease.
4, heart failure
Patients often have valvular heart disease or other types of heart disease. Although there is an increase in jugular vein engorgement and venous pressure, the Kussmaul sign is negative; the heart is enlarged or accompanied by murmur of heart valve disease; and the lower extremity edema is more obvious than the ascites. .
5. Restricted cardiomyopathy
Primary or secondary restricted cardiomyopathy due to infiltration of the endocardium and myocardium or fibrosis of the heart, loss of myocardial compliance causes ventricular diastolic filling limitation, hemodynamics and clinical manifestations similar to constrictive pericarditis Differential diagnosis is extremely difficult (Table 1). Because of the different treatment methods, the prognosis is completely different, so the differential diagnosis is very important. If it is difficult to identify, the diagnosis can be confirmed by open chest exploration.
