chronic constrictive pericarditis
Introduction
Introduction to chronic constrictive pericarditis Chronic constrictive pericarditis is a disease caused by chronic pericardial inflammation, which is caused by pericardial thickening, adhesion and even calcification, which causes diastole, limited contraction, and decreased heart function, causing systemic blood circulation disorders. Mainly manifested as labor dyspnea, liver and ascites. X-ray examination of common pericardial calcification, echocardiography showed pericardial thickening, calcification and double room enlargement. The main treatment is to perform surgery as soon as possible to relieve the restraint of the pericardium on the myocardium. basic knowledge The proportion of illness: 0.001% Susceptible people: no special people Mode of infection: non-infectious Complications: electrolyte imbalance, arrhythmia, acute renal failure
Cause
Causes of chronic constrictive pericarditis
Tuberculosis infection (85%):
The main cause of chronic constrictive pericarditis is tuberculosis infection, bacteriological and histological examination confirmed that tuberculosis is 30%, about 50% of cases can not identify the cause of disease, but many cases are because of long-term anti-tuberculosis drugs Treatment, in the occurrence of pericardial constriction, evidence of tuberculosis has disappeared, therefore, it is believed that most of these cases are tuberculous pericarditis.
Suppurative infection (10%):
Followed by suppurative infection, traumatic and non-traumatic pericardial effusion caused by contraction of pericarditis accounted for about 10%, in recent years, the number of patients with this disease increased after cardiac surgery.
pathology
The main pathophysiological changes of constrictive pericarditis are due to the narrowing of the pericardium, which limits the normal activities of the bilateral ventricles. In the early stage of the disease, the main manifestations of ventricular diastolic diastolic relaxation are limited. As the disease progresses, the middle diastolic phase is also significantly affected. During left ventricular diastolic, intraventricular pressure increased rapidly, left and right ventricular reflux blood blocked, venous pressure increased, manifested as jugular vein engorgement, hepatomegaly, ascites, pleural effusion and systemic edema, a small number of patients may have splenomegaly Large, heart discharge is slightly lower than normal, stroke volume is significantly reduced, during physical activity or when severely narrowed, mainly by increasing heart rate to maintain cardiac output per minute, appearing in the atrioventricular sulcus and large blood vessels When the ring is narrowed, it can produce the murmurs and signs of the valve dysfunction in the corresponding part. The degree of ascites and surrounding edema is disproportionate. It is a major feature of this disease. The mechanism of ascites production has the following three points:
1 liver reflex congestion, obstruction of hepatic venous return.
2 Pericardial adhesions on the diaphragm surface affect lymphatic drainage.
3 plasma albumin decreased.
Prevention
Chronic constrictive pericarditis prevention
The pericardial stripping surgery should be performed as early as possible. Most patients can get satisfactory results. The longer course of the disease may be due to myocardial atrophy and cardiogenic cirrhosis, and the prognosis is poor. If the patient is not treated by surgery, the condition deteriorates, and a few cases have long-term illness. Life and work are severely restricted, and anti-tuberculosis treatment is needed for patients with tuberculosis.
Complication
Chronic constrictive pericarditis complications Complications electrolyte disorder arrhythmia acute renal failure
Common complications and postoperative complications of this disease include low cardiac output, electrolyte imbalance, arrhythmia, acute renal failure, hemorrhage, etc. Once these complications occur, they should be treated promptly.
(1) Due to chronic contraction of the pericardium, the pericardium binds the heart for a long time, leading to myocardial atrophy, prone to low cardiac output, and adequate diuresis in the early postoperative period. After avoiding pericardial exfoliation, a large amount of peripheral fluid deposits into the heart, aggravating cardiac load; Limiting the amount of liquid, especially crystals, strictly limits the rapid rehydration in a short period of time to prevent low cardiac output due to excessive capacity overload.
(2) Postoperative central venous pressure test, under the premise of maintaining the circulation, try to make CVP at a low level. Due to a large amount of diuretic, be highly alert to low potassium and low magnesium, pay attention to timely supplement electrolyte and prevent arrhythmia.
(3) The disease is associated with the risk of acute renal failure, so the appropriate application of vasodilators can reduce the burden on the heart, especially in the early postoperative period.
(4) The disease is easy to complicated with pulmonary complications, so proper ventilator assist is especially important for patients with moderate to severe disease and those with pulmonary complications.
Symptom
Chronic constrictive pericarditis symptoms Common symptoms Difficult bloating bloating end sitting breathing liver enlargement Pericardial fiber thickening splenomegaly pleural water ascites shortness of fatigue
First, clinical symptoms
The generally thickened pericardium binds the heart, the whole body is bruised, and there are signs of jugular vein engorgement, hepatomegaly, ascites, pleural effusion, etc. Tuberculous pericarditis can develop symptoms 3 to 6 months after the acute phase, often with fatigue. Shortness of breath, low urine, bloating, loss of appetite, ascites, liver enlargement, systemic edema, increased difficulty in breathing.
Half of the patients had slow onset, unconsciously developed symptoms, and no history of acute pericarditis. About 30% of patients had a history of acute pericarditis a few months ago, and gradually worsened after treatment symptoms were relieved. First, the elderly for more than ten years, most patients have a history of one and a half to two years in the main symptoms and a clear diagnosis, the main symptoms are dyspnea, bloating, peripheral edema, fatigue and cough, all Patients have different levels of dyspnea, mild physical activity is shortness of breath, severe cases can be expressed as sitting breathing, dyspnea is mostly caused by decreased pleural effusion or ascites with diaphragmatic muscles, although pulmonary venous pressure Increased, but pulmonary interstitial edema rarely occurs, therefore, paroxysmal nocturnal dyspnea and acute pulmonary edema are relatively rare, abdominal distension is caused by liver, ascites and visceral congestion, renal blood flow is reduced, body water and Sodium retention, resulting in peripheral edema, mostly manifested as ankle edema, and may have palpitations, fatigue, loss of appetite and upper abdominal discomfort In addition, cough and chest pain are more common.
In addition to the heart, the lungs, liver, spleen and other organs may have passive hyperemia and fibrotic changes, similar to changes caused by long-term heart failure.
Second, physical signs
The patient presented with chronic disease, facial edema, superficial vein filling, and jugular vein engorgement. The Friedreich sign was observed, that is, the jugular vein pulsation showed early diastolic depression. When the narrowing seriously affected the right ventricular return blood flow, it can be observed when inhaling. Obvious to the jugular vein engorgement (Kussmaul sign), such as the amount of pleural effusion, the rib space can be widened, half of the patients with apical beats weakened or disappeared, the heart boundary percussion is normal or slightly increased, and sometimes the apex can be observed during systole The area on the left side of the sternum and the left side of the sternum showed a retractive change, while in the early stage of diastole, there was a rapid outward movement and a rapid heart rate. About 2/3 of the patients could hear the third heart sound in early diastole due to rapid filling of the early ventricular diastole. The patients have abdominal distension, liver enlargement, ascites sign positive, about 10% of patients have splenomegaly, normal or low blood pressure, showing decreased systolic blood pressure, increased venous pressure, prolonged circulation time, patients often There is a strange pulse, the pulse is weakened or unclear when inhaling. The sphygmomanometer measures that the systolic pressure during inhalation is 10mmHg lower than that of exhalation. Some people think that the above change is a thickened pericardium. Muscle adhesions secured together, pulling the diaphragm down inspiratory pericardium, the tension increases and cardiac filling limit, thus the cardiac output is smaller, resulting in decreased systolic blood pressure.
The pericardium is generally thickened, but the degree of thickening of different parts is inconsistent. The bilateral ventricular manifestations and facial pericardial thickening are more significant. The thickened pericardium is composed of fibrous tissue, and the deposition of calcium salts can form plaque or strip calcification. It can also form a complete bony shell. The early pericardial cavity can have effusion, and a thin layer of cellulose or fibrous tissue is attached to the epicardium. As the disease progresses, the visceral layer of the pericardium gradually develops into a slight adhesion. , tightly adhered, or even tightly fused, the latter has no obvious interface between the pericardial visceral layer, thickened pericardium can adhere to the diaphragm, pleura and mediastinal structure, early constrictive pericarditis occurs subepicardial myocardial atrophy, late Extensive atrophy, ventricular wall thickness is significantly thinner than normal, but also due to chronic inflammatory infiltration, focal myocarditis, partial myocardial fibrosis, in a few cases, annular stenosis can occur in the atrioventricular groove.
Examine
Chronic constrictive pericarditis
The examination methods that are helpful in the diagnosis of this disease are:
(1) Electrocardiogram examination: all patients have abnormal electrocardiogram, but no specific ECG changes. Most patients have ventricular complex wave low voltage, about 70% of patients have P wave abnormality, P wave broadens or P wave has notch Or both, T wave is low or inverted, 1/3 to 2/3 patients have atrial arrhythmia, and 75% of atrial arrhythmias are atrial fibrillation.
(2) Echocardiography: visible thickening or adhesion of the pericardium, echo enhancement; left ventricular wall diastolic middle and late movement in a straight shape; early mitral valve closure; pulmonary valve opening in advance; abnormal ventricular septal motion The ventricular end diastolic diameter is reduced. Some people think that the early rapid filling of ventricular diastolic is the evidence for the diagnosis of pericardial constriction, and the inferior vena cava is abnormally dilated.
(3) X-ray examination: the heart image of the heart is normal or slightly larger, or smaller, the outline of the heart is irregular, stiff, and the upper mediastinum is widened, which is caused by the expansion of the superior vena cava. The surrounding lung field is clear, 50%-90 Percent pleural effusion, such as unilateral pleural effusion without mediastinal shift, is an important sign of constrictive pericarditis. Pericardial calcification is also the main evidence of X-ray changes. Coexistence with clinical features can confirm the diagnosis, calcification The site is widely characterized. About 70% of patients have signs of calcification. Common calcifications are coronary sulcus, the right ventricular septum and sternal surface, and the left ventricular surface except the apex. X-ray faults also help to define pericardial calcification.
(4) CT and magnetic resonance: can clearly show the degree of pericardial thickening, the positive rate accounts for about 80%, high-speed CT (UFCT) is more accurate, magnetic resonance is the best non-invasive examination for the diagnosis of constrictive pericarditis, Accurate measurement of pericardial thickness and extent of right atrial dilation and right ventricular dilation.
(5) Cardiac catheterization: If the non-invasive examination method is not clearly diagnosed, right heart catheterization can be performed. The equal pressure of the right atrium, pulmonary artery and left atrium at the end of diastole is a sign of diagnosis of the disease, and the right ventricle is pressed. Early diastolic rapid decline, followed by rapid increase, and then in the diastolic, late pressure is flat, called the "square root sign" (squareroot sign), also supports the diagnosis of this disease.
(6) Laboratory examination: Some patients may present with severe hypoproteinemia and have anemia changes. Individual cases may have abnormal liver function and jaundice.
Diagnosis
Diagnosis and differentiation of chronic constrictive pericarditis
diagnosis
According to the patient's dyspnea, hepatomegaly, ascites, increased venous pressure, reduced pulse pressure difference and odd pulse, peripheral edema and other clinical manifestations, plus X-ray examination, ECG and echocardiography and other auxiliary methods, generally A correct diagnosis can be made.
Differential diagnosis
1. Congestive heart failure in the past history of heart disease, heart enlargement, heart valve murmur often, lower extremity edema and relatively low abdominal distension, venous pressure decreased significantly after diuretics, and diuretic used in chronic constrictive pericarditis It has little effect on venous pressure.
2. Portal hypertension with cirrhosis or hepatic vein thrombosis may have hepatomegaly and/or ascites. According to clinical symptoms and head, the upper extremity venous pressure is increased, which is easy to differentiate from constrictive pericarditis. In patients with portal hypertension, esophageal barium meal examination was performed, and the lower esophageal varices were seen.
3. Patients with primary cardiomyopathy with dilated cardiomyopathy can see a marked increase in the heart, apical beats to the left, auscultation of the mitral or tricuspid valve may have systolic murmur, ECG left ventricular hypertrophy or left bundle branch conduction resistance Hysteresis, or pathological Q wave and T wave inversion, the X-ray heart image expands to the sides, especially in the left ventricle, the pulsation is weakened, the superior vena cava is not dilated, and the right ventricular and biventricular type restricts cardiomyopathy and constriction. The hemodynamic changes and clinical manifestations of pericarditis are quite similar, but the restrictive cardiomyopathy echocardiography can have myocardial, endocardial characteristic thickening and reflex enhancement, chamber narrowing and apical occlusion. Identification, a small number of patients after a comprehensive examination, the diagnosis is still difficult to determine, you can re-do the pericardial biopsy, through the left fifth intercostal space to do all the mouth, remove a pericardium for pathological examination, such as confirmed constrictive pericarditis, The original incision can be enlarged for pericardectomy.
4. Tricuspid stenosis with characteristic murmur and related valvular lesions (aortic valve and mitral valve), jugular vein without early diastolic depression, Doppler ultrasound and tricuspid diastolic transvalvular pressure gradient, With tricuspid regurgitation, systolic jugular pulsation, hepatic pulsation and full systolic murmur can occur.
