bubble_chart Overview

Acute pericarditis is an acute inflammation of the visceral and parietal layers of the pericardium, sometimes accompanied by myocarditis and endocarditis.

bubble_chart Etiology

Acute pericarditis is almost always secondary, with some disease causes still unknown. Among them, nonspecific, subcutaneous nodule-related, purulent, and wind-dampness pericarditis are relatively common. Common pathogenic bacteria causing purulent pericarditis include pneumococcus, staphylococcus, and streptococcus. There are four pathways for infection to invade the pericardium: ① In cases of pneumonia and empyema, bacteria enter the pericardial cavity directly or via lymphatic pathways from the lungs and pleura. ② Septicemia caused by purulent infections such as boils, abscesses, and osteomyelitis allows pathogenic bacteria to enter the pericardial cavity through the bloodstream. ③ Chest trauma introduces bacteria into the pericardial cavity, and postoperative hemopericardium leads to infection. ④ Subphrenic or liver abscesses rupture through the diaphragm into the pericardial cavity.

bubble_chart Pathogenesis

Pericardial effusion increases the pressure within the pericardial cavity. When it reaches a certain level, it restricts the expansion of the heart, reduces ventricular diastolic filling volume, and decreases stroke volume. As the pressure in the pericardial cavity further rises and the stroke volume drops to a critical level, compensatory mechanisms fail. Elevated venous pressure can no longer increase ventricular filling or cardiac output per minute, leading to a decline in {|###|} pulse pressure and resulting in circulatory failure, which manifests as acute cardiac tamponade. The symptoms of cardiac tamponade depend on the rate of effusion {|###|} abdominal mass. If the effusion accumulates rapidly and the heart lacks compensatory capacity, cardiac tamponade may occur. During cardiac tamponade, the pulse intensity may significantly weaken or disappear during inspiration due to the following reasons: ① Pericardial effusion restricts right ventricular filling, reducing output and pulmonary venous return, thereby decreasing left ventricular filling; ② During inspiration, increased blood filling in the right ventricle enlarges its volume, causing the interventricular septum to shift backward, further reducing left ventricular volume and filling; ③ During inspiration, the descent of the diaphragm pulls on the pericardium, further increasing pericardial pressure and reducing left ventricular filling. These three factors sharply decrease left ventricular output, causing a drop in {|###|} pulse pressure and resulting in pulsus paradoxus.

bubble_chart Pathological Changes

The extent and characteristics of pericardial inflammatory reactions vary with the disease cause. The disease cause can manifest as fibrinous (dry) or exudative (wet). During acute episodes, the pericardial serous membrane becomes congested and edematous between the parietal and visceral layers of the pericardium, forming exudates composed of large numbers of white blood cells, endothelial cells, and fibrin. These may be localized or diffuse. As fluid increases in the exudate, it transitions into serofibrinous effusion, ranging from 100ml to 2–3L in volume. The appearance is typically yellow and clear but may become cloudy due to white blood cells and shed endothelial cells; occasionally, a higher red blood cell count gives it a bloody appearance. The effusion is usually absorbed within 2–3 weeks. The subpericardial myocardium may be affected, leaving small patches and varying degrees of adhesion after healing. If improperly treated, granulation tissue in the pericardium may organize, replaced by connective tissue or forming scars that constrict the heart, leading to constrictive pericarditis.

bubble_chart Diagnosis

(1) Symptoms In the early stages of infection, there may be shivering, fever, sweating, and general malaise. Later, pericarditis develops, with precordial pain localized to the precordial area and the lower part of the sternum, radiating to the left shoulder and back. Cardiac tamponade causes dyspnea, dysphoria, restlessness, cyanosis, and shock. Pericardial effusion compresses the lungs and trachea, restricting ventilation and exacerbating dyspnea.

(2) Signs The patient experiences shortness of breath and cannot lie flat, with distended neck veins, elevated venous pressure, rapid and weak pulse, paradoxical pulse, and decreased pulse pressure. The cardiac dullness border expands, heart sounds weaken, and pericardial friction rub may sometimes be heard. A large amount of pericardial effusion may lead to hepatomegaly, ascites, and lower limb edema.

(3) Laboratory Tests Purulent pericarditis shows an increased white blood cell count and neutrophilia. Serum aspartate aminotransferase and lactate dehydrogenase levels are normal or slightly elevated.

(4) X-ray Examination The cardiac shadow expands bilaterally, with weak pulsations under fluoroscopy. In the upright position, the pus or abdominal mass accumulates in the lower part of the pericardial cavity, causing the lower half of the cardiac shadow to widen, resembling a flask or pear shape. In the supine position, the pus is evenly distributed in the upper and lower parts of the pericardial cavity, making the heart appear spherical. Changes in body position can help differentiate it from cardiac enlargement.

(5) Electrocardiogram Low-voltage QRS waves, flattened or inverted T waves, and sometimes atrial premature beats, atrial tachycardia, atrial flutter, or atrial fibrillation may be observed.

(6) Ultrasound Examination Echocardiography can display the fluid level reflection of pericardial effusion and determine the volume and location of fluid in the pericardial cavity.

(7) Pericardial Puncture Examination Pericardiocentesis is a reliable method for diagnosing pericarditis. Approaches include the left parasternal route or the subxiphoid left costal margin route. The aspirated fluid should undergo bacteriological examination. If necessary, 100–200 ml of CO₂ can be injected into the pericardial cavity, followed by immediate X-ray examination to assess the size and thickness of the pericardial cavity and detect any masses protruding into it.

bubble_chart Treatment Measures

Prompt and effective treatment of acute pericarditis includes addressing the primary disease cause and symptomatic relief for cardiac tamponade, with the expectation of full recovery. Some cases may leave behind myocardial damage or progress to constrictive pericarditis.

(1) Systemic antibiotic therapy is generally employed, along with pericardiocentesis to drain pus and intrapericardial antibiotic injection. There are two puncture methods: ① Left parasternal approach: The patient is placed in a semi-recumbent position, with the left anterior chest sterilized and draped. Under local anesthesia, the puncture needle is inserted 2–3 cm from the sternum in the fourth or fifth left intercostal space. The needle is advanced posteriorly and medially while aspirating the syringe. Advancement stops once pus is aspirated to avoid injuring the heart and coronary vessels. Drainage should not be too rapid. After fluid removal, an appropriate amount of antibiotics can be injected into the pericardial cavity. ② Subxiphoid left costal margin approach: The patient is placed in a semi-recumbent position with a thin pillow under the lower back, sterilized and draped. Under local anesthesia, a 10 cm long puncture needle is inserted at the angle between the xiphoid process and the left costal margin. The needle is advanced upward, posteriorly, and medially at a 45° angle to the abdominal wall while aspirating the syringe until pus is withdrawn from the pericardial cavity. The left parasternal approach risks puncturing the pleural membrane, contaminating the pleural cavity, and potentially injuring coronary vessels, whereas the subxiphoid left costal margin approach is more convenient and safer. To prevent cardiac injury, an ECG chest lead can be clipped to the base of the puncture needle for continuous ECG monitoring. When the needle tip contacts the heart surface, the QRS complex inverts, and it normalizes upon needle withdrawal.

(2) Pericardial drainage: If pericardial effusion and toxemia symptoms do not improve after puncture and pus drainage, or if the pus is too thick for effective drainage, pericardiotomy and drainage should be performed. A left parasternal curved incision is made, and after resecting the fourth and fifth costal cartilages, the pleural membrane is pushed laterally. Before incising the pericardium, a confirmatory puncture is performed, followed by a cruciform incision to open the pericardial membrane and excise a piece for biopsy. After aspirating the pus, the finger is used to separate loculated abscesses, and a rubber drain is placed for pus drainage. Alternatively, subxiphoid pericardial drainage can be performed. With adequate drainage, healing typically occurs within 4–6 weeks.