The excess fluid from pericardial effusion can cause intense pressure on your heart and damage it. A pericardial cyst is a noncancerous, fluid-filled growth in the pericardium. This type of cyst is very rare, affecting only 1 in , people. However, if they press on your lungs or other structures in your chest, they can cause complications like inflammation or severe bleeding. Rarely , a pericardial cyst can lead to heart failure. Acute pericarditis starts suddenly and lasts only a few weeks.
Chronic pericarditis develops more slowly and can last longer. Usually pericarditis is mild and heals over time. Sometimes it will improve with plenty of rest. More severe pericarditis may need to be treated with medication or surgery to prevent it from damaging your heart. This buildup places pressure on your heart, which prevents it from filling and emptying properly. Cardiac tamponade is not the same as pericardial effusion, though it can be a complication of fluid buildup from pericardial effusion.
One sign of cardiac tamponade is a large drop in blood pressure. The pericardium is important because it protects the heart from trauma, shock, stress, and even infections from the nearby lungs.
The pericardium lubricates the heart and prevents it from becoming too large if blood volume is overloaded though it will not prevent chronic heart enlargement. Despite these functions, the pericardium is still vulnerable to problems of its own. Pericarditis is the term for inflammation in the pericardium, typically due to infection.
Pericarditis is often a severe disease because it can constrict and apply pressure on the heart and work against its normal function.
Pericarditis comes in many types depending on which tissue layer is infected. Learning Objectives Distinguish between the fibrous and serous layers of the pericardium. Key Points The pericardium is a mesothelium tissue of the thoracic cavity which surrounds the heart. The cause of acute pericarditis is often difficult to establish, and idiopathic pericarditis remains the most common diagnosis.
Most cases are presumed to have a viral etiology. Coxsackievirus B and echovirus are the most common viruses, and a fourfold increase in antiviral titers is required for the diagnosis. Patients often experience a prodrome of an upper respiratory tract infection. The prognosis of viral pericarditis is generally good, with a self-limited course, and if uncomplicated, patients may be treated on an outpatient basis.
Before the antibiotic era, pneumonia was the prime cause of purulent pericarditis. Currently, causes include thoracic surgery, chemotherapy, immunosuppression, and hemodialysis, as well as extension from pneumonia and empyema.
Presentation is usually acute with high fevers, chills, night sweats, and dyspnea, but the classic findings of chest pain or friction rub are rare. If purulent pericarditis is suspected, hospital admission, treatment with intravenous, broad-spectrum antibiotics and urgent drainage is recommended.
It remains the leading cause of pericarditis in some developing countries. A patient with suspected or diagnosed pericardial tuberculosis should be hospitalized and antituberculous therapy started promptly. A pericardial biopsy with acid-fast bacilli polymerase chain reaction testing is recommended for all patients with suspected tuberculous pericarditis.
However, a normal pericardial biopsy does not exclude the diagnosis. A large hemorrhagic effusion facilitated by impaired platelet function may occur, although tamponade is rare. Alternatively, a serous pericardial effusion related to fluid overload may occur. With both forms, initiation or intensification of hemodialysis is indicated, usually leading to improvement in 1 to 2 weeks.
Its development correlates with the extent of necrosis, is more common with anterior than inferior infarcts, and is associated with a higher 1-year mortality rate as well as a higher incidence of congestive heart failure. The diagnosis of post-MI pericarditis requires symptoms or a new pericardial friction rub; a pericardial effusion alone is nonspecific.
In addition to the typical ST elevation seen with acute pericarditis that may be difficult to differentiate from the actual MI in this setting, findings on the ECG are persistently positive T waves more than 2 days after MI or normalization of previously inverted T waves.
Dressler's syndrome typically occurs 2 to 3 weeks after MI or open heart surgery. An autoimmune component involving sensitization to myocardial self-antigens at the time of infarction is believed to be responsible. The fully expressed syndrome consists of pleuritic chest pain, fever, leukocytosis, and a pericardial friction rub. Pleural effusions or pulmonary infiltrates may be seen.
Pericarditis associated with malignancy is caused mainly by metastatic disease. Pericarditis is common in metastasized bronchogenic or breast carcinoma, Hodgkin's disease, and lymphoma Figure 3 ; it is rare in primary mesothelioma and angiosarcoma.
Recent or remote mediastinal radiation can cause pericarditis at any time from weeks to months after the exposure. Sharp or blunt trauma Figures 4 and 5 and invasive cardiac procedures such as electrophysiological ablation procedures, cardiac diagnostic, or interventional catheterization have been associated with pericardial irritation and inflammation. The diagnosis of acute pericarditis remains a clinical one based on history, physical examination, ECG and the echocardiogram. Other imaging studies, including computed tomography CT and magnetic resonance imaging MRI may be used in selected cases to investigate the pericardium.
The ECG in acute pericarditis has four consecutive stages Table 1. Stage 1, characterized by diffuse concave-upwards ST elevation and PR segment deviation in the direction opposite from the P polarity, is the most useful stage for the diagnosis of acute pericarditis Figure 6. The distinction between pericarditis and acute MI is difficult at times, but there exist several helpful electrocardiographic clues Table 2. Depending on presentation and clinical evaluation, additional blood testing may be necessary such as viral titers, blood cultures, thyroid-stimulating hormone, antinuclear antibodies, HIV serology, or QuantiFERON-TB assay.
The chest radiograph may be entirely normal unless there is a pericardial effusion causing cardiomegaly Figure 7A-B or there are changes caused by an underlying disease. Trans-thoracic echocardiography TTE is used to detect and evaluate for pericardial effusion and any concomitant cardiac disease. Assessment of regional wall motion abnormalities can help differentiate acute pericarditis from myocardial ischemia.
Echocardiography is essential in the presence of hemodynamic abnormalities, history of recent cardiac surgery, or if there is a clinical suspicion of a large or increasing pericardial effusion. Advanced imaging modalities are increasingly used in the diagnotic assessment of patients with acute pericarditis, and to help guide their management. Cardiac computed tomography CCT is useful to assess for loculated effusions and to evaluate for increased thickness of the pericardium, although these features are not diagnostic of acute pericarditis.
If there is clinical suspicion, CCT is useful in diagnosing the underlying etiology of acute pericarditis such as in the assessment of suspected malignancy-induced pericarditis. Inflammation of the pericardium produces characteristic changes that can be detected on cardiac magnetic resonance CMR imaging with very high sensitivity. Specifically, T2 weighted short-tau inversion recovery STIR imaging is useful for visualizing edema, while detection of a bright pericardium on late gadolinium enhancement LGE imaging is highly sensitive for pericardial inflammation Figure 8A-B.
Most cases of acute pericarditis are uncomplicated and self-limited, and may be treated on an outpatient basis. Indications for an advanced imaging modality, hospital admission, or both include clinical suspicion of a large effusion, hemodynamic instability, severe pain or other symptoms, suspicion of a serious underlying condition, or any other signs or symptoms of clinical instability or impending deterioration.
In acute idiopathic and viral pericarditis, the aim of treatment is the resolution of pain and inflammation. For other etiologies of acute pericarditis treatment of the underlying disease is the mainstay of therapy. Ibuprofen mg or indomethacin 50 mg every 8 hours for one to two weeks followed by a gradual taper until resolution of symptoms and inflammatory markers, in combination with colchicine 0.
Due to the risk of gastrointestinal toxicity, addition of gastrointestinal protection with a proton pump inhibitor is recommended in higher risk patient. Unless their use is mandatory, anticoagulants should be avoided during the acute phase of pericarditis to reduce the risks of intra-pericardial bleeding and tamponade.
Treatment with glucocorticoids should only be considered in recurrent pericarditis for patients with symptoms refractory to standard therapy, or in immune-mediated or uremic pericarditis. As with non-aspirin NSAIDs, steroids should be avoided in post-MI pericarditis due to their impairment of scar formation and a consequently increased incidence of myocardial wall rupture.
Patients with uncomplicated acute pericarditis should have regular follow-up after the initial visit to ensure resolution of symptoms and rule out the development of constrictive symptoms. The etiology of a pericardial effusion can often be deduced from the clinical presentation Box 1 ; for example, in patients who present with severe hypothyroidism, end-stage kidney failure, acute myocardial infarction, or who underwent a recent invasive cardiac procedure.
The relative frequency of different etiologies of pericardial effusions depends on the geography and the patient population.
The pericardial sac normally contains up to 50 mL of fluid; it can hold 80 to mL of fluid acutely, and even up to 2 L if the fluid accumulates slowly. Pericardial effusions may be asymptomatic unless associated with inflammation or tamponade physiology. Other symptoms arise from the compression of surrounding structures lung, stomach, phrenic nerve or diastolic heart failure and include chest pressure or pain, dyspnea, nausea, abdominal fullness, and dysphagia. Phrenic nerve irritation can cause hiccups.
With a small effusion, the physical examination is unremarkable. Larger effusions cause muffled heart sounds and, rarely, Ewart's sign dullness to percussion, bronchial breath sounds, and egophony below the angle of the left scapula.
Low voltage and electrical alternans Figure 9 may be seen if the effusion is large — the former due to increased distance from the chest leads, the latter caused by swinging of the heart within the effusion. These features in combination with sinus tachycardia should raise concern regarding the potential hemodynamic impact of the effusion and urgent assessment for tamponade physiology should be performed.
It is this fluid that provides lubrication between the two layers, and allows the heart to expand and contract. The classic picture of the way in which the serous pericardium works is if you push your fist into a balloon. The layer of rubber covering your hand is analogous with the visceral layer, the inside of the balloon is analogous to the pericardial cavity, and the outer layer of the balloon not in contact with your hand is equivalent to the parietal pericardium. Pericarditis is an inflammation of the serous pericardium of the heart.
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