8.1: Pericardial Disease - Acute
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An increase in intrapericardial pressure, resulting in compression of the heart, and thereby a resitriction of cardiac inflow, is termed cardiac tamponade. Tamponade may result from pericardial effusion of any cause. The intrapericardial pressure importantly determines to what extent cardiac inflow is decreased, but two factors need to be taken into consideration. First, intrapericardial pressure is determined not only on the amount of fluid that accumulates, but also on the rate with which this accumulation proceeds, and the available distensibility of the pericardium. Chronic effusions may therefore lead to small increases in intrapericardial pressures in the presence of large fluid accumulations, and small accumulations may directly lead to severe cardiac tamponade for example after free wall rupture. Second, the intravascular volume and intra-atrial, and -ventricular pressures determine at what pressure inflow becomes impaired. When intrapericardial pressure exceeds right atrial pressure (approximately 8 mmHg), tamponade typically follows. However, in patients in whom intra-atrial pressure is decreased, for example due to volume depletion, tamponade may already occur at lower intrapericardial pressures; low-pressure cardiac tamponade.
With increasing intrapericardial pressure, clinical features increase with severe hemodynamic compromise as its end stage. First, small changes in intrapericardial pressure induce subtle changes in arterial pressure, cardiac output, and variations in arterial pressure with inspiration (pulsus paradoxus). When intrapericardial pressure reaches levels similar to right atrial and diastolic right ventricular pressure echocardiographic evidence of tamponade may be found in diastolic collapsing of the right atrium, and increased variations of blood flow velocity over the cardiac valves with respiration. Fulminant clinical tamponade presents with symptoms that depend on its etiology. Acute cardiac tamponade based upon aortic or free wall rupture presents with syncope and sudden collapse, whereas tamponade in the setting of an acute inflammatory pericardits may present with pericardial chest pain, and dyspnoea. Therefore, in patients presenting with chest discomfort, dyspnoea, tachycardia or tachypnoea, cardiac tamponade should be suspected when jugular distension, hypotension or pulsus paradoxus is present. Auscultation may reveal pericardial friction rub, and heart sounds may be faint. Echocardiography shows pericardial effusion, the previously mentioned diastolic collapsing of the cardiac cavities, increased flow velocity over tricuspid and pulmonary valves, and decreased flow velocity over the aortic and mitral valves.
When secondary to inflammatory pericarditis, tamponade up to moderate severity may be treated by anti-inflammatory drugs. In severe tamponade, pericardiocentesis should be performed to immediately alleviate intrapericardial pressure. Surgical drainage should be considered when pericardiocentesis is unsuccessful, or when tamponade recurs.
Acute pericarditis
Acute inflammation of the pericardium may result from a wide variety of etiologies (Table 8.2.1), and typically presents with chest pain, a pericardial friction rub on auscultation, and repolarization changes on the electrocardiogram.
| Causes of Acute Pericarditis |
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Patients present with a rapid-onset chest pain syndrome located precordial and retrosternal, and radiating to the subclavian region, the back and the trapezoid region. Chest pain is of moderate severity, lasting for several days, and increases with inspiration or chest movement. Patients typically alleviate the pain by sitting and leaning forward.
A pericardial friction rub is pathognomonic of pericarditis, and ECG changes are frequently present, which comprise diffuse concave ST-segment elevation, with positive T-waves in several leads. Atrial injury is accompanied by PR-segment depression. After several hours to a few days, ST-segments return iso-electric, and negative T-waves may occur subsequently, which may persist for several weeks although they frequently normalize within days. Pericardial effusion may be present, and can be diagnosed by chest X-ray when fluid accumulation exceeds 250mL, or by echocardiography.
Although initial presentation may mimic ST-segment elevation myocardial infarction (STEMI). Onset of chest pain is less abrupt in acute pericarditis, and varies with respiration. Furthermore, diffuse ST-segment changes are present in pericarditis, whereas STEMI presents with ST-segment elevation, and reciprocal depression, in leads corresponding to the ischemic myocardium. Biomarkers can be positive in both syndromes.
Treatment consists of aspirin while pain and fever are present, which usually adequately alleviates symptoms. Another option is NSAIDs, which are recommended when aspirin in insufficient or contraindicated. Corticosteroids should, however, be avoided as they are associated with relapsing pericarditis. Hospital admission may be necessary in patients with high fever, large effusions or cardiac tamponade.
Recurrent pericarditis
In 8 to 80% of patients, pericarditis recurs after a first episode of acute pericarditis. A continuous type, in which symptoms recur shortly after cessation of anti-inflammatory therapy, and an intermittent type, in which symptom-free periods of more than 6 weeks separate recurrences, can be distinguished. Frequently resulting from inadequate therapy or corticosteroid-use during the initial episode, subsequent recurrences are usually less severe. A recurrence should be treated according to the same procedures as for the first event. Pericardiectomy may be considered the last resort in severely refractory recurrent pericarditis, but its results are unpredictable. Prognosis of the disease is excellent, as severe complications are rare.
Pericardial effusion
Fluid accumulation in the pericardium, pericardial effusion, is a common finding on routine echocardiography, and is asymptomatic in the absence of inflammation or cardiac tamponade. It may result from any disease of the pericardium, or be iatrogenic. Most frequently it results from idiopathic pericarditis, malignancy, or iatrogenic defects (Table 8.2.2).
| Causes of Pericardial Effusion |
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Where the use of electrocardiography and chest radiography is limited in pericardial effusion, echocardiography may reveal an echo-free space in the anterior or posterior sacs, present throughout the cardiac cycle. The absence of cavity collaps indicates the absence of tamponade.
Treatment of pericardial effusion depends on the extent of symptoms, and the etiology underlying the effusion. Asymptomatic mild pericardial effusion (<10mm sum of echo-free spaces in anterior and posterior sacs) may be left untreated. Control echocardiography is indicated at 3-6 months. In moderate (10-20mm sum of echo-free space) to large effusions, a complete history, routine physical examination, ECG, chest radiography and routine blood analysis is indicated. Treatment is then based upon its expected etiology, standard treatment with aspirin or NSAIDs to relief pain, with invasive procedures indicated in case of tamponade with hemodynamic compromise or recurrent pericarditis as discussed previously. Specific etiologies of pericardial effusion must be managed accordingly.
Chronic pericardial effusion
Pericardial effusion is considered chronic when moderate to large effusions persist for at least 3 months. Resulting most frequently from idiopathic cause, intrapericardial pressure is frequently elevated in these patients, which may lead to unexpected tamponade in up to 30% of patients. Hence, pericardiocentesis is indicated to alleviate the fluid accumulation, and pericardiectomy should be considered when large effusions recur. Long term outcome is excellent with this approach.