If follow-up echocardiography documents fluid reaccumulation, a pericardial window should be considered, because the infection risk associated with a pericardial drain increases after 48 hours.
Constrictive pericarditis refers to an abnormal scarring and loss of elasticity of the pericardium, resulting in impaired ventricular filling and decreased cardiac output. The frequency of different causes of constrictive pericarditis depends on the population and geography in question. In developed countries, cardiac surgery and idiopathic constriction are the leading cause, while in certain developing countries tuberculous remains the number one etiology. The initiating event results in a chronic inflammatory pericardial process, resulting in fibrinous scarring and occasionally calcification of the pericardium Figure As the heart becomes encased with a non-compliant pericardium, ventricular interdependance and dissociation between the intrathoracic and intracardiac pressure occurs.
In constriction, normal expansion of the right heart is restricted by the pericardium and the septum shifts to the left to accommodate the increase in venous return with inspiration; the opposite movement occurs with expiration.
Normally, there is a reduction in intrathoracic and intracardiac pressure with inspiration. The rigid pericardium impedes normal ventricular expansion and therefore venous return and pulmonary venous pressure.
Because intrathoracic pressure drops but left ventricular pressure does not decrease with inspiration there is a reduction in the transpulmonary gradient. This leads to impaired ventricular filling and decreased cardiac output. Ultimately, right and then left ventricular heart failure develop. Distinguishing heart failure caused by constrictive physiology from diastolic restrictive physiology is a classic diagnostic dilemma. Symptoms are often vague and their onset is insidious; they include malaise, fatigue, and decreased exercise tolerance.
With progression of constrictive pericarditis, symptoms of right-sided heart failure eg, peripheral edema, nausea, abdominal discomfort, ascites become apparent and usually precede signs of left-sided failure eg, exertional dyspnea, orthopnea, paroxysmal nocturnal dyspnea. Increased ventricular filling pressures cause jugular venous distention and Kussmaul's sign paradoxical rise in jugular venous pressure on inspiration , which is sensitive but not specific for constrictive pericarditis.
Constrictive effusive pericarditis consists of a tense pericardial effusion in the presence of pericardial constriction, and both tamponade and constrictive signs and symptoms are present. Brain natriuretic peptide BNP is a serum biomarker that can help distinguish constrictive pericarditis from restrictive cardiomyopathy. Despite elevated filling pressures in both conditions, levels of BNP are significantly higher in restrictive cardiomyopathy.
Pericardial calcifications Figure 10 , pleural effusions, and biatrial enlargement may be noted on the chest radiograph. Echocardiography is the best imaging modality for assessing hemodynamic parameters noninvasively.
M-mode echocardiography is useful for looking for rapid motion followed by abrupt flattening of the left ventricular free wall in early and mid diastole respectively. Two-dimensional echocardiography may demonstrate a thickened pericardium about one third of cases , myocardial tethering, abrupt cessation of left ventricular and right ventricular diastolic filling, biatrial enlargement, tubular deformity of the left ventricle, respirophasic septal shift, septal bounce and inferior vena cava plethora with absent inspiratory collapse.
Doppler echocardiographic findings have the highest sensitivity and specificity for detecting constrictive physiology. Excessive respiratory variations in transmitral, transtricuspid, pulmonary venous, and hepatic vein flow are characteristic. Low tissue velocity at both medial and lateral annuli suggests restriction.
More recently developed echocardiographic modalities such as strain imaging have enhanced the ability to discriminate between restriction and constriction. Direct pressure measurements are performed if there is doubt about the diagnosis. Characteristic features in the right atrium include: elevated right atrial pressures, prominent x and y decents and Kussmaul's sign.
Square-root or dip-and-plateau right ventricular pressure waveforms reflect impaired ventricular filling. Because of the fixed and limited space within the stiff pericardium, end-diastolic pressure equalization typically within 5 mmHg occurs between these cardiac chambers. Pulmonary artery systolic pressures are usually normal in pericardial constriction; higher pulmonary pressures suggest a restrictive cardiomyopathy.
The ratio of the right ventricular to left ventricular systolic pressure-time area during inspiration compared to expiration is a highly sensitive and specific means of differentiating constriction from restriction Figure Computed tomography is the imaging modality of choice to evaluate the thickness of the pericardium and for pericardial calcification.
While echocardiography is the first choice imaging modality for assesssment of constriction, for many patients CMR is becoming increasingly utilized in the initial evaluation, particularly if any ambiguity remains regarding the diagnosis, if there is suggestion of active inflammation, or if the duration of symptoms has been brief.
Cardiac magnetic resonance is very useful to differentiate a small pericardial effusion from pericardial thickening. The superior signal-to-noise and contrast-to-noise ratio of CMR allows precise evaluation of the morphological and hemodynamic changes seen in pericardial constriction.
Real-time cine sequences allow evaluation of the features described above in the 2D echocardiographic evaluation of pericardial constriction, which is useful if echocardiographic images are sub-optimal. Phase encoding velocity imaging potentially provides similar data to Doppler echocardiography but is not yet generally employed in routine practice.
The degree of constrictive physiology occurs along a spectrum of severity. Early forms may be difficult to diagnose without a high degree of clinical suspicion.
It is increasingly recognized that some of these patients may respond to medical therapy, without surgical intervention; this is referred to as transient constrictive pericarditis.
Medical treatment is limited in chronic constrictive pericarditis in the absence of active inflammation. Diuretics and a low-sodium diet may be tried for patients with mild to moderate New York Heart Association Class I or II heart failure symptoms or contraindications to surgery.
For effusive-constrictive pericarditis therapy includes pericardiocentesis initially, followed by treatment with anti-inflammatory agents. Frequently, pericardiectomy is necessary for long-term management. Recurrence following surgery is caused mainly by incomplete resection of the pericardium. Without surgical treatment, biventricular failure develops. Long-term survival after pericardiectomy is worse than matched controls but this is mainly related to the underlying etiology.
Grimm, DO Published: July Summary Suggested Readings References. Figure 1: Click to Enlarge. Figure 2: Click to Enlarge. Figure 3: Click to Enlarge. Figure 4: Click to Enlarge.
Figure 5: Click to Enlarge. R and V 1 leads and PR depression elsewhere. Figure 7A: Click to Enlarge. Figure 7B: Click to Enlarge. Figure 8A: Click to Enlarge.
Figure 8B: Click to Enlarge. Figure 9: Click to Enlarge. Evaluation of patients with acute pericarditis should include a history, physical examination, electrocardiography, chest radiography, and baseline laboratory studies i. Additional laboratory testing and imaging are dictated by clinical presentation and risk factors. Transthoracic echocardiography should be performed in all patients with suspected acute pericarditis to exclude pericardial effusion and cardiac tamponade.
Patients with acute pericarditis should be treated empirically with nonsteroidal anti-inflammatory drugs. Colchicine may be used as monotherapy or in combination with a nonsteroidal anti-inflammatory drug for the first episode of acute pericarditis.
Information from references 4 through 6. Healthy pericardium consists of the inner serous visceral layer and the outer fibrous parietal layer that envelop the heart. About 15 to 50 mL of fluid, an ultrafiltrate of plasma, separates these layers. Acute pericarditis can result from a systemic disease or a process isolated to the pericardium Table 2. Systemic conditions, such as malignancy, inflammatory responses, autoimmune disorders e. External causes other than viral infections include pharmacologic agents e.
Coxsackie virus A and B. Epstein-Barr virus. Human immunodeficiency virus. Streptococcus pneumoniae in children. Whipple disease. Direct pericardial injury. Cardiac injury e. Pericardial perforation e. Indirect pericardial injury. Blunt chest trauma. Phenytoin Dilantin. Renal insufficiency i. Postmyocardial infarction Dressler syndrome. Postpericardiotomy syndrome. Ankylosing spondylitis. Familial Mediterranean fever.
Polyarteritis nodosa. Rheumatoid arthritis. Systemic lupus erythematosus. Wegener granulomatosis. Acute pericarditis: diagnostic cues and common electrocardiographic manifestations. Cardiol Rev. In contrast to the pain from myocardial ischemia, chest pain from acute pericarditis is exacerbated in the supine position, by coughing, and with inspiration. The pain usually improves in the seated position or by leaning forward, which reduces pressure on the parietal pericardium, but it is not relieved with nitrates.
Dull, oppressive chest pain radiating to the trapezius ridges or shoulders may occur with acute pericarditis, making it difficult to differentiate from other common or life-threatening causes of chest pain, such as MI or aortic dissection Tables 3 11 and 4 9. Information from reference Reprinted with permission from Massachusetts Medical Society.
Clinical practice. Acute pericarditis [published correction appears in N Engl J Med. N Engl J Med. Additional clinical findings reflective of the underlying etiology, such as those consistent with specific autoimmune disorders or malignancies, may occur in patients with acute pericarditis. Patients with a bacterial etiology may present with fever, chills, and leukocytosis, whereas those with a viral etiology may present with influenza-like or gastrointestinal symptoms.
The intensity of the friction rub may be increased during auscultation by having the patient lean forward or rest the elbows on the knees, applying firm pressure on the stethoscope diaphragm during suspended respiration. Classic changes include widespread concave upward ST-segment elevation and PR-segment depression without T-wave inversions. In contrast, pathologic Q waves, regional convex ST-segment elevations, and reciprocal changes commonly occur with myocardial ischemia or infarction.
When the ratio of ST-segment elevation to T-wave amplitude in mm in lead V 6 exceeds 0. Acute pericarditis electrocardiographic changes, stage 1. Information from references 2 and 9. Information from references 2 , 9 , and Diagnosis requires at least two of the following criteria: characteristic sharp, pleuritic chest pain; pericardial friction rub; suggestive changes on electrocardiography; and a new or worsening pericardial effusion.
Chest radiography can rule out abnormalities of the lungs and mediastinum, specifically pericardial effusion. Cardiomegaly in the absence of known cardiac disease indicates a pericardial effusion of at least mL. A chest X-ray is done mainly to exclude other important differential diagnoses, such as pneumothorax, or to rule out certain complications of pericarditis, such as large pericardial effusions.
Alternative causes of this finding would include dilated cardiomyopathy. It is also important to note that a chest X-ray may appear normal despite the patient having small or moderate-sized effusions. A negative, cardiac-specific troponin level is an important finding. AP was diagnosed with viral pericarditis on the basis of the findings described above, and was prescribed ibuprofen mg three times a day with food for one week and colchicine 0.
AP was referred for a transthoracic echocardiogram. He was also advised to refrain from strenuous activity until his symptoms had completely resolved. He noted clinical improvement in his symptoms later that night and slept very well in his bed. The mainstay of treatment for acute pericarditis is pain relief and resolution of inflammation.
Clinicians should aim to use safer NSAIDs at their lowest effective dose for the shortest duration required. Such patients include those who are over the age 65 years, have a prior history of peptic ulcers, or who are taking concurrent aspirin, corticosteroids or anticoagulants.
Low-dose colchicine is usually well tolerated and has infrequent side effects, mainly of gastrointestinal nature, although high doses, specifically with prolonged use, can lead to irreversible toxicity. It is now common practice to use colchicine for the first episode of pericarditis, unless there are specific contraindications. The use of glucocorticoids is controversial. A simple lifestyle factor such as activity restriction, especially in cases of athletes, is important as well.
Refraining from strenuous activity until symptom resolution is recommended for all patients, and for at least three months after resolution of symptoms for competitive athletes. When AP presented for the transthoracic echocardiogram, he seemed diaphoretic, clammy and tachypnoeic. Assessment of his vital signs revealed tachycardia and hypotension.
AP had an elevated JVP, difficult-to-hear heart sounds on auscultation and a pulsus paradoxus of 30 mmHg. An ambulance was called to take him the emergency department. A bedside transthoracic echocardiogram was performed in the emergency department and revealed a large circumferential pericardial effusion.
The development of cardiac tamponade is not dependent on the quantity of fluid accumulated, but rather on the rate of fluid accumulation in the pericardium. Other features include tachypnoea, tachycardia and atrial arrhythmias, such as atrial fibrillation, Kussmaul sign a paradoxical rise in JVP on inspiration , positive hepatojugular reflux, weakened peripheral pulses, peripheral oedema and cyanosis.
Pulsus paradoxus is one of the key clinical features of cardiac tamponade, when measured correctly. To measure pulsus paradoxus, the sphygmomanometer cuff is inflated above systolic pressure.
Korotkoff sounds are sought over the brachial artery while the cuff is slowly deflated. Initial Korotkoff sounds are heard only intermittently during expiration. The cuff is then deflated slowly to the pressure at which Korotkoff sounds become audible continuously during inspiration and expiration.
When the difference between these two levels exceeds 10 mmHg during quiet respiration, pulsus paradoxus is present. Electrical alternans is an alternation in the amplitude of QRS complexes. It is thought to be due to the swinging movement of the heart within the pericardial cavity, which creates changes in the vectors measured on surface ECG.
However, low-amplitude QRS complexes and tachycardia are more commonly seen on ECGs and should raise suspicion of possible cardiac tamponade.
Urgent pericardiocentesis was performed, and about 1 L of fluid was drained. AP improved clinically and was monitored in hospital for the next 48 hours. On repeat transthoracic echocardiograpy, there was only mild re-accumulation of the pericardial effusion. AP was discharged home with plans to repeat the transthoracic echocardiogram in seven to 10 days for monitoring.
Get medical advice if you have chest pain. Pericarditis often follows a viral infection, such as a sore throat or cold. Contact NHS A GP will listen to your heart. Pericarditis can change the sound it makes.
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