Acute Pericarditis Clinical Presentation
- Author: Sean Spangler, MD; Chief Editor: Richard A Lange, MD, MBA more...
Palpitations may be the presenting complaint, but chest pain is the cardinal symptom of pericarditis, usually precordial or retrosternal with referral to the trapezius ridge, neck, left shoulder, or arm. The quality of the pain is usually pleuritic, but it range from sharp, dull, aching, burning, or pressing, and the intensity varies from barely perceptible to severe. The pain is worse during inspiration, when lying flat, or during swallowing and with body motion, and it may be relieved by leaning forward while seated.
Common associated signs and symptoms include low-grade intermittent fever, dyspnea/tachypnea (a frequent complaint and may be severe with myocarditis, pericarditis, and tamponade), cough, and dysphagia. In tuberculous pericarditis, fever, night sweats, and weight loss were commonly noted (80%).
Children may present with abdominal pain.
Interestingly, symptomatic rheumatoid arthritis–pericardial disease tends to occur in patients with arthritis, pleuritis, and other complications who are already being treated with anti-inflammatory agents such as corticosteroids, gold, and antimalarial drugs.
In uremic patients, heart rates may be deceptively slow with tamponade, fever, and hypotension due to autonomic impairment. Symptoms of neoplastic pericarditis develop over days to weeks; dyspnea is common and is the most significant symptom.
Patients with cardiac tamponade may present subacutely with symptoms of anxiety, dyspnea, fatigue, or altered mental status. They may have a history of medical illnesses associated with pericardial involvement, particularly end-stage renal disease (ESRD).
A waxing and waning clinical picture may be present in intermittently decompressing tamponade, and traumatic tamponade may present with acute dyspnea or altered mental status.
Physical findings in acute pericarditis and cardiac tamponade are discussed in this section.
A pericardial friction rub is pathognomonic for acute pericarditis; the rub has a scratching, grating sound similar to leather rubbing against leather. Serial examinations may be necessary for detection, as a friction rub may be transient from one hour to the next and is present in approximately 50% of cases.
Auscultation with the diaphragm of the stethoscope over the left lower sternal edge or apex during end expiration with the patient sitting up and leaning forward (or on hands and knees) allows the best detection of the rub and increases the likelihood of observing this finding.
More than 50% of pericardial friction rubs are triphasic: (1) An atrial systolic rub that precedes S1, (2) a ventricular systolic rub occurs between S1 and S2 and is coincident with the peak carotid pulse, and (3) an early diastolic rub occurs after S2 (usually the faintest).
The biphasic to-and-fro rub is less common (24%). It can occur with tachycardia and is due to summation of the atrial and early diastolic rub. Monophasic rubs (the ventricular systolic) are the least common but may occur in patients with atrial fibrillation.
Especially when the pericardial friction rub is monophasic, it can be mistaken for a systolic murmur. Pericardial rubs may be differentiated if the rub does not change with usual respiratory or positional maneuvers, if 3 components are present, and if the findings on the electrocardiograms are typical. That is, a friction rub has a changing character from heartbeat to heartbeat and with patient position changes. In addition, a friction rub is closer to the ear on auscultation than a murmur.
Other physical findings may include dyspnea/tachypnea, particularly in patients with sizable effusions, and Ewart sign (dullness and bronchial breathing between the tip of the left scapula and the vertebral column) Fever (usually low grade but occasionally reach 104°F [40°C]), cyanosis, and varying degrees of consciousness may also be present, as well as hepatomegaly and ascites. Tachycardia and cardiac arrhythmias, such as premature atrial and ventricular contractions, are occasionally present.
Cardiac tamponade is influenced by the volume and rate of fluid accumulation. The Beck triad (ie, hypotension; elevated systemic venous pressure, often with jugular venous distention; muffled heart sounds) may occur in affected patients, especially from sudden intrapericardial hemorrhage.
Pulsus paradoxus occurs in 70-80% of patients with pericardial tamponade and is measured by careful auscultation with a blood pressure cuff. The first sphygmomanometer reading is recorded at the point when the beats are audible during expiration and disappear with inspiration. The second reading is taken when each beat is audible during the respiratory cycle.
A difference of more than 10 mm Hg defines pulsus paradoxus. This decrease is important in patients with more slowly developing tamponade, because they may lack findings of the Beck triad. If an associated hemorrhage is outside pericardial sac, hypotension and tachycardia without elevated jugular venous distension may be found.
Pulsus paradoxus also occurs in patients with severe asthma, constrictive pericarditis, and severe congestive heart failure. See the image below.
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