Pericarditis is an inflammation of the pericardium, a two-layered structure that surrounds the heart. The inner layer adheres to the heart. There is usually about 15 to 35 mL of serous fluid in the pericardial space. This fluid provides lubrication during the contraction of the heart. The pericardial sac functions as a barrier to protect the heart from infection from the lungs, fix the heart to the mediastinum, prevent extreme dilation of the heart, equalize compliance between the right and left sides of the heart, and reduce friction between the heart and the surrounding structures. Pericarditis can be acute or chronic, and has a variety of causes.
Pericarditis can present along a wide spectrum of symptoms ranging from mild chest pain to severe cardiovascular compromise and shock, depending on the size of the effusion and the rate at which it accumulates. However, there are features that are common to most cases. Acute pericarditis typically presents with fever, tachypnea, and chest pain. However, in studies of patients presenting to the emergency department with chest pain, the vast majority of patients do not have pericarditis.1 The chest pain is located in the midsternal or left precordial region, occasionally radiates to the left shoulder, has a sharp or stabbing quality, and is positional, increased when the patient is supine and less intense when the patient is sitting or leaning forward. The chest pain may get worse with inspiration. Some patients with acute pericarditis will report abdominal pain, either isolated or with chest pain.
On physical examination, patients may be tachpneic and tachycardic. Patients with a small or moderate pericardial effusion may have a pericardial friction rub, a high-pitched sound commonly described as crinkling paper or rubbing two pieces of sandpaper together. This sound is best heard over the third to fourth left intercostal interspace with the patient sitting, leaning forward in expiration. Patients with large effusions do not have a rub because the pericardial and epicardial surfaces do not contact each other. Patients with large effusions can also have pallor, altered mental status, hypotension, narrowed pulse pressure, distant muffled heart sounds, jugular venous distension, prolonged capillary refill, and hepatomegaly.
Increased pulsus paradoxus is an early sign of cardiac tamponade (Figure 56-1). There is normally a change in the blood pressure during the respiratory cycle and this is exaggerated in cardiac tamponade. With inspiration, there is increased filling of the right atrium and increased capacity in the pulmonary vascular bed, resulting in decreased left-sided filling and decreased cardiac output. Clinically this produces a difference in systolic blood pressure during inspiration and expiration that is normally <10 mmHg. In patients with cardiac tamponade, the systolic blood pressure difference is >10 mmHg. To check for pulsus paradoxus, the patient should be seated comfortably and the blood pressure checked manually on the brachial artery. The cuff pressure should be released until the first Korotkoff sound is heard only during expiration. Once this systolic pressure ...