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 is noted, the cuff pressure should be lowered until the first Korotkoff sound is heard throughout the respiratory cycle; the difference between these two systolic pressures represents the pulsus paradoxus. Patients with pericarditis can develop tamponade with a variable amount of pericardial fluid; the faster the fluid accumulates, the lower volume that is necessary to cause tamponade. If the fluid collection increases very slowly, a larger volume of fluid can accumulate without signs of tamponade.

The history and presentation provide clues to the cause of pericarditis. Viral pericarditis generally is associated with a history of a viral upper respiratory infection or gastroenteritis 10 days to 2 weeks before presentation with symptoms of pericarditis. Patients with purulent pericarditis present with a more acute course and generally appear toxic. These patients may present with signs of another infection such as pneumonia. It is important to remember that purulent pericarditis can develop in a patient who is being treated for another infection. If there is a worsening of the patient’s condition with an enlarged heart size on chest radiography, pericarditis should be suspected. Patients who are immune-­compromised may present with purulent pericarditis from an opportunistic infection, such as fungus or tuberculosis.

In patients with symptoms of pericarditis, a history of collagen vascular disease or a history of symptoms consistent with collagen vascular disease should increase the suspicion of pericarditis. Likewise, a patient with a history of preceding open heart surgery in the prior 2 weeks presenting with chest pain, fever, and a pericardial friction rub should be evaluated for post-pericardiotomy syndrome.

VIRAL AND IDIOPATHIC

The vast majority of cases of pericarditis will be considered idiopathic after a workup to determine the cause. Identifiable causes of pericarditis are listed in Table 56-1. The most common infectious cause of pericarditis is viral infection. Many patients present with an antecedent history of an upper respiratory infection. Viral infection can result in direct infection of the pericardium or produce a secondary immune mediated inflammation of the pericardium. This may be the basis for idiopathic pericarditis. The viruses most commonly associated with pericarditis are adenovirus or coxsackie virus.

BACTERIAL PERICARDITIS

Bacterial pericarditis is a direct infection of the pericardial space with a bacterial agent. This is also referred to as purulent pericarditis. It can develop spontaneously, in relation to a concurrent infection and result from direct spread (e.g. pneumonia), or from hematologic spread (e.g. osteomyelitis). These patients are extremely ill appearing. Common etiologic agents include Staphylococcus aureus and Group A streptococcus.² Streptococcus pneumoniae and Haemophilus influenzae type B were common causes of purulent pericarditis before the vaccines were developed. Meningococcus can also be associated with purulent pericarditis. It has also been reported in association with the smallpox vaccine, and in one case with the meningococcus vaccine.³

TUBERCULOUS PERICARDITIS

Tuberculous pericarditis is most commonly reported in the third world but has been increasing in frequency due to human immunodeficiency virus infection in the United States. It can spread directly from the lungs or lymph nodes in the chest. Most often it is an insidious infection that can lead to constrictive pericarditis. It can less frequently present with the rapid development of pericardial effusion and tamponade. The rapid diagnosis and treatment of tuberculous pericarditis can prevent the development of constrictive pericarditis. In cases of constrictive pericarditis, it is often necessary to biopsy the pericardium to confirm the diagnosis of tuberculosis.⁴