or inflammation of the pericardium, is most oftencaused by viral infection.It can also develop as a result of bacterialor other infection, autoimmune disease, renalfailure, injury to themediastinal area, and the effects of certain drugs (notably hydrala-zine and procainamide). The clinical features of pericarditis dependon its cause, as wellas the volume and type of effusion. Patients withuncomplicated pericarditis have pleu-ritic-type chest pain that radiates to the left shoulder and may be relieved byleaningforward. Chest radiographs, Doppler studies, andlaboratory tests confirm the diagno-sis and provide informationabout the degree of effusion. In most patients, pericarditisis mildand resolves spontaneously, although treatment with anonsteroidal anti-inflam-matory drug or a short course of acorticosteroid may be helpful. When a large peri-cardial effusion isproduced, cardiac function may be compromised, and cardiac tam-ponade can occur. In patients with longstanding inflammation, thepericardiumbecomes fibrous or calcified, resulting in constriction of the heart. Drainage or surgicalintervention may be necessary inpatients with complicated pericarditis. (Am Fam Physi-cian2002;66:1695-702. Copyright© 2002 American Academy of Family PhysiciansPericarditis is inflammation of thepericardial sac surroundingtheheart and the origins of the greatvessels.The condition is mostoften caused by a viral infectionand generallyresolves in a few weeks with nosequelae.
Pathophysiology and Classification
Depending on the underlying cause, theacute inflammatoryresponse in pericarditismay produce serous fluid,pus,or densefibrin-ous material. Viral pericarditis usually resultsin smallaccumulations of serous fluid thatresolve spontaneously or requireminimaltherapeutic intervention. Even large volumesof serousfluid (up to 250 mL) may not cause significant clinical signs orsymptoms if accu-mulation is gradual.The effusion may onlybeapparent as an enlarged cardiac silhouette onthe chest radiograph.Conversely, large acute accumulations of pericardial fluid may causeintrapericardialpressure to rise,thereby impeding filling of theright side of the heart through the superiorvena cava and inferior vena cava.Acutely, thissituation can result in cardiac tamponade. If the pericarditis processcontinues and the fluidorganizes into a thickened (even calcified)coating, theresultant constrictive pericarditismay mimic restrictive cardiomyopathy.Thus, pericarditis may be classified as acute,subacute,or chronic,dependingon the under-lying pathophysiologic process.
Changes in the jugular veins and the rela-tionship of those changesto respiration can beextremely useful in differentiatingpericarditisfrom other causes of chest pain
Etiology of Pericarditis
Idiopathic (nonspecific, probably viral)InfectiouscausesViruses: coxsackievirus A and B, hepatitis viruses,human immunodeficiencyvirus, measles virus, mumpsvirus, varicella virusBacteria: gram-positive and gram-negative organisms; rarely, Mycobacteriumspecies(tuberculosis)Fungi (most often inimmunocompromised patients):Blastomyces dermatitidis,Candida species,Histoplasma capsulatumNoninfectious causesAcute myocardial infarction*Renalfailureclosed procedures and pacemakerimplantation(puncture of myocardium)Drugs: hydralazine (Apresoline), procainamide (Pronestyl),phenytoin(Dilantin), isoniazid (e.g., Nydrazid); withrifampin (Rifamate),phenylbutazone, dantrolene(Dantrium), doxorubicin (Adriamycin,Rubex),methysergide (Sansert), penicillin, mesalamine(Rowasa)Pericardial effusion may occur on the second to fourthday after acutemyocardial infarction as a reaction tounderlying necrotic myocardium in up to25 percent of patients. It can also develop weeks to months aftermyocardial infarction in patients with postmyocardialinfarction syndrome (Dresslers syn-drome); in thissituation, pericarditis occurs because of a lateautoimmune reac-tion stimulated by the entry of necrotic myocardial tissue into the circulation,where it acts as an antigen.Pericarditis in uremia indicates a need for dialysis;pericarditis may also beassociated with hemodialysis.Listed in relative order of frequency..descent duringventricular systole). During inspiration, lungexpansioncauses negative intrathoracic pres-sure that is transmitted to the pericardiumandcardiac chambers, leading to dilation of thechambers. As aresult, the right chambers of the heart fill with blood from the superiorvenacava and the inferior vena cava, and the leftchambers fill because of forwardflow in thepulmonary veins.Even with a moderately largeeffusion,mildacute pericarditis usually has no hemody-namicimpact on the heart. Hence, jugularvenous profiles are generallynormal.Conversely, cardiac tamponade and con-strictive pericarditis lead toimportant and dis-tinctive hemodynamic changes. Because theheart is constrictedby fluid or a rigid fibrinousor calcified pericardium, negative intratho-racicpressure during inspiration is not trans-mitted to the pericardial sac.Consequently,intrapericardial and intracardiac pressuresremainelevated, and intrapericardial pressureequals or exceeds right atrial pressure.Incardiac tamponade, this situation resultsin early right ventricular diastolic collapseandlate diastolic right atrial collapse,because pres-sures are lowest indiastole. Thedescent isblunted because the right ventricle cannotexpand, but thedescent remains normal. Incardiac tamponade, some blood (though lessthannormal) still flows toward the right side of the heart during inspiration. Because thecar-diac chambers are inhibited from dilating, theinflow causes the intraventricularseptum toshift to the left, which further decreases leftventricular capacity.Thehemodynamic changes can cause sys-tolic blood pressure to fall by10 mm Hg ormore during inspiration. Thissituation,termed pulsus paradoxus, is the classic hall-mark of cardiactamponade.Pulsus paradoxusis detectable in 70 to 80 percent of patientswith cardiac tamponade and in about onethird of patientswith pericarditis.
In constrictive pericarditis
,no forward flowoccurs from thesuperior vena cava and theinferior vena cava during inspiration.Thisresults in Kussmauls sign, which is a para-doxic inspiratory