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Pericarditis,

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.

Hemodynamic Considerations

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 (Dresslers 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 Kussmauls sign, which is a para-doxic inspiratory

swelling of the neck veins.Because blood flow to the right side of theheart does not increase,no septal shift occurs,and pulsusparadoxus is not common in con-strictive pericarditis.

Clinical Features

Patients usually recall a nonspecific pro-drome of malaise, fever,and chest pain, espe-cially in viral or idiopathic pericarditis.Thechest pain is typically pleuritic and radiates tothe left shoulderand,characteristically,the lefttrapezius musculature. The pain isexacer-bated by inspiration or recumbency andrelieved tosome extent by leaning forward.Patients may have additionalsymptoms,depending on the etiology of the pericarditisand thepresence of complications.Clinical signs may be subtle. Apericardialfriction rub may or may not be present.Largeeffusionsare unlikely to produce a pericardialrub. With large, slowlyaccumulating effu-sions, there may be dullness to percussion inPericarditisClassification of PericarditisAcute pericarditis (<6weeks)EffusiveFibrinousSubacute pericarditis (>6weeks to 6 months)Chronic pericarditis (>6months)EffusiveAdhesiveEffusive-adhesiveConstrictivethe scapular region because of compression of the left lung (Ewartssign).As previously noted,acute,rapid accumula-tion of fluid in thepericardium causes signs of acute hemodynamic compromise incardiactamponade. Patients with this conditiondeveloptachycardia,hypotension,pulsus para-doxus, and distended neck veins. Althoughthese patients appear to be in acute distress(similar tocardiac failure and pulmonary edema),their lungs are clear onauscultation.In chronic constrictive pericarditis,theneck veins are markedly distended, butpatientsdo not appear distressed and showno evidence of pulsusparadoxus. Duringinspiration, the neck veins becomedistended(normally, they collapse). The jugular venouspulseshows a sharpdescent because of rapid right ventricular filling in early diastole.Asharp heart sound called a pericardialknockis heard in earlydiastole.Unless otherproblems are present, the lungs areusually clear on auscultation. Because of congestionof the inferiorvena cava, the liver is enlarged,and ascites and peripheral legedema are evi-dent. Clinical features may mimic those of restrictivecardiomyopathy.DiagnosisThe diagnosis of pericarditis and its compli-cations requires a highindex of suspicion.Clinical features and the probability of a causeof pericarditismay assist in recogni-tion. Potential confirmatory studiesincludethe electrocardiogram (ECG),the chest radio-graph, Dopplerstudies, and selected labora-tory tests. A suggested approach to thediag-nosis of pericarditis is provided inIn this situation, the differential diagnosisincludes acute myocardialinfarction and nor-mal-variant repolarization abnormality. It isparticularly important to distinguish peri-carditis from acutemyocardial infarction,because thrombolytic therapy could havedis-astrous effects in patients with pericarditis.Characteristicfeatures of acute pericarditis,acute myocardial infarction, and earlyrepo-larization are summarized inin c ardiac tamponade, the ECG shows elec-trical alternans as the heart floatsin relationto the recording leads. Chronic constrictivepericarditispresents with low voltage of theQRS complex and diffuse flattening or inver-sionof the T waves.Atrial fibrillation occurs inone third of patients withpericardial disease.CHEST RADIOGRAPHYIf more than 250 mL of fluid has accumu-lated, the cardiac silhouette is usuallyenlargedon the chest radiograph.Smaller accumulationsmay appear normal.Inconstrictive pericarditis,calcification may be seen around the heart.DOPPLER STUDIESThe diagnostic test of choice for large effu-sions, cardiac tamponade, andconstrictivepericarditis is two-dimensional Doppler echo-cardiography.This imaging modality candemonstrate moderate or large effusions.Incardiac tamponade,Doppler examination may show the characteristicswinging motion of theheart that gives rise to electrical alternans.Dopplerexamination can also show thereversal of inflow velocities in thetricuspidand mitral valves during inspiration and expi-ration.Divergence of right and left ventricularsystolic pressures isdemonstrated in cardiactamponade and constrictivepericarditis.Doppler studies differentiate pericarditisfromrestrictive cardiomyopathy.

Symptoms

Chest pain, caused by the inflamed pericardium rubbingagainst the heart.

Usually relieved by sitting up and leaning forward

Pleuritistype: a sharp, stabbing pain

May radiate to the neck, shoulder, back or abdomen

Often increases with deep breathing and lying flat, and mayincrease with coughing and swallowing

Breathing difficulty when lying down

Need to bend over or hold the chest while breathing

Drycough

Ankle, feet and leg swelling(occasionall y)

Anxiety

Fatigue

Signs and tests When listening to the heart with a stethoscope,the health care provider can hear a typical sound called a pericardial rub. Theheart soundsmay be muffled or distant.There may be other signs of fluid in the pericardium(pericardial effusion).If the disorder is severe, there may be crackles in the lungs,decreasedbreath sounds, or other signs of fluid in the space around the lungs ( pleural effusion).If fluid has accumulated in the pericardial sac, it may show on:

Chest x-ray

Echocardiogram

Chest MRI scan

Heart MRIor heartCTscan

Radionuclide scanningThese tests showenlargement of the heartfrom fluid collectionin the pericardium, and signs of inflammation. They may also show scarring andcontrac tureof the pericardium (constrictive pericarditis). Other findings vary depending on the cause of pericarditis.

AnECGis abnormal in 90% of patients with acute pericarditis.ECG changes generally evolveduring the disease process, and they may mimic the ECGchanges of aheart attack . To rule outheart attack, serial cardiac marker levels (CK -MB andtroponin I) may be ordered. Other laboratory tests may include:

Pericardiocentesis, with chemical analysis andpericardialfluid cultureTreatmentThe cause of pericarditis must be identified, if possible. inmost types of pericarditis, it is necessary to treat the painwithanalgesics(pain killers). Theinflammation of the pericardium is treated with anti-inflammatory drugs(NSAIDS) such as aspirinand ibuprofen. Iin some cases, corticosteroids may be prescribed.Diuretics may be used to remove excess fluid accumulated inthe pericardial sac. If the buildup of pericardial fluid makes theheart function poorly or producescardiac tamponade, it isnecessary to drain the fluid from the sac. This procedure,called pericardiocentesis, may be done using anechocardiography-guided needle or surgically in a minor procedure.Bacterial pericarditis must be treated with antibiotics. Fungal pericarditis is treated with antifungalagents.If the pericarditis ischronic, recurrent, or causes constrictive pericarditis, cutting or removing partof the pericardium may be recommended.Expectations (prognosis)Pericarditis can range from mild cases that resolve on their own to life-threatening casescomplicated by significant fluid buildup around the heart and poor heart function. The outcome isgood if the disorder is treated promptly. Most people recover in2 weeks to 3 months.Complications

Arrhythmias, such as atrial fibrillation. When pericarditisaccompanies myocarditis, other arrhythmias may be present, such as supraventricular tachycardia (SVT) or completeheart block.

Cardiac tamponade

Constrictive pericarditis, where inflammation of the pericardialsac results in fibrosis and thickening of the pericardium withadhesions (sticky scars) between the pericardium and the heart.The pericardium creates a rigid "case" around the heart, whichcan severely limit the ability of the heart to fill with blood.Patients with constrictive pericarditis may developheartfailure, which responds poorly to treatment. Constrictive pericarditis must be differentiated from a chronic heartcondition calledrestrictive cardiomyopathy, which producessymptoms and signs similar to constrictive pericarditis.