Morning ReportSteven Hart, MD

HistoryCC: increasing DOEHPI49 y/o AAFIncreasing SOB over 1-2 weeksIntermittent Chest painLeg swelling starting to develop

HistoryAny thing else you like to know?

HistoryChest painNon-exersionalPleuritic in natureImproves by leaning forwardWorsened when laying downRecent URI symptoms, low grade fevers, malaiseRecent orthopnea, now PND

HistoryPMHxHTNHyperlipidemiaSocialNon-smokerWorks as secretarySocial ETOH (1-2 times per month)

Physical ExamWhat things might you look for?

Physical ExamVS T 99.1 P 108 R 22 BP 102/64+ JVDCVTachy, distant heart soundsRub heard intermittently by examinersLower extremity edemaResp sits up to breathCrackles at basesMildly increased effortable to speak full sentences sitting up

Physical ExamExtremities - +1 edemaPulsesExaggerated drop in pulses with inspiration

LabsCardiac enzymes slightly elevatedWBC 12

EKGNote diffuse ST seg elevations

ImagingCXR any guesses

ECHO any guesses

IntroductionThe Pericardium is a fibroelastic tissue made up of parietal and visceral layersThese two layers are separated by the pericardial cavityPericardial cavity usually contains 15-50 ml of plasma ultrafiltrate in healthy individuals

Diseases of the PericardiumAcute Fibrinous PericarditisPericardial Effusion without major hemodynamic compromiseCardiac Tamponade Constrictive Pericarditis

Etiology of Pericardial DiseasesViral InfectionsPurulent PericarditisTBMediastinal radiationMICardiac surgeryTraumaCardiac proceduresDrugs and ToxinsMetabolic disordersMalignancies (breast, lung, Hodgkins, mesothelioma)Collagen Vascular DiseaseIdiopathic

Etiologies of PericarditisNeoplastic-35%Immune Mediated- 23%Viral- 21% Bacterial-6%Uremia-6%TB- 4%Idiopathic-4%

Viral PericarditisCommon bugsCocksackie A and BEchovirusAdenovirus

Viral infections uncommon in patients presenting with pericardial effusion w/o pericarditisException is HIV- frequently presents with significant effusion w/o pericaritisseen in 7 % of patients hospitalized with effusions

Bacterial PericarditisStaphylococcusPneumococccusStreptococcus(rheumatic pancarditis)HaemophilusM.TuberculosisCan occur as systemic spread or direct extensionFrequently purulent

Fungal PericarditisHistoplasma- most common fungus in immunocompetent patientsEspecially the Ohio River ValleyIn immunocompromisedAspergillus CandidaCoccidoidesFrequently purulent

Other Infectious EtiologiesRickettsia RicketsiiChlamydia PsittaciBorrelia burgdorferiTreponema PallidumActinomycosisMycoplasma PneumoniaNocardia

Post MIPericardial involvement is related to infarct sizeEarly stage - inflammatory etiologyLate stageImmune mediated weeks to months outKnown as Post Cardiac Injury syndrome (PCIS) or Dresslers syndromeRare in modern time due to reperfusion therapies

Iatrogenic CausesMediastinal Radiation-wide spectrum of diseases seenCardiac SurgeriesCardiac ProceduresTraumatic

DrugsLupus like sydromesProcainamideHydralazinePhenytoinINHPenicillins- Hypersensitivity PericarditisChemotherapyDoxorubicin/Daunorubicin-cardiomyopathy/pericardiopathyBleomycin - sclerosing agent

ToxinsAsbestosis can cause pericardial lesionsScorpion fish venom can cause pericarditis

Metabolic DisordersUremia- Most common metabolic cause6-10 % of ESRD patients not on HD can have PericarditisDialysis related Pericardial Effusions (seen in 13% of patients)Severe Hypothyroidism effusion usually not significantrarely pericarditisOvarian hyperstimulation syndrome complication of gonadotropin therapyDue to fluid shifts

MalignancyResponsible for 6% of acute pericardial disease (pericarditis and tamponade)Accounts for 15-20% of moderate to large pleural effusionsMets - Lung, Breast, Hodgkins metastasesPrimary - Mesotheliomas and lipomas

Collagen Vascular DiseaseSLE- pericardial involvement in up to 50%Rheumatoid ArthritisProgressive Systemic SclerosisMCTDPolyarteritisGiant Cell ArteritisInflammatory Bowel Disease

IdiopathicIn two large series (331 patients), only 16 % had an identifiable cause of pericarditisMany of these cases are presumed viralOnly 7-29% of patients have idiopathic pericardial effusions

Clinical Presentation of PericarditisChest Pain-sudden onset over anterior chestsharp and pleuriticImproves by leaning forwardRadiates commonly to trapezius ridgesPericardial Friction RubEKG findings depend on stage2 of 3 needed to make diagnosis +/- effusion.

Diagnostic evaluationHistoryPhysicalSearch for systemic disordersECGCXRANA in selected cases

PPDHIVBCx if febrileNo routine viral culturesWorkup for malignancy if history suggestsEcho-Class Ia

Pericardial Friction RubAuscutationScratchy or squeaky sound LLSB most frequent site Use the diaphragmsuspended respirationHighly specific for pericarditis (up to 85%). Intermittent sensitivity can vary.Heard better in patients without effusion. Result of friction from 2 inflamed layers of pericardium

EKG FindingsStage IST elevation in most leadsExceptions aVR and V1 Depression of PR segmentLow voltage QRS usually assoc with tampanode

Stage II Transition or pseudonormalization or ST/PR segments

Stage III T wave inversions.

Stage IV Normalization vs persistent changes

*No changes in metabolic causes

EKG changesArrhythmias uncommon. Arryhthmias suggest myocarditis or ischemia

Distinction From AMIST elevations in pericarditis: begin at J point, rarely exceed 5 mm, and retain normal concavityST elevations / T wave changes are more generalized No reciprocal lead changesST elevations and T wave inversions do not occur at the same timePR segment changes commonQ waves/QT prolongation/Hyperacute T waves uncommon

Cardiac BiomarkersCan see elevation in CK, MB, TpnI22% of patients with Acute Pericarditis in one trial were above TpnI thresholdTransient rise, resolving within the first 7 daysPatients with higher TpnI did not have higher complication rates

CXR findingsTypically normal in Pericarditis200ml of pericardial fluid needed to accumulate before enlargement of the cardiac silhouette seenCalcification in chronic cases may be appreciated

Lateral CXR of a person with chronic calcified pericarditis due to TB

A cystic massB calcified pericardium

Echocardiogram Should be done in all casesOften normal in patients with pericarditis, unless associated with pericardial effusionPresence of pericardial effusion helps support diagnosis, while absence does not exclude it

Pericardial Effusion

Diagnostic evaluationNot needed in all patients- Viral and idiopathic usually follow a benign course after treatmentIt is important to rule out significant effusion and tamponade in patients

ManagementSimple, uncomplicated pericarditisNo high risk featuresMedical managementoutpatient if proper F/U is established

High Risk FeaturesSubacute onsetFever >100.4LeukocytosisCardiac tamponadeLarge pericardial effusion (>2cm) not decreased after NSAIDSImmunosuppressedHx of anticoagulationAcute TraumaFailure to respond to NSAIDS

TreatmentsASA-Class I (2-6g/day) or (800mg q6h tapered by 800mg /week for 3-4 weeks)ASA resistance at 1 week should prompt further investigationNSAIDS- ClassI (Ibuprofen 300-800mg q6h)GI prophylaxisColchicine- Class IIaIntrpericardial Steroids Class IIaCorticosteroids if refractory to NSAIDS

PericardiocentesisIf moderate to severe tamponade is present Class IA recommendationIf purulent, TB, or neoplastic pericarditis is suspected- Class II a recommendationPersistent symptomatic pericardial effusion

ComplicationsConstrictionscarring and consequent loss of elasticity of the pericardial sac Tamponadeaccumulation of pericardial fluid under pressure Effusive-constrictive pericarditisRecurrent Pericarditis- seen in 15-30% of patients with idiopathic pericarditis. Immune autoreactivity thought to play a primary role.

Pericardial TamponadeIncreased Pericardial Pressures leading to compression of all cardiac chambersPericardial elasticity maybe limited (Acute vs Chronic)Cardiac chambers become small and chamber diastolic compliance is reducedDecreased cardiac filling

Physiologic significanceEarly diastolic filling decreases, leading to the majority of venous return occuring during ventricular systoleWhen tamponade is severe, total venous return falls and cardiac chambers shrink

Physical Exam of TamponadeSinus TachycardiaElevated JVPPulsus ParadoxusRub possibleKussmaul's signLess likely w/o constrictive component

Pulsus ParadoxusAn exaggerated fall in systemic blood pressure during inspiration Inspiratory decline in thoracic pressure is transmitted through the pericardium to the right side of the heartSystemic Venous return increases with inspirationIn tamponade, the rigid pericardium prevents the RV free wall from expanding during diastole causing the pressure transmission to the septal wall and decreased LV filling during inspiration

Acute vs chronic accumulationAs little as 20-50 ml acutely can cause tamponade acutelyAs much as 2 liters can accumulate chronically prior to causing tamponade

ConclusionPericarditis has many causesA good history and physical will often lead to diagnosisECHO, EKG, HIV, CXR and PPD should be doneOutpatient management may be reasonableAnti-inflammatories key for medical management