1 MAGDI AWAD SASI PERICARDIAL DISEASES 2013PERICARDIAL DISEASESFunctions of pericardium:PERCARDITISEssential for diagnosisESSENTIALS OF DIAGNOSIS_ Anterior pleuritic chest pain that is worse supine than upright.Pericardial rub.Fever common.Erythrocyte sedimentation rate usually elevated.ECG - diffuse ST segment elevation with associated PR depression.
2 MAGDI AWAD SASI PERICARDIAL DISEASES 2013 Pericaditis refers to an inflammation of a visceral pericardium which is amembranous sac enveloping the heart .Pericarditis can be acute or chronic. Acute pericarditis(< 2 weeks) occurs due tocomplications of infections or may be due to systemic diseases (autoimmunesyndromes, uremia), neoplasm, radiation, drug toxicity, hemopericardium,postcardiac surgery, or contiguous inflammatory processes in the myocardiumor lung. In many of these conditions, the pathologic process involves both thepericardium and the myocardium.Chronic pericarditis is however less common a form of constrictive pericarditis.It can also be a primary illness which develop as a result of medical and surgicaldisorders . More common in men Occurs between the ages of 20 to 50 yearsPathology:Depends on underlying cause and severity of inflammationSerous pericarditisSerofibrinous pericarditisSuppurative (purulent) pericarditisHemorrhagic pericarditis
3 MAGDI AWAD SASI PERICARDIAL DISEASES 2013AETIOLOGY:I. INFECTIVE A.viral illnessCoxsackie A & B((the commonest)), Echovirus, Hepatitis B ,HIV, Influenza,Mononucleosis ,Mumps ,Varicella ,EBV ,Adeno.B.Bacterial infections-Stab wounds, pneumonia, endocarditis, sepsis, surgical contamination,Tuberculosis, Diphtheria, Staphylococcus, pneumococus.C .Fungal- Candida D. Parasitic- AmoebaII. AUTOIMMUNE1. Systemic lupus erythematosus (SLE)2. Drug-Induced lupus (e.g. Hydralazine, Procainamide, ioniazide.minoxidil, penicillins, clozapine)3. Rheumatoid Arthritis4. Post Cardiac Injury Syndromes i.e. postmyocardial Infarction(Dresslers) Syndrome, postcardiotomy syndrome, TraumaIII. NEOPLASM1. Primary mesothelioma2. Secondary, metastatic breast cancer, renal cell carcinoma,Hodgkin disease, and lymphomas3. Direct extension from adjoining tumorIV. RADIATION PERICARDITISV. RENAL FAILURE (uremia)VI. TRAUMATIC CARDIAC INJURY1. Penetrating - stab wound, bullet wound2. Blunt non-penetrating - automobile steering wheel accidentVII. Chemotherapy VIII IDIOPATHIC (exclude others 1s)
4 MAGDI AWAD SASI PERICARDIAL DISEASES 2013Pericarditis & AMI• If occurs within 2 – 7 days following an AMI– Considered a pericardial inflammatory response to the AMI.• Dressler Syndrome– May occur 2 weeks to several months after the event aftermyocardial infarction or open heart surgery, may be recurrent– Autoimmune response to myocardial necrosis involving both thepleura and the pericardium.– Patients present with typical pain, fever, malaise, and leukocytosis.Occasionally, the syndrome will occur within days of surgery.Rarely, other symptoms of an autoimmune disorder, such as jointpain and fever, may occur. Tamponade is rare with Dresslersyndrome after myocardial infarction but not when it occurspostoperatively. PATHOPHYSIOLOGYACUTEIn acute pericarditis when microbes are inhaled or ingested, they migrate tomyocardium and cause inflammation. So when these membranes are inflamed,they rub against each other and cause classic sounds of which the patientcomplains of severe chest pains which increases when the patient lies supineand decreases when in sitting position.This acute inflammation causes accumulation of fluid in the pericardial saccalled pericardial effusion. The fluid may be serous which accompanies heartfailure, purulent accompanying tuberculosis and haemorrhage accompanyingtrauma in the heart.The excessive accumulation of fluid in the sac causes compression of the heart,resulting in decrease venous retain of the heart resulting in ventricular fillingand a decrease in stroke volume. These events will eventually lead to cardiacfailure( right 1st), shock and death.
5 MAGDI AWAD SASI PERICARDIAL DISEASES 2013CHRONICChronic pericarditis occurs when the layers adhere to each other causingfibrosis of the pericardial sac due to surgery which later restricts movementof the heart. So the fibrotic pericardium tightens the heart decreasing cardiacfilling and output and later patient may report symptoms of heart failure. CLINICAL MANIFESTATION:The presentation and course of inflammatory pericarditis depend on itscause, but most syndromes have associated chest pain.Sharp chest pain- with a rapid onset that worsens with breathing, coughingand changes position(( pleuritic in nature)) , relief obtained by sittingupright and leaning forward((postural chest pain)).The pain is substernal /? radiate to the neck, shoulders, back, or epigastrium.OFTEN- fever of 37.5 to 38 degrees and precede the chest pain.o Bacterial percarditis- toxic and are often critically ill.o Uremic pericarditis can present with or without symptoms;fever is absent.o Often neoplastic pericarditis is painless, and the presenting symptomsrelate to hemodynamic compromise or the primary diseaseo Chills, Night sweatsDyspnea, coughPERICARDIAL RUB------------to-and-fro rubbing be heard over the entireprecordial region or a very small area.It may be heard in both phases of the cardiac cycle. Pericardial friction rub isunaffected by respiration and is thus differentiated from a pleural frictionrub. It is also increased as pressing the stethoscope firmly against thepatient’s chest wall. A rub may be readily heard at one moment and beabsent several minutes later. The intensity of the rub is usually increasedwhen the subject is sitting upright and leaning forward.
6 MAGDI AWAD SASI PERICARDIAL DISEASES 2013Differentiating Chest PainPericarditis• Pain is often sharp,piercing• Located between theneck and shoulder• Dyspnea unrelated toexertion• Pericardial friction rubAcute MI• Pain is described aspressure• Dyspnea related toexertion• Pain is in the chest andmay sometimes radiateTuberculous Pericarditis 4-10% of All Acute Pericarditis is Caused by TB (Reported up to 80% inSome 3rdWorld Countries) Lymphatic or haematogenous spread. Nonspecific symptoms (fever, night sweats, fatigue) may be present fordays to months. 1-8% of Patients with TB Have Pericardial Involvement Etiology of 20% of Constrictive Pericarditis Cases 93% of all Pericardial Effusions in HIV PatientsFour Pathologic Stages of TB Pericarditis I-Dry: Fibrin Deposition & Granulomatous Reaction. Clinically Silent II-Effusive: Serous Fluid Accumulation Caused by Hypersensitivity toTuberculoprotein and Impaired Resorption III- Absorptive: Effusion Resolves and Fibrous Tissue ReplacesGranulomas, Pericardium Thickens
7 MAGDI AWAD SASI PERICARDIAL DISEASES 2013 IV-Constrictive: Parietal Pericardial CalcificationPresentation Dyspnea 45-90% Rub 30-85% Chest Pain 40-75% Cough 50-95% Orthopnea 20-65% Fever 80-100% Distant Heart Sounds 25-55% 50% of Patient Have Slowly Progressive Insidious Presentation 95% Have Cardiomegally, 30% Have Active Pulmonary TB, 39-71% HavePleural Effusions L>R. Bilateral Pleural Effusions More Common than Rub. “Because of the variable and nonspecific features of TB pericarditis,establishing the diagnosis on clinical grounds alone is impossible. Diagnosis by Pericardial Fluid or Biopsy: Positive AFB Smear, Culture,Caseating Granulomas, TB DNA PCRTreatment Antibiotics: Isoniazid, Rifampin, Pyrazinamide, Ethambutol Corticosteroids: Reduces Mortality and Need for SubsequentPericardiocentisis DIAGNOSTIC EVALUATIN STUDIES OF PERICARDITIS:The diagnosis of viral pericarditis is usually clinical, and leukocytosis is oftenpresent. Rising viral titers in paired sera may be obtained for confirmationbut are rarely done.12-Lead EKG• Most definitive test in acute pericarditis
8 MAGDI AWAD SASI PERICARDIAL DISEASES 2013• The ECG usually shows generalized ST and T wave changes and maymanifest a characteristic progression beginning with diffuse ST elevation,followed by a return to baseline and then to T wave inversion.• Atrial injury is often present and manifested by PR depression especiallyin the limb leads.• ST-segment elevation(saddle shaped) in most leads except V1 and AVR.• NO RECIPROCAL CHANGES OR T INVERSION IN ACUTE DURATION.• PR segment depressed• Electrical alternans– QRS varies from beat to beat(( IN PERICARDIAL EFFUSION))• Atrial dysrhythmias common( IF EXTEND TO MYOCARDIUM))
9 MAGDI AWAD SASI PERICARDIAL DISEASES 2013• Four stages of EKG changesStage 1 S-T elevation seen globally, but more prominent in the precordial leadsStage 2 S-T segment starts to normalize and T-wave increases in amplitudeStage 3 Normal S-T segments and inverted T-wavesStage 4 Resolution of repolarization abnormalities
10 MAGDI AWAD SASI PERICARDIAL DISEASES 2013Chest X-Ray• The chest radiograph is frequently normal.• Cardiac silhouette enlarged if there is pericardial effusion, As well as signsof related pulmonary disease. Mass lesions and enlarged lymph nodesmay suggest a neoplastic process.– If more than 250 ml is presentEchocardiogram Evaluates hemodynamic changes associated with cardiac tamponadeTransesophageal Echocardiogram (TEE) Pericarditis is a clinical diagnosis, not an Echo diagnosis! The echocardiogram is often normal or reveals only a trivial amount offluid during the acute inflammatory process. The diagnosis of tuberculouspericarditis can be inferred if acid-fast bacilli are found elsewhere. Thetuberculous pericardial effusions are usually small or moderate but maybe large. Helpful in evaluating the size of an effusion & compromised ventricularFilling
11 MAGDI AWAD SASI PERICARDIAL DISEASES 2013 Large pericardial effusions and accompanying pleural effusions arefrequent.Labs1.Erhythrocyte Sedimentation Rate (ESR) & Complete Blood Count (CBC)– Non-specific elevation2. Cardiac Profile (CK-MB, troponins)---Rule out AMI /raised TroponinCardiac enzymes may be slightly elevated, reflecting an epicardialmyocarditis component.3. PPD, HIV-AIDS screening4.Rheumatoid factors (RF), Antinuclear Antibodies (ANA)5.CT scan / MRI – locate neoplastic lesions Biopsy of pericardium to obtain tissue sample for culture andmicroscopic examination If bacterial pericarditis is suspected on clinical grounds, diagnosticpericardiocentesis may be of value. In uremic patients not on dialysis, theincidence of pericarditis correlates roughly with the level of blood ureanitrogen (BUN) and creatinine. The pericardium is characteristically“shaggy” in uremic pericarditis, and the effusion is hemorrhagic andexudative. The diagnosis of neoplastic pericarditis can occasionally be made bycytologic examination of the effusion or by pericardial biopsy, but it maybe difficult to establish clinically if the patient has received mediastinalradiation within the previous year. Neoplastic pericardial effusionsdevelop over a long period of time and may become quite huge (> 2 L).Clinical ManagementUncomplicated Viral Pericarditis• Treatment of viral pericarditis is generally symptomatic. Aspirin (650 mgevery 3–4 hours) or other nonsteroidal agents (eg, indomethacin, 100–150mg daily in divided doses) are usually effective.
12 MAGDI AWAD SASI PERICARDIAL DISEASES 2013• Indomethacin & Colchicine --Allergy to NSAIDs or aspirin• Narcotic analgesia• Corticosteroids may be beneficial in unresponsive cases.Complicated pericarditis• In general, symptoms subside in several days to weeks. The major earlycomplication is tamponade, which occurs in less than 5% of patients.There may be recurrences in the first few weeks or months.• Rarely, acute pericarditis may lead to constrictive pericarditis, which maynecessitate pericardial resection• Uremic pericarditis usually resolves with the institution of aggressivedialysis. Tamponade is common, and partial pericardiectomy (pericardialwindow) may be necessary.• Whereas anti-inflammatory agents may relieve the pain and feverassociated with uremic pericarditis, indomethacin and systemiccorticosteroids do not affect its natural history.• The prognosis with neoplastic effusion is dismal, with only a smallminority surviving 1 year. If it is compromising the clinical comfort of thepatient, the effusion is initially drained percutaneously. Early attempts atballooning the pericardium from a subxiphoid approach have been mostlyabandoned in favor of surgical approaches. A pericardial window, eitherby a subxiphoid approach or via video-assisted thoracic surgery, allowsfor partial pericardiectomy. Instillation of chemotherapeutic agents ortetracycline may occasionally be used to reduce the recurrence rate.• Relapses do occur and may require slow withdrawal of anti-inflammatorytherapy over several months. Colchicine may be required for months tohelp prevent recurrences.• Post-MI Pericarditis• Avoid use of corticosteroids and anti-inflammatory agents– May cause rupture of the infarcted areaPericarditis (recurrent pain or connective tissue disorders)• Corticosteroids are most effectiveMedication-Related Pericarditis Stop the medication
13 MAGDI AWAD SASI PERICARDIAL DISEASES 2013Pericardial Effusion• Accumulation of excessive fluid in the pericardial space• May happen slowly overtime and the pericardialsac accommodates.• The fluid may press onthe heart enough to limitits movement within thesac.• Rapid fluid accumulationresults in CardiacTamponade.Pericardial effusion causes an enlarged heart shadow that is often globularshaped (transverse diameter is disproportionately increased).A lateral film and close-up of a pericardial effusion showing the anteriormediastinal fat (blue arrows) and epicardial fat (red arrows) separated by asoft tissue stripe ( "fat pad" sign) reflecting the pericardial effusion seenedge-on.
14 MAGDI AWAD SASI PERICARDIAL DISEASES 2013The speed of accumulation determines the physiologic importance of theeffusion. Because the pericardium stretches, large effusions (> 1000 mL)that develop slowly may produce no hemodynamic effects. Conversely,smaller effusions that appear rapidly can cause tamponade. Tamponadeis characterized by elevated intrapericardial pressure (> 15 mm Hg), whichrestricts venous return and ventricular filling. As a result, the strokevolume and pulse pressure fall, and the heart rate and venous pressurerise. Shock and death may result.AETIOLOGY:Any cause for pericarditis can cause pericardial effusion and temponade.S&S:Pericardial effusions may be associated with pain if they occur as part ofan acute inflammatory process OR may be painless, as is often the casewith neoplastic or uremic effusion. Dyspnea and cough are common,especially with tamponade. Other symptoms may result from the primarydisease. A pericardial friction rub may be present even with largeeffusions. Diagnosis Same line of investigations for pericarditis. CXR , ECG, ECHO, CTSCAN CHEST ,CBC,ESR,ANA,TB TEST CHEST X RAY Although an effusion is often described as producing a globular-shaped heart, it is usually not possible to differentiate a pericardialeffusion from cardiac enlargement on a chest radiograph. May appear normal in acute situations. Approximately 250 ml of fluid must be in the pericardium to lead toa detectable change in the size of the heart shadow on PA CXR
15 MAGDI AWAD SASI PERICARDIAL DISEASES 2013 small effusions (100–200 mL) may not cause cardiomegaly eventhough they can cause tamponade when they accumulate rapidly orwhen the pericardial membrane is stiffened from fibrosis. Pericardial effusion can be definitively diagnosed with eitherechocardiography (can be bedside in the emergency department inthe critically ill patient patient) or CT chest. ECG The ECG often reveals nonspecific T wave changes and low QRSvoltage. Electrical alternans is present uncommonly but ispathognomonic. It is due to the heart swinging within the largeeffusion. ECHOEchocardiography is the primary method for demonstrating pericardialeffusion and is quite sensitive. Cardiac CT and MRI also demonstrate pericardial fluid and any associatedcontiguous lesions. Diagnostic pericardiocentesis or biopsy is often indicated formicrobiologic and cytologic studies; a pericardial biopsy may beperformed relatively simply through a small subxiphoid incision. Unfortunately, the quality of the pericardial fluid rarely leads to adiagnosis, and any type of fluid (serous, serosanguinous, bloody, etc) canbe seen in most diseases
16 MAGDI AWAD SASI PERICARDIAL DISEASES 2013TreatmentSmall effusions can be followed clinically by careful observations of theJVP and by testing for a paradoxical pulse.Serial echocardiograms are indicated if no intervention is immediatelycontemplated.Continued or repeat drainage may be indicated, especially in malignanteffusions. Pericardial windows via video-assisted thorascopy have beenparticularly effective in preventing recurrences. Additional therapy isdetermined by the nature of the primary process. Recurrent effusion inneoplastic disease and uremia, in particular, may require partialpericardiectomy as noted earlier.Trivial pericardial effusions are common, especially in CHF, and need notbe referred.• Hypotension or a paradoxical pulse suggesting the pericardial effusion ishemodynamically compromising the patient should prompt an immediatereferral._
17 MAGDI AWAD SASI PERICARDIAL DISEASES 2013Cardiac TamponadeIt is an impairment of ventricular filling during diastole due to someexternal pressure on the heart by pericardial effusion. Tamponade ischaracterized by elevated intrapericardial pressure (> 15 mm Hg), whichrestricts venous return and ventricular filling. As a result, the strokevolume and pulse pressure fall, and the heart rate and venous pressurerise. This leads to obstructive shock. Shock and death may result.Tamponade can occur acutely (eg, due to rupture of the heart or aorta,trauma, or as a complication of catheter or pacemaker procedures) orsubacutely (eg, due to neoplasm, uremia, or idiopathic pericarditis).Accumulation of fluid under high pressure:compresses cardiac chambers & impairsdiastolic filling of both ventriclesSV venous pressuresCO systemic& pulmonary congestionHypotension/shock JVD ralesReflex tachycardia HepatomegalyAscitesPeripheral edema
18 MAGDI AWAD SASI PERICARDIAL DISEASES 2013Symptomatology of Cardiac Tamponade:((Low cardiac output symptoms with heart failure))Acute: (trauma, LV rupture)profound hypotension-Fatigue, dizziness, syncope, lose of effortconfusion/agitationSlow/Progressive large effusion (weeks)Fatigue ( CO)DyspneaJVD1. LVF:.Chest pain _oppressive precordial , positional as it is preceded bypericarditis, stabbing in quality..Fullness in chest pushing on her heart.Dyspnea on exertion , at rest , PND.Cough dry irritant positional( more on laying )2. RVF:. Abdominal pain , dysphagia.Early statiety. Abdominal distention. Nausea hoarsness.Edema or ascites are rarely present; these signs favor a more chronicprocess.
19 MAGDI AWAD SASI PERICARDIAL DISEASES 2013Clinical Signs of Cardiac Tamponade:Tamponade has a spectrum of presentations ranging from circulatorycollapse to mildly reduced cardiac output with symptoms of dyspnea andchest or abdominal discomfort depending on the rate of fluid collection.• Generalo Anxiouso Apprehensiveo Ashen gray facieso Cool perspiration• Tachycardia• Tachypnea• Jugular venous distension-NO Y DESCENT IN RA/RV• Peripheral Cyanosis• Quiet precordium with both inspection and palpation• muffled heart sounds• Rub• Right upper quadrant tenderness• The venous pressure tracing shows absence of diastolic y descent (i.e.there is a deep x descent but y descent is absent) . Cardiac tamponadealso causes a raised JVP, Kussmaul’s sign and pulsus paradoxus.• Summary signs of cardiac tamponade are:1. Rapid x descent2. Kussmaul’s sign3. Pulsus paradoxus
20 MAGDI AWAD SASI PERICARDIAL DISEASES 2013• Bamberger-Pins-Ewart signo Variable dullness and bronchial breathing at one or both basesmost frequently the left below the 9th rib and between the midscapular line and the spine(( lung collapse)).o Becks triad (1) systemic hypotension(2) elevated systemic venous pressure(3) muffled heart sounds is typical of acute tamponadewhich may be due to abrupt intrapericardial hemorrhage frompenetrating trauma, invasive cardiac procedures, or rupture of anascending aortic dissection or myocardial infarction. The completetriad is rarely present• Pulsus Paradoxuso First described by Kussmaul in 1873 as a palpable decrease orabsence of the radial pulse during inspiration.o Physiological bases (in normal person)o Intrapericardial pressure (IPP) tracks intrathoracic pressure.o Inspiration:o Negative intrathoracic pressure is transmitted to the pericardialspace.o IPP blood return to the right ventricleo jugular venous and right atrial pressureso right ventricular volume interventricular septum shiftstowards the left ventricle left ventricular volumeo LV stroke volumeo blood pressure (<10mmHg is normal) during inspiration
21 MAGDI AWAD SASI PERICARDIAL DISEASES 2013o Pulsus paradoxicus, an accentuated fall in the systolic pulsepressure (>10 mm Hg) during inspiration, is not present in one-quarter of patients with tamponade.o A greater than10 mm Hg decline in systolic pressure duringinspiration due to further impairment of LV filling—is the classicfinding• Place the patient in a position of comfort and conduct manometric studies• Raise sphygmomanometer pressure until Korotkoff sounds disappear.• Lower pressure slowly until first Korotkoff sounds are heard during earlyexpiration with their disappearance during inspiration.• Record this pressure.• Very slowly lower pressure until Korotkoff sounds are heard throughoutthe respiratory cycle with even intensity and Record this pressure.• The difference B/W the two recorded pressures is the Pulsus Pardoxus.• Significant pulsus paradox is greater than or equal to 10% of the pressureat which all Korotkoff sounds are heard with even intensity.• Pulsus Paradoxus is felt to be present when the paradoxus is greater than10% of the pressure at which all Korotkoff sounds are heard with evenintensity(( > 10 mm Hg drop in BP with inspiration)).Conditions in which Cardiac Tamponade presents without a Pulsus Paradoxus• Septal Defect• Severe Aortic Stenosis• Severe Left Ventricular Dysfunctiono Cardiomyopathyo Myocardial infarction
22 MAGDI AWAD SASI PERICARDIAL DISEASES 2013Other Etiologies of Pulsus Paradoxus• Large pulmonary embolus• Severe COPDexacerbation• Labored respiration• Constrictive pericarditis• Restrictivecardiomyopathy• Right ventricularinfarction• Circulatory shock• Large pleural effusions• Tense ascites• Extreme obesitySUMMARY:i. Acute cardiac tamponade is generally sudden in onset, may beassociated with chest pain and dyspnea, and is life-threatening if notpromptly treated. The central venous pressure is typically markedlyelevated, while hypotension is common due to the decline in cardiacoutput. The heart sounds are often muted.ii. Subacute cardiac tamponade is a less dramatic process. Patients maybe asymptomatic or may complain of dyspnea, chest discomfort orfullness, peripheral edema, fatiguability, or other symptoms referableto increased filling pressures and limited cardiac output. The physicalexamination in subacute tamponade may reveal hypotension with anarrow pulse pressure, reflecting the limited stroke volume. However,patients with preexisting hypertension may remain hypertensive dueto increased sympathetic discharge.
23 MAGDI AWAD SASI PERICARDIAL DISEASES 2013DIAGNOSIS:ECG FINDINGEKG in the setting of tamponade often shows sinus rhythm with low voltage(QRS amplitude in the limb leads <5 mm) suggestive of tamponadephysiology.Electrical alternans, a more specific sign of tamponade occurs when there is avery large pericardial effusion in which the heart swings during cardiaccontraction causing a beat-to-beat variation in the ECG axis (QRS amplitude).ElectricalalternansLow voltageP-R depressionEtiologies ofElectricalAlternans:1. Pericardial effusion2. Constrictive pericarditis3. Tension pneumothorax4. Myocardial dysfunction– Severe cardiomyopathy– Myocardial infarction
24 MAGDI AWAD SASI PERICARDIAL DISEASES 2013Echocardiographic• If tamponade is present, the high intrapericardial pressure may collapselower pressure cardiac structures, such as the RA and RV. In tamponade,the normal inspiratory reduction in LV filling is accentuated due to RV/LVinteraction and there is a > 25% reduction in maximal mitral inflowvelocities.• Pericardial effusion,Right atrial collapse,Right ventricular diastoliccollapse,Swinging heart• Respiratory variation of tricuspid and mitral valve flow velocities.• Right ventricular diastolic collapse is a highly sensitive and specificindicator of Cardiac Tamponade.• Right atrial collapse although specific for Cardiac Tamponade was lesssensitive for the detection of Cardiac Tamponade.• Right heart collapse may not be seen in patients with pulmonary HTN andCardiac TamponadeCONCLUSIONS:• The gold standard for the diagnosis of pericardial effusion isechocardiography.• The diagnosis of Cardiac Tamponade is based solely on PHYSICAL EXAM.
25 MAGDI AWAD SASI PERICARDIAL DISEASES 2013TREATMENT:When tamponade is present, urgent pericardiocentesis is required.Because the pressure– volume relationship in the pericardial fluid iscurvilinear and up sloping, removal of a small amount of fluid oftenproduces a dramatic fall in the intrapericardial pressure and immediatehemodynamic benefit; but complete drainage with a catheter ispreferable.Surgical Care• Pericardiocentesis:• Indicated in pt’s• With effusions > 250 mL or• Effusion increases despite intensive dialysis for 10-14 days or• Evidence of tamponade.•• Pericardial window is a modification of balloon valvuloplasty:In which an uninflated balloon is passed inside the pericardial space,where it is opacified, inflated, and then pulled through the pericardium tocreate a window through which pericardial fluid drains into the peritonealor pleural space• Subxiphoid pericardiotomy:• Is performed under local anesthesia and has a lower risk ofcomplications compared to pericardiectomy. Consider subxiphoidpericardiotomy for large effusions that do not resolve.• Pericardiectomy:• Is the most effective procedure managing large effusions because ithas the lowest associated risk of recurrent effusions.• It requires general anesthesia & thoracotomy; therefore, should beconsidered only if pericardiotomy cannot be performed or has beenunsuccessful.
26 MAGDI AWAD SASI PERICARDIAL DISEASES 2013EDIAGNOSIS Constrictive PericarditisESSENTIAL FOR DIAGNOSISEvidence of right heart failure with an elevated JVP, edema,hepatomegaly, and ascites.No fall or an elevation of the JVP with inspiration (Kussmaul sign).Echocardiographic evidence for septal bounce and reduced mitral inflowvelocities with inspiration.Catheterization evidence for RV-LV interaction, a “square root” sign,equalization of diastolic pressures, normal pulmonary artery pressure,and narrow RV pressure tracing that increases with inspiration.PATHOPHYSIOLOGY:Inflammation can lead to a thickened, fibrotic, adherent pericardium thatrestricts diastolic filling and produces chronically elevated venous pressures. Inthe past, tuberculosis was the most common cause of constrictive pericarditis,but the process now more often occurs after radiation therapy, cardiac surgery,or viral pericarditis; histoplasmosis is another uncommon causeFibrous scar formationFusion of pericardial layersCalcification further stiffens pericardiumRigid, scarred pericardium encircles heart:Systolic contraction normalInhibits diastolic filling of both ventriclesSV venous pressuresCOSystemic & pulmonary congestionHypotension/shock JVD RalesReflex tachycardia HepatomegalyAscitesPeripheral edema
27 MAGDI AWAD SASI PERICARDIAL DISEASES 2013Clinical FindingsA. Symptoms and Signs:The principal symptoms are slowly progressive dyspnea, fatigue, andweakness. Chronic edema, Right hypochondrial pain or fullness,abdominal distention, lose of apetite are common symptoms.Physical finding-HR, BPascites, edema, hepatomegalyHepatic congestion and ascites are usually present.Ascites often seems out of proportion to the degree of peripheral edema.The examination reveals these signs and a characteristically elevatedjugular venous pressure with a rapid y descent. This can be detected atbedside by careful observation of the jugular pulse and noting anapparent increased pulse wave at the end of systole (due to accentuationof the v wave by the rapid y descent).Kussmaul sign—inspiration: intrathoracic pressure, venous return to thoraxintrathoracic pressure not transmitted though to RVNo pulsus paradoxus!( unusual).No inspiratory augmentation of RV filling (rigid pericardium)Intrathoracic systemic veins become distendedJVP rises with inspiration (normally falls)Definition-a failure of the JVP to fall with inspiration—is also a frequentfinding. The apex may actually retract with systole and a pericardial“knock” may be heard in early diastole.((sudden cessation of ventricular diastolic filling imposed by rigidpericardial sac)).Atrial fibrillation is common.Summary = RT HEART FAILURE + JVP + PERICARDIAL KNOCK.
28 MAGDI AWAD SASI PERICARDIAL DISEASES 2013DIAGNOSISAt times constrictive pericarditis is extremely difficult to differentiate fromrestrictive cardiomyopathy. When unclear, the use of noninvasive testing andcardiac catheterization is required to sort out the difference.1. CHEST X RAY:The chest radiograph mayshow normal heart size orcardiomegaly. Pericardialcalcification is best seenon the lateral view and isuncommon. It rarelyinvolves the LV apex, andfinding of calcification atthe LV apex is moreconsistent with LVaneurysm.2. Cardiac CT and MRI are only occasionally helpful. Pericardialthickening of > 4 mm must be present to establish the diagnosis, yet nopericardial thickening is demonstrated in 20–25% of patients withconstrictive pericarditis
29 MAGDI AWAD SASI PERICARDIAL DISEASES 20133. Echocardiography—Echocardiography rarely demonstrates a thickened pericardium. Aseptal “bounce” reflecting the rapid early filling is common, though.RV/LV interaction may be demonstrated by a reduction in the mitralinflow pattern of > 25%, much as in tamponade.4. Cardiac catheterization-Because of the need to demonstrate RV/LV interaction, cardiaccatheterization should include simultaneous measurement of both theLV and RV. Hemodynamically, patients with constriction haveequalization of end-diastolic pressures throughout their cardiacchambers, there is rapid early filling then an abrupt increase indiastolic pressure (“square-root” sign), the RV end-diastolic pressure ismore than one-third the systolic pressure, simultaneousmeasurements of RV and LV systolic pressure reveal a discordanceWith inspiration (the RV rises as the LV falls), and there is usually aKussmaul sign (failure of the RA pressure to fall with inspiration).The width (or area) of the RV pressure tracing may also be less inexpiration and greater during inspiration, reflecting the variability infilling of the RV with respiration.In restrictive cardiomyopathy, the LV diastolic pressure is usuallygreater than the RV diastolic pressure by 5 mm Hg, there is pulmonaryhypertension, and simultaneous measurements of the RV and LVsystolic pressure reveal a concordant drop in the peak systolic pressurein both with inspiration.Aetiology Tuberculous Pericarditis Cardiac Sarcoidosis Cardiac Amyloidosis Giant Cell Myocarditis Radiation Post-surgery Neoplasm
30 MAGDI AWAD SASI PERICARDIAL DISEASES 2013TREATMENT:Diuretics- Initial treatment consists of diuresis. As in other disorders of rightheart failure, the diuresis should be aggressive, using loop diuretics (torsemideif bowel edema is suspected), thiazides ,and aldosterone antagonists (especiallyif ascites is present).Surgical pericardiectomy should be done when diuretics are unable to controlsymptoms. symptoms are usually dramatically improved.Most experts recommend earlier rather than later pericardiectomy if symptomsare presentTAMPONADE• Low cardiac output state• JVD present• NO Kussmaul’s sign• Equalized diastolicpressures• RA: blunted y descent• Decreased heart soundsCONSTRICTION• Low cardiac output state• JVD present• Kussmaul’s sign• Equalized diastolicpressures• RA: rapid y descent• Pericardial “knock”Constriction vs. TamponadeSummaryConstriction vs. TamponadeSummaryTAMPONADEPulsus paradoxus:PresentEcho/MRI:• Normal systolic function• Large effusion• RA & RV compressionTreatment:PericardiocentesisCONSTRICTIONPulsus paradoxus:AbsentEcho/MRI:• Normal systolic function• No effusion• Pericardial thickeningTreatment:Pericardial stripping