2Dr. Mirdamadi Cardiologist,Fellowship of Echocardiography Pericardial diseaseDr. MirdamadiCardiologist,Fellowship of Echocardiography
3Pericardium The normal pericardium is a double-layered sac the visceral and parietal pericardium that is separated by a small quantity (15–50 cc) of fluid.
4pericardial functions 1. Prevents sudden dilation of the cardiac chambers, especially the right atrium and ventricle, during exercise and with hypervolemia.2.Restricts the anatomic position of the heart3.Minimizes friction between the heart and surrounding structures4. Prevents displacement of the heart and kinking of the great vessels5. Retards the spread of infections from the lungs and pleural cavities to the heart.
6Clinical Classification I. Acute pericarditis (<6 weeks) A. Fibrinous B. Effusive (serous or sanguineous) II. Subacute pericarditis (6 weeks to 6 months) A. Effusive-constrictive B. Constrictive III. Chronic pericarditis (>6 months) A. Constrictive B. Effusive C. Adhesive (nonconstrictive)
7Etiologic Classification I. Infectious pericarditisA. Viral (coxsackievirus A and B, echovirus, mumps, adenovirus, hepatitis, HIV)B. Pyogenic (pneumococcus, streptococcus, staphylococcus, Neisseria, Legionella)C. TuberculousD. Fungal (histoplasmosis, coccidioidomycosis, Candida, blastomycosis)E. Other infections (syphilitic, protozoal, parasitic)
8II. Noninfectious pericarditis A. Acute myocardial infarctionB. UremiaC. Neoplasia1. Primary tumors (benign or malignant,mesothelioma)2. Tumors metastatic to pericardium(lung and breast cancer, lymphoma, leukemia)D. MyxedemaE. CholesterolF. Chylopericardium
9G. Trauma 1. Penetrating chest wall 2. Nonpenetrating H G. Trauma 1. Penetrating chest wall 2. Nonpenetrating H. Aortic dissection (with leakage into pericardial sac) I. Postirradiation J. Familial Mediterranean fever K. Familial pericarditis L. Acute idiopathic M. Whipple's disease N. Sarcoidosis
10III. Pericarditis related to hypersensitivity or autoimmunity A. Rheumatic feverB. Collagen vascular diseaseC. Drug-inducedD. Post-cardiac injury1. Postmyocardial infarction (Dressler's syn.)2. Postpericardiotomy3. Posttraumatic
11DefinitionAcute Pericarditis defined as symptoms or signs resulting from pericardial inflammation of no more than 1-2 weeksThe majority of causes is idiopathicMost cases of acute idiopathic pericarditis are viral but testing for specific virus is not routine
12Acute pericarditis almost always presents with chest pain The pain can be severe.It is almost always pleuritic. It is not similar to myocardial ischemia.Pericardial pain typically has a relatively rapid onsetIt is most commonly substernal but can be centered in the left anterior chest or epigastrium.Left arm radiation is not unusual. The radiation is to the trapezius ridge, which is highly specific for pericarditis.Pericardial pain is relieved by sitting forward andworsened by lying down.
13Associated symptoms : dyspnea, cough, and hiccoughs. history of symptoms suggesting a viral syndrome is common.It is important to review the past medical history for clues to specific diagnoses. A history of cancer or an autoimmune disorder, high fevers with shaking chills, rash, or weight loss should alert the physician to specific diseases that can cause pericarditis.
14Differential Diagnosis pneumonia or pneumonitis with pleurisy (which may coexist with pericarditis),pulmonary embolus or infarction,costochondritis,gastroesophageal reflux disease.myocardial ischemia or infarctionaortic dissectionintraabdominal processespneumothoraxherpes zoster pain before skin lesions appear.Acute pericarditis due to recent silent MI.
15Physical ExaminationPatient is uncomfortable and anxious and may have low grade fever and sinus tachycardia.The only abnormal physical finding is the friction rub caused by contact between visceral and parietal pericardium.It consists of three components corresponding to ventricular systole, early diastolic filling, and atrial contraction .The rub is usually loudest at the LSB and is best heard with the patient leaning forward.
16It is often dynamic, disappearing and returning during short periods. Thus, it is often rewarding to listen frequently to a patient with suspected pericarditis who does not have an audible rub initially.
18ElectrocardiographyST-segment elevation in all leads except aVR and often V1.The ST segment is usually coved upward and resembles the hyper acute MI(differentiation with more extensive lead involvement in pericarditis and the presence of reciprocal ST depression in ischemia.)However, ST elevation in pericarditis sometimes involves a smaller number of leadsSomtimes, the ST segment is similar to early repolarization. Here again, pericarditis usually involves more leads than typical early repolarization
19As with the rub, electrocardiographic changes can be dynamic.
20PR segment depression is also common . PR depression can occur without ST elevation and be the initial or sole ECG manifestation of acute pericarditis.
21In some, the ECG reverts to normal during days or weeks. In others, the elevated ST segment progresses to ST-segment depression and T wave inversions in leads with upright QRS complexes.These changes can persist for weeks or even months .
22In patients presenting late after the onset of symptoms, these findings can be difficult to distinguish from ischemia
24Laboratory DataModest elevations of the white blood cell count with mild lymphocytosisElevated creatine kinase MB fraction or troponin I valuesSerum ANA evaluation in young woman is recommended.
25The CXR is usually normal in uncomplicated acute idiopathic pericarditis but pulmonary disease,TB,malignancy or pericardial effusion may be detected by CXR
26Echocardiography Echo is normal in the most patients . The main reason for it is to exclude silent effusion. Most patients do not have effusions, but small ones are fairly common .Moderate or larger effusions are unusual and may signal a diagnosis other than idiopathic pericarditis.Echo is also useful to rule out associated myocarditis.
27TreatmentAcute idiopathic pericarditis is a self-limited disease without significant complications or recurrence in 70% to 90% of patients.
28Treatment with NSAIDs should be initiated Ibuprofen (600 to 800 mg orally three times daily) with discontinuation if pain is no longer present after 2 weeks.
29Patients who respond slowly or inadequately to NSAIDs may require supplementary narcotic analgesics to allow time for a full response or a course of colchicine.Colchicine is administered as a 2- to 3-mg oral loading dose followed by 1 mg daily for 10 to 14 days
30Poorly responding patients have typically been treated with short courses of corticosteroids. However, corticosteroids should be avoided as they appear to encourage recurrences.Prednisone 60 mg orally daily for 2 days with tapering to zero during a week.
33The accumulation of fluid in the pericardial space in a quantity sufficient to cause serious obstruction to the inflow of blood to the ventricles results in cardiac tamponade.This complication may be fatal if it is not recognized and treated promptly.
34The most common causes of tamponade : neoplastic diseaseidiopathic pericarditisrenal failure.Tamponade may also result from bleeding into the pericardial space after cardiac operations, trauma, and treatment of patients with acute pericarditis with anticoagulants.
35The three principal features of tamponade (Beck's triad) : HypotensionSoft or absent heart soundsJugular venous distention with a prominent x descent but an absent y descent
36The quantity of fluid necessary to produce tamponae may be as small as 200 mL when the fluid develops rapidly or >2000 mL in slowly developing effusions .Tamponade may also develop more slowly, and in these circumstances the clinical manifestations may resemble those of heart failure, including dyspnea, orthopnea, and hepatic engorgement
38presence of cardiac tamponade consists of a greater than normal (10 mmHg) inspiratory decline in systolic arterial pressure
39Since both ventricles share a tight incompressible covering, the inspiratory enlargement of the right ventricle in cardiac tamponade compresses and reduces left ventricular volumeleftward bulging of the IVS further reduces the left ventricular cavity as well.
40Thus, the normal inspiratory augmentation of right ventricular volume causes an exaggerated reciprocal reduction in left ventricular volume.
41respiratory distress increases the fluctuations in intrathoracic pressure, which exaggerates the mechanism just described.RV MI may resemble cardiac tamponade with hypotension, elevated JVP, an absent y descent in the JVP, and, occasionally, pulsus paradoxus.
42Differential Diagnosis of Paradoxical Pulse constrictive pericarditishypovolemic shock,acute and chronic obstructive airway diseasepulmonary embolus.RV MI
43Electrocardiographic abnormalities 1.reduced voltage2.electrical alternansElectrical alternans caused by anterior-posterior swinging of the heart with each heart beat.
45TreatmentPatients with acute pericarditis should be observed frequently for the development of an effusionif a large effusion is present, the patient should be hospitalized and pericardiocentesis carried out or the patient should be watched closely for signs of tamponade
47Constrictive Pericarditis(CP)results of healing a fibrinous or serofibrinous pericarditis or the resorption of a chronic pericardial effusionThe latter gradually contracts and forms a firm scar, which may be calcified, encasing the heart and interfering with filling of the ventricles
48EtiologiesCP may follow acute or relapsing viral or idiopathic pericarditisTrauma with organized blood clotCardiac surgery of any typeMediastinal irradiationPurulent infection,TBHistoplasmosisNeoplastic disease (especially breast cancer, lung cancer, and lymphoma)Rheumatoid arthritis, SLEChronic renal failure with uremia treated by dialysis.
49The basic abnormality in this patients is the inability of the ventricles to fill because of the limitations imposed by the rigid, thickened pericardiummyocardial function is normal or only slightly impairedHowever, the fibrotic process may extend into the myocardium and cause myocardial scarring and atrophy
50In constrictive pericarditis, JVP display an M-shaped contour, with prominent x and y descents. The y descent, which is absent or diminished in cardiac tamponade, is the most prominent deflection in constrictive pericarditis
51The usual presentation consists of signs and symptoms of right-sided heart failure. Include lower extremity edema, vague abdominal complaints, and passive hepatic congestion.As the disease progresses, hepatic congestion worsens and can progress to ascites, anasarca, and jaundice due to cardiac cirrhosis.
52In end-stage , the effects of a chronically low cardiac output are prominent, including severe fatigue, muscle wasting, and cachexia.Other findings include recurrent pleural effusions and syncope.
53CP can be mistaken for any cause of right-sided heart failure As well as end-stage primary hepatic disease. venous pressure is not elevated in the latter circumstance.
54Physical Examinationmarkedly elevated JVP with a prominent, rapidly collapsing y descent.This, combined with a normal x descent, results in an M- or W-shaped contour
55The cervical veins are distended and may remain so even after intensive diuretic treatment, and venous pressure may fail to decline during inspiration (Kussmaul's sign).The latter may occur in chronic pericarditis , tricuspid stenosis, right ventricular infarction, and restrictive cardiomyopathy.
56The pulse pressure is normal or reduced. In 1/3 of cases, a paradoxical pulse can be detected.Congestive hepatomegaly is pronounced and may impair hepatic function and cause jaundiceascites is common and is usually more prominent than dependent edema
57The apical pulse is reduced and may retract in systole (Broadbent's sign). The heart sounds may be distantPericardial knock, in early diastole occurs with the abrupt cessation of ventricular filling.A systolic murmur of tricuspid regurgitation may be present.
58The ECG frequently displays : Low voltage of the QRS complexesDiffuse flattening or inversion of the T waves.Atrial fibrillation is present in about one-third of patients.
59The CXR shows a normal or slightly enlarged heart Pericardial calcification is most common in tuberculous pericarditis.Pericardial calcification may,occur in the absence of constriction.
61More accurate modalities EchocardiographyMRICT-scan
62TreatmentPericardial resection is the only definitive treatment of constrictive pericarditis and should be as complete as possible. Dietary sodium restriction and diuretics are useful during preoperative preparation.