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Acute pericarditis.pptx
- 1. PERICARDIAL EFFUSION Dr Sandeep Bansal, MD ( Internal Medicine )-PGIMER,Chandigarh DM(Cardiology),DNB(Cardiology),MNAMS, FESC,FSCAI,FCAPSC,FAPSIC,FIMSA,FISC Consultant in Cardiology Professor and Head Department of Cardiology Vardhman Mahavir Medical College and Safdarjung Hospital, New Delhi-110029, Indi
- 2. CASE • RAJU • 30/M • PLUMBER BY OCCUPATION • ALCOHOLIC, SMOKER
- 3. CHIEF COMPLAINTS • CHEST PAIN SINCE 6-8HRS • SWEATING AND GHABRAHAT • HOPI: • FEVER SINCE 1 DAY • TRAUMA 1 WEEK BACK
- 5. RELEVANT INVESTIGATIONS • 2D ECHO: NO RWMA, EF: NORMAL • TROP I: 0.63 DIAGNOSED AS ANTERIOR WALL M.I.: STARTED ON TREATMENT FOR ACUTE CORONARY SYNDROME, THROMBOLYSED
- 6. FOLLOW UP • GENERAL CONDITION DETERIORATED • SUBSEQUENT ECG
- 9. • 2D ECHO AFTER 2DAYS SHOWS MODERATE PERICARDIAL EFFUSION
- 10. INTRA ARTERIAL B.P. TRACING
- 11. • CORONARY ANGIOGRAPHY: NORMAL CORONARIES • URGENT PERICARDIOCENTESIS WAS DONE: • 400ML OF STRAW COLORED FLUID • DEVELOPED COAGULUM ON STANDING • (REPORTS AWAITED)?TUBERCULAR
- 13. Pathophysiology: Disorders of pericardium Etiology Change the permeability of pericardial vascularity Influx of neutrophils & other chemical mediators Inflammatory response Restriction of heart motion and pain with breathing Pericardial inflammation & edema
- 14. • distinction between acute pericarditis and acute myocardial infarction (AMI) is a difficult one. • Clinically, both presentations cause chest pain that is often described as severe in nature. • Classic, textbook descriptions of the conditions (eg, pleuritic, positional pain radiating to the trapezius ridge in pericarditis; substernal pressure radiating to the left jaw/neck/arm in AMI) are often absent in real patients.
- 15. Acute pericarditis • in contrast with acute myocardial infarction, typically induces diffuse ST-segment elevation, usually in most of the chest leads and also in leads I, aVL, II, and aVF. • Reciprocal ST-segment depression is seen in lead aVR. • Important clue to acute pericarditis is the frequent presence of PR- segment elevation in aVR, with reciprocal PR-segment depression in other leads, caused by a concomitant atrial current of injury • Abnormal Q waves do not occur with acute pericarditis, and the ST- segment elevation may be followed by T wave inversion after a variable period.
- 18. Major causes of pericardial disease Idiopathic Infections Viral , tubercular Neoplasm A. Metastatic - Lung or breast cancer, Hodgkin's disease, leukemia, melanoma B. Primary - Rhabdomyosarcoma, teratoma, fibroma, lipoma, leiomyoma, angioma C. Paraneoplastic Cardiac A. Early infarction pericarditis B. Late postcardiac injury syndrome (Dressler's syndrome) C. Myocarditis D. Dissecting aortic aneurysm Autoimmune A. Rheumatic diseases - Including lupus, rheumatoid arthritis, vasculitis, scleroderma, mixed connective disease B. Other - Granulomatosis with polyangiitis (Wegener's), polyarteritis nodosa, sarcoidosis,IBD (Crohn's, ulcerative colitis), Whipple's, giant cell arteritis, Behcet's disease, rheumatic fever Drugs Procainamide, isoniazid, hydralazine, phenytoin, penicillin, phenylbutazone, doxorubicin Metabolic A. Hypothyroidism - Primarily pericardial effusion B. Uremia C. Ovarian hyperstimulation syndrome Trauma A. Blunt, Penetrating C. Iatrogenic - Catheter and pacemaker perforations, cardiopulmonary resuscitation Radiation
- 19. Causes of pericardial disease: infection Infection A. Viral - Coxsackievirus, echovirus, adenovirus, EBV, CMV, influenza, varicella, rubella, HIV, hepatitis B, mumps, parvovirus B19, B. Bacterial - Staphylococcus, Streptococcus, pneumococcus, Haemophilus, Neisseria (gonorrhoeae or meningitidis), Chlamydia (psittaci or trachomatis), Legionella, tuberculosis, Salmonella, Lyme disease C. Mycoplasma D. Fungal - Histoplasmosis, aspergillosis, blastomycosis, coccidiodomycosis, actinomycosis, nocardia, candida E. Parasitic - Echinococcus, amebiasis, toxoplasmosis F. Infective endocarditis with valve ring abscess
- 20. Pericarditis: Chest Pain • Sudden in onset • Retrosternal in location • Pleuritic and sharp in nature • Exacerbated by inspiration and coughing • Worsens when supine and improves upon sitting upright or leaning forward. • Can often radiate to the neck, arms, or left shoulder, trapezius muscle.
- 21. MI Pulmonary infarction Pericarditis Chest pain location Retrosternal Ant, post or lat Retrosternal onset sudden sudden sudden character Pressure like heavy squeezing Sharp, stabbing Sharp, stabbing and sometimes dull Change with respiration no Worse with inspiration Change with position no no Worse in supine , improve c sitting up Radiation Jaw, neck, shoulder or arms shoulder Jaw, neck, shoulder, arms, trapezius Duration Min to hours Hours to days Hours to days Response to NTG improved No change No change others Pericardial rub absent rare present S3, pul cong present absent absent
- 22. Pericardial Friction Rub • Present in 85% of cases of pericarditis • Highly specific with a variable sensitivity • A high-pitched scratchy or squeaky sound best heard with the diaphragm at the LSB with the patient leaning forward. • Has 3 components, which correspond to atrial systole, ventricular systole, and early diastole.1 • Pericardial friction rub is audible throughout the respiratory cycle, whereas the pleural rub disappears when respirations are on hold.
- 23. ECG findings with pericarditis • Stage 1 (1st hrs-dys) :characterized by diffuse ST elevation (typically concave up). • Stage 2(1st wk): characterized by normalization of the ST & PR segments. • Stage 3: diffuse T wave inversions. • Stage 4 :normalization of the ECG or indefinite persistence of T wave inversions. • Typical ECG evolution in AP has been shown in up to 60% of pts in a clinical series, & stage 1 changes have been observed in 80% of pts with pericarditis
- 24. Others • Echocardiogram — Echocardiography is often normal unless there is a/w pericardial effusion. • Chest x-ray — typically normal • Cardiac biomarkers — may be a/w increases in biomarkers of myocardial injury such as cardiac T I or T. • Signs of inflammation — elevations in the WBC , ESR , and serum CRP concentration. • An elevated troponin level is not associated with a worse prognosis, and troponin levels usually return to normal within 1 to 2 weeks.
- 25. TREATMENT: Acute pericarditis • The therapy of AP should be targeted as much as possible to the underlying etiology. • Most patients with AP can be managed effectively with medical therapy alone. However, patients with a large pericardial effusion, a hemodynamically significant pericardial effusion, or evidence of CP should be evaluated for invasive therapies, such as pericardial drainage and/or pericardiotomy. • NSAIDS • Glucocorticoids
Editor's Notes
- Chest pain that results from acute pericarditis is typically fairly sudden in onset and occurs over the anterior chest. Unlike pain from myocardial ischemia, chest pain due to pericarditis is most often sharp and pleuritic in nature, with exacerbation by inspiration or coughing. One of the most distinct features is the tendency for a decrease in intensity when the patient sits up and leans forward . This position (seated, leaning forward) tends to reduce pressure on the parietal pericardium, particularly with inspiration, and may also allow for splinting of the diaphragm. Note: Radiation to one or both trapezius muscle ridges, suggests a probable pericarditis (phrenic nerve traverses the pericardium). The chest pain of pericarditis must always be distinguished from other common and/or life-threatening causes of chest pain such as myocardial ischemia, pulmonary embolism, aortic dissection, gastroesophageal reflux disease, and musculoskeletal pain. Note: however,radiation of the pain to 1 or both trapezius muscle ridges is probably due to pericarditis because the phrenic nerve that innervates these muscles traverses the pericardium.
- The presence of a pericardial friction rub on physical examination is highly specific for acute pericarditis . The classic friction rub consists of three phases, corresponding to movement of the heart during atrial systole (which is not heard in patients with atrial fibrillation), ventricular systole(most loudest), and in the rapid filling phase of early ventricular diastole. However, some rubs are present only during one (one component) or two phases (two components) of the cardiac cycle . The intensity of the rub frequently increases after application of firm pressure with the diaphragm, during suspended respiration, and with the patient leaning forward or resting on elbows and knees .
- Stage 1, seen in the first hours to days, is characterized by diffuse ST elevation (typically concave up) with reciprocal ST depression in leads aVR and V1 ). There is also an atrial current of injury, reflected by elevation of the PR segment in lead aVR and depression of the PR segment in other limb leads and in the left chest leads, primarily V5 and V6. Thus, the PR and ST segments typically change in opposite directions. Stage 2, typically seen in the first week, is characterized by normalization of the ST and PR segments. Stage 3 is characterized by the development of diffuse T wave inversions. Stage 4 is represented by normalization of the ECG or indefinite persistence of T wave inversions.
- Echocardiogram — Echocardiography is often normal in patients with the clinical syndrome of acute pericarditis unless there is an associated pericardial effusion. Chest x-ray — typically normal in patients with acute pericarditis. Although patients with a substantial pericardial effusion may exhibit an enlarged cardiac silhouette with clear lung fields , this finding is uncommon in acute pericarditis since at least 200 mL of fluid must accumulate before the silhouette enlarges. Cardiac biomarkers — Acute pericarditis may be a/w increases in serum biomarkers of myocardial injury such as cardiac T I or T. Signs of inflammation — Since pericarditis is an inflammatory disease, laboratory signs of inflammation are common in patients with acute pericarditis. These include elevations in the WBC , ESR , and serum CRP concentration.