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Morning Report

Morning Report. Steven Hart, MD. History. CC: increasing DOE HPI 49 y/o AAF Increasing SOB over 1-2 weeks Intermittent Chest pain Leg swelling starting to develop. History. Any thing else you like to know?. History. Chest pain Non-exersional Pleuritic in nature

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Morning Report

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  1. Morning Report Steven Hart, MD

  2. History • CC: increasing DOE • HPI • 49 y/o AAF • Increasing SOB over 1-2 weeks • Intermittent Chest pain • Leg swelling starting to develop

  3. History • Any thing else you like to know?

  4. History • Chest pain • Non-exersional • Pleuritic in nature • Improves by leaning forward • Worsened when laying down • Recent URI symptoms, low grade fevers, malaise • Recent orthopnea, now PND

  5. History • PMHx • HTN • Hyperlipidemia • Social • Non-smoker • Works as secretary • Social ETOH (1-2 times per month)

  6. Physical Exam What things might you look for?

  7. Physical Exam • VS T 99.1 P 108 R 22 BP 102/64 • + JVD • CV • Tachy, distant heart sounds • Rub heard intermittently by examiners • Lower extremity edema • Resp • sits up to breath • Crackles at bases • Mildly increased effort • able to speak full sentences sitting up

  8. Physical Exam • Extremities - +1 edema • Pulses • Exaggerated drop in pulses with inspiration

  9. Labs • Cardiac enzymes slightly elevated • WBC 12

  10. EKG Note diffuse ST seg elevations

  11. Imaging • CXR – any guesses • ECHO – any guesses

  12. Introduction • The Pericardium is a fibroelastic tissue made up of parietal and visceral layers • These two layers are separated by the pericardial cavity • Pericardial cavity usually contains 15-50 ml of plasma ultrafiltrate in healthy individuals

  13. Diseases of the Pericardium • Acute Fibrinous Pericarditis • Pericardial Effusion without major hemodynamic compromise • Cardiac Tamponade • Constrictive Pericarditis

  14. Viral Infections Purulent Pericarditis TB Mediastinal radiation MI Cardiac surgery Trauma Cardiac procedures Drugs and Toxins Metabolic disorders Malignancies (breast, lung, Hodgkin’s, mesothelioma) Collagen Vascular Disease Idiopathic Etiology of Pericardial Diseases

  15. Etiologies of Pericarditis • Neoplastic-35% • Immune Mediated- 23% • Viral- 21% • Bacterial-6% • Uremia-6% • TB- 4% • Idiopathic-4%

  16. Viral Pericarditis • Common bugs • Cocksackie A and B • Echovirus • Adenovirus • Viral infections uncommon in patients presenting with pericardial effusion w/o pericarditis • Exception is HIV- frequently presents with significant effusion w/o pericaritis • seen in 7 % of patients hospitalized with effusions

  17. Bacterial Pericarditis • Staphylococcus • Pneumococccus • Streptococcus(rheumatic pancarditis) • Haemophilus • M.Tuberculosis • Can occur as systemic spread or direct extension • Frequently purulent

  18. Fungal Pericarditis • Histoplasma- most common fungus in immunocompetent patients • Especially the Ohio River Valley • In immunocompromised • Aspergillus • Candida • Coccidoides • Frequently purulent

  19. Other Infectious Etiologies • Rickettsia Ricketsii • Chlamydia Psittaci • Borrelia burgdorferi • Treponema Pallidum • Actinomycosis • Mycoplasma Pneumonia • Nocardia

  20. Post MI • Pericardial involvement is related to infarct size • Early stage - inflammatory etiology • Late stage • Immune mediated weeks to months out • Known as Post Cardiac Injury syndrome (PCIS) or Dressler’s syndrome • Rare in modern time due to reperfusion therapies

  21. Iatrogenic Causes • Mediastinal Radiation-wide spectrum of diseases seen • Cardiac Surgeries • Cardiac Procedures • Traumatic

  22. Drugs • Lupus like sydromes • Procainamide • Hydralazine • Phenytoin • INH • Penicillins- Hypersensitivity Pericarditis • Chemotherapy • Doxorubicin/Daunorubicin-cardiomyopathy/pericardiopathy • Bleomycin - sclerosing agent

  23. Toxins • Asbestosis can cause pericardial lesions • Scorpion fish venom can cause pericarditis

  24. Metabolic Disorders • Uremia- • Most common metabolic cause • 6-10 % of ESRD patients not on HD can have Pericarditis • Dialysis related Pericardial Effusions (seen in 13% of patients) • Severe Hypothyroidism • effusion – usually not significant • rarely pericarditis • Ovarian hyperstimulation syndrome • complication of gonadotropin therapy • Due to fluid shifts

  25. Malignancy • Responsible for 6% of acute pericardial disease (pericarditis and tamponade) • Accounts for 15-20% of moderate to large pleural effusions • Mets - Lung, Breast, Hodgkin’s metastases • Primary - Mesotheliomas and lipomas

  26. Collagen Vascular Disease • SLE- pericardial involvement in up to 50% • Rheumatoid Arthritis • Progressive Systemic Sclerosis • MCTD • Polyarteritis • Giant Cell Arteritis • Inflammatory Bowel Disease

  27. Idiopathic • In two large series (331 patients), only 16 % had an identifiable cause of pericarditis • Many of these cases are presumed viral • Only 7-29% of patients have idiopathic pericardial effusions

  28. Clinical Presentation of Pericarditis • Chest Pain- • sudden onset over anterior chest • sharp and pleuritic • Improves by leaning forward • Radiates commonly to trapezius ridges • Pericardial Friction Rub • EKG – findings depend on stage • 2 of 3 needed to make diagnosis +/- effusion.

  29. History Physical Search for systemic disorders ECG CXR ANA in selected cases PPD HIV BCx if febrile No routine viral cultures Workup for malignancy if history suggests Echo-Class Ia Diagnostic evaluation

  30. Pericardial Friction Rub • Auscutation • Scratchy or squeaky sound • LLSB most frequent site • Use the diaphragm • suspended respiration • Highly 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

  31. EKG Findings • Stage I • ST elevation in most leads • Exceptions aVR and V1 • Depression of PR segment • Low voltage QRS – usually assoc with tampanode • Stage IITransition or “pseudonormalization” or ST/PR segments • Stage IIIT wave inversions. • Stage IVNormalization vs persistent changes • *No changes in metabolic causes

  32. EKG changes • Arrhythmias uncommon. Arryhthmias suggest myocarditis or ischemia

  33. Distinction From AMI • ST elevations in pericarditis: begin at J point, rarely exceed 5 mm, and retain normal concavity • ST elevations / T wave changes are more generalized • No reciprocal lead changes • ST elevations and T wave inversions do not occur at the same time • PR segment changes common • Q waves/QT prolongation/Hyperacute T waves uncommon

  34. Cardiac Biomarkers • Can see elevation in CK, MB, TpnI • 22% of patients with Acute Pericarditis in one trial were above TpnI threshold • Transient rise, resolving within the first 7 days • Patients with higher TpnI did not have higher complication rates

  35. CXR findings • Typically normal in Pericarditis • 200ml of pericardial fluid needed to accumulate before enlargement of the cardiac silhouette seen • Calcification in chronic cases may be appreciated

  36. Lateral CXR of a person with chronic calcified pericarditis due to TB A – cystic mass B – calcified pericardium

  37. Echocardiogram • Should be done in all cases • Often normal in patients with pericarditis, unless associated with pericardial effusion • Presence of pericardial effusion helps support diagnosis, while absence does not exclude it

  38. Pericardial Effusion

  39. Diagnostic evaluation • Not needed in all patients- Viral and idiopathic usually follow a benign course after treatment • It is important to rule out significant effusion and tamponade in patients

  40. Management • Simple, uncomplicated pericarditis • No high risk features • Medical management • outpatient if proper F/U is established

  41. Subacute onset Fever >100.4 Leukocytosis Cardiac tamponade Large pericardial effusion (>2cm) not decreased after NSAIDS Immunosuppressed Hx of anticoagulation Acute Trauma Failure to respond to NSAIDS High Risk Features

  42. ASA-Class I (2-6g/day) or (800mg q6h tapered by 800mg /week for 3-4 weeks) ASA resistance at 1 week should prompt further investigation NSAIDS- ClassI (Ibuprofen 300-800mg q6h) GI prophylaxis Colchicine- Class IIa Intrpericardial Steroids –Class IIa Corticosteroids if refractory to NSAIDS Treatments

  43. Pericardiocentesis • If moderate to severe tamponade is present –Class IA recommendation • If purulent, TB, or neoplastic pericarditis is suspected- Class II a recommendation • Persistent symptomatic pericardial effusion

  44. Complications • Constriction • scarring and consequent loss of elasticity of the pericardial sac • Tamponade • accumulation of pericardial fluid under pressure • Effusive-constrictive pericarditis • Recurrent Pericarditis- seen in 15-30% of patients with idiopathic pericarditis. Immune autoreactivity thought to play a primary role.

  45. Pericardial Tamponade • Increased Pericardial Pressures leading to compression of all cardiac chambers • Pericardial elasticity maybe limited (Acute vs Chronic) • Cardiac chambers become small and chamber diastolic compliance is reduced • Decreased cardiac filling

  46. Physiologic significance • Early diastolic filling decreases, leading to the majority of venous return occuring during ventricular systole • When tamponade is severe, total venous return falls and cardiac chambers shrink

  47. Sinus Tachycardia Elevated JVP Pulsus Paradoxus Rub possible Kussmaul's sign Less likely w/o constrictive component Physical Exam of Tamponade

  48. Pulsus Paradoxus • An exaggerated fall in systemic blood pressure during inspiration • Inspiratory decline in thoracic pressure is transmitted through the pericardium to the right side of the heart • Systemic Venous return increases with inspiration • In 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

  49. Acute vs chronic accumulation • As little as 20-50 ml acutely can cause tamponade acutely • As much as 2 liters can accumulate chronically prior to causing tamponade

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