Pericarditis

Pericarditis, pericardial effusion, constrictive pericarditis

1. Pericarditis :a complete guide Pratap Sagar Tiwari , MD, internal Medicine

2. Pericardium  The pericardium is a fibroelastic sac made up of visceral and parietal layers separated by a (potential) space, the pericardial cavity. In healthy individuals, the pericardial cavity contains 15 to 50 mL of an ultrafiltrate of plasma. http://www.nhlbi.nih.gov/health/health-topics/topics/peri/

3. 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

4. Diseases of pericardium Diseases of the pericardium present clinically in one of four ways : Acute and recurrent pericarditis Pericardial effusion without major hemodynamic compromise Cardiac tamponade Constrictive pericarditis Note: AP refers to inflammation of the pericardial sac. The term myopericarditis , or perimyocarditis , is used for cases of AP that also demonstrate myocardial inflammation. 

5. 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

6. 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

7. Pericarditis Acute pericarditis refers to inflammation of the pericardial sac . Acute pericarditis is the most common disorder involving the pericardium.

8. Pericarditis : classification Acute Subacute Chronic < 6 weeks 6 weeks – 6 months > 6 months Effusive Fibrinous Effusive-constrictive COnstrictive Effusive Adhesive Constrictive Reference: Harrison’s 18 th edition

9. 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.

10. 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

11. 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 . Ref 1. Spodick DH. Pericardial rub. Prospective, Multiple observer investigation of pericardial friction in 100 patients. Am J Cardiol 1975; 35:357.

12. Reference: www.fpnotebook.com

13. Pericardial rub Sound Pericardial Friction Rub Audio from youtube by Pombero123

14. Pleural rub sound Pleural rub sound from youtube by Drparth2008

15. 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 ,(1) & stage 1 changes have been observed in 80% of pts with pericarditis .(2) Imazio M, Demichelis B, Parrini I, et al. Day-hospital treatment of acute pericarditis: a management program for outpatient therapy. J Am Coll Cardiol . 2004;43(6):1042-1046. Bruce MA, Spodick DH. Atypical electrocardiogram in acute pericarditis:characteristics and prevalence. J Electrocardiol . 1980;13(1):61-66.

16. Electrocardiogram (ECG) in pericarditis Electrocardiogram in acute pericarditis showing diffuse upsloping ST segment elevations seen best here in leads II, III, aVF , and V2 to V6. There is also subtle PR segment deviation (positive in aVR , negative in most other leads). ST segment elevation is due to a ventricular current of injury associated with epicardial inflammation; similarly, the PR segment changes are due to an atrial current of injury which, in pericarditis, typically displaces the PR segment upward in lead aVR and downward in most other leads.

17. ECG ; AMI Vs Pericarditis AMI Percarditis Morphology Convex (dome-shaped) ST elevation May be > 5 mm in height Concavity. Rarely >5 mm Distribution limited to anatomical groupings of leads Generalized Reciprocal changes often A/w reciprocal ST seg changes Not seen Conc ST & T wave changes Common Uncommon Hyperacute T waves May occur Donot Q waves May occur Donot PR segment depression Absent Frequently seen

18. 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 .(1) Lange RA, Hillis LD. Clinical practice: acute pericarditis [published correction appears in N Engl J Med. 2005;352(11):1163]. N Engl J Med. 2004;351(21):2195-2202.

19. Myopericarditis   When acute pericarditis is present, myopericarditis has been diagnosed by the detection of one or both of the following in the absence of evidence of another cause. Elevation in serum cardiac biomarkers, such as cardiac troponin I or T. New or presumed new focal or global left ventricular systolic dysfunction on imaging studies

20. DETERMINATION OF RISK AND NEED FOR HOSPITALIZATION Fever (>38ºC [100.4ºF]) and leukocytosis Evidence suggesting cardiac tamponade A large pericardial effusion ( ie , an echo-free space of more than 20 mm) Immunosuppressed state A history of oral anticoagulant therapy Acute trauma Failure to respond within seven days to NSAID therapy Elevated cardiac troponin, which suggests myopericarditis

21. 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

22. TREATMENT  : NSAID In the treatment of AP, the goals of therapy are the relief of pain and resolution of inflammation (and, if present, pericardial effusion). NSAIDs is recommended for all patients without a contraindication, with the duration of treatment based upon the persistence of symptoms, which is usually for 2 wks. Failure to respond to aspirin or NSAID therapy within 1 week ( defined as persistence of fever, pericarditic chest pain, a new pericardial effusion, or worsening of general illness ) suggests that a cause other than idiopathic or viral pericarditis is present.

23. NSAID regimens  

24. Glucocorticoids European Society of Cardiology guidelines  — The 2004 European Society of Cardiology (ESC) guidelines recommended that systemic steroid therapy be restricted to patients with the following conditions : Patients with symptoms refractory to standard therapy Acute pericarditis due to connective tissue disease Autoreactive (immune-mediated) pericarditis Uremic pericarditis 

25. Sequele /complications Cardiac tamponade –which may be acute or subacute , is characterized by accumulation of pericardial fluid under pressure. Variants include low pressure (occult) and regional tamponade . Constrictive pericarditis –is the result of scarring and consequent loss of the normal elasticity of the pericardial sac. PC is typically chronic, but variants include subacute , transient, and occult constriction.

26. Effusive-constrictive pericarditis is characterized by underlying constrictive physiology with a coexisting pericardial effusion, often with cardiac tamponade . This usually results in a mixed hemodynamic picture with features of both constriction and tamponade . Such patients may be mistakenly thought to have only CT; however, elevation of the right atrial and pulmonary wedge pressures after drainage of the pericardial fluid points to the underlying constrictive process.

27. Masud H. Khandaker . Pericardial Disease: Diagnosis and Management.June 2010;85(6):572-593

28. Cardiac Tamponade Cardiac tamponade is characterized by the accumulation of pericardial fluid under pressure. Tamponade occurs when all cardiac chambers are compressed as a result of increased intrapericardial pressure to the point of compromising systemic venous return to the right atrium (RA ).(1,2) Spodick DH. Acute cardiac tamponade . N Engl J Med. 2003;349(7):684-690. Troughton RW, Asher CR, Klein AL. Pericarditis. Lancet. 2004;363(9410):717-727.

29. Tamponade : Physical Examination Symptoms Chest pain Shoulder discomfort Abdominal discomfort Nausea Examination findings Sinus tachycardia Elevated JVP Pulsus paradoxus Friction rub

30. Cardiac Tamponade Acute Subacute /chronic Beck’s triad Low bp Distended neck veins Muffled heart sounds Some acute features in variability with features of biventricular heart failure ,usually right sided heart failure. Acute vs. subacute tamponade : small volumes at fast rates vs. abilility for pericardial stretch if fluid gradually accumulates.

31. JVP A. www.ottawaheart.ca B. soperedi.wordpress.com C. www.zen104556.zen.co.uk C B A

32. JVP Changes in the jugular veins can be crucial in recognizing CT and CP. The normal jugular vein examination shows 2 positive waves (the a wave during atrial systole and the v wave during ventricular systole) and two negative waves (the x descent during atrial diastole and the y descent during ventricular diastole). Normally, During inspiration, lung expansion causes -VE intrathoracic pressure that is transmitted to the pericardium and cardiac chambers, leading to dilation of the chambers. As a result, the right chambers of the heart fill with blood from the SVC and IVC, and the left chambers fill because of forward flow in the pulmonary veins. In mild acute pericarditis or even in pericardial effusion until the filling pressure is > intrapericardial pressures there is usually no hemodynamic impact on the heart. Hence, JVP:generally N. In CT: The JVP is almost always elevated . In CT, the primary abnormality is compression of all cardiac chambers due to ↑ pericardial pressure . The pericardium has some degree of elasticity; but once the elastic limit is reached, As CT progresses , the cardiac chambers become smaller and chamber diastolic compliance is ↓ . There is limited venous return that leads to raised JVP.

33. CVP in constrictive pericarditis vs tamponade constrictive pericarditis vs tamponade http://www.derangedphysiology.com/php/CVC/The-abnormal-central-venous-pressure-waveforms.php

34. JVP In CP, as there is fix constriction the early diastolic fiiling is normal or more rapid (rapid y decent) and then as the ventricles are filled and can no more stretch there is impaired mid diastolic and late diastolic filling( plateu phase) . So, In early diastole there is an abnormally rapid filling which suddenly stops (this suddenly halt results in pericardial knock ) when the fibrous pericardium reaches its maximum distensibility . On pressure tracings this filling pattern is recognised as dip-plateau or square-root sign . There is also Abnormal interventricular septum motion ( septal bounce) which is seen with echo . How ever in tamponade the filling is impaired from the early diastole itself so rapid y decent is blunted . and pericardial knock is also not a feature of tamponade .

35. Etiologies of Cardiac Tamponade Acute tamponade : Usually due to traumatic rupture of ventricle due to procedure/blunt trauma; aortic dissection or MI with ventricular rupture Subacute tamponade : Infection: More commonly purulent than viral Malignancy: Particularly lung, breast, Hodgkin’s, mesothelioma Post-MI, post-CT surgery, post-procedure Uremia Post- XRT,Drugs Collagen-vascular disease: in particular SLE Idiopathic, HIV,

36. Pulsus paradoxus In the next 2 slides ,first know the normal hemodynamics change with repiration .

37. Normal hemodynamic change with respiration Inspiration ITP becomes more - ve Pressure transmitted to cardiac chambers ICP becomes more - ve ↑ inflow of venous return to rt heart RV dilate in all direction IVS bulges to the left ↓ stretch ↓ contractility ↓ LVEDV ↓ SV / CO / SBP ITP: Intrathoracic pressure IVS : Intraventricular septum LVEDV :Left ventricular end diastolic pressure Refer to starling mechanism So there is ↓ in SBP during inspiration ,but not >10 mmhg A Checkout mechanism B in next slide

38. Normal hemodynamic change with respiration Inspiration as pul vasculature in highly compliant structure ↑ blood pooling in the pulmonary vasculature ↓ pul venous flow to left side of heart ↓ stretch ↓ contractility ↓ LVEDV ↓ SV / CO / SBP LVEDV :Left ventricular end diastolic pressure Refer to starling mechanism So there is ↓ in SBP during inspiration ,but not >10 mmhg B

39. Hemodynamic change with respiration in Cardiac tamponade In CT , the increased intrapericardial pressure prevents the ventricle from expansing . There is impaired diastolic filling of the RV (why RV only ? Though the pressure due to effusion is transmitted to both ventricular walls but LV is more thicker than the rt ,so effect on RV is more pronounced). There is more bulging of IVS to the left. The mechanism presented in previous 2 slides are exagerrated . Finally there is decrease in SBP >10 mmhg = pulsus paradoxus .

40. Pulsus paradoxus in constrictive pericarditis CP is the result of scarring and consequent loss of the normal elasticity of the pericardial sac.However , in Tamponade the elasticity of pericardial sac is not lost as in CP. Moreover, in CP ,there is overall constriction in a fixed manner ,the early diastolic filling is rapid and not impaired and the effect of constriction is only in the mid/late diastolic filling. Moreover intrathoracic pressure is not transmitted to cardiac chamber through rigid collagenous stiff pericardium. Pulsus paradoxus (an exaggerated drop in systemic blood pressure greater than 10 mmHg during inspiration) occurs in <20 percent of patients with CP.

41. Pulsus paradoxus Pulsus paradoxus has been shown to be predictive of the sever ity of cardiac tamponade .(1 ) A pericardial friction rub , while not common, can also be heard in cardiac tamponade if the underlying cause is an inflammatory pericarditis.(2) Curtiss EI, Reddy PS, Uretsky BF, Cecchetti AA. Pulsus paradoxus : definition and relation to the severity of cardiac tamponade . Am Heart J .1988;115(2):391-398. Troughton RW, Asher CR, Klein AL. Pericarditis. Lancet . 2004;363(9410 ):717-727 .

42. PP: how to measure ? Get a manual BP cuff and inflate until above SBP; then very slowly release until you start to hear Korotkoff sounds. At first, you should just hear them during expiration; slowly release until you hear a sound with every beat in the cardiac cycle. The difference between when you first hear the sounds and when you hear them with every cycle is the pulsus paradoxus .

43. Pulsus Paradoxus Video Taken from youtube : Stanford medicine

44. Kussmaul sign Kussmaul sign is an elevation in the jugular venous pressure during inspiration and can be seen in tamponade , but not usually in the absence of pericardial constriction.

45. Kussmaul's sign Kussmaul's sign (the lack of an inspiratory decline in JVP) is present in patients with CP, but does not distinguish CP from severe tricuspid valve disease or right-sided heart failure.  A pericardial knock , an accentuated heart sound occurring slightly earlier than an S3 which may be audible and rarely is palpable, has been reported in 47 %of pts with CP in 1 series [1]. 16 % of pts in the same series had a pericardial friction rub. Profound cachexia, peripheral edema, ascites, pulsatile hepatomegaly (part of the syndrome of congestive hepatopathy ), and pleural effusion are common findings with more severe CP[2 ]. Ling LH, Oh JK, Schaff HV, et al. Constrictive pericarditis in the modern era: evolving clinical spectrum and impact on outcome after pericardiectomy . Circulation 1999; 100:1380. Maisch B, Seferović PM, Ristić AD, et al. Guidelines on the diagnosis and management of pericardial diseases executive summary; The Task force on the diagnosis and management of pericardial diseases of the European society of cardiology. Eur Heart J 2004; 25:587.

46. Kussmaul’s sign Kussmaul’s sign is not seen in patients with CT because even though the ↑ in PP exerts an inward force compressing the entire heart during inspiration, the increase in -VE ITP is still able to be transmitted to the rt side of heart and subsequent ↑ in bld flow to the RA ensues.1 Conversely , the restriction to diastolic filling of the RV in CP and RCM by the fixed, less compliant constricting pericardium or myocardium respectively at higher chamber volumes, results in the paradoxical ↑ in JVP referred to as Kussmaul’s sign.2 Roy, CL, Minor, MA, Brookhart , MA, Choudhry , NK. Does This Patient With a Pericardial Effusion Have Cardiac Tamponade ? JAMA 2007;297:1810-1818. Myers, RBH, Spodick , DH. Constrictive pericarditis: Clinical and pathophysiologic characteristics. Am Heart J 1999;138:219-232.

47. Kussmaul Sign Taken from youtube : Atikun Limsukon

48. Tamponade :ECG Sinus tachycardia Low-voltage QRS Widespread concave ST-segment elevation and PR-segment depression Electrical alternans Low-voltage QRS complex, defined as a maximum QRS amplitude of <0.5 mV in the limb leads, has been shown to resolve within 1 wk after Rx of tamponade by pericardiocentesis or anti-inflammatory medications.(1) Electrical alternans , defined as the alteration of the QRS complex amplitude between beats, is specific but not very sensitive for CT. (2) Electrical alternans reflects the swinging motion of the heart in pericardial fluid . Bruch C, Schmermund A, Dagres N, et al. Changes in QRS voltage in cardiac tamponade and pericardial effusion: reversibility after pericardiocentesis and after anti-inflammatory drug treatment. J Am Coll Cardiol . 2001;38(1 ):219-226 . Spodick DH. Acute cardiac tamponade . N Engl J Med. 2003;349(7 ):684-690.

49. Tamponade : 2-Dimensional ECHO Pericardial effusion Late diastolic collapse of RA Early diastolic collapse of RV Collapse of LA Ventricular interdependence IVC dilatation with <50% inspiratory collapse

50. TAMPONADE Low cardiac output state JVD present NO Kussmaul’s sign Equalized diastolic pressures RA: blunted y descent Decreased heart sounds CONSTRICTION Low cardiac output state JVD present Kussmaul’s sign Equalized diastolic pressures RA: rapid y descent Pericardial “knock” Constriction vs. Tamponade Summary

51. Constriction vs. Tamponade Summary TAMPONADE Pulsus paradoxus: Present Echo/MRI: Normal systolic function Large effusion RA & RV compression Treatment: Pericardiocentesis CONSTRICTION Pulsus paradoxus : Absent Echo/MRI: Normal systolic function No effusion Pericardial thickening Treatment: Pericardial stripping