Pericarditis

Pericarditis :a complete guide

Pratap Sagar Tiwari, MD, internal Medicine

Pericardium

• The pericardium is a fibroelastic sac made upof visceral and parietal layers separated by a(potential) space, the pericardial cavity.

• In healthy individuals, the pericardial cavitycontains 15 to 50 mL of an ultrafiltrate ofplasma.

http://www.nhlbi.nih.gov/health/health-topics/topics/peri/

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

Diseases of pericardium

Diseases of the pericardium present clinically in one offour ways :1. Acute and recurrent pericarditis2. Pericardial effusion without major hemodynamic

compromise3. Cardiac tamponade4. Constrictive pericarditisNote: AP refers to inflammation of the pericardial sac.The term myopericarditis, or perimyocarditis, is used forcases of AP that also demonstrate myocardialinflammation.

Major causes of pericardial diseaseIdiopathic

Infections Viral , tubercular

Neoplasm A. Metastatic - Lung or breast cancer, Hodgkin's disease, leukemia, melanomaB. Primary - Rhabdomyosarcoma, teratoma, fibroma, lipoma, leiomyoma, angiomaC. Paraneoplastic

Cardiac A. Early infarction pericarditisB. Late postcardiac injury syndrome (Dressler's syndrome)C. MyocarditisD. Dissecting aortic aneurysm

Autoimmune A. Rheumatic diseases - Including lupus, rheumatoid arthritis, vasculitis, scleroderma, mixed connective diseaseB. Other - Granulomatosis with polyangiitis (Wegener's), polyarteritis nodosa, sarcoidosis,IBD (Crohn's, ulcerative colitis), Whipple's, giant cell arteritis, Behcet'sdisease, rheumatic fever

Drugs Procainamide, isoniazid, hydralazine, phenytoin, penicillin, phenylbutazone, doxorubicin

Metabolic A. Hypothyroidism - Primarily pericardial effusionB. UremiaC. Ovarian hyperstimulation syndrome

Trauma A. Blunt, PenetratingC. Iatrogenic - Catheter and pacemaker perforations, cardiopulmonary resuscitation

Radiation

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 diseaseC. MycoplasmaD. Fungal - Histoplasmosis, aspergillosis, blastomycosis, coccidiodomycosis, actinomycosis, nocardia, candidaE. Parasitic - Echinococcus, amebiasis, toxoplasmosisF. Infective endocarditis with valve ring abscess

Pericarditis

• Acute pericarditis refers to inflammation ofthe pericardial sac.

• Acute pericarditis is the most commondisorder involving the pericardium.

Pericarditis : classification

Acute Subacute Chronic

< 6 weeks 6 weeks – 6 months > 6 months

1. Effusive2. Fibrinous

1. Effusive-constrictive2. COnstrictive

1. Effusive2. Adhesive3. Constrictive

Reference: Harrison’s 18th edition

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 sittingupright or leaning forward.

• Can often radiate to the neck, arms, or left shoulder,trapezius muscle.

MI Pulmonaryinfarction

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

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.

Reference: www.fpnotebook.com

Pericardial rub Sound

Pericardial Friction Rub Audio from youtube by Pombero123

Pleural rub sound

Pleural rub sound from youtube by Drparth2008

ECG findings with pericarditis

• Stage 1 (1st hrs-dys) :characterized by diffuse STelevation (typically concave up).

• Stage 2(1st wk): characterized by normalization ofthe 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% ofpts with pericarditis.(2)

1. Imazio M, Demichelis B, Parrini I, et al. Day-hospital treatment of acute pericarditis: a management program for outpatienttherapy. J Am Coll Cardiol. 2004;43(6):1042-1046.

2. Bruce MA, Spodick DH. Atypical electrocardiogram in acute pericarditis:characteristics and prevalence. J Electrocardiol.1980;13(1):61-66.

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 epicardialinflammation; 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.

ECG ; AMI Vs PericarditisAMI 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

Others

• Echocardiogram — Echocardiography is often normalunless there is a/w pericardial effusion.

• Chest x-ray — typically normal

• Cardiac biomarkers — may be a/w increases inbiomarkers 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)

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.

Myopericarditis

When acute pericarditis is present,myopericarditis has been diagnosed by thedetection of one or both of the following in theabsence of evidence of another cause.

• Elevation in serum cardiac biomarkers, such ascardiac troponin I or T.

• New or presumed new focal or global leftventricular systolic dysfunction on imagingstudies

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

TREATMENT: Acute pericarditis

• The therapy of AP should be targeted as much aspossible to the underlying etiology.

• Most patients with AP can be managedeffectively with medical therapy alone. However,patients with a large pericardial effusion, ahemodynamically significant pericardial effusion,or evidence of CP should be evaluated forinvasive therapies, such as pericardial drainageand/or pericardiotomy.

• NSAIDS• Glucocorticoids

TREATMENT : NSAID

• In the treatment of AP, the goals of therapy are therelief of pain and resolution of inflammation (and, ifpresent, pericardial effusion). NSAIDs is recommendedfor all patients without a contraindication, with theduration of treatment based upon the persistence ofsymptoms, which is usually for 2 wks.

• Failure to respond to aspirin or NSAID therapy within1 week (defined as persistence of fever, pericarditicchest pain, a new pericardial effusion, or worsening ofgeneral illness) suggests that a cause other thanidiopathic or viral pericarditis is present.

NSAID regimens

Glucocorticoids

European Society of Cardiology guidelines — The2004 European Society of Cardiology (ESC)guidelines recommended that systemic steroidtherapy be restricted to patients with the followingconditions :• Patients with symptoms refractory to standard

therapy• Acute pericarditis due to connective tissue

disease• Autoreactive (immune-mediated) pericarditis• Uremic pericarditis

Sequele/complications

• Cardiac tamponade –which may be acute orsubacute, is characterized by accumulation ofpericardial fluid under pressure. Variants includelow pressure (occult) and regional tamponade.

• Constrictive pericarditis –is the result of scarringand consequent loss of the normal elasticity ofthe pericardial sac. PC is typically chronic, butvariants include subacute, transient, and occultconstriction.

Effusive-constrictive pericarditis

• is characterized by underlying constrictivephysiology with a coexisting pericardial effusion,often with cardiac tamponade .

• This usually results in a mixed hemodynamicpicture with features of both constriction andtamponade.

• Such patients may be mistakenly thought to haveonly CT; however, elevation of the right atrial andpulmonary wedge pressures after drainage of thepericardial fluid points to the underlyingconstrictive process.

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

Cardiac Tamponade

• Cardiac tamponade is characterized by theaccumulation of pericardial fluid underpressure.

• Tamponade occurs when all cardiac chambersare compressed as a result of increasedintrapericardial pressure to the point ofcompromising systemic venous return to theright atrium (RA).(1,2)

1. Spodick DH. Acute cardiac tamponade. N Engl J Med. 2003;349(7):684-690.

2. Troughton RW, Asher CR, Klein AL. Pericarditis. Lancet. 2004;363(9410):717-727.

Tamponade: Physical Examination

Symptoms• Chest pain• Shoulder discomfort• Abdominal discomfort• NauseaExamination findings• Sinus tachycardia• Elevated JVP• Pulsus paradoxus• Friction rub

Cardiac Tamponade

Acute Subacute/chronic

Beck’s triad1. Low bp2. Distended neck veins3. 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.

JVP

A. www.ottawaheart.caB. soperedi.wordpress.comC. www.zen104556.zen.co.uk

C

B

A

JVP

1. Changes in the jugular veins can be crucial in recognizing CT and CP.2. 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).

3. Normally, During inspiration, lung expansion causes -VE intrathoracic pressure thatis transmitted to the pericardium and cardiac chambers, leading to dilation of thechambers. As a result, the right chambers of the heart fill with blood from the SVCand IVC, and the left chambers fill because of forward flow in the pulmonary veins.

4. 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.

5. In CT: The JVP is almost always elevated .6. In CT, the primary abnormality is compression of all cardiac chambers due to ↑

pericardial pressure . The pericardium has some degree of elasticity; but once theelastic limit is reached, As CT progresses, the cardiac chambers become smaller andchamber diastolic compliance is ↓. There is limited venous return that leads toraised JVP.

CVP in constrictive pericarditis vstamponade

constrictive pericarditis vs tamponade

http://www.derangedphysiology.com/php/CVC/The-abnormal-central-venous-pressure-waveforms.php

JVP

1. In CP, as there is fix constriction the early diastolic fiiling is normalor more rapid (rapid y decent) and then as the ventricles are filledand can no more stretch there is impaired mid diastolic and latediastolic filling(plateu phase) .

2. So, In early diastole there is an abnormally rapid filling whichsuddenly stops(this suddenly halt results in pericardial knock)when the fibrous pericardium reaches its maximumdistensibility.

3. On pressure tracings this filling pattern is recognised as dip-plateau or square-root sign. There is also Abnormalinterventricular septum motion (septal bounce) which is seen withecho.

4. How ever in tamponade the filling is impaired from the earlydiastole itself so rapid y decent is blunted. and pericardial knockis also not a feature of tamponade.

Etiologies of Cardiac TamponadeAcute 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,

Pulsus paradoxus

• In the next 2 slides ,first know the normal hemodynamics change with repiration.

Normal hemodynamic change with respiration

Inspiration ITP becomes more -vePressure transmitted to cardiac chambers

ICP becomes more -ve

↑ inflow of venous

return to rtheart

RV dilate in all direction

IVS bulges to the left

↓ stretch↓ contractility

↓ LVEDV

↓ SV / CO / SBP

Refer to starling mechanism

So there is ↓ in SBP during inspiration ,but not >10 mmhg

A

Checkout mechanism B in next slide

Normal hemodynamic change with respiration

Inspirationas 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

Refer to starling mechanism

So there is ↓ in SBP during inspiration ,but not >10 mmhg

B

Hemodynamic change with respiration in Cardiac tamponade

• In CT , the increased intrapericardial pressure preventsthe ventricle from expansing .

• There is impaired diastolic filling of the RV (why RVonly ? Though the pressure due to effusion istransmitted to both ventricular walls but LV is morethicker than the rt ,so effect on RV is morepronounced).

• 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.

Pulsus paradoxus in constrictive pericarditis

• CP is the result of scarring and consequent loss of the normalelasticity of the pericardial sac.However, in Tamponade theelasticity of pericardial sac is not lost as in CP.

• Moreover, in CP ,there is overall constriction in a fixedmanner ,the early diastolic filling is rapid and not impairedand the effect of constriction is only in the mid/late diastolicfilling.

• Moreover intrathoracic pressure is not transmitted to cardiacchamber through rigid collagenous stiff pericardium.

• Pulsus paradoxus (an exaggerated drop in systemic bloodpressure greater than 10 mmHg during inspiration) occurs in<20 percent of patients with CP.

Pulsus paradoxus

• Pulsus paradoxus has been shown to bepredictive of the severity of cardiactamponade.(1 )

• A pericardial friction rub, while not common,can also be heard in cardiac tamponade if theunderlying cause is an inflammatorypericarditis.(2)

1. 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.

2. Troughton RW, Asher CR, Klein AL. Pericarditis. Lancet. 2004;363(9410):717-727.

PP: how to measure ?

• Get a manual BP cuff and inflate until aboveSBP; then very slowly release until you start tohear Korotkoff sounds.

• At first, you should just hear them duringexpiration; slowly release until you hear asound with every beat in the cardiac cycle.

• The difference between when you first hearthe sounds and when you hear them withevery cycle is the pulsus paradoxus.

Pulsus Paradoxus Video

Taken from youtube : Stanford medicine

Kussmaul sign

• Kussmaul sign is an elevation in the jugularvenous pressure during inspiration and can beseen in tamponade, but not usually in theabsence of pericardial constriction.

Kussmaul's sign

• Kussmaul's sign (the lack of an inspiratory decline in JVP) ispresent in patients with CP, but does not distinguish CP fromsevere tricuspid valve disease or right-sided heart failure.

• A pericardial knock, an accentuated heart sound occurringslightly earlier than an S3 which may be audible and rarely ispalpable, has been reported in 47 %of pts with CP in 1 series[1]. 16 % of pts in the same series had a pericardial frictionrub.

• Profound cachexia, peripheral edema, ascites, pulsatilehepatomegaly (part of the syndrome of congestivehepatopathy), and pleural effusion are common findings withmore severe CP[2].

• Ling LH, Oh JK, Schaff HV, et al. Constrictive pericarditis in the modern era: evolving clinical spectrum and impact on outcome afterpericardiectomy. Circulation 1999; 100:1380.

• Maisch B, Seferović PM, Ristić AD, et al. Guidelines on the diagnosis and management of pericardial diseases executive summary; TheTask force on the diagnosis and management of pericardial diseases of the European society of cardiology. Eur Heart J 2004; 25:587.

Kussmaul’s sign

• Kussmaul’s sign is not seen in patients with CT becauseeven though the ↑ in PP exerts an inward force compressingthe entire heart during inspiration, the increase in -VE ITP isstill able to be transmitted to the rt side of heart andsubsequent ↑ in bld flow to the RA ensues.1

• Conversely, the restriction to diastolic filling of the RV in CPand RCM by the fixed, less compliant constrictingpericardium or myocardium respectively at higher chambervolumes, results in the paradoxical ↑ in JVP referred to asKussmaul’s sign.2

1. Roy, CL, Minor, MA, Brookhart, MA, Choudhry, NK. Does This Patient With a Pericardial Effusion Have CardiacTamponade? JAMA 2007;297:1810-1818.

2. Myers, RBH, Spodick, DH. Constrictive pericarditis: Clinical and pathophysiologic characteristics. Am Heart J1999;138:219-232.

Kussmaul Sign

Taken from youtube : Atikun Limsukon

Tamponade :ECG

1. Sinus tachycardia2. Low-voltage QRS3. Widespread concave ST-segment elevation and PR-segment

depression4. 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 wkafter Rx of tamponade by pericardiocentesis or anti-inflammatorymedications.(1)

• Electrical alternans, defined as the alteration of the QRS complexamplitude between beats, is specific but not very sensitive for CT.(2) Electrical alternans reflects the swinging motion of the heart inpericardial fluid.

1. 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.

2. Spodick DH. Acute cardiac tamponade. N Engl J Med. 2003;349(7):684-690.

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

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

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