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 :
1. Acute and recurrent pericarditis
2. Pericardial effusion without major hemodynamic
compromise
3. Cardiac tamponade
4. 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
1. Effusive
2. Fibrinous
1. Effusive-constrictive
2. COnstrictive
1. Effusive
2. Adhesive
3. Constrictive
Reference: Harrison’s 18th 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)
1. 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.
2. 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)
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.

20. 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

21. 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

22. 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

23. 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.

24. NSAID regimens

25. 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

26. 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.

27. 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.

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

29. 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)
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.

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

31. Cardiac Tamponade
Acute Subacute/chronic
Beck’s triad
1. Low bp
2. Distended neck veins
3. 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.

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

33. 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 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.
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 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.

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

35. JVP
1. 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) .
2. 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.
3. 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.
4. 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.

36. 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,

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

38. 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
Refer to starling mechanism
So there is ↓ in SBP during
inspiration ,but not >10 mmhg
A
Checkout mechanism B in next slide

39. 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
Refer to starling mechanism
So there is ↓ in SBP during
inspiration ,but not >10 mmhg
B

40. 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.

41. 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.

42. Pulsus paradoxus
• Pulsus paradoxus has been shown to be
predictive of the severity 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)
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.

43. 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.

44. Pulsus Paradoxus Video
Taken from youtube : Stanford medicine

45. 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.

46. 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.

47. 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
1. Roy, CL, Minor, MA, Brookhart, MA, Choudhry, NK. Does This Patient With a Pericardial Effusion Have Cardiac
Tamponade? JAMA 2007;297:1810-1818.
2. Myers, RBH, Spodick, DH. Constrictive pericarditis: Clinical and pathophysiologic characteristics. Am Heart J
1999;138:219-232.

48. Kussmaul Sign
Taken from youtube : Atikun Limsukon

49. Tamponade :ECG
1. Sinus tachycardia
2. Low-voltage QRS
3. Widespread concave ST-segment elevation and PR-segment
depression
4. 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.
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.

50. 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

51. 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

52. 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