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
http://www.nhlbi.nih.gov/health/health-topics/topics/peri/
Inflamed and thickened layers
of pericardium rub against each
3. Pathophysiology: Disorders of
pericardium
Restriction of heart
motion and pain
with breathing
Inflammatory
response
Pericardial
inflammation &
edema
Influx of neutrophils &
other chemical
mediators
Change the permeability
of pericardial vascularity
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.
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. 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.
11. 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 inversion
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)
12. 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.
13. ECG ; AMI Vs Pericarditis
AMI
Morphology Convex (dome-shaped) ST elevation
May be > 5 mm in height
Percarditis
Concavity.
Rarely >5 mm
Distribution limited to anatomical groupings of Generalized
leads
Reciprocal changes often A/w reciprocal ST seg changes Not seen
Conc ST & T wave Common Uncommon
changes
Hyperacute T waves May occur Donot
Q waves May occur Donot
PR segment Absent Frequently seen
depression
14. 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.
15. Diagnostic criteria for acute pericarditis and myopcricarditis in the clinical
setting
Acute pericarditis (at least 2 criteria of 4 should be present)11:
1. Typical chest pain
2. Pericardial friction rub
3. Suggestive ECG changes (typically widespread ST-segment elevation)
4. New or worsening pericardial effusion Myopcricarditis:
1. Definite diagnosis of acute pericarditis, PLUS
2. Suggestive symptoms (dyspnea, palpitations, or chest pain) and ECG
abnormalities beyond normal variants, not documented previously (ST/T
abnormalities, supraventricular or ventricular tachycardia or frequent ectopy,
atrioventricular block), OR focal or diffuse depressed LV (unction of
uncertain age by an imaging study
3. Absence of evidence of any other cause
4. One of the following features: evidence of elevated cardiac enzymes
(creatine kinase-M B fraction, or troponin I or T), OR new onset of focal or
diffuse depressed LV function by an imaging study, OR abnormal imaging
consistent with myocarditis (MRI with gadolinium, gallium-67 scanning,
anti-myosin antibody scanning)
Case definitions for myopcricarditis [30] include:
> Suspected myopericarditis: criteria 1 plus 2 and 3
> Probable myopericarditis: criteria 1,2,3, and 4
> Continued myopericarditis:b histopathologic evidence of myocarditis by
endomyocardial biopsy or on autopsy
a Pericardial effusion is added as diagnostic criteria in some papers [12,30],
The effusion confirms the clinical diagnosis but its absence does not exclude
it.
b A con finned diagnosis would require an endomyocardial biopsy [30,31 ]
that is not warranted in self-limited cases with predominant pericarditis.
16. 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 orT.
• New or presumed new focal or global left
ventricular systolic dysfunction on imaging studies
17. DETERMINATION OF RISK AND NEED
FOR HOSPITALIZATION
• Fever (>38°C [100.4°F]) 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
18. 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
19. 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.
21. 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
22. 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.
23. 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.
24.
25. 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).
27. Cardiac Tamponade
Acute Subacute/chronic
Beck's triad Some acute features in variability
1. Low bp with features of biventricular heart
2. Distended neck veins failure ,usually right sided heart
3. Muffled heart sounds failure.
Acute vs. subacute tamponade: small volumes at fast rates vs.
abilility for pericardial stretch if fluid gradually accumulates.
28. TopofjugUarvenouspulsations
Look for jugular
venous pulsations
internal
Jugular
Vein
External
JugUar
Vein
Distance
from RA
lo
sternal
angle:
approx.
5 cm
SternalAngle
Atria
diastole
Atria
systole
ventricular systole
r
maximum atrial
tricu spid
filling
coses at start pressure
before ventricular diastok
of ventricular systole
JVP
'S.'f
A. www.ottawaheart.ca
B. soperedi.wordpress.com
C. www.zen104556.zen.co.uk
29. 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 j. There is limited venous return that leads to raised JVP.
31. 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.
32. 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,
33. Pulsus paradoxus
• In the next 2 slides ,first know the normal
hemodynamics change with repiration.
34. 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.
35. Pulsus paradoxus
• Pulsus paradoxus has been shown to be
predictive of the severity of cardiac
tamponade.
• A pericardial friction rub, while not common, can
also be heard in cardiac tamponade if the
underlying cause is an inflammatory pericarditis.(2)
36. 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.
37. 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.
38. 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. 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.
39. Kussmaul's sign
• Kussmaul's sign is not seen in patients with CT because even
though the t 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 t in bld flow to
the RA ensues.
• 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 t in JVP referred to as Kussmaul's sign.
41. 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.
2.
42. 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
43. Constriction vs. Tamponade
Summary
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"
44. Constriction vs. Tamponade
Summary
TAMPONADE CONSTRICTION
| 1 | ■ 1 p ■ ■ /"*« ^ ^ ^ ^ ^ W 1 | p •
Present
•
Absent
• Normal systolic function • Normal systolic function
• Large effusion • No effusion
• RA & RV compression • Pericardial thickening
Pericardiocentesis Pericardial stripping
