Transcript Pericardial Disease

Pericardial Disease
Dr. Mozhgan Parsaee
Department of Echocardiography
Shahid Rajaei Cardiovascular Center
Normal Function of Pericardium
 Fibrous sac surrounding heart-dense network of
collagen fibres.
 Serous membrane – two continuous layers separated
by a small amount of fluid lubricant , ultrafiltration of
plasma (10-50 mL).
 Layers are called visceral and parietal
 Visceral
is inner layer (epicardium)
 Parietal is continuous with diaphragm and outer
walls of great arteries.
Normal Function of Pericardium
 Limit cardiac dilatation
 Limit cardiac displacement
 Reduce friction to cardiac movement
 Barrier to inflamation
 Not needed to sustain life
Acute Pericarditis
Acute Pericarditis
 Acute pericarditis, defined as symptoms or signs
resulting from pericardial inflammation of no more
than 1 to 2 weeks in duration.
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
Serous
Fibrinous
Purulent
Hemorrhagic
Etiology
 Infectious pericarditis
A. Viral : coxackievirus A&B, echovirus, mumps,HIV,
adenovirus, hepatitis
B.
Pyogenic: pneumococcus, streptococcus,
staphylococcus
C.
Fungal: histoplasma, candida
Etiology
 Non infectious pericarditis
A. acute MI
B. Uremia
C. Cancer (commonly lung or breast)
D. Trauma
E. Myxedema
F. Postirradiation
G. Aortic dissection
H.Acute idiopathic
I. Connective tissue disease
Etiology
 Pericarditis related to hypersensivity or
autoimmunity
A. Rheumatic fever
B.
Collagen vascular disease(SLE, RA)
C. Drug induced (phenytoin, procainamide, hydralazine,
isoniazide, minoxidil, anticoagulant)
D. Post cardiac injury (posttraumatic, Dressler’s syn, post
pericardiotomy)
Signs, Symptoms and Investigations
How can we diagnose this?
 Clinical examination
 Auscultation
 Chest x-ray
 ECG
 Echo
 Catheter laboratory investigations
Acute Pericarditis
 Chest pain
 Pericardial friction rub
 ECG changes
 Pericardial effusion
Chest Pain
 Usually present in the acute infectious types and in
many of the forms related to hypersensivity and
autoimmunity
 Often absent pain in slowly developing TB, post
irradiation, cancer, or uremic pericarditis
Chest Pain
 The pain of acute pericarditis is often severe,
retrosternal and left precordial and reffered to the
neck, arms or the left shoulder; the most
characteristic radiation is to the trapezius ridge.
 Almost always the pain is pleuritric (sharp and
aggravated by inspiration, coughing, and changes in
body positions).
 Pain may be relieved by sitting up and leaning
forward and is intensified by lying supine.
Pericardial Friction Rub
 Pericardial friction rub is audible in 85% of patients.
 Is high pitch and scratching.
 Has three components per cardiac cycle
presystolic rub during atrial filling
ventricular systolic rub (loudest)
ventricular diastolic rub (after A2P2)
Pericardial Friction Rub
 Most frequently is audible at end-expiration with
the patient upright and leaning forward.
 is audible when the diaphragm of the stethoscope
is applied firm to the chest wall at the LLSB.
 The rub is often inconstant.
Clinical signs differential diagnosis pleurisy
 Pleuritic pain has similar sharp quality but is usually
more specific in location
 Pleural rub is heard over the area where the pain
occurs
 A pericardial rub is heard throughout the respiratory
cycle, while a pleural rub disappears when
respiration is suspended.
ECG differential diagnosis - MI
 What leads is the ST elevation in?
 What shape is the elevation?
 Are there Q waves?
 Do the ST –T changes evolve with time?
 History of the patient
 Cardiac enzymes etc
 But REMEMBER that you can get more than one
pathology at the same time!
ECG Features
 ECG display changes secondary to acute
subepicardial inflammation and shows typically
four stages.
Stage I (first hours to days)
 Diffuse up sloping ST elevation with reciprocal ST
depression(aVR,V1)
 PR depression in the inferolateral leads
 PR elevation in aVR
ECG Features
Stage II (after several days)
 Normalization of the ST and PR segments
Stage III
 Diffuse T wave inversions, generally after the ST segment
have become isoelectric, however, this phase is not seen in
some patients
Stage IV
 ECG may become normal or the T inversion may persist
indefinitely
ECG in AMI
 ST elevation are convex
 Reciprocal depression is usually more prominent
 QRS changes occurs (development of Q wave and
loss of R-wave amplitude)
 T wave inversion are seen within hours before the ST
segment have become isoelectric.
ECG in Early Repolarization
 Early repolarization is a normal variant and
may also associated with widespread ST-T
segment elevation, most prominent in left
precordial leads.
 T wave are usually tall.
 ST/T ratio is <0.25
(this ratio is higher in pericarditis)
ST/T ratio in Pericarditis
ECG in Early Repolarization
Diagnosis of pericarditis
 Patient will have 2 or more of the following;
 Characteristic
 Pericardial
 ECG
chest pain
friction rub (auscultation)
showing characteristic ST elevation (caused
by epicardial injury)
Treatment
 Search for the underlying disease
 Patients require bed rest
 NSAIDs: Iboprofen (600 to 800 mg orally three
times daily) with discontinuation if pain is no
longer present after 2 weeks
 Reliable patients with no more than small PE who
respond well to NSAIDs need not to be admitted
to the hospital.
Indication for Hospital Admission
 Patients who do not respond well initially to NSAIDs
 Patients have larger effusion
 Patients have a suspected cause other than idiopathic
pericarditis
Should be hospitalized for additional observation, diagnostic
testing, and treatment as necessary
Prognosis
 Pericarditis is usually a benign and self-limited
disease (usually over 1 to 3 weeks) without
significant complication or recurrence in 70% to
90% of patients
 Diagnosis relates to underlying cause
 But any cause can lead to an effusion and
tamponade which can lead to death
 Pericarditis can also progress to pericardial
constriction and heart failure
Management
 In young women, it is not unreasonable to test for SLE.
 However, low ANA titers appear to be common in
patients with recurrent idiopathic pericarditis who do
not meet other criteria for SLE.
 Thus, the significance of low ANA titers in the setting
of an initial presentation in somewhat uncertain.
Cardiac Enzymes
 Cardiac troponin I was detectable in 49% and
above 1.5 ng/ml−1 in 22%.
 Elevated troponin values were felt to reflect
superficial myocardial inflammation and were not
an adverse prognostic marker after a mean
follow‐up of 24 months.
Pericarditis of Renal Failure
 Occurs in to one-third of patients (uremic pericarditis)
 Occurs in patients undergoing chronic dialysis with normal
level of BUN, CR (dialysis associated pericarditis)
 Pain is absent or mild.
 The ECG does not usually show the typical ST and T wave
elevation.
 Treatment: NSAID, intensification of dialysis.
Early Post-MI Pericarditis
 It is associated with large, transmural MIs, but it is almost
invariably a benign process that does not affect in-hospital
mortality.Treatment is based on symptoms.
 Augmentation of usual post-MI aspirin doses (650 mg TID
or QID for 2-5 days) or acetaminophen is usually effective.
 Because significant hemopericardium is rare with early post-
MT pericarditis and there is no evidence that heparin or other
antithrombotic drugs increase its risk, their administration
need not be modified.
Pericardial Effusion
Pericardial Effusion
 It is important clinically when it develops within a
relatively short time as it may lead to tamponade.
 Heart sounds may be fainter with PE.
 The friction rub may disappear.
 Apex impulse may vanish.
Pericardial Effusion: Symptoms
 Dull constant left chest ache
 Dyspnea (shortness of breath)
 Less common: Hiccups (phrenic nerve)
 Hoarseness (recurrent laryngeal nerve)
 Dysphagia (esophageal compression)
Pericardial Effusion
 Ewart’s sign:
the base of the left lung may be compressed by PE,
a patch of dullness and increased fremitus
(egophony) beneath the angle of the left scapula.
 CXR:
- Enlargemnt of cardiac silhouette (effusion>250 mL)
- Water bottle configuration of the cardiac cilhouette.
Pericardial Effusion
Echo:
 Is the most effective imaging.
 A echo free space between the posterior pericardium
and LV epicardium
 In the latter, the heart may swing freely within the
pericardial space.(electrical alternans)
CT,MRI:
 Loculated PE, pericardial thickening and mass
Myxedema
 25-35% of patients with severe hypothyroidism develop PE.
 PE has a high concentration of protein-cholestrole and like
other serous effusions ,its pathogenesis is not fully
understood (accumulation of mucopolysaccharides or a combination of
extravasation of albumin and decreased lymph flow( .
 The effusion gradually resolve with thyroid replacement.
 PE occasionally occur in subclinical hypothyrodism.
 Rarely, PE can occur in hyperthyrodism.
PE in hypothyroidy
 May cause of large
chronic pericardial
effusion (rarely is
massive and lead to
tamponade).
Management of Pericardial Effusion
 The management of small or moderate pericardial
effusions, without tamponade, is usually conservative.
 The routine diagnostic pericardiocentesis in the absence of
cardiac tamponade is not indicated.
 If the pericardial effusion is likely to be purulent then it
should be drained.
 If the effusion is felt to be malignant, pericardiocentesis is
recommended if confirmation would change management
and can be performed safely.
Taomponade
Tamponade
 Tamponade is life-threatening, slow (2000 mL) or
rapid (150-200 mL) compression of the heart due to
the pericardial accumulation of the fluid.
 There are limitation of ventricular filling and
reduction of cardiac output.
The causes of Raised Intra Pericardial Pressure
 Raised intrapericardial pressure can occur by 3 main
mechanisms:
1. Increased fluid within the intrapericardial space (PE)
2. Increased volume of the cardiac chambers (PTE)
3. Increased stiffness of the pericardium (CP)
Consequences of raised IPP
 Raised intrapericardial pressure has 3 potential
adverse effect on the heart:
1. A compressive effect with limits diastolic filling of the
heart
2. Increased diastolic filling pressure
3. Reduced stroke volume and cardiac output
Etiology
Causes of tamponade :
 Cancer
 Idiopathic pericarditis (receive anticoagulant)
 Renal failure
 Cardiac operation
 Trauma
 PCI
 Insertion PPM
Tamponade
 The clinical manifestation of tamponade may be
resemble of heart failure (dyspnea, orthopnea,
hepatic engorgement)
 When tamponade more slowly a high index of
suspicious is necessary because sometimes no
obvious cause for pericardial disease is apparent
 It should be considered in any patient with
hypotention and increased JVP.
Suspicious to Tamponade
 Hypotention+increased JVP
 Unexplained enlargement of the cardiac silhouette
 Reduction in amplitude of the QRS complex
 Electrical alternance of the P,QRS,T
Beck’s triad
 Hypotension
 Soft or absent heart sounds
 Jugular venous distention (prominent x)
Ventricular interdependence
 Normal subjects – there is normally small augmentation of
right-sided transvalvular flows accompanying inspiration.
 Explanation – combination of
 increased venous return due to decreases intrathoracic pressure
 fall in PVR
Enhanced Ventricular interdependence in
Tamponade
Pulse paradox
 A more than 10 mmHg (normal) inspiratory decline
in systolic arterial pressure
 When severe, it may be detected by palpating
weakness or disappearance of the arterial pulse
during inspiration.
 DD: RVMI, 1/3 patients with constrictive
pericarditis, hypovolemic shock, PTE, acute and
chronic obstructive lung disease
How to measure Pulsus Paradoxus
 When severe, it may be detected by palpating weakness or
disappearance of the arterial pulse during inspiration.
Ask the subject to breath normally
 Auscultate Korotkoff’s sounds as the BP cuff is slowly
lowered. Time respiration simultaneously
 Mark when BP sounds are heard only in expiration
 Mark when BP sounds are heard both in expiration &
inspiration. Korotkoff’s sounds seem to double at this
point.
 The difference is the measured pulsus paradoxus

Echocardiography
 Both ventricles is a tight incompressible covery




(pericardial sac)
Inspiratory enlargement of the RV in tamponade
Compress and reduce LV volume due to left ward
bulging of the IVS
Normal inspiratory augmentation of RV volume
causes an exaggerated reciprocal reduction in LV
volume
Respiratory distress increases the fluctuation in
transthoracic pressure
Ventricular interdependence in Tamponade
Echocardiography
 % respiratory variation=
E exp- E ins
E exp
Echocardiography
 An exaggerated respiratory variation in
inflow and outflow velocities:
MV:25% increase with expiration (normally 15%)
TV :50% increase with inspiration (normally 25%)
AV :14% increase with expiration (normally 4%)
PV :16% increase with inspiration (normally 5%)
Echocardiography
 Doppler ultrasound shows the TV and PV flow
velocities increase markedly in inspiration
 MV and AV and PVs flow velocities diminish
 RA and RV collapse in late diastole
Management
 In patient with clinical finding of tamponade if there
is RV collapse , immediate therapy is needed
 In patient without clinical finding of tamponade if
there is RV collapse it means intrapericardial
pressure is greater than RV pressure and there is
potential for acute hemodynamic deterioration,
urgent therapy is needed
Management
 Medical emergency – intensive care environment
needed.
 Oxygen
 Volume expansion
 Bed rest with leg elevation
 Inotropic drugs if necessary
Management
 Pericardiocentesis is the
definitive therapy to remove the
excessive fluid
 Commonly performed in the cath
lab but may be done ‘blind’ in an
intensive care environment
Constrictive Pericarditis
Chronic constrictive pericarditis
 Tuberculous constrictive pericarditis was common cause of
constriction pre 1960 – decline in incidence.
 Post-radiotherapy constriction features prominently today along
with post-surgical causes.
 Needs to be differentiated from restrictive cardiomyopathy
when making diagnosis.
Chronic constrictive pericarditis
 Formation of granulation tissue after desorption of
effusion or healing of a acute fibrinous pericarditis.
 The ventricles are enable to fill because of the
limitations imposed by rigid, thickened pericardium
 Ventricular filling is only in early diastole and is
reduced abruptly when the elastic limit of the
pericardium is reached
 In tamponade ventricular filling is impeded
throughout diastole
Investigations
 Clinical picture– prime symptoms weakness,
fatigue, weight gain, edema, ascitis, exertional
dyspnea, ortopnea (not severe)
 The cervical veins are distended and may remain
so even after intensive diuretic treatment
 Auscultation may reveal a pericardial knock(0.09-
0.12 after AV closure) , audible in apex, it occurs
due to abrupt cessation of ventricular filling
Investigations
 Heart sounds may be distant
 Audible systolic murmur due to TR
 Congestive hepatomagaly that cause LFT
impairment and jaundice
 Broadbent’s sign: reduced apical pulce and
sometimes retract in systole
Kussmaul’s sign
 Normal subjects – inspiration causes a decrease in
chest pressure. Increase in venous return – JVP falls
 Constrictive pericarditis – Increased venous return
cannot be accommodated in RV because of high EDP
 So JVP rises on inspiration
 D.D: tricuspid stenosis, RVMI, RCM
Investigations
 ECG may not show characteristic ST elevation,
display low voltage of the QRS complexes and
diffuse flattening or inversion of the T waves, AF is
present in one-third of patients
 CXR may see calcification(23-50%), calcification
in CXR is more common in TB and there is normal
or only mild enlarged heart that helps to rule out
coexisting effusion
 Echo to identify hemodynamic effects on heart
and coexisting effusion
Respiratory Variation in CP
 Ventricular interdependence
is found in CP but not RCM
Respiratory Variation in CP
Echo Finding
 Normal subjects – increase in TV flow velocity on
inspiration, and decrease in MV flow
 Due to increased vascular capacity of lungs venous
return and RV output increases while return to LA is
reduced
 This is exaggerated in tamponade/sig constriction –
RV output can’t increase because of high EDP +
pulmonary return is reduced further
Septal Bounce
TDI of the Mitral Annulus
CP
RCM
CT/MRI
 MRI/CT scan – data about the thickness of the
pericardium and display calcification.
 Pericardial thickening and even calcification are
not synonymous with CP since they may occur
without seriously impairing ventricular filling.
Normal Right Atrial Pressure Tracing
• “a” wave
Atrial systole
• “x” descent
– Relaxation of RA
– Downward pulling of tricuspid
annulus by RV contraction
• “v” wave
– RV contraction
• “y” descent
– TV opening and RA emptying
–
CVP Tracing in Normal Subjects
Bimodal with x > y
Constrictive Pericarditis
Constrictive Pericarditis vs. Tamponade
Tamponade
CP
Dip and Plateau in Diastolic Waveform
No respiratory variation in RCM
Treatment
 The only effective treatment for chronic constrictive
pericarditis is complete surgical resection of the
pericardium.
 Mortality for procedure ranges from 5-16%
 Symptomatic improvement in ~90%
 5 year survival rate is 74-87% depending on co-
morbidities pre-op
Treatment
 Radiation-induced disease is considered a relative
contraindication for pericardiectomy.
 Healthy older patients with very mild constriction
may also be managed nonsurgically (salt restriction
and diuretics consumption).
Pericardial cyst
 Appear as rounded or lobulated deformities of the
cardiac silhouette, most commonly at the right
cardiophernic angle
 No symptom
 May be confused by tumor, ventricular aneurysm, or
cardiomegaly
 Management is conservative