REZA KIANI,MD, Invasive Cardiologist & Interventionist Rajaei Heart Center.
Dr. Mozhgan Parsaee Department of Echocardiography Shahid Rajaei Cardiovascular Center Pericardial...
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Transcript of Dr. Mozhgan Parsaee Department of Echocardiography Shahid Rajaei Cardiovascular Center Pericardial...
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Dr. Mozhgan ParsaeeDepartment of Echocardiography
Shahid Rajaei Cardiovascular Center
Pericardial Disease
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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.
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Normal Function of Pericardium
Limit cardiac dilatation
Limit cardiac displacement
Reduce friction to cardiac movement
Barrier to inflamation
Not needed to sustain life
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Acute Pericarditis
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Acute Pericarditis
Acute pericarditis, defined as symptoms or signs resulting from pericardial inflammation of no more than 1 to 2 weeks in duration.
Serous Fibrinous Purulent Hemorrhagic
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Etiology
Infectious pericarditisA.Viral : coxackievirus A&B, echovirus,
mumps,HIV, adenovirus, hepatitis
B. Pyogenic: pneumococcus, streptococcus, staphylococcus
C. Fungal: histoplasma, candida
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Etiology
Non infectious pericarditisA. acute MIB. UremiaC. Cancer (commonly lung or breast) D. TraumaE. MyxedemaF. PostirradiationG. Aortic dissectionH.Acute idiopathicI. Connective tissue disease
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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)
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Signs, Symptoms and Investigations
How can we diagnose this?
Clinical examinationAuscultationChest x-rayECGEchoCatheter laboratory investigations
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Acute Pericarditis
Chest pain
Pericardial friction rub
ECG changes
Pericardial effusion
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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
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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.
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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)
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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.
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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.
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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 patientCardiac enzymes etcBut REMEMBER that you can get more
than one pathology at the same time!
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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 leadsPR elevation in aVR
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ECG Features
Stage II (after several days)Normalization of the ST and PR segments
Stage IIIDiffuse T wave inversions, generally after the ST
segment have become isoelectric, however, this phase is not seen in some patients
Stage IVECG may become normal or the T inversion may
persist indefinitely
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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.
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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)
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ST/T ratio in Pericarditis
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ECG in Early Repolarization
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Diagnosis of pericarditis
Patient will have 2 or more of the following;
Characteristic chest pain
Pericardial friction rub (auscultation)
ECG showing characteristic ST elevation (caused by epicardial injury)
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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.
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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
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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 causeBut any cause can lead to an effusion and
tamponade which can lead to deathPericarditis can also progress to pericardial
constriction and heart failure
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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.
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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.
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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.
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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.
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Pericardial Effusion
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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.
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Pericardial Effusion: Symptoms
Dull constant left chest acheDyspnea (shortness of breath)Less common: Hiccups (phrenic
nerve)Hoarseness (recurrent laryngeal
nerve)Dysphagia (esophageal compression)
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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.
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Pericardial Effusion
Echo:Is the most effective imaging.A echo free space between the posterior
pericardium and LV epicardiumIn the latter, the heart may swing freely within
the pericardial space.(electrical alternans)
CT,MRI:Loculated PE, pericardial thickening and mass
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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.
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PE in hypothyroidy
May cause of large chronic pericardial effusion (rarely is massive and lead to tamponade).
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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.
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Taomponade
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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.
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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)
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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 pressure3.Reduced stroke volume and cardiac output
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Etiology
Causes of tamponade :CancerIdiopathic pericarditis (receive anticoagulant)Renal failureCardiac operationTraumaPCIInsertion PPM
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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.
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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
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Beck’s triad
Hypotension
Soft or absent heart sounds
Jugular venous distention (prominent x)
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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
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Enhanced Ventricular interdependence in Tamponade
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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
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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
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Echocardiography
Both ventricles is a tight incompressible covery (pericardial sac)
Inspiratory enlargement of the RV in tamponadeCompress and reduce LV volume due to left
ward bulging of the IVSNormal inspiratory augmentation of RV volume
causes an exaggerated reciprocal reduction in LV volume
Respiratory distress increases the fluctuation in transthoracic pressure
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Ventricular interdependence in Tamponade
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Echocardiography
% respiratory variation= E exp- E ins E exp
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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%)
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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
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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
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Management
Medical emergency – intensive care environment needed.
OxygenVolume expansionBed rest with leg elevationInotropic drugs if necessary
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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
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Constrictive Pericarditis
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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.
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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
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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
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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
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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
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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
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Respiratory Variation in CP
Ventricular interdependence is found in CP but not RCM
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Respiratory Variation in CP
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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
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Septal Bounce
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TDI of the Mitral Annulus
CP RCM
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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.
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Normal Right Atrial Pressure Tracing
• “a” wave– Atrial systole
• “x” descent– Relaxation of RA– Downward pulling of
tricuspidannulus by RV contraction
• “v” wave– RV contraction
• “y” descent– TV opening and RA emptying
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CVP Tracing in Normal Subjects
Bimodal with x > y
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Constrictive Pericarditis
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Constrictive Pericarditis vs. Tamponade
Tamponade CP
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Dip and Plateau in Diastolic Waveform
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No respiratory variation in RCM
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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
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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).
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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
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The End Result