Download Pericarditis

2 OF THE ABOVE CRITERIA ARE NECESSARY FOR THE DIAGNOSIS
ABSENCE OF A PERICARDIAL EFFUSION DOES NOT EXCLUDE THE DX
PERICARDITIS SHOULD BE SUSPECTED WITH PERSISTANT FEVER
PERICARDIAL EFFUSION
OR CADIOMEGALLY
SINCE THE SAME VIRUSES CAN CAUSE BOTH PERICARDITIS/ AND MYOCARDITIS THERE
ARE COMMON ELEMENTS TERM: PERIMYOCARDITIS SOMETIMES USED
CHEST PAIN: - FAIRLY SUDDEN
- OVER ANT. CHEST WALL
- PLEURITIC/SHARP
- DEC. LEANING FORWARD
PERICARDIAL FRICTION RUB:- VERY SPECIFIC (85% OF CASES)
CARDIAC BIOMARKERS: ACUTE PERICARDITIS- INCR. TROPONIN I (MYOCARDITIS)
SIGNS OF INFLAMMATION: WBC/ SED RATE/CRP/
EKG: STAGE1- SEEN HOURS/DAYS- ST ELEV. CONCAVE UP
ATRIAL INJURY- PR CHANGE (ST:PR CHANGE IN OPPOSITE DIRECTION)
STAGE2- NORMALIZATION ST AND PR
STAGE3- DIFFUSE T WAVE INVERSION (CAN BE ABSENT)
STAGE4- MAY NORMALIZE OR T WAVES MAY PERSIST INDEFINITELY)
CXR: USUALLY NORMAL
INITIAL EVALUATION– STANDARD APPROACH
PERICARDITIS IS USUALLY BRIEF AND BENIGN
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INITIAL HISTORY AND PHYSICAL
ECHOCARDIOGRAPHY
EKG
CHEST X-RAY
TB TEST
ANA
HIV
BLOOD CULTURES IF TEMP.> 100.4
VIRAL STUDIES-USUALLY NOT DONE SINCE COURSE IS NOT ALTERED
TREATMENT
IF IDENTIFIED CAUSE OTHER THAN VIRAL/ OR IDIOPATHIC- TX UNDERLYING CAUSE
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VIRAL OR IDIOPATHIC: NO THERAPY HAS PROVEN TO PREVENT SERIOUS SEQUELLA
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IF NO HIGH RISK FEATURES- CAN BE TREATED AS AN OUTPATIENT
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NSAIDS- RELIEF OF PAIN AND DECREASE INFLAMMATION/ OR EFFUSION ESC 2004
A) IBUPROFEN 300-800 MG/Q6-8HR. Days or wks. OR ASA 2-5 G/DAY—ALTHOUGH DOESN’T CHANGE NATURAL HX
B) KETOROLAC- IV
5. IF NO RESPONSE X 1WK. – LOOK FOR OTHER CAUSES/ AUTOIMMUNE DISORDERS
6. IN AMI- USE ONLY ASA/ NOT NSAID---( INDOMETHICIN)
7. COLCHICINE: - MAY HELP PREVENT RECURRENCE OF ACUTE IDIOPATHIC OR VIRAL ? FOR 1ST EPISODE
0.5-1MG TWICE ON THE 1ST DAY, THEN 0.5 1OR 2 X DAY FOR THREE MONTHS
8. GLUCOCORTICOIDS: USE ONLY IF REFRACTORY TO NSAIDS OR COLCHICINE
- ACUTE PERICARDITIS DUE TO CONNECTIVE TISSUE DISEASE
- IMMUNE MEDIATED PERICARDITIS
- UREMIC PERICARDITIS
HIGH DOSES OF STEROIDS WITH RAPID TAPERING
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Pericardial Disease
Acute Pericarditis
Chronic Relapsing Pericarditis
Constrictive Pericarditis
Cardiac Tamponade
Localized and Low Pressure Tamponade
Restrictive Cardiomyopathy
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Pericardial Anatomy
Two major components
serosa (viceral pericardium)
mesothelial monolayer
facilitate fluid and ion exchange
fibroa (parietal pericardium)
fibrocollagenous tissue
Pericardial Fluid
15 - 50 ml of clear plasma ultrafiltrate
Ligamentous attachments
to the sternum, vertebral column, diaphragm
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Pericardial Physiology
not needed to sustain life
physiologic functions
limit cardiac dilatation
maintain normal ventricular compliance
reduce friction to cardiac movement
barrier to inflammation
limit cardiac displacement
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Acute Pericarditis
common causes
Outpatient setting
usually idiopathic
probably due to viral infections
Coxsackie A and B (highly cardiotropic) are the most common viral cause of
pericarditis and myocarditis
Others viruses: mumps, varicella-zoster, influenza, Epstein-Barr, HIV
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Acute Pericarditis
Non-infectious
Post-myocardial infarction
Uremia
Neoplastic disease
Radiation induced
Connective tissue diseases
Drug induced
Acute Pericarditis
common causes
Inpatient setting
= Trauma, TUMOR
U = Uremia
M = Myocardial infarction (acute, post)
Medications (hydralazine, procain)
O = Other infections (bacterial, fungal, TB)
R = Rheumatoid, autoimmune disorder
T
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Radiation
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Acute Pericarditis
Diagnostic Clues
History
sudden onset of anterior chest pain that
is pleuritic and substernal
Physical exam
presence of two- or three-component rub
ECG
most important laboratory clue
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Acute pericarditis: clinical findings
Chest pain
Pleuritic, positional, may mimic MI
Fever, tachycardia, dyspnea
Pericardial friction rub
3 component “scratchy” sound
Abnormal ECG
Diffuse ST elevation
PR depression
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Heart Murmurs of Pericarditis
Pericardial friction rub is pathognomic for pericarditis
scratching or grating sound
Classically three components:
presystolic rub during atrial filling
ventricular systolic rub (loudest)
ventricular diastolic rub (after A2P2)
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Acute Pericarditis
ECG features
ST-segment elevation
reflecting epicardial inflammation
leads I, II, aVL, and V3-V6
lead aVR usually shows ST depression
ST concave upward
ST in AMI concave downward like a “dome”
PR segment depression (early stage)
T-wave inversion
occurs after the ST returns to baseline
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Acute Pericarditis:
Electrocardiogram
Viral Pericarditis
Coxsackievirus and Echovirus
Often diagnosed as idiopathic
Seasonal variation
Can occur with AIDS as a result of CMV
History
Usually self-limited
Complications: myocarditis, recurrence, tamponade,
constriction
Treat underlying disorder
Acute Pericarditis
Management
Treat underlying cause
Analgesic agents
codeine 15-30 mg q 4-6 hr
Anti-inflmmatory agents
ASA 648 mg q 3-4 hrs
NSAID (indomethacin 25-50 mg qid)
Corticosteroids are symptomatically effective , but preferably avoided
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Chronic Relapsing Pericarditis
occurs in a small % of patients with acute idiopathic pericarditis
steroid dependency requiring gradual tapering over 3-12 months; NSAIDs, analgesics,
and colchicine may be beneficial
pericardiectomy for relief of symptoms is not always effective
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Dressler’s Syndrome
Described by Dressler in 1956
fever, pericarditis, pleuritis
(typically with a low grade fever and a pericardial friction rub)
occurs in the first few days to several weeks following MI or heart surgery
incidence of 6-25%
treat with high-dose aspirin
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Acute Pericarditis
Differential Diagnosis
Acute myocardial infarction
Pulmonary embolism
Pneumonia
Aortic dissection
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Recurrent Pericarditis
Incidence ~25%
Treatment
NSAID’s initially
Steroids Rarely
Colchicine
Well Tolerated
60% effective long-term, more effective if taken chronically
Fewer side effects than long-term steroids
Large pericardial effusion: signs
Soft heart sounds
Reduced intensity of friction rub
Ewart’s sign: Dullness, decreased breath sounds, and egophony over posterior L
lung due to compression by large pericardial sac
Electrical alternans on ECG
ECG in Pericardial Effusion
Diffuse low voltage
amount of fluid
electrical conductivity of the fluid
Electrical alternans
alternating amplitude of the QRS
produced by heart swinging motion
also seen in PSVT, HTN, ischemia
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Dignostic Evaluation
Chest x-ray
usually requires > 200 ml of fluid
cannot distinguish between pericardial effusion and
cardiomegly
Echocardiography
standard for diagnosing pericardial effusion
convenient, highly reliable, cost effective
false positives (M-mode)- left pleural effusion, epicardial fat,
tumor tissue, pericardial cysts
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Pericardial effusion
L
Pericardial tamponade:
pathophysiology
Increased intra-pericardial pressure
Exceeds ventricular diastolic pressure
Causing impaired diastolic filling
Elevated venous pressure
Increased JVP, hepatomegaly, edema
Dyspnea
Decreased filling decreased stroke volume
Reflex tachycardia, hypotension
Cardiac Tamponade
Early stage
mild to moderate elevation of central venous pressure
Advanced stage
intrapericardial pressure
ventricular filling, stroke volume
hypotension
impaired organ perfusion
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Beck’s Triad
Described in 1935 by thoracic surgeon Claude S. Beck
3 features of acute tamponade
Decline in systemic arterial pressure
Elevation in systemic venous pressure (e.g. distended neck vein)
A small, quiet heart
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Pulsus paradoxus
Exaggerated (>10mmHg) cyclic decrease in systolic BP during normal inspiration
Inspiration: increased venous return increased RV volume.
Interventricular septum shifts left, decreased LV volume decreased stroke volume
systolic pressure falls.
Pulsus Paradoxus
an exaggerated drop in SBP with inspiration (>10mmHg)
Berliner Klinische Wochenschrift 1878; 10:461
Cardiac Tamponade
clinical features
Symptoms
dyspnea, fatigue, cough, agitation and restlessness, syncope, shock, anuria
Physical examination
pulsus paradoxus
tachycardia
increased jugular venous pressure
hypotension
Echocardiographic Diagnosis
Pericardial effusion
highly reliable
Cardiac tamponade
RA and RV diastolic collapse
reduced chamber size
distension of the inferior vena cava
exaggerated respiratory variation of the mitral and tricuspid
valve flow velocities
RA and RV diastolic collapse
RA and RV walls are thin with relatively low intracavitary pressures
Absence of compression virtually excludes tamponade
Presence of compression is suggestive but not diagnostic
When to treat pericardial effusion ?
Tamponade is not an all-or-non-phenomena
Echo more sensitive than clinical criteria
Limited data exist with respect to the optimal timing
of intervention for pericardial effusion
Cardiogenic shock must be aggressively addressed
Infusion of large volume of IV fluids may temporarily
stabilize the patient
Echo-guided Pericardiocentesis
SAFE and EFFECTIVE
locating the optimal site of puncture
determining the depth of the pericardial effusion and the distance form the puncture
site to the effusion
monitoring the results of the pericardiocentesis
Pericardiocentesis
Diagnostic tap
not always indicated
Pericardial biopsy may be more definitive
Therapeutic drainage
indicated for tamponade
Clearance for percutaneous pericardiocentesis
Subcostal view
At least 1 cm fluid between visceral and parietal pericardium
No significant adhesions
Effusion not consolidated
Path to pericardium not THROUGH the liver
Constrictive pericarditis
Fibrous thickening, adhesion, calcification of the pericardium.
Most common etiologies:
TB
Idiopathic
Post pericarditis of any etiology
Constriction
Thickening of the pericardium that limits diastolic volume
Resultant syndrome mimicking right heart failure
Difficult to separate from Restriction
Constriction
Etiology
Idiopathic
33%
Post-pericarditis 18%
Post-surgical
16%
Radiation
14%
Rheumatic
6%
Infection
3%
Constrictive pericarditis: clinical
findings
Fatigue, hypotension, tachycardia
Elevated JVP
Kussmaul’s sign
Pericardial “knock”
Ascites, edema
Constrictive pericarditis: Diagnosis
Calcified pericardium on Xray
Image thickened pericardium:
scan, MRI
Cardiac cath:
Elevated, equalized diastolic pressures
Restricted filling pattern in RV (“dip and plateau”)
Prominent “y” descent on RA pressure tracing
CT
MRI- Constriction
RV
LV
Echocardiographic signs of constriction
Thickened and adherent pericardium
Respiratory “bounce” of septum
Diastolic mitral regurgitation
Dilated IVC without respiratory variation
Normal E’ and loss of A’ on tissue Doppler
Constriction Treatment
Medical management-palliative
Diuretics to minimize edema
Anti TB drugs x 4 weeks before surgery
Surgical management-Pericardiectomy
Mortality ~10%
Symptomatic improvement 90%
Poor Prognostic Indicators:
NYHA class III or IV
Incomplete resection
Radiation induced