Pericarditis - PowerPoint

							Acute Pericarditis
Emory Family Medicine




                Susan Schayes M.D.
               Assistant Professor-CT
       Family Medicine, Emory University School
                     of Medicine
             The Pericardium
 A fibroelastic sac composed of visceral and
  parietal layers
 Both these layers are separated by a pericardial
  cavity.
 The cavity normally contains 15 to 50 ml of
  straw-colored fluid.
 Visceral layer is in contact with the epicardium
  (ST elevation)
             The Clinical problem


 Can be an isolated entity or part of a systemic
  disease
 0.1% of all hospitalized patients
 5% of ER visits for chest pain without an MI
               Etiology-Acute Pericarditis
 Infectious
       Viral : Coxsackie, Echo, EBV, Influenza, HIV
       Bacterial: TB, staph, hemophilus, pneumococcal, salmonella
       Fungal/other: histo/blasto/coccidio, rickettsial
 Rheumatologic
     SLE, Sarcoid, RA, Dermatomyositis, Ankylosing Spondylitis, Scleroderma,
      PAN
 Neoplastic
     Primary: angiosarcoma, mesothelioma
     Metastatic: breast, lung, lymphoma, melanoma, leukemia
 Immunologic
     Celiac sprue, Inflammatory Bowel Disease
 Drug
     Hydralazine, Procainamide
 Other
     MI, Dressler’s, Post Pericardiotomy, Chest Trauma, Aortic dissection
     Uremic, Post Radiation
     IDIOPATHIC
                    Other Pearls

 Viral and Autoimmune causes constitute > 50% of
  cases of acute pericarditis

 Pericardial disease is the most frequent
  cardiovascular manifestation of AIDS

 The typical diffuse ST elevation is not seen in uremic
  pericarditis,in which there is fibrin deposition in the
  parietal layer but no epicardial inflammation.
            Clinical Presentation
 Chest pain
 Pericardial friction rub
 Diffuse ST segment elevation on EKG
 Pericardial effusion


Presence of at least two of the above features is necessary
to make the diagnosis
                    Chest Pain
 Retrosternal in location
 Sudden in onset
 Pleuritic and sharp in nature
 Exacerbated by inspiration
 Worsens when supine and improves upon sitting
  upright or leaning forward.
 Can often radiate to the neck, arms, or left shoulder.
 Radiation to one or both trapezius muscle ridges,
  suggests a probable pericarditis (phrenic nerve
  traverses the pericardium)
            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.
 Corresponds temporally to the movement of heart within the
  pericardial sac.
 Has 3 components, which correspond to atrial systole,
  ventricular systole, and early diastole.
 Pericardial friction rub is audible throughout the respiratory
  cycle, whereas the pleural rub disappears when respirations are
  on hold.
           EKG in Pericarditis
 Widespread upward concave ST-segment
  elevation and PR-segment depression
 If the ratio of ST-segment elevation to T-wave
  amplitude in V6 > 0.24, acute pericarditis is
  almost always present.
 The EKG changes have 4 phases during the
  course of illness
                          EKG Stages
 Stage I
    first few days  2 weeks
    ST elevation, PR depression
    up to 50% of pt with symptoms / rub do NOT have or evolve into stage I
 Stage II
    last days  weeks
    Normalization of ST and PR segments
    ST returns to baseline, flat T waves
 Stage III
    after 2-3 weeks, lasts several weeks
    Widespread T wave inversion
 Stage IV
    lasts up to several months
    gradual resolution of T wave changes
Acute pericarditis – Stage I
            Pericarditis-Stage II




60 y/o man with acute pericarditis on presentation and after 1 month
of resolution of symptoms
         Pericarditis-Stage III




T wave inversions
              Differential Diagnoses

          Clinical                 EKG (ST elev)

   Myocardial Infarction      AMI
   Myocarditis                Early Repolarization
   Pulmonary embolism         Myocarditis
   Pneumothorax               Hyperkalemia
   Pneumopericardium          Ventricular Aneurysm
   Musculoskeletal            Normal Variant
      Pericarditis vs Early Repolarization
                Acute           Early
                Pericarditis    Repolarization
Sex             Either          Usually Male
Age             Any             Usually < 40
PR segment dev Common           Uncommon
T waves         nl, blunt       tall, peaked
J-ST / T ampl   > 25%           <25%

Tallest         Usually V5      Usually V4
precordial R
                 Early Repolarization




J point and ST segment elevation is most prominent in V4 to V6.
The ST segment maintains its normal configuration and is slightly concave
                   Pericarditis vs AMI
                Pericarditis                       MI

ST segment      Diffuse,concave elevation in all   Localized, convex, with
                leads except aVR+ V6 w/o           reciprocal changes in infarct
                reciprocal changes
                Height Not > 5mm                   Height may be > 5 mm

PR depression   Frequent                           Almost never


Q waves         Not usual, unless with infarct     Common with q wave infarct


T waves         Inverted after J returns to        Inverted while ST still elevated
                baseline                           T inversions and ST ↑ can be
                T inversions and ST ↑ are not      seen simultaneously on the
                seen simultaneously on the         same EKG
                same EKG
Arrhythmias     Rare                               Frequent


Conduction      Rare                               frequent
disturbances
Acute Anterior MI
                 Laboratory testing
 Laboratory abnormalities
       CBC – very high WBC (purulent pericarditis)
       ↑ESR
       Chem-7 (uremic etiology)
       ↑CRP
       HIV in selected cases
       ANA
       Rheumatoid factor
       Blood cultures if febrile
       Viral cultures and antibody testing not indicated
          Cardiac Isoenzymes - ? helpful
 MB fraction of CK and Troponin I are modestly elevated
 The rise in TnI is related to the extent of myocardial
  inflammation.
 Features associated with a rise in Tn I are younger age,male
  gender,presence of effusion and a recent infection
 Enzyme rise is transient,resolving within the first week,
  persistent ↑ suggest myopericarditis
 Not reliable to differentiate MI vs pericarditis

 • Two studies that included 187 patients with idiopathic pericarditis ,TnI
 was detectable in 32-49% and in 8-22% it was >1.5 mcg/ml

 • Another 2 year ER based study-
     Out of 14 pts with 2/3 findings (typical CP, rub, and ECG changes)
      71% had elevated Tn I with negative CAD workup
                    Other Studies
 Tuberculin skin testing
 Echocardiogram
       Normal unless there is an effusion
       Presence of effusion supports the diagnosis, but absence
        does not exclude it.
       The ACC/AHA/ASE all recommend to obtain an echo
        in any suspected pericardial disease
 Chest X-ray
       Recommended in all cases
       Typically normal
       Enlarged cardiac silhouette in effusion (with clear lung
       fields)
                Need for hospitalization
 Many physicians tend to admit them, but this may not be
  necessary.
 Uncomplicated acute pericarditis can undergo initial
  evaluation in a same day hospital facility or clinic, with an
  outpatient follow-up
 Features of high risk include:
       Subacute symptoms (eg, developing over several days or weeks)
       High fever (>38ºC [100.4ºF]) and leukocytosis
       Evidence suggesting cardiac tamponade
       A large pericardial effusion
       Immunosuppressed state
       A history of oral anticoagulant therapy
       Acute trauma
       Failure to respond within seven days to NSAID therapy, a generous
          allocation of time
         Elevated cardiac troponin, suggestive of myopericarditis
                  Complications

 Pericardial Effusion/ Tamponade
 Constrictive Pericarditis
   can be “transient” – 10% may have transient
    within 1st month, resolves by 3 months
 Recurrent Pericarditis (15-32%)
   Recurrent sx after the initiating event is no longer
    active
   Most likely an autoimmune etiology
   Rx : NSAIDS/ Colchicine +/- steroids
                       Treatment
 Goals of acute therapy:
     Relieve Pain
     Treat the inflammation
     Prevent Cardiac tamponade
   Most viral infections are self-limited
   Treat the underlying disease process
   Drain purulent effusions
   Symptomatic therapy
   None of the treatments unfortunately, have not been
    proven to prevent the complications.
                            NSAIDs
 May require weeks to months of treatment with high doses of
    NSAIDs
   The choice is usually empiric, based on the physician’s
    familiarity with the agent and/or its availability.
   Rapidly titrate the dose within 1–2 days to achieve maximum
    symptomatic relief
   Evaluate for a response within 1–2 wks,Sx usually subside in a
    week.
   If adequate clinical response,continue NSAIDs for 1 wk after
    complete resolution of Sx and then taper in 2–3 days.
                                                    NSAIDs
       Aspirin
             2-6 gm daily650mg Q3-4 hrs
             Preferred in patients with CAD
       Ibuprofen
             1600-3200 mg daily400-800 mg q 6-8 hrs
             above average response rate and has a very good side
              effect profile
       Indomethacin
             75-225 mg daily
             Try to avoid, unless absolutely needed as it can ↓
              coronary blood flow.

Nonsteroidal Anti-inflammatory Drugs in the Treatment of Pericarditis: Clinical Review
SCHIFFERDECKER, BRANISLAV MD; SPODICK, DAVID H. MD, DSc
Cardiology Review ; Volume 11(4), July/August 2003, pp 211-217
                                             Colchicine
      A prospective, randomized, open-label design was
       used.
      120 patients with a first episode of acute pericarditis
       were randomly assigned to
            conventional treatment with aspirin (group I) or
            conventional treatment plus colchicine 1.0 to 2.0 mg for the first day
             and then 0.5 to 1.0 mg/d for 3 months (group II).
            Colchicine significantly reduced the recurrence rate (10.7% vs 32.3%;
             P=0.004;) and presence of symptoms at 72 hours (11.7% vs 36.7%;
             P=0.003).
            Based upon this, addition of it to the Rx regimen for an initial episode
             of acute pericarditis is an option for physicians.


Colchicine in Addition to Conventional Therapy for Acute Pericarditis
Results of the COlchicine for acute PEricarditis (COPE) Trial
Circulation. 2005;112:2012-2016 10.1161/CIRCULATIONAHA.105.542738eeeeew
                          Steroids
 In patients refractory to NSAIDs and colchicine
 Steroid therapy with initial episode is more likely
  associated with recurrent episodes.
 Evidence available argues against the routine
  administration of corticosteroids during a first
  episode of acute pericarditis
 Specific conditions that will benefit:
       Acute pericarditis due to connective tissue diseases
       Auto-immune pericarditis
       Uremic pericarditis
  Myocardial Infarction-Associated Pericarditis
 Early post MI pericarditis is a consequence of transmural
  infarction.
        Aspirin is the drug of choice in this setting. (650 mg
         Q4h)
 Late MI associated pericarditis (Dressler syndrome), occurs
  days to months after infarction,
        Autoimmune in etiology.
        NSAIDs are the treatment of choice.
        Colchicine seems to be the most effective if NSAIDs fail
        Corticosteroids seem to provide symptomatic benefit but do not
          prevent recurrence.
         Pericardiectomy is only rarely curative
               Summary
 Etiology of Acute Pericarditis
 Clinical Presentation and EKG findings
 Differential Diagnosis
 Evaluation
 Treatment