Myocarditis _amp; Pericarditis

Document Sample
Myocarditis _amp; Pericarditis Powered By Docstoc
					Myocarditis & Pericarditis
      Resident Rounds
       March 6, 2003
        Aric Storck
Case 1
  57 year old man
  n   previously healthy
  n   No cardiac risk factors
  One week history of
  n   General malaise, fever/chills, myalgias, coryza
  Yesterday
  n   Gradual onset of 6/10 pleuritic chest pain
       w   Worst lying down
       w   Better sitting forward
       w   Not exacerbated by exertion
       w   Slightly SOB
Physical exam
  HR 105 RR 20 BP 130/80 T 38.2
  H&N – some palpable lymph nodes
  CVS – sounds like velcro
  Chest – Normal
  Abdo - Normal
Could this be a heart attack?
 Should I call the cath lab?
     What’s going on?
Pericardial Disease
           Chest Pain - Ischemic vs
                 Pericarditis
                 pericarditis      ischemic pain
Location     Precordium, L       Retrosternal, L
             trapezius ridge     shoulder, arm
Quality      Pleuritic           Pressure, tightness,
                                 burning
Duration     Hours to days       1-15 minutes

Exacerbation Lying down, chest   exertion
             wall motion
Relief       Leaning forward     Rest
          Ischemic vs Pericarditis
                    Pericarditis     Ischemic Pain

Associated SSx   SOB, diaphoresis, N/V, diaphoresis,
                 no N/V            SOB
Vital signs      Often febrile     High fever rare
Pericardial Disease
  Pericarditis
  n   Non-specific inflammation of pericardium
  n   Rarely emergent
  Pericardial effusion
  n   Accumulation of fluid in pericardial space
  n   Serous, purulent, fibrinous, hemorrhagic
  Cardiac tamponade
  n   Impairment of ventricular filling due to fluid
      in pericardial space
  n   Emergent
Pericardial physiology
  Parietal layer
  n   Thick, collagenous, stiff
  n   Adventitial attachments to sternum,
      diaphragm, mediastinum

  Visceral layer
  n   Thin
  n   Closely adherent to epicardial surface
Pericardial fluid
  Potential space between layers
   n   Normally 15-60 cc fluid
  Functions
   n   Reduces friction
   n   Prevention of infection
   n   Augmentation of atrial filling
   n   Maintains normal pressure-volume
       relationship of chambers
  No physiological consequence to absent
  pericardium
Pericardial innervation
  Parasympathetic
  n   Vagus
  n   Left-recurrent laryngeal nerve
  Sympathetic
  n   Stellate
  n   First thoracic ganglia
  Little somatic sensory innvervation
  n   Thus visceral nature of chest pain
Pericarditis - etiology
  Viral
  Bacterial
  Traumatic
  Malignant
  Post-irradiation
  Post-MI
  Drug-induced
  Collagen vascular disease
          Viral Pericarditis
Most common cause
n   Enteroviruses
     w Coxsackie A & B
     w Echovirus
n   HIV
Mechanism of injury
n   Direct viral cytotoxicity
n   Indirect auto-antibody mediated effects
Viral Pericarditis - SSx
  Syndrome may be immediate or
  develop 2-4 weeks post viral illness
   n   Chest pain
   n   Pericardial friction rub
        w Heard with diaphragm over LLSB, leaning
          forward, breath held
        w Scratchy
        w Triphasic (presystolic, systolic, diastolic)
   n   Fever
   n   Tachycardia
   n   Tachypnea,dyspnea
   n   diaphoresis
Bacterial Pericarditis
  Common in less developed countries
  More commonly associated with
  tamonade
  Higher mortality than viral
  Streptococcus, staphylococcus, gram
  negs, anaerobes
  TB
  Lyme disease
Concomitant pneumonia / empyema
Often not diagnosed until tamponade
Definitive Dx requires pericardiocentesis
Treatment Abx
ICU admission indicated
Uremic Pericarditis
  ESRD / Underdialysis
  Bloody pericardial effusions
  ECG often normal (little epicardial involvement)
  Cardiac tamponade common
  n   Often loculated - therapeutic pericardiocentesis
      difficult
  Treatment
  n   ICU admission
  n   NSAIDS (caution b/c bleeding diathesis of uremia)
Post-MI Pericarditis
  May occur within days of MI
  n   Direct extension of myocardial inflammation
  n   Presents as “different” chest pain
  n   Must distinguish from reinfarction
  n   Incidence 7-16%
  n   Tx: NSAIDs
  Dressler’s syndrome
  n   Thought to be autoimmune
  n   Weeks to months
  n   Fever, chest pain, leukocytosis, pleuritis,
      pericardial/pleural effusions
  n   Tx: NSAIDs, steroids for resistant cases
Collagen Vascular Disease
       Pericarditis
Common in many CVDs
n   RA
    w Incidence 30-50% - many clinically silent
n   SLE
    w 50% incidence
Dx: CP, R CHF, echo
n   ECG/CXR often normal
Tx: steroids
Commonly progress to constrictive
pericarditis
Malignant pericarditis
  Primary tumours rare
  Metastatic disease common
  n   Incidence 10% in cancer patients
  n   Lung, breast, lymphoma, leukemia, MM
  n   Children – Hodgkin’s, leukemia,
      lymphosarcoma
  Progress to tamponade in 50-85%
  Dx: pericardiocentesis / cytology
  Tx: symptomatic
Post-Irradiation Pericarditis
  Early (days – months)
  n   Dose related pericardial effusion
  n   Must distinguish from malignant effusion
  n   SSx:
       w SOBOE
       w can mimic infectious pericarditis (fever, CP, friction rub)
  n   Tx:
       w Often resolves spontaneously
       w NSAIDs, steroids, pericardiocentesis
  Late (years)
  n   Constrictive pericarditis
  n   Tx:
       w Often requires pericardiectomy
Drug-induced pericarditis
  SLE-like syndrome     Methysergide
  n   Procainamide      n   constrictive pericarditis
  n   Hydralazine           / generalized
  n   Isoniazid             mediastinal fibrosis
  n   Methyldopa        Doxorubicin
  n   Reserpine         n   Chemotherapy
  Hypersensitivity      n   Pericarditis /
                            cardiomyopathy
  reaction
  n   Penicillin
  n   Cromolyn sodium
    Back to our case

You order an ECG on your
         patient
                        His ECG




•STE – I, II, aVF, V2-V6
•Reciprocal STD – aVR
•PR depression
Pericarditis – ECG
4 Stages
  Evolution over 3-4 weeks
  n   Only 50% have all 4 phases
Stage 1
  Hours to days
  Diffuse ST elevation
  n   ventricular subepicardial injury
  n   I, II, III, aVL, aVF, V2 to V6
       w Concave upwards
       w No distinct J-point
       w No T-wave inversions
  Reciprocal ST depression
  n   aVR, V1
  Diffuse PR depression
  n   atrial injury
Stage 2
  Variable timeline
  ECG transiently normal
  n   ST / PR return to baseline
  Some T-wave flattening
Stage 3
  Variable timeline
  T-wave inversion
  n   Deep, uniform
Stage 4
  Weeks to months
  Return to normal
  Some patients will have residual T-wave
  inversion
        ECG – ECG vs Pericarditis
                   Pericarditis   Ischemia/Infarction
ST elevation   Diffuse, concave   Anatomical, convex

ST changes     few reciprocal     Reciprocal changes
               changes
PR segment     Depression         No depression

Q-T            Rarely without     More commonly seen
prolongation   myocarditis
Evolution      Normalization in   MI progression with
               stage 2            development of Q-
                                  waves
Electrical     Present with       absent
Alternans      tamponade
 What if your patient was an
18 year old male athlete with
burning chest discomfort after
  one too many seven-layer
          burritos?
His ECG
BER vs Pericarditis
Pericarditis – Ancillary tests
  Most useful for ruling out other
  diagnoses
  Troponin / CK-MB
   n   Normal to mildly elevated (damage of
       subepicardial myocardium)
  ESR – elevated or normal
  WBC – elevated or normal
Echocardiogram
  Gold standard for pericarditis with
  effusion
  Can also evaluate
  n   Pericardial thickness
  n   Tamponade
  n   Tumours / cysts
  n   Constrictive pericarditis
Trans-thoracic echocardiogram

                   •Large pericardial
                   effusion
                   •RV compressed
     You suspect a viral
        pericarditis.

How are you going to treat it?
Viral Pericarditis - treatment
  All need to be followed to monitor for
  effusion
  n   Effusion suspected if:
       w Dyspnea, fatigue, findings of tamponade
       w Must distinguish between purulent & viral
          n   May need diagnostic pericardiocentesis
  n   NSAIDS – good relief of pain & fever
  n   Colchicine – 1-2mg po od
  n   Steroids – only if NSAID resistant
  n   Admit if: cannot rule out MI, pain control
Pericardial Effusion
  Collection of fluid in indistensible pericardium
  Secondary to pericarditis
  n   infectious, uremic, malignant, post irradiation
  Secondary to hemorrhage / trauma
  n   aortic dissection, penetrating trauma
  Symptoms related to size and acuity of
  collection
  n   80-100cc required before decompensation begins
      (15-60cc fluid normal)
  n   Chronic effusions rarely progress to tamponade
Pericardial tamponade
  Physiologic decompensation due to pericardial
  effusion
  Acute surgical tamponade
  n   Penetrating injury
  n   aortic dissection
  n   Iatrogenic (central line insertion)
  Medical tamponade
  n   Due to pericardial effusions due to pericarditis
  Low-pressure tamponade
  n   Due to severe dehydration
  n   LV pressure lowered to equilibrate with RV
      pressure
Pericardial tamponade
  Early
  n   <200cc, h CVP, tachycardia
  Moderate
  n   ~200cc, hh CVP, tachycardia, i cardiac
      output, i BP
  Severe
  n   >200cc, hhh CVP (unless hypovolemic), ii
      BP, i i cardiac output, +/- bradycardia
Traumatic Tamponade
   2% of penetrating thoracic trauma
   80-90% of stab wounds to heart
   20% of GSW to heart
   Large instruments cause exsanguination
   Foreign bodies, rib fractures
   Iatrogenic – cardiac catheterization,
   pacemaker insertion, pericardiocentesis,
   cardiac surgery
Clinical features
   Beck’s triad:
    n   hypotension
    n   distended neck veins (>15mm H20 with
        hypotension is diagnostic)
    n   muffled heart sounds (unlikely to be heard
        in trauma room)
   pulsus paradoxus – difficult to measure
   during resuscitation
   no response to vigorous fluid
   resuscitation
Diagnosis
  Echocardiography
  n   available at some centres, but difficult to
      perform during resuscitation
  n   TTE better than TEE
  n   98.1% sensitive, 99.9% specific
  n   Also useful for evaluation of valves and
      wall motion
Diagnosis
  Ultrasound
  n   Features include
       w fluid in pericardial sac
       w dilated IVC
       w Compression of RA
       w Collapse of RV during diastole
Diagnosis
  ECG
  n   Generalized low voltage
       w R-wave height <1cm in all leads
  n   Electrical alternans
       w specific but not sensitive
       w more likely seen in chronic than acute effusions
       w Morphology/amplitude of P, QRS, ST-T wave
         alternate every beat in any single lead
       w Likely due to inability of heart to return to a
         single position following each beat because of
         pericardial fluid
Diagnosis
  CXR
  n   May show enlarged cardiac shadow if lots
      of fluid (>200-250cc)
  n   Generally not useful for acute early
      tamponade as only a small amount of fluid
      is required to create significant
      hemodynamic compromise
Large Pericardial
    Effusion
•Loss of customary heart
borders
•“water-bottle” heart
Management
 Prehospital care
  n   Same as any trauma patient
  n   Consider tension pneumothorax and needle
      thoracostomy
Management
 Emergency Department
  n   vigorous fluid resuscitation
  n   CVP monitoring
  n   Treat concomitant injuries
  n   Pericardiocentesis
  n   ED thoracotomy
Pericardiocentesis
Pericardiocentesis
  Diagnostic and therapeutic
  Many false positives / false negatives (clotted
  blood)
  Improvement possible with small volume of
  blood removed
  Complications
  n   Pericardial tamponade
  n   Laceration of coronary artery / lung
  n   Induction of dysrhythmia
  Continued deterioration may necessitate
  thoracotomy
Pericardiocentesis
Technique
 n   18 gauge, 10 cm spinal needle, 20 cc
     syringe
 n   Continuous ECG monitoring
 n   Needle enters subxyphoid area
 n   Aim for left scapula
 n   Aspirate every 1-2 mm
 n   Stop if blood aspirated, cardiac pulsations
     felt, ECG changes
 n   NB: if more than 20 cc blood is removed
     easily you are probably in the RV (ooops!)
Case 2
  28 year old man
  n   previously healthy
  8 day history
  n   Fever
  n   Fatigue
  n   Myalgias
  n   Progressive SOBOE
  n   Vague chest discomfort
Physical examination
 HR 140 RR 20 BP 100/70 T 38.3 SaO2 91%
 diaphoretic
 H&N
  n Some cervical lymphadenopathy

 Chest
  n Coarse crackles in bases bilaterally

 CVS
  n Apex inferolaterally displaced

  n No murmurs

  n No friction rub

  n Is that an S4?????
ECG
 Sinus tachycardia
 Frequent premature atrial and
 ventricular beats
 Non-specific ST & T wave changes
CXR
Troponin
n   0.05


CBC
n   WBC 13
n   Some atypical lymphocytes
n   No left shift


ESR 29
Echocardiogram
n   Dilated chambers
n   Global wall motion abnormalities
n   Decreased LV and RV function
n   Mild tricuspid and mitral insufficiency
n   No pericardial effusion

Cardiac Catheterization
n   Totally normal coronary arteries
What’s going on?

What are you going to do
about it?
Myocarditis
Etiology
  Viral – most common
  n   Mostly enteroviruses – esp. Coxsackie B
  n   Adenovirus
  n   Influenza A/B
  n   CMV / EBV / VZV
  Bacterial
  n   S. aureus, Streptococcus
  n   Mycoplasma
  n   Diphtheria
Spirochetal
n   Lyme disease
Mycotic
n   Candida
n   Aspergillus
Rickettsial
n   Rocky Mountain Spotted Fever
Helminthic
n   Trichinosis
n   Schistosomiasis
Protozoal
 Chagas disease
 n   most common cause
     worldwide
 Trypanosoma cruzi
 Insect vector
 Dx:
 n   Demonstration of serum
     parasites
 Tx:
 n   Nifurtimox
     (antitrypanosomal)
HIV and myocarditis
  Myocarditis in 46% on autopsy
  Multifactorial
  n   HIV, CMV, toxoplasma, TB, aspergillus
  n   Kaposi’s sarcoma- may involve myocardium
  n   Cardiac B-cell lymphoma
  n   Treatment toxicity
       w Pentamidine, zidovudine, dideoxyinosine
Drugs
 Cocaine
 Emetine
 Doxorubicin
 HIV treatment
Systemic Diseases
  Collagen Vascular Disease
  n   SLE
  n   PAN
  n   RA
  n   Dermatomyositis
  Sarcoidosis
  Kawasaki’s Disease
Pathophysiology
   Three major mechanisms
  n   Myocardial necrosis from direct invasion
  n   Autoimmune destruction
      •   Beta myosin chain & coxsackie B share 50%
          same amino acid sequences
  n   Endotoxins produced by pathogens
Clinical Features
  VERY NON-SPECIFIC!

  Wide spectrum of disease
  n   Subclinical (most)
       w overshadowed by other manifestations of
         illness
  n   Fulminant cardiac failure +/- death
History
  Fever
  Fatigue
  Myalgias (**suggestics myotropic virus)
  Vomiting / diarrhea
  Chest pain
  n   May mimic ischemic or pericardial pain
Physical Exam
  Cardiac exam may be normal
  Tachycardia disproportionate to fever
  Cardiomegaly
  Atrial or ventricular dysrhythmias
  S3, S4, TR/MR
  +/- pericardial rub
  CHF
  n   Usually biventricular
  n   SSx of RV dysfunction (JVD, edema, hepatic
      congestion, etc.)
  n   SSx of LV dysfunction if predominant LV
      involvement
Children
n   Respiratory distress (grunting respirations,
    intercostal retractions)
n   Lungs clear / wheeze
n   Ventricular dysrhythmias
Infants
n   Often fulminant syndrome
     w Fever, cyanosis, respiratory distress,
       tachycardia, cardiac failure
ECG
  n   NON-SPECIFIC!
  n   Sinus tachycardia
  n   Low voltages
  n   Prolonged QTc
  n   AV block
  n   AMI patterns
  n   ST changes
  n   T wave inversions
CXR
 Often normal
 Cardiomegaly
 +/- pulmonary congestion
  n   Depends on relative RV vs LV dysfunction
Laboratory
  Cardiac enzymes
  n   May or may not be elevated
  n   Troponin
       w elevated in 34% of patients with biopsy proven
         myocarditis
  n   CK-MB
       w Elevated in 5.7% of patients with biopsy
         proven myocarditis


  Bottom Line …. Not really very helpful
WBC
n   Normal to elevated
ESR
n   Normal to elevated
Viral titres
n   May suggest a viral infection, but don’t
    confirm etiology of cardiac disease
Echocardiography
  Non-specific
  May mimic AMI
  Usually multichamber dysfunction
  n   Reduced LVEF
  n   Global hypokinesis
  n   Wall motion abnormalities
  Can evaluate for thrombi and pericardial
  involvement
That all sounds pretty non-
          specific…

      I’m confused?

  When should I suspect
      myocarditis?
Suspect myocarditis if …
  Systemic infection is associated with
  new cardiovascular problems.
  Young patient with few coronary RF’s
  Tachycardia out of proportion to fever
  Severe myalgias
  n   Suggests myotropic pathogen
Non-anatomical ECG changes
Continued pain with no ECG evolution
Global (vs segmental) wall motion
abnormalities on echo
Unexplained CHF / dysrhythmias in
previously healthy patient
I suspect myocarditis.

How do I confirm the
    diagnosis?
MRI
n   Contrast enhanced (gadopentate dimeglumine)
    shown to be useful
n   Maybe the future?


Antimyosin scintigraphy (Indium-111)
n   Binds to exposed myosin in damaged myocardium
n   Diffuse, faint uptake of antimyosin antibody
n   (AMI typically has intense, localized uptake)
n   Normal antimyosin scan excludes AMI and
    myocarditis
Endomyocardial biopsy
  Gold standard
  One report …
  n   Sensitivity 79%, Specificity 63%
  Dallas criteria used to standardize diagnosis
  n   Histologic criteria for myocarditis
       w 5-30% of patients with suspected myocarditis
       w 41% of patients with acute dilated cardiomyopathy
       w 63% of patients with chronic dilated cardiomyopathy

  Worse prognosis for patients with histological
  changes
I’m pretty sure it’s myocarditis
…. How do I treat it?
Treatment
  ED treatment
  n   Bed rest
  n   Cardiac monitoring
  n   Management of arrhythmias
      w No treatment of PAC’s, PVC’s
      w Electrical cardioversion for supraventricular
        arrhythmias with rapid ventricular response
      w Drugs for serious ventricular ectopy /
        arrhythmias
      w Pacing for high grade conduction blocks
CHF
n   Treat very cautiously
n   Aggressive preload or afterload reduction
    may cause cardiogenic shock
Anticoagulation
n   If intracardiac thrombi detected on echo
Definitive Treatment
  Treat specific cause if possible
  n   Eg: Chagas disease, Lyme disease, etc.

  Anti-viral agents & immunosuppression
  are controversial

  IVIG may be helpful in certain subsets

  Cardiac transplantation if fulminant
Disposition
  Admission to monitored bed
  n   All patients with symptomatic suspected
      myocarditis


  ICU / CCU
  n   All hemodynamically unstable patients
Prognosis
  Many cases subclinical and benign
  Wide spectrum
  n   Complete recovery to any of many
      permanent cardiac problems
  n   Dilated cardiomyopathy common sequelae
  NIH myocarditis trial
  n   20% mortality at 1 year
  n   56% mortality at 4.3 years
  LVEF & RV function 1 year after
  presentation best predictor of outcome
The End

				
DOCUMENT INFO
Shared By:
Categories:
Tags:
Stats:
views:0
posted:7/25/2013
language:English
pages:91