Transcript Pericarditis and Myocarditis

Pericarditis
&
Myocarditis
April 6th, 2006
Shawn Dowling
Objectives

Review
– Dx
– Tx
– ECG’s changes
Anatomy and Physiology

Parietal layer
– Thick, collagenous, stiff
– Adventitial attachments to
sternum, diaphragm,
mediastinum

Visceral layer
– Thin
– Closely adherent to
epicardial surface
Pericardial
Anatomy/Physiology

Pericardial space
– Normally 15-60 cc fluid

Functions
– Reduces friction
– Prevention of infection
– Augmentation of atrial filling & maintains normal
pressure-volume relationship of chambers

But…No physiological consequence to absent
pericardium
Innervation/Sensation
Case #1

You’re working in the ED and have a
patient that is sent in from their family doc
with a diagnosis of perdicarditis (based on
the history). He’s a 26 yo M.
– Describe the classic symptoms of Pericarditis.
Pericarditis - History

Hx:

– Sudden onset severe
CP, x 24H
– Pleuritic, worsened
w/lying flat
– Rads to back area
– No SOB, not
exertional, no PND
ROS:
– fevers, recent URTI
Sx,

PMHx:
– Otherwise healthy

Meds:
– Tylenol for the pain –
not really working
Quality
Pericarditis
Precordium, L
trapezius ridge
Pleuritic
Duration
Hours to days
Exacerbation
Lying down, chest exertion
wall motion
Leaning forward
Rest
Location
Relief
Associated SSx SOB, diaphoresis,
no N/V
Ischemic pain
Retrosternal, L
shoulder, arm
Pressure, tightness,
burning
1-15 minutes
N/V, diaphoresis,
SOB
Aric™
Pericarditis is…
– An inflammation of the pericardium
– IR 2-6%, adults>children, Male>female,
– # of disease processes/agents responsible
– Classic Dx is pleuritic CP, pericardial rub & ECG 


Can have ischemic quality and positional component
For research purposes usually 2 of 3
– Usually benign condition, but there are a few
complications
– But, you need to consider a few very important Dx
before diagnosing pericarditis
DDx to consider…

Pneumonia or pneumonitis with pleurisy
 PE
 Costochondritis
 GERD
 MI
 Aortic dissection
 Pneumothorax

You’re about to examine the patient when
the your staff asks you
– What physical examine finding is most helpful
in making the diagnosis of pericarditis?
– Does your inability to illicit this p/e finding rule
out the disease?
Physical Exam

Looks to be in pain, not toxic looking
 VS–HR 110,RR-12(98%),T – 38.7°, 138/75
 Cardiac: S1+,S2+, (link), JVP 2 ASA, no
peripheral edema, PMI N.
 Lungs – clear, no c or w, no WOB,
shallow respirations
 Rest of exam N
What’s that sound?

Mono-,Bi-,Tri-phasic Rub
1.
2.
3.



Atrial systolic rub that precedes S1,
Ventricular systolic rub between S1 and S2 and coincident with the peak
carotid pulse, and
Early diastolic rub after S2 (usually the faintest).
Best heard at LLSB, pt sitting forward
Intermittent and migratory (unlike murmur)
Spec 100%, Sens  Poor
Investigations

What are you going to order?
– Labs?
– Imaging?
– CV investigations?
Labs

WBC usually elevated
 ESR usually elevated - do not order
 Troponin
– What does it signify if +ve?
– Does this change disposition?
Imaging

CXR
 CT scan Not our
domain
 MRI
What phase of ECG changes are these?
aVR PR segment 
PR  (most specific)
What are the other phases?
ST  (diffuse, concave)
ECG Findings of Pericarditis

What are the 4 phases of pericarditis?
– Which findings are most specific?

The staging is not very helpful – but
popular question to be asked
Stage 1 (hours  days)

Hours to days (often only ECG findings since we
Tx and pt may not progress to next stage)
 Diffuse ST elevation
– ventricular subepicardial injury
– I, II, III, aVL, aVF, V2 to V6




Concave upwards
No distinct J-point
No T-wave inversions
PR Elevation
– aVR

Diffuse PR depression
– atrial injury
Stage 2 (variable timeline)

ST / PR return to baseline
 Some T-wave flattening
Stage 3 (Variable timeline)
• T-wave inversion
–Deep, uniform
Stage 4 (Weeks to months)

Return to normal
– Some patients may have residual T-wave
inversion
But how do we distinguish
these ST changes from BER?
ST=PR-Jp pt
T=J pt to peak of Twave
Pericarditis versus AMI

Pericarditis

AMI
– Concave STE
– Convex
– <5mm
– Variable amt STE
– No reciprocal STD
– Often see reciprocal 
– ECG changes usually
– ECG can evolve very
over hours to days
rapidly
His CXR
What is the significance of this
ECG in the setting of his CXR?
Criteria for this?
ECG Findings of Pericardial
Effusion

When should a pericardiocentesis be done
–
–
–
–

Diagnostically – i.e. concerned about CA, TB,
Purulent Pericarditis
Unresponsive to treatment
Severe symptoms: SOBtamponade
Pericardectomy/window: Consider for
traumatic hemopericardium and purulent
pericarditis
Etiology of pericarditis?


Idiopathic
Infectious
–
–
–

Immune-inflammatory
–
–
–



Secondary: breast and lung carcinoma, lymphomas, leukemias
Radiation induced
Trauma
–

Connective tissue disease (SLE, RA, scleroderma)
Early post-myocardial infarction
Late post-myocardial infarction (Dressler syndrome), late post-cardiotomy/thoracotomy, late posttrauma
Drug induced (e.g., procainamide, hydralazine, isoniazid, cyclosporine)
Neoplastic disease
–

Viral: enterovirus (MC), CMV, hepatitis B, infectious mononucleosis, HIV/AIDs)
Bacterial
(Pneumococcus, Staphylococcus, Streptococcus, Mycoplasma, Lyme disease,
Hemophilus influenzae, Neisseria meningitidis)
Mycobacteria
(Mycobacterium tuberculosis, Mycobacterium avium-intracellulare)
Blunt and penetrating, post-cardiopulmonary resuscitation
Miscellaneous
–
–
–
–
Chronic renal failure, dialysis related
Hypothyroidism
Amyloidosis
Aortic dissection
Pericarditis - etiology
INFECTIOUS
 Viral
– Coxsackie, adeno,
Echoviruses, HIV,
mumps, EBV, etc.

– Days to mths after

Pneumococcus, Staphylococcus,
Streptococcus, Mycoplasma, Lyme
disease, Hemophilus influenzae, Neisseria
meningitidis
Fungal
Post-MI
– Early
– Late: Dressler’s
Bacterial
–

NON-INFECTIOUS
 IDIOPATHIC (MC)
 Traumatic



Auto-immune dz: RA,
SLE, vasculitides, sarcoid
Malignant Post-irradiation
Drug-induced
Pericarditis
Acute
Consider broad Ddx
Chronic (>3/12)
Usually inflammatory
Recurrent
Reasons to investigate further:
1)prolonged latent period before recurrence
2)presence of anti-heart antibodies (one way to have ER nurses hate ya –
order anti-sarcollemmal/antifibirllary antibodies and keep pt in ED until
results come back)
3)Rapid response to steroids in setting of auto-immune
disease
Mainstay’s of Tx

Drugs
– NSAID’s (level B, Class 1)
 Mainstay of treatment for idiopathic/viral cause
 Advil 600-800mg TID or ASA 650 QID
 Indocid – avoid since some evidence of coronary flow
 Duration: recommend x 2wks and discontinue once
asymptomatic
– Steroids – traditionally recommended, but some
evidence that ↑ with stopping steroids
Viral/Idiopathic

MC cause of pericarditis
– Tx: symptomatic treatment with ibuprofen 600mg PO
TID until ASx or 2 wks, whichever comes first
– ECHO?



if considerably symptomatic
?pericardial effusion
If being admitted
– Trop?



If concerned about ischemia
If concerned about Myocarditis
At your discretion (cardiologist here recommend trop in all
cases of pericarditis to ensure no myocarditis)
Recurrent Pericarditis or
Refractory to initial Tx

What other options do you have?
– 1st line for recurrent
 Colchicine (Adler) 2mg PO 1st day, then 0.5 BID
until ASx

Prednisone (especially when underlying autoimmune process)
What do the (french)
cardiologist do…
• Survey of French cardiologist in 2005
• initial investigations ECG in 100% of cases, ECHO in
95%, b.w. in 93% of cases.
• Hospitalisation was advised by only 24% of
cardiologists.
• Aspirin was prescribed as first choice treatment in
92.5% of cases.
• Duration of treatment recommendations varied widely,
from <5 days by 2.5%, between 5 and 10 days by
25.5%, 11 and 15 days by 23.0%, 16 to 21 days by
35.3%,
days by 14% of cardiologists.
•Arch
Mal Coeurand
Vaiss.for
2006>21
Jan;99(1):61-4.
[Acute pericarditis: results of a survey of treatment practices of cardiologists]
Pericarditis to watch out
for…
Bacterial pericarditis
– Rare, but universally fatal if not Tx(abx, +/-
surgery), otherwise MR 40% (tamponade, sepsis)
– Hx/exam/labs: ↑ fever, short duration (2 to 3/7),
↑HR, dyspnea, ↑CVP, CP, friction rub, and ↑WBC
– Source:




1) spread from an adjacent infection (i.e.pneumonia)
2) hematogenous spread from a distant site (MC),
3) direct inoculation of bacteria (trauma or procedure),
4) spread from an intracardiac source
– RF: immunocompromised, chronic dz
(i.e.EtOH, rheumatoid), CV surgery, chest
trauma
– Tx: as per mgnt of sick/septic pts, CCU/ICU


Vanco + cipro (Sanford Guide)
Pericardial tap (urgent) +/-pericardectomy
Pericarditis and HIV +

Can be infectious, non-infective (i.e Rx)
and neoplastic (Kaposi’s, lymphoma)
– Tx Sx
– ECHO to assess for these causes
 +/-pericardiocentesis depending on ECHO findings
– Steroids contra-indicated unless TB pericarditis
Uremic Pericarditis

Usually seen with ARF/CRF prior to
dialysis
 Correlates with degree of azotemia
 +/- pericardial rub, usu no ECG changes
 Tx with dialysis
– +/- pericardial drain/pericardectomy if not
improving
Auto-Immune Disease

MC with RA, SLE, Scleroderma
 Only Tx if Sx (I.e. don’t Tx if only have
mild ECG/ECHO findings)
 Tx
– Optimize auto-immune disease Tx
– NSAID’s
 Consider steroids for RA
Pericarditis Prognosis

Excellent
 60% of patients have complete recovery
within 1 week, 78% have complete recovery
within 3 weeks.
 Only 3% have a prolonged course with
symptoms for more than 3 weeks before
complete resolution
Case #2

A 47M presents to the ED feeling presyncopal and extremely SOB. It’s 3:00am.
– Recently Dx with pericarditis and had been
doing okay until the past 24 hrs
– Patient appears moribund
– VS: sBP 75, sats 85%, obvious resp distress

Cardiac: unable to hear his HS, JVP at his jaw
– What do you think is going on?
Physical Exam
What is Beck’s triad?
 What is the pathophysiology of pulsus
paradoxus?

– How do you check for it?

How much pericardial fluid
Beck’s
Triad
Management of
Tamponade?

Temporizing measures?
– Non-invasive?
– Invasive?

Definitive tx
– Surgical or pericardial drain
Complications of
Pericarditis

Pericardial Effusion (unsure of IR, but
likely <5% for moderate – severe)
 Constrictive Pericarditis
 Recurrence (15-30%)
Disposition of Pericarditis

Most can be sent home
– Clear d/c instructions: return if Sx not improving within
next few days, SOB, feeling generally unwell

Admission
– Intractable pain
– Peri-myocarditis: ↑trop – risk of arrhythmia
– Moderate-severe effusion or Tamponade
– To r/o other Dx (ischemia, PE)
Case #3

Myocarditis
Myocarditis

Epi, etiology
 Dx (hx, p/e, labs, imaging)
 Tx (general and disease specific)
 Px
Epidemiology and Etiology

IR: unknown but 10% of autopsies have
evidence (??how many had clinical Sx),
50% of HIV patients have evidence
Etiology


INFECTIOUS*

NON- INFECTIOUS
– Viruses (MC):
– Medications (i.e.
enteroviruses (MC in
Western world), Chagas
(MC worldwide) also
adeno, influeza, parainfluenza, EBV, mumps,
– Bacteria: strep, chlamydia,
– Others: mycobacterium,
adriamycin)
– Toxins (i.e. cocaine)
– Rheumatologic
*Pathophys is felt to be
molecular mimicry
History
– Viral prodrome described in 50-90%
– Fever 60%
– Chest pain (40%)
 Can be pericardial- suggests peri-myocarditis
 Ischemic Quality
– Resp Sx/CHF Sx
 Dyspnea, PND, orthopnea, Pedal edema,
– Dysrhythmia Sx
 Palpitations, pre-syncope, syncope,
Physical Exam

VS: ↑HR, ↑RR, +/- BP
– Resp: crackles,
– Cardiac: EHS - S3, +/- rub, JVP ↑
– Extremities: pedal edema
ECG

Extremely non-specific
– Can be normal
– Non-specific ST changes, I-V blocks
– Pericarditis changes
– Ischemic changes
Labs

Elevated cardiac enzymes
– Trop better than CK-MB early on

Evidence of MODS
– Liver, kidneys, lactic acidosis, resp failure
Imaging

CXR
– Findings usually consistent with pulm edema
but…
– Are dependent on what stage of myocarditis:



Initially may be normal
Intermediate – pulm edema with normal heart size
Late/Fulminant – pulm edema + cardiogemaly
Imaging

ECHO
– EF
– Pericardial effusion
– Wall motion abnormalities (focal or segmental)
Tx – in the ED

ABC’s
– May BiPAP to try and avoid intubation
– Fluids/Pressors/Inotropes if in cardiogenic
shock
– Manage CHF as per usual
– Manage any arrhythmias as per usual
Tx – out of the ED

Balloon pump, ventricular assist device,
bypass as a bridge to transplantation
 IVIG
 Cardiac Transplantation
Myocarditis Complications

Dysrhythmias (including VT/VF)
 Mechanical (DCM, aneurysm)
 Cardiogenic shock
 Death
 Thromboembolic (from akinesis)
Prognosis

Difficult to say based on ED presentation
– Of those who present with shock & rhythm
disturbances MR 15-20% @ 1 yr, 50% at 4 yrs

Those who are transplanted have particular
bad outcomes and high-graft rejection rates
Disposition

All should be admitted
– Most are likely to go to CCU
Summary
References

Adler Y, Finkelstein Y, Guindo J, et al: Colchicine treatment for recurrent pericarditis: A
decade of experience. Circulation 97:2183, 1998.