Morning Report

Steven Hart, MD

History
CC: increasing DOE
HPI

49 y/o AAF
Increasing SOB over 1-2 weeks
Intermittent Chest pain
Leg swelling starting to develop

History

Any thing else you like to know?

History

Chest pain
Non-exersional
Pleuritic in nature
Improves by leaning forward
Worsened when laying down

Recent URI symptoms, low grade

fevers, malaise
Recent orthopnea, now PND

History

PMHx
HTN
Hyperlipidemia

Social
Non-smoker
Works as secretary
Social ETOH (1-2 times per month)

Physical Exam
What things might you look for?

Physical Exam

VS T 99.1
+ JVD
CV

P 108

R 22 BP 102/64

Tachy, distant heart sounds

Rub heard intermittently by examiners
Lower extremity edema

Resp

sits up to breath
Crackles at bases
Mildly increased effort
able to speak full sentences sitting up

Physical Exam
Extremities - +1 edema
Pulses

Exaggerated drop in pulses with

inspiration

Labs
Cardiac enzymes slightly elevated
WBC 12

EKG
Note diffuse ST seg
elevations

Imaging

CXR any guesses

ECHO any guesses

Introduction
The Pericardium is a fibroelastic
tissue made up of parietal and
visceral layers
These two layers are separated by
the pericardial cavity
Pericardial cavity usually contains
15-50 ml of plasma ultrafiltrate in
healthy individuals

Diseases of the Pericardium

Acute Fibrinous Pericarditis
Pericardial Effusion without major
hemodynamic compromise
Cardiac Tamponade
Constrictive Pericarditis

Etiology of Pericardial
Diseases

Viral Infections
Purulent
Pericarditis
TB
Mediastinal
radiation
MI
Cardiac surgery
Trauma

Cardiac procedures
Drugs and Toxins
Metabolic disorders
Malignancies (breast,
lung, Hodgkins,
mesothelioma)
Collagen Vascular
Disease
Idiopathic

Etiologies of Pericarditis
Neoplastic-35%
Immune Mediated- 23%
Viral- 21%
Bacterial-6%
Uremia-6%
TB- 4%
Idiopathic-4%

Viral Pericarditis

Common bugs

Cocksackie A and B
Echovirus
Adenovirus

Viral infections uncommon in patients

presenting with pericardial effusion w/o
pericarditis

Exception is HIV- frequently presents with

significant effusion w/o pericaritis
seen in 7 % of patients hospitalized with effusions

Bacterial Pericarditis

Staphylococcus
Pneumococccus
Streptococcus(rheumatic pancarditis)
Haemophilus
M.Tuberculosis
Can occur as systemic spread or direct
extension
Frequently purulent

Fungal Pericarditis

Histoplasma- most common fungus

in immunocompetent patients

Especially the Ohio River Valley

In immunocompromised
Aspergillus
Candida
Coccidoides

Frequently purulent

Other Infectious Etiologies

Rickettsia Ricketsii
Chlamydia Psittaci
Borrelia burgdorferi
Treponema Pallidum
Actinomycosis
Mycoplasma Pneumonia
Nocardia

Post MI

Pericardial involvement is related to

infarct size
Early stage - inflammatory etiology
Late stage

Immune mediated weeks to months out

Known as Post Cardiac Injury syndrome
(PCIS) or Dresslers syndrome
Rare in modern time due to reperfusion
therapies

Iatrogenic Causes
Mediastinal Radiation-wide spectrum
of diseases seen
Cardiac Surgeries
Cardiac Procedures
Traumatic

Drugs

Lupus like sydromes

Penicillins- Hypersensitivity Pericarditis

Chemotherapy

Procainamide
Hydralazine
Phenytoin
INH

Doxorubicin/Daunorubicincardiomyopathy/pericardiopathy

Bleomycin - sclerosing agent

Toxins
Asbestosis can cause pericardial
lesions
Scorpion fish venom can cause
pericarditis

Metabolic Disorders

Uremia

Severe Hypothyroidism

Most common metabolic cause

6-10 % of ESRD patients not on HD can have
Pericarditis
Dialysis related Pericardial Effusions (seen in 13% of
patients)
effusion usually not significant
rarely pericarditis

Ovarian hyperstimulation syndrome

complication of gonadotropin therapy

Due to fluid shifts

Malignancy

Responsible for 6% of acute pericardial

disease (pericarditis and tamponade)
Accounts for 15-20% of moderate to large
pleural effusions
Mets - Lung, Breast, Hodgkins
metastases
Primary - Mesotheliomas and lipomas

Collagen Vascular Disease

SLE- pericardial involvement in up to
50%
Rheumatoid Arthritis
Progressive Systemic Sclerosis
MCTD
Polyarteritis
Giant Cell Arteritis
Inflammatory Bowel Disease

Idiopathic
In two large series (331 patients),
only 16 % had an identifiable cause
of pericarditis
Many of these cases are presumed
viral
Only 7-29% of patients have
idiopathic pericardial effusions

Clinical Presentation of
Pericarditis

Chest Pain

sudden onset over anterior chest

sharp and pleuritic
Improves by leaning forward
Radiates commonly to trapezius ridges

Pericardial Friction Rub

EKG findings depend on stage
2 of 3 needed to make diagnosis +/effusion.

Diagnostic evaluation

History
Physical
Search for
systemic disorders
ECG
CXR
ANA in selected
cases

PPD
HIV
BCx if febrile
No routine viral
cultures
Workup for
malignancy if
history suggests
Echo-Class Ia

Pericardial Friction Rub

Auscutation

Scratchy or squeaky sound

LLSB most frequent site
Use the diaphragm
suspended respiration

Highly specific for pericarditis (up to 85%).

Intermittent sensitivity can vary.
Heard better in patients without effusion.
Result of friction from 2 inflamed layers of
pericardium

EKG Findings
Stage I
ST elevation in most leads
Exceptions aVR and V1
Depression of PR segment
Low voltage QRS usually assoc with
tampanode
Stage II
Transition or pseudonormalization or
ST/PR segments
Stage III
T wave inversions.
Stage IV
Normalization vs persistent changes
*No changes in metabolic causes

EKG changes

Arrhythmias uncommon.
Arryhthmias suggest myocarditis or
ischemia

Distinction From AMI

ST elevations in pericarditis: begin at J point,

rarely exceed 5 mm, and retain normal concavity
ST elevations / T wave changes are more
generalized
No reciprocal lead changes
ST elevations and T wave inversions do not occur
at the same time
PR segment changes common
Q waves/QT prolongation/Hyperacute T waves
uncommon

Cardiac Biomarkers
Can see elevation in CK, MB, TpnI
22% of patients with Acute
Pericarditis in one trial were above
TpnI threshold
Transient rise, resolving within the
first 7 days
Patients with higher TpnI did not
have higher complication rates

CXR findings
Typically normal in Pericarditis
200ml of pericardial fluid needed to
accumulate before enlargement of
the cardiac silhouette seen
Calcification in chronic cases may be
appreciated

Lateral CXR of a person

with chronic calcified
pericarditis due to TB
A cystic mass
B calcified
pericardium

Echocardiogram
Should be done in all cases
Often normal in patients with
pericarditis, unless associated with
pericardial effusion
Presence of pericardial effusion
helps support diagnosis, while
absence does not exclude it

Pericardial Effusion

Diagnostic evaluation
Not needed in all patients- Viral and
idiopathic usually follow a benign
course after treatment
It is important to rule out significant
effusion and tamponade in patients

Management

Simple, uncomplicated pericarditis

No high risk features
Medical management
outpatient if proper F/U is established

High Risk Features

Subacute onset
Fever >100.4
Leukocytosis
Cardiac
tamponade
Large pericardial
effusion (>2cm)
not decreased
after NSAIDS

Immunosuppressed
Hx of
anticoagulation
Acute Trauma
Failure to respond
to NSAIDS

Treatments

ASA-Class I (2-6g/day) or
(800mg q6h tapered by
800mg /week for 3-4
weeks)
ASA resistance at 1 week
should prompt further
investigation
NSAIDS- ClassI (Ibuprofen
300-800mg q6h)
GI prophylaxis

Colchicine- Class
IIa
Intrpericardial
Steroids Class IIa
Corticosteroids if
refractory to
NSAIDS

Pericardiocentesis
If moderate to severe tamponade is
present Class IA recommendation
If purulent, TB, or neoplastic
pericarditis is suspected- Class II a
recommendation
Persistent symptomatic pericardial
effusion

Complications

Constriction

Tamponade

scarring and consequent loss of elasticity of the

pericardial sac
accumulation of pericardial fluid under pressure

Effusive-constrictive pericarditis
Recurrent Pericarditis- seen in 15-30% of
patients with idiopathic pericarditis.
Immune autoreactivity thought to play a
primary role.

Pericardial Tamponade

Increased Pericardial Pressures leading to

compression of all cardiac chambers
Pericardial elasticity maybe limited (Acute
vs Chronic)
Cardiac chambers become small and
chamber diastolic compliance is reduced
Decreased cardiac filling

Physiologic significance
Early diastolic filling decreases,
leading to the majority of venous
return occuring during ventricular
systole
When tamponade is severe, total
venous return falls and cardiac
chambers shrink

Physical Exam of
Tamponade

Sinus Tachycardia
Elevated JVP
Pulsus Paradoxus
Rub possible
Kussmaul's sign

Less likely w/o

constrictive
component

Pulsus Paradoxus

An exaggerated fall in systemic blood pressure

during inspiration
Inspiratory decline in thoracic pressure is
transmitted through the pericardium to the right
side of the heart
Systemic Venous return increases with
inspiration
In tamponade, the rigid pericardium prevents
the RV free wall from expanding during diastole
causing the pressure transmission to the septal
wall and decreased LV filling during inspiration

Acute vs chronic
accumulation

As little as 20-50 ml acutely can cause

tamponade acutely
As much as 2 liters can accumulate
chronically prior to causing tamponade

Conclusion

Pericarditis has many causes

A good history and physical will often
lead to diagnosis
ECHO, EKG, HIV, CXR and PPD should
be done
Outpatient management may be
reasonable
Anti-inflammatories key for medical
management