ACUTE PERICARDITIS

BY :
AFDALIA
C111 07 114
SUPERVISOR :
DR. PENDRIK TANDEAN, SPPD-KKV.FINASIM

Patient Identity
Name

: Mr. Y

Age

: 41 years old

Address

: Takallar Pattalasang

Medical record : 536023

Admitted

: January 1th 2013

History Taking
Chief complaint: Chest pain
History taking:
Experienced since 2 days ago before admitted to the

hospital, feel like stab and penetrate to the back. The

patient feel comfortable when in bend position and the
pain was not improved by rest. Shortness of breath (-)
accompanied by sweating, nausea. PND (-), DOE (-)
Fever (+), since 2 days before admitted to the hospital,
Headache (-)
Epigastric pain (-), Cough (-)
No history of previous chest pain,
Defecation & urination normal

History of illness
Hypertension history (-), DM (-), heart

disease (-)
History of smoking (-)
Post. Op urolithiasis December 2012

Physical Examination
General Status :

Moderate-illness/normal Body
Weight/conscious
Vital Sign :
Blood Pressure

: 110/70 mmHg

Pulse

: 88 bpm, regular

Respiratory rate

: 20 tpm,

abdominothoracal
Body temperature : 36,8 C

Head Examination

Eyes
Lip
Neck

: anemic -/-, icterus -/: cyanosis (-)

: lymphadenopathy (-), JVP R +2 cmH2O

Chest Examination

Inspection
Palpation
Percussion
Auscultation

: symmetric R=L, normochest

: mass (-), tenderness (-), VF R=L
: sonor
: breath sound
: vesicular
additional sound : ronchi - /wheezing -/-

Cardiac Examination

Inspection
Palpation
Percussion
Auscultation
(-)

: IC not visible
: IC not palpable
: Normal
: Heart sound I/II regular, murmur

Abdominal Examination
- Inspection

: flat and following breath

movement
- Auscultation
: peristaltic sound (+) ,
normal
- Palpation
: liver and spleen
unpalpable
- Percussion
: tympani, ascites (-)

Extremities
- Oedema

: pretibial -/dorsum pedis -/-

Interpretation
-

Rhythm
Hearth Rate
P wave
PR Interval
QRS Complex
Axis
ST Segment
-

Conclusion

: Sinus rythm
: 85 x/minute
: 0,08
: 0,12 ms
: 0,08
: Normoaxis
: - L1+aVL = ST Depresion
- II, III, aVF = ST Elevation Inferior
- V1+V2 = ST Elevation Septal
- V3+V4 = ST Elevation Anterior
- V5+V6 = ST Elevation Lateral

: Sinus rhythm, HR 85x/minute,

normoaxis, ST elevation mostly
in all leads.

LABORATORY FINDINGS
(01/01/2013)

Routine Blood Test

RBC
WBC
HB
HCT
PLT

: 4,40 x106/mm3
: 24,1 x103/mm3
: 12,1 g/dl
: 37,41 %
:386.103/mm3

Biochemical blood test

GDS
Ureum
Creatinin
SGOT
SGPT
Tot.Chol
HDL
LDL
TG

: 118 mg/dl
: 78 mg/dl
: 5,4 mg/dl
: 24 U/L
: 35 U/L
: 96 mg/dl
: 6 mg/dl
: 32 mg/dl
: 195 mg/dl

Electrolyte (01/01/2013)

Sodium
Potassium
Chloride

: 138 mmol/L
: 4,4 mmol/L
: 110 mmol/L

Cardiac Enzyme (03/01/2013)

CK-MB : 151 U/L
Trop. T : 1,5

WORKING DIAGNOSIS
CHEST PAIN e.c SUSPC. ACUTE
PERICARDITIS

PLANNING
Thorax PA
Echocardiography

MANAGEMENT

O2 2 L/min
IVFD NaCl 0.9% 500cc/24h/iv
Ceftriaxone 2 gr/24h/iv
Ibuprofen 4x400 mg

Acute pericarditis

DEFINITION
Acute pericarditis is an inflammation of the

pericardium characterized by chest pain,

pericardial
friction
rub,
and
serial
electrocardiographic (ECG) changes (see an
example of such an ECG below).
Happened more man than woman

Causes

Idiopathic (idio and pathy) 86%

Infective (viral or bacterial) 7%
Following a myocardial infarction or cardiac

surgery (Dresslers syndrome)

Radiation therapy
Neoplastic disease (commonly lung or breast)
6%
Connective tissue disease

PATHOPHYSIOLOGY
Pericardial tissue damaged by bacteria or other substances releases

chemical mediators of inflammation (prostaglandins, histamines,

bradykinins, and serotonin) into the surrounding tissue, thereby
initiating the inflammatory process. Friction occurs as the inflamed
pericardial layers rub against each other. Histamines and other
chemical mediators dilate vessels and increase vessel permeability.
Vessel walls then leak fluids and protein (including fibrinogen) into
tissues, causing extracellular edema. Macrophages already present
in the tissue begin to phagocytize the invading bacteria and are
joined by neutrophils and monocytes. After several days, the area
fills with an exudate composed of necrotic tissue and dead and dying
bacteria, neutrophils, and macrophages. If the cause of pericarditis
isn't infection, the exudate may be serous (as with autoimmune
disease) or hemorrhagic (as seen with trauma or surgery).
Eventually, the contents of the cavity autolyze and are gradually
reabsorbed into healthy tissue.

RISK FACTORS
Pericarditis occurs in people of all ages.
However, men between the ages of 20 and
50 are more likely to get it.
People who are treated for acute pericarditis
may get it again. This may happen in 15 to
30 percent of people who have the
condition. A small number of these people
go on to develop chronic pericarditis.

CLINICAL FEATURES
Chest pain
Retrosternal chest pain
more likely to be sharp and pleuritic
with coughing, inspiration, swallowing
worse by lying supine, relieved by sitting and leaning forward
Can often radiate to the neck, arms, or left shoulder.
Sudden in onset
Pleuritic and sharp in nature
Exacerbated by inspiration

Mild fever
Dyspnea, orthopnea, tachycardia
Pericardial friction rub

Present in 85% of cases of pericarditis

Pericardial friction rub is audible throughout the respiratory cycle,
whereas the pleural rub disappears when respirations are on hold.

ECG (acute pericarditis)

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

Treatment
Bed rest as long as fever and pain persist
Treatment of the underlying cause, if it can be

identified
Nonsteroidal anti-inflammatory drugs, corticosteroids
Antibacterial, antifungal, or antiviral therapy
NSAID (aspirin, indomethacin) are generally accepted
as effective for relieving symptoms of chest pain
NSAID ketorolac tromethamine rapid results
Colchicine may be a useful adjunct in those who do not
respond to NSAIDs alone

Complication

Pericardial effusion
Cardiac Tamponade
Constrictive pericarditis

Prognosis
Pericarditis is usually a benign disorder
Diagnosis relates to underlying cause
But any cause can lead to an effusion and tamponade

which can lead to death

Pericarditis can also progress to pericardial
constriction and heart failure

Deferential diagnosis
MI
Angina Pectoris
Pulmonary Emboli

Pericarditis vs AMI
Pericarditis

MI

Diffuse,concave elevation in all

leads except aVR+ V6 w/o
reciprocal changes
Height Not > 5mm

Localized, convex, with

reciprocal changes in infarct

PR depression

Frequent

Almost never

Q waves

Not usual, unless with infarct

Common with q wave infarct

T waves

Inverted after J returns to

baseline
T inversions and ST are not
seen simultaneously on the
same EKG

Inverted while ST still elevated

T inversions and ST can be
seen simultaneously on the
same EKG

Arrhythmias

Rare

Frequent

Conduction
disturbances

Rare

Frequent

ST segment

Height may be > 5 mm

THANK YOU