Pericardial Diseases Diagnosis and Causes

1 MAGDI AWAD SASI PERICARDIAL DISEASES 2013
PERICARDIAL DISEASES
Functions of pericardium:
PERCARDITIS
Essential for diagnosis
ESSENTIALS OF DIAGNOSIS
_ Anterior pleuritic chest pain that is worse supine than upright.
Pericardial rub.
Fever common.
Erythrocyte sedimentation rate usually elevated.
ECG - diffuse ST segment elevation with associated PR depression.

 Pericaditis refers to an inflammation of a visceral pericardium which is a
membranous sac enveloping the heart .
Pericarditis can be acute or chronic. Acute pericarditis(< 2 weeks) occurs due to
complications of infections or may be due to systemic diseases (autoimmune
syndromes, uremia), neoplasm, radiation, drug toxicity, hemopericardium,
postcardiac surgery, or contiguous inflammatory processes in the myocardium
or lung. In many of these conditions, the pathologic process involves both the
pericardium and the myocardium.
Chronic pericarditis is however less common a form of constrictive pericarditis.
It can also be a primary illness which develop as a result of medical and surgical
disorders .
 More common in men
 Occurs between the ages of 20 to 50 years
Pathology:
Depends on underlying cause and severity of inflammation
Serous pericarditis
Serofibrinous pericarditis
Suppurative (purulent) pericarditis
Hemorrhagic pericarditis

AETIOLOGY:
I. INFECTIVE A.viral illness
Coxsackie A & B((the commonest)), Echovirus, Hepatitis B ,HIV, Influenza
,Mononucleosis ,Mumps ,Varicella ,EBV ,Adeno.
B.Bacterial infections-
Stab wounds, pneumonia, endocarditis, sepsis, surgical contamination,
Tuberculosis, Diphtheria, Staphylococcus, pneumococus.
C .Fungal- Candida D. Parasitic- Amoeba
II. AUTOIMMUNE
1. Systemic lupus erythematosus (SLE)
2. Drug-Induced lupus (e.g. Hydralazine, Procainamide, ioniazide.
minoxidil, penicillins, clozapine)
3. Rheumatoid Arthritis
4. Post Cardiac Injury Syndromes i.e. postmyocardial Infarction
(Dressler's) Syndrome, postcardiotomy syndrome, Trauma
III. NEOPLASM
1. Primary mesothelioma
2. Secondary, metastatic breast cancer, renal cell carcinoma,
Hodgkin disease, and lymphomas
3. Direct extension from adjoining tumor
IV. RADIATION PERICARDITIS
V. RENAL FAILURE (uremia)
VI. TRAUMATIC CARDIAC INJURY
1. Penetrating - stab wound, bullet wound
2. Blunt non-penetrating - automobile steering wheel accident
VII. Chemotherapy VIII IDIOPATHIC (exclude others 1s)

Pericarditis & AMI
• If occurs within 2 – 7 days following an AMI
– Considered a pericardial inflammatory response to the AMI.
• Dressler Syndrome
– May occur 2 weeks to several months after the event after
myocardial infarction or open heart surgery, may be recurrent
– Autoimmune response to myocardial necrosis involving both the
pleura and the pericardium.
– Patients present with typical pain, fever, malaise, and leukocytosis.
Occasionally, the syndrome will occur within days of surgery.
Rarely, other symptoms of an autoimmune disorder, such as joint
pain and fever, may occur. Tamponade is rare with Dressler
syndrome after myocardial infarction but not when it occurs
postoperatively.
 PATHOPHYSIOLOGY
ACUTE
In acute pericarditis when microbes are inhaled or ingested, they migrate to
myocardium and cause inflammation. So when these membranes are inflamed,
they rub against each other and cause classic sounds of which the patient
complains of severe chest pains which increases when the patient lies supine
and decreases when in sitting position.
This acute inflammation causes accumulation of fluid in the pericardial sac
called pericardial effusion. The fluid may be serous which accompanies heart
failure, purulent accompanying tuberculosis and haemorrhage accompanying
trauma in the heart.
The excessive accumulation of fluid in the sac causes compression of the heart,
resulting in decrease venous retain of the heart resulting in ventricular filling
and a decrease in stroke volume. These events will eventually lead to cardiac
failure( right 1st
), shock and death.

CHRONIC
Chronic pericarditis occurs when the layers adhere to each other causing
fibrosis of the pericardial sac due to surgery which later restricts movement
of the heart. So the fibrotic pericardium tightens the heart decreasing cardiac
filling and output and later patient may report symptoms of heart failure.
 CLINICAL MANIFESTATION:
The presentation and course of inflammatory pericarditis depend on its
cause, but most syndromes have associated chest pain.
Sharp chest pain- with a rapid onset that worsens with breathing, coughing
and changes position(( pleuritic in nature)) , relief obtained by sitting
upright and leaning forward((postural chest pain)).
The pain is substernal /? radiate to the neck, shoulders, back, or epigastrium.
OFTEN- fever of 37.5 to 38 degrees and precede the chest pain.
o Bacterial percarditis- toxic and are often critically ill.
o Uremic pericarditis can present with or without symptoms;
fever is absent.
o Often neoplastic pericarditis is painless, and the presenting symptoms
relate to hemodynamic compromise or the primary disease
o Chills, Night sweats
Dyspnea, cough
PERICARDIAL RUB------------to-and-fro rubbing be heard over the entire
precordial region or a very small area.
It may be heard in both phases of the cardiac cycle. Pericardial friction rub is
unaffected by respiration and is thus differentiated from a pleural friction
rub. It is also increased as pressing the stethoscope firmly against the
patient’s chest wall. A rub may be readily heard at one moment and be
absent several minutes later. The intensity of the rub is usually increased
when the subject is sitting upright and leaning forward.

Differentiating Chest Pain
Pericarditis
• Pain is often sharp,
piercing
• Located between the
neck and shoulder
• Dyspnea unrelated to
exertion
• Pericardial friction rub
Acute MI
• Pain is described as
pressure
• Dyspnea related to
exertion
• Pain is in the chest and
may sometimes radiate
Tuberculous Pericarditis
 4-10% of All Acute Pericarditis is Caused by TB (Reported up to 80% in
Some 3rd
World Countries) Lymphatic or haematogenous spread.
 Nonspecific symptoms (fever, night sweats, fatigue) may be present for
days to months.
 1-8% of Patients with TB Have Pericardial Involvement
 Etiology of 20% of Constrictive Pericarditis
 Cases 93% of all Pericardial Effusions in HIV Patients
Four Pathologic Stages of TB Pericarditis
 I-Dry: Fibrin Deposition & Granulomatous Reaction. Clinically Silent
 II-Effusive: Serous Fluid Accumulation Caused by Hypersensitivity to
Tuberculoprotein and Impaired Resorption
 III- Absorptive: Effusion Resolves and Fibrous Tissue Replaces
Granulomas, Pericardium Thickens

 IV-Constrictive: Parietal Pericardial Calcification
Presentation
 Dyspnea 45-90% Rub 30-85%
 Chest Pain 40-75% Cough 50-95%
 Orthopnea 20-65% Fever 80-100%
 Distant Heart Sounds 25-55%
 50% of Patient Have Slowly Progressive Insidious Presentation
 95% Have Cardiomegally, 30% Have Active Pulmonary TB, 39-71% Have
Pleural Effusions L>R. Bilateral Pleural Effusions More Common than Rub.
 “Because of the variable and nonspecific features of TB pericarditis,
establishing the diagnosis on clinical grounds alone is impossible.
 Diagnosis by Pericardial Fluid or Biopsy: Positive AFB Smear, Culture,
Caseating Granulomas, TB DNA PCR
Treatment
 Antibiotics: Isoniazid, Rifampin, Pyrazinamide, Ethambutol
 Corticosteroids: Reduces Mortality and Need for Subsequent
Pericardiocentisis
 DIAGNOSTIC EVALUATIN STUDIES OF PERICARDITIS:
The diagnosis of viral pericarditis is usually clinical, and leukocytosis is often
present. Rising viral titers in paired sera may be obtained for confirmation
but are rarely done.
12-Lead EKG
• Most definitive test in acute pericarditis

• The ECG usually shows generalized ST and T wave changes and may
manifest a characteristic progression beginning with diffuse ST elevation,
followed by a return to baseline and then to T wave inversion.
• Atrial injury is often present and manifested by PR depression especially
in the limb leads.
• ST-segment elevation(saddle shaped) in most leads except V1 and AVR.
• NO RECIPROCAL CHANGES OR T INVERSION IN ACUTE DURATION.
• PR segment depressed
• Electrical alternans
– QRS varies from beat to beat(( IN PERICARDIAL EFFUSION))
• Atrial dysrhythmias common( IF EXTEND TO MYOCARDIUM))

• Four stages of EKG changes
Stage 1 S-T elevation seen globally, but more prominent in the precordial leads
Stage 2 S-T segment starts to normalize and T-wave increases in amplitude
Stage 3 Normal S-T segments and inverted T-waves
Stage 4 Resolution of repolarization abnormalities

Chest X-Ray
• The chest radiograph is frequently normal.
• Cardiac silhouette enlarged if there is pericardial effusion, As well as signs
of related pulmonary disease. Mass lesions and enlarged lymph nodes
may suggest a neoplastic process.
– If more than 250 ml is present
Echocardiogram
 Evaluates hemodynamic changes associated with cardiac tamponade
Transesophageal Echocardiogram (TEE)
 Pericarditis is a clinical diagnosis, not an Echo diagnosis!
 The echocardiogram is often normal or reveals only a trivial amount of
fluid during the acute inflammatory process. The diagnosis of tuberculous
pericarditis can be inferred if acid-fast bacilli are found elsewhere. The
tuberculous pericardial effusions are usually small or moderate but may
be large.
 Helpful in evaluating the size of an effusion & compromised ventricular
Filling

 Large pericardial effusions and accompanying pleural effusions are
frequent.
Labs
1.Erhythrocyte Sedimentation Rate (ESR) & Complete Blood Count (CBC)
– Non-specific elevation
2. Cardiac Profile (CK-MB, troponins)---Rule out AMI /raised Troponin
Cardiac enzymes may be slightly elevated, reflecting an epicardial
myocarditis component.
3. PPD, HIV-AIDS screening
4.Rheumatoid factors (RF), Antinuclear Antibodies (ANA)
5.CT scan / MRI – locate neoplastic lesions
 Biopsy of pericardium to obtain tissue sample for culture and
microscopic examination
 If bacterial pericarditis is suspected on clinical grounds, diagnostic
pericardiocentesis may be of value. In uremic patients not on dialysis, the
incidence of pericarditis correlates roughly with the level of blood urea
nitrogen (BUN) and creatinine. The pericardium is characteristically
“shaggy” in uremic pericarditis, and the effusion is hemorrhagic and
exudative.
 The diagnosis of neoplastic pericarditis can occasionally be made by
cytologic examination of the effusion or by pericardial biopsy, but it may
be difficult to establish clinically if the patient has received mediastinal
radiation within the previous year. Neoplastic pericardial effusions
develop over a long period of time and may become quite huge (> 2 L).
Clinical Management
Uncomplicated Viral Pericarditis
• Treatment of viral pericarditis is generally symptomatic. Aspirin (650 mg
every 3–4 hours) or other nonsteroidal agents (eg, indomethacin, 100–150
mg daily in divided doses) are usually effective.

• Indomethacin & Colchicine --Allergy to NSAIDs or aspirin
• Narcotic analgesia
• Corticosteroids may be beneficial in unresponsive cases.
Complicated pericarditis
• In general, symptoms subside in several days to weeks. The major early
complication is tamponade, which occurs in less than 5% of patients.
There may be recurrences in the first few weeks or months.
• Rarely, acute pericarditis may lead to constrictive pericarditis, which may
necessitate pericardial resection
• Uremic pericarditis usually resolves with the institution of aggressive
dialysis. Tamponade is common, and partial pericardiectomy (pericardial
window) may be necessary.
• Whereas anti-inflammatory agents may relieve the pain and fever
associated with uremic pericarditis, indomethacin and systemic
corticosteroids do not affect its natural history.
• The prognosis with neoplastic effusion is dismal, with only a small
minority surviving 1 year. If it is compromising the clinical comfort of the
patient, the effusion is initially drained percutaneously. Early attempts at
ballooning the pericardium from a subxiphoid approach have been mostly
abandoned in favor of surgical approaches. A pericardial window, either
by a subxiphoid approach or via video-assisted thoracic surgery, allows
for partial pericardiectomy. Instillation of chemotherapeutic agents or
tetracycline may occasionally be used to reduce the recurrence rate.
• Relapses do occur and may require slow withdrawal of anti-inflammatory
therapy over several months. Colchicine may be required for months to
help prevent recurrences.
• Post-MI Pericarditis
• Avoid use of corticosteroids and anti-inflammatory agents
– May cause rupture of the infarcted area
Pericarditis (recurrent pain or connective tissue disorders)
• Corticosteroids are most effective
Medication-Related Pericarditis Stop the medication

Pericardial Effusion
• Accumulation of excessive fluid in the pericardial space
• May happen slowly over
time and the pericardial
sac accommodates.
• The fluid may press on
the heart enough to limit
its movement within the
sac.
• Rapid fluid accumulation
results in Cardiac
Tamponade.
Pericardial effusion causes an enlarged heart shadow that is often globular
shaped (transverse diameter is disproportionately increased).
A lateral film and close-up of a pericardial effusion showing the anterior
mediastinal fat (blue arrows) and epicardial fat (red arrows) separated by a
soft tissue stripe ( "fat pad" sign) reflecting the pericardial effusion seen
edge-on.

The speed of accumulation determines the physiologic importance of the
effusion. Because the pericardium stretches, large effusions (> 1000 mL)
that develop slowly may produce no hemodynamic effects. Conversely,
smaller effusions that appear rapidly can cause tamponade. Tamponade
is characterized by elevated intrapericardial pressure (> 15 mm Hg), which
restricts venous return and ventricular filling. As a result, the stroke
volume and pulse pressure fall, and the heart rate and venous pressure
rise. Shock and death may result.
AETIOLOGY:
Any cause for pericarditis can cause pericardial effusion and temponade.
S&S:
Pericardial effusions may be associated with pain if they occur as part of
an acute inflammatory process OR may be painless, as is often the case
with neoplastic or uremic effusion. Dyspnea and cough are common,
especially with tamponade. Other symptoms may result from the primary
disease. A pericardial friction rub may be present even with large
effusions.
 Diagnosis
 Same line of investigations for pericarditis.
 CXR , ECG, ECHO, CTSCAN CHEST ,CBC,ESR,ANA,TB TEST
 CHEST X RAY
 Although an effusion is often described as producing a globular-
shaped heart, it is usually not possible to differentiate a pericardial
effusion from cardiac enlargement on a chest radiograph.
 May appear normal in acute situations.
 Approximately 250 ml of fluid must be in the pericardium to lead to
a detectable change in the size of the heart shadow on PA CXR

 small effusions (100–200 mL) may not cause cardiomegaly even
though they can cause tamponade when they accumulate rapidly or
when the pericardial membrane is stiffened from fibrosis.
 Pericardial effusion can be definitively diagnosed with either
echocardiography (can be bedside in the emergency department in
the critically ill patient patient) or CT chest.
 ECG
 The ECG often reveals nonspecific T wave changes and low QRS
voltage. Electrical alternans is present uncommonly but is
pathognomonic. It is due to the heart swinging within the large
effusion.
 ECHO
Echocardiography is the primary method for demonstrating pericardial
effusion and is quite sensitive.
 Cardiac CT and MRI also demonstrate pericardial fluid and any associated
contiguous lesions.
 Diagnostic pericardiocentesis or biopsy is often indicated for
microbiologic and cytologic studies; a pericardial biopsy may be
performed relatively simply through a small subxiphoid incision.
 Unfortunately, the quality of the pericardial fluid rarely leads to a
diagnosis, and any type of fluid (serous, serosanguinous, bloody, etc) can
be seen in most diseases


Treatment
Small effusions can be followed clinically by careful observations of the
JVP and by testing for a paradoxical pulse.
Serial echocardiograms are indicated if no intervention is immediately
contemplated.
Continued or repeat drainage may be indicated, especially in malignant
effusions. Pericardial windows via video-assisted thorascopy have been
particularly effective in preventing recurrences. Additional therapy is
determined by the nature of the primary process. Recurrent effusion in
neoplastic disease and uremia, in particular, may require partial
pericardiectomy as noted earlier.
Trivial pericardial effusions are common, especially in CHF, and need not
be referred.
• Hypotension or a paradoxical pulse suggesting the pericardial effusion is
hemodynamically compromising the patient should prompt an immediate
referral.
_

Cardiac Tamponade
It is an impairment of ventricular filling during diastole due to some
external pressure on the heart by pericardial effusion. Tamponade is
characterized by elevated intrapericardial pressure (> 15 mm Hg), which
restricts venous return and ventricular filling. As a result, the stroke
volume and pulse pressure fall, and the heart rate and venous pressure
rise. This leads to obstructive shock. Shock and death may result.
Tamponade can occur acutely (eg, due to rupture of the heart or aorta,
trauma, or as a complication of catheter or pacemaker procedures) or
subacutely (eg, due to neoplasm, uremia, or idiopathic pericarditis).
Accumulation of fluid under high pressure:
compresses cardiac chambers & impairs
diastolic filling of both ventricles
SV venous pressures
CO systemic& pulmonary congestion
Hypotension/shock JVD rales
Reflex tachycardia Hepatomegaly
Ascites
Peripheral edema

Symptomatology of Cardiac Tamponade:
((Low cardiac output symptoms with heart failure))
Acute: (trauma, LV rupture)
profound hypotension-Fatigue, dizziness, syncope, lose of effort
confusion/agitation
Slow/Progressive large effusion (weeks)
Fatigue ( CO)
Dyspnea
JVD
1. LVF:
.Chest pain _oppressive precordial , positional as it is preceded by
pericarditis, stabbing in quality.
.Fullness in chest pushing on her heart
.Dyspnea on exertion , at rest , PND
.Cough dry irritant positional( more on laying )
2. RVF:
. Abdominal pain , dysphagia
.Early statiety
. Abdominal distention
. Nausea hoarsness
.Edema or ascites are rarely present; these signs favor a more chronic
process.

Clinical Signs of Cardiac Tamponade:
Tamponade has a spectrum of presentations ranging from circulatory
collapse to mildly reduced cardiac output with symptoms of dyspnea and
chest or abdominal discomfort depending on the rate of fluid collection.
• General
o Anxious
o Apprehensive
o Ashen gray facies
o Cool perspiration
• Tachycardia
• Tachypnea
• Jugular venous distension-NO Y DESCENT IN RA/RV
• Peripheral Cyanosis
• Quiet precordium with both inspection and palpation
• muffled heart sounds
• Rub
• Right upper quadrant tenderness
• The venous pressure tracing shows absence of diastolic y descent (i.e.
there is a deep x descent but y descent is absent) . Cardiac tamponade
also causes a raised JVP, Kussmaul’s sign and pulsus paradoxus.
• Summary signs of cardiac tamponade are:
1. Rapid x descent
2. Kussmaul’s sign
3. Pulsus paradoxus

• Bamberger-Pins-Ewart sign
o Variable dullness and bronchial breathing at one or both bases
most frequently the left below the 9th rib and between the mid
scapular line and the spine(( lung collapse)).
o Beck's triad (1) systemic hypotension
(2) elevated systemic venous pressure
(3) muffled heart sounds is typical of acute tamponade
which may be due to abrupt intrapericardial hemorrhage from
penetrating trauma, invasive cardiac procedures, or rupture of an
ascending aortic dissection or myocardial infarction. The complete
triad is rarely present
• Pulsus Paradoxus
o First described by Kussmaul in 1873 as a palpable decrease or
absence of the radial pulse during inspiration.
o Physiological bases (in normal person)
o Intrapericardial pressure (IPP) tracks intrathoracic pressure.
o Inspiration:
o Negative intrathoracic pressure is transmitted to the pericardial
space.
o IPP blood return to the right ventricle
o jugular venous and right atrial pressures
o right ventricular volume  interventricular septum shifts
towards the left ventricle left ventricular volume
o LV stroke volume
o blood pressure (<10mmHg is normal) during inspiration

o Pulsus paradoxicus, an accentuated fall in the systolic pulse
pressure (>10 mm Hg) during inspiration, is not present in one-
quarter of patients with tamponade.
o A greater than10 mm Hg decline in systolic pressure during
inspiration due to further impairment of LV filling—is the classic
finding
• Place the patient in a position of comfort and conduct manometric studies
• Raise sphygmomanometer pressure until Korotkoff sounds disappear.
• Lower pressure slowly until first Korotkoff sounds are heard during early
expiration with their disappearance during inspiration.
• Record this pressure.
• Very slowly lower pressure until Korotkoff sounds are heard throughout
the respiratory cycle with even intensity and Record this pressure.
• The difference B/W the two recorded pressures is the Pulsus Pardoxus.
• Significant pulsus paradox is greater than or equal to 10% of the pressure
at which all Korotkoff sounds are heard with even intensity.
• Pulsus Paradoxus is felt to be present when the paradoxus is greater than
10% of the pressure at which all Korotkoff sounds are heard with even
intensity(( > 10 mm Hg drop in BP with inspiration)).
Conditions in which Cardiac Tamponade presents without a Pulsus Paradoxus
• Septal Defect
• Severe Aortic Stenosis
• Severe Left Ventricular Dysfunction
o Cardiomyopathy
o Myocardial infarction

Other Etiologies of Pulsus Paradoxus
• Large pulmonary embolus
• Severe COPD
exacerbation
• Labored respiration
• Constrictive pericarditis
• Restrictive
cardiomyopathy
• Right ventricular
infarction
• Circulatory shock
• Large pleural effusions
• Tense ascites
• Extreme obesity
SUMMARY:
i. Acute cardiac tamponade is generally sudden in onset, may be
associated with chest pain and dyspnea, and is life-threatening if not
promptly treated. The central venous pressure is typically markedly
elevated, while hypotension is common due to the decline in cardiac
output. The heart sounds are often muted.
ii. Subacute cardiac tamponade is a less dramatic process. Patients may
be asymptomatic or may complain of dyspnea, chest discomfort or
fullness, peripheral edema, fatiguability, or other symptoms referable
to increased filling pressures and limited cardiac output. The physical
examination in subacute tamponade may reveal hypotension with a
narrow pulse pressure, reflecting the limited stroke volume. However,
patients with preexisting hypertension may remain hypertensive due
to increased sympathetic discharge.

DIAGNOSIS:
ECG FINDING
EKG in the setting of tamponade often shows sinus rhythm with low voltage
(QRS amplitude in the limb leads <5 mm) suggestive of tamponade
physiology.
Electrical alternans, a more specific sign of tamponade occurs when there is a
very large pericardial effusion in which the heart swings during cardiac
contraction causing a beat-to-beat variation in the ECG axis (QRS amplitude).
Electrical
alternans
Low voltage
P-R depression
Etiologies of
Electrical
Alternans:
1. Pericardial effusion
2. Constrictive pericarditis
3. Tension pneumothorax
4. Myocardial dysfunction
– Severe cardiomyopathy
– Myocardial infarction

Echocardiographic
• If tamponade is present, the high intrapericardial pressure may collapse
lower pressure cardiac structures, such as the RA and RV. In tamponade,
the normal inspiratory reduction in LV filling is accentuated due to RV/LV
interaction and there is a > 25% reduction in maximal mitral inflow
velocities.
• Pericardial effusion,Right atrial collapse,Right ventricular diastolic
collapse,Swinging heart
• Respiratory variation of tricuspid and mitral valve flow velocities.
• Right ventricular diastolic collapse is a highly sensitive and specific
indicator of Cardiac Tamponade.
• Right atrial collapse although specific for Cardiac Tamponade was less
sensitive for the detection of Cardiac Tamponade.
• Right heart collapse may not be seen in patients with pulmonary HTN and
Cardiac Tamponade
CONCLUSIONS:
• The gold standard for the diagnosis of pericardial effusion is
echocardiography.
• The diagnosis of Cardiac Tamponade is based solely on PHYSICAL EXAM.

TREATMENT:
When tamponade is present, urgent pericardiocentesis is required.
Because the pressure– volume relationship in the pericardial fluid is
curvilinear and up sloping, removal of a small amount of fluid often
produces a dramatic fall in the intrapericardial pressure and immediate
hemodynamic benefit; but complete drainage with a catheter is
preferable.
Surgical Care
• Pericardiocentesis:
• Indicated in pt’s
• With effusions > 250 mL or
• Effusion increases despite intensive dialysis for 10-14 days or
• Evidence of tamponade.
•
• Pericardial window is a modification of balloon valvuloplasty:
In which an uninflated balloon is passed inside the pericardial space,
where it is opacified, inflated, and then pulled through the pericardium to
create a window through which pericardial fluid drains into the peritoneal
or pleural space
• Subxiphoid pericardiotomy:
• Is performed under local anesthesia and has a lower risk of
complications compared to pericardiectomy. Consider subxiphoid
pericardiotomy for large effusions that do not resolve.
• Pericardiectomy:
• Is the most effective procedure managing large effusions because it
has the lowest associated risk of recurrent effusions.
• It requires general anesthesia & thoracotomy; therefore, should be
considered only if pericardiotomy cannot be performed or has been
unsuccessful.

EDIAGNOSIS Constrictive Pericarditis
ESSENTIAL FOR DIAGNOSIS
Evidence of right heart failure with an elevated JVP, edema,
hepatomegaly, and ascites.
No fall or an elevation of the JVP with inspiration (Kussmaul sign).
Echocardiographic evidence for septal bounce and reduced mitral inflow
velocities with inspiration.
Catheterization evidence for RV-LV interaction, a “square root” sign,
equalization of diastolic pressures, normal pulmonary artery pressure,
and narrow RV pressure tracing that increases with inspiration.
PATHOPHYSIOLOGY:
Inflammation can lead to a thickened, fibrotic, adherent pericardium that
restricts diastolic filling and produces chronically elevated venous pressures. In
the past, tuberculosis was the most common cause of constrictive pericarditis,
but the process now more often occurs after radiation therapy, cardiac surgery,
or viral pericarditis; histoplasmosis is another uncommon cause
Fibrous scar formation
Fusion of pericardial layers
Calcification further stiffens pericardium
Rigid, scarred pericardium encircles heart:
Systolic contraction normal
Inhibits diastolic filling of both ventricles
SV venous pressures
CO
Systemic & pulmonary congestion
Hypotension/shock JVD Rales
Reflex tachycardia Hepatomegaly
Ascites
Peripheral edema

Clinical Findings
A. Symptoms and Signs:
The principal symptoms are slowly progressive dyspnea, fatigue, and
weakness. Chronic edema, Right hypochondrial pain or fullness,
abdominal distention, lose of apetite are common symptoms.
Physical finding-
HR, BP
ascites, edema, hepatomegaly
Hepatic congestion and ascites are usually present.
Ascites often seems out of proportion to the degree of peripheral edema.
The examination reveals these signs and a characteristically elevated
jugular venous pressure with a rapid y descent. This can be detected at
bedside by careful observation of the jugular pulse and noting an
apparent increased pulse wave at the end of systole (due to accentuation
of the v wave by the rapid y descent).
Kussmaul sign—
inspiration: intrathoracic pressure, venous return to thorax
intrathoracic pressure not transmitted though to RV
No pulsus paradoxus!( unusual).
No inspiratory augmentation of RV filling (rigid pericardium)
Intrathoracic systemic veins become distended
JVP rises with inspiration (normally falls)
Definition-a failure of the JVP to fall with inspiration—is also a frequent
finding. The apex may actually retract with systole and a pericardial
“knock” may be heard in early diastole.
((sudden cessation of ventricular diastolic filling imposed by rigid
pericardial sac)).
Atrial fibrillation is common.
Summary = RT HEART FAILURE + JVP + PERICARDIAL KNOCK.

DIAGNOSIS
At times constrictive pericarditis is extremely difficult to differentiate from
restrictive cardiomyopathy. When unclear, the use of noninvasive testing and
cardiac catheterization is required to sort out the difference.
1. CHEST X RAY:
The chest radiograph may
show normal heart size or
cardiomegaly. Pericardial
calcification is best seen
on the lateral view and is
uncommon. It rarely
involves the LV apex, and
finding of calcification at
the LV apex is more
consistent with LV
aneurysm.
2. Cardiac CT and MRI are only occasionally helpful. Pericardial
thickening of > 4 mm must be present to establish the diagnosis, yet no
pericardial thickening is demonstrated in 20–25% of patients with
constrictive pericarditis

3. Echocardiography—
Echocardiography rarely demonstrates a thickened pericardium. A
septal “bounce” reflecting the rapid early filling is common, though.
RV/LV interaction may be demonstrated by a reduction in the mitral
inflow pattern of > 25%, much as in tamponade.
4. Cardiac catheterization-
Because of the need to demonstrate RV/LV interaction, cardiac
catheterization should include simultaneous measurement of both the
LV and RV. Hemodynamically, patients with constriction have
equalization of end-diastolic pressures throughout their cardiac
chambers, there is rapid early filling then an abrupt increase in
diastolic pressure (“square-root” sign), the RV end-diastolic pressure is
more than one-third the systolic pressure, simultaneous
measurements of RV and LV systolic pressure reveal a discordance
With inspiration (the RV rises as the LV falls), and there is usually a
Kussmaul sign (failure of the RA pressure to fall with inspiration).
The width (or area) of the RV pressure tracing may also be less in
expiration and greater during inspiration, reflecting the variability in
filling of the RV with respiration.
In restrictive cardiomyopathy, the LV diastolic pressure is usually
greater than the RV diastolic pressure by 5 mm Hg, there is pulmonary
hypertension, and simultaneous measurements of the RV and LV
systolic pressure reveal a concordant drop in the peak systolic pressure
in both with inspiration.
Aetiology
 Tuberculous Pericarditis
 Cardiac Sarcoidosis
 Cardiac Amyloidosis
 Giant Cell Myocarditis
 Radiation
 Post-surgery
 Neoplasm

TREATMENT:
Diuretics- Initial treatment consists of diuresis. As in other disorders of right
heart failure, the diuresis should be aggressive, using loop diuretics (torsemide
if bowel edema is suspected), thiazides ,and aldosterone antagonists (especially
if ascites is present).
Surgical pericardiectomy should be done when diuretics are unable to control
symptoms. symptoms are usually dramatically improved.
Most experts recommend earlier rather than later pericardiectomy if symptoms
are present
TAMPONADE
• Low cardiac output state
• JVD present
• NO Kussmaul’s sign
• Equalized diastolic
pressures
• RA: blunted y descent
• Decreased heart sounds
CONSTRICTION
• Low cardiac output state
• JVD present
• Kussmaul’s sign
• Equalized diastolic
pressures
• RA: rapid y descent
• Pericardial “knock”
Constriction vs. Tamponade
Summary
Constriction vs. Tamponade
Summary
TAMPONADE
Pulsus paradoxus:
Present
Echo/MRI:
• Normal systolic function
• Large effusion
• RA & RV compression
Treatment:
Pericardiocentesis
CONSTRICTION
Pulsus paradoxus:
Absent
Echo/MRI:
• Normal systolic function
• No effusion
• Pericardial thickening
Treatment:
Pericardial stripping

Pericardial Diseases Diagnosis and Causes

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