DISEASES OF THE

PERICARDIUM
 Pericardium
• Fibroelastic sac contains 25-50 ml of fluid.
• Parietal AKA Fibrous Pericardium whereas Visceral AKA Serous
Pericardium separated by cavity.
• Innervated by Phrenic Nerve, which provides sensory information of
touch and pain to the pericardium, hence pericarditis can cause
referred pain to neck, arms or shoulders.
They present in several ways-
I. Acute Pericarditis
II. Recurrent Pericarditis
III. Pericardial Effusion without hemodynamic compromise
IV. Cardiac Tamponade
V. Constrictive Pericarditis
VI. Effusion-constrictive Pericarditis
A. Acute Pericarditis
• Inflammation of the pericardial sac.
• Etiology involves-
1. Viral- Coxsackie Coxsackie after an upper respiratory infection, Echovirus,
Adenovirus; Bacterial due to Pneumonia; TB; Fungal
2. Uremia
3. Acute MI, Dressler
4. Autoimmune- Collagen Vascular Disease
Lupus
Diffuse Cutaneous Systemic Sclerosis(Scleroderma)
5. Surgery/Trauma/Radiation
 Uremic Pericarditis
• A complication of Chronic Kidney disease that causes Fibrinous
Pericarditis, which is a type of inflammation when exudation allows
for fibrinogen and leukocytes to extravasate into pericardial space,
• Clinical Features- Chest pain worsened by inhalation,
• Physical Findings- Frictional rub on Ausculation,
• ECG is normal because inflammatory cells do not invade the
myocardium to produce changes like diffuse ST Elevation.
The pericardium is covered
with linear, fibrinous
exudates consisting of fibrin
strands and leukocytes.
• Clinical Features-
1. Severe, pleuritic chest pain that improves with leaning forward,
2. Pericardial Friction Rub- Highly Specific, Triphasic- can be heard in
atrial and ventricular systole and early diastole.
3. ECG shows PR depressions and ST Elevation,
4. TTE shows an effusion in 50 percent of the cases.

• Diagnosis- Clinical Criteria (≥ 2 out of 4 of the following)

1. Classic Positional Chest Pain
2. Friction Rub
3. Typical ECG Changes
4. Pericardial Effusion
• Management- Generally self-limited (1-3 week resolution)
1. Idiopathic---- NSAIDs (Ibuprofen or Indomethacin) + Colchicine
2. Post MI------- ASA + Colchicine
3. Uremic-------- Dialysis

Glucocorticoids reserved for those with contraindication for NSAIDs

• Contraindications for NSAIDs-
1. Gastroduodenal Ulcers
2. Renal Failure
3. Recent MI, Unstable angina, Heart Failure
4. Discontinued 1-3 days prior to Surgery because of their antiplatelet
effect
5. Pregnancy- avoided in Second and Third Trimester because they
cause premature closure of Ductus Arteriosus and inhibit uterine
contractility.
B. Recurrent Pericarditis
• Recurrent pericarditis occurs when symptoms of acute pericarditis return after a
symptom-free interval of least four to six weeks. Four to six weeks has been established
as the minimum required symptom-free interval as it represents the typical duration of
antiinflammatory therapy (including taper).
• Key features — Recurrent pericarditis is manifested by recurrence of the symptoms and
signs of acute pericarditis after a symptom-free interval of at least four to six weeks. The
presenting symptoms of recurrent pericarditis are generally similar to those for acute
pericarditis, although the presenting symptoms may not be consistent for each
individual patient and are frequently less intense during recurrences.
• The predominant feature of recurrent pericarditis is usually pleuritic chest pain (often
sharp, worse when lying flat, and alleviated when leaning forward), which may follow
exertion. Some patients may also report dyspnea or malaise. Other clinical
manifestations of acute pericarditis are often absent.
• Management-
1. Activity Restriction
2. 1st Line- Colchicine + NSAID/ASA
3. 2nd Line- Glucocorticoid + Colchicine for recurrence despite 1st Line
4. Triple Therapy- Glucocorticoid + Colchicine + ASA for recurrence
despite 2nd Line
5. Fourth Line-
if Inflammatory phenotype present- Treat with Interleukin 1 Inhibitor
such as Rilonacept
Non inflammatory but Autoimmune disease- IVIG
Non inflammatory and non autoimmune- Azathioprine
• Inflammatory phenotype — Patients with recurrent pericarditis may
present with an inflammatory or non-inflammatory phenotype.
• An inflammatory phenotype is characterized by the presence of one
or more of signs of an inflammatory process when presenting with a
recurrence: fever, elevated CRP, elevated WBC count, elevated ESR,
pericardial LGE on CMR, or pericardial contrast enhancement on CT.
• Patients presenting without any of these signs of inflammation have a
non-inflammatory phenotype.
C. Pericardial Effusion
• Fluid between the visceral and parietal layers of the pericardial sac
• Risk-
1. Pericarditis (of any cause)
2. Malignancy
3. Volume Overloaded (as seen with CHF, Cirrhosis, Nephrotic
Syndrome)
• Clinical
1. Often asymptomatic, but can develop signs of impaired cardiac function.
2. Muffled heart sounds, soft PMI, dullness at left lung base (compressed by pericardial fluid), friction
rub,
3. CXR shows water bottle appearance
4. ECG shows low voltage and electrical alternans- consecutive QRS complexes that alternate in
height due to the swinging motion of the heart when surrounded by large amounts of pericardial
 fluid.

• Diagnosis-
1. TTE- best at establishing and assess hemodynamic compromise,
2. Pericardial Fluid Analysis if etiology is unknown

• Management-
1. Treat underlying cause.
2. Sample fluid if etiology is unclear.
3. Avoid Diuretics
4. Follow with TTE
Fluid Analysis
Ascitic Fluid Analysis
 Pericardial Fluid Analysis

• Cell Count- WBCs elevated in Infection whereas RBCs elevated in

hemorrhagic effusions
• Gram stain and culture; Cytology (for malignancy), Acid-fast stain
• Glucose level < 60-80mg/dl suggestive of malignant, parapneumonic or
tuberculous effusions, or connective tissue disease.
• Protein level > 6g/dl is associated with purulent, parapneumonic, and
tuberculous effusions.
• LDH: Isolated pericardial fluid LDH elevation of >300 units/dl suggests
malignant effusion.
• Light Criteria can be used for interpretation.
 Interpretation of Pericardial Fluid Samples
• Transudate-------- Clear Appearance- Heart Failure, Renal Failure,
Hypoalbuminemia, Postradiationtherapy
• Exudate-----------Cloudy, chylous- Viral infection, Inflammation, Malignancy,
Autoimmune disease, Chylopericardium
• Blood---------------Hemorrhagic- Postcardiac surgery, cardiac rupture, aortic
dissection, TB, Malignancy (Malignant pericardial effusions are more
commonly caused by metastatic disease (in particular, lymphomas
, leukemias, melanoma, lung cancer, and breast cancer) than primary
malignancies)
• Purulent-----------Thick, yellowish-white, cloudy- TB, bacterial infection
Hemorrhagic Pericardial Effusion
D. Cardiac Tamponade
• Impaired diastolic function of heart due to pericardial effusion that is
under pressure. Results from either a large effusion (>2L) OR rapid
accumulation of smaller effusion.
• Equalization of cardiac pressures and decrease cardiac output
• Ventricular Interdependence
• Clinical-
1. Presents with signs of hemodynamic compromise, chest, SOB- not
due to Pulmonary Edema, mechanism is unclear
2. Cardiogenic shock, Tx with Ino-Dilators and No fluids
3. Obstructive Shock,
4. Pulsus paradoxus, narrowed pulse pressure, distant heart sounds
5. Beck’s Triad- Hypotension + JVD + Muffled Heart Sounds
6. ECG with decreased voltage and electrical alternans
• Diagnosis-
TTE confirms effusion + Elevated Pulsus Paradoxus

• Management-
1. IV Fluids- because they are preload dependent, they need fluid
filling the ventricles because the ventricles are struggling to get
filled.
2. Non-hemorrhagic ---- Urgent Pericardiocentesis or surgical drainage
3. Hemorrhagic (Traumatic)------- Surgical Drainage and Repair
E. Constrictive Pericarditis
• Fibrous scarring of pericardium resulting in rigid and thick pericardium.
• Restricts diastolic filling of the heart.
• Increased ventricular interdependence.
• Etiology-
1. TB
2. Connective Tissue Disease
3. Surgery
4. Radiation
• Clinical Features-
1. Presents with SOB because of low cardiac output, prominent Right Heart Failure, Congestive Hepatopathy
(progressive right V failure symptoms)
2. Elevated JVP, Kussmaul sign and Pericardial Knock
3. Dyspnea and fatigue from low cardiac output.

• Diagnosis-
1. CXR-enlarged Cardiac silhouette
2. Cardiac MRI or CT revealing Pericardial thickening +/- Calcification

• Management-
Pericardiectomy
Calcification
Similarities between CP and CD

Greatly enhanced Ventricular Interdependence

What is Ventricular Interdependence?
 Normally-
• normal pericardium allows for its distention by the right heart during
inspiration which is why the increased venous return does not impede
left ventricular filling.

• Just because more blood goes to the right heart, more blood pooled
in lungs and less flows to the left heart, the SBP decreases mildly.

• This is not Ventricular Interdependence.

 Ventricular Interdependence in Constrictive Pericarditis
• Abnormal, restrictive, pericardium cannot expand to accommodate
increased VR due to inspiration. So the negative thoracic pressures
are not transmitted to heart chambers,
• Lung inflation during inspiration would stretch pulmonary vasculature
and decrease their resistance lowering the pressure.
• Because pulmonary venous pressure drops, the gradient between
Pulmonary veins and left ventricule decreases which impairs filling of
left ventricle,
• As a result left ventricular filling is reduced allowing for right heart to
accommodate blood by shifting Interventricular septum.
 Ventricular Interdependence in Tamponade
• Systemic venous return to the right heart increases with inspiration, and
pulmonary venous return to the left heart decreases with inspiration.
• In cardiac tamponade, the rigid pericardium prevents the free wall from
expanding.
• The ensuing distension of the right ventricle is limited to the
interventricular septum, which along with relative underfilling of the left
ventricle causes the septum to bulge to the left, reducing left ventricular
compliance and contributing to further decreased filling of the left
ventricle during inspiration.
 Differences
• In CP because there is no transmission of negative pressures to the heart as such we get Kussmaul’s
Sign.
• In Tamponade, negative pressure is transmitted to the heart, so the bulging of interventricular septum
into left ventricular (instead of distending the pericardium) will cause a serious drop in BP more than
10mmHg. We get Pulsus Paradoxus.
• In CP, , Because of exaggerated Longitudinal Annulus, we see a prominent X descent. Early right
ventricular filling is enhanced while the rest of the filling is impaired, because of equalized pressures
diastolic pressures there is descent from a higher right atrial pressure hence a rapid Y descent,
• In Tamponade, the Jugular venous pulse changes are as follows:
Right ventricular filling is impaired throughout diastole, and therefore the Y-descent (which represents
the fall in right atrial pressure immediately after tricuspid valve opening as blood rushes into the right
ventricle) is blunted.
X descent is rapid because During systole, the pericardial pressure becomes a little negative (ventricle
contracts so space in the pericardium increases) which momentarily relieves the tamponade.
This negative wave is transmitted to the atria which causes an exaggerated atrial relaxation, pulling all
the blood inside the atrium, leading to a prominent X descent.
Video for Double Inward Collapsing
Deflections of Patient’s JVP
• https://www.escardio.org/Journals/E-Journal-of-Cardiology-Practice/
Volume-15/Constrictive-pericarditis-prevalence-causes-and-clinical-
presentation
F. Effusive-constrictive Pericarditis
• Rare clinical syndrome characterised by concurrent pericardial
effusion and pericardial constriction with constrictive hemodynamics
persistent even after pericardial effusion is removed.
• Hallmark is Elevated RAP post-pericardiocentesis.
• Failure of RAP to fall by 50% or to postPCCentesis level below 10mm
Hg.
• Patients with effusive-constrictive pericarditis may have tamponade-
like pressure tracings, which change to constrictive-like tracings after
pericardiocentesis
• Etiology
1. Most cases are idiopathic,
2. Other reported causes include- radiation, malignancy,
chemotherapy, infection and post-surgical pericardial disease.
3. TB is frequent cause in endemic regions. (IL-10 was high)
• Features- Common with Tamponade
1. Pulsus Paradoxus is common finding, uncommon in Constrictive Pericarditis.
2. Knock is absent
3. Tachycardia
4. Tachypnea
5. Hepatomegaly
6. Ascites
7. Peripheral edema
8. Y descent is less marked than expected
X descent is rapid just like in Tamponade- Because During systole, the pericardial pressure becomes a little
negative (ventricle contracts so space in the pericardium increases) which momentarily relieves the
tamponade.
This negative wave is transmitted to the atria which causes an exaggerated atrial relaxation, pulling all the
blood inside the atrium, leading to a prominent x descent
• Diagnosis-
1. RAP abnormally elevated post pericardiocentesis despite lowering
pericardial pressure to 0, other findings postPCC include Pulsus
Paradoxus and marked rapid y descent.
2. Persistence of v wave in RAP recording prior to PCC.
• Treatment-
1. Randomized data are lacking, Success with NSAIDs, Colchicine and
Corticosteroids use is established,
2. PCC is temporary relief
3. Pericardiectomy- remove the visceral one,
Thank You