Acute Pericarditis, Pericardial Effusion and Cardiac Tamponade, Constrictive Pericarditis

1. PERICARDIAL DISEASES
Dr Dilmo Yeldo
DNB Resident
General Medicine

3. ACUTE PERICARDITIS
• Pericarditis is inflammation of the pericardium with or without an
associated pericardial effusion.
• While in west idiopathic causes account for a greater number of
cases, with viral infections being the most frequent cause; in the
developing countries, tuberculosis accounts for 60% to 80% of the
acute pericarditis (dry or effusive).

5. CLINICAL FEATURES
• Chest pain is usually present in acute infectious pericarditis.
• Pain is often absent in slowly developing tuberculous, post-
irradiation, neoplastic, and uremic pericarditis.
• The pain of acute pericarditis is often severe, retrosternal and/or left
precordial, and referred to the neck, arms, or left shoulder.
• But sometimes it is steady pain which radiates to the trapezius ridge,
or into either arm, and resembles that of myocardial ischemia;
therefore, confusion with acute myocardial infarction is common.
• Characteristically, pericardial pain may be intensified by lying supine,
and relieved by sitting up and leaning forward

6. • A pericardial friction rub is audible at some point in the illness in
about 85% of patients with acute pericarditis, it may have up to
three components per cardiac cycle, is rasping, scratching, or grating.
• It is heard most frequently at end expiration with the patient upright
and leaning forward.
• Complications of acute pericarditis include:
1. Recurrent Pericarditis : M/C common complication(15-30%)
2. Pericardial effusion
3. Tamponade
4. Constrictive Pericarditis

7. DIAGNOSIS

9. TREATMENT
• Treatment for pericarditis should be targeted towards the specific
etiology but most cases are idiopathic or viral.
• Empirical therapy in form of NSAIDs or aspirin is the first-line
approach and mainstay of treatment.
• Anti-tubercular and antibiotic treatment should be instituted
whenever required along with supportive therapy in the form of
salicylates and corticosteroids to bring about early relief and to
prevent formation of adhesions.
• Colchicine is recommended for 3 months as an adjunct to NSAIDs.
• Colchicine added to standard anti-inflammatory therapy improves the
response and reduces recurrences by approximately half during
follow-up.

11. PERICARDIAL EFFUSION AND
CARDIAC TAMPONADE
• Pericardial effusion occurs when fluid accumulates in the intra-
pericardial space.
• Virtually any disease that can cause pericarditis can cause an effusion.
• The accumulation of fluid in the pericardial space in a quantity
sufficient to cause serious obstruction of the inflow of blood into the
ventricles results in cardiac tamponade.
• The quantity of fluid necessary to produce cardiac tamponade may be
as small as 200 mL when the fluid develops rapidly to as much as
>2000 mL in slowly developing effusions when the pericardium has
had the opportunity to stretch and adapt to an increasing volume.

12. • Effusion causes compression and collapse of the right heart and
caval vessels. This reduced right heart output which in turn causes
underfilling of the left heart and finally decreased CO
• As fluid accumulates, left- and right-sided atrial and ventricular
diastolic pressures rise, and in severe tamponade they equalize at a
pressure similar to that in the pericardial sac, typically 20 to 25 mmHg.
• Characteristics of Tamponade
• Elevated and equal intracavitary filling pressures,
• Low transmural filling pressures,
• Small cardiac volumes,
• Loss of the y descent of the RA or systemic venous pressure.

13. • The three principal features of tamponade (Beck’s triad) are
• hypotension,
• soft or absent heart sounds,
• jugular venous distention with a prominent x (early
systolic) descent but an absent y (early diastolic) descent.
• The limitations to ventricular filling are responsible for
reductions of cardiac output and arterial pressure.
• Patients with tamponade appear uncomfortable and display
varying signs of reduced cardiac output and shock, including
tachypnea, diaphoresis, cool extremities, peripheral cyanosis
and depressed sensorium.

14. • Paradoxical pulse: This important clue to the presence of cardiac
tamponade consists of a greater than normal (10 mmHg)
inspiratory decline in systolic arterial pressure.
• Because both ventricles share a tight incompressible covering,
i.e., the pericardial sac, the inspiratory enlargement of the right
ventricle causes leftward bulging of the interventricular septum,
compresses and reduces left ventricular volume; stroke volume,
and arterial systolic pressure.

15. • BP: Low. May be
undetectable on
inspiration.
• Pulse: Sinus tachycardia, low
volume pulse. Pulsus paradoxus.
• Heart sounds are soft. There
may be a pericardial rub in
tamponade.
• Oliguria or anuria rapidly
develops with tamponade, and
a brisk diuresis occurs when
tamponade is relieved.

17. DIAGNOSIS
• ECG abnormalities : Reduced voltage and Electrical alternans.
• Chest radiograph
 Normal cardiac silhouette until effusions are at least moderate in
size.
 With larger effusions
 PA view : flask-like appearance
 Lateral views : fat pad sign
 The lungs are oligemic.

19. • M-mode and two-dimensional Doppler echocardiography are
the standard noninvasive methods for detection of pericardial
effusion and tamponade.
• A significant effusion appears as a lucent separation between
the parietal and visceral pericardium for the entire cardiac cycle.
• Small effusions are usually first evident over the posterobasal
left ventricle.
• Ultimately, the separation becomes circumferential.
• Circumferential effusions are graded as:
• Small (echo-free space in diastole < 10 mm)
• Moderate (10 to 20 mm)
• Large (> 20 mm)

21. • When pericardial effusion causes tamponade, Doppler ultrasound
shows:
• tricuspid and pulmonic valve flow velocities increase markedly
during inspiration, whereas pulmonic vein, mitral, and aortic
flow velocities diminish.
• there is late diastolic inward motion (collapse) of the right
ventricular free wall and the right atrium.
• Trans-esophageal echocardiography, CT, or cardiac MRI may be
necessary to diagnose a loculated effusion responsible for cardiac
tamponade.

22. TREATMENT

23. Emergency subxiphoid percutaneous drainage
A 16- or 18-gauge needle, angle
of 30-45° to the skin, near the
left xiphocostal angle, aiming
towards the left shoulder.
Mortality rate of approximately
4%, complication rate of 17%

25. • The pericardial fluid should be analyzed for red and white blood cells
and cytology for neoplastic cells.
• Cultures should be obtained.
• The presence of DNA of Mycobacterium tuberculosis determined by
the polymerase chain reaction strongly supports the diagnosis of
tuberculous pericarditis

26. CHRONIC CONSTRICTIVE PERICARDITIS
• This disorder results when the healing of an acute fibrinous or
serofibrinous pericarditis or the resorption of a chronic pericardial
effusion is followed by obliteration of the pericardial cavity with the
formation of granulation tissue.
• Chronic constrictive pericarditis may follow
• acute or relapsing viral or idiopathic pericarditis,
• trauma with organized blood clot, or cardiac surgery of any type,
• results from mediastinal irradiation,
• purulent infection, histoplasmosis,
• neoplastic disease (especially breast cancer, lung cancer, and lymphoma),
• rheumatoid arthritis, SLE,
• chronic renal failure treated by chronic dialysis.

27. • The basic physiologic abnormality in patients with chronic
constrictive pericarditis is the inability of the ventricles to fill
because of the limitations imposed by the rigid, thickened
pericardium.
• Ventricular filling is unimpeded during early diastole but is
reduced abruptly when the elastic limit of the pericardium is
reached, whereas in cardiac tamponade, ventricular filling is
impeded throughout diastole.
• Despite these hemodynamic changes, systolic function may
be normal or only slightly impaired at rest

28. • In constrictive pericarditis, the right and left atrial pressure pulses
display an M-shaped contour, with prominent x and y descents.
• The y descent is the most prominent deflection in constrictive
pericarditis; it reflects rapid early filling of the ventricles.
• In constrictive pericarditis, the ventricular pressure pulses in both
ventricles exhibit characteristic “square root” signs during diastole.

29. CLINICAL FEATURES
• Weakness, fatigue, weight gain, increased abdominal girth, abdominal
discomfort, and edema are common.
• The patient often appears chronically ill, and in advanced cases,
anasarca, skeletal muscle wasting, and cachexia may be present.
Exertional dyspnea is common.
• The cervical veins are distended and may remain so even after
intensive diuretic treatment.

30. • Kussumaul’s sign: Systemic venous pressure (JVP) may fail to decline
or may increase during inspiration.
• It is seen in: Chronic pericarditis, tricuspid stenosis, right ventricular
infarction, and restrictive cardiomyopathy.
• Congestive hepatomegaly is pronounced and may impair hepatic
function and cause jaundice; ascites is common.
• Broadbent’s sign: The apical pulse is reduced and may retract in
systole.
• An early third heart sound (i.e., a pericardial knock) occurring at the
cardiac apex with the abrupt cessation of ventricular filling is often
conspicuous

31. DIAGNOSIS
• The ECG frequently displays low voltage of the QRS complexes and
diffuse flattening or inversion of the T waves.
• Atrial fibrillation is present in about one-third of patients.
• The chest x-ray shows a normal or slightly enlarged heart.
Pericardial calcification is most common in tuberculous pericarditis.
• The transthoracic echocardiogram often shows pericardial
thickening, dilation of the inferior vena cava and hepatic veins, and
a sharp halt to rapid left ventricular filling in early diastole, with
normal ventricular systolic function and flattening of the left
ventricular posterior wall.
• CT or MRI confirms the diagnosis.

32. TREATMENT
• Pericardial resection is the only definitive treatment of constrictive
pericarditis and should be as complete as possible.
• Dietary sodium restriction and diuretics are useful during
preoperative preparation.
• Coronary arteriography should be carried out preoperatively in
patients aged >50 years to exclude unsuspected accompanying
coronary artery disease.

33. SUBACUTE EFFUSIVE-CONSTRICTIVE PERICARDITIS
• This form of pericardial disease is characterized by the
combination of a tense effusion in the pericardial space and
constriction of the heart by thickened pericardium.
• It may be caused by tuberculosis, multiple attacks of acute
idiopathic pericarditis, radiation, traumatic pericarditis, renal
failure, scleroderma, and neoplasms.
• The heart is generally enlarged, and a paradoxical pulse is usually
present.
• The diagnosis can be established by pericardiocentesis followed
by pericardial biopsy.
• Wide excision of both the visceral and parietal pericardium is
usually effective therapy.

34. TUBERCULOUS PERICARDIAL DISEASES
• A common cause of chronic pericardial effusion, especially in the
developing world where active tuberculosis and HIV are endemic.
• Tuberculous pericarditis may present as pericardial effusion,
chronic constrictive pericarditis, or subacute effusive constrictive
pericarditis.
• It is important to consider this diagnosis in a patient with known
tuberculosis, with HIV, and with fever, chest pain, weight loss, and
enlargement of the cardiac silhouette of undetermined origin.

35. • If the etiology of chronic pericardial effusion remains
obscure despite detailed analysis including culture of the
pericardial fluid, a pericardial biopsy, preferably by a
limited thoracotomy, should be performed.
• ATT is the treatment.
• If the biopsy specimen shows a thickened pericardium
after 2–4 weeks of antituberculous therapy,
pericardiectomy should be carried out to prevent the
development of constriction.

36. THANK YOU