Pericardial effusion around the heart sufficient to make cardiac tampnode

1. Cardiac Tamponade
Moderator –Dr Nagaraj kotli Sir,

2. • ANATOMY
• DEFINITION OF CARDIAC TAMPONADE
• ETIOLOGY
• PATHOPYSIOLOGY AND HAEMODYNAMICS
• CLINICAL FEATURES
• DIAGNOSIS
• MANAGEMENT
• D/D

3. INTRODUCTION
• The heart is surrounded by double layered sac called
pericardium.
1. The Parietal layer- Outer layer (Fibrous )
2. The Visceral layer – Inner layer (Serous membrane )

4. PERICARDIUM
• Layers of pericardium are separated by pericardial space.
• A small quantity of fluid measuring 15-50ml will be present
in the pericardial space
• Its an ultra filtrate of plasma

5. NORMAL FUNTIONS OF PERICARDIUM
1. Maintaining an optimal cardiac shape
2. Prevents sudden dilatation of the cardiac chambers,
3. Protecting the heart from spread of infections from lungs
and pleural cavities
4. Prevents over filling of heart

6. LAYERS OF PERICARDIUM

7. CARDIAC TAMPONADE
• 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 fluid which can be blood,pus ,or air in the pericardial
space. Accumalates fast enough and In sufficient quatity to
compress the heart and restrict blood flow in and out of the
ventricles.

8. • The quantity of fluid necessary to produce cardiac tamponade
may be small as 150 -200ml when the fluid develops rapidly
or
be as much as more than 2000ml in slowly developing
effusions when the pericardium has had the oppurtunity to
stretch and adapt to an increasing volume.

9. LAYERS OF PERICARDIUM

10. LOCALIZED PERICARDIAL EFFUSION

11. Causes for Cardiac Tamponade
1. Idiopathic pericarditis
2. Non infective causes
a)Renal failure
b)Neoplasia -Primary tumors(benign/malignant)
-Metastatic tumors(lung/breast/leukemia)
c)Aortic dissection (leakage into the pericardial sac)
d)Trauma-Penetrating chest wall
e)Post radiation, AMI,
f)Metabolic –Myxedema ,Cholesterol

12. 3. Infections
a)Viral-Coxsackie virus A and B
Herpesvirus ,Hepatitis ,HIV
mumps ,adenovirus ,
b)Bacterial- Pneumococcus ,Streptococcus,
legionella, Chlamydia ,Neisseria
Staphylococcus,Tuberculosis,
c)Fungal –Histoplasmosis,candida,Blastomycosis
d)syphilitic,parasitic infections,

13. Other Causes for Cardiac Tamponade
1. Cardiac operation
2. Treatment with Anticoagulant
3. Drug induced –phenytoin ,isoniazid ,minoxidil,
4. Collagen vascular disease –SLE , Rheumatoid arthritis,
scleroderma ,wegners granulomatosis.

14. PATHOPHYSIOLOGY AND HAEMODYNAMICS
• Formation of an effusion in response to
inflammatory,infectious,or neoplastic disease involving the
pericardium lymphomas occasionally causes effusion by
obstructing lymphatic outflow by enlarged mediastinal
lymphnodes.
• Effusion when there is no inflammation (uremia ,idiopathic
disease)is very poorly understood.

15. HAEMODYNAMICS
1. Increased pericardial fluid and pressure
2. Compression and collapse of the right heart and caval
vessels
3. Underfilling of left heart due to decreased right heart
output
4. Decreased diastolic volume and cardiac output
5. Eventually decreased BP/SV/CO

16. PERICARDIAL EFFUSION

17. CLINICAL PRESENTATION
1. Chest pain due to pericarditis(Sharp, pleuritic and positional
dependent)
2. Dyspnea
3. Tachypnea ,diaphoresis, cool extremities ( decreased CO and
Shock)
4. Peripheral cyanosis ,depressed sensorium,
5. A loud pericardial friction rub is the most striking clinical
finding seen in pericarditis but reduced in cardiac tamponade
due to fluid.

18. BECK’S TRIAD
1. Hypotension – due to limitation to ventricular filling are responsible
for reduction cardiac output and arterial pressure.
2. Soft or absent heart sound.
3. Jugular venous distension with a prominent x (early systolic)descent
but an absent y(early diastolic)descent.

19. • Paradoxical pulse - This is the important clue to the presence
of cardiac tamponade consist of a greater than normal
(10mmhg)inspiratory decline in systolic arterial pressure .
• Due to inspiratory enlargement of the right ventricle causes
leftward bulging of interventricular septum,there by
reducing left ventricular volume.
• Seen in cardiac tamponade ,constrictive
pericarditis,hypovolemic shock,COPD,Pulmonary embolism

20. CLASSICAL SIGNS OF CARDIAC TAMPONADE
1. Absence of diastolic venous flow
2. JVP-Loss of Y descent –due to total heart volume is fixed in
severe cardiac tamponade.

21. ECG
1. Low QRS voltage(reductuion in amplitude of the QRS
complexes)
2. Electrical alterens-Consecutive ,normally conducted QRS
complexes that alternate in height, Due to Heart swings
backwards and forwards within a large fluid filled
pericardium.
3. Tachycardia

22. ECG

23. 1.CHEST X RAY OF PERICARDIAL EFFUSION

24. WATER BOTTLE SIGN

25. 2. 2D ECHO- It’s the standard noninvasive method for detection of
cardiac tamponade,
-Significant effusion appears as lucent separation between two
layers.
-In cardiac tamponade early diastolic collapse of the right ventricle
and late diastolic indentation or collapse of the right atrium
-Exaggerated respiratory variation in RV and LV size and
interventricular septal shifting during inspiration causing bulge or
bounce.
-distended IVC does not diminish with inspiration is an important
sign.

29. Grading of Cardiac tamponade
• Based on circumferential effusion in 2D Echo
1. Small effusion -echo free space in diastole <10mm
2. Moderate effusion -10 to 20mm
3. Large effusion – more than 20mm

30. 3. CT AND CARDIAC MRI are more precise than transthoracic echo
cardiography for estimating pericardial thickness and loculated cardiac
effusion.

31. MANAGEMENT
• APPROACH TO THE PATIENT WITH PERICARDIAL EFFUSION
1. Determine If tamponade is present or threatened based on
history ,physical examination ,echocardiography
2. If tamponade is not present or threatened :
If etiology is not apparent ,consider diagnostic test as
acute pericarditis
If effusion large ,consider a course of an NSAIDS plus
colchicine or corticosteroid ;if no response consider closed
pericardiocentesis.

32. • 3.If tamponade is present or threatened
urgent or emergent closed pericardiocentesis or careful
monitoring if trial of medical treatment to reduce effusion is
appropriate.

33. PERICARDIOCENTESIS
1. Open pericardiocentesis
2. Closed pericardiocentesis

34. Closed pericardiocentesis
• In vast majority cases closed pericardiocentesis is the
treatment of choice.
• Most common approach is subxiphoid approach.
• It has a success rate of 95% and rate serious complication of
less than 2%.
• Pericardial decompression syndrome following
pericardiocentesis is serious complication ,charcterised by
cardiogenic pulmonary edema.

36. C/I FOR OPEN PERICARDIOCENTESIS
1. TRAUMATIC CARDIAC TAMPONADE
2. POST MI
3. LV RUPTURE
4. HAEMOPERICARIUM
5. CARCINOMA WITH NEED OF BIOPSY.

37. ANALYSIS OF PERICARDIAL FLUID
• Normal pericardial fluid has the features of a plasma
ultrafiltrate.
• Lymphocytes are predominant cell type.
1. In tubercular pericardial disease
- caseous fluid
- raised ADA ,Unstimulated interferon gamma ,lysozyme
- staining (AFB)and culture
- PCR for genomic material identification

38. 2. Malignant
- hemorrhagic fluid (seen in bleeding diathesis also)
- cytology may reveal neoplastic cells
3.Bacterial
- purulent fluid
- exudate fluid with marked inflammatory cells
- culture and sensitivity can be done.

39. • 4.Chylous effusion seen in surgical injury to thoracic duct and
obstructive neoplasma.
• 5.gold paint (cholesterol rich )effusion seen in
hypothyroidism
• Percutaneous biopsy
-pericardioscopically guided biopsy taken and applied
immunologic and molecular methods to yield diagnosis.

40. D/D
1. Right ventricular infarction
2. Constrictive pericarditis
3. Restrictive cardiomyopathy
4. Effusive constrictive pericarditis

41. REFERENCES
1. HARRISON’S PRINCIPLES OF INTERNAL MEDICINE 21ST
EDITION
2. BRAUNWALD’S HEART DISEASE 11TH EDITION
3. ROBBINS AND COTRAN PATHOLOGY BASIS OF DISEASE.

42. THANK YOU