1. Cardiac Tamponade
Francesca N. Delling
October 17, 2007

2. Tamponade Etiology Physiology
- comparison with constrictive pericarditis
Types of tamponade
Diagnosis
- clinical presentation, physical exam, EKG, CXR, echo
Treatment

3. Etiologies Infectious Neoplastic Uremic
Viral (coxsackie B, echovirus, influenza)
Bacterial
Others: TB, fungal, toxoplasmosis
Neoplastic
Uremic
Trauma / cardiac surgery / aortic dissection / cardiac procedures
Radiation
Connective tissue disease (RA, SLE, scleroderma)
Myocardial ischemia / infarct
Myxedema
Idiopathic

4. Physiology Exaggerated ventricular interaction
During inspiration  greater RV inflow and outflow and concurrent decrease in LV size, outflow tract flow velocity profile and mitral valve inflow
During expiration  LV filling and LV outflow augmented at the expense of reduced RV volume and Doppler flow velocities

5. Increasing pericardial
Physiology
Normal pericardium
Increasing pericardial
pressure
Increasing filling
pressures
RVEDP = LVEDP
Equalization of
diastolic pressures

6. Comparison with constrictive pericarditis
Features in common
- diastolic dysfunction and preserved ventricular ejection fraction
- heightened ventricular interaction
- increased respiratory variation of ventricular inflow and outflow manifested clinically by pulsus paradoxus (less frequent in constrictive pericarditis)
- equally elevated central venous, pulmonary venous, and ventricular diastolic pressures
Distinctive features
- tamponade  pericardial space is open and transmits respiratory variation in thoracic pressure to heart (pericardium does not see fluctuation in thoracic pressure in constrictive pericarditis)
- constrictive pericarditis: venous return does not increase with inspiration. Diminished LV and increased RV volume are 2/2 lesser pressure gradient from the pulmonary veins

7. Types of tamponade Acute tamponade
- Due to trauma, rupture of the heart or aorta or complication of an invasive diagnostic or therapeutic intervention
- Sudden in onset
- Hypotension common
Subacute tamponade
- Pericardial fluid accumulates slowly
- Hypotension with a narrow pulse pressure, reflecting limited stroke volume. However, patients with preexisting hypertension may remain hypertensive due to increased sympathetic activity

8. Acute vs chronic tamponade
Pericardial pressure-volume curves are shown. On the left, rapidly increasing pericardial fluid first reaches the limit of pericardial reserve, then exceeds the limit of pericardial strech, causing a steep rise in pressure which becomes even steeper as smaller increments in fluid cause a disproportionate increase in pericardial pressure. On the right, aslower rate of pericardial filling takes longer to exceed the limit of pericardial stretch, because there is more time for the pericardium to stretch.

9. Types of tamponade (continued)
Low pressure tamponade
- Severely hypovolemic pts (hemorrhage, hemodyalisis, or overdiuresis)  intracardiac and pericardial diastolic pressures are only 6 to 12 mmHg  fluid challenge usually elicits typical tamponade hemodynamics
Regional tamponade
- caused by a loculated, eccentric effusion
- typical physical, hemodynamic, and echocardiographic signs of tamponade may be absent

10. Clinical Presentation
Tachypnea and exertional dyspnea  rest air hunger
Weakness
Presyncope
Dysphagia
Cough
Anorexia
(Chest pain)

11. Physical Exam Findings
Tachycardia
Hypotension  shock
Elevated JVP with blunted y descent
Muffled heart sounds
Pulsus paradoxus
(Pericardial friction rub)

12. JVP and pulsus paradoxus in tamponade
Prominent X descent (first deflectio of jugular pulse during systole due to atrial relaxation and TV descent) and blunted Y descent (second deflection of jugular pulse due to diastolic inflow of blood into the right ventricle) because of the limited or absent late diastolic filling of the ventricle.
A fall in systolic pressure with inspiration in pulsus paradoxus is associated with decrease in LV filling
Y descent blunted because of limited or absent lated diastolic
filling of the right ventricle

13. Other causes of pulsus paradoxus
Obstructive airway disease
Acute and chronic
Constriction
Restriction
Pulmonary embolism
RV infarction
Circulatory failure

14. EKG pericarditis
Electrical alternans, low voltage, tachycardia

15. EKG tamponade
Electrical alternans, low voltage, tachycardia

16. EKG electrical alternans
Simply secondary to large pericardial effusion (swinging of the heart with variation of cardiac position within the pericardium from beat to beat)

17. Chest X-ray
Enlarged cardiac silhouette

18. Echocardiography 2D and M-mode RV diastolic collapse
RA collapse/inversion
IVC plethora
Doppler
Exaggerated respiratory variation in mitral and tricuspid inflow velocities
Phasic variation in right ventricular outflow tract/left ventricular outflow tract flow
Exaggerated respiratory variation in inferior vena cava flow

19. Echocardiogram: RVDC
Most commonly involves the RV outflow tract (more compressible area of RV)
Occurs in early diastole, immediately after closure of the pulmonary valve, at the time of opening of the tricuspid valve
When collapse extends form outflow tract to the body of the right ventricle, this is evidence that intrapericardial pressure is elevated more substantially

20. Parasternal long axis view

21. M-mode
Beginning of systole ES DC

22. Short axis view

23. 4 chamber view

24. Subcostal view

25. M-mode
Beginning of systole ES DC

26. Echocardiogram: RA Inversion
Right atrium normally contracts in volume with atrial systole
In the presence of marked elevation of intrapericardial pressure, RA wall will remain collapsed throughout atrial diastole (early ventricular systole)
Isolated RA inversion occurs during late diastole
Very sensitive but specificity = 86%
Positive predictive value = 50%
RA Inversion Time Index (RAITI)
- Calculated by dividing
- Using 33% as the threshold
Specificity = 100%
Sensitivity = 94%
Total # frames with inversion
Total # frames in the cardiac cycle

27. M-mode across RA

28. Peak velocity of mitral inflow varies > 15%
with respiration

29. Peak velocity of tricuspid inflow varies > 25% with respiration

30. IVC plethora

31. Predictable hierarchy of events
Exaggerated respiratory variation of tricuspid inflow
Exaggerated respiratory variation of mitral inflow
Abnormal right atrial collapse
Right ventricular free wall collapse

32. Instances when echo abnormalities
are not seen
Significant RV hypertrophy, usually due to PHTN
Thickening of the ventricular wall due to malignancy, overlying inflammatory response or thrombus in hemorrhagic pericarditis
Low-pressure tamponade (hypovolemic patients)

33. Echocardiogram: Additional roles
Confirm size of the pericardial effusion
Small defined as < 100 mL
Moderate defined as 100 – 500 mL
Large defined as > 500 mL
Confirm location of the pericardial effusion
Rule out loculated effusions
Assist pericardiocentesis

34. Assessment of the patient
Insignificant effusion
Flat neck veins
Normal BP, HR, RR, good perfusion
Hemodynamically significant-Compensated
Elevated JVP
Mild paradox, No hypotension or tachycardia
Good perfusion
Mild RV collapse

35. Assessment of the patient
Hemodynamically Severe-Max Compensation
Elevated JVP
Prominent paradox, Tachycardia
No hypotension-adequate perfusion
Chamber collapse on ECHO
Hemodynamically Severe-Decompensated
Tachycardia, tachypnea
Hypotension with paradox
Chamber collapse, swinging heart

36. Pericardiocentesis Usually performed if more than 1 cm effusion
Also performed if effusion smaller in the setting of acute trauma and hemodynamic compromise
Pericardial window if need for biopsies and if evidence of coaugulopathy

37. RB 74 yo male with recently diagnosed adenocarcinoma
of undetermined primary who presented to ED on 10/6
with chest pain

38. RB BP 125/65, pulsus paradoxus of 12 JVP 12 cm
PMI located in 5th ICS, distant heart sounds
Faint crackles lung bases

39. RB
CT chest consistent with large pericardial effusion and moderate compression of right ventricle
Worsened metastatic disease including enlargement of subclavicular, mediastinal, right hilar lymph nodes and pulmonary nodules
Stat echo showing…

40. 10/6 TTE
Large pericardial effusion. Effusion is loculated (4.6 anterior to the right atrium and RV). Stranding visualized within the pericardial space c/w organization. Sustained RA diastolic collapse c/w low filling pressures or early tamponade. RV diastolic collapse c/w impaired filling/tamponade physiology

41. 10/6 TTE
Large pericardial effusion. Effusion is loculated (4.6 anterior to the right atrium and RV). Stranding visualized within the pericardial space c/w organization. Sustained RA diastolic collapse c/w low filling pressures or early tamponade. RV diastolic collapse c/w impaired filling/tamponade physiology

42. 10/6 TTE
Large pericardial effusion. Effusion is loculated (4.6 anterior to the right atrium and RV). Stranding visualized within the pericardial space c/w organization. Sustained RA diastolic collapse c/w low filling pressures or early tamponade. RV diastolic collapse c/w impaired filling/tamponade physiology

43. 10/6 pericardiocentesis Drainage of 400 cc of bloody fluid
Pre-procedure: pulsus 20 mmHg, cardiac output 3.8
Post-procedure: pulsus < 10 mmHg, cardiac output 5.0

44. TTE post-procedure

47. Thank you