Cardiac tamponade occurs when fluid accumulates in the pericardial space, reducing cardiac filling and output. It can develop acutely or subacutely. Echocardiography is key for diagnosis, showing pericardial effusion, chamber collapse, and respiratory variations in flow velocities. Treatment involves drainage of fluid, usually by pericardiocentesis under ultrasound guidance. Subxiphoid approach carries liver/vessel injury risk but is safest in emergencies, while apical is easiest but risks heart wall puncture. Drainage resolves tamponade, and catheters are typically removed within 2 days if drainage is low.

1. Cardiac tamponade
pathophysiology and management
Dr ODAY ABDOW

2. pericardium
• The pericardium is composed of two layers:
• Visceral pericardium: monolayer of
mesothelial cells and collagene and elastin
fibers adherent to the epicardial surface of the
heart
• The parietal layer: acellular and contains
elastin and collagen, it is about 2 mm thick and
surrounds most of the heart

3.  The visceral pericardium reflects back and is
continuous with and forms the inner layer of the
parietal pericardium
 The parietal pericardium has ligamentous
attatchments to the sternum,diaphragm.and
other stuctures
 Normally the pericardial space or sac contains
up to 50 ml of serous fluid

5. Functions of the pericardium
1- maintain the heart at relatively constant position
within the thorax via its attachments
2- serves as a barrier to infection and injury
3- modulate cardiac reflexes and coronary tone via
secretion of prostaglandins
4- restrains cardiac volumes and readily transmits
changes in intrathoracic pressure to the heart

6. Cardiac tamponade
cardiac tymponade is a Clinical syndrome
caused by the accumulation of fluid,
pus,blood or gas in the pericardial space
resulted in reduced ventricular filling and
subsequent hemodynamic copromise.

7. Causes of pericardial effusion
-Idiopathic
-Infections
Viral: enteroviruses (coxsackie,echo),herpsviruses, adenoviruses,
influenza ,hepatitis B,HIV
Bacterial(purulent) :stappylococcus ,streptococcus ,haemophilus
influenza, salmonella, legionella pneumophila ,neisseria
meningitidis ,lyme disease
Tuberculosis
Fungal :(histopasmosis,aspergillosis,blastomucosis,
Other infections: amebiasis,echinococcus

8. autoimmune/inflammatory disorders:
-SLE ,ankylosing spondylitis ,rheumatoid arthritis ,
scleroderma
-Systemic vasculitis( polyarteritis nodusa ,eosinophilic
granulomatosis with polyangitis ,giant cell ateritis)
-Sarcoidosis, mamyloidosis
-IBD , whipple disease
-Behcet disease ,Reiter syndrome , FMF

9. Post myocardial infarction pericarditis
Iatrogenic/traumatic
-Postpericardiotomy/postcardiac surgery
-After PCI,pacemaker lead insertion,radiofrequency ablation
-Indirect trauma to the chest
Neoplastic
Primary(rare): mesothelioma,teratoma,fibroma,sarcoma,angioma
Metastatic( common): lung and breast cancer,
lymphoma,leukemia,melanoma

10. Drugs
hydralazine, minoxidil ,procainamide
doxorubicin,phenytoin,penicillin(hypersensitivity pericarditis with
eosinophilia), heparin ,warfarin,dantroline,
methysergide,interleukin2
Metabolic
Uremia,myxedemam,hypoalbominemia
Radiation
Dissecting thoracic aneurysm
PAH

11. ESC 2015

12. pathophysiology
-the pericardium is able to distend in response to fluid
accumulation until a limit on its ability to stretch is
reached,beyond this small increments in pericardial
fluid volume result in large increases in
intrapericardial pressure.
Intracardiac volume becomes fixed,and there is
equalization of intracardiac diastolic pressures with
those within the pericardium,this causes an absolute
reduction in intracardiac volums,ventricular diastolic
filling,and stroke volume.

13. Cardiac pressure-volume curves
a slower fluid accumulation takes longer time to reach limit of pericardial
stretch contrary to the rapid accumulation because there is more time for the
pericardium to stretch and activate compensatory mechanisms

14. Types of tamponade and Clinical
presentation
The presentation of patients with tymponade largely
depends upon the length of time over which
pericardial fluid accumulates and the clinical situation:
Acute tymponade occurs within minutes due to
trauma,rupture of the heart or as a complication of
an invasive diagnostic or therapeutic procdures
This generally results in a picture resembling
cardiogenic shock (tachypnea,diaphoresis,cool
extremities,peripheral cyanosis,depressed sensorium)

15. Subacute cardiac tamponade occurs over days to
weeks and can be associated with neoplastic,uremic,or
idiopathic pericarditis symptoms include: dyspnea,
chest discomfort,peripheral edema and fatigability
Low pressure cardiac tamponade a subset of
subacute tamponade occures in patients who are
severly hypovolemic because of traumatic hemorrhage
,hemodialysis, overduresis
Regional (occult)cardiac tamponade(loculated
eccentric effusion or localized hematoma is most often
seen after pericadictomy or myocardial infarction and
can produce regional cardiac compression and
tamponade,typical physical and hemodynamic and
echocardiographic findings are often absent

16. Physical examination
Beck’s triad: (suggests sever tamponade)
1- Jugular venous distension
2- Hypotension
3- Distant heart sounds

17.  compensatory tachycardia because of decreased
diastolic filling(exceptions heart rate drugs have
been adminestered,conduction system disease
coexists,hypothyroidism in subacute tymponade
,preterminal bradycardia reflex
 prominent x discent and attenuated or abscent y
descent
 Pulsus paradoxus(respiratory drop in systolic
BP>10 mm Hg)
 Pericardial rub

18. Pulsus paradoxus
What is happening during inspiration:
1- Increased venous return to the right heart
2- RV is unable to expand outward >>results in
bulging of the IVS into the LV
3- Reduction in LV filling
[bulging of the IVS +reduction in blood return
to the left heart >>>reduction in SBP
>10mmHG (pulsus paraduxus)]

20. Pulsus paradoxus is not specific to
cardiac tamponade
Causes include:
cardiac
-constrictive pericarditis , RV infarction , RCM
pumonary
-Asthma and COPD
-pulmonary embolism, tension pneumothorax
other
-Marked obesity, hypovolemic shock
-Pectus excavatum, extrinsic cardiac compression

21. Cardiac tyamponade without
pulsus paradoxus
 Elevated LV diastolic pressure such as
aortic regurgitation,chronic LV dysfunction
• Pulmonary hypertension with cor
pulmonale
 Asd
 Aortic dissection with retrograde
bleeding in the pericardium and AR
 Low pressure tymponade such as
dehydration or hypovolemia

26. ECG
Typically shows:
-Sinus tachycardia
-May also show low voltage
-Electrical alternans(relatively specific but
not very sensitive)
-Signs of pericarditis may be seen

29. Chest radiograph
•Findings on a chest radiograph are neither
sensitive nor specific for the diagnosis of cardiac
tymponade
•Enlarged cardiac silhouette with clear lung fields
may be seen in slowly developing tymponade
•Cardiomegaly is not usually seen in acute
tymponade since at least 200ml of pericardial
effusion must accumulate before the cardiac
silhouette enlarges

31. Fat pad sign

32. Water bottle sign in very large pericardial
effusion(rigt inferior)and cardiomegaly( left
inferior) of the image

33. examples of HF with pulmonary congestion and plueral effusion
note :(in tymponade there are oligemic lungs or clear lung fields)

34. echocardiography

35. 1-Quantification of pericardial
effusion
 Small effusions(50-100ml)are only seen
posteriorly , typically less than 10mm
thickness
 Moderate effusions (100 to 500ml)tend to be
seen along the length of the posterior wall but
not anteriorly (10-20mm thickness)
 Large effusions(>500ml)tend to be seen
circumferentially(the free echo space is
greater than 20 mm at greatest width)

37. 2-chamber collapse
-RA will collapse first due to having the lowest pressure
-RA collapse in end ventricular diastole
-Highly sensitive marker that indicate the presense of
tamponade
-RV collapse will occure when the pericardial pressure is
even higher
-Occuring at early diastole
-Less sensitive marker than RA collapse but more specific

38. RA collapse

39. Early diastolic RV collapse

40. M mode RV diastolic collapse

41. 3- IVC collapsipility for<50% during inspiration/sniff
highly sensitive marker but not specific

43. 4-respiratory variations of the TV and MV inflow
doppler velocities
Tricuspid valve :>60% change in E wave
velocity
Inspiration>>> increase
Expiration>>>> decrease
Mitral valve:>30% change in E wave
velocity
Inspiration>>> decrease
Expiration>>> increase

45. Differential diagnosis
- acute cardiac tamponade with elevated JVP and
hypotension must be distinguished from RV
infarction,massive PE,aortic dissection
- Subacute tamponade with dyspnea , elevated JVP
and fatigue,and edema must be ditinguished from
constrictive pericarditis,congestive heart failure,
advanced liver disease with cirrhosiss
echocardiography is crtically important in making this
distinction

46. management
- prompt drainage of pericardial fluid is the most
important intervention
- the options include pericardiocentesis
underechocardiographic or fluroscopic guidance and
surgical drainage
- Additional management includes volume
expansion,inotropic support if the patient is
hypotensive,and avoidance of duiretics and
vasodilators

47. pericardiocentesis

48. contraindications
Absolute:
in emergent scenarios of cardiac tymponade with circulatory
collapse there are no absolute contraindications,in these
instances pericardiocentesis is lifesaving intervention
Relative:
1- Type A aortic dissection(in case of circulatory collapse small
volume pericardiocentesis (10-25ml)may be necessary to
stabilize patient before surgery)
2- Traumatic hemipericardium (surgical)
3- Subacute free wall rupture( as with dissections drainage a
small amount of pericardial fluid may be necessary before
surgery)

49. 4- Small loculated,or posteriorly located effusions
5- Purulent effusions(best treated surgically)
6- Anticoagulations: if time permits(INR >1.8 or
PTT>twice normal should be corrected before
pericardiocentesis,if the patient is coagulopathic the
subxiphoid approuch is best avoided because
berforations of hepatic vessels could be life threating)
7- Thrombocytopenia (plt counts should be more than
50,000)

50. Selecting the approach for
pericardiocentesis
In general there are three different
approaches:
1-Apical
2-Subcostal(subxiphoid)
3-parasternal

51. Subxiphoid pericardiocentesis
•It is safest approach in
emergent situation when
ultrasound is not available
• has the Less risk of
pneumothorax
•Has the greatest risk of
injuring the liver or right
coronary artery

52. Apical approach
•Echo guided
•The insertion point is at
least 5 cm lateral to the
parasternal approach
within the fifth, sixth or
seventh intercostal space
Advance the needle over
the cephalad border of the
rib towards the patients
right shoulder
•Easiest to performe
•Less possibility of injuring
adjacent organs or vascular
structures
•Higher risk of injuring the
LV wall or inducing
ventricular fibrillation

53. Parasternal approach
•Echo guided
•Higher risk of injury the
internal thoracic artery
•Higher risk of
pneumothorax

54. Monitoring :
- patients should be observed for 1-2 hours
following the pericardiocentesiss
Drain care:
- the drain should be aspirated every 6 hours
following by flushing the catheter with saline ,
continuous drainage can also be used but the risk of
catheter obstruction is higher
- The catheter is typically left in place for 1-2 days ,
when drainage is<25-50ml the catheter can be
removed
- Before pulling the drain ,an echocardiogram should
be obtained to ensure the effusion resolution

55. references
-Braunwald ‘s heart disease Eleventh
edition
-Manual of cardiovascular medicine
Fifth edition
-Uptodate
-Medscape
ESC guideline pericardial diseases 2015