Cardiac Tamponade Detailed Pericardial anatomy and physiology Detailed Tamponade pathophysiology Diagnosis Pathophysiology of beck's triad, pulsus paradoxus Tamponade Management Pericardiocentasis Closed and Open method

1. CARDIAC
TAMPONADE
PATHOPHYSIOLOGY
AND MANAGEMENT
Dr Satyam Rajvanshi
SR Cardiology, Dr. RML Hospital, New Delhi

2. CARDIAC TAMPONADE
 Pericardial Anatomy and Physiology
 Pericardial Pathology
 Tamponade
 Physics and Pathology
 Presentation, Diagnosis and Differential
 Management

3. Pericardial Pathology
Tamponade
Physics and Pathology
Presentation, Diagnosis and Differential
Management
PERICARDIAL ANATOMY AND
PHYSIOLOGY

4. PERICARDIUM - ANATOMY
• Resilient Fibro-serous sac – envelops heart and great
vessels
• 2 layers
• Inner visceral layer – Serous Pericardium
• Monolayer membrane of mesothelial cells, collagen & elastin
fibres.
• Over the heart, same as the Epicardium - contains the
epicardial coronary arteries and veins, autonomic nerves,
lymphatics, and a variable amount of adipose tissue.
• Reflects over the great vessels - forms delicate inner lining
of Fibrous Pericardium

5. • Outer parietal layer – Fibrous Pericardium
• Acellular, mainly collagenous fibrous tissue, little elastin fibrils.
• 2 mm thick normally. Contains the epicardial coronary arteries
and veins, autonomic nerves, lymphatics, variable amount of
adipose tissue.
• The junctions between the visceral and parietal pericardium
lie along the great vessels - pericardial reflections -
continuous along the pulmonary veins and vena cavae
• Posterior to LA, midline cul-de-sac known as the Oblique Sinus.
• Behind the great arteries, the Transverse Sinus forms a tunnel-
like passageway.

6. • Between these 2 layers lies the Pericardial Space – 10-50
ml of fluid - ultrafiltrate of the plasma.
• Intrapericardial
• All 4 Chambers except posterior part of LA
• Almost entire Ascending Aorta, Main Pulmonary Artery, all 4
Pulmonary Veins
• In case of TAPVC, PV confluence is intrapericardial
• Extrapericardial
• Right and Left Pulmonary Artery
• Ductus Arteriosus

7.  Only noncardiovascular macrostructure associated with the
pericardium - the Phrenic Nerves, enveloped by parietal
pericardium.
 Drainage of pericardial fluid is via right lymphatic duct and
thoracic duct.

12. PERICARDIUM: FUNCTIONS
Hurst’s The Heart, 12th ed. 2008

13.  Pericardiectomy – No obvious negative consequences, the
normal pericardium does have functions.
 Maintains the position of the heart relatively constant -
Ligamentous attachments to the diaphragm, sternum, and
other structures Ensure a fixed position of heart within the
thoracic cavity regardless of respiration and body position.
 Barrier to infection and provides lubrication between visceral
and parietal layers.
 Pericardium is well innervated with mechanoreceptors and
chemoreceptors and phrenic afferents - probably participate
in reflexes arising from the pericardium and epicardium (e.g.,
the Bezold-Jarisch reflex) as well as in transmission of
pericardial pain.

14.  Secretes prostaglandins and related substances - may
modulate neural traffic and coronary tone by effects on
coronary receptors.
 BNP Level in pericardial fluid is a more sensitive and
accurate indicator of ventricular volume and pressure than is
either plasma BNP or atrial natriuretic factor; it may play an
autocrine–paracrine role in heart failure.
 Finally, the pericardial space has been used as a vehicle for
drug delivery and gene therapy; studies using radiolabeled
growth factors indicate that substances more consistently and
reproducibly gain access to the coronary arteries via
pericardial fluid than via endoluminal delivery.
J Am Coll Cardiol 1998;31(2):399–403
Catheter Cardiovasc Interv 2003;58:375–381

15.  Pressure-volume relation of the parietal pericardial sac
Relatively flat, compliant segment transitioning relatively abruptly
to a noncompliant segment, with the transition in the range of the
upper limit of normal total cardiac volume.

16.  Pressure-volume relation of the parietal pericardial sac
Pericardial Reserve Volume is relatively small. When it is
exceeded, the pressure within the sac operating on the surface
of the heart increases rapidly and is transmitted to the inside of
the cardiac chambers – Direct Contact Pressure.

17.  Pressure-volume relation of the parietal pericardial sac
Inference - Once a critical level of effusion is reached, relatively
small amounts of additional fluid cause large increases in
intrapericardial pressure and have marked effects on cardiac
function. Conversely, removal of small amounts of fluid can result
in striking benefit.

18.  Pressure-volume relation of the parietal pericardial sac
Inference - Once a critical level of effusion is reached, relatively
small amounts of additional fluid cause large increases in
intrapericardial pressure and have marked effects on cardiac
function. Conversely, removal of small amounts of fluid can result
in striking benefit.

19.  Pressure-volume relation of the parietal pericardial sac
Marked shift to the right and flattening - Pericardial compliance
ed
After chronic volume overload
After slowly developing effusions

20. Tamponade
Physics and Pathology
Presentation, Diagnosis and Differential
Management
PERICADIAL PATHOLOGY
Pericardial Anatomy and Physiology

21. PERICADIAL PATHOLOGY
 Few clinicopathologic processes involve pericardium
 Pericardial heart disease includes only
 Pericarditis (an acute, subacute, or chronic fibrinous,
"noneffusive," or exudative process)
 Complications of pericarditis - Tamponade and Constriction (an
acute, subacute, or chronic adhesive, fibrocalcific response)
 Congenital lesions.
 Despite a limited number of clinical syndromes, the
pericardium is affected by virtually every category of disease -
infectious, neoplastic, immune–inflammatory, metabolic,
iatrogenic, traumatic, and congenital etiologies.

22. Categories of Pericardial Disease
 Idiopathic
 Infectious - Viral/Bacterial/Mycobacterial/Fungal/Protozoal
 Immune-inflammatory Connective tissue disease, Early post–myocardial
infarction, Dressler syndrome, Post-cardiotomy/thoracotomy, Late post-
trauma, Drug induced,
 Early post–cardiac surgery and post–orthotopic heart transplantation
 Hemopericardium - Trauma, Post–myocardial infarction free wall rupture,
Device and procedure related (percutaneous coronary procedures,
implantable defibrillators, pacemakers, post–arrhythmia ablation, post–atrial
septal defect closure, post–valve repair or replacement), Dissecting aortic
aneurysm
 Trauma - Blunt and penetrating, Post–cardiopulmonary resuscitation
 Congenital - Cysts, congenital absence
 Miscellaneous - Chronic renal failure, dialysis related, Chylopericardium,
Hypothyroidism and hyperthyroidism, Amyloidosis, Neoplastic, Radiation

23.  Idiopathic pericarditis and any infection, neoplasm, and
autoimmune or inflammatory process that can cause
pericarditis can cause an effusion
 Tamponade
Common
•Bacterial / Mycobacterial /
Fungal
•Hemopericardium
Traumatic
Iatrogenic
Asc Aortic Dissection
•HIV
•Uremia / Dialysis associated
•Malignancy
Uncommon/Less Common
•Common Viral
•Post-MI pericarditis
•Post cardiotomy, Post cardiac transplant
•Autoimmune
•Drug-induced

24. Tamponade
Presentation, Diagnosis and Differential
Management
TAMPONADE : PHYSICS AND PATHOLOGY
Pericardial Anatomy and Physiology
Pericardial Pathology

25.  CARDIAC TAMPONADE - life-threatening, slow or rapid
compression of the heart due to the pericardial accumulation
of fluid, pus, blood, clots, or gas, as a result of effusion,
trauma, or rupture of the heart.
 Pericardial compressive - Tamponade
syndromes - Constrictive Pericarditis
- Effusive-Constrictive Pericarditis
 Hemodynamics of pericardial tamponade, constriction, and
restrictive physiology governed by complex interactions
between
- transmyocardial pressure gradients
- diastolic coupling of cardiac chambers
- pericardial restraint/pericardial contact pressure

26.  Transmyocardial Pressure Gradient (Intracavitary pressure
- Pericardial pressure)
 Normal pericardial pressure – subatmospheric (negative),
it tracks intrapleural pressure during the respiratory cycle.
Maintains a positive transmyocardial pressure gradient
 Results in a net chamber-distending pressure that is
slightly higher than the intracavitary pressure.
 Facilitates diastolic filling, particularly in the low-pressure
right heart.

27.  Inspiration > reduction in intrapleural pressure that affects
all structures within the thorax, associated with a fall in
chamber pressures and pulmonary wedge pressure > The
reduction in intrapericardial pressure tends to be larger
than the fall in systemic venous pressure , and with
descent of the diaphragm, intra-abdominal pressure
increases , resulting in an increase in the pressure gradient
from extrathoracic veins to the right atrium > collectively
serve to enhance right atrial and right ventricular
filling.
 Inspiration > Decrease in intrapleural pressure more
effectively transmitted to the pulmonary venous bed than to
the left ventricle > the pressure gradient from pulmonary
vein to left atrium decreases slightly > slight drop in the
transmitral pressure gradient > decrease in LV preload ,
and transmission of the negative intrathoracic pressure to
the aorta > mild decrease in systemic arterial pressure.

29.  Inter-Ventricular Dependence/Diastolic Coupling
 The right and left ventricles share the intraventricular septum and
are contained in the relatively indistensible pericardial sac
 When the pericardium becomes diseased or when the heart
becomes enlarged to the pericardial limits > Enhanced diastolic
ventricular interaction
 An increase in volume of one ventricle (in the setting of a
compliant septum and an intact pericardium) will affect filling and
volume of the other ventricle.

30.  Pericardial contact pressure/pericardial restraint
 Pericardial contact pressure can be estimated by
- flattened balloons in pericardial sac
- quantifying the change in the right- and left-sided heart
diastolic pressure-volume relation before and after
pericardiectomy
 There is negligible pericardial restraint at low normal filling volumes,
with contact pressures in the range of 2 to 4 mm Hg at the upper
end of the normal range.
 With additional filling, contact pressure rapidly increases - At left-
sided filling pressure of ∼25 mm Hg, estimated contact pressure is
∼10 mm Hg, accounting for most of the right-sided heart pressure at
this level of filling.
 Thus, if cardiac volume or pericardial sac volume and pressure
increase above the physiologic range - Pericardial Reserve
Volume is exhausted - - acute restraint on cardiac volume
- increasing contribution to intracavitary filling pressures, directly
because of the external contact pressure and indirectly because
of increased diastolic interaction.

32. Tamponade physiology
develops when the size of
the effusion becomes
sufficient to increase total
pericardial volume from the
shallow, compliant portion
of the Pericardial pressure-
volume relationship to the
steep, noncompliant
portion.

33. In pericardial tamponade, as intrapericardial pressure increases,
an increase in venous return (1st compensatory
mechanism) will initially serve to maintain cardiac filling and
prevent diastolic collapse of cardiac chambers.
Adrenergic stimulation causes Tachycardia (2nd compensatory
mechanism)

34. Further increase in pericardial pressure will lead to a
progressive impairment in atrial emptying and ventricular
filling, with blunting or disappearance of the y descent (atrial
emptying) while the x descent is typically preserved or
enhanced.

35. There is also loss of the early dip in minimal LV diastolic
pressure and equalization between right atrial and LV
pressure at the onset of diastole.

36. Enhanced Diastolic Interaction – RV and LV filling 180º out of
phase

37. This leads to PULSUS PARADOXUS!

39. As pericardial pressure continues to increase, diastolic filling
pressures will equalize across the four cardiac chambers,
eventually culminating in diastolic compression of the right
side and then the left-side cardiac chambers – Cardiogenic
Shock!

40. Tamponade
Management
TAMPONADE : PRESENTATION,
DIAGNOSIS AND DIFFERENTIAL
Pericardial Anatomy and Physiology
Pericardial Pathology
Tamponade : Physics and Pathology

41. The presentation of patients with cardiac tamponade largely
depends upon the length of time over which pericardial fluid
accumulates and the clinical situation.
From Shoemaker WC, Carey SJ, Yao ST, et al: Hemodynamic monitoring for physiologic evaluation, diagnosis, and
therapy of acute hemopericardial tamponade from penetrating wounds. J Trauma 13:36, 1973.
Grade
Pericardial
Volume
(mL)
Cardiac
Index
MAP CVP HR Beck's Triad
I <200 Normal or ↑ Normal ↑ ↑
usually not
present
II ≥200 ↓
Normal
or ↓
↑
(≥12 cm H2O)
↑
May or may not be
present
III >200 ↓↓ ↓↓
↑↑
(≤30–40 cm
H2O)
↓ Usually present

43.  Acute cardiac tamponade occurs within minutes, due to
trauma, rupture of the heart or aorta, or as a complication of
an invasive diagnostic or therapeutic procedure. This
generally results in a picture resembling cardiogenic shock
that requires urgent reduction in pericardial pressure
 Subacute cardiac tamponade occurs over days to weeks
and can be associated with infective, neoplastic, uremic, or
idiopathic pericarditis.
Maybe asymptomatic early in course.
Symptoms include dyspnea, chest discomfort or fullness,
peripheral edema, and fatigability.

44. Clinical Symptoms
Clinical Symptoms – Nonspecific and Nonsensitive
 Apprehension
 Chest pain
 Oppressive precordial
 Positional
 Dyspnea
 Dry Cough
 Hoarseness
 Dysphagia
 Singultus
 Early Satiety, Nausea, Abdominal Pain

45. Clinical Signs
Clinical Signs – More specific
 General
 Anxious
 Apprehensive
 Ashen gray facies
 Cool perspiration
 Tachypnea
 Tachycardia - Exceptions include patients with bradycardia during uremia and
patients with hypothyroidism
 Tachypnea
 Jugular venous distension
 Quiet precordium with both inspection and palpation, Impure muffled heart sounds
 Rub
 Peripheral Cyanosis
 Bamberger-Pins-Ewart sign
 Variable dullness and bronchial breathing at one or both bases most frequently
the left below the 9th rib and between the mid scapular line and the spine.

46. Physical findings in 56 patients diagnosed with Cardiac Tamponade at the bedside.
Circulation. 1981: 64, 633-9

47.  Pulsus Paradoxus – Key diagnostic finding
 First described by Kussmaul in 1873 as a palpable
decrease or absence of the radial pulse during
inspiration.
Kussmaul, A. Puls. Klin. Wchnschr. 1873: 10, 433-5, 445-9, 461-4.

48. Conditions in which Cardiac Tamponade presents without a
Pulsus Paradoxus
 Septal Defect
 Ascending Aortic Dissection with AR
 Preexisting elevations in Diastolic pressures
 Severe Left Ventricular Dysfunction
 Severe AR
 Myocardial infarction

49. NEJM 349;7 www.nejm.org august 14, 2003

50. ECG Signs
ECG Finding Sensitivity
Specificity
Electrical Alternans 76 - 93 % 8 - 33 %
Low Voltage 99% 25%
P-R depression 86% 42%
187 patients with echocardiographically diagnosed pericardial effusion.
Eisenberg, M.J. et. al. Chest. 1996: 110, 318-24.

54. Radiographic Signs
 The cardiac silhouette is normal until effusions are at least
moderate in size.

55.  With moderate and larger effusions, the anteroposterior
cardiac silhouette assumes a rounded, flasklike appearance.
The lungs appear oligemic.
 "Differential density sign" is increase in lucency at heart
margin secondary to slight difference in contrast between
pericardial fluid and heart muscle

56. Red arrow points to fat outside of pericardium. Green arrow points to pericardial space which is 8 mm
in this patient (<3 mm is normal.) The yellow arrow points to fat outside of heart and the blue
arrow to the myocardium.
Lateral views may reveal the pericardial fat pad sign, a linear lucency
between the chest wall and the anterior surface of the heart
representing separation of parietal pericardial fat from epicardium.

57. Echocardiographic Signs
Echocardiographic findings may suggest a hemodynamic
abnormality that may be the substrate for tamponade, but
echocardiographic abnormalities alone do not establish
the diagnosis of cardiac tamponade.
One of the earliest signs of cardiac tamponade is evidence of a
swinging heart, detected on either M-mode or two-
dimensional echocardiography - simply a marker of a large
pericardial effusion in which the four cardiac chambers are
free to float within the pericardial space in a phasic manner –
indirect evidence of elevated pressure.

58.  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

59.  RV Diastolic Collapse
 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
Circulation. 1977, 56: 774-9.

60. Systole
Early Diastole
Late Diastole

61. Parasternal long axis view

62. Beginning of systole
ES DC
M-mode

63. Short axis view
Feigenbaum's Echocardiography, 6th Edition

64. Subcostal view

65.  Right atrial collapse / 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
 specificity (86%)
 The specificity rose to 100% when the duration of atrial
collapse was > 34% of the cycle length.
Gillam, et. al. 1983. Circulation. 1983, 68: 294-301.

66. Apical 4C view

67.  Right ventricular diastolic collapse is a highly sensitive
and specific indicator of Cardiac Tamponade.
 Right atrial collapse although specific for Cardiac
Tamponade was less sensitive for the detection of
Cardiac Tamponade.
 Right heart collapse may not be seen in patients with
pulmonary HTN and Cardiac Tamponade.
Circulation 1984, 70: 966-71.

68.  Variation of the blood flow velocities across the tricuspid and
mitral valves
 pulsed wave doppler ultrasound

70. Inspiratory increase of tricuspid flow velocities

71. Expiratory increase of mitral (B) and aortic (C) flow velocities.

72. Doppler echocardiograms of pulmonary venous flow velocity from a dog
before (A) and after (B) creation of cardiac tamponade. Note the
predominance of systolic flow after tamponade. J, systolic flow; K,
diastolic flow on control flow velocity (A).

73. Pulsed Doppler imaging of the hepatic vein recorded in a patient with a
hemodynamically significant pericardial effusion. Note the loss of
forward flow in the hepatic veins during the expiratory (E) phase
of the respiratory cycle. Flow out of the hepatic veins is confined
exclusively to the early inspiratory (I) phase.

74. Other Modalities: Less useful
 Fluoroscopy
 CT and CMR –
 valuable when echocardiography is technically inadequate.
 especially useful for loculated effusions and in the
presence of coexistent pleural effusions.
 Real-time CT or CMR cine displays provide information
similar to that of echocardiography for assessment of
tamponade (e.g., septal shifting and chamber collapse).

75. Tamponade Variants
 Low-pressure tamponade occurs at diastolic pressures of 6 to 12
mm Hg and is virtually confined to patients with hypovolemia and
severe systemic diseases, hemorrhage, or cancer, or in patients
with hypovolemia after diuresis. Patients are weak and generally
normotensive, with dyspnea on exertion and no diagnostic pulsus
paradoxus, but with characteristic respiratory fluctuations in
transvalvular diastolic Doppler flows. The low-pressure effusion
equilibrates only with right-sided diastolic pressures and does so at
first only during inspiration (“inspiratory tracking”). A fluid challenge
with a liter of warm saline can evoke tamponade dynamics.
 Hypertensive cardiac tamponade with all the classic features of
tamponade, occurs at high and very high arterial blood pressures
(even over 200 mm Hg) and is ascribed to excessive
betaadrenergic drive. Affected patients typically have had
antecedent hypertension.
 Regional cardiac tamponade occurs when any cardiac zone is
compressed by loculated effusions, which are usually accompanied
by localized pericardial adhesions, especially after cardiac surgery.
Sometimes the typical hemodynamic abnormalities are found only
in the compressed chambers or zones.

76.  Loculation can also produce classic tamponade, presumably by
tightening the uninvolved pericardium; for example, loculated
effusions after cardiac surgery may include hematomas over the
right atrium and atrioventricular groove.
 After right ventricular infarction, loculated effusion can cause
selective right-heart tamponade in which right atrial pressure is
higher than left atrial pressure. The absence of pulsus paradoxus
makes this form difficult to recognize.
 Effusive–constrictive pericarditis is characterized by mixed
clinical, imaging, and hemodynamic signs, because a constrictive
epicarditis underlies the pericardial effusion. In some patients with
scarred, rigid parietal and visceral pericardium, tamponade can
occur with relatively little accumulation of fluid. Effusive–constrictive
pericarditis is revealed in these patients when drainage of
pericardial fluid does not cause intracardiac pressures to return to
normal.

78. TAMPONADE : MANAGEMENT
Pericardial Anatomy and Physiology
Pericardial Pathology
Tamponade : Physics and Pathology
Tamponade : Presentation, Diagnosis And Differential

79. Acute Cadiac Tamponade
The treatment of cardiac tamponade is drainage of the
pericardial contents, preferably by needle paracentesis, with
the use of echocardiographic or another type of imaging,
such as fluoroscopy or CT.

80. Medical treatment of acute cardiac tamponade, including
inotropic support with or without vasodilators, is relatively
controversial, no specific guideline.
Aimed at supporting compensatory mechanisms to reduce the
elevated vascular resistance. Thus, dobutamine,
administered to reverse the hypotension, is theoretically
ideal.
During tamponade, however, endogenous inotropic stimulation
of the heart is often already maximal.
Increasing the volume may help only in patients with
hypovolemia, since in patients with normovolemia and
hypervolemia, volume infusion may increase intracardiac
pressures as well as heart size, which in turn increases
pericardial pressure, further reducing or eliminating the low
transmural myocardial pressures supporting the circulation.

81. Fluid overload with intravenous administration of 500 mL of
normal saline over 10 minutes. Cardiac index increased by
>10% in (47%), remained unchanged in (22%), and
decreased in (31%). No patient developed clinical
complications. Predictors of this favorable response were
systolic blood pressure <100 mm Hg and low cardiac index.
Circulation.2008; 117: 1545-1549
Hydration and positive inotropes are thus temporizing measures
and should not be allowed to substitute for or to delay
pericardiocentesis.

82. Mechanical ventilation with positive airway pressure should be
avoided in patients with tamponade, because this further
decreases cardiac output.
In patients with cardiac arrest and a large amount of pericardial
fluid, external cardiac compression has little or no value,
because there is little room for additional filling and because
even if systolic pressure rises, diastolic pressure falls and, in
doing so, reduces coronary perfusion pressure.

83.  In most circumstances, closed pericardiocentesis is the
treatment of choice. Before proceeding, it is important to be
confident that there is an effusion large enough to cause
tamponade, especially if hemodynamics are atypical.
 One of the more difficult management decisions is whether to
perform closed versus open pericardiocentesis in patients
with known or suspected bleeding into the pericardial space.
The danger of a closed approach is that lowering the
intrapericardial pressure will simply encourage more bleeding
without affording an opportunity to correct its source. In
cases of trauma or rupture of the wall of the left ventricle
after MI, closed pericardiocentesis should in general be
avoided. However, if bleeding is slower (e.g., due to a
procedural coronary perforation or puncture of a cardiac
chamber), closed pericardiocentesis is often appropriate
because bleeding may stop spontaneously or the procedure
can provide temporary relief before definitive repair.
NEJM 349;7 www.nejm.org august 14, 2003

84.  Needle drainage of pericardial fluid, is best done with
imaging, to determine which anterior landmarks, usually
paraxiphoid or apical, are closest to the fluid.
 Whenever possible, the procedure should be performed in
the cardiac catheterization laboratory with experienced
personnel in attendance.
 The paraxiphoid approach is also most often used for
pericardiocentesis that is performed without imaging.

85. NEJM 349;7 www.nejm.org august 14, 2003

86. From Custalow CB: Color Atlas of Emergency Department Procedures.
Philadelphia, Elsevier Saunders, 2005, p 123.
Pericardiocentesis

91. For prolonged drainage, a guide wire passed through the
sheath will facilitate the introduction of a pigtail angiographic
catheter.
Thereafter, patients should be followed with the use of Doppler
echocardiography to ensure that the pericardial space has
been adequately drained and to avert a recurrence. When the
amount of fluid drained is less than 50 ml a day, the catheter
may be withdrawn; the patient should continue to be
observed.

92. Hemodynamic monitoring before and after pericardiocentesis is
useful for several reasons. Initial measurements confirm and
document the severity of tamponade. Assessment after
completion establishes a baseline to assess reaccumulation.
If a pulmonary artery catheter has been inserted, pulmonary
capillary wedge and systemic arterial pressures and cardiac
output should be monitored before, during, and after the
procedure. Ideally, pericardial fluid pressure should also be
measured.
Filling pressures that remain elevated after pericardiocentesis
and the appearance of venous waveforms typical of
constriction (rapid x and y descents) indicate coexistent
constriction.

93. Procedural success rate 97% and complication rate 4.7% (major,
1.2%; minor, 3.5%).
In 89%, only 1 attempt at needle passage necessary to gain access
into the pericardial space.
Major complications (1.2%) occurred included fatal hemorrhagic
tamponade. Nonfatal complications included chamber lacerations
requiring surgery, injury to an intercostal vessel necessitating
surgery, pneumothoraces requiring chest tube placement,
ventricular tachycardia, and bacteremia possibly related to
pericardial catheter placement.
Minor complications (3.5%) occurred that required no specific
interventions, except for monitoring and appropriate follow-up.
These included transient chamber entries, small pneumothorax
noted on radiographs, vasovagal response with transient decrease
in blood pressure, nonsustained supraventricular tachycardia,
pericardial catheter occlusion, and probable pleuropericardial
fistulas.
Mayo Clin Proc 2002; 77:429.

94. After pericardiocentesis, repeated echocardiography and in
many cases continued hemodynamic monitoring are useful to
assess reaccumulation. Ideally atleast for 24 hours.
Leaving intrapericardial catheters in place for several days to
allow continued fluid removal has been shown to minimize
recurrences and facilitates delivery of intrapericardial drugs if
indicated.

95. Open pericardiocentesis is occasionally preferred for initial
removal of pericardial fluid.
 Bleeding due to trauma and rupture of the left ventricular free
wall.
 Loculated effusions or effusions that are borderline in size are
drained more safely in the operating room.
 Recurring effusions, especially those causing tamponade,
may initially be drained by a closed approach because of
logistical considerations. However, open pericardiocentesis
with biopsy and establishment of a pericardial window are
preferred for most recurrences that are severe enough to
cause tamponade.

96. More recently, percutaneous balloon techniques have been
used for drainage {Pediatric valvuloplasty balloon - diameter
20 mm, length 30 mm}.
Particularly useful in patients with malignant effusions, in whom
the incidence of recurrence is high and a definitive approach
without a surgical procedure is desirable.
Available only at few centers.
Rev Esp Cardiol. 2002;55:25-8. - Vol. 55 Num.01

97. CONCLUSIONS
 Acute cardiac tamponade is a life-threatening, slow or rapid
compression of the heart due to the pericardial accumulation
of fluid, pus, blood, clots, or gas, as a result of effusion,
trauma, or rupture of the heart.
 The gold standard for the diagnosis of pericardial effusion is
echocardiography.
 The diagnosis of Cardiac Tamponade is based solely on
PHYSICAL EXAM.
 In most circumstances, closed pericardiocentesis is the
treatment of choice, and is life-saving when performed with
adequate precautions.

100. How to Check Pulsus
Paradoxus
 Place the patient in a position of comfort and conduct manometric
studies during baseline respiration.
 Raise sphygmomanometer pressure until Korotkoff sounds
disappear.
 Lower pressure slowly (2 mmHg per sec) until first Korotkoff sounds
are heard during early expiration with their disappearance during
inspiration.
 Record this pressure.
 Lower pressure until Korotkoff sounds are heard throughout the
respiratory cycle with even intensity.
 Record this pressure.
 The difference between the two recorded pressures is the Pulsus
Pardoxus.
 Conventionally differnce >10 mmHg considered significant.
 Other definition: Pulsus paradox is greater than or equal to 10% of
the pressure at which all Korotkoff sounds are heard with even
intensity.

101.  Other Etiologies of Pulsus Paradoxus
 Large pulmonary embolus
 Severe COPD exacerbation
 Labored respiration
 Constrictive pericarditis
 Restrictive cardiomyopathy
• Right ventricular infarction
• Circulatory shock
• Large pleural effusions
• Tense ascites
• Extreme obesity

102.  Conditions in which Cardiac Tamponade presents
without a Pulsus Paradoxus
 Septal Defect
 Severe Aortic Stenosis
 Severe Left Ventricular Dysfunction
 Cardiomyopathy
 Myocardial infarction
 When there are pre-existing elevations in diastolic pressures
or volume, tamponade can occur without a paradoxical
pulse.[18,22] Examples are patients with left ventricular
dysfunction, aortic regurgitation, and atrial septal defect. In
patients with retrograde bleeding into the pericardial sac due
to aortic dissection, tamponade can occur without a
paradoxical pulse because of aortic valve disruption and
regurgitation.

103. NEJM 349;7 www.nejm.org august 14, 2003

104.  Fluoroscopy is useful in the cardiac catheterization laboratory for detection of
procedure-related effusions because they may cause damping or abolition of cardiac
pulsation.
 CT (see Chap. 19) and CMR (see Chap. 18) are useful adjuncts to echocardiography
in the characterization of effusion and tamponade.[26,27] Neither is ordinarily required
or advisable in sick patients who require prompt management and treatment
decisions. They have an important ancillary role in situations in which hemodynamics
are atypical, other conditions complicate interpretation, and the presence and
severity of tamponade are less certain. They are of course invaluable when
echocardiography is technically inadequate.
 CT and CMR provide more detailed quantitation and regional localization than
echocardiography does and are especially useful for loculated effusions and in the
presence of coexistent pleural effusions.
 Clues to the nature of pericardial fluid can be gained from CT attenuation
coefficients. Attenuation similar to water suggests transudative; higher than water,
malignant, bloody, or purulent; and lower than water, chylous. CMR can be used to
make similar distinctions.
 Real-time CT or CMR cine displays provide information similar to that of
echocardiography for assessment of tamponade (e.g., septal shifting and chamber
collapse).