Intensive Care Med
https://doi.org/10.1007/s00134-018-5191-z
UNDERSTANDING THE DISEASE
Cardiac tamponade
Armand Mekontso Dessap1,2* and Michelle S. Chew3
© 2018 Springer-Verlag GmbH Germany, part of Springer Nature and ESICM
Introduction
Cardiac tamponade (CT) is characterized by hemody-
namic instability due to heart compression by accu-
mulation of fluid, blood, clots, or gas in the pericardial
space [1]. In this article, we focus on understanding
pathophysiology, clinical and echocardiographic find-
ings of non-loculated pericardial fluid accumulation,
in order to answer the following question: In a patient
with pericardial effusion, how do I recognize and man-
age tamponade? Loculated intrapericardial effusions or
extrapericardial tamponade (by mediastinal or pleural
processes) that may cause local compression on any heart
chamber will not be extensively discussed here.
Epidemiology
The pericardium may be affected by all categories of dis-
eases, including infectious, autoimmune, neoplastic, iat-
rogenic, traumatic, and metabolic [1]. The true incidence
of CT is difficult to estimate but pericardial diseases
likely to progress to CT include some infectious diseases
(e.g., human immunodeficiency virus infection or tuber-
culosis), malignancies, renal failure, trauma/iatrogenic,
and hemopericardium in aortic dissection and rupture
of the heart after acute myocardial infarction [2]. Other
important associated conditions are bacterial infections,
autoimmune disorders, radiation-induced, and pneumo-
pericardium [1]. Large (> 20 mm) idiopathic chronic peri-
cardial effusions (which occur mostly in women at least
50 years of age) are also associated with a high incidence
of tamponade [3].
Pathophysiology
Normally, only a small amount of fluid (< 30  mL) exists
between the two pericardial layers, with intrapericardial
*Correspondence: armand.dessap@aphp.fr
1
AP‑HP, Hôpitaux universitaires Henri Mondor, DHU A‑TVB, Service de
Réanimation Médicale, 94010 Créteil, France
Full author information is available at the end of the article
pressure approximating pleural pressure. CT develops
when intrapericardial pressure exceeds intracardiac
pressures. This is not necessarily related to the volume
of pericardial fluid, as the development of tamponade is
more dependent on the rate of accumulation. Thus, large
effusions may be tolerated if the intrapericardial pres-
sure does not exceed right heart filling pressures. The
steep rise at the end of the pericardial volume–pressure
relationship illustrates how small increases in pericar-
dial volume may produce sudden, critical hemodynamic
compromise, and why the first decrement during drain-
age produces the largest relative decompression (Fig. 1).
At  postmortem, CT is most often related to hemoperi-
cardium, attributable to either ruptured acute myocardial
infarction or dissecting aortic aneurysm [4].
In a study investigating patients with pericardial effu-
sions greater than 150  mL, Reddy et  al. described three
phases of hemodynamic changes in tamponade [5]. In
phase I, the accumulation of pericardial fluid “stiffens”
the ventricles and impairs their relaxation. Ventricular
filling pressures are increased but remain higher than the
intrapericardial pressure. In phase II, further fluid accu-
mulation increases intrapericardial pressure above right
ventricular filling pressure. Systemic venous pressure is
unable to fill the right heart, resulting in a decrease in
cardiac output. In phase III, a further decrease in cardiac
output leading to circulatory collapse occurs when intra-
pericardial pressure equilibrates with left ventricle filling
pressure.
Low pressure tamponade develops when intraperi-
cardial pressure exceeds right heart filling pressure in a
hypovolemic patient [6]. Here, the low right ventricular
filling pressure may be normalized by volume loading.
The increase in systemic venous return restores right
heart filling pressure, allowing forward flow of blood.
During CT, the physiological interdependence of the
left and right ventricles is often exaggerated. Serial inter-
dependence means that the stroke volume, which is
maximal during spontaneous inspiration at the output
 Haemodynamic compromise when
pericardial pressure > right-sided filling pressure
Acute
Intrapericardial pressure
Pericardial
reserve
volume
Volume of pericardial fluid
Fig. 1  Pericardial volume–pressure relationship illustrating an initial slow rise followed by a steep rise in intrapericardial pressure. At the steep por-
tion of the curve, only small additional volumes are required to precipitate tamponade. Modified with courtesy of Prof. Stephen Huang, Critical Care
Echocardiography Group, Nepean Hospital, Sydney University
of the right ventricle (secondary to increased venous
return), is maximal at the output of the left ventricle dur-
ing the following expiration (and vice versa), because the
pulmonary transit time is long (several seconds) [7]. As
a result of parallel interdependence, an increase in right
ventricle size during spontaneous inspiration will induce
a septal shift of the interventricular septum towards the
left ventricle, resulting in decreased left ventricle dimen-
sion and output [7]. During positive pressure ventilation,
however, right ventricular preload becomes limited and
intraventricular pressures may be exceeded by intratho-
racic pressure making mechanical ventilation potentially
dangerous especially in the hypovolemic patient.
Presentation
CT often presents as a cardiogenic obstructive shock
with shortness of breath, tachycardia, hypotension with
a narrow pulse pressure (but blood pressure may be pre-
served in some cases) [8], venous jugular distension (with
increased central venous pressure), and muffled heart
sounds. The exaggeration of the biventricular interde-
pendence induces pulsus paradoxus (an inspiratory fall
of systolic blood pressure of more than 10  mmHg dur-
ing normal spontaneous breathing), which is an impor-
tant diagnostic finding in CT [9], although it can also
be found during constrictive pericarditis, severe acute
asthma, pneumothorax, or exacerbations of chronic
obstructive pulmonary disease [10].
Electrocardiography may show signs of large peri-
cardial effusion, with especially low QRS voltage and
Chronic
Right-sided filling
pressure
electrical alternans. An enlarged cardiac silhouette may
be present on chest X-ray in slow-accumulating hence
large-volume effusions.
Echocardiography
Echocardiography is the main diagnostic method for
detection of pericardial effusion and tamponade (see
video S1). The transthoracic approach is often sufficient,
but the transesophageal route must be preferred in intu-
bated patients following trauma or cardiac surgery in
whom loculated or extrapericardial tamponade may
result in nonspecific clinical presentation [11]. Pericar-
dial effusion is usually visualized as an echo-free space
between the visceral and parietal pericardium surround-
ing the heart, but hemorrhagic or purulent fluid may be
more echogenic than simple serous fluid. The fluid first
accumulates posterior to the heart, when the patient is
examined in the supine position. A “swinging” heart may
be observed when the effusion is massive. Pericardial
effusion should be distinguished from left pleural effu-
sion (which appears behind the descending aorta on
a parasternal long axis view) and from pericardial fat
(which is often seen only anteriorly).
The main echocardiographic sign of CT is heart col-
lapse. It mainly occurs in low pressure cardiac chambers
with thin walls, namely the right atria at end diastole
(early sign, very sensitive, but poorly specific unless sus-
tained at least one-third of the cardiac cycle) [12], and the
right ventricle outflow tract at early diastole (late sign,
very specific) [13]; left atrium and left ventricle collapses
are less common because intra-cavitary pressures are
higher. The heart collapse is enhanced during the sponta-
neous expiratory phase, because of the decreased venous
return; conversely, it may be mitigated by hypervolemia,
pulmonary hypertension, and right ventricle hypertrophy
[14].
Echocardiography can also easily document the exag-
gerated respiratory reciprocation of flows within the
heart (echographic pulsus paradoxus). In a spontaneously
breathing individual with CT, the inspiratory increase
of right-sided flows (tricuspid or pulmonary) and the
concomitant decrease on the left side (mitral or aortic)
often exceed +  25% and −  15%, respectively [15, 16].
This echographic pulsus paradoxus is complex to ana-
lyze during mechanical ventilation [17]. Other echocar-
diographic signs of CT often include (1) an inferior vena
cava plethora with blunted respiratory variations [18];
(2) a paradoxical motion of the interventricular septum,
which is usually accompanied by a relaxation impairment
seen on transmitral inflow (with an early to late peak flow
ratio < 1); (3) a diminished stroke volume.
Management
Echocardiographic diagnosis of CT is difficult, even in
experienced hands, because images are frequently not
caricatural. The clinical assessment remains essential to
drive the management. A triage strategy has been pro-
posed for the clinical management of CT [2]. The treat-
ment involves urgent drainage of the pericardial fluid,
triggered by the integration of clinical and echocardio-
graphic findings. CT represents a continuous spectrum
of hemodynamic abnormalities, but not an all-or-none
phenomenon [5, 10]. Real-time echocardiography guid-
ance with microbubbles injection can be used by expe-
rienced staff for safe bedside pericardiocentesis [19].
When possible, surgical drainage is preferable in some
cases like purulent pericarditis or bleeding (e.g., type A
aortic dissection, ventricular free wall rupture) [2]. In
some patients presenting with CT and large pleural effu-
sion, drainage of the pleural effusion may be given prior-
ity [20]. Fluid loading may improve cardiac index in half
of patients with CT, one predictor of a favorable response
being a systolic blood pressure  below 100  mmHg [21].
Vasodilators and diuretics are not recommended in this
setting [1]. The comparative effects of catecholamines in
CT are controversial, but norepinephrine seems the most
indicated to increase blood pressure [22]. The reduction
in venous return induced by positive pressure mechani-
cal ventilation and general anesthetics may decompen-
sate cardiac tamponade. Intubation should therefore be
cautious (with some authors suggesting the use of local
anesthetics or ketamine) and high ventilatory pressures
avoided [23].
Electronic supplementary material
The online version of this article (https://doi.org/10.1007/s00134-018-5191-z)
contains supplementary material, which is available to authorized users.
Author details
1
 AP‑HP, Hôpitaux universitaires Henri Mondor, DHU A‑TVB, Service de Réani-
mation Médicale, 94010 Créteil, France. 2 Université Paris Est Créteil, Faculté de
Médecine de Créteil, IMRB, GRC CARMAS, 94010 Créteil, France. 3 Department
of Anesthesiology and Intensive Care, Medical and Health Sciences, Linköping
University, 58185 Linköping, Sweden.
Received: 1 March 2018 Accepted: 18 April 2018
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