Cardiac tamponade: a clinical challenge

escardio.org/Journals/E-Journal-of-Cardiology-Practice/Volume-15/Cardiac-tamponade-a-clinical-challenge

Vol. 15, N° 17 - 27 Sep 2017

Dr. Jesper K. Jensen

Assoc. Prof Steen Hvitfeldt Poulsen

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 Prof. Henning Mølgaard

Cardiac tamponade results from an accumulation of pericardial fluid under pressure,

leading to impaired cardiac filling and haemodynamic compromise. Findings during
physical examination are included in Beck´s triad (sinus tachycardia, elevated jugular
venous pressure, low blood pressure) and pulsus paradoxus. Cardiac tamponade is a
clinical diagnosis, but assessment of the patient’s condition and diagnosis of the
underlying cause of the tamponade can be obtained through lab studies,
electrocardiography, echocardiography, or other imaging techniques. The treatment of
cardiac tamponade is the removal of pericardial fluid to help relieve the pressure
surrounding the heart.

Pericardial Disease

Causes
The pericardium is a double-walled sac containing the heart and the roots of the great
vessels and is composed of a visceral and parietal component. The pericardial space
enclosed between the two serosal layers normally contains up to 50 mL of serous fluid. It
provides lubrication and protection from infection. Pericardial diseases may be isolated or
part of a systemic disease. Cardiac tamponade is a life-threatening condition due to slow
or rapid pericardial accumulation of fluid with subsequent compression of the heart [1].

The causes of pericardial fluid accumulation leading to cardiac tamponade are idiopathic,
infectious, immune-inflammatory, neoplastic disease, post-cardiac surgery, trauma, renal
failure, aortic dissection and miscellaneous (chronic renal failure, thyroid disease,
amyloidosis) [2-4]. The most common causes of tamponade are pericarditis (infection and
non-infection), iatrogenic (cardiac invasive procedures and post-surgery), and malignancy
[5]. More rare causes are collagen diseases (systemic lupus erythematosus, rheumatoid
arthritis, scleroderma), radiation, aortic dissection, uraemia, post-myocardial infarction
and bacterial infection [2]. Causes of effusion with a high incidence of progression to
tamponade include bacterial, fungal, human immunodeficiency virus-associated
infections, bleeding, and cancer involvement [3]. For all patients, infectious diseases are
still the most common cause of pericardial tamponade but, due to an increasing number
of cardiac interventional procedures (cardiac ablation, device lead implantation and
percutaneous coronary intervention), the incidence of haemopericardium seems to be
increasing.

Signs
The key element which determines the clinical presentation is the rate of fluid
accumulation relative to pericardial stretch and the effectiveness of compensatory
mechanisms. Thus, cardiac tamponade comprises a continuum from an effusion causing

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minimal effects to one causing circulatory collapse. The stiffness of the pericardium
determines fluid increments precipitating tamponade [6,7]. The pericardial strain-stress
curve is depicted in Figure 1. There is a slow phase and a steep rise, leading to critical
cardiac compression. Thus, rapid accumulation of as little as 150 mL of fluid can result in
a marked increase in pericardial pressure and can severely impede cardiac output. In
contrast, 1,000 mL of fluid may accumulate over a longer period without any significant
effect on diastolic filling of the heart. This is due to adaptive stretching of the pericardium
over time. A compliant pericardium can allow considerable fluid accumulation over time
without haemodynamic compromise.

Figure 1. Cardiac tamponade.

Pericardial strain-stress curves illustrating that the pericardium has some degree of
elasticity. When the elastic limit is reached the intrapericardial pressure rises. The left-
hand panel shows the pressure-volume curve with rapidly increasing pericardial fluid
whereas the right-hand panel shows a slower rate of pericardial effusion.

Several signs may be present during examination depending on the time of fluid
accumulation. The classic signs in cardiac tamponade are included in Beck’s triad of
hypotension, jugular venous distension, and muffled heart sounds. Other clinical signs in
a patient with cardiac tamponade include tachycardia, pulsus paradoxus, decreased
electrocardiographic voltage with electrical alternans and an enlarged cardiac silhouette
on chest X-ray with slow-accumulating effusions [8-10].

The pathophysiological and haemodynamic explanation for the above-mentioned findings

is as follows.

During fluid accumulation, left- and right-sided atrial and ventricular diastolic pressures
rise, and equalise the pressure similar to the pericardial sac (20-25 mmHg). The
equalisation is closest during inspiration. Thus, pericardial pressure dictates intracavitary
pressure leading to a progressive decline in cardiac volumes. The decreased preload

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accounts for the reduced stroke volume and compensatory increased contractility, and
tachycardia is not enough to maintain stroke volume, thus leading to reduced cardiac
output. Since the filling pressure in the right side of the heart is lower than in the left side
of the heart, filling pressure increases more rapidly in the right than in the left side of the
heart. Pulsus paradoxus is an abnormal decline (>10 mmHg) in systemic arterial pressure
during inspiration. Normally, the intrathoracic pressure decreases during inspiration which
allows blood to flow easily into the right heart. Conversely, the left heart filling decreases
during inspiration, as the intrapericardial volume is fixed. During expiration, the
intrathoracic pressure increases which leads to less right heart filling and augments filling
of the left heart chambers. When fluid accumulates in the pericardial space, the
intrapericardial pressure increases. This leads to a compression of the right heart,
increasing the right heart pressure. Thus, the right heart filling is now relying more heavily
on the decreased intrathoracic pressures during inspiration to fill, exaggerating the blood
pressure change. The interventricular septum shifts to the left during inspiration and
encroaches on the left ventricle, leading to a further reduction in stroke volume of the left
ventricle [11].

The underlying process for the development of tamponade is a marked reduction in

diastolic filling, which results when transmural distending pressures become insufficient to
overcome increased intrapericardial pressures. Tachycardia is the initial cardiac response
to these changes to maintain the cardiac output.

Systemic venous return is also altered during tamponade. Because the heart is
compressed throughout the cardiac cycle due to the increased intrapericardial pressure,
systemic venous return is impaired and right atrial and right ventricular collapse occurs.
Because the pulmonary vascular bed is a vast and compliant circuit, blood preferentially
accumulates in the venous circulation, at the expense of left ventricular filling. This results
in reduced cardiac output and venous return.

The amount of pericardial fluid needed to impair diastolic filling of the heart depends on
the rate of fluid accumulation and the compliance of the pericardium.

Small effusions are seen posteriorly and are typically less than 10 mm in thickness
(pericardial pressure <10 mmHg). Moderate effusions tend to be posterior and may be
circumferential and are usually 10-20 mm in thickness (pericardial pressure <10 mmHg),
whereas large effusions tend to be circumferential and greater than 20 mm in thickness
(pericardial pressure >15 mmHg).

Symptoms
The symptoms of cardiac tamponade vary with the length of time over which pericardial
fluid accumulates. As depicted in Figure 1, a rapid accumulation of fluid in the
pericardium quickly leads to a steep rise in pericardial pressure, whereas a slower
accumulation of fluid takes longer to reach critical or symptomatic pericardial pressure
[12,13]. Thus, the haemodynamic impact of an effusion ranges from none or mild to
cardiogenic shock which leads to a clinical presentation ranging from acute to subacute.
Acute or rapid cardiac tamponade is a form of cardiogenic shock and occurs within

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minutes. The symptoms are sudden onset of cardiovascular collapse and may be
associated with chest pain, tachypnoea, and dyspnoea. The decline in cardiac output
leads to hypotension and cool extremities. The jugular venous pressure rises which may
show as venous distension at the neck and head. Acute cardiac tamponade is usually
caused by bleeding due to trauma, aortic dissection or is iatrogenic.

Chronic fluid accumulation or subacute cardiac tamponade is characterised by the

patients being more asymptomatic in the early phase but, when the pressure rises above
the pericardial stretch point (Figure 1), they complain of dyspnoea, chest discomfort,
peripheral oedema, fatigue, or tiredness, all symptoms attributable to increased
pericardial pressure and limited cardiac output.

Diagnosis
Prompt diagnosis is the key to reducing the mortality risk for patients with cardiac
tamponade. Although cardiac tamponade is a clinical diagnosis, echocardiography
(Figure 2) provides useful information and is the cornerstone during evaluation
(availability, bedside, and treatment). However, cardiac tamponade is associated with a
variety of abnormalities that lead to changes on the electrocardiogram (ECG), chest X-
ray, and on echocardiography. Abnormalities of tamponade on the ECG are typically low
voltage and electrical alternans. However, reduced voltage can also be seen among other
conditions such as infiltrative myocardial disease and emphysema, whereas electrical
alternans characterised by beat to beat alterations in the QRS complex caused by
swinging of the heart is specific, but not sensitive for tamponade. The chest X-ray reveals
a normal cardiac silhouette until the effusions are at least moderate in size (~200 mL). In
general, an enlarged cardiac silhouette is neither sensitive nor specific for the diagnosis
of cardiac tamponade.

Echocardiographic techniques remain the standard non-invasive method to establish the

diagnosis and can be used to visualise ventricular and atrial compression abnormalities
as blood cycles through the heart [14]. An effusion appears as a transparent separation
between the parietal and visceral pericardium during the cardiac cycle. Physiologic
pericardial fluid may only be visible during ventricular systole, whereas effusions
exceeding 75-100 mL are visualised throughout the cardiac cycle.

Figure 2. Two-dimensional echocardiogram illustrating cardiac tamponade with

right atrium collapse or indentation (arrow).

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The following may be observed with two-dimensional echocardiography:-

1) Early diastolic collapse of the right ventricular free wall

2) Late diastolic compression/collapse of the right atrium

3) Swinging of the heart in the pericardial sac

4) Dilated inferior vena cava with minimal or no collapse with inspiration

5) A greater than 40% relative inspiratory augmentation of blood flow across the tricuspid
valve

6) A greater than 25% relative decrease in inspiratory flow across the mitral valve

7) Septal bounce into the left ventricle during inspiration

Transoesophageal echocardiography is also useful in patients where transthoracic

echocardiography is non-diagnostic. It is typically used in post-cardiac surgery patients
suspected of having loculated effusions containing clots. Additional imaging with magnetic
resonance or computed tomography is normally not necessary to diagnose cardiac
tamponade, but can be used as second-line imaging in cases of complex or loculated
effusions and evaluation of associated or extracardiac diseases or findings. Depending on
the underlying cause of the pericardial fluid, lab test and analysis of the pericardial fluid
can supply diagnostics. However, most effusions are transudate and do not yield the
underlying cause, but it is good practice to analyse the pericardial fluid for white blood cell
count, haematocrit, malignant cells and protein content [14,15].

Treatment
When tamponade is present or threatened, clinical decision making requires urgency, and
the threshold for pericardiocentesis should be low. The treatment of cardiac tamponade is
drainage, preferably by needle paracentesis with the use of echocardiographic or another

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type of imaging, such as fluoroscopy [14,16]. The needle tip is evident on imaging, and
imaging can thus be used to identify the optimal point to perform the centesis [17].
Imaging guidance allows the operator to select the shortest and safest route to the
effusion. Open surgical drainage is normally not necessary, but based upon local
preference and experience, and is desirable if intrapericardial bleeding is present, when
there is a clotted pericardium and if needle centesis is difficult or ineffective. Treatment
should be individualised, and thoughtful clinical judgement is essential. Patients with large
effusions with minimal or no evidence of haemodynamic compromise may be treated
conservatively with careful follow-up and monitoring, and therapy aimed towards the
underlying cause. Thus, patients with apparently idiopathic pericarditis and mild
tamponade could be treated for a period with non-steroidal anti-inflammatory drugs
(NSAID) and colchicine in the hope that the effusion will shrink. The same approach or
strategy could be performed in patients with connective tissue or inflammatory diseases.
Unfortunately, there are no proven effective medical therapies to reduce an isolated
effusion. In the absence of inflammation, NSAID, colchicine and corticosteroids are
generally not effective [14]. Pericardiocentesis alone may be necessary for the resolution
of large effusions, but recurrences are also common, and surgical pericardiectomy or less
invasive options (i.e., pericardial window) should be considered whenever fluid
reaccumulates, becomes loculated, coagulopathy is present, or biopsy material is
required [14]. Loculated effusions due to bleeding are difficult to drain sufficiently with a
closed approach, whereas surgical drainage affords the opportunity to correct the source
of the bleeding.

Once tamponade is diagnosed, management should be orientated toward urgent

pericardiocentesis. Preparing the pericardiocentesis, intravenous hydration and positive
inotropes can be used temporarily, but should not be allowed to substitute for or delay
pericardiocentesis. The risk and benefits of needle centesis should be considered in
patients with anticoagulation therapy or if coagulopathy is present. Mechanical ventilation
should be avoided due to a further decrease in cardiac output [16]. In case of cardiac
arrest due to tamponade, external cardiac compression has limited or no value because
there is little room for additional filling [18].

A triage system has been proposed by the ESC Working Group on Myocardial and
Pericardial Diseases in order to guide the timing of the intervention and the possibility of
transferring the patient to a referral centre [1]. This triage system is essentially based on
expert consensus and requires additional validation in order to be recommended in
clinical practice.

References

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 1. Ristic AD, Imazio M, Adler Y, Anastasakis A, Badano LP, Brucato A, Caforio AL,
Dubourg O, Elliott P, Gimeno J, Helio T, Klingel K, Linhart A, Maisch B, Mayosi B,
Mogensen J, Pinto Y, Seggewiss H, Seferović PM, Tavazzi L, Tomkowski W,
Charron P. Triage strategy for urgent management of cardiac tamponade: a position
statement of the European Society of Cardiology Working Group on Myocardial and
Pericardial Diseases. Eur Heart J. 2014 Sep 7;35(34):2279-84.
2. Imazio M, Gaita F. Diagnosis and treatment of pericarditis. Heart. 2015
Jul;101(14):1159-68.
3. Dudzinski DM, Mak GS, Hung JW. Pericardial diseases. Curr Probl Cardiol. 2012
Mar;37(3):75-118.
4. LeWinter MM. Clinical practice. Acute pericarditis. N Engl J Med. 2014 Dec
18;371(25):2410-6.
5. Imazio M, Cecchi E, Demichelis B, Ierna S, Demarie D, Ghisio A, Pomari F, Coda L,
Belli R, Trinchero R. Indicators of poor prognosis of acute pericarditis. Circulation.
2007 May 29;115(21):2739-44.
6. Reddy PS, Curtiss EI, Uretsky BF. Spectrum of hemodynamic changes in cardiac
tamponade. Am J Cardiol. 1990 Dec 15;66(20):1487-91.
7. Spodick DH. Threshold of pericardial constraint: the pericardial reserve volume and
auxiliary pericardial functions. J Am Coll Cardiol. 1985 Aug;6(2):296-7.
8. Fitchett DH, Sniderman AD. Inspiratory reduction in left heart filling as a mechanism
of pulsus paradoxus in cardiac tamponade. Can J Cardiol. 1990 Oct;6(8):348-54.
9. Bruch C, Schmermund A, Dagres N, Bartel T, Caspari G, Sack S, Erbel R. Changes
in QRS voltage in cardiac tamponade and pericardial effusion: reversibility after
pericardiocentesis and after anti-inflammatory drug treatment. J Am Coll Cardiol.
2001 Jul;38(1):219-26.
10. Spodick DH. Images in cardiology. Truly total electric alternation of the heart. Clin
Cardiol. 1998 Jun;21(6):427-8.
11. Guntheroth WG, Morgan BC, Mullins GL. Effect of respiration on venous return and
stroke volume in cardiac tamponade. Mechanism of pulsus parodoxus. Circ Res.
1967 Apr;20(4):381-90.
12. Ditchey R, Engler R, LeWinter M, Pavelec R, Bhargava V, Covell J, Moores W,
Shabetai R. The role of the right heart in acute cardiac tamponade in dogs. Circ
Res. 1981 May;48(5):701-10.
13. Singh S, Wann LS, Schuchard GH, Klopfenstein HS, Leimgruber PP, Keelan MH Jr,
Brooks HL. Right ventricular and right atrial collapse in patients with cardiac
tamponade--a combined echocardiographic and hemodynamic study. Circulation.
1984 Dec;70(6):966-71.

8/9
 14. Adler Y, Charron P, Imazio M, Badano L, Barón-Esquivias G, Bogaert J, Brucato A,
Gueret P, Klingel K, Lionis C, Maisch B, Mayosi B, Pavie A, Ristić AD, Sabaté Tenas
M, Seferovic P, Swedberg K, Tomkowski W, Achenbach S, Agewall S, Al-Attar N,
Angel Ferrer J, Arad M, Asteggiano R, Bueno H, Caforio AL, Carerj S, Ceconi C,
Evangelista A, Flachskampf F, Giannakoulas G, Gielen S, Habib G, Kolh P,
Lambrinou E, Lancellotti P, Lazaros G, Linhart A, Meurin P, Nieman K, Piepoli MF,
Price S, Roos-Hesselink J, Roubille F, Ruschitzka F, Sagristà Sauleda J, Sousa-Uva
M, Uwe Voigt J, Luis Zamorano J; European Society of Cardiology (ESC). 2015
ESC Guidelines for the diagnosis and management of pericardial diseases: The
Task Force for the Diagnosis and Management of Pericardial Diseases of the
European Society of Cardiology (ESC)Endorsed by: The European Association for
Cardio-Thoracic Surgery (EACTS). Eur Heart J. 2015 Nov 7;36(42):2921-64.
15. Ben-Horin S, Shinfeld A, Kachel E, Chetrit A, Livneh A. The composition of normal
pericardial fluid and its implications for diagnosing pericardial effusions. Am J Med.
2005 Jun;118(6):636-40.
16. Cooper JP, Oliver RM, Currie P, Walker JM, Swanton RH. How do the clinical
findings in patients with pericardial effusions influence the success of aspiration? Br
Heart J. 1995 Apr;73(4):351-4.
17. Callahan JA, Seward JB. Pericardiocentesis Guided by Two-Dimensional
Echocardiography. Echocardiography. 1997 Sep;14(5):497-504.
18. Hashim R, Frankel H, Tandon M, Rabinovici R. Fluid resuscitation-induced cardiac
tamponade. J Trauma. 2002 Dec;53(6):1183-4.

Notes to editor

Authors:

Jesper K. Jensen, MD, PhD; Steen Hvitfeldt Poulsen, MD, DMSc, PhD; Henning
Mølgaard, MD, DMSc

Department of Cardiology, Aarhus University Hospital, Skejby, Denmark

Address for correspondence:

Dr Jesper K. Jensen, Palle Juul-Jensens Blv. 99, Skejby, 8200 Aarhus N, Denmark

E-mail: jesperkjensen@dadlnet.dk

Author disclosure:

None of the authors has any conflicts of interest to declare.

The content of this article reflects the personal opinion of the author/s and is not
necessarily the official position of the European Society of Cardiology.

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