Cardiac
tamponade: a clinical challenge 
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.
Topic(s):
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 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 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 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).
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 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.
