Introduction:
Cardiac
tamponade is the compression of the heart muscle, caused by a build-up of blood
or fluid between the myocardium and the Pericardium, this pressure prevents the
ventricles from fully expanding, which can have a large range of effects on the
body, it effects 2 in 10,000 people in the UK, therefore, medical imaging has begun
to play an important role in diagnosing cardiac tamponade and techniques have
been developed in many of the different imaging modalities to help with this process.
Anatomy
and Physiology of the Heart wall and the Pericardium:
The
heart walls muscle tissues, or myocardium, is composed of specialised
involuntary muscle cells, known as “myocardial cells”, these cells are
grouped in bundles in a connective tissue framework (Tortora, 2011 Pg. 760). Within this framework are; small blood
and lymphatic vessels and autonomic nerve fibres, the density of the
capillaries found in the myocardium is much denser than in skeletal muscle
tissue, according to Wear (1927 Pg. 280) there is one capillary to each muscle
fibre, this is to supply enough oxygen to the muscle so as they can carry out
the many contractions required per minute (average of 60-70 BPM) resulting in a
high requirement of blood and its energy providing nutrients
The Pericardium, consists of
two layers, the outermost fibrous pericardium, and the innermost serous
pericardium, (O'Rahilly 2008)
these two layers encase the entire heart, as well as the cardiac portion of the
great vessels; superior vena cava, Inferior vena cava, Pulmonary arteries,
Pulmonary veins, Aorta (Drake et al. 2010 Pg. 177)
Structure of the Pericardium
in relation to the great vessels (Drake et
al. 2010 Pg. 179) note the pericardium is tightly adhered to the surfaces
of the great vessels.
The fibrous pericardium is
the most external layer, it is made up of tough, inelastic, connective tissue
that resembles a bag and it rests on, and attaches to the diaphragm (Drake et al. 2010 Pg. 177) where it is
partially fused to the central tendon of the diaphragm (O’Rahilly 2008),
meaning that, upon heavy breathing the motion of the heart aids the movement of
blood. The open end of the fibrous pericardium is fused to the connective
tissues of the great vessels
The serous pericardium is
much thinner than the fibrous pericardium and it forms a double layer around
the heart, Drake et al. (2010 Pg.
178) names these layers as the outer
parietal layer and the inner visceral layer ;
The outer parietal layer is made up of connective tissue which is fused to the
fibrous pericardium (Sinclair, 1975 Pg.163), this helps to maintain the
position of the serous pericardium during contractions.
The inner visceral layer,
also known as the “epicardium”, is classed as one of the layers of the heart wall,
(Tortora 2011 Pg. 758). As
it adheres tightly to the surface of the myocardium, sliding smoothly beneath
the parietal layer, with little friction between the two, (Sinclair 1961
Pg.163) due to the pericardial fluid within in space between them (Tortora, 2011 Pg. 758).
Between the two layers in
the “pericardial cavity” is found a thin film (a few millilitres) of serous
fluid (Tortora, 2011 Pg. 758),
this slippery substance, is produced by the pericardial cells of both the
parietal and visceral layers of the serous pericardium, its function is to
reduce friction between the 2 layers when the heart moves.
Pathophysiology of Cardiac
Tamponade:
In classic cardiac tamponade,
the pressure within the pericardial sac increases due to an accumulation of
fluid within the pericardial space (known as a pericardial effusion) (Saito et al. 2008) , as a result of ,this ventricular
diastolic, right atrial and wedge pressures all increase in equal proportions
to the increase in pericardial pressure in an attempt to prevent any chambers
from collapsing,( Blum and Bella, 2012), this equalization of pressure is the “haemodynamic
hallmark” of cardiac tamponade, (Blum and Bella, 2012) however, eventually, if
left un-treated, the pericardial pressure will become greater than the pressure
in the chambers, resulting in chamber collapse of at least one of the cardiac
chambers. (Spodick 2003 Pg. 686)
Also found in cases of
classic cardiac tamponade, the pericardium becomes stretched due to the excess
fluid build-up, (Blum and Bella, 2012) and due to the inelastic nature of the
fibrous pericardium, any increases in pressure within the pericardium can lead
to a greatly exaggerated respiratory variation of the filling of the right and
left ventricles (Spodick 2003 Pg. 685) . During inspiration, the
negative intra-thoracic pressures lead to an increase in the venous return of
blood to the right side of the heart, (Blum and Bella 2012) this leads to an
increase in blood volume in the right side of the heart, which, in turn, exerts
a pressure on the intra-ventricular and intra-atrial septum’s (Restrepo et al. 2007 ), pushing them towards the
left side of the heart, encroaching on the space within the left side of the
heart, this is known as “Ventricular Interdependence” and leads to a decreased
cardiac output with each inspiration.
As there is less
blood in the left ventricle to be transported around the body, a decrease in
systemic blood pressure is often seen in cardiac tamponade cases, if this
decrease in pressure is greater than 10mmHg it is known as the “pulus
paradoxus”. (Blum and Bella 2012)
Cardiac tamponade can also occur when there is localised tamponade without
a generalised effusion throughout the pericardium, in patients with low central
venous pressures, when there is an accumulation of fluid within a stiffened
pericardium or when there is a large pleural effusion which impacts of
ventricular filling, however, these causes are less common than classic Cardiac
Tamponade (Blum and Bella 2012)
Aetiology of Cardiac
Tamponade
Cardiac tamponade is
normally a symptom of one of many different causes, some of which, among
others, include;
·
Dissecting thoracic aortic aneurysm
·
Heart attack
·
Heart surgery
·
Pericarditis (swelling of the pericardium)
caused by infaction
·
Heart tumors
·
Kidney failure (Medline Plus, 2012)
2 in 10,000 people are
likely to suffer from cardiac tamponade at some point in their lives, (Medline
Plus, 2012) however, people who put
extra strain upon their heart; smokers, obese patients for example, who
increase their risk of needing heart surgery or having a heart attack, also
increase their risk of suffering a cardiac tamponade. (University of Maryland
Medical Centre, 2010)
Clinical presentation of
Cardiac Tamponade:
When an effusion has
developed within the pericardial sac over time, there are often few noticeable
symptoms, the patient may complain of dyspnoea (laboured breathing), a dull
pain in the chest, swollen ankles, and some abdominal bloating, (Yarlagadda, 2012) chronic effusions are often detected as an
incidental findings during other imaging of the thoracic cavity.
Acute effusions occur when
there is a rapidly accumulating smaller effusion within the pericardial sac,
acute effusions often present with cardiac tamponade, (Blum and Bella, 2012)
patients present with similar symptoms to that as in chronic effusions with a
few extra symptoms such as elevated neck veins, which are due to the increased
venous return of blood to the heart. (Avşar et al. 2008)
The heart loses its ability
to fully relax and contract due to the increased pressure placed upon it by the
pericardial fluid, there is also often a threatened or actual, collapse within
the circulatory system, (Spodick 2003 Pg.688) normally within the heart itself
due to the increased pressure within the right side of the heart, it is during
an acute effusion that the patient may potentially suffer from “pulsus
paradoxus” (Blum and Bella 2012)
A chest x-ray of an acute
effusion may demonstrate globular cardiomegaly with sharp heart margins, known
as a “waterbottle silhouette” (Restrepo et
al. 2007 ), and an ECG study may demonstrate small complexes and electrical
alternans may be seen (Appendix i). (Restrepo et al. 2007 )
Patients may also present
with;
- Palpitations
- Pale/Grey/Blue
skin
- Dizziness/Drowsiness
(Medline plus 2012)
Imaging studies
On a chest x-ray of a
patient with cardiac tamponade, the cardiac silhouette may be enlarged and it
may or may not present with an epicardial fat pad sign, which would normally
suggest a pericardial effusion (C. S. Restrepo et al. 2007 ) The lungs, are normally clear in cardiac tamponade,
however some causes of cardiac tamponade may have other symptoms affecting the
lungs (Medline plus, 2012). While X-ray is both relatively cheap and quick, chest
imaging with plain film X-ray may not be useful in early cases, as at least
200mL of the pericardial fluid must have accumulated before there is any
enlargement that can be seen on a chest radiograph. (Restrepo et al. 2007 )
Chest x-ray of cardiac tamponade secondary to
tuberculosis
Echocardiography
A transthoracic echocardiogram (TTE) uses ultrasound to capture real time
images of the patients heart (Medline Plus, 2011), in cases with cardiac
tamponade, there can be seen to be restricted contraction and relaxation of the
heart walls due to the increase in pericardial pressure (Lindqvist and Calcuttea and
Henein, 2007), images produced can be either three-dimensional or
two-dimensional depending on the area of the heart that is being imaged and the
typed hardware being used. However,
occasionally the patients; ribs, lungs or other bodily tissues may interfere
with the sound waves meaning a diagnostic image cannot be acquired, in such a
case either IV contrast can be used, or a Transoesophageal
echocardiogram (TEE) is
performed. (Medline Plus, 2011)
During a TEE an ultrasonic scope is inserted down the
patients, anesthetized, oral cavity, the scope can be guided down the esophagus
by a radiologist to acquire a clearer image of the patient’s heart. (Bupa,
2012)
Showing collapse of the
right ventricle suggestive of cardiac tamponade (Chatterji, 2009)
|
|
(Avşar et al. 2008)
Whilst echocardiography still remains the gold standard for evaluating pericardial disease,
Computed Tomography gives the advantage of a larger field of view (Restrepo et al. 2007 ),
allowing for assessments of the entire chest, and detection of any associated abnormalities
in the surrounding tissues (Restrepo et al. 2007 ), CT also has the added benefit of being
less operator dependent and, due to the ever increasing resolution of multi-detector
CT scanners (http://old.ctisus.com/multidetector/syllabus/multidetector_article1.html, no date),
acquiring high-quality motion-free images of the pericardium is easier particularly beneficial
with patients who have a limited breath-hold capacity.
CT provides information about the nature of some of the
underlying causes of Cardiac Tamponade, such as pericardial effusions, by using
the attenuation measurements of the fluid collecting in the pericardial cavity.
(Restrepo
et al. 2007), (Appendix 1)
 |
Cardiac Tamponade in a male who
complained of shortness of breath,
Axial CT shows a large pericardial
Effusion. (Restrepo et al. 2007 ), |
 |
Cardiac Tamponade in a
patient following a
RTA, Contrast CT shows a bowing of the interventricular
septum towards the left ventricle, and a
large pericardial effusion (Restrepo et al. 2007 ),
|
 |
Non-Hodgkin lymphoma patient presented
with cardiactamponade, Non-Contrast CT
shows concave deformity of anterior wall of
right ventricle, and a moderate-sized
pericardial effusion,
(Restrepo et al. 2007 ),
|
 |
Cardiac tamponade in a patient with pericardial
metastasis, Contrast CT
shows a large pericardial
fluid collection with a single solid metastatic
nodule (Restrepo et al. 2007 ),
|
Magnetic Resonance Imaging (MRI) allows pericardial
effusions to be detected with a very high sensitivity (Restrepo
et al. 2007) with the ability to gather signals from fluid collections
as small as 30 mL, however, due to the potential acute onset, and life-threatening
nature of the condition (J.P. Surg, 1998), MRI has a limited role in diagnosing
cardiac tamponade, although, there have been cases of imminent cardiac
tamponade and cardiac rupture that have been discovered as incidental findings
(J.H. Sohn et al. 2005 Pg. 448), the
heart may have a “paradoxical septal bounce”, which can easily be seen on short
or long-axis MR images. (Restrepo
et al. 2007)
 |
Patient referred for cardiac MRI to investigate suspected
pericarditis, MRI scan shows a large pericardial effusion
and classic signs of cardiac tamponade with right ventricular
and right atrial diastolic collapse (Restrepo
et al. 2007) |
Summary
Cardiac tamponade is a rare heart complication, caused by an acute
pericardial effusion, its main impact is the increased pressure upon the heart
muscle, reducing its ability to contract and relax, it can also cause cardiac
chambers to collapse. Diagnostic imaging plays an important role in diagnosis
of cardiac tamponade, as well as the possible causes behind it, with
echocardiography being the “gold standard” for diagnosis, despite Computed
Tomography’s ever increasing detail.
References:
Bruch, C., Schmermund, A.,
Dagres, N., Bartel, T., Caspari, G., Sack, S., Erbel, R. (2001) ‘Changes in QRS
voltage in cardiac tamponade and pericardial effusion: reversibility after
pericardiocetesis and after anti-inflammatory drug treatment’ Journal of the American College of
Cardiology, 38, pp.219-226 [Online] DOI: 10.1016/S0735-1097(01)01313-4
(Accessed : 21st January 2013)
Drake, R.L., Vogl, A.W.,
Mitchell, A.W.M. (2010) Gray’s Anatomy
for students. 2nd edn. Philadelphia: Churchill Livingstone
Elsevier.
Friedman, H.S., Gomes, J.A.,
Tardio, A.R. Haft, J.I. (1974) ‘The electrocardiographic features of acute
cardiac tamponade’ Circulation – Journal
of the American Heart Association, 50, 260-265 [Online] DOI:
10.1161/01.CIR.50.2.260 (Accessed: 15th January 2013)
Restrepo, C. S., Lemos,
D.F., Lemos, J.A., Velasquez, E., Diethelm, L., Ovella, T.A., Martinez, S.,
Carrillo, J., Moncada, R., Klein, J.S. (2007) ‘Imaging Findings in cardiac
tamponade with emphasis on CT’ RadioGraphics
Journal, 27 pp. 1595-1610. [Online] DOI: 10.1148/rg.276065002
Saito, Y., Donohue, A.,
Attai, S., Vahdat, A., Brar, R., Handapangoa, I., Chandraratna, P.A. (2008)
‘The syndrome of cardiac tamponade with “small” pericardial effusion’, Echocardiography, 25, pp 237-351.
[Online] DOI: 10.1111/j.1540-8175.2007.00567.x. (Accessed 19th
January 2013)
Sinclair , D. (1975) An introduction to functional anatomy. 5th
edn. Holland: Blackwell Scientific publications
Sohn,
J.H., Song, J.W., Seo, J.B., Do, K.H., Lee, J.S., Kim, D.K., Song, K.S., Lim,
T.H. (2005) ‘Pericardial rupture and cardiac herniation after blunt trauma: a
case diagnosed using cardiac MRI’ The
British Journal of Radiology, 78, pp. 447-499. [Online] DOI:
10.1259/bjr/31146905 (Accessed: 29th January 2013)
Surg, J.P. (1998) ‘Cardiac
tamponade: a rare but life-threatening complication of central venous catheters
in children.’ Department of Paediatric
surgery, University Hospital of Nijmegen 33(12), pp. 1822-4 [Online].
Available at: http://www.ncbi.nlm.nih.gov/pubmed/9869062
(Accessed: 21st January 2013)
Tortora, G.J., Derrickson,
B. (2011) Principles of anatomy and
physiology. 13th edn.Aisa: John Wiley and Sons
Appendix 1
ECG
An Echocardiogram of a patient’s heart who is suffering from cardiac tamponade may have changes in all 4
main sections of the ECG (Friedman, 1974 Pg. 261-262);
P wave voltages are either maintained, or will increase,
and in the majority of cases the p wave contour will become peaked however, the
appearance of an atrial rhythm prior to the electromagnetic dissociation
develops could obscure any P wave changes, the increase of P wave voltage
normally correlates with the change in venous pressure, but this is not true in
all cases. (Friedman, 1974 Pg.261)
The mean QRS complex axis shifts towards the left and
upwards when fluid is added to the pericardial space ( Friedman, 1974
Pg. 262), these shifts quickly reverse upon removal of the fluid, electrical
alternans of the QRS complex can sometimes be demonstrated due to the movement
of the heart within the pericardial fluid. (Lau, 2002, Pg. 66)
Often, one of the first changes on an ECG of a patient
with cardiac tamponade is the deep T wave inversions (Friedman, 1974 Pg. 260),
this is often seen within the first 2-3 beats after the start of the fluid
buildup (Friedman, 1974 Pg. 262), however, T wave changes do not appear to
alter depending on the amount of fluid within the pericardial sac.(
Friedman, 1974 Pg. 262)
In some cases, there can sometimes be ST segment changes
noted, either becoming elevated or depressed, however, these changes are only
seen after prolonged hypotension. (Friedman, 1974 Pg. 262),
