Saturday, 23 February 2013

So i was bored

And ended up looking at my stats for this,
they've slowed down a bit but so have my posts :P
still, over 200 this month so i'm happy


but put together a pie chart of my views per browser, shocked to see chrome on top (i'm a firefox guy)


If you don't use the skills, you lose them :P

Liam
Out!

Cardiac Tamponade with a focus on medical imaging



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:
Avşar, A., Günay, N.K., Çelik, A., Melek, M. (2008) ‘A case of cardiac tamponade caused by tuberculous pericarditis’  Turkish Society of Cardiology [Online] Available at: http://www.tkd.org.tr/english.asp?pg=:dergi/dergi_content&plng=eng&id=1735&dosya=167 (accessed: 17th January 2013)

Bella, J., Blum, L. (2012) Cardiac Tamponade – Pathophysiology Available at: http://bestpractice.bmj.com/best-practice/monograph/459/basics/pathophysiology.html (Accessed: 16th January 2013)

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)

Chatterji, A. (2009) ‘An unusual cause of pericardial tamponade ‘ Scottish medical Journal  54(1) pp. 58 [Online]. Available at: http://www.smj.org.uk/0209/pericardial%20cr5.htm (Accessed: 22nd 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)

Lau, T.K., Civitello, A.B., Hernandez, A., Coulter, S.A. (2002) ‘Cardiac Tamponade and Electrical Alternans’  Texas Heart Institute 29(1) pp. 66-67 [Online] Available at: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC101278/pdf/20020300s00020p66.pdf (Accessed 25th January 2013)

Medline Plus (2012) Cardiac Tamponade Available at: http://www.nlm.nih.gov/medlineplus/ency/article/000194.htm (Accessed: 18th January 2013)

Medline Plus (2011) Echocardiogram Available at: http://www.nlm.nih.gov/medlineplus/ency/article/003869.htm (Accessed: 19th January 2013)
O’Rahilly, R., (2008) Chapter 23: The Pericardium and the heart. Available at: http://www.dartmouth.edu/~humananatomy/part_4/chapter_23.html (Accessed 18th 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)

Spodick, D.H., (2003) ‘Acute Cardiac Tamponade’ The New England Journal of Medicine 349(7) pp. 684 – 690 [Online] Available at: http://www.uthsc.edu/cardiology/articles/cardiac%20tamponade.pdf (Accessed: 18th 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
University of Maryland Medical centre (2010)  Cardiac Tamponade – All Information Available at: http://www.umm.edu/ency/article/000194all.htm (Accessed : 14th January  2013)

Wearn, J.T, (1927) ‘The extent of the capillary bed of the heart’ Pp. 13-16 [Online]. Available at: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2131359/pdf/273.pdf (Accessed: 25th January 2013)

Yarlagadda, C. (2012) Cardiac Tamponade Clinical Presentation. Available at: http://emedicine.medscape.com/article/152083-clinical (Accessed: 7th February  2013)


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),