Cardiac tamponade has appeared in the fellowship exam directly in a couple of scenarios; for instance Question 11 from the second paper of 2015 , and Question 15 from the first paper of 2011 where the college asked the candidates to describe how they would perform blind pericardiocentesis.
From peer-reviewed journals, if one had to choose one article it would have to be the NEJM paper by Spodick from 2003. It of course is paywalled. Spodick co-authored a subsequent paper in 2007, which was thankfully published in the somewhat less prestigious Texas Heart Institute Journal, and is therefore free. Unless otherwise stated, most of the information here comes from these two excellent articles. For minutiae regarding the various eponymous physical signs, a great article by Lange et al (1966) is also freely available online.
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The chronicity of the effusion plays a role in tamponade physiology. The pericardium is a fibrous sack which is described as "inextensible", that is to say at any given moment there is little stretch. Ergo, small volumes quickly will give rise to a rapid increase in pericardial pressure, giving rise to tamponade physiology. This produces decreased cardiac output because the stroke volume is limited by the presence of incompressible pericardial fluid. Interaction of respiratory variation in right atrial venous return with this decreased diastolic filling gives rise to all the interesting clinical and echocardiographic signs of cardiac tamponade.
The y descent is usually absent in tamponade because early diastolic blood flow from the right atrium to the right ventricle is impaired by the compressive effect of the surrounding pericardial fluid.
Realistically, these changes are often lost in the noise. Published waveforms (eg. those grainy scans reproduced below from Shabetai et al, 1970) and real bedside observations (on the right) demonstrate that though the a and v components are objectively elevated the whole waveform is elevated by an even greater degree, so that these fine structures are obliterated by the respiratory pressure variation and the "zoomed out" effect of having to scale your waveform into the 20-30 mmHg range.
These images are probably more interesting in their representation of pulsus paradoxus, which will be the next topic of discussion.
For whatever reason, pulsus paradoxus was a dominant feature of Question 11 from the second paper of 2015. The candidates were called upon to define it, and to describe the mechanism by which it occurs. Spodick (2003) defined it as
"an inspiratory systolic fall in arterial pressure of 10 mm Hg or more during normal breathing"
This is also the definition seen in such sources as Wikipedia, UpToDate and LITFL. It differs slightly from the way the college examiners described it in Question 11 :
"an exaggeration (> 12 mmHg or 10%) of the normal inspiratory decrease in systemic blood pressure"
Of course the CICM examiner's definition as definitive as the official Scrabble dictionary. But why is it different and where did they get it? Moreover, how does a 2 mmHg difference in the definition influence management (or marking of your SAQ)? Well. It turns out, 12 mmHg and 9% systolic variation (not 10%) are the 95% confidence limits for diagnosis of moderate or severe tamponade (Curtiss et al, 1988). In the vast majority of patients with these findings, pericardiocentesis increased cardiac output by 50%. 10mmHg is a convenient rounding figure, described by Swami and Spodick (2003) as "a quasi arbitrary but practical level".
So, where is the paradoxus? Apparently, the paradox in the pulsus is the fact that during inspiration (of a spontaneously breathing patient) you can hear the heart sounds but can't feel the radial pulse. The term was coined by Adolf Kussmaul in 1873 on the basis of the observations he made in three patients with constrictive pericarditis (Wagner, 1973).
According to the college examiners, the main mechanism of inspiratory pulsus paradoxus is related to ventricular interdependence.
This importance of right ventricular venous return was demonstrated by Shabetai et al (1970), who found that pusus paradoxus disappeared when the right atrial pressure was kept constant during respiration.
The college examiners also make allusions to other mechanisms in the confusing sentence, "the relatively higher negative pressure in the pulmonary circulation compared to the left atrium in patients with pericardial pathology pooling of blood in pulmonary veins during inspiration resulting in decreased LV stroke volume". This mechanism was well described by Ruskin et al (1973). "It is possible that pooling of blood in the pulmonary veins during inspiration may additionally decrease left ventricular filling and contribute to the paradoxical pulse seen in patients with pericardial tamponade", they wrote. Likely, this pooling occurs due to the decreased intrathoracic pressure in inspiration. The pressure in the thoracic cavity (and thus in the pulmonary circulation) ends up being lower than the pressure in the left atrium, which means that pulmonary venous blood does not feel compelled to flow into the left side of the heart.
Obviously all this is relevant only for the spontaneously breathing patient. In mechanical ventilation, everything is backwards. Positive pressure ventilation decreases preload to the RV, which means the ventricular bulge occurs during expiration. The resulting inspiratory increase in systolic blood pressure has been called "reverse" pulsus paradoxus.
Again, it is something which occurs in all mechanically ventilated patients, but to a lesser extent. The excellent diagram to the left is from the 1979 study by Möller et al. These investigators got a hold of five Cape Chacma baboons (Papio ursinus) and then introduced saline into their pericardia. Saline was added until there was significant pulsus paradoxus and the arterial pressure was halved.The baboons were ventilated using a model 607 Harvard Animal Respirator, which generated a sine-wave inspiratory pressure pattern. The waveforms carefully recorded by the investigators clearly show that whenever pleural pressure was positive, the arterial systolic pressure was at its highest.
In Question 11 from the second paper of 2015, the college wanted trainees to list several methods by means of which one may be able to elicit pulsus paradoxus. If the trainee did not come to the exam with a prefabricated list of such methods committed to memory, a zero mark was virtually guaranteed. The following list is an expansion of the college answer.
Khasnis et al (2002) list the following conditions in which pulsus paradoxus will be absent even in cardiac tamponade:
The college asked for four electrocardiographic findings suggestive of pericarditis with cardiac tamponade, rather than tamponade on its own. Unlike virtually everything else in this chapter, this area can be answered with a single reference. The 1974 article by Howard Friedman describes the echocardiographic features of acute cardiac tamponade in great detail. Another more recent article (Eisenberg, 1996) describes their diagnostic value. These features are as follows are:
Pérez-Casares et al (2017) describes this topic very well.
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Ariyarajah, Vignendra, and David H. Spodick. "Cardiac tamponade revisited: a postmortem look at a cautionary case." Texas Heart Institute Journal 34.3 (2007): 347.
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Friedman, Howard S., et al. "The electrocardiographic features of acute cardiac tamponade." Circulation 50.2 (1974): 260-265.
Eisenberg, Mark J., et al. "The diagnosis of pericardial effusion and cardiac tamponade by 12-lead ECG: a technology assessment." Chest 110.2 (1996): 318-324.
Badiger, Sharan, Prema T. Akkasaligar, and M. S. Biradar. "Electrocardiography–pericarditis, pericardial effusion and cardiac tamponade." International Journal of Internal Medicine1.4 (2012): 37-41.
Pérez-Casares, Alejandro, et al. "Echocardiographic evaluation of Pericardial effusion and Cardiac Tamponade." Frontiers in pediatrics 5 (2017): 79.
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Roy, Christopher L., et al. "Does this patient with a pericardial effusion have cardiac tamponade?." Jama 297.16 (2007): 1810-1818.
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