You are most welcome. Busy prepping the medical school course. Looking forward to ramping up production in the Spring. Best of luck, HS

That is a fabulous point! You'll have to think in terms of a 'leathery' heart/pericardium in constrictive disease compared to tamponade, where the heart is in a fluid filled. Although there is entrapped, the septum is still 'expansile (or rubbery)' Again, fabulous point in the sense that constrictive pericarditis is a disease of the pericardium, not the heart per se. Yet, if you consider external beam radiation as the prototype, you can envision that leathery septum. Finally, and in fairness, I've discussed this with cardiologists who have a tough time reconciling Kussmaul's in constrictive pericarditis v tamponade so it is okay to use your imagination a little bit (and appreciate that the NBME likes this little nugget). Thank you so much for the consideration...HS

Not positive I understand the question but the appearance/disappearance of pulse (pressure) relates to increased venous return to the right heart but only during inspiration (i.e. lower intrathoracic pressure). That increased volume of blood is entering the right ventricle, which would normally expand 'outwardly' (e.g. picture an enlarging RV accommodating more blood). If the right ventricle can't expand outward (due to the high pericardial pressure in tamponade), it must expand into the space occupied by the LV (i.e. bowing of the IV septum). The process of 'occupying' the LV territory results in decreased LV output, reflected by decreased pulse/pressure during systole BUT this only occurs during inspiration (when the RV is accommodating the larger blood volume). In tamponade, it is a zero sum gain. The RV/LV are working in a confined space (e.g. tamponade physiology). If more blood goes to one chamber (i.e. RV during inspiration), less blood must go to the other. Inspiration favors filling of the RV; expiration favors filling of the LV. It is all related to intrathoracic pressures during respiration and venous return. OK?

Yes, you are correct. It looks like I was describing them as components of the triad, rather than defining the triad per se. I don't know why I didn't just spell out the triad as you describe BUT I am a creature of habit and don't dig eponyms. As the recording highlighted, 'they won't ask you what the triad is, rather they will...' essentially set you up with pulsus paradoxus. So thank you, you are correct (and 6000 viewers later, you are the first to make mention!). I do appreciate your feedback. Best of luck with your studies, HS

Why is Kussmaul sign absent?

A very confusing concept for students. Best way to answer it is with this question: Why is pulsus paradoxus (PP) present? Right...PP is present as a result of blood returning to the right heart, with bowing of the septum that reduces cardiac output (CO) in the left ventricle. So, by definition, blood is returning to the heart and is accommodated at the expense of the LV. Kussmaul's, but definition, is paradoxical distension of the jugular vein during inspiration because the blood can NOT return to the heart. So in tamponade, there is definitely JVD but with inspiration it does not get worse (compared with constriction which cannot accommodate the additional venous return with inspiration). If you consider the pathophysiology of PP in the setting of tamponade, absence of Kussmaul's makes sense. Subtle point but it is testworthy. Best of luck, HS

@@HowardSachs12DaysinMarch thanks. makes sense

Not quite following the question...jugular venous distension (JVD) = elevation of the central (jugular) venous pressure. I have become aware, over the years, that students aren't necessarily on board with the hundreds of medical abbreviations that we use daily (and take for granted). I try to avoid abbreviations with newer material (but its almost impossible!). You will be using abbreviations with your medical students one day. Best of luck, HS

@@HowardSachs12DaysinMarch thank you so much sir