14:29 In constrictive pericarditis, if the interventricular septum is able to bulge toward right ventricle to compensate the inability of pericardium diastole (JUST LIKE tamponade), why is Kussmaul sign present?? I'm genuinely confused.
Yeah, took me a while to figure that one out. The bulging septum in constrictive pericarditis reflects blood returning to the RV against fixed filling pressures (as with tamponade). But why Kussmaul's? Simply put, in constrictive pericarditis, the blood returning from the IVC displaces blood returning from the SVC. Whereas inspiration reduces intrathoracic pressure, it increases intra-abdominal pressure. In this manner, Kussmaul's behaves similar to hepatojugular reflux. In tamponade, if you will, the bulging septum permits (accommodates) RV filling from both the SVC and IVC. I know it is confusing. The sentinel paper on Kussmaul's comes from a cardiologist on UMass staff (Theo Meyer). The paper is entitled 'Mechanism underlying Kussmaul's sign in chronic constrictive pericarditis' was published in the AJC in Nov 1989. The distinction between tamonade and constriction continues to be defined in the Q-banks but this subtle distinction. Not so sure the NBME harps on this fact but it is worth hanging onto. Thank you for the note. 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
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
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
Viciously intelligent , thanks much for taking the time to make these awesome videos
Thanks a ton! You explained the absence of Kussmaul's sign in tamponade so well and clear! :)
Very great sir…… Thanks a lot
WOW. yes. thank you. this is so helpful for USMLE questions!
lol the beginning, "if you order now...jk" lol had me laughing!
Thank you for the simple and easy to understand videos. =)
WONDERFUL YOU NAILED IT
14:29 In constrictive pericarditis, if the interventricular septum is able to bulge toward right ventricle to compensate the inability of pericardium diastole (JUST LIKE tamponade), why is Kussmaul sign present?? I'm genuinely confused.
Yeah, took me a while to figure that one out. The bulging septum in constrictive pericarditis reflects blood returning to the RV against fixed filling pressures (as with tamponade). But why Kussmaul's? Simply put, in constrictive pericarditis, the blood returning from the IVC displaces blood returning from the SVC. Whereas inspiration reduces intrathoracic pressure, it increases intra-abdominal pressure. In this manner, Kussmaul's behaves similar to hepatojugular reflux. In tamponade, if you will, the bulging septum permits (accommodates) RV filling from both the SVC and IVC. I know it is confusing. The sentinel paper on Kussmaul's comes from a cardiologist on UMass staff (Theo Meyer). The paper is entitled 'Mechanism underlying Kussmaul's sign in chronic constrictive pericarditis' was published in the AJC in Nov 1989.
The distinction between tamonade and constriction continues to be defined in the Q-banks but this subtle distinction. Not so sure the NBME harps on this fact but it is worth hanging onto.
Thank you for the note. HS
This was amazing. Thank you!
Amazing lecture !!!!!!
Why can’t the interventricular septum bulge into the left ventricle in constrictive pericarditis? Wouldn’t that eliminate kussmauls sign?
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
Hi, I don’t understand the part at 7:37 where the sound is heard at expiration and then later throughout.
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?
thank you!!
Thank you , very helpful
You are most welcome. Busy prepping the medical school course. Looking forward to ramping up production in the Spring. Best of luck, HS
AMAZING THANK ALOT FOR HELP
Awesome
that intro got me dying lol
Isn't Beck's Triad JVD, hypotension, and muffled heart sounds?
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
nice
Jvd?
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
Awesome