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How is it possible that you would see BOTH signs with cardiac tamponade and constrictive pericarditis if they are pretty much the opposite processes on inspiration?
The way I think about pulsus paradoxus is its a problem on top of a primary problem-a heart that has difficulty expanding into the pericardial space (i.e.- tamponade or pericarditis), hence when you inspire (the secondary problem) you --> increase VR --> increase filling of the RV which buldges out into the LV and thus you hear anything when a patient inspires when listening for the Kortkoff sounds.
However, in Kussmauls sign, on inspiration, you see an increase in JVP because the VR doesn't return to the heart and instead stays in the jugular vein so you see a rise in JVP...how can both processes coexist in tamponade and constrictive pericarditis?
The way I think about pulsus paradoxus is its a problem on top of a primary problem-a heart that has difficulty expanding into the pericardial space (i.e.- tamponade or pericarditis), hence when you inspire (the secondary problem) you --> increase VR --> increase filling of the RV which buldges out into the LV and thus you hear anything when a patient inspires when listening for the Kortkoff sounds.
However, in Kussmauls sign, on inspiration, you see an increase in JVP because the VR doesn't return to the heart and instead stays in the jugular vein so you see a rise in JVP...how can both processes coexist in tamponade and constrictive pericarditis?
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