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As far as I remember from my medical school the mechanism of decrease in systolic BP during inspiration was the expantion of lungs that subsequently result in decreased pulmonary venous flow to left atrium and hence to left venticle and thus decreased stroke volume, which results in decrease in systolic BP. However the Kap IM notes explain it another way i.e., there is increased venous flow to right atrium due to negative intrathoracic pressure and this increased amount of blood in the right atrium renders interatrial septum to be pushed to the left atrium and hence decrease the size of left atrial cavity and thereby cause a decrease in systemic systolic BP.

What do u guys think? Is the first mechanism ok or the second or both?:confused::notsure:
 

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pathophysiology

How does the pathophysiology of pulsus paradoxus differ in cardiac tamponade from constrictive pericarditis from asthma.

I understood that of normal systolic pressure decrease in normal inspiration and tamponade but not of asthma and pericarditis
 

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It sounds like normally the first mechanism is in play, i.e. normally the inflation of the lungs is causing decreased LV filling but this is by less than 10mmhg and thus no pulsus paradoxus. However, when restrictive disease mechanisms are at play, such as in restrictive pericarditis, or in obstructive lung diseases due to increased expansion of the lungs, then mechanism two is adding to the decreased LV filling and increasing the difference in systolic BP over 10mmhg = pulsus paradoxus.
 
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