Peripheral edema + *no* intra-thoracic edema + normal LVEF does not always= isolated R.-sided CHF.
Other major culprit? HFpEF!
Why?
First, ⏫ LVEDP (>15 mmHg) causes pulmonary venous HTN...
Other major culprit? HFpEF!
Why?
First, ⏫ LVEDP (>15 mmHg) causes pulmonary venous HTN...
Pulmonary venous HTN results in PA vasoconstriction & a sustained increase in mPAP. This ultimately causes ⏫ RVEDP via high afterload, often w/ RV systolic dysfunction.
The reflex PA vasoconstriction allows right-to-left forward flow in the face of high LVEDP:
The reflex PA vasoconstriction allows right-to-left forward flow in the face of high LVEDP:
High RVEDP causes ⏫ RAP & CVP, which initially causes peripheral edema.
Once LVEDP & pulm venous pressures are roughly >18 mmHg, you see interstitial edema, followed by pulmonary edema at >25 mmHg.
If sustained, b/l pleural effusions begin to accumulate, followed by ascites.
Once LVEDP & pulm venous pressures are roughly >18 mmHg, you see interstitial edema, followed by pulmonary edema at >25 mmHg.
If sustained, b/l pleural effusions begin to accumulate, followed by ascites.
This sequence of events is what allows edematous HFpEF patients to present *without* intra-thoracic edema *early* into their disease's decompensation!
A mind-blowing realization after some @LandsbergManual reading. Not sure how I've made it this far w/o hearing of this...
A mind-blowing realization after some @LandsbergManual reading. Not sure how I've made it this far w/o hearing of this...
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