Transition from sinus rhythm to atrial fibrillation - A mechanism inducing or delaying pulmonary congestion and edema

Cardiogenic pulmonary edema (PEd) is a life-threatening condition where fluid accumulates in the lungs due to increasing hydrostatic pressure building up in the pulmonary vasculature (PV): veins, venules and capillaries. Atrial fibrillation (AF) is accepted as an arrhythmia which triggers and promotes the pathophysiological processes leading to pulmonary congestion and its final expression: PEd. We propose a different view, where AF is actually a physiological solution temporarily protecting from PEd. We hypothesize that the compliance of the left atrium (LA) increases with the onset of AF. Thus, it is possible that even if the volume of blood within the LA increases due to loss of atrial contraction, the pressure within the LA would still be lower than that prior to AF (because of the increased LA compliance during AF). Decreased LA pressure allows more blood to flow from the PV to the LA, abating the hydrostatic pressure buildup in the PV compartment. The ratio, R, between the LA volume gained from the transition to AF provided by the greater LA compliance, and the volume of blood retained in the LA due to loss of atrial contraction, determines the instant pressure in the LA, as AF begins. If R is >1, then the LA pressure will instantly decrease with the transition to AF and this may be beneficial in delaying PEd.