Hey Ven0m,
The way I think about preload is the overall force/relaxation felt by the chamber (in this case the RV in a patient with an ASD), which is often dictated by the overall concentric stress by the cardiac myocytes, often due to the experienced volume state. If a patient has an ASD, the blood will flow from the LA into the RA because like everything in life, the path of least resistance is sought out. The reason why the RV experiences an increased preload is because the increased volume coming in from the LA is already added to the systemic, low O2 blood from the venous return to the R side of the heart. The RA will dump off the increased volume into the RV. This is already leading to an increased volume state on the R side of the heart relative to what is usually experienced. This is the cause of the increased preload felt in the R side of the heart. With an increased volume state, the RV will react by getting gainz, hypertrophy-ing, in an attempt to get the extra volume out to the lungs.
The pulmonary circulation is really sensitive, so pulmonary HTN would occur early with its associated symptoms. The pulmonary HTN goes hand in hand with explaining the increased after load experienced by the RV as it pumps blood to the lungs. Again, this all started out because the increased volume coming into the R heart initially increased the preload while the heart still attempted to get the blood into the lungs. The heart ain't a wimp and knows tissues are depending on it to send out freshly oxygenated blood for perfusion. Eventually this compensation craps out, the RV has hypertrophied as much as it can to handle the increased stress, but the pulmonary HTN coupled with a hypertrophied RV that can hardly relax has gotten so bad that some blood starts to spill over from the R side of the heart to the L side of the heart. Now the path of least resistance is for some of the blood to actually flow from the RA --> LA --> LV. The big worry here is that the patient (often a child) will begin to receive some blood from its cardiac output that has not even seen the lungs--hence, late cyanosis.
Also, it's interesting to note that early on in an ASD, cyanosis is not seen (why it's called late cyanosis). This is because blood coming into the LA via the pulmonary veins is already oxygenated, but since there is a hole in between the LA and RA, blood will simply flow into the R side of the heart and go right back to the lungs, which is useless. However, some of the oxygenated blood does in fact go from the LA --> LV --> body (it doesn't have to flow either/or in an all or nothing fashion), which is enough to prevent cyanosis in the early stage.
