Thread by @Thind888

1/ **Septal kinetics in acute cor pulmonale (ACP)**

I'm glad @load_dependent brought this up. I think it's helpful to analyze the mechanistic reasoning behind why 'diastolic' flattening is seen in ACP

In general, septal position depends on the relative RV/LV pressures.

2/
Normally, LV pressures during the entire cardiac cycle are higher than RV pressures so the curvature of septum is towards the RV.

Now let's consider what happens in acute massive PE:
(i) Acute pressure overload results in prolongation of RV systole, compared to LV systole.

3/
This has been shown in multiple clinical studies (e.g. PMID: 19561027), but I have not been able to track down the precise mechanism (?altered calcium cycling with increased afterload).

In any case, this leads to a brief *early-diastolic* septal flattening: first sign of ACP.

4/
(ii) Next, RV function falls due to sudden increase in afterload --> RV stroke volume is decreased --> RVEDV gradually increases over the next few beats.

This is initially helpful as the RV is able to utilize the Frank-Starling mechanism to augment its function.

5/
However, if the increase in RV afterload is severe enough, RVEDV/RVEDP increases drastically. This is why we see a "blown RV" on ECHO in ACP.

This is nothing but "RV volume overload"!

Eventually, RVDP may exceed LVDP --> leading to *pan-diastolic* septal flattening.

6/ However, if the RV is normal at baseline, RV systolic pressure can almost never exceed LV systolic pressure (irrespective of afterload). This is because normal RV architecture is drastically different from LV (thin).

With chronic pressure overload, RV remodeling occurs.

7/ Due to RV eccentric hypertrophy, the thick RV is now able to generate high enough pressures to cause *systolic* septal flattening (RVSP > LVSP) if the afterload is high enough

This is also the rationale behind the 60/60 sign.

(Here's a classic paper on this - PMID: 12421740)