The causal hemodynamic audit for surgery.
Per-subject neural-ODE physiological estimator. Reads continuous intraoperative physiology — arterial waveform or NIBP cuff, ECG, pleth, capnography, drug record — and classifies the causal endotype driving each hypotension event. The data layer the field has been missing.
The current AI-in-healthcare stack splits two ways. The first wave — Abridge, Nuance DAX, Hippocratic AI, Glass — runs language models over clinical notes for scribing, billing, and summary generation. Useful documentation products. They never see physiology. The second wave — gradient-boosted and transformer time-series predictors like Edwards's HPI, the only FDA-cleared example in intraoperative care — has two structural problems. First, it only runs on Edwards's proprietary HemoSphere monitor + Acumen IQ sensor: capital purchase per OR, per-case disposables, and gated to invasive-arterial-line cases — a small fraction of US ORs and zero ambulatory surgery centers. Second, even where it does run, it pattern-matches on waveform surface signals to predict BP will drop in 15 minutes — without modeling the cardiovascular physics underneath. It can warn that something is coming, but it can't say why, and a warning without a cause doesn't change what the clinician does.
Each year ~30 million U.S. patients undergo surgery, and roughly half develop intraoperative hypotension at clinically meaningful thresholds (MAP <65 mmHg). The AKI, myocardial injury, prolonged stays, and SNF discharges that follow drive tens of billions of dollars in direct cost and a large share of anesthesia malpractice claims. The largest randomized trial to date — IMPROVE-multi, n=8,520 — just confirmed that better blood-pressure targeting alone doesn't reduce any of those outcomes. The number isn't enough.
The reason is structural. The same low BP number is driven by four physiologically distinct causes, each requiring a different clinical intervention. Clinicians already reason in mechanism, not in numbers — case-by-case, at the bedside. What's missing is the comprehensive record: retrospective detection of every intraoperative event from the lead-up vital-sign changes, the interventions delivered in response, and the surrounding labs that captured the downstream impact — attributed to the cause that drove it. That is the quality-improvement, safety, and care-optimization layer this product is.
Treatment: vasopressor (phenylephrine, vasopressin)
Treatment: volume (crystalloid / colloid / blood)
Treatment: inotrope (epinephrine, dobutamine)
Treatment: chronotrope (atropine, ephedrine, pacing)
Sources: Sessler et al., IMPROVE-multi (2026). Walsh et al., Anesthesiology 2013. Bijker et al., Anesthesiology 2009.
Anesthesia groups upload existing case data; we return the comprehensive record of what drove every intraoperative event in their last quarter — the QI, safety, and care-optimization documentation quality committees, malpractice carriers, and value-based-care contracts actually need.
Every intraoperative event reconstructed from its full context: vital-sign trajectories, the interventions delivered in response (drug record, fluids, pressors, inotropes), and the surrounding labs (creatinine, troponin, lactate, ABG). Returns per-case cause attribution, site-level pattern reports ("63% of last quarter's IOH-driven AKI was vasodilation-mediated, clustered in long cases with high MAC + propofol"), clinician-level outlier identification, and defensible QI, safety, and care-optimization documentation. Three things shift downstream: site protocols change, individual practice patterns change, malpractice/regulatory exposure drops.
The audit relationship and the dataset it produces unlock a pre-op risk stratifier downstream — also under the FD&C Act §520(o)(1)(E) CDS carve-out, no 510(k) required. Same QI / safety / care-optimization category. Ships after the wedge wins, not before.
The audit covers the full intraoperative emergency catalog — not just hypotension. Events from the Stanford EPIC manual the audit identifies:
ETCO2 waveform morphology change, peak inspiratory pressure rise, SpO2 lag against ventilation, recent drug exposure (β-blockers, NSAIDs in atopic patients), induction agent.
Distinguishes IgE-mediated reaction (timing post-induction agent, skin signs, biphasic course) from inflammatory vasoplegia (long bypass, high-MAC, sepsis prior). Different cause, identical pressor response.
Tension pneumothorax vs. pulmonary embolism vs. cardiac tamponade. Same presentation, different intervention, different fatal-if-wrong window. ETCO2 trajectory + ventilation pressure + position resolves it.
Cardiovascular collapse + neurologic signs after regional block dosing. Drug record + timing + bupivacaine-specific QRS-widening signature. Catches under-recognized cases that drive the malpractice tail.
Healthcare reimbursement is moving off volume and onto outcomes. Hospitals and the anesthesia groups that staff them now carry direct financial exposure for the post-op complications that intraoperative hypotension drives — AKI, MI, prolonged length of stay, SNF discharges, 30-day readmissions. Three CMS programs already put that exposure on the books:
Mandatory January 2026. ~700 hospitals on the hook for the full 30-day cost of major surgical episodes (lower-extremity joint replacement, CABG, hip/femur fracture, spinal fusion, major bowel). Post-op complications eat the bundle.
1% Medicare withhold for bottom-quartile performers on hospital-acquired conditions. On a hospital with $100M of Medicare revenue, that's ~$1M/year of straight penalty for being on the wrong side of the curve.
Voluntary bundled payments across 30+ surgical episode types. Hospitals carry full financial risk for the complete episode. Anesthesia-driven complications eat the bundle margin first — one bad case can flip an episode from positive to negative.
Anesthesia is the highest-severity claim line in medicine. IOH-driven AKI and myocardial injury sit at the top of the catastrophic-claim distribution. Carriers price coverage on group-level risk profile; defensible cause-attribution moves the actuarial inputs.
The audit converts that exposure into something a quality committee can act on: which cases drove which complications, which causal pattern clustered where, which protocol changes would have prevented the events that incurred the penalty. That is why anesthesia groups and hospitals will pay for the wedge product today — the audit is a budget defense, not a research tool.
Sources: CMS TEAM Final Rule (CMS-1808-F, August 2024). HAC Reduction Program (Section 3008, ACA). BPCI-A program documentation. Anesthesia Quality Institute (AQI) closed-claims analysis 2022.
That substrate powers the retrospective audit shipping today, the prospective stratifier downstream, and the broader QI / safety / care-optimization tools the audit relationship and dataset unlock. CF2 is the architecture: a 63,975-parameter compartmentalized neural-ODE estimator with three compartments — cardio (27 params), respiratory (8), pharmacokinetic (14) — that encode the actual physics of preload, afterload, contractility, ventilation, and drug PK. The encoder is trained once on population data; at inference, it ingests each patient's streaming signals (waveforms, vitals, drug record, labs) and produces per-subject parameter estimates that fit that patient's physiology. Those parameter estimates feed the audit's cause-attribution layer alongside clinical-rule triangulation across vitals, interventions, and labs — CF2's contractility / SVR / preload outputs combined with drug-record timing, SpO2 drift, EKG morphology, and lab markers to assign each event to its driving cause. The model learns physiology. Notes-LLMs and time-series predictors pattern-match on the output of physiology.
On retrospective benchmarks, CF2 outperforms the only FDA-cleared incumbent. HPI remains the relevant scientific benchmark — it's the only FDA-cleared AI predictor in this space — even though it failed to change practice. CF2 reads what the OR already produces — arterial waveform or NIBP cuff, ECG, pleth, capnography, drug record. No new hardware, no proprietary sensor, no per-case disposable. The same trained CF2 model produces per-subject estimates across both signal regimes without retraining; HPI is structurally locked to Edwards's HemoSphere + Acumen IQ in invasive-arterial-line cases. The same model carries from inpatient hospital cases into ambulatory surgery centers — into a regime HPI cannot operate in.
| Dataset | Validation N | Prevalence | AUROC@15min | Brier (Platt-CV5) | Brier Skill Score |
|---|---|---|---|---|---|
| MOVER | 188,370 windows | 44.5% | 0.979 | 0.048 | ~0.81 |
| VitalDB | 47,717 windows | 41.1% | 0.944 | 0.070 | ~0.71 |
| MIMIC-IV | running | running | running | running | running |
| eICU | queued | queued | queued | queued | queued |
Methodology disclosure: prevalence is window-level (samples around hypotension events), not patient-level — standard in the published HPI literature and the rest of the IOH-prediction field. Patient-level intraoperative hypotension base rate is roughly 10–30% per Walsh et al. and Bijker et al. Brier Skill Score >0.7 is publication-grade calibration. Patent: USPTO Provisional App #64/011,899, "Compartmentalized Neural Ordinary Differential Equation System for Dynamical State Prediction," filed 2026-03-20, 109 clauses, sole inventor Anish Joseph.
Land first paid retrospective-audit pilot (Q4 2026). Brier-Platt-CV5 calibration paper submitted. Founders bridge to full-time on seed close.
3–5 paid audit contracts. First annual contract from pilot conversion. AMSO + value-based-care channel conversations open.
Pre-op risk stratifier ships under §520(o)(1)(E) CDS carve-out (no 510(k) required). 10+ annual audit contracts. First TEAM / BPCI-A workflow integrations.
25+ enterprise contracts across audit + stratifier. Malpractice carrier risk-pricing data licenses. The cause-attributed intraop dataset is the durable moat.
Practicing Certified Anesthesiologist Assistant — administers the vasopressors, fluids, and inotropes the model classifies the response to, on the patients in the populations the model is trained on. Sole inventor on the CF2 patent (109 clauses on compartmentalized neural-ODE systems for dynamical state prediction). Co-author on prior peer-reviewed work in neural prosthetics (Biomaterials, Bellamkonda lab GT/Emory, 2015) and developmental neuroscience (Lin Mei lab, GHSU). Erdős Institute alumnus; two more ML publications in progress with Algoverse. The 2013 ASEE paper that originated the LINCR name is mine — Georgia Tech BME, twelve years of continuity to the company name.