LINCR is the causal hemodynamic audit for surgery.
Anesthesia groups upload existing case data, and we return every intraoperative event reconstructed from its full context — vital trajectories, the interventions delivered, the surrounding labs — attributed to the cause that drove it. The model behind it is CF2, our compartmentalized neural-ODE that produces per-subject estimates of intraoperative cardiovascular physics from the signals the OR already collects (arterial waveform or NIBP cuff, ECG, pleth, capnography, drug record), so no new hardware is required.
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. They are useful documentation products that never see the patient's 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 roughly 30 million U.S. patients undergo surgery, and about half develop intraoperative hypotension (IOH) at clinically meaningful thresholds (mean arterial pressure, or MAP, below 65 mmHg). The acute kidney injury (AKI), myocardial injury, prolonged hospital stays, and skilled-nursing-facility (SNF) discharges that follow drive tens of billions of dollars in direct cost and a large share of anesthesia malpractice claims. The published HPI-guided RCTs have shown the same structural result: warning the clinician earlier reduces hypotension duration, but it does not consistently translate into fewer post-operative complications. Knowing the number is about to drop is not the same as knowing what to do about it.
This is a structural problem, and it is not specific to hypotension. The Stanford EPIC manual — the field-standard reference for intraoperative emergencies — catalogs roughly 30 of these events, from anaphylaxis to bronchospasm to obstructive shock to local anesthetic systemic toxicity. They share a common pattern: the same surface presentation can be driven by several different underlying causes, and each cause requires a different clinical intervention. Clinicians already reason in those causal terms, case by case, at the bedside. What hasn't existed is the systematic record across an entire group's caseload: each event reconstructed from the lead-up vital-sign changes, the interventions delivered in response, and the surrounding labs that captured the downstream impact, then attributed to the cause that drove it. That is the quality-improvement, safety, and care-optimization layer LINCR provides.
A drop in blood pressure can be driven by vasodilation, hypovolemia, myocardial depression, or bradycardia. Each cause requires a different drug and a different clinical decision.
Wheezing and a rise in airway pressure can come from an asthma flare, anaphylaxis, aspiration, a mucous plug, or β-blocker effect. The right intervention depends entirely on which one it is.
A sudden hypotensive collapse with tachycardia can be an IgE-mediated allergic reaction or an inflammatory vasoplegia (long bypass, sepsis). The presentation looks identical; the underlying mechanism and durable treatment are not.
A sudden hemodynamic collapse can come from tension pneumothorax, pulmonary embolism, or cardiac tamponade. Each requires a different intervention with a different fatal-if-wrong window.
Sources: Stanford EPIC manual (Goldhaber-Fiebert et al.). HYPE Trial (Wijnberge et al., JAMA 2020) and subsequent HPI-guided RCTs. 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.
What the audit attributes for hypotension events — the wedge chapter, where CF2's AUROC 0.972 validation lives. Each event is assigned to one of four causes, each requiring a different clinical intervention:
Treatment: vasopressor (phenylephrine, vasopressin)
Treatment: volume (crystalloid / colloid / blood)
Treatment: inotrope (epinephrine, dobutamine)
Treatment: chronotrope (atropine, ephedrine, pacing)
The same audit also identifies other intraoperative emergencies from the Stanford EPIC manual covered in Section 02 — bronchospasm, anaphylaxis vs. vasoplegia, obstructive shock differential, LAST — with cause-attribution from the same per-subject estimator + clinical-rule triangulation pipeline.
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 IOH drives — AKI, myocardial infarction (MI), prolonged length of stay, SNF discharges, and 30-day readmissions. Three CMS programs already put that exposure on the books:
The Transforming Episode Accountability Model becomes mandatory in January 2026. Roughly 700 hospitals will be 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.
The Hospital-Acquired Conditions Reduction Program withholds 1% of Medicare payments from bottom-quartile performers. On a hospital with $100M of Medicare revenue, that is roughly $1M per year of straight penalty for being on the wrong side of the curve.
The Bundled Payments for Care Improvement Advanced program covers more than 30 voluntary surgical episode types. Hospitals carry full financial risk for the complete episode — one bad case can flip an episode from positive to negative, and anesthesia-driven complications eat the bundle margin first.
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 a group's overall risk profile, and 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 — with no new hardware, no proprietary sensor, and no per-case disposable. The same trained CF2 model produces per-subject estimates across both signal regimes without retraining, while HPI is structurally locked to Edwards's HemoSphere + Acumen IQ in invasive-arterial-line cases. The same CF2 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.
Trained as a biomedical engineer at Georgia Tech; practicing Certified Anesthesiologist Assistant — administers the vasopressors, fluids, and inotropes the audit attributes 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).
Trained in applied ML at the Erdős Institute; two ML publications in progress with Algoverse. Just completed Techstars Catalyst at Emory University. Founder/organizer of the annual Lifebox Chili Cook-Off fundraiser, supporting Lifebox's global anesthesia training and surgical-safety-checklist mission.