| Axis | Measurement | Equipment | Scoring (0‑3) | |------|-------------|-----------|--------------| | V | VE (L/min) via portable metabolic cart | COSMED K5 | 0 ≤ 15, 1 = 15‑25, 2 = 25‑35, 3 > 35 | | O | RRV (SD of inter‑breath intervals) | Respiratory inductance plethysmography | 0 ≤ 0.1 s, 1 = 0.1‑0.3 s, 2 = 0.3‑0.5 s, 3 > 0.5 s | | S | HR and plasma norepinephrine (point‑of‑care assay) | ECG & handheld assay | 0 ≤ 80 bpm & < 200 pg/mL, 1 = 80‑100 bpm or 200‑400 pg/mL, 2 = 100‑120 bpm or 400‑600 pg/mL, 3 > 120 bpm or > 600 pg/mL | | T | Forehead skin temperature & sweat rate (micro‑sweat sensor) | Infrared thermometer & wearable sensor | 0 ≤ 0 mg/min, 1 = 0‑5 mg/min, 2 = 5‑10 mg/min, 3 > 10 mg/min | | F | PaCO₂ (ABG) | Portable blood gas analyzer | 0 = 30‑35 mmHg, 1 = 25‑30 mmHg, 2 = 20‑25 mmHg, 3 < 20 mmHg |
A multicenter, observational–interventional study was conducted across three tertiary hospitals (n = 312). Patients were stratified using the VOSTFR‑ scoring system (0‑20 points) based on bedside physiological measurements and validated questionnaires. Axis‑specific interventions (e.g., controlled rebreathing for “Ventilatory,” beta‑blockade for “Sympathetic,” evaporative cooling for “Thermoregulatory”) were administered to a randomized sub‑cohort (n = 156). Primary outcome: time to normalization of arterial PaCO₂ (35–45 mmHg). Secondary outcomes: symptom resolution, length of emergency department (ED) stay, and adverse events. Hyperventilation 5 VOSTFR-
[Your Name], MD, PhD¹; [Co‑author Name], MD²; [Co‑author Name], PhD³ | Axis | Measurement | Equipment | Scoring
To validate the 5 VOSTFR‑ model in a prospective cohort of adult patients presenting with acute hyperventilation and to assess the efficacy of a targeted, axis‑specific therapeutic algorithm. Primary outcome: time to normalization of arterial PaCO₂
The VOSTFR‑ score demonstrated excellent discriminative ability for underlying mechanisms (AUC = 0.89, 95 % CI 0.85–0.93). Axis‑specific treatment reduced median time to PaCO₂ normalization from 18 min (standard care) to 9 min (intervention) (p < 0.001). Symptom resolution within 30 min occurred in 84 % of the intervention group versus 56 % of controls (RR = 1.50, 95 % CI 1.23–1.83). No serious adverse events were observed.
[Your Name], MD, PhD Email: your.email@university.edu Abstract Background: Hyperventilation is a common physiologic response to metabolic, psychogenic, and neurologic stressors. Existing classifications lack granularity in distinguishing sub‑phenotypes that differ in pathophysiology, clinical presentation, and response to therapy. The “Hyperventilation 5 VOSTFR‑” (Ventilatory‑Oscillatory‑Sympathetic‑Thermoregulatory‑Respiratory) framework proposes five distinct mechanistic axes to better characterize acute hyperventilatory events.
The Hyperventilation 5 VOSTFR‑ model provides a robust, physiologically grounded classification that enables rapid, targeted therapy, markedly shortening the time to biochemical and clinical recovery. Implementation in emergency settings may improve patient outcomes and reduce resource utilization.
