Hyperventilation 5 Vostfr- -

Hyperventilation, VOSTFR, respiratory physiology, acute care, targeted therapy, ventilatory control 1. Introduction Hyperventilation, defined as an increase in alveolar ventilation that exceeds metabolic CO₂ production, leads to arterial hypocapnia (PaCO₂ < 35 mmHg) and a cascade of neuro‑vascular and metabolic effects (Brown & Smith, 2021). While often benign, severe or prolonged episodes can precipitate cerebral vasoconstriction, tetany, arrhythmias, and, in extreme cases, loss of consciousness (Klein et al., 2020).

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-

Current clinical practice typically categorizes hyperventilation into , metabolic , and neurologic types (American Thoracic Society, 2019). However, this taxonomy does not capture the multidimensional nature of the response, which involves intertwined ventilatory, autonomic, thermoregulatory, and respiratory‐muscle components. Primary outcome: time to normalization of arterial PaCO₂

Each axis can be scored (0 = absent, 1 = mild, 2 = moderate, 3 = severe) yielding a composite (0–15). The suffix “‑” denotes the presence of a dominant axis (the one with the highest individual score) that guides therapeutic priority. physiologically grounded classification that enables rapid

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.

[Your Name], MD, PhD¹; [Co‑author Name], MD²; [Co‑author Name], PhD³

| 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 |