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.
¹ Department of Pulmonary Medicine, University Hospital, City, Country ² Department of Emergency Medicine, University Hospital, City, Country ³ Institute of Clinical Physiology, University of Science, City, Country
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. 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).
| Axis | Physiologic Domain | Representative Markers | |------|--------------------|------------------------| | (Ventilatory) | Central respiratory drive, lung mechanics | Minute ventilation (VE), tidal volume (VT) | | O (Oscillatory) | Respiratory rhythm stability | Respiratory rate variability (RRV) | | S (Sympathetic) | Autonomic tone | Heart rate (HR), catecholamine levels | | T (Thermoregulatory) | Body temperature regulation | Skin temperature, sweat rate | | F (Respiratory) | Gas exchange efficiency | PaCO₂, alveolar‑arterial gradient | To validate the 5 VOSTFR‑ model in a
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.
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. | Axis | Physiologic Domain | Representative Markers
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.
Hyperventilation 5 VOSTFR‑: A Novel Classification and Therapeutic Framework for Acute Respiratory Dysregulation
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.