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.
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‑: A Novel Classification and Therapeutic Framework for Acute Respiratory Dysregulation Hyperventilation 5 VOSTFR-
| 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 |
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. Patients were stratified using the VOSTFR‑ scoring system
[Your Name], MD, PhD¹; [Co‑author Name], MD²; [Co‑author Name], PhD³
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 PhD³ ¹ Department of Pulmonary Medicine
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.
[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.
Baseline characteristics were balanced (Table 1).
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.
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‑: A Novel Classification and Therapeutic Framework for Acute Respiratory Dysregulation
| 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 |
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
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
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.
[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.
Baseline characteristics were balanced (Table 1).