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 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). To validate the 5 VOSTFR‑ model in a
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. While often benign, severe or prolonged episodes can
The framework proposes a five‑axis model:
Baseline characteristics were balanced (Table 1).
| 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 |