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Stage021’s product range focuses on blending healthcare with advanced technology to enhance patient care. Our medical devices are designed with precision, innovation, and ease of use in mind, enabling healthcare professionals to diagnose, monitor, and treat patients more efficiently.
AGM100
AGM100 is here to enhance your cardiopulmonary diagnostic support by measuring pulmonary gas exchange quickly and non-invasively. In just 90 seconds, it delivers objective insights into a patient’s cardiac and respiratory function through a simple tidal breath sampling procedure, answering key health questions with ease.
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How AGM100 Helps In Better Management of Sarcoidosis
AGM100 Enables Better COPD Care by Early Detection
Hantavirus Infection: From Viral Prodrome to Sudden Pulmonary Decline
End-Tidal CO₂: Key to Detecting Respiratory Diseases
AGM100 for Impaired Gas Exchange Detection in COVID-19
Oxygen Deficit: Key to Early Detection of Respiratory Diseases
What is the AGM100 and how does it work without taking a blood sample?
The AGM100 is a non-invasive pulmonary gas exchange analyser, the first FDA-cleared, CDSCO-approved and WHO-recognised device of its kind. Traditional arterial blood gas (ABG) tests require drawing blood from an artery to measure oxygen and CO₂ levels. The AGM100 achieves equivalent results through a simple tidal breath sampling procedure: the patient breathes normally through a specialised breathing circuit, and the device captures and analyses exhaled air in real time.
Internally, advanced algorithms process the composition of expired gas alongside pulse oximetry (SpO₂) data to derive arterial oxygen partial pressure, a technique grounded in the physiological relationship between alveolar ventilation and blood-gas exchange first formalised by respiratory physiologist Dr John West. The entire process takes under 90 seconds and requires no needles, no lab infrastructure, and no specialised training.
What is Oxygen Deficit, and why is it considered the most important parameter the AGM100 measures?
Oxygen Deficit (OD) is defined as the difference between the partial pressure of oxygen in the alveoli (PAO₂ — what the lung has available) and the calculated partial pressure of oxygen in arterial blood (gPaO₂ — what actually reaches the bloodstream). In a perfectly healthy lung, this gap approaches zero. In a diseased lung, it widens — and the size of the gap directly reflects the severity of gas exchange impairment.
What makes OD uniquely powerful is its sensitivity. A landmark study in the American Journal of Physiology found the mean OD in healthy young adults was just 2.0 mmHg, rising to 7.5 mmHg in healthy older subjects — but jumping to 42.7 mmHg in patients with confirmed lung disease. This sensitivity makes it an early-warning metric capable of detecting impairment before conventional tools like pulse oximetry (SpO₂) register a change.
Clinically, OD has been shown to be elevated in patients who required hospital admission versus those who were safely discharged (55 ± 20 vs. 32 ± 14 mmHg, p = 0.041) and significantly higher in those needing supplemental oxygen (65 ± 9 vs. 30 ± 1 mmHg, p < 0.001). In a prospective study across two academic emergency departments, OD achieved an AUC of 0.98 in predicting which patients required immediate clinical intervention.
The AGM100 derives Oxygen Deficit non-invasively — from expired gas composition and pulse oximetry — in under 90 seconds. No blood draw. No arterial puncture. No lab wait time.
Deriving arterial PO₂ and OD from expired gas and pulse oximetry — Journal of Applied Physiology
What is gPaO₂ (arterial oxygen), what are normal values, and why can the AGM100 estimate it without a blood draw?
gPaO₂ — the partial pressure of oxygen dissolved in arterial blood — is a direct measure of how much oxygen has successfully crossed from the alveoli into the bloodstream. It is one of the most clinically actionable numbers in respiratory medicine: it tells a clinician not just whether a patient is hypoxaemic, but how severe that hypoxaemia is and whether it is likely to be causing end-organ stress.
80-100 mmHg – Normal (Young Adult)
60-79 mmHg – Mild Hypoxemia
40-59 mmHg – Moderate (Oxygen therapy usually needed)
<40 mmHg – Severe – Urgent intervention
Traditionally, measuring gPaO₂ requires an arterial blood gas (ABG) test — an arterial puncture, typically at the wrist — which carries risks of pain, haematoma, arterial spasm, and infection, and requires laboratory processing that delays results by 15–30 minutes. The AGM100 eliminates all of this.
The device uses the physiological relationship between end-tidal alveolar oxygen (measured from expired gas) and arterial oxygen, corrected for CO₂ levels, to calculate gPaO₂ (a derived, non-invasive estimate of PaO₂). Validated in a pivotal multi-institutional study published in CHEST — involving researchers from the University of British Columbia, Duke University, and Bangor University — the AGM100’s gPaO₂ demonstrated near 1:1 correlation with invasive ABG-measured PaO₂ under resting, hypoxic, and exercise conditions.
gPaO₂ is particularly critical in COPD, ARDS, and pulmonary embolism — conditions where a falling gPaO₂ can precede clinical deterioration by hours. The AGM100 makes serial monitoring of gPaO₂ practical for the first time without repeated arterial punctures.
Alveolar Gas Equation and PaO₂ physiology — StatPearls / NCBI
FAQ
Frequently Asked Questions
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