2L Smallest Oxygen Machine for Pregnant Women

During pregnancy, the mother initiates a series of delicate physiological adjustments to accommodate fetal growth and development. Changes in blood volume and respiratory function are crucial factors that affect fetal oxygen supply. This is the core logic behind the precise function of our 2L/30% concentration oxygen concentrator. Its scientific basis can be further analyzed through the following medical mechanisms:

The underlying mechanism of physiological hypoxia during pregnancy: a chain reaction from the mother to the placenta

During the second and third trimesters (after 20 weeks), maternal blood volume increases by 40%-50% compared to pre-pregnancy (approximately 1.5-2L). However, red blood cell production lags behind plasma volume expansion, resulting in a decrease in hematocrit (HCT) by approximately 10% (from 38% pre-pregnancy to approximately 34%), resulting in “physiological anemia of pregnancy.” This “dilution anemia” directly leads to a relative decrease in the blood’s oxygen-carrying capacity: While the normal adult arterial oxygen partial pressure (PaO₂) is approximately 95-100 mmHg, during pregnancy, due to dilution of blood volume, PaO₂ can drop to 85-90 mmHg. If accompanied by mild anemia (Hb <110 g/L), PaO₂ may further drop below 80 mmHg.

At the same time, as the uterus enlarges (the uterine fundus can reach below the xiphoid process in late pregnancy), the diaphragm is pushed upward by 3-4 cm, resulting in a decrease in vital capacity by approximately 20%. Although tidal volume increases (by approximately 30%), respiratory reserve (maximum ventilation) decreases, making the mother susceptible to “inefficient breathing” after even minimal activity—manifested by a temporary drop in arterial oxygen saturation (SpO₂) (below 95%). This fluctuation is directly transmitted to the placenta.

The placenta serves as the fetus’s sole oxygen delivery hub. The oxygen partial pressure difference between maternal blood in the intervillous space and fetal umbilical cord blood is the core driving force for oxygen diffusion (according to Fick’s law: oxygen transport capacity = placental blood flow × oxygen partial pressure difference). Under normal circumstances, maternal uteroplacental blood flow is approximately 600 ml/min, while fetal umbilical artery blood flow is approximately 400 ml/min. Gas exchange occurs between the two via the chorionic plate: maternal blood PaO₂ is approximately 80-90 mmHg, while fetal umbilical venous PaO₂ is only 25-30 mmHg. This pressure difference of approximately 50-60 mmHg ensures continuous oxygen diffusion to the fetus. However, when maternal PaO₂ drops below 80 mmHg due to the aforementioned physiological changes, this “diffusion gradient” is significantly reduced, directly causing the fetal umbilical artery oxygen saturation (SaO₂) to drop from the normal 70%-75% to below 65%, triggering a chain reaction of fetal tissue hypoxia.

Precision Intervention with Oxygen Concentrators: Targeted Improvement of Maternal PaO₂ to Fetal Oxygen Delivery

Inhaling 2 L/min of 30% oxygen-enriched gas (the oxygen concentration in air is 21%) through a nasal cannula can elevate the maternal inspired oxygen fraction (FiO₂) to approximately 30%. Through alveolar exchange, this can steadily increase the maternal arterial PaO₂ by 10-15 mmHg (from 80 mmHg to 90-95 mmHg). This seemingly modest increase can have a “multiplier effect” on placental oxygen transport:

According to clinical research data, for every 10 mmHg increase in maternal PaO₂, the oxygen partial pressure difference between the placental intervillous space and fetal umbilical cord blood increases by 8-10 mmHg. Combined with stable uteroplacental blood flow (600 ml/min), this can result in a 3-5% increase in fetal umbilical artery SaO₂ (from 65% to 68-70%). This improvement is not a “quantitative change”, but a “qualitative change” that directly affects the metabolism of fetal tissues – the efficiency of aerobic metabolism (glucose → ATP) of important organs such as the fetal myocardium and brain can be increased by 15%-20%, and the accumulation of anaerobic metabolic products such as lactic acid is reduced, fundamentally reducing the risk of “fetal growth restriction (FGR)” caused by chronic hypoxia (clinical data show that when the mother’s PaO₂ is lower than 80mmHg for a long time, the incidence of FGR is 2.3 times higher than that of normal pregnancy).

Safety and Clinical Suitability: Why 30% Concentration is the “Golden Range” for Oxygen Supplementation During Pregnancy

The core principle of oxygen supplementation during pregnancy is “physiological regulation” rather than “excessive intervention.” A 30% oxygen concentration (2 L/min) is considered “low-flow physiological oxygen supplementation,” and its safety has been confirmed in multiple clinical studies:

For the mother, this concentration does not cause oxygen toxicity (oxygen toxicity requires a FiO₂ > 60% for more than 24 hours) or respiratory depression (the respiratory center is more sensitive to CO₂ during pregnancy, and low oxygen concentrations do not affect respiratory drive).
For the fetus, this concentration maintains the fetal umbilical artery SaO₂ at around 70% (the upper limit of the normal range), avoiding the potential for excessive retinal vascular proliferation induced by high oxygen concentrations (a risk associated with high oxygen concentrations in premature infants, a concern not associated with low-concentration oxygen supplementation during pregnancy).

This is also consistent with the International Federation of Gynecology and Obstetrics (FIGO) guidelines for oxygen therapy during pregnancy: They recommend that when physiological hypoxia during pregnancy causes SpO₂ <95%, low-flow oxygen therapy at 2L/min be used to maintain maternal PaO₂ above 90mmHg, thereby ensuring oxygen reserves in the fetal umbilical artery blood flow. (Doppler ultrasound can monitor that the fetal umbilical artery pulsatility index (PI) can decrease by 8-10% after oxygen supplementation, indicating reduced blood flow resistance and improved oxygen supply.)

In short, our oxygen concentrator addresses the unique physiological characteristics of pregnancy by precisely increasing maternal arterial oxygen partial pressure, enhancing the “driving force” of placental oxygen diffusion, and maintaining a stable oxygen supply environment for the fetus within a safe threshold. Its mechanism of action is not to “add additional oxygen,” but rather to “repair the oxygen supply gap caused by physiological fluctuations during pregnancy,” which is the core of its professionalism and reliability.