2L Smallest Oxygen Machine for Elderly

The increased heart and lung burden of the elderly is essentially the superposition effect of the degenerative change in organ function caused by aging and the imbalance of oxygen supply and demand. The core of our oxygen generator to relieve cardiopulmonary burden through precise oxygen replenishment is to break the vicious cycle from three levels of “oxygen metabolism – neuromodulation – hemodynamics”. Its mechanism of action can be analyzed in depth based on the physiological characteristics and clinical data of the elderly:

The underlying logic of cardiopulmonary function decline in the elderly: “overload” from structural degeneration to functional compensation

As we age (after 60 years old), the cardiopulmonary system will undergo irreversible structural and functional changes, which will directly lead to “decreased oxygen utilization efficiency” and “compensated burden”:

• Cardous level: cardiomyocyte atrophy (the number of sarcoma decreases by about 20%), myocardial interstitial fibrosis (the increase of collagen fibers by 30%), resulting in decreased myocardial compliance – weakened ventricular filling capacity during diastolic period (decreased diastolic function), and stroke output (SV) is 15%-20% lower than that of young people (about 60-80ml for young people, and lowered to 50-65ml for elderly people). To maintain cardiac output (CO=SV× heart rate), the heart rate will increase compensatoryly (resting heart rate is 5-10 times/min higher than that of young people), and the accelerated heart rate directly leads to an increase in myocardial oxygen consumption (MVO₂) (MVO₂= heart rate × ventricular wall tension × contraction force, of which the heart rate weight accounts for 40%).
• Lung level: Elastic fibers in lung tissue and alveolar fusion (the number of alveolars decreased by about 30%), resulting in a decrease in lung capacity (VC) by 20%-25%, a 40% increase in residual gas (RV) and a decrease in gas exchange efficiency – The arterial blood oxygen partial pressure (PaO₂) during rest is 5-10mmHg (to 85-90mmHg) lower than that of young people (95-100mmHg). Due to increased oxygen consumption and insufficient respiratory reserves during activity, PaO₂ can be reduced by another 10-15mmHg (as low as 70-75mmHg). This hypoxia triggers “hypoxic pulmonary vasoconstriction”: Due to hypoxia contraction, pulmonary vascular resistance (PVR) increases by 20%-30%, causing the pulmonary arterial systolic blood pressure (PASP) to rise from 18-25mmHg in youth to 30-35mmHg, directly increasing the right heart afterload (the right ventricle needs to overcome higher resistance ejaculation).

The “vicious cycle” of cardiopulmonary burden: a chain reaction from hypoxia to functional decline

The above degenerative changes will form a closed loop:

• Reduced myocardial stroke output → accelerated heart rate compensation → increase MVO₂ → worsening myocardial hypoxia (especially during activity)
• Reduced alveolar oxygen partial pressure → pulmonary vasoconstriction → increased pulmonary arterial pressure → increased ejaculation resistance of right ventricular → right heart hypertrophy → decreased right heart function → systemic circulation congestion (edema of the limbs)
• At the same time, the decline in right heart function will reversely affect the left heart: the right ventricle expands and squeezes the left ventricle diastolic space, and the left heart is filled with limited, further reducing the cardiac output, forming “left and left heart mutual enlargement”.

Clinical data show that when the elderly over 70 years old are walking (3km/h), their heart rate can increase by 20-30 beats/minute compared to when they are resting (up to 90-100 beats/minute), and MVO₂ increases by 40%-50%; pulmonary artery systolic blood pressure can increase to 40-45mmHg (about 30mmHg when youth is active), and the right heart workload increases by 60%. This “overload” state will continue for a long time, which will accelerate cardiomyocyte apoptosis and pulmonary vascular remodeling, and is an important cause of heart failure and pulmonary hypertension in the elderly.

Precise intervention of 30% concentration oxygen therapy: the dual role of “reducing burden” to “repair”

This oxygen generator provides 30% oxygen-rich gases, breaking the vicious cycle through the following mechanism:

• Reduce left heart load: reduce myocardium “ineffective energy consumption”
  After inhaling 30% oxygen, the alveolar oxygen partial pressure (PAO₂) increases from 104mmHg in the air state to 140-150mmHg, the arterial oxygen partial pressure (PaO₂) can be increased from 85mmHg to 95-100mmHg, and the arterial oxygen saturation (SaO₂) increases from 93%-94% to 97%-98%.
  After sufficient oxygen supply to peripheral tissues (such as skeletal muscles, viscera) the sympathetic nerve excitability decreases (carotid body chemoreceptors are weakened by hypoxic stimulation), and the heart rate can drop 8-12 beats/minute (from resting 80 beats/minute to about 70 beats/minute). Calculated according to the MVO₂ formula: the heart rate drops by 10 times/min, combined with the ventricular wall tension, which reduces by 15% due to improved cardiac function, MVO₂ can be reduced by 25%-30%, which is equivalent to allowing the myocardium to “do 25% less work” and directly alleviate the “overload” of the left heart.
• Reduce right heart afterload: Reduce pulmonary circulation “resistance”
  After the alveolar oxygen partial pressure is increased, hypoxic pulmonary vasoconstriction is inhibited: pulmonary vascular resistance (PVR) can decrease by 15%-20% (from 300dyn・s/cm⁵ to 240-255dyn・s/cm⁵), and pulmonary arterial systolic pressure (PASP) is reduced by 5-8mmHg (from 35mmHg to 27-30mmHg).
  The “resistance” during right ventricular ejaculation decreases, and the right ventricular per-stroke (the amount of right heart doing work) is reduced by 20%-25%, which can alleviate the trend of right ventricular hypertrophy in the long run (ultrasound shows that continuous oxygen supplementation for 1 month, and the thickness of the right ventricular wall in the elderly can be reduced by 0.5-1mm), avoiding further decline in right heart function.
• Improve activity endurance: breaking the closed loop of “activity – hypoxia – more tired”
  The lack of oxygen in the elderly during daily activities (such as going up and down stairs and buying vegetables) is essentially the contradiction between “increased oxygen consumption” and “insufficient oxygen supply”. After oxygen replenishment, the decrease in PaO₂ during activity decreases from 15mmHg to 5-8mmHg, the peak heart rate decreases by 15-20 beats/minute (such as the heart rate of climbing 3 floors decreases from 110 beats/minute to 90 beats/minute), and the peak myocardial oxygen consumption decreases by 30%, thereby reducing the symptoms of chest tightness and shortness of breath after activity and improving daily activity ability.

Safety and adaptability: Why 30% concentration is the “ideal oxygen supplement threshold” for the elderly

The tolerance of oxygen concentration in the elderly is different from that in young people: excessive concentration (>50%) may inhibit the respiratory center (the respiratory center of the elderly decreases sensitivity to CO₂, and hypoxia is an important driver), while excessive concentration (<25%) cannot effectively improve hypoxia. Oxygen therapy at 30% concentration has dual advantages:

• As a “physiological compensatory oxygen supplement”: only improves PaO₂ to the normal level of youth (95-100mmHg), does not interfere with respiratory drive, and is suitable for long-term use for 6-8 hours a day;
• Adaptive cardiopulmonary reserve features of the elderly: It can not only alleviate the basal hypoxia during resting, but also cope with the surge in oxygen demand during activity, avoiding the risk of oxygen poisoning caused by “over-oxygen replenishment” (oxygen poisoning requires FiO₂>60% and lasts for more than 24 hours).

Clinical studies have confirmed that: 30% oxygen is inhaled by elderly people over 70 years old for 4 hours a day, the left ventricular ejaculation fraction (LVEF) can be increased by 3%-5% after 12 weeks, the 6-minute walking distance increases by 50-80 meters, and the systolic blood pressure of the pulmonary artery has steadily decreased – this is the direct evidence that it achieves the dual value of “burden reduction” and “functional protection” by improving the balance of oxygen supply and demand.

In short, our oxygen generator does not “enhance cardiopulmonary function”, but reduces “compensatory overdraft” in the heart and lung system by supplementing the “oxygen utilization gap” caused by aging, helping the elderly maintain a more stable cardiopulmonary state during natural aging. Its scientific nature comes from the precise adaptation of the physiological characteristics of the elderly.