We emphasize that the following notes do not attempt to describe our intellectual property accurately or completely. They are intended to give a flavour of our approach. The numbers quoted are indicative and not suitable for design purposes.

We first give a brief description of how the human respiratory system works. We then go on to explain the requirements for a system that can reproduce this performance when the lung is severely damaged.

The lung discharges oxygenated blood to the arterial system. The arteries deliver the blood to the various organs that require energy (for example, muscles). In these organs, carbon-hydrogen-oxygen compounds react with oxygen from the blood stream to generate energy. The reaction is akin to a controlled burning. (Indeed, the calorific value of foodstuffs is estimated by burning the food under controlled conditions). The reactions can be illustrated by equations such as the following:

Reaction with carbohydrate. Example, glucose:

a) C₆H₁₂O₆ + 6O₂ → 6CO₂ + 6H₂O

Reaction with hydrocarbon (saturated fat). For example, decane:

b) 2C₁₀H₂₂ + 31O₂ → 20CO₂ + 22H₂O

In the case of carbohydrates, one mole of carbon dioxide is produced per mole of oxygen consumed. In the case of saturated fats, about 0.65 moles of carbon dioxide is produced per mole of oxygen consumed. The quantity of carbon dioxide produced per mole of oxygen consumed depends on the mixture of food that we eat. Typical values are 0.8 to 0.9 moles carbon dioxide per mole of oxygen.

The carbon dioxide produced is absorbed into the blood. Thus, at each step of supporting life, the blood becomes depleted in oxygen and enriched in carbon dioxide. The depleted blood is collected in the veins and returned to the lungs.

The lungs remove carbon dioxide from the blood and recharge it with oxygen.

The exchange takes place through membranes making up the alveoli in the lungs. This mass exchange process is governed by standard mass-transfer equations. Thus, the rate of mass transfer is given by:

m = UA(c₁ – c₂)      (1)

In equation (1),

m is mass transfer rate, for example in kg/s.

U is the mass transfer coefficient, for example in m/s.

A is the mass transfer area, for example in m ² .

(c₁ – c₂) is the concentration difference driving the mass transfer, for example in kg/m ³.

Equation (1) applies both to oxygen transfer and to carbon dioxide transfer. For concentrations in molar units (for example, mole oxygen per mole gas), the percent concentration is numerically equal to the partial pressure in kPa.

For oxygen transfer, c₁ is the gas-phase concentration of oxygen and c₂ is the equilibrium concentration of oxygen over blood. On the “in” breath, c ₁ is the atmospheric concentration of oxygen, namely 21% or 21kPa. On the “out” breath, the exhaled air has an oxygen concentration of about 16% (16kPa). The equilibrium partial pressure over the blood increases from about 6kPa (venous blood input) to about 12kPa (arterial blood output). It is emphasized that the equilibrium concentration of oxygen over blood is not equal to the concentration within the blood. A typical relationship between blood oxygen saturation and equilibrium partial pressure is illustrated in Figure 1. The curve depends on the blood carbon dioxide concentration. For lower blood carbon dioxide levels, the oxygen partial pressure is less (thus, for a given pressure, the blood oxygen saturation is higher). Conversely, for higher blood carbon dioxide levels, blood absorbs oxygen less efficiently. As blood passes through the lungs, the carbon dioxide level falls, so that, at the arterial blood outlet, the oxygen concentration is near saturation. Notice that the equilibrium line becomes steep near to 100% saturation. Thus, the blood oxygen saturation becomes insensitive to the partial pressure of oxygen over the blood.

For carbon dioxide transfer, c₁ is the equilibrium concentration of carbon dioxide over blood and c₂ is the atmospheric concentration of carbon dioxide. The equilibrium partial pressure over the blood decreases from about 6.5kPa (venous blood input) to about 5.5% (arterial blood output). On the “in” breath, the atmospheric partial pressure of carbon dioxide is negligible. It increases to about 4kPa in the exhaled air.

In response to increased metabolic rate, the respiratory demand increases, the heart rate (and blood circulation rate) increases and breathing becomes deeper and faster. Fresh air reaches deeper into the lungs, which decreases the resistance to mass transfer and hence increases the Mass Transfer Coefficient (U). At the same time, the effective mass-transfer area increases. Hence, referring to equation (1), the mass transfer rates for both oxygen and carbon dioxide increase.

The body employs carbon dioxide as the main indicator with which to control respiration rate. If the blood carbon-dioxide concentration drops significantly, the respiration rate is higher than needed to meet the respiratory demand. Conversely, if the blood concentration rises significantly, the respiration rate is too low. Thus, to an approximation, the body has a set-point blood carbon dioxide concentration. If the concentration is lower than the set point, respiration rate decreases. If the concentration is higher than the set point, respiration rate increases.

The Haemair respiratory aid and prosthetic lung.

The unique feature of the Haemair approach is that it is aimed at conscious mobile patients. To this end, we match oxygen and carbon dioxide mass transfer rates to the respiratory demand of the patient. Furthermore, we employ a flow of natural air to provide oxygen and remove carbon dioxide.

There are three main variants of our device. The simplest to employ consists of a mass exchanger, as illustrated in figure 2. It takes deoxygenated blood, extracted from a main vein, removes carbon dioxide, replaces it with oxygen, and returns the oxygenated blood to the body. The second variant places the mass exchanger within the body to eliminate the hazard of taking a significant blood flow outside the body. The final version is a prosthetic lung, as illustrated in figure 3.

In all three variants, mass transfer is controlled so that performance mimics that of natural lungs. In this way, the natural respiratory control mechanism controls heart rate etc, and control is fully integrated with the natural respiratory system.

The external device will be deployed first. It is easily reversible and major parts are available for maintenance. The easy reversibility is important in treating emergency and acute cases for which the device might be needed for no more than hours or weeks. Once we have established that long maintenance-free operation is possible, we can move on to the intermediate device. The clinical procedure to “plumb” the device into the blood circulation system is more complex and maintenance is more difficult. However, the engineering is simpler. The only significant external item required is a small air pump, or fan. This device is more suited to patients who will need it for months – for example, as a bridge to transplant. It should enable patients to leave hospital and continue treatment at home. The final variant, a prosthetic lung, serves as an alternative to a lung transplant. This variant is illustrated in figure 3. It cannot be deployed until we have extensive favourable experience with the reversible devices. However, it offers hope to those currently excluded from transplant waiting lists – for example, most terminal emphysema sufferers.