Dr Rob Law,
Bristol Royal Infirmary, Bristol, UK
Dr H Bukwirwa,
Mulago Hospital, Kampala, Uganda

Introduction		Delivery
Oxygen transport		Consumption
Atmosphere to alveolus		Stores
Alveolus to blood		Effects of Anaesthesia
Ventilation/perusuion mismatch		Practical uses
Diffusion		Problems with administration
Carriage by the blood		References
Cascade

Introduction

In order to survive humans have to be able to extract oxygen from the atmosphere and transport it to their cells where it is utilised for essential metabolic processes. Some cells can produce energy without oxygen (anaerobic metabolism) for a short time, although it is inefficient. Other organs (e.g.brain) are made up of cells that can only make the energy necessary for survival in the presence of a continual supply of oxygen (aerobic metabolism). Tissues differ in their ability to withstand anoxia (lack of oxygen). The brain and the heart are the most sensitive. Initially a lack of oxygen affects organ function but with time irreversible damage is done (within minutes in the case of the brain) and revival is impossible.   

OXYGEN TRANSPORT FROM AIR TO TISSUES

Oxygen is transported from the air that we breathe to each cell in the body. In general, gases move from an area of high concentration (pressure) to areas of low concentration (pressure). If there are a mixture of gases in a container, the pressure of each gas (partial pressure) is equal to the pressure that each gas would produce if it occupied the container alone.    

Atmosphere to alveolus

The air (atmosphere) around us has a total pressure of 760 mmHg (1 atmosphere of pressure = 760mmHg = 101kPa = 15lbs/sq. in). Air is made up of 21% oxygen, 78% nitrogen and small quantities of CO2, argon and helium. The pressure exerted by the main two gases individually, when added together, equals the total surrounding pressure or atmospheric pressure. The pressure of oxygen (PO2) of dry air at sea level is therefore 159 mmHg (21/100 x 760=159). However by the time the inspired air reaches the trachea it has been warmed and humidified by the upper respiratory tract. The humidity is formed by water vapour which as a gas exerts a pressure. At 37^oC the water vapour pressure in the trachea is 47 mmHg. Taking the water vapour pressure into account, the PO2 in the trachea when breathing air is (760-47) x 21/100 = 150 mmHg. By the time the oxygen has reached the alveoli the PO2 has fallen to about 100 mmHg. This is because the PO2 of the gas in the alveoli (PAO2) is a balance between two processes: the removal of oxygen by the pulmonary capillaries and its continual supply by alveolar ventilation (breathing).    

Alveolus to blood

Blood returning to the heart from the tissues has a low PO2 (40 mmHg) and travels to the lungs via the pulmonary arteries. The pulmonary arteries form pulmonary capillaries, which surround alveoli. Oxygen diffuses (moves through the membrane separating the air and the blood) from the high pressure in the alveoli (100 mmHg) to the area of lower pressure of the blood in the pulmonary capillaries (40 mmHg). After oxygenation blood moves into the pulmonary veins which return to the left side of the heart to be pumped to the systemic tissues. In a 'perfect lung' the PO2 of pulmonary venous blood would be equal to the PO2 in the alveolus. Three factors may cause the PO2 in the pulmonary veins to be less than the PAO2: ventilation/perfusion mismatch, shunt and slow diffusion.    

Ventilation/perfusion mismatch

In a 'perfect lung' all alveoli would receive an equal share of alveolar ventilation and the pulmonary capillaries that surround different alveoli would receive an equal share of cardiac output ie.ventilation and perfusion would be perfectly matched.
Diseased lungs may have marked mismatch between ventilation and perfusion. Some alveoli are relatively overventilated while others are relatively overperfused (the most extreme form of this is shunt where blood flows past alveoli with no gas exchange taking place (figure 1). Well ventilated alveoli (high PO2 in capillary blood) cannot make up for the oxygen not transferred in the underventilated alveoli with a low PO2 in the capillary blood. This is because there is a maximum amount of oxygen which can combine with haemoglobin (see haemoglobin-oxygen dissociation curve figure 2a). The pulmonary venous blood (mixture of pulmonary capillary blood from all alveoli) will therefore have a lower PO2 than the PO2 in the alveoli (PAO2). Even normal lungs have some degree of ventilation/perfusion mismatch; the upper zones are relatively overventilated while the lower zones are relatively overperfused and underventilated.

Shunt occurs when deoxygenated venous blood from the body passes unventilated alveoli to enter the pulmonary veins and the systemic arterial system with an unchanged PO2 (40 mmHg). (Figure 1.) Atelectasis (collapsed alveoli), consolidation of the lung, pulmonary oedema or small airway closure (see later) will cause shunt.

 

Diffusion

Oxygen diffuses from the alveolus to the capillary until the PO2 in the capillary is equal to that in the alveolus. This process is normally complete by the time the blood has passed about one third of the way along the pulmonary capillary.
In the normal lung, the diffusion of oxygen into the blood is vary rapid and is complete, even if the cardiac output is increased (exercise) and the blood spends less time in contact with the alveolus. This may not happen when the alveolar capillary network is abnormal (pulmonary disease). However, the ability of the lung to compensate is great and problems caused by poor gas diffusion are a rare cause for hypoxia, except with diseases such as alveolar fibrosis.
In order to decrease the detrimental effect that shunt and ventilation/perfusion mismatch have on oxygenation, the blood vessels in the lung are adapted to vasoconstrict and therefore reduce blood flow to areas which are underventilated. This is termed hypoxic pulmonary vasoconstriction and reduces the effect of shunt.    

Oxygen carriage by the blood

Oxygen is carried in the blood in two forms. Most is carried combined with haemoglobin (figure 2b) but there is a very small amount dissolved in the plasma. Each gram of haemoglobin can carry 1.31 ml of oxygen when it is fully saturated. Therefore every litre of blood with a Hb concentration of 15g/dl can carry about 200 mls of oxygen when fully saturated (occupied) with oxygen (PO2 >100 mmHg). At this PO2 only 3 ml of oxygen will dissolve in every litre of plasma.

If the PO2 of oxygen in arterial blood (PAO2) is increased significantly (by breathing 100% oxygen) then a small amount of extra oxygen will dissolve in the plasma (at a rate of 0.003 ml O2/100ml of blood /mmHg PO2) but there will normally be no significant increase in the amount carried by haemoglobin, which is already >95% saturated with oxygen. When considering the adequacy of oxygen delivery to the tissues, three factors need to be taken into account, haemoglobin concentration, cardiac output and oxygenation.  

  Oxygen cascade

Oxygen moves down the pressure or concentration gradient from a relatively high level in air, to the levels in the respiratory tract and then alveolar gas, the arterial blood, capillaries and finally the cell. The PO2 reaches the lowest level (4-20 mmHg) in the mitochondria (structures in cells responsible for energy production). This decrease in PO2 from air to the mitochondrion is known as the oxygen cascade and the size of any one step in the cascade may be increased under pathological circumstances and may result in hypoxia (figure 3).

 

Oxygen delivery

The quantity of oxygen made available to the body in one minute is known as the oxygen delivery and is equal to the cardiac output x the arterial oxygen content (see previously) ie. 5000ml blood/min x 200 mlO2/1000 ml blood = 1000ml O2/min.

Oxygen delivery (mls O2/min) = Cardiac output (litres/min) x Hb concentration (g/litre) x 1.31 (mls O2/g Hb) x % saturation    

Oxygen consumption

Approximately 250 ml of oxygen are used every minute by a conscious resting person (oxygen consumption) and therefore about 25% of the arterial oxygen is used every minute. The haemoglobin in mixed venous blood is about 70% saturated (95% less 25%).

In general there is more oxygen delivered to the cells of the body than they actually use. When oxygen consumption is high (eg. during exercise) the increased oxygen requirement is usually provided by an increased cardiac output - see formula above for how this works. However, a low cardiac output, a low haemoglobin concentration (anaemia) or a low haemoglobin O2 saturation will result in an inadequate delivery of oxygen, unless a compensatory change occurs in one of the other factors. Alternatively, if oxygen delivery falls relative to oxygen consumption the tissues extract more oxygen from the haemoglobin (the saturation of mixed venous blood falls below 70%)(a-b in figure 4). A reduction below point 'c' in figure 4 cannot be compensated for by an increased oxygen extraction and results in anaerobic metabolism and lactic acidosis.

(Continued ...)

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