Alveolar gases and diffusion

A run-down of ventilation and medical implications.

1. Alveolar Gases and Diffusion HDT 2:2 – Semester 2

2. Introduction to Terms PACO 2 is the partial pressure (gas concentration) of CO 2 in the alveoli. PAO 2 is therefore the partial pressure (gas concentration) of O 2 in the alveoli. PaCO 2 is the partial pressure (gas concentration) of CO 2 in the arteries. PaO 2 is therefore the partial pressure (gas concentration) of O 2 in the arteries. Hypoventilation (under-breathing) is where the ventilation of the alveoli does not meet the metabolic demand for removal of CO 2 , leading to increased PACO 2 and PaCO 2 . Hyperventilation (over-breathing) is where the ventilation of the alveoli exceeds the demand for removal of CO 2 from the blood, resulting in decreased PACO 2 and PaCO 2 . Hyperpnoea is an increase in respiration rate, in line with an increased metabolic demand both form removal of carbon dioxide and supply of oxygen. Patients presenting with hyperventilation will be dizzy due to vasoconstriction of cerebral blood vessels, caused by a fall in PaCO 2 . Patients will potentially present with carpopedal spasm (check the hands) caused by decreased levels of ionised calcium resulting in increased excitability. Dyspnoea is shortness of breath, apnoea is absence of breathing and tachypnoea is fast breathing.

3. Alveolar and Arterial Oxygen The PAO 2 is usually 100mmHg and the PACO 2 is usually 40mmHg. The PaO 2 is usually 95mmHg and the PaCO 2 is usually 40mmHg. The similarity of the blood and alveolar gases indicates that there diffusion is occurring across the respiratory membrane at a high efficiency. Alveolar levels DETERMINE the arterial levels. Quite logically, the PO 2 in the alveoli depends on three factors; the concentration of oxygen in the environment (usually stable, but changes with altitude), the level of replenishment of oxygen in the alveoli (determined by ventilation rate and depth) and also the rate of removal of oxygen from capillary blood vessels. Decreasing ventilation rate will decrease PAO 2 and increasing ventilation rate will increase PAO 2 . As these levels directly influence the PaO 2, then blood gases can be said to be directly affected by ventilation rate, assuming that the environmental oxygen concentration doesn’t change. This is significant in terms of how breathing can affect the carbonic acid buffer system and lead to disorders of blood pH. If metabolism and therefore the rate of removal of oxygen from capillaries were to increase, then PAO 2 would also decrease, assuming that ventilation rate does not change. In reality, respiratory compensation kicks in and ventilation rate increases to account for the increased consumption of oxygen by respiring tissues.

4. Alveolar and Arterial CO 2 The PAO 2 is usually 100mmHg and the PACO 2 is usually 40mmHg. The PaO 2 is usually 95mmHg and the PaCO 2 is usually 40mmHg . Levels of carbon dioxide in the alveoli are determined by two factors; the rate of elimination through ventilation (affected by the ventilation rate – VA) and the rate of delivery of carbon dioxide to the alveoli from capillaries (affected by the rate of metabolism and blood flow – VCO 2 ). Increasing the rate of alveolar ventilation will decrease the concentration or carbon dioxide in the alveoli and will lead to a decrease in the arterial carbon dioxide concentration, assuming that metabolic demand does not change. PACO 2 is proportional to 1/VA. Increasing the supply of carbon dioxide to the alveoli (i.e. an increase in metabolism) will increase alveolar concentrations if ventilation rate is unchanged. PACO 2 is proportional to VCO 2 . The above quoted values for partial pressures of oxygen and carbon dioxide are normal resting values where metabolic rate is constant and the alveolar ventilation is 4L/min.

5. Gases The alveolar gas equation is PAO 2 = PIO 2 – (PaCO 2 /R). This equation demonstrates that the level of oxygen in the alveoli (and therefore the blood) depends on the oxygen concentration of inspired air and the removal of carbon dioxide from blood (breathing). R is the respiratory gas quotient and is assumed to be the same in all patients, with a value of 0.8. The only variable in this equation that changes is the PaCO 2 . The difference in PAO 2 and PaO 2 should be less than 10mmHg (1kPa). Differences larger than this indicate that either diffusion is not occurring as efficiently as it should be (damage to or thickening of the respiratory membrane) or that a shunt system is in effect. A shunt system means that deoxygenated blood is mixing with oxygenated blood at some point and being pumped into systemic circulation. This can occur via thebesian veins or changes in bronchial-pulmonary circulation. The difference in arterial and alveolar oxygen can be useful but where both are low, a normal difference will be seen despite a problem existing. This could be alveolar hypoventilation.

6. Gases Diffusion across the respiratory membrane is governed by Fick’s Law, which is dependent on the thickness of the barrier, the gradient, the diffusion coefficient and the surface area. Carbon dioxide diffuses across the barrier 20x more efficiently than oxygen due to MW and charge, and so changes in O 2 will be seen in disease states much quicker than carbon dioxide. Alveolar gases are able to set blood gases through equilibration of the gradient across the respiratory membrane. Thickening of the diffusion barrier as part of a disease state can occur, i.e. emphysema, which leads to less efficient exchange and inability of the system to equilibrate. This means that at rest, a patient may be able to breathe normally and achieve acceptable levels of arterial oxygen, however during exercise the system is less able to compensate for the increased demand (due to inefficiency of exchange), which leads to fatigue on exertion and exercise intolerance.

7. Ventilation – Perfusion Matching When alveolar ventilation and lung perfusion (V/Q) are matched, then gas exchange, oxygen delivery and carbon dioxide removal are optimised. Assuming that alveolar ventilation in a healthy individual is 4L/min and that blood flow to the lungs from cardiac output is 5L/min, then the V/Q ratio is 0.8. In a perfect scenario, this value would be 1. Values much less than 1 could be caused by poor alveolar ventilation or excessive perfusion of the alveoli. This would be problematic, as oxygen would be rapidly stripped from the alveoli, lowering the concentration of oxygen, whilst simultaneously increasing the concentration of carbon dioxide. This would eventually lead to PAO 2 equating with venous blood gases, causing the patient to be become hypoxic and hypercapnic. Values higher than 1 could be caused by excessive ventilation of the alveoli or poor/no perfusion. This would mean that the alveolar gases would equilibrate with inspired gases, leaving the patient with hypocapnia and hyperoxia. Adjustments are made in the lung to accommodate changes in V/Q, for example; hypoxic blood causes localised vasoconstriction which limits the oxygen carried from the lungs back to the heart and allows alveolar concentrations to increase again so that equilibration occurs at the desired oxygen levels. Another adjustment made is the local bronchoconstriction that occurs when PCO 2 concentrations are low in the lungs, which limits the removal of alveolar CO 2 and allows concentrations to build again so that equilibration occurs at the desired level.