- Updated on December 20, 2021
By Dr. Artour Rakhimov, Alternative Health Educator and Author
McFadden & Lyons (1968) showed that in mild and severe asthmatic patients, some parts of the lungs could not carry out adequate air exchange due to airway obstruction. This causes an ineffective exchange of CO2 for O2 in venous blood in the obstructed alveoli of the lung. Therefore, this venous blood, after leaving the lungs almost unchanged, is mixed with oxygenated arterial blood. This effect is called “blood shunting”. As a result, hypoxia of such patients becomes worse since less O2 is present in the blood. Meanwhile, aCO2 rises to or even exceeds, in severe cases, the physiological norm (40 mm Hg). Thus, with further deterioration of health, large aCO2 (hypercapnia) is observed. In spite of increased aCO2 pressure and greatly improved Bohr effect, tissue hypoxia is greater than before due to very low arterial oxygenation (it would not be correct to expect that higher aCO2 concentrations can compensate for lack of oxygenation in the damaged lung areas. The balance between these two gases is indeed delicate.) This problem of ventilation/perfusion mismatch (inadequate air supply to some lung parts) and corresponding blood shunting is especially severe in patients with emphysema.
Normally, in healthy lungs, each lung area requires air ventilation, which is approximately proportional to its volume. Meanwhile, in severe cases of ventilation/perfusion mismatch, the working lung part can hyperventilate, but the total ventilation can be less than the norm. Indeed, if, for example, only one-third of the lungs are functional, as in emphysema, this third may use, say, about 3-4 l of air per minute, indicating general hypoventilation (3-4 l/min is less than the physiological norm). Meanwhile, under normal conditions, this working lung part would need only about 2 l/min.
Ventilation/perfusion mismatch is common in patients with mild or severe asthma, emphysema, and cystic fibrosis, and for some patients with obesity, hypertension, and diabetes. However, for most people very low aCO2 does not cause severe airway obstruction and corresponding blood shunting. Taking into account individual variability of the effects of CO2 depletion (discussed in section 1.3), it is possible that asthmatics and other groups of people as above have air passages, which are more sensitive to hyperventilation due to their genetically inherited characteristics.
Hypoxic hypoxia can also be the result of ventilatory failure due to fatigue of respiratory muscles or depression of the respiratory neurons in the brain by morphine and other drugs. (Hypoxic hypoxia is hypoxia resulting from a defective mechanism of oxygenation in the lungs.)