where VT - tidal volume, amount of air inhaled during each inspiration, and f - number of breaths per minute.
In an adult male subject VT is about 500 ml, and f is about 12 breaths/minute, and therefore VE is about 6000 ml/minute. However, not all the air inhaled into the lungs reaches the lung area where the gas exchange takes place, (i.e. the respiratory zone). Some of the air remains in the conducting airways i.e. in the anatomical dead space. The volume of the anatomical dead space (VD) in an adult subject is about 150 ml. Thus, in approximation, the volume of air that reaches the respiratory zone each minute is (500-150 ml) x 12 = 4200 ml/min. This is the amount of inspired air available for gas exchange each minute, and is called alveolar ventilation (VA). The difference between minute ventilation and alveolar ventilation is the dead space ventilation that is wasted from the gas exchange point of view. Anatomical dead space is not easy to measure. A close approximation of the dead space in ml is a subject's weight in pounds.
Under some pathological conditions a certain amount of inspired air,
although reaching the respiratory zone, does not take part in the gas exchange.
Figure 5 illustrates
two examples (B and C) of these pathologies. In these circumstances, i.e.
alveoli with a significantly decreased or no blood supply, represent
alveolar dead space. The sum of alveolar and anatomical dead spaces
is called the physiological dead space.
Because the inspired air contains essentially no CO2, the CO2 in the alveoli must reflect the balance between what is produced by metabolism (CO2 production, VCO2) and what is eliminated by VA. The alveolar ventilation equation describes the exact relation between alveolar ventilation and PACO2 for any given metabolic rate (VCO2).
VA (ml/min) x PACO2 (mmHg) = VCO2 (ml/min) x K
where PACO2 is partial pressure of CO2 in alveoli; K is barometric pressure. Because CO2 in the arterial blood is rapidly in equilibrium with alveolar CO2, PACO2 can be substituted by the arterial value, PaCO2.
Alveolar Ventilation matches VCO2
and keeps PaCO2 at a constant level.
Alveolar hyperventilation occurs when more O2 is supplied and more CO2 removed than the metabolic rate requires: alveolar and arterial partial pressures of O2 rise and those of CO2 decrease.
Alveolar hypoventilation : A fall in the overall level of ventilation can reduce alveolar ventilation below that required by the metabolic activity of the body. Under the condition of alveolar hypoventilation, the rate at which oxygen is added to the alveolar gas, and CO2 is eliminated, is lowered, so that the alveolar partial pressure of O2 (PAO2) falls and PACO2 rises. As a result of this, capillary blood is less well oxygenated, and PaO2 falls below normal values. Similarly, PaCO2 rises above the normal value (Fig. 6).
Fig. 6. Effects of ventilation of blood gases. Under normal conditions (A), PO2 and PCO2 in mixed venous blood reaching the pulmonary capillaries is 40 mmHg and 46 mmHg, respectively. In the arterial blood, PO2 increases to 100 mHg and PCO2 drops to 40 mmHg. During hyperventilation (B) PO2 increases and PCO2 decreases in venous and arterial blood. It is because ventilation delivers more O2 and eliminates more CO2 than it is used and produced, respectively, by tissues. During hypoventilation (C), PO2 drops and PCO2 increases in venous and arterial blood because ventilation does not match the metabolic demands of tissues: less CO2 is eliminated from, and less O2 is delivered to tissues than it is necessary for a given metabolic rate. Arrows indicate direction of blood flow.
Alveolar hypoventilation may occur during severe disorders of the lungs (e.g. chronic obstructive lung disease) and when the chest cage is injured and the lung collaps. It can also occur when the central nervous system is depressed by the administration of narcotics, sedatives and anesthetics or when the central respiratory activity is normal but transmission at the neuromuscular junction within the respiratory muscles is impaired.