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VENTILATION
The amount of air inspired into the lungs over some period of time is called ventilation. Usually it is measured for one minute, and therefore we call it minute ventilation. Minute ventilation (VE) is the amount of air inspired (or expired) during one minute. Therefore,
VE = VT x f

where VT - tidal volume, amount of air inhaled during each inspiration, and f - number of breaths per minute.

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.

Fig. 5
Fig. 5. Types of respiratory dead space. A: anatomical dead space. Air in the conducting airways does not contribute to gas exchange. B. alveolar dead space. Air in alveoli witout blood supply does not contribute to gas exchange ("wasted" ventilation). C: gas exchange is limited in alveoli with insufficient blood flow. Therefore, some air in these alveoli is also "wasted" and adds to the alveolar dead space. The sume of the anatomical and alveolar dead space represent the physiological dead space. Arrows indicate direction of blood flow.

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

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.