Ventilation lung volumes

Lung volume reduction surgery is a rarely performed treatment option for heterogeneous emphysema patients with high hyperinflation. Novel semi-invasive and invasive alternatives are being developed, such as bronchial valves for heterogeneous emphysema treatment, and bronchial stents for homogeneous emphysema to reduce counteiproductive collateral ventilation. 

Ventilation is the exchange of air between the external atmosphere and the alveoli. It is typically defined as the volume of air entering the alveoli per minute. A complete understanding of ventilation requires the consideration of lung volumes. 

Total ventilation. The total ventilation (minute volume) is the volume of air that enters the lungs per minute. It is determined by tidal volume and breathing frequency ... 

The inhaled air volume (V in L) depends on the extent of chest enlargement. During normal breathing, the inhaled and exhaled volumes (tidal volume) are only part of the total lung volume [8,21]. The different parameters that describe pulmonary ventilation are shown in Figure 3.2. Table 3.1 presents a definition of the different parameters. Normal adults have a tidal... 

Q7 If the embolus is quite large and obstructs a significant area of the pulmonary circulation, the affected area of lung will be underperfused or non-perfused. The area may continue to be ventilated for some time, causing a ventilation-perfusion mismatch, which leads to poor gas exchange and abnormal blood gas tensions. The lung volume in the affected area decreases, and this decrease in size can sometimes be seen on a chest X-ray. After some hours, surfactant production declines in the non-perfused area of lung and the alveoli collapse. 

In poorly ventilated lung areas, perfusion is diminished (= von Euler-Liljestrand reflex). This reflex is impaired in liver cirrhosis. The decrease in or loss of hypoxia-induced pulmonary vasoconstriction leads to the greater perfusion of poorly ventilated lung areas this results in an increase in the intrapulmonary shunt volume and... 

Thus, alveoli in the apices of the lung are well inflated but poorly ventilated, whereas those toward the base are poorly inflated but better ventilated. In normal subjects in the erect posture, the ratio of alveolar ventilation to volume in the upper parts of the lung is approximately 60% of that at the lung bases. In the lateral (decubitus) posture, the inferior (dependent) lobe has better ventilation than that which is superior whereas in the supine position, the ventilation per unit of lung volume is relatively uniform. These gravitational differences disappear at total lung capacity, when all alveoli are fully expanded. 

Spirometry has its limitations, however. It can measure only ventilated volumes. It cannot measure lung capacities that contain the residual volume. Measurements of TLC, FRC, and RV have diagnostic value in defining lung overdistension or restrictive pulmonary disease the body plethysmograph can determine these absolute lung volumes. 

In addition to the static lung volumes just identified, there are several time-dependent volumes associated with the respiratory act. The minute volume (MV) is the volume of air per breath (tidal volume) multiplied by the respiratory rate (R), that is, MV = (TV) R. It is obvious that the same minute volume can be produced by rapid shallow or slow deep breathing. However, the effectiveness is not the same, because not all the respiratory air participates in gas exchange, there being a dead space volume. Therefore the alveolar ventilation is the important quantity which is defined as the tidal volume (TV) minus the dead space (DS) multiphed by the respiratory rate R, that is, alveolar ventilation = (TV-DS) R. In a normal adult subject, the dead space amounts to about 150 mL, or 2 mL/kg. 

The carotid body is the primary sensor of hypoxemia across many species. When stimulated by a decrease in Pa02 or hypoxic perfusates, it promotes many cardiopulmonary responses. Ventilation, static lung volumes, airway resistance, and airway secretions increase. The hypoxic pulmonary vasoconstrictor response and the systemic vascular vasodilator responses are attenuated bronchial vascular resistance decreases (for review see Ref 1). A current question is How does the carotid body transduce a low Pa02 stimulus into increased neural output traveling to the nucleus tractus sohtarii Here the increased neural traffic is processed and distributed to various other nuclei responsible for the increased breathing and the autonomicaUy regulated changes in the cardiopulmonary system. 

In this chapter we will discuss recommendations from the hterature regarding dec-aruiulation as well as our personal clinical experience. We will comment on the pathophysiology of ventilator dependence, the determination of candidates for weaning from ventilation and tracheostomy, and a stepwise approach to decannulation. Lastly, we will discuss the choices of noninvasive ventilatory supports and techniques that clinicians may utilize, such as lung volume recruitment (LVR), assisted coughing and mechanical airway clearance. 

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