V D is the sum of the anatomic dead space and the alveolar dead space.Physiologic dead space (V D): volume of inspired air that does not participate in gas exchang e.Volume of air that a person breathes per minute.Tidal volume ( V T): the volume of air that is inspired or expired in a single breath.Respiratory rate (RR): number of breaths per minute.See “ Chest wall dynamics” for details.Intrathoracic pressure becomes positive to expel the air ( passive elastic recoil of the lungs).passive elastic recoil of the lungs) but expiratory muscles (e.g., intercostal muscles, subcostal muscles) can assist. Expiration is primarily a passive process (i.e.Air reaches the respiratory zone of the respiratory tree (site of gas exchange): respiratory bronchioles → alveolar ducts → alveoli.Intrathoracic pressure becomes even more negative to fill the lungs with air.Inspiratory muscles (mainly external intercostal muscles and the diaphragm) elevate the ribs and sternum and increase the intrathoracic volume.Inspiration of air into the conducting zone of the respiratory tree ( anatomic dead space): nose → pharynx → larynx → trachea → bronchi → bronchioles → terminal bronchioles.Definition: movement of air through the respiratory tract into (inspiration) and out of (expiration) the respiratory zone ( lungs) to facilitate gas exchange (O 2 and CO 2).Inspiration is an active process driven by the respiratory musculature while expiration is passive at rest, driven by the elastic properties of lung tissue. Central regulation of respiration is provided by the respiratory center located in the reticular formation of the medulla oblongata and pons. CO 2 diffuses into the alveoli and is exhaled. In the capillaries, oxygen binds to hemoglobin in erythrocytes or dissolves into the plasma (oxygenation). The gases diffuse across the barrier following pressure gradients. Gas exchange occurs via simple diffusion across the blood-air barrier. Diseases that affect the perfusion (e.g., pulmonary embolism) or ventilation (e.g., foreign body aspiration) can cause a V/Q mismatch. The Euler-Liljestrand mechanism regulates the perfusion of nonventilated alveoli: if a lung section is perfused but not ventilated, there will be a drop in the oxygen concentration in the blood, resulting in hypoxic vasoconstriction. The ventilation-perfusion ratio is higher in the apex of the lung than at its base. Perfusion of the pulmonary capillaries is closely regulated to match ventilation in order to maximize gas exchange. The physiologic dead space is the volume of inspired air that does not participate in gas exchange. Ventilation is the movement of air through the respiratory tract into (inspiration) and out of (expiration) the respiratory zone ( lungs). Two potential strategies are an initial sustained inflation and ventilation with a positive end-expiratory pressure.The main function of the respiratory system is gas exchange (O 2 and CO 2). In particular, such strategies should initially focus on moving liquid rather than air through the airways because liquid has a much higher resistance and should assist in establishing and maintaining functional residual capacity. Based on the knowledge that transpulmonary pressures primarily regulate airway liquid clearance after birth, it is possible to devise ventilation strategies that facilitate this process in very preterm infants. The level of contribution of each mechanism likely depends on the timing and mode of delivery. This indicates that airway liquid clearance is not solely dependent on sodium reabsorption and that a variety of mechanisms that may act before, during, and after birth are involved. Recent imaging studies have demonstrated that after birth, airway liquid clearance and lung aeration are intrinsically linked and regulated primarily by transpulmonary pressures generated during inspiration. Because preterm infants commonly have difficulty in making the transition to neonatal life, it is important to understand the mechanisms of lung aeration and how this action can be facilitated to improve the transition in these very immature infants. Major changes in cardiovascular and respiratory physiology underpin the successful transition from fetal to neonatal life, and it is now apparent that lung aeration and the onset of pulmonary ventilation trigger such changes.
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