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Airflow Resistance

  • Ultimately, airflow between two points in a closed space is actuated by differences in the air pressure between those two points. However, the rate at which this movement occurs is dependent on the relative resistance of the environment to air movement. In many ways, resistance to airflow follows the same principles as resistance to blood flow (See: Resistance). The most important principle to consider is that the resistance of a tube, such as a pulmonary airway, is most influenced by the airway's diameter. Reduction of the airway diameter drastically increases its resistance, whereas dilation of the airway can significantly reduce its resistance. As discussed below, a number of factors can influence airway resistance and can play important roles in certain pathologies.
Lung Volume
  • Small bronchi and bronchioles in the lung have little to no supporting cartilage and depend on radial stretching by the elastic lung parenhcyma to maintain their patency. Because the elastic recoil of the lungs increases as the lung is expanded, this radial traction is also enhanced and thus smaller airways are rendered more patent. Conversely, at lower lung volumes, the reduced radial traction may result in critical narrowing of these smaller airways. Many individuals whose airways display pathologically excessive resistance to airflow may breathe at higher lung volumes to enhance this radial traction.
Bronchial Smooth Muscle
  • Bronchial smooth muscle surrounding bronchi and bronchioles can significantly modulate the diameter and thus resistance of these airways. Bronchoconstriction is mediated by neurons of the Parasympathetic Nervous System which travel via the Vagus nerve and release acetylcholine on bronchial smooth muscle cells. Bronchodilation is mediated by neurons of the Sympathetic Nervous System which activate beta2 receptors on bronchial smooth muscle cells. In this way, the autonomic nervous system can exert powerful effects on airflow and can be used to pharmacologically intervene in scenarios of pathological bronchoconstriction.

Dynamic Compression of Airways
The pressure of air inside airways gradually declines as it moves from the alveoli to the upper respiratory tract. This is a result of the progressive resistance to airflow that any airway will cause. In normal quiet expiration, the intra-airway pressure never declines below that of the intrapleural pressure and thus airways remain patent throughout their length. However, during forced expiration the intrapleural pressure in a healthy lung can sufficiently rise above the intra-airway pressure to overcome the natural radial traction maintaining airway patency. This yields dynamic airway collapse and limits airflow. In certain pathologies, such as emphysema, the radial traction of the lung maintaining airway patency can become so tenuous that even normal quiet expiration can yield dynamic airway collapse. These individuals can display airflow limitation even at rest.

  • In addition to the diameter, the length of a tube is an important factor in determining its resistance to flow (See: Resistance). As air passes through an airway, the progressive resistance it encounters gradually reduces the pressure gradient between the distally moving air and atmospheric pressure. Consequently, during expiration, the highest intra-airway pressures are found near the alveoli and these values gradually decline as air arrives near the mouth and nose. As described previously, small airways are not supported by any cartilage and depend on the elastic recoil of the lung to remain patent.
  • However, even small external pressures exerted by the intrapleural space can collapse the airway. During normal expiration the pressures within the intrapleural space are negative and thus aid in maintaining airway patency; however, during forced expirations powerful contraction of the chest wall can give the intrapleural space substantial positive pressures, above that of atmospheric pressure. At a certain distance within the airway, the declining intra-airway pressure will dip far enough below the positive intrapleural pressure during forced expiration that the elastic recoil of the lung maintaining airway patency will be overcome. In normal individuals, the elastic recoil of the lung is strong enough that this threshold segment is reached at a point where cartilage exists within the airways, thus preventing airway collapse.
  • However, in individuals with emphysema who display reduced elastic recoil this threshold segment may be reached at a point where no cartilage exists, resulting in bona fide airways collapse. For these individuals, strong expirations may result in trapping of air behind collapsed airways. In many cases, patients will purse their lips as they exhale. This action appears to help increase the intra-airway pressure during expiration and thus prevent airway collapse.