75
Chapter four: Pressure regulation
resistance to compression (Fahlman et al. 2014a; Leith 1976). Whether cetaceans also show
high chest compliance is not known, but studies in the pilot whale (Olsen et al. 1969), beluga
whale, and bottlenose dolphin (Fahlman, unpub. obs.) indicate that the chest recoils to low
lung volumes. Thus, whereas for humans, pulmonary vascular engorgement is required to
fill the space left by the compressed lungs, the pinniped, and possibly the cetacean, chest
offers little resistance toward compression regardless of the depth to which they dive. The
venous thoracic rete that exists in many cetaceans may help pool blood in the thoracic cavity
and prevent excessive negative intra-thoracic pressures from developing (Hui 1975; Vogl
and Fisher 1982). In addition, dolphins and sperm whales have a tracheal lumen lined with
transitional epithelia (Cozzi et al. 2005; Leith 1989), and it has been suggested that this structure may engorge with blood and so offset the limited compression of a stiff trachea. Thus,
both the chest and trachea may resist compression in some species, but blood engorgement
may help fill the space caused by reduced gas volume and thereby prevent barotrauma.
The second problem relates to gas uptake by the pressurized lung. As depth increases, the
lung volume reduces and the pulmonary pressure and the partial pressure of the gases in the
respiratory system increase (Boyle’s and Dalton’s laws). This increases the solubility of these
gases within the blood (Henry’s law), potentially causing a problem with uptake of N 2 and the
risk of forming inert gas bubbles during ascent and decompression (i.e., DCS symptoms).
Marine mammals show modifications to their lungs compared to terrestrial mammals.
In general, marine mammals have reinforced upper airways and a lack of smaller respiratory
bronchii compared to terrestrial mammals (Kooyman 1973). However, there is great variation in tracheal stiffness between species and some appear not very different from terrestrial
mammals (Moore et al. 2014). Dolphins show the most extreme modifications including the
presence of a series of bronchial sphincter muscles found in the terminal segments of the
airways (Kooyman 1973). The function of these is largely unknown, but it is hypothesized to
relate to management of lung air (Belanger 1940; Ninomiya et al. 2004). In combination with
chest wall musculature, compression/expansion of the chest could be used to help control
volume (and thus buoyancy) without the need to exhale (Garcia-Parraga, pers. comm.)
Otariids (fur seals and sea lions) have robust cartilaginous airway reinforcement
extending to the alveolar sac, whereas phocids have no cartilage in the terminal airway,
but the walls are thickened by connective tissue and smooth muscle (Kooyman 1973). Thus
for all marine mammals, the thin-walled alveoli compress under increasing hydrostatic
pressure causing a graded decrease in the amount of respiratory gases absorbed by the
blood stream as the depth of diving increases. Effective gas exchange between lungs and
blood ceases when all alveoli are collapsed. This reinforced lung structure may also facilitate high ventilation rates at the surface (Denison and Kooyman 1973; Denison et al. 1971).
The mechanism leading to alveolar collapse (previously called lung collapse) was first
proposed by Scholander (1940): “It seems almost evident that the compression of such a system would begin with the alveols and end with the most rigid parts.” In this hypothetical situation, compression would result in a gradual reduction of the alveolar surface area
and increasing alveolar thickness reducing diffusion (i.e., a pulmonary shunt) and eventually leading to a termination of gas exchange (Kooyman and Sinnett 1982; McDonald and
Ponganis 2012). Progressive compression of alveoli was thus thought to reduce gas uptake
by the blood up to some critical depth of alveolar collapse at which gas uptake would cease
(Figure 4.2). Early empirical work supported this, suggesting alveolar collapse in bottlenose
dolphins at 70 m depth would lead to the muscle N 2 washout rates observed (Ridgway and
Howard 1979). Similarly, use of an arterial N 2 blood sampler during Weddell seal dives suggested alveolar collapse at approximately 30 m (Falke et al. 1985). More recently, continuous arterial partial pressure of O 2 during diving has shown suggested depth of alveolar
Chapter four: Pressure regulation
resistance to compression (Fahlman et al. 2014a; Leith 1976). Whether cetaceans also show
high chest compliance is not known, but studies in the pilot whale (Olsen et al. 1969), beluga
whale, and bottlenose dolphin (Fahlman, unpub. obs.) indicate that the chest recoils to low
lung volumes. Thus, whereas for humans, pulmonary vascular engorgement is required to
fill the space left by the compressed lungs, the pinniped, and possibly the cetacean, chest
offers little resistance toward compression regardless of the depth to which they dive. The
venous thoracic rete that exists in many cetaceans may help pool blood in the thoracic cavity
and prevent excessive negative intra-thoracic pressures from developing (Hui 1975; Vogl
and Fisher 1982). In addition, dolphins and sperm whales have a tracheal lumen lined with
transitional epithelia (Cozzi et al. 2005; Leith 1989), and it has been suggested that this structure may engorge with blood and so offset the limited compression of a stiff trachea. Thus,
both the chest and trachea may resist compression in some species, but blood engorgement
may help fill the space caused by reduced gas volume and thereby prevent barotrauma.
The second problem relates to gas uptake by the pressurized lung. As depth increases, the
lung volume reduces and the pulmonary pressure and the partial pressure of the gases in the
respiratory system increase (Boyle’s and Dalton’s laws). This increases the solubility of these
gases within the blood (Henry’s law), potentially causing a problem with uptake of N 2 and the
risk of forming inert gas bubbles during ascent and decompression (i.e., DCS symptoms).
Marine mammals show modifications to their lungs compared to terrestrial mammals.
In general, marine mammals have reinforced upper airways and a lack of smaller respiratory
bronchii compared to terrestrial mammals (Kooyman 1973). However, there is great variation in tracheal stiffness between species and some appear not very different from terrestrial
mammals (Moore et al. 2014). Dolphins show the most extreme modifications including the
presence of a series of bronchial sphincter muscles found in the terminal segments of the
airways (Kooyman 1973). The function of these is largely unknown, but it is hypothesized to
relate to management of lung air (Belanger 1940; Ninomiya et al. 2004). In combination with
chest wall musculature, compression/expansion of the chest could be used to help control
volume (and thus buoyancy) without the need to exhale (Garcia-Parraga, pers. comm.)
Otariids (fur seals and sea lions) have robust cartilaginous airway reinforcement
extending to the alveolar sac, whereas phocids have no cartilage in the terminal airway,
but the walls are thickened by connective tissue and smooth muscle (Kooyman 1973). Thus
for all marine mammals, the thin-walled alveoli compress under increasing hydrostatic
pressure causing a graded decrease in the amount of respiratory gases absorbed by the
blood stream as the depth of diving increases. Effective gas exchange between lungs and
blood ceases when all alveoli are collapsed. This reinforced lung structure may also facilitate high ventilation rates at the surface (Denison and Kooyman 1973; Denison et al. 1971).
The mechanism leading to alveolar collapse (previously called lung collapse) was first
proposed by Scholander (1940): “It seems almost evident that the compression of such a system would begin with the alveols and end with the most rigid parts.” In this hypothetical situation, compression would result in a gradual reduction of the alveolar surface area
and increasing alveolar thickness reducing diffusion (i.e., a pulmonary shunt) and eventually leading to a termination of gas exchange (Kooyman and Sinnett 1982; McDonald and
Ponganis 2012). Progressive compression of alveoli was thus thought to reduce gas uptake
by the blood up to some critical depth of alveolar collapse at which gas uptake would cease
(Figure 4.2). Early empirical work supported this, suggesting alveolar collapse in bottlenose
dolphins at 70 m depth would lead to the muscle N 2 washout rates observed (Ridgway and
Howard 1979). Similarly, use of an arterial N 2 blood sampler during Weddell seal dives suggested alveolar collapse at approximately 30 m (Falke et al. 1985). More recently, continuous arterial partial pressure of O 2 during diving has shown suggested depth of alveolar