In horses, the displacement of the caudal border of the soft palate to a position above the epiglottis, called dorsal displacement of the soft palate, is not physiologic, except when it occurs during swallowing, coughing, or whinnying (see Figure 9-1). (l: nasal cavity 2: nasopharynx 3: oropharynx 4: soft palate 5: intrapharyngeal ostium (“button hole”) 6: epiglottis 7: corniculate cartilage 8: larynx 9: trachea 10: guttural pouch 11: frontal sinus 12: sphenopalatine sinus 13: esophagus 14: tongue 15: food bolus 16: closed larynx 17: endoscope.) (Modified with permission from Cook WR: Specifications for speed in the racehorse: in the airflow factors, Menasha, WI, 1989, Russell Meerdink.) Depending on the disease condition, additional mechanisms that can contribute to an elevated physiological dead space measurement include shunt, a substantial increase in overall V'A/Q' ratio, diffusion impairment, and ventilation delivered to unperfused alveolar spaces.FIGURE 9-1 Lateral view of the pharyngolaryngeal area during ( A) normal breathing, ( B) swallowing, and ( C) dorsal displacement of the soft palate.
For the range of physiological abnormalities associated with an increased physiological dead space measurement, increased alveolar ventilation/perfusion ratio (V'A/Q') heterogeneity has been the most important pathophysiological mechanism. Although a frequently cited explanation for an elevated dead space measurement has been the development of alveolar regions receiving no perfusion, evidence for this mechanism is lacking in both of these disease settings. An elevated physiological dead space, calculated from measurements of arterial CO2 and mixed expired CO2, has proven to be a useful clinical marker of prognosis both for patients with acute respiratory distress syndrome and for patients with severe heart failure.
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