![]() ![]() We performed volumetric capnography ( V cap), and calculated V d,phys and V A when arterial blood sampling was necessary. ![]() Intubated infants ( n = 33 mean birth weight, 2257 ± 641 g mean gestational age, 35.0 ± 3.3 weeks) were enrolled. We investigated the relationship between dead space and partial pressure of carbon dioxide (PaCO 2) and assessed V A. We hypothesised that increased physiological dead space ( V d,phys) caused decreased minute alveolar ventilation ( V A alveolar ventilation ( V A) × respiratory rate) in well-ventilated infants with hypercapnia. 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.Hypercapnia occurs in ventilated infants even if tidal volume ( V T) and minute ventilation ( V E) are maintained. 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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