The ICC revealed an excellent consistency for both methods. Linear regression analysis revealed a correlation coefficient (r(2)) of 0.79, 0.94, and 0.83 for PēCO(2), V(D) and V(D)/V(T), respectively. Intra-class correlation coefficient (ICC) was used to measure consistency of each method.įour measurement pairs were obtained in all 20 dogs for method SBT and MC. Method MC and SBT were compared using Bland-Altman plots and linear regression. Physiologic dead space variables (V(D) and V(D)/V(T)) were calculated manually (method MC) or automatically (method SBT) using the Bohr-Enghoff equation.

At four time points arterial partial pressure of CO(2) (PaCO(2)) was measured. Mixed expired CO(2) partial pressure (PēCO(2)) was measured by two methods: method MC by analysis, using an infrared capnograph, of the expired gas collected in a mixing box and method SBT which calculated it automatically by a device consisting of a mainstream capnograph and a pneumotachograph.

Twenty client-owned dogs, ASA I and II undergoing anaesthesia for clinical purposes.įollowing pre-medication, induction of anaesthesia, and intubation of the trachea, intermittent positive pressure ventilation was commenced. 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.To compare physiologic dead space (V(D)) and physiologic dead space to tidal volume (V(T)) ratio (V(D)/V(T)) obtained by an automated single breath test for carbon dioxide (CO(2)) (method SBT) and a manual calculation (method MC) in ventilated healthy dogs. 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.

What is physiologic dead space