The assessment of gas exchange by automated analysis of O2 and CO2 alveolar to arterial differences

Abstract

A computer program to measure breath by breath alveolar pressure (PA) and alveolar to arterial difference (AaD) for O2 and CO2, by a mass-spectrometer has been implemented. The program allows the determination of alveolar gas by different methods: 1. Bohr's equation (BE); 2. ideal alveolar air equation for O2 (IDO2); 3. end-tidal (ET); 4. by the Rahn's definition of 'mean alveolar gas', i.e., alveolar pressures are defined when instantaneous respiratory exchange ratio (IRQ) equals mean respiratory exchange ratio (MRQ). This automated technique has been used in 16 patients with chronic obstructive lung disease (COLD) and 15 patients with pulmonary embolism (APE). In both groups of patients it was always possible to find in each breath the point where IRQ = MRQ and therefore to measure AaD by RD. IDO2 was significantly lower than PAO2 by the other methods. Also ET values of O2 and CO2 were significantly different from RD and BE in both groups of patients, however the difference was consistently higher in COLD patients. The different shape of the expirograms (steeper expirograms in COLD) is responsible for this different result. RD and BE AaD characterize gas exchange more precisely than ET, because the contribution of high VA/Q units is also evaluated. This is particularly important in COLD patients. Consideration on dead space measurements are also reported both for COLD and APE patients. In conclusion this automated technique provides the assessment of gas exchange for the use in clinical respiratory physiology and for the monitoring of gas-exchange in critically ill patients.

Inhibition of prostaglandin synthesis during polystyrene microsphere-induced pulmonary embolism in the rat

“…Pulmonary gas exchange was estimated primarily by the V D/VTalv, calculated using etCO2 in the Severinghaus equation (1,14,25). Use of the etCO2 to estimate the alveolar dead space fraction as opposed to the mixed-expired CO2 was chosen because the end-tidal equation provides a more specific estimate of the alveolar dead space fraction compared with the physiological dead space fraction, which measures both airway and alveolar dead space (25).…”

“…Use of the etCO2 to estimate the alveolar dead space fraction as opposed to the mixed-expired CO2 was chosen because the end-tidal equation provides a more specific estimate of the alveolar dead space fraction compared with the physiological dead space fraction, which measures both airway and alveolar dead space (25). VD/VTalv correlates with pulmonary vascular resistance (22), and perfusion defects in humans with PE (17) decreases in parallel with reduction in perfusion defects during treatment (25) and correlates with the plasma concentration of TxB2 in dogs with PE (39).…”

Use of genetic programming to diagnose venous thromboembolism in the emergency department

“…From 13 unique candidate variables, our selection process found that end-tidal CO 2 , end-tidal O 2 , and flow yielded the genome with highest overall diagnostic accuracy. End-tidal CO 2 concentrations have previously been used to diagnose pulmonary embolism [11,20]. Similarly, higher end-tidal O 2 concentrations are associated with pulmonary embolism [11].…”

“…The D-dimer test has excellent diagnostic sensitivity but has poor specificity in most patients with risk factors for pulmonary embolism [5]. Several studies have been conducted utilizing the knowledge that pulmonary embolism increases pulmonary deadspace and affects partial pressures of exhaled CO 2 or O 2 [11,20]. Recently, development of a portable device that measures exhaled CO 2 and O 2 concentrations along with flows and volumes has shown promise in predicting thromboembolism [12].…”

Measurement of expired carbon dioxide, oxygen and volume in conjunction with pretest probability estimation as a method to diagnose and exclude pulmonary venous thromboembolism

“…Other drawbacks to the use of the Enghoff equation include the requirement for a painful arterial blood gas stick, and the occurrence of negative values suggesting non-steady-state collection of end-tidal CO 2 and arterial blood pCO 2 (Kline et al, 2004). Prior work has provided concept framework suggesting that end-tidal CO 2 decreases and end-tidal O 2 increases in rats subjected to experimental PE, and in humans diagnosed with pulmonary thromboembolism (Paoletti et al, 1986;Jones et al, 2003). This project was designed to non-invasively measure the effect of high ventilation-perfusion relationships imparted by pulmonary thromboembolism by measuring the decrease without the need for arterial blood gas sampling.…”