During this study, we did not observe any adverse effects from or patient discomfort with the heating electrode. There was no need to recalibrate, and, because it was a short-term study, the accuracy of the data recording was not influenced by patient motion.
Comparison Between Transcutaneous and Arterial Gas Pressures When Breathing Spontaneously in the Stable State
In this study, arterial O2 values were assessed over a range of 51 to 138 mm Hg, and arterial CO2 values were assessed over a range of 37 to 58 mm Hg. The correlation between Ptcco2 and Paco2 measures is shown in Figure 1. Both measurements were highly correlated (r = 0.848; p 56 mm Hg were less correlated with PtcC02. When PaC02 values of > 56 mm Hg were removed (n = 7), the correlation between PaC02 and PtcC02 improved substantially (r = 0.930; p < 0.0001). Ptc02 and Pa02 values were highly correlated, and linear regression was close to the identity line (r = 0.751; p 115 mm Hg were much less correlated with Ptc02.
According to the analysis technique described by Bland and Altman, we calculated the PC02 bias (ie, the mean PtcC02-PaC02 gradient) [Fig 2]. For all of the patients and all of the PC02 measurements (n = 48), the mean observed bias was —0.72 ± 2.98 mm Hg and the limits of agreement between both techniques were —6.68 and 5.24 mm Hg. The bias was lower for PaC02 values of < 56 mm Hg (mean bias, 0.07 ± 1.95 mm Hg; limits of agreement, —3.73 and 3.96 mm Hg). The difference between PaC02 and PtcC02 reached a maximum of 9.62 mm Hg in one patient. Similarly, the mean Ptc02-Pa02 gradient was found to be 7.89 ± 19.3 mm Hg, and the limits of agreement between both techniques were —30.7 and 46.5 mm Hg. The bias was lower for Pa02 values of < 115 mm Hg (mean bias, 7.06 ± 8.57 mm Hg; limits of agreement, —10.1 and 24.2 mm Hg). Mechanical ventilation is very important in case of breathing impossibility. It may save the life of the patient. More info for read on – www.infohealthcaremall.com.
Evolution of Transcutaneous Pressure and Arterial Blood Measures Among Responder Patients During Mechanical Ventilation
During mechanical ventilation, seven patients decreased PaC02 > 4 mm Hg between T0 and T35/ T40. These patients were considered to be PaC02 responders. The early PtcC02 response was observed during the first 5 min following the initiation of mechanical ventilation. Afterward, arterial CO2 and PtcC02 pressures evolved simultaneously and in a parallel manner in these responder patients (Fig 3). Stability was obtained after 20 min for both arterial and transcutaneous PC02 values. However, PtcC02 values always underestimated PaC02 values.
We also assessed four patients who were receiving mechanical ventilation with an increased Pa02 > 7.5 mm Hg between T0 and T35/T40. These patients were considered to be Pa02 responders. The initial changes in Ptc02 were observed during the first 5 min following the initiation of mechanical ventilation. Afterward, arterial O2 and Ptc02 pressures evolved simultaneously and in a similar manner in responder patients (data not shown). Stability was obtained after as soon as 5 min for both arterial and transcutaneous P02 values (data not shown).
In order to further assess the accuracy of PtcC02 variations during mechanical ventilation, we compared the respective PaC02 and PtcC02 decrements during all consecutive 5-min epochs after initiating mechanical ventilation in responder patients. As shown in Figure 4, PtcC02 variations during the 5-min period were significantly correlated with arterial variations (r = 0.8966; p = 0.0033). The results were similar for Po2 variations (data not shown).
Figure 1. Ptcco2 and Paco2 correlations in the 12 patients when breathing spontaneously (n = 48). Arterial and transcutaneous values were assessed every 10 min during 40 min of spontaneous breathing in the stable state and with room air, except for three patients who did not tolerate room air and were receiving low-flow O2.
Figure 2. Differences against mean for Pco2 data according to Bland and Altman (n = 48). Arterial and transcutaneous values were assessed every 10 min during 40 min of spontaneous breathing in the stable state and with room air, except for three patients who did not tolerate room air and were receiving low-flow oxygen.
Figure 3. Parallel evolution of Paco2 and Ptcco2 among responders (n = 7) and nonresponders (n = 5) to mechanical ventilation. Responder patients were defined as patients whose Paco2 decreased by > 4 mm Hg between T0 and T35, and also between T0 and T40 during mechanical ventilation (n = 7).
Figure 4. Correlation between PaC02 and PtcC02 variations during 5-min epochs in responder patients (n = 7). Responders were defined as patients whose PaC02 decreased by > 4 mm Hg between T0 and T35, and also between T0 and T40 during mechanical ventilation (n = 7).