Is there an alliance between body mass index and end-tidal carbon dioxide partial pressure?

2016 ◽  
Author(s):  
Serkan Doğru ◽  
Tuğba Karaman ◽  
Aynur Şahin ◽  
Hakan Tapar ◽  
Serkan Karaman ◽  
...  
Keyword(s):  
Carbon Dioxide ◽  
Body Mass Index ◽  
Partial Pressure ◽  
Body Mass ◽  
Carbon Dioxide Partial Pressure ◽  
End Tidal Carbon Dioxide ◽  
End Tidal

Only Carbon Dioxide Absorbents Free of Both NaOH and KOH Do Not Generate Compound A during In Vitro  Closed-system Sevoflurane

2001 ◽  
Vol 95 (3) ◽  
pp. 750-755 ◽  
Author(s):  
Linda F. M. Versichelen ◽  
Marie-Paule L. A. Bouche ◽  
Georges Rolly ◽  
Jan F. P. Van Bocxlaer ◽  
Michel M. R. F. Struys ◽  
...  
Keyword(s):  
Carbon Dioxide ◽  
Partial Pressure ◽  
Closed System ◽  
Breathing Circuit ◽  
Lithium Hydroxide ◽  
Lung Model ◽  
Carbon Dioxide Partial Pressure ◽  
Compound A ◽  
End Tidal Carbon Dioxide ◽  
End Tidal

Background Insufficient data exist on the production of compound A during closed-system sevoflurane administration with newer carbon dioxide absorbents. Methods A modified PhysioFlex apparatus (Dräger, Lübeck, Germany) was connected to an artificial test lung (inflow at the top of the bellow approximately/= 160 ml/min CO2; outflow at the Y piece of the lung model approximately/= 200 ml/min, simulating oxygen consumption). Ventilation was set to obtain an end-tidal carbon dioxide partial pressure of approximately 40 mmHg. Various fresh carbon dioxide absorbents were used: Sodasorb (n = 6), Sofnolime (n = 6), and potassium hydroxide (KOH)-free Sodasorb (n = 7), Amsorb (n = 7), and lithium hydroxide (n = 7). After baseline analysis, liquid sevoflurane was injected into the circuit by syringe pump to obtain 2.1% end-tidal concentration for 240 min. At baseline and at regular intervals thereafter, end-tidal carbon dioxide partial pressure, end-tidal sevoflurane concentration, and canister inflow (T degrees(in)) and canister outflow (T degrees(out)) temperatures were measured. To measure compound Ainsp concentration in the inspired gas of the breathing circuit, 2-ml gas samples were taken and analyzed by capillary gas chromatography plus mass spectrometry. Results The median (minimum-maximum) highest compound Ainsp concentrations over the entire period were, in decreasing order: 38.3 (28.4-44.2)* (Sofnolime), 30.1 (23.9-43.7) (KOH-free Sodasorb), 23.3 (20.0-29.2) (Sodasorb), 1.6 (1.3-2.1)* (lithium hydroxide), and 1.3 (1.1-1.8)* (Amsorb) parts per million (*P < 0.01 vs. Sodasorb). After reaching their peak concentration, a decrease for Sofnolime, KOH-free Sodasorb, and Sodasorb until 240 min was found. The median (minimum-maximum) highest values for T degrees(out) were 39 (38-40), 40 (39-42), 41 (40-42), 46 (44-48)*, and 39 (38-41) degrees C (*P < 0.01 vs. Sodasorb), respectively. Conclusions With KOH-free (but sodium hydroxide [NaOH]-containing) soda limes even higher compound A concentrations are recorded than with standard Sodasorb. Only by eliminating KOH as well as NaOH from the absorbent (Amsorb and lithium hydroxide) is no compound A produced.

scholarly journals Dependency of Blood Flow Velocity in the Middle Cerebral Artery on End-Tidal Carbon Dioxide Partial Pressure—A Transcranial Ultrasound Doppler Study

1984 ◽  
Vol 4 (3) ◽  
pp. 368-372 ◽  
Author(s):  
Thomas-Marc Markwalder ◽  
Peter Grolimund ◽  
Rolf W. Seiler ◽  
Fritz Roth ◽  
Rune Aaslid
Keyword(s):  
Carbon Dioxide ◽  
Partial Pressure ◽  
Middle Cerebral Artery ◽  
Flow Velocity ◽  
Cerebral Artery ◽  
Cerebrovascular Reactivity ◽  
Carbon Dioxide Partial Pressure ◽  
Doppler Study ◽  
End Tidal Carbon Dioxide ◽  
End Tidal

The end-tidal carbon dioxide partial pressure (PCO2) response curves for the flow velocity in the middle cerebral artery were studied in 31 normal subjects with transcranial Doppler techniques. An exponential curve with an exponent of 0.034 mm Hg−1 was found to be a good fit to the recorded data. By means of this relationship, recordings of flow velocity in cerebral arteries can be normalized to a standard value of PCO2. Physiological aspects of cerebrovascular reactivity to PCO2 and the clinical implications of the PCO2 response curve are discussed. The normal material provides a reference for assessing pathological responses.

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