- Library Home /
- Search Collections /
- Open Collections /
- Browse Collections /
- UBC Theses and Dissertations /
- End-tidal-to-arterial gas gradients during dynamic...
Open Collections
UBC Theses and Dissertations
UBC Theses and Dissertations
End-tidal-to-arterial gas gradients during dynamic end-tidal forcing Tymko, Michael Martin
Abstract
The end-tidal gas partial pressure is often considered a surrogate for the partial pressure of arterial blood gas; however, in healthy humans an end-tidal-to-arterial gradient normally exists for O₂ (PET–PaO₂) and CO₂ (Pa–PETCO₂). We sought to determine if the Pa-PETCO₂ affects the measurement of cerebrovascular reactivity (CVR) and the hypercapnic ventilatory response (HCVR), and whether it could be corrected for in subjects with (n=8) and without (n=7) a patent foramen ovale (PFO) during a CO₂ reactivity test. It was hypothesized that (1) the Pa-PETCO₂ would be greater in the background of hypoxia compared to normoxia during a CO₂ reactivity test, (2) the PET-PaCO₂ would be similar while the PET-PaO₂ gradient would be greater in those with a PFO, (3) the HCVR and CVR would be lower when plotted against PETCO₂ compared to PaCO₂, and (4) a PaCO₂ prediction algorithm will correct for the Pa-PETCO₂. PETCO₂ was controlled by dynamic end-tidal forcing in steady-state steps of -8, -4, 0, +4, and +8mmHg from baseline in normoxia (NX1; PETO2 = 94.3 ± 1.3 mmHg) and hypoxia (HX1; PETO₂ = 50.8 ± 0.1 mmHg). Tests were repeated following correction for the Pa-PETCO₂ (NX2 and HX2). Internal carotid artery blood flow (Q̇ICA), middle cerebral artery blood flow velocity (MCAv) and temperature-corrected end-tidal and arterial blood gases were measured throughout each protocol. CVR was calculated using linear regression analysis in the hypocapnic and hypercapnic ranges by indexing the percent change in Q̇ICA, and MCAv against PETCO₂ and PaCO₂. In both conditions, a Pa-PETCO₂ was present in hypercapnia but not hypocapnia, and was unchanged by PFO (P>0.05), however, the PET-PaO₂ was greater in PFO+ participants in normoxia (P=0.003). Relative Q̇ICA CVR, MCAv CVR, and HCVR assessed using PETCO₂ were less compared to using PaCO₂ during both normoxia and hypoxia (P>0.05). A previously derived prediction equation minimized the difference between measured and predicted PaCO₂ during +4mmHg (NX2: 0.0 ± 0.2 mmHg, P=0.894; HX2: -0.2 ± 0.2 mmHg, P=0.403) and +8mmHg for HX2 (0.0 ± 0.3 mmHg, P=0.860). In conclusion, care must be taken when indexing reactivity measures to PETCO₂ compared to PaCO₂.
Item Metadata
Title |
End-tidal-to-arterial gas gradients during dynamic end-tidal forcing
|
Creator | |
Publisher |
University of British Columbia
|
Date Issued |
2015
|
Description |
The end-tidal gas partial pressure is often considered a surrogate for the partial pressure of arterial blood gas; however, in healthy humans an end-tidal-to-arterial gradient normally exists for O₂ (PET–PaO₂) and CO₂ (Pa–PETCO₂). We sought to determine if the Pa-PETCO₂ affects the measurement of cerebrovascular reactivity (CVR) and the hypercapnic ventilatory response (HCVR), and whether it could be corrected for in subjects with (n=8) and without (n=7) a patent foramen ovale (PFO) during a CO₂ reactivity test. It was hypothesized that (1) the Pa-PETCO₂ would be greater in the background of hypoxia compared to normoxia during a CO₂ reactivity test, (2) the PET-PaCO₂ would be similar while the PET-PaO₂ gradient would be greater in those with a PFO, (3) the HCVR and CVR would be lower when plotted against PETCO₂ compared to PaCO₂, and (4) a PaCO₂ prediction algorithm will correct for the Pa-PETCO₂. PETCO₂ was controlled by dynamic end-tidal forcing in steady-state steps of -8, -4, 0, +4, and +8mmHg from baseline in normoxia (NX1; PETO2 = 94.3 ± 1.3 mmHg) and hypoxia (HX1; PETO₂ = 50.8 ± 0.1 mmHg). Tests were repeated following correction for the Pa-PETCO₂ (NX2 and HX2). Internal carotid artery blood flow (Q̇ICA), middle cerebral artery blood flow velocity (MCAv) and temperature-corrected end-tidal and arterial blood gases were measured throughout each protocol. CVR was calculated using linear regression analysis in the hypocapnic and hypercapnic ranges by indexing the percent change in Q̇ICA, and MCAv against PETCO₂ and PaCO₂. In both conditions, a Pa-PETCO₂ was present in hypercapnia but not hypocapnia, and was unchanged by PFO (P>0.05), however, the PET-PaO₂ was greater in PFO+ participants in normoxia (P=0.003). Relative Q̇ICA CVR, MCAv CVR, and HCVR assessed using PETCO₂ were less compared to using PaCO₂ during both normoxia and hypoxia (P>0.05). A previously derived prediction equation minimized the difference between measured and predicted PaCO₂ during +4mmHg (NX2: 0.0 ± 0.2 mmHg, P=0.894; HX2: -0.2 ± 0.2 mmHg, P=0.403) and +8mmHg for HX2 (0.0 ± 0.3 mmHg, P=0.860). In conclusion, care must be taken when indexing reactivity measures to PETCO₂ compared to PaCO₂.
|
Genre | |
Type | |
Language |
eng
|
Date Available |
2015-07-24
|
Provider |
Vancouver : University of British Columbia Library
|
Rights |
Attribution-NonCommercial-NoDerivs 2.5 Canada
|
DOI |
10.14288/1.0166430
|
URI | |
Degree | |
Program | |
Affiliation | |
Degree Grantor |
University of British Columbia
|
Graduation Date |
2015-09
|
Campus | |
Scholarly Level |
Graduate
|
Rights URI | |
Aggregated Source Repository |
DSpace
|
Item Media
Item Citations and Data
Rights
Attribution-NonCommercial-NoDerivs 2.5 Canada