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Intramucosal-arterial PCO2 gap fails to reflect intestinal dysoxia in hypoxic hypoxia.

Dubin A, Murias G, Estenssoro E, Canales H, Badie J, Pozo M, Sottile JP, Barán M, Pálizas F, Laporte M - Crit Care (2002)

Bottom Line: Both progressive bleeding and hydrochloric acid aspiration provoked critical reductions in systemic and intestinal oxygen delivery and consumption.DeltaPCO2 increased in the IH group (12 +/- 10 [mean +/- SD] versus 40 +/- 13 mmHg; P < 0.001), but remained unchanged in HH and in the sham group (13 +/- 6 versus 10 +/- 13 mmHg and 8 +/- 5 versus 9 +/- 6 mmHg; not significant).These results suggest that DeltaPCO2 might be determined primarily by blood flow.

View Article: PubMed Central - PubMed

Affiliation: Cátedra de Farmacologia, Facultad de Ciencias Médicas, Universidad Nacional de La Plata, Argentina. adee@infovia.com.ar

ABSTRACT

Introduction: An elevation in intramucosal-arterial PCO2 gradient (DeltaPCO2) could be determined either by tissue hypoxia or by reduced blood flow. Our hypothesis was that in hypoxic hypoxia with preserved blood flow, DeltaPCO2 should not be altered.

Methods: In 17 anesthetized and mechanically ventilated sheep, oxygen delivery was reduced by decreasing flow (ischemic hypoxia, IH) or arterial oxygen saturation (hypoxic hypoxia, HH), or no intervention was made (sham). In the IH group (n = 6), blood flow was lowered by stepwise hemorrhage; in the HH group (n = 6), hydrochloric acid was instilled intratracheally. We measured cardiac output, superior mesenteric blood flow, gases, hemoglobin, and oxygen saturations in arterial blood, mixed venous blood, and mesenteric venous blood, and ileal intramucosal PCO2 by tonometry. Systemic and intestinal oxygen transport and consumption were calculated, as was DeltaPCO2. After basal measurements, measurements were repeated at 30, 60, and 90 minutes.

Results: Both progressive bleeding and hydrochloric acid aspiration provoked critical reductions in systemic and intestinal oxygen delivery and consumption. No changes occurred in the sham group. DeltaPCO2 increased in the IH group (12 +/- 10 [mean +/- SD] versus 40 +/- 13 mmHg; P < 0.001), but remained unchanged in HH and in the sham group (13 +/- 6 versus 10 +/- 13 mmHg and 8 +/- 5 versus 9 +/- 6 mmHg; not significant).

Discussion: In this experimental model of hypoxic hypoxia with preserved blood flow, DeltaPCO2 was not modified during dependence of oxygen uptake on oxygen transport. These results suggest that DeltaPCO2 might be determined primarily by blood flow.

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Systemic and intestinal oxygen supply dependence. (a) Relationship between systemic oxygen transport and consumption during ischemic and hypoxic hypoxia, and in the sham group. (b) Relationship between intestinal oxygen transport and consumption during ischemic and hypoxic hypoxia, and in the sham group. Data are expressed as means ± SEM. *P < 0.05 versus basal oxygen consumption. §P < 0.05 versus sham group.
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Figure 1: Systemic and intestinal oxygen supply dependence. (a) Relationship between systemic oxygen transport and consumption during ischemic and hypoxic hypoxia, and in the sham group. (b) Relationship between intestinal oxygen transport and consumption during ischemic and hypoxic hypoxia, and in the sham group. Data are expressed as means ± SEM. *P < 0.05 versus basal oxygen consumption. §P < 0.05 versus sham group.

Mentions: Systemic and intestinal supply dependence was induced in both the IH and HH groups. There were no significant changes in systemic and intestinal DO2 and VO2 in the sham group (Figure 1). In the IH group, supply dependence appeared with critical decreases in CO and superior mesenteric artery blood flow (0.104 ± 0.024 versus 0.048 ± 0.006 l/min per kg, and 0.664 ± 0.227 versus 0.258 ± 0.082 l/min per kg, respectively; P < 0.0001). In the HH group it was due to a progressive decrease in arterial oxygenation. CO and intestinal blood flow were maintained (0.446 ± 0.085 versus 0.431 ± 0.140 ml/min per kg, respectively; not significant), owing to the administration of normal saline (median 630 ml; range 20–1310 ml). Arterial and intra-mucosal pH fell significantly in the IH and HH groups. In the HH group it was primarily related to systemic respiratory and metabolic acidosis (Tables 1 and 2), because ΔPCO2 did not increase. In addition, systemic and intestinal venoarterial PCO2 gradients were not modified. CO2 content differences also did not change (Table 2 and Figure 2). In contrast, in the IH group, ΔPCO2, systemic and intestinal venoarterial PCO2, and CO2 content gradients increased significantly (Table 2 and Figure 2). In the sham group, CO2 gradients and pHi remained unchanged.


Intramucosal-arterial PCO2 gap fails to reflect intestinal dysoxia in hypoxic hypoxia.

Dubin A, Murias G, Estenssoro E, Canales H, Badie J, Pozo M, Sottile JP, Barán M, Pálizas F, Laporte M - Crit Care (2002)

Systemic and intestinal oxygen supply dependence. (a) Relationship between systemic oxygen transport and consumption during ischemic and hypoxic hypoxia, and in the sham group. (b) Relationship between intestinal oxygen transport and consumption during ischemic and hypoxic hypoxia, and in the sham group. Data are expressed as means ± SEM. *P < 0.05 versus basal oxygen consumption. §P < 0.05 versus sham group.
© Copyright Policy
Related In: Results  -  Collection

Show All Figures
getmorefigures.php?uid=PMC153432&req=5

Figure 1: Systemic and intestinal oxygen supply dependence. (a) Relationship between systemic oxygen transport and consumption during ischemic and hypoxic hypoxia, and in the sham group. (b) Relationship between intestinal oxygen transport and consumption during ischemic and hypoxic hypoxia, and in the sham group. Data are expressed as means ± SEM. *P < 0.05 versus basal oxygen consumption. §P < 0.05 versus sham group.
Mentions: Systemic and intestinal supply dependence was induced in both the IH and HH groups. There were no significant changes in systemic and intestinal DO2 and VO2 in the sham group (Figure 1). In the IH group, supply dependence appeared with critical decreases in CO and superior mesenteric artery blood flow (0.104 ± 0.024 versus 0.048 ± 0.006 l/min per kg, and 0.664 ± 0.227 versus 0.258 ± 0.082 l/min per kg, respectively; P < 0.0001). In the HH group it was due to a progressive decrease in arterial oxygenation. CO and intestinal blood flow were maintained (0.446 ± 0.085 versus 0.431 ± 0.140 ml/min per kg, respectively; not significant), owing to the administration of normal saline (median 630 ml; range 20–1310 ml). Arterial and intra-mucosal pH fell significantly in the IH and HH groups. In the HH group it was primarily related to systemic respiratory and metabolic acidosis (Tables 1 and 2), because ΔPCO2 did not increase. In addition, systemic and intestinal venoarterial PCO2 gradients were not modified. CO2 content differences also did not change (Table 2 and Figure 2). In contrast, in the IH group, ΔPCO2, systemic and intestinal venoarterial PCO2, and CO2 content gradients increased significantly (Table 2 and Figure 2). In the sham group, CO2 gradients and pHi remained unchanged.

Bottom Line: Both progressive bleeding and hydrochloric acid aspiration provoked critical reductions in systemic and intestinal oxygen delivery and consumption.DeltaPCO2 increased in the IH group (12 +/- 10 [mean +/- SD] versus 40 +/- 13 mmHg; P < 0.001), but remained unchanged in HH and in the sham group (13 +/- 6 versus 10 +/- 13 mmHg and 8 +/- 5 versus 9 +/- 6 mmHg; not significant).These results suggest that DeltaPCO2 might be determined primarily by blood flow.

View Article: PubMed Central - PubMed

Affiliation: Cátedra de Farmacologia, Facultad de Ciencias Médicas, Universidad Nacional de La Plata, Argentina. adee@infovia.com.ar

ABSTRACT

Introduction: An elevation in intramucosal-arterial PCO2 gradient (DeltaPCO2) could be determined either by tissue hypoxia or by reduced blood flow. Our hypothesis was that in hypoxic hypoxia with preserved blood flow, DeltaPCO2 should not be altered.

Methods: In 17 anesthetized and mechanically ventilated sheep, oxygen delivery was reduced by decreasing flow (ischemic hypoxia, IH) or arterial oxygen saturation (hypoxic hypoxia, HH), or no intervention was made (sham). In the IH group (n = 6), blood flow was lowered by stepwise hemorrhage; in the HH group (n = 6), hydrochloric acid was instilled intratracheally. We measured cardiac output, superior mesenteric blood flow, gases, hemoglobin, and oxygen saturations in arterial blood, mixed venous blood, and mesenteric venous blood, and ileal intramucosal PCO2 by tonometry. Systemic and intestinal oxygen transport and consumption were calculated, as was DeltaPCO2. After basal measurements, measurements were repeated at 30, 60, and 90 minutes.

Results: Both progressive bleeding and hydrochloric acid aspiration provoked critical reductions in systemic and intestinal oxygen delivery and consumption. No changes occurred in the sham group. DeltaPCO2 increased in the IH group (12 +/- 10 [mean +/- SD] versus 40 +/- 13 mmHg; P < 0.001), but remained unchanged in HH and in the sham group (13 +/- 6 versus 10 +/- 13 mmHg and 8 +/- 5 versus 9 +/- 6 mmHg; not significant).

Discussion: In this experimental model of hypoxic hypoxia with preserved blood flow, DeltaPCO2 was not modified during dependence of oxygen uptake on oxygen transport. These results suggest that DeltaPCO2 might be determined primarily by blood flow.

Show MeSH
Related in: MedlinePlus