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Esophageal capnometry during hemorrhagic shock and after resuscitation in rats.

Totapally BR, Fakioglu H, Torbati D, Wolfsdorf J - Crit Care (2002)

Bottom Line: Base deficit increased significantly following severe hemorrhage and remained significantly elevated after blood reinfusion.Significant correlations were found between base deficit and PeCO2-PaCO2 (P < 0.002) and PeCO2 (P < 0.022).Blood bicarbonate concentration decreased significantly following mild and severe hemorrhage, but its recovery was not complete at 60 min after blood reinfusion.

View Article: PubMed Central - PubMed

Affiliation: Associate Professor and Research Director, Division of Critical Care Medicine, Miami Children's Hospital, Miami, Florida, USA. Dan.Torbati@MCH.Com

ABSTRACT

Background: Splanchnic perfusion following hypovolemic shock is an important marker of adequate resuscitation. We tested whether the gap between esophageal partial carbon dioxide tension (PeCO2) and arterial partial carbon dioxide tension (PaCO2) is increased during graded hemorrhagic hypotension and reversed after blood reinfusion, using a fiberoptic carbon dioxide sensor.

Materials and method: Ten Sprague-Dawley rats were anesthetized, tracheotomized, and cannulated in one femoral artery and vein. A calibrated fiberoptic PCO2 probe was inserted into the distal third of the esophagus for determination of luminal PeCO2 during maintained anesthesia (pentobarbital 15 mg/kg per hour), normothermia (38 +/- 0.5 degrees C), and fluid balance (saline 5 ml/kg per hour). Three out of 10 rats were used to determine the limits of hemodynamic stability during gradual hemorrhage. Seven of the 10 rats were then subjected to mild and severe hemorrhage (15 and 20-25 ml/kg, respectively). Thirty minutes after severe hemorrhage, these rats were resuscitated by reinfusion of the shed blood. Arterial gas exchange, hemodynamic variables, and PeCO2 were recorded at each steady-state level of hemorrhage (at 30 and 60 min) and after resuscitation.

Results: The PeCO2-PaCO2 gap was significantly increased after mild and severe hemorrhage and returned to baseline (prehemorrhagic) values following blood reinfusion. Base deficit increased significantly following severe hemorrhage and remained significantly elevated after blood reinfusion. Significant correlations were found between base deficit and PeCO2-PaCO2 (P < 0.002) and PeCO2 (P < 0.022). Blood bicarbonate concentration decreased significantly following mild and severe hemorrhage, but its recovery was not complete at 60 min after blood reinfusion.

Conclusion: Esophageal-arterial PCO2 gap increases during graded hemorrhagic hypotension and returns to baseline value after resuscitation without complete reversal of the base deficit. These data suggest that esophageal capnometry could be used as an alternative for gastric tonometry during management of hypovolemic shock.

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Changes in partial arterial carbon dioxide tension (PaCO2), partial esophageal carbon dioxide tension (PeCO2) and esophageal–arterial PCO2 gap in seven anesthetized, spontaneously breathing rats subjected to mild and severe hemorrhagic hypotension followed by blood reinfusion. *P < 0.05, by repeated measures of analysis of variance followed by Dunnett multiple comparison test, using baseline as controls.
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Figure 1: Changes in partial arterial carbon dioxide tension (PaCO2), partial esophageal carbon dioxide tension (PeCO2) and esophageal–arterial PCO2 gap in seven anesthetized, spontaneously breathing rats subjected to mild and severe hemorrhagic hypotension followed by blood reinfusion. *P < 0.05, by repeated measures of analysis of variance followed by Dunnett multiple comparison test, using baseline as controls.

Mentions: Mild and severe homorrhagic hypotension created average reductions of 33% and 53% in MABP, respectively. Reinfusion of the blood restored MABP to the normal range. Blood hemoglobin concentration followed a pattern similar to that of blood pressure (Table 1). The HR was significantly increased following severe hemorrhage (29%). After blood reinfusion, the HR remained significantly higher than its prehemorrhagic baseline value (Table 1). The partial arterial oxygen tension was increased significantly during both mild and severe hemorrhagic hypotension, apparently caused by hyperventilation. The latter also reduced the PaCO2 significantly (Fig. 1). Arterial saturation following blood reinfusion was not significantly different from baseline. Blood bicarbonate concentrations decreased significantly following hemorrhage, but recovery was not complete at 60 min after blood reinfusion (Table 1).


Esophageal capnometry during hemorrhagic shock and after resuscitation in rats.

Totapally BR, Fakioglu H, Torbati D, Wolfsdorf J - Crit Care (2002)

Changes in partial arterial carbon dioxide tension (PaCO2), partial esophageal carbon dioxide tension (PeCO2) and esophageal–arterial PCO2 gap in seven anesthetized, spontaneously breathing rats subjected to mild and severe hemorrhagic hypotension followed by blood reinfusion. *P < 0.05, by repeated measures of analysis of variance followed by Dunnett multiple comparison test, using baseline as controls.
© Copyright Policy
Related In: Results  -  Collection

Show All Figures
getmorefigures.php?uid=PMC154116&req=5

Figure 1: Changes in partial arterial carbon dioxide tension (PaCO2), partial esophageal carbon dioxide tension (PeCO2) and esophageal–arterial PCO2 gap in seven anesthetized, spontaneously breathing rats subjected to mild and severe hemorrhagic hypotension followed by blood reinfusion. *P < 0.05, by repeated measures of analysis of variance followed by Dunnett multiple comparison test, using baseline as controls.
Mentions: Mild and severe homorrhagic hypotension created average reductions of 33% and 53% in MABP, respectively. Reinfusion of the blood restored MABP to the normal range. Blood hemoglobin concentration followed a pattern similar to that of blood pressure (Table 1). The HR was significantly increased following severe hemorrhage (29%). After blood reinfusion, the HR remained significantly higher than its prehemorrhagic baseline value (Table 1). The partial arterial oxygen tension was increased significantly during both mild and severe hemorrhagic hypotension, apparently caused by hyperventilation. The latter also reduced the PaCO2 significantly (Fig. 1). Arterial saturation following blood reinfusion was not significantly different from baseline. Blood bicarbonate concentrations decreased significantly following hemorrhage, but recovery was not complete at 60 min after blood reinfusion (Table 1).

Bottom Line: Base deficit increased significantly following severe hemorrhage and remained significantly elevated after blood reinfusion.Significant correlations were found between base deficit and PeCO2-PaCO2 (P < 0.002) and PeCO2 (P < 0.022).Blood bicarbonate concentration decreased significantly following mild and severe hemorrhage, but its recovery was not complete at 60 min after blood reinfusion.

View Article: PubMed Central - PubMed

Affiliation: Associate Professor and Research Director, Division of Critical Care Medicine, Miami Children's Hospital, Miami, Florida, USA. Dan.Torbati@MCH.Com

ABSTRACT

Background: Splanchnic perfusion following hypovolemic shock is an important marker of adequate resuscitation. We tested whether the gap between esophageal partial carbon dioxide tension (PeCO2) and arterial partial carbon dioxide tension (PaCO2) is increased during graded hemorrhagic hypotension and reversed after blood reinfusion, using a fiberoptic carbon dioxide sensor.

Materials and method: Ten Sprague-Dawley rats were anesthetized, tracheotomized, and cannulated in one femoral artery and vein. A calibrated fiberoptic PCO2 probe was inserted into the distal third of the esophagus for determination of luminal PeCO2 during maintained anesthesia (pentobarbital 15 mg/kg per hour), normothermia (38 +/- 0.5 degrees C), and fluid balance (saline 5 ml/kg per hour). Three out of 10 rats were used to determine the limits of hemodynamic stability during gradual hemorrhage. Seven of the 10 rats were then subjected to mild and severe hemorrhage (15 and 20-25 ml/kg, respectively). Thirty minutes after severe hemorrhage, these rats were resuscitated by reinfusion of the shed blood. Arterial gas exchange, hemodynamic variables, and PeCO2 were recorded at each steady-state level of hemorrhage (at 30 and 60 min) and after resuscitation.

Results: The PeCO2-PaCO2 gap was significantly increased after mild and severe hemorrhage and returned to baseline (prehemorrhagic) values following blood reinfusion. Base deficit increased significantly following severe hemorrhage and remained significantly elevated after blood reinfusion. Significant correlations were found between base deficit and PeCO2-PaCO2 (P < 0.002) and PeCO2 (P < 0.022). Blood bicarbonate concentration decreased significantly following mild and severe hemorrhage, but its recovery was not complete at 60 min after blood reinfusion.

Conclusion: Esophageal-arterial PCO2 gap increases during graded hemorrhagic hypotension and returns to baseline value after resuscitation without complete reversal of the base deficit. These data suggest that esophageal capnometry could be used as an alternative for gastric tonometry during management of hypovolemic shock.

Show MeSH
Related in: MedlinePlus