Patients in hemorrhagic shock often require emergent airway management. Clinical experience suggests that oxygen desaturation occurs rapidly in these patients; however, data are scant. The hypothesis of this study was that increasing levels of hemorrhagic shock, varying levels of fraction of inspired oxygen (Fio2) for preoxygenation, and fluid resuscitation significantly affect the duration until critical desaturation occurs.
Fifteen pigs were studied in a hemorrhagic shock model with controlled hemorrhage (15, 30, and 45 ml/kg blood loss) and randomized to standard fluid resuscitation or no fluids. At each shock level, three apnea experiments (in randomized order) were performed after 5 min of preoxygenation at 21, 50, or 100% Fio2. After preoxygenation, ventilation was discontinued and the time to peripheral oxygen saturation of 70% or less was measured.
During normovolemia, peripheral oxygen desaturation to less than 70% occurred after 33+/-7 s (Fio2=0.21, mean+/-SD), 89+/-12 s (Fio2=0.5), and 165+/-22 s (Fio2=1.0; P<0.001). During increasing blood loss, peripheral oxygen desaturation to Spo2 less than 70% occurred significantly (P<0.001) faster compared with normovolemia, but no effect of fluid resuscitation was observed. With 45 ml/kg blood loss, peripheral oxygen desaturation to less than 70% occurred after approximately 15 (Fio2=0.21) to 65 (Fio2=0.5) to 140 s (Fio2=1.0).
Findings from this swine hemorrhagic shock model confirm that Fio2 and the level of hemorrhagic shock, but not fluid resuscitation, influence the rate of apneic desaturation. A five-fold increase in time until critical oxygen desaturation occurs can be achieved when preoxygenating with 100% oxygen compared with room air, underscoring the importance of adequate preoxygenation before emergent airway management.
[Show abstract][Hide abstract] ABSTRACT: Treatment of polytrauma patients remains a medical as well as socioeconomic challenge. Although diagnostics and therapy improved during the last decades, multiple injuries are still the major cause of fatalities in patients below 45 years of age. Organ dysfunction and organ failure are major complications in patients with major injuries and contribute to mortality during the clinical course. Profound understanding of the systemic pathophysiological response is crucial for innovative therapeutic approaches. Therefore, experimental studies in various animal models are necessary. This review is aimed at providing detailed information of common trauma models in small as well as in large animals.
BioMed Research International 01/2011; 2011:797383. DOI:10.1155/2011/797383 · 2.71 Impact Factor
[Show abstract][Hide abstract] ABSTRACT: The interaction between neutrophils and activated endothelium is essential for the development of multiple organ dysfunction in patients with hemorrhagic shock (HS). Mechanical ventilation frequently is used in patients with HS. The authors sought to investigate the consequences of mechanical ventilation of mice subjected to HS on microvascular endothelial activation in the lung and kidney.
Anesthetized wild type C57BL/6 male mice were subjected to controlled hemorrhage; subgroups of mice were mechanically ventilated during the HS insult. To study the effect of acute hypoxia on the mice, the animals were housed in hypoxic cages. Gene expression levels was assessed by quantitative real-time polymerase chain reaction. Protein expression was assessed by immunohistochemistry and enzyme-linked immunosorbent assay.
Ninety minutes after the shock induction, a vascular bed-specific, heterogeneous proinflammatory endothelial activation represented by E-selectin, vascular cell adhesion molecule 1, and intercellular adhesion molecule 1 expression was seen in kidney and lung. No differences in adhesion molecules between the spontaneously breathing and mechanically ventilated mice were found. Concentrations of the proinflammatory cytokines chemokine (C-X-C motif) ligand 1 (11.0-fold) and interleukin-6 (21.7-fold) were increased after 90 min of HS. Two hours of 6% oxygen did not induce the expression of E-selectin, vascular cell adhesion molecule 1, and intercellular adhesion molecule 1 in the kidneys and the lung.
Hemorrhagic shock leads to an early and reversible proinflammatory endothelial activation in kidney and lung. HS-induced endothelial activation is not changed by mechanical ventilation during the shock phase. Hypoxia alone does not lead to endothelial activation. The observed proinflammatory endothelial activation is mostly ischemia- or reperfusion-dependent and not related to hypoxia.
Data provided are for informational purposes only. Although carefully collected, accuracy cannot be guaranteed. The impact factor represents a rough estimation of the journal's impact factor and does not reflect the actual current impact factor. Publisher conditions are provided by RoMEO. Differing provisions from the publisher's actual policy or licence agreement may be applicable.