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Direct hepatic tissue PO2 measurements in sepsis and tamponade models

Introduction

Tissue hypoxia diagnosis at the bedside remains a huge challenge for intensivists, and surrogate markers of tissue oxygen utilization are used instead. The precise correlation between them is not well defined.

Objective

To verify the correlation between portal blood flow, O2 and CO2 gradients, hepatic lactate gradient with hepatic tissue PO2.

Methods

This is an observational experimental study, in which 16 large, male, white pigs, about 35 kg, were allocated into two groups: sepsis (n = 8), and tamponade (n = 8). All protocols were approved by the institutional review board for animal experiments. Anesthesia: premedication with intramuscular ketamine (10 mg/kg) plus midazolam (0.25 mg/kg); induction with intravenous propofol 5 mg/kg (at maximum) followed by continuous isoflurane (1.5%), fentanil 2.5 μg/kg/hour and pancuronium 0.24 mg/kg/hour. Mechanical ventilation settings: Vt 10 ml/kg, PEEP 5 cmH2O, respiratory rate set to normocapnia and FiO2 adjusted to arterial oxygen partial pressure 60 to 100 mmHg. Continuous gas analysis was also performed. Electrocardiography, invasive pressure in dissected femoral artery, right atria and ventricular pressures after left internal jugular dissection; etCO2 (by gas analyzer), pulmonary artery catheter, portal vein flow Doppler ultrasound, and small bowel tonometry, after median laparotomy. Liver tissue pO2 monitoring: pO2 - fluorescence quenching optode - and LDF - laser Doppler fluxometry - probes were directly inserted inside liver parenchyma (Oxford-Optronix, UK). Other procedures: cistostomy (to monitor diuresis), inferior vena cava (by femoral) and superior vena cava (by right jugular) vein catheterizations. Portal vein catheter, after liver hilus dissection (Seldinger) and fluoroscopy-guided right suprahepatic vein catheterization. After experiments, pigs were sacrificed with sedative overdose and 20 ml KCl 19.1% injection. Sepsis was induced by spread of 150 ml warm saline diluted 1 g/kg feces in the peritoneal cavity. Tamponade: mini-thoracotomy and a mono-lumen intrapericardium catheter positioning to arouse cardiac tamponade, targeting 20% of baseline decrease in cardiac output at each time phase. Data were analyzed in Excel 2007.

Results

In both groups, there was a progressive decrease in portal blood flow, an increase in jejune-portal CO2 gap, and a decrease in hepatic tissue PO2. Interestingly, there was a progressive hepatic lactate consumption as hepatic tissue PO2 decreases. Figure 1 (overleaf) depicts the behavior of the above variables.

Figure 1
figure 1

Portal blood flow, hepatic CO 2 gap, hepatic lactate gradient, jejune CO 2 gap and hepatic tissue PO 2 over time in both groups, sepsis and tamponade.

Conclusion

Hepatic tissue PO2 paralleled portal blood flow and was inversely related to the jejune tissue PCO2 gap. Liver has increased lactate consumption as hepatic tissue PO2 decreased.

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Silva, E., Rehder, P., Pereira, A. et al. Direct hepatic tissue PO2 measurements in sepsis and tamponade models. Crit Care 15 (Suppl 2), P3 (2011). https://doi.org/10.1186/cc10151

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