Year in review in Intensive Care Medicine, 2008: II. Experimental, acute respiratory failure and ARDS, mechanical ventilation and endotracheal intubation

SCOPUS: re.jinfo:eu-repo/semantics/publishe

Acute hypoxia during propofol-anesthesia, but not during sevoflurane-anesthesia, stimulates macro- and microcirculatory hemodynamics in dogs

Background & Goal: To study the response to acute hypoxia in micro- and macrocirculatory variables during propofol- (PROPO) vs. sevoflurane- (SEVO) anesthesia. Materials and methods: In randomized cross over design, chronically instrumented dogs (24-32 kg, n=6 per group) were anesthetized with PROPO or SEVO (equi-anesthetic dosages), mechanically ventilated (FiO2 ~0.3) and underwent a hypoxemic episode (FiO2 ~0.1 for 15 min [1] ), followed by normoxic recovery (FiO2 ~0.3; 90 min). Microcirculatory perfusion of oral mucosa (µ-mucosa) and hindlimb skin (µ-skin) were measured by laser Doppler fluxmetry. Regional gastric intraluminal PCO2 (PgiCO2) was measured by tonometry. Macro-hemodynamics (cardiac output (CO), blood pressures), metabolism (O2-consumption (VO2); indirect alorimetry) and blood-derived variables (art. O2-content (CaO2), acid/base variables) were also measured. Statistics: Data are mean±sem for n=6 experiments per group, and compared by two-way-ANOVA, corrected for multiple comparisons (Bonferroni). A p< 0.05 was significant. Results and Discussion: During normoxia, both CO and CaO2 were similar (both N.S.) under PROPO and SEVO. In addition, the hypoxia model achieved comparable drops in CaO2 (N.S.) under both anesthesia types. However, hypoxia elicited markedly different responses between PROPO and SEVO: Hypoxia during PROPO significantly increased µ-mucosa and µ-skin, but decreased both during SEVO. After hypoxia under PROPO, PgiCO2 was preserved, whereas under SEVO, PgiCO2 significantly accumulated. During PROPO, hypoxia generally stimulated macro-hemodynamics (e.g., CO increased from 86±3 to 123±8 ml/kg/min), whereas in contrast during SEVO-hypoxia hemodynamics were unresponsive (CO, 72±8 vs. 71±6 ml/kg/min) or even depressed. On the metabolic level, VO2 was maintained during PROPO/hypoxia, but significantly decreased with SEVO/hypoxia. Conclusion:  In this dog model, only PROPO permitted hemodynamic stimulation by acute hypoxia, resulting in (compensatory) increased micro- and macrocirculatory perfusion. In line, PROPO-hypoxia maintained VO2 , without aggravating anaerobiosis markers (lactate), and with preservation of PgiCO2. In contrast, SEVO failed to permit hemodynamic stimulation by hypoxia and failed to preserve PgiCO2. If our data can be transferred to the clinical setting, PROPO appears beneficial (vs. SEVO) to support the systemic and regional circulation during acute hypoxia. Reference: 1. Schwarte LA et al, Int Care Med 2011;37:701-1

Sevoflurane and propofol anaesthesia differentially modulate the effects of epinephrine and norepinephrine on microcirculatory gastric mucosal oxygenation

Background: Adequate gastrointestinal mucosal oxygenation is regarded to be crucial in the prevention and therapy of critical illness. Epinephrine and norepinephrine are used for perioperative haemodynamic support. However, their per se effects on gastromucosal haemoglobin oxygenation (mu HbO(2)) remain unclear. Moreover, respective effects of epinephrine and norepinephrine may be affected by the type of underlying anaesthesia. Thus, we studied the effects of epinephrine and norepinephrine during anaesthesia with sevoflurane or propofol on regional gastromucosal mu HbO(2) and systemic O(2)-derived variables. Methods: In a double-randomized cross-over study, chronically instrumented dogs (n=6 per group) were anaesthetized randomly with sevoflurane or propofol, ventilated, and then randomly received either epinephrine or norepinephrine (0, 0.05, 0.1, and 0.2 mu g kg(-1) min(-1)). We measured gastromucosal mu HbO(2), systemic haemodynamics, and O(2)-derived variables. Results: During sevoflurane anaesthesia, norepinephrine markedly increased mu HbO(2) (P <0.0001) and systemic oxygen transport (DO(2)) (P=0.0006). In contrast, epinephrine failed to increase mu HbO(2), despite doubling DO(2) (P=0.0002). During propofol anaesthesia, in contrast to sevoflurane, neither epinephrine nor norepinephrine affected mu HbO(2), although epinephrine, but not norepinephrine, again resulted in markedly increased DO(2) (P <0.0001). Conclusions: The effects of epinephrine and norepinephrine depended on the type of anaesthesia. In addition, regional effects (i.e. mu HbO(2)) were not predictable from systemic effects (i.e. DO(2))

Moderate hypercapnia exerts beneficial effects on splanchnic energy metabolism during endotoxemia.

PURPOSE: Low tidal volume ventilation and permissive hypercapnia are required in patients with sepsis complicated by ARDS. The effects of hypercapnia on tissue oxidative metabolism in this setting are unknown. We therefore determined the effects of moderate hypercapnia on markers of systemic and splanchnic oxidative metabolism in an animal model of endotoxemia. METHODS: Anesthetized rats maintained at a PaCO(2) of 30, 40 or 60 mmHg were challenged with endotoxin. A control group (PaCO(2) 40 mmHg) received isotonic saline. Hemodynamic variables, arterial lactate, pyruvate, and ketone bodies were measured at baseline and after 4 h. Tissue adenosine triphosphate (ATP) and lactate were measured in the small intestine and the liver after 4 h. RESULTS: Endotoxin resulted in low cardiac output, increased lactate/pyruvate ratio and decreased ketone body ratio. These changes were not influenced by hypercapnia, but were more severe with hypocapnia. In the liver, ATP decreased and lactate increased independently from PaCO(2) after endotoxin. In contrast, the drop of ATP and the rise in lactate triggered by endotoxin in the intestine were prevented by hypercapnia. CONCLUSIONS: During endotoxemia in rats, moderate hypercapnia prevents the deterioration of tissue energetics in the intestine