Anesthesiology · 2012
Cutaneous vasoconstriction affects near-infrared spectroscopy determined cerebral oxygen saturation during administration of norepinephrine.
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Sørensen Henrik, Secher Niels H, Siebenmann Christoph, Nielsen Henning B, Kohl-Bareis Matthias, Lundby Carsten, Rasmussen Peter
Аннотация
BACKGROUND: Perioperative optimization of spatially resolved near-infrared spectroscopy determined cerebral frontal lobe oxygenation (scO2) may reduce postoperative morbidity. Norepinephrine is routinely administered to maintain cerebral perfusion pressure and, thereby, cerebral blood flow, but norepinephrine reduces the scO2. We hypothesized that norepinephrine-induced reduction in scO2 is influenced by cutaneous vasoconstriction.
METHODS: Fifteen healthy male subjects (25 ± 5 yr, mean ± SD) were studied during: hyperventilation (1.5 kPa end-tidal PcO2 reduction), whole-body heating, administration of norepinephrine (0.15 μg · kg · min; with and without end-tidal carbon dioxide correction), and hypoxia (FiO2: 0.12%). Arterial (saO2), skin, and internal jugular venous oxygen saturations (sjO2) were recorded, and the average cerebral capillary oxygen saturation (scapO2) was calculated.
RESULTS: This study indicates that scO2 is influenced by skin oxygen saturation because whole-body heating increased scO2 by 3.6% (2.1-5.1%; 95% CI) and skin oxygen saturation by 3.1% (1.3-4.9%), whereas scapO2 remained unaffected. Conversely, hyperventilation decreased scO2 by 2.1% (0.4-3.7%) and scapO2 by 5.3% (3.8-6.9%), whereas skin oxygen saturation increased 1.8% (0.5-3.1%). In response to hypoxia, scO2 (10.2%; 6.6-13.7%), scapO2 (7.9%; 6.4-9.4%), and skin oxygen saturation (8.9%; 6.3-11.6%) all decreased. With administration of norepinephrine there was a 2.2% (1.0-4.3%) decrease in skin oxygen saturation and scO2 decreased 6.2% (4.2-8.0%), with scapO2 remaining unaffected.
CONCLUSION: The results confirm that spatially resolved near-infrared spectroscopy detects cerebral deoxygenation with systemic hypoxic exposure and hyperventilation. However, a commonly used vasopressor norepinephrine disturbs skin oxygen saturation to an extent that influences scO2.
METHODS: Fifteen healthy male subjects (25 ± 5 yr, mean ± SD) were studied during: hyperventilation (1.5 kPa end-tidal PcO2 reduction), whole-body heating, administration of norepinephrine (0.15 μg · kg · min; with and without end-tidal carbon dioxide correction), and hypoxia (FiO2: 0.12%). Arterial (saO2), skin, and internal jugular venous oxygen saturations (sjO2) were recorded, and the average cerebral capillary oxygen saturation (scapO2) was calculated.
RESULTS: This study indicates that scO2 is influenced by skin oxygen saturation because whole-body heating increased scO2 by 3.6% (2.1-5.1%; 95% CI) and skin oxygen saturation by 3.1% (1.3-4.9%), whereas scapO2 remained unaffected. Conversely, hyperventilation decreased scO2 by 2.1% (0.4-3.7%) and scapO2 by 5.3% (3.8-6.9%), whereas skin oxygen saturation increased 1.8% (0.5-3.1%). In response to hypoxia, scO2 (10.2%; 6.6-13.7%), scapO2 (7.9%; 6.4-9.4%), and skin oxygen saturation (8.9%; 6.3-11.6%) all decreased. With administration of norepinephrine there was a 2.2% (1.0-4.3%) decrease in skin oxygen saturation and scO2 decreased 6.2% (4.2-8.0%), with scapO2 remaining unaffected.
CONCLUSION: The results confirm that spatially resolved near-infrared spectroscopy detects cerebral deoxygenation with systemic hypoxic exposure and hyperventilation. However, a commonly used vasopressor norepinephrine disturbs skin oxygen saturation to an extent that influences scO2.