Pulse oxymetry noninvasively estimates arterial oxygen saturation (SaO2) spectrophotometically by processing a pulse added light absorbance signal from transilluminated tissue and provides continuous information. So the device is rapidly becoming
a
standard in clinical monitoring.
Preganglionic sympathetic denervation during spinal and lumbar epidural anesthesia causes dilatation of both resistance and capacitance vessels of the lower limbs, with a reflex increase in efferent sympathetic activity above the level of the
block.
Skin temperature elevation corresponds with the upper limit of diminished sympathetic activity and is in agreement with the view that skin temperature increase is a useful indicator of sympathetic blockade.
Pulse oximetry is dependent upon the presence of a pulsating vascular bed. The signal detection will be impaired in the presence of vasoconstriction or venous congestion, conditions which occur in spinal and lumbar epidural anesthesia.
We compared the oximetric measurements (SpO2) at the hand and the foot with arterial oxygen saturation (SaO2) during spinal and lumbar epidural anesthesia. After administration of a crystalloid solution, 10 patients received γ-10mg of 0.5%
tetracaine
into the subarachnoid space and 10 patients received 10-20ml of 2% lidocaine into the lumbar epidural space in 20 adult patients, scheduled for operation.
Two temperature probes and two pulse oximeter probes were applied to the finger and toe of the patients, and the temperature and SpO2 values were recorded continuously. Arterial oxygen saturation (SaO2) was measured using M288 before and 30 min
after
the onset of sensory block.
In all patients, intraoperative decreasing of heart rate and arterial blood pressure was 15% from baseline. During anesthesia, the decreasing of temperature recorded from sympathetically unaffected areas could be related to vasoconstriction,
counterbalancing sympathetic block. But no significant differences were detected between SaO2 and SpO2 basal values recorded from the hand and foot before anesthesia. After the onset of spinal and lumbar epidural anesthesia, SpO2 values recorded
from
the hand were not changed significantly. Otherwise significant difference in SaO2 were detected between two groups before and 30 min after anesthesia, because the age in lumbar epidural group (63.8±90.1) was older than the age in spinal group
(44.6±121.1).
Therefore, we concluded that SaO2 must be confirmed when there are clinically significant changes during spinal and lumbar epidural anesthesia, although SpO2 in hand are neither changed nor decreased below normal range.
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