Physiologic Factors Influencing Sensory Evoked Responses
A number of physiologic variables, including systemic blood pressure,
temperature (local and systemic), and blood gas tensions, can influence SEP recordings.
With decreases in mean arterial blood pressure to below levels of cerebral autoregulation
due to blood loss or vasoactive agents, progressive changes in SERs have been observed.
The SSEP changes observed are progressive decreases in amplitude until loss of the
waveform with no changes in latency.[154]
[155]
BAEPs are relatively resistant to even profound levels of hypotension (i.e., mean
arterial pressure of 20 mm Hg in dogs).[154]
Cortical
(synaptic) function necessary to produce cortical SERs appears to be more sensitive
to hypoperfusion than spinal cord or brainstem nonsynaptic transmission.[155]
Rapid decreases in blood pressure to levels above the lower limit of autoregulation
have also been associated with transient SSEP changes of decreased amplitude that
resolve after several minutes of continued hypotension at the same level.[156]
Reversible SSEP changes at systemic pressures within the normal range have been
observed in patients undergoing spinal distraction during scoliosis surgery. These
changes resolved with increases of systemic blood pressure to slightly above the
patient's normal pressure, suggesting that the combination of surgical manipulation
with levels of hypotension generally considered "safe" could result in spinal cord
ischemia.[157]
Changes in temperature also affect SERs. Hypothermia causes increases
in latency and decreases in amplitude of cortical and subcortical SERs after all
types of stimulation.[158]
[159]
[160]
Hyperthermia also alters SERs, with increases
in temperature leading to decreases in the amplitude of SSEPs and loss of SSEPs at
42°C during induced hyperthermia.[161]
Changes in arterial blood gas tensions can alter SERs, probably
in relation to changes in blood flow or oxygen delivery to neural structures.[162]
[163]
Hypoxia produces SSEP changes (i.e., decreased
amplitude) similar to those seen with ischemia.[163]
Decreased oxygen delivery associated with anemia during isovolemic hemodilution
results in progressive increases in the latencies of SSEPs and VEPs, which become
significant at hematocrits below 15%. Changes in amplitude were variable until very
low hematocrits (≅7%) were reached, at which point the amplitude of all waveforms
decreased.[164]
