A comparison of the transient hyperemic response test and the static autoregulation test to assess graded impairment in cerebral autoregulation during propofol, desflurane, and nitrous oxide anesthesia.
ABSTRACT The transient hyperemic response (THR) test has been used to assess cerebral autoregulation in anesthesia and intensive care. To date it has not been compared with the static autoregulation test for assessing graded changes in cerebral autoregulation. We compared the two tests during propofol, desflurane, and nitrous oxide anesthesia. Seven subjects were studied. For the THR test, changes in the middle artery blood flow velocity were assessed during and after a 10-s compression of the ipsilateral common carotid artery. Two indices of autoregulation--THR ratio (THRR) and strength of autoregulation (SA)--were calculated. For the test of static autoregulation, changes in the middle cerebral artery flow velocity after a phenylephrine-induces increase in mean arterial pressure were assessed, and the static rate of regulation (sROR) was calculated. The tests were performed before induction and after equilibrium at 0.5 minimum alveolar anesthetic concentration (MAC) and then at 1.5 MAC of desflurane. THRR, SA and sROR decreased significantly (P < 0.001) at 0.5 MAC and then at 1.5 MAC desflurane. CHanges in THRR and SA reflected the changes in sROR with a sensitivity of 100%. Implications: When compared with the established test of static autoregulation, the transient hyperemic response test provides a valid method for assessing graded impairment in cerebral autoregulation.
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ABSTRACT: The effect of surgical decompression of tumor on autoregulation and CO2 reactivity is not known. We examined the effect of elective tumor resection on cerebral autoregulation and CO2 reactivity. Patients with supratentorial tumors undergoing elective craniotomy for tumor resection under standard anesthesia underwent cerebral autoregulation and CO2 reactivity testing immediately before and between 6 and 24 hours after surgery. Transient hyperemic response of the middle cerebral artery after the release of 10 second compression of the ipsilateral common carotid artery was used to calculate the transient hyperemic response ratio (THRR). THRR>1.1 defined the normal autoregulation. Voluntary hyperventilation was titrated to reduce the ETCO2 by 10 mm Hg below baseline and CO2 reactivity was calculated. Thirty-five patients (26 male and 9 female) were studied. Overall, cerebral autoregulation was intact before and after tumor resection for the cohort (THRR 1.27+/-0.10 and 1.30+/-0.12, P=0.11). However, cerebral autoregulation was impaired preoperatively in 7 (20%) patients and remained impaired in all 7 patients after tumor resection. Larger tumor size (P=0.002), and midline shift more than 5 mm (P<0.001) were associated with impaired cerebral autoregulation. Twenty-eight (80%) patients who had intact preoperative cerebral autoregulation maintained autoregulation postoperatively. CO2 reactivity was within normal limits before and after surgery in all patients and did not change between the 2 periods (3.41+/-0.46/mm Hg and 3.60+/-0.63%/mm Hg, P=0.07). Preoperative cerebral autoregulation was impaired in a significant number of patients with large supratentorial tumor size and midline shift more than 5 mm and was associated with postoperative impaired cerebral autoregulation during the first 24 hours after the surgery.Journal of neurosurgical anesthesiology 04/2010; 22(2):132-7. · 2.41 Impact Factor
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ABSTRACT: The effects of hyperthermia on the human brain are incompletely understood. This study assessed the effects of whole body hyperthermia on cerebral oxygen extraction and autoregulation in humans. Nineteen patients with chronic hepatitis C virus infection, not responding to interferon treatment, were subjected to experimental therapy with extracorporeal whole body hyperthermia at 41.8 degrees C for 120 min under propofol anesthesia (23 sessions total). During treatment series A (13 sessions), end-tidal carbon dioxide was allowed to increase during heating. During series B (10 sessions), end-tidal carbon dioxide was maintained approximately constant. Cerebral oxygen extraction (arterial to jugular venous difference of oxygen content) and middle cerebral artery blood flow velocity were continuously measured. Cerebral pressure-flow autoregulation was assessed by static tests using phenylephrine infusion and by assessing the transient hyperemic response to carotid compression and release. For treatment series A, cerebral oxygen extraction decreased 2.2-fold and cerebral blood flow velocity increased 2.0-fold during heating. For series B, oxygen extraction decreased 1.6-fold and flow velocity increased 1.5-fold. Jugular venous oxygen saturation and lactate measurements did not indicate cerebral ischemia at any temperature. Static autoregulation test results indicated loss of cerebrovascular reactivity during hyperthermia for both series A and series B. The transient hyperemic response ratio did not decrease until the temperature reached approximately 40 degrees C. Per degree Celsius temperature increase, the transient hyperemic response ratio decreased 0.07 (95% confidence interval, 0.05-0.09; P = 0.000). This association remained after adjustment for variations in arterial partial pressure of carbon dioxide, mean arterial pressure, and propofol blood concentration. Profound hyperthermia during propofol anesthesia is associated with decreased cerebral oxygen extraction, increased cerebral blood flow velocity, and impaired pressure-flow autoregulation, indicating transient partial vasoparalysis.Anesthesiology 06/2004; · 6.17 Impact Factor
- Seminars in Anesthesia Perioperative Medicine and Pain 09/2004; 23(3):174–180.