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Timothy J McCulloch

Publications and source records attributed to Timothy J McCulloch.

4 recordsLinked to original sources
PubMed2007

A randomized crossover comparison of the effects of propofol and sevoflurane on cerebral hemodynamics during carotid endarterectomy.

BACKGROUND: Intravenous and inhalational anesthetic agents have differing effects on cerebral hemodynamics: Sevoflurane causes some vasodilation, whereas propofol does not. The authors hypothesized that these differences affect internal carotid artery pressure (ICAP) and the apparent zero flow pressure (critical closing pressure) during carotid endarterectomy. Vasodilation is expected to increase blood flow, reduce ICAP, and reduce apparent zero flow pressure. METHODS: In a randomized crossover study, the gradient between systemic arterial pressure and ICAP during carotid clamping was measured while changing between sevoflurane and propofol in 32 patients. Middle cerebral artery blood velocity, recorded by transcranial Doppler, and ICAP waveforms were analyzed to determine the apparent zero flow pressure. RESULTS: ICAP increased when changing from sevoflurane to propofol, causing the mean gradient between arterial pressure and ICAP to decrease by 10 mmHg (95% confidence interval, 6-14 mmHg; P<0.0001). Changing from propofol to sevoflurane had the opposite effect: The pressure gradient increased by 5 mmHg (95% confidence interval, 2-7 mmHg; P=0.002). Ipsilateral middle cerebral artery blood velocity decreased when changing from sevoflurane to propofol. Cerebral steal was detected in one patient after changing from propofol to sevoflurane. The apparent zero flow pressure (mean+/-SD) was 22+/-10 mmHg with sevoflurane and 30+/-14 mmHg with propofol (P<0.01). There was incomplete drug crossover due to the limited duration of carotid clamping. CONCLUSIONS: Compared with sevoflurane, ipsilateral ICAP and apparent zero flow pressure are both higher with propofol. Vasodilatation associated with sevoflurane can cause cerebral steal.

Anesthetics, Inhalation↗
PubMed2005

The effect of hypocapnia on the autoregulation of cerebral blood flow during administration of isoflurane.

Isoflurane impairs autoregulation of cerebral blood flow in a dose-related manner. Previous investigations in several other conditions have demonstrated that impaired autoregulation can be restored by hyperventilation. We hypothesized that hypocapnia may restore cerebral autoregulation impaired by isoflurane anesthesia. We administered isoflurane in 100% oxygen to 12 healthy patients aged 21-59 yr scheduled for elective nonneurological surgery. Isoflurane end-tidal concentration was individualized at 0.1% to 0.2% less than that required to induce short periods of isoelectric electroencephalogram. This resulted in an end-tidal isoflurane concentration of 1.6% +/- 0.2% (mean +/- sd) corresponding to an age-adjusted minimum alveolar anesthetic concentration multiple of 1.4. Mean arterial blood pressure was reduced to <80 mm Hg, by infusion of remifentanil if required. Cerebral autoregulation was assessed by infusing phenylephrine to increase mean arterial blood pressure to 100 mm Hg while monitoring middle cerebral artery blood flow velocity with transcranial Doppler ultrasonography. The change in flow velocity was used to calculate the autoregulation index (ARI). The ARI ranges between 0 and 1 and an ARI < or =0.4 indicates significantly impaired autoregulation. Autoregulation was tested twice in randomized order: once during normocapnia (Paco(2) 38-43 mm Hg) and once during hypocapnia (Paco(2) 27-34 mm Hg). The median (interquartile range) ARI was 0.29 (0.23-0.64) during normocapnia and 0.77 (0.70-0.78) during hypocapnia (P < 0.005). Of the 12 subjects, autoregulation was significantly impaired in 8 subjects during normocapnia and none during hypocapnia (P = 0.001). Hypocapnia restored cerebral autoregulation in normal subjects during isoflurane-induced impairment of autoregulation.

Adult↗
PubMed2003

Cerebral hemodynamics immediately following carotid occlusion.

During carotid endarterectomy, we routinely monitor internal carotid artery pressure (P(ICA)) and middle cerebral artery flow velocity (V(MCA)). P(ICA) has been previously shown to accurately reflect pressure at the origin of the middle cerebral artery, even during times of rapidly changing pressure such as occurs with sudden occlusion of the common carotid artery. We retrospectively analyzed pressure recordings around the time of carotid cross clamping in 29 consecutive carotid endarterectomy operations. Suitable transcranial Doppler recordings of V(MCA) were available from eight of the operations. Comparing the cardiac cycle prior to cross clamping with the first complete cardiac cycle after cross clamping, the mean P(ICA) fell from 93 mm Hg to 62 mm Hg and the mean V(MCA) fell from 41 cm x sec-1 to 25 cm x sec-1. Over the subsequent 10 seconds, there was a further decrease in P(ICA) to 51 mm Hg (P <.0001), while V(MCA) changed in the opposite direction, increasing to 32 cm x sec-1 (P <.01). The patients with the greatest decrease in P(ICA) immediately on cross clamping also had the greatest additional decrease over the following 10 seconds (r = 0.74). The increase in V(MCA) during the first 10 seconds after carotid occlusion is well recognized and is presumed to be due to autoregulatory vasodilatation. The simultaneous decrease that we observed in P(ICA) indicates an increase in the pressure gradient along the collateral vessels, which is to be expected during a period of increasing flow along those vessels.

Anesthesia, Intravenous↗