Cerebral Arterial Diameters during Changes in Blood Pressure and Carbon Dioxide during Craniotomy

Giller, Cole A.; Bowman, Gary; Dyer, Hunter; Mootz, Lee; Krippner, William

doi:10.1097/00006123-199305000-00006

Cited by 258 publications

(293 citation statements)

References 17 publications

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“…In addition the diameter of the proximal segment of the middle cerebral artery has been shown to remain constant during moderate changes in MAP and PaCO2 [26,27]. However, vasospasm of the middle cerebral artery is frequently observed after SAH and may increase MFVMCA, as confirmed previously [28].…”

Section: Discussionsupporting

confidence: 53%

Therapeutic Hypothermia Reduces Middle Cerebral Artery Flow Velocity in Patients with Severe Aneurysmal Subarachnoid Hemorrhage

et al. 2013

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Background: Transcranial Doppler (TCD) is widely used to detect and follow up cerebral vasospasm after sub-arachnoid hemorrhage (SAH). Therapeutic hypothermia might influence blood flow velocities assessed by TCD. The aim of the study was to evaluate the effect of hypo-thermia on Doppler blood flow velocity after SAH. Methods: In 20 patients treated with hypothermia (33°) due to refractory intracranial hypertension or delayed cerebral ischemia (DCI), mean flow velocity of the middle cerebral artery (MFVMCA) was assessed by TCD. Thirteen patients were treated with combined hypothermia and barbiturate coma and seven with hypothermia alone. MFVMCA was obtained within 24 h before and after induction of hypothermia as well as before and after rewarming. Results: Hypothermia was induced on average 5 days after SAH (range 1-12) and maintained for 144 h (range 29-270). After hypothermia induction, MFVMCA decreased from 113.7 ± 49.0 to 93.8 ± 44.7 cm/s (p = 0.001). The decrease was independent of SAH-related complications and barbiturate coma. MFVMCA further decreased by 28.2 cm/s between early and late hypothermia (p < 0.001). This second decrease was observed in patients with DCI (p < 0.001), but not in patients with intracranial hypertension (p = 0.715). Compared to late hypothermia, MFVMCA remained unchanged after rewarming (65.6 ± 32.1 vs 70.3 ± 36.8 cm/s; p = 0.219). However, patients treated with hypothermia alone showed an increase in MFVMCA after rewarming (p = 0.016). Conclusion: Therapeutic hypothermia after SAH decrea-ses Doppler blood flow velocity in both intracranial hypertension and DCI cases. The results can be the effect of hypothermiarelated mechanisms or resolving cerebral vasospasm during prolonged hypothermia. AbstractBackground: Transcranial Doppler (TCD) is widely used to detect and follow up cerebral vasospasm after sub-arachnoid hemorrhage (SAH). Therapeutic hypothermia might influence blood flow velocities assessed by TCD. The aim of the study was to evaluate the effect of hypo-thermia on Doppler blood flow velocity after SAH. Methods: In 20 patients treated with hypothermia (33°) due to refractory intracranial hypertension or delayed cerebral ischemia (DCI), mean flow velocity of the middle cerebral artery (MFVMCA) was assessed by TCD. Thirteen patients were treated with combined hypothermia and barbiturate coma and seven with hypothermia alone. MFVMCA was obtained within 24 h before and after induction of hypothermia as well as before and after rewarming. Results: Hypothermia was induced on average 5 days after SAH (range 1-12) and maintained for 144 h (range 29-270). After hypothermia induction, MFVMCA decreased from 113.7 ± 49.0 to 93.8 ± 44.7 cm/s (p = 0.001). The decrease was independent of SAH-related complications and barbiturate coma. MFVMCA further decreased by 28.2 cm/s between early and late hypothermia (p < 0.001). This second decrease was observed in patients with DCI (p < 0.001), but not in patients with intracranial hypertension (p = 0.715). Compared to late hypotherm...

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Section: Discussionsupporting

confidence: 53%

Therapeutic Hypothermia Reduces Middle Cerebral Artery Flow Velocity in Patients with Severe Aneurysmal Subarachnoid Hemorrhage

et al. 2013

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“…This assumption is only valid if the diameter of the insonated vessel remains constant. Measurements of MCA diameters in humans have shown that the diameters do not change during alterations in PET CO 2 (14,36). Therefore, it is likely that alterations in MCA V mean reflect changes in cerebral blood flow in the present study.…”

Section: Limitationsmentioning

confidence: 60%

Cerebrovascular responsiveness to steady-state changes in end-tidal CO₂ during passive heat stress

Low

Wingo

Keller

et al. 2008

Journal of Applied Physiology

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CG. Cerebrovascular responsiveness to steady-state changes in end-tidal CO2 during passive heat stress. J Appl Physiol 104: 976-981, 2008. First published January 24, 2008 doi:10.1152/japplphysiol.01040.2007.-This study tested the hypothesis that passive heat stress alters cerebrovascular responsiveness to steady-state changes in end-tidal CO2 (PETCO 2 ). Nine healthy subjects (4 men and 5 women), each dressed in a water-perfused suit, underwent normoxic hypocapnic hyperventilation (decrease PETCO 2 ϳ20 Torr) and normoxic hypercapnic (increase in PETCO 2 ϳ9 Torr) challenges under normothermic and passive heat stress conditions. The slope of the relationship between calculated cerebrovascular conductance (CBVC; middle cerebral artery blood velocity/mean arterial blood pressure) and PETCO 2 was used to evaluate cerebrovascular CO2 responsiveness. Passive heat stress increased core temperature (1.1 Ϯ 0.2°C, P Ͻ 0.001) and reduced middle cerebral artery blood velocity by 8 Ϯ 8 cm/s (P ϭ 0.01), reduced CBVC by 0.09 Ϯ 0.09 CBVC units (P ϭ 0.02), and decreased PETCO 2 by 3 Ϯ 4 Torr (P ϭ 0.07), while mean arterial blood pressure was well maintained (P ϭ 0.36). The slope of the CBVC-PET CO 2 relationship to the hypocapnic challenge was not different between normothermia and heat stress conditions (0.009 Ϯ 0.006 vs. 0.009 Ϯ 0.004 CBVC units/Torr, P ϭ 0.63). Similarly, in response to the hypercapnic challenge, the slope of the CBVC-PETCO 2 relationship was not different between normothermia and heat stress conditions (0.028 Ϯ 0.020 vs. 0.023 Ϯ 0.008 CBVC units/Torr, P ϭ 0.31). These results indicate that cerebrovascular CO2 responsiveness, to the prescribed steady-state changes in PETCO 2 , is unchanged during passive heat stress. brain blood flow; hyperthermia; hypocapnia; hypercapnia ORTHOSTATIC TOLERANCE IS REDUCED under heat stress, relative to normothermic, conditions (1,8,19,40,41). Although mechanisms responsible for reduced orthostatic tolerance during heat stress are unclear, they are likely associated with factors that directly or indirectly affect cerebral perfusion pressure, cerebral blood flow, and thus cerebral oxygenation (20, 24,38). Cerebral perfusion is very sensitive to changes in arterial carbon dioxide tension (Pa CO 2 ), such that increases in Pa CO 2 increase cerebral perfusion, whereas decreases in Pa CO 2 decrease cerebral perfusion (16, 36). Previously, our laboratory identified decreases in end-tidal carbon dioxide (PET CO 2 ; surrogate of Pa CO 2 ) of ϳ2 Torr in response to whole body passive heat stress, as well as significant reductions in cerebral perfusion and cerebral vascular conductance (40,41). Decreased cerebral perfusion would theoretically reduce the functional reserve by which cerebral blood flow can decrease further, before the onset of syncopal symptoms.It is unlikely that the relatively small decrease in PET CO 2 (i.e., ϳ2 Torr) in response to passive heat stress is the sole mechanism leading to the observed reduction in cerebral perfusion. However, this assumption is based on ca...

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“…10,12 In addition, in contrast to the traditional concept of cerebral autoregulation, which suggests that steady-state CBF remains relatively constant despite large changes in arterial pressure, 1,14 we 15 and others 16,17 have found that beat-to-beat CBF velocity measured in the MCA in humans fluctuates spontaneously in response to dynamic changes in arterial pressure. If MCA diameter remains relatively constant, as has been shown by numerous studies, 18,19 these changes in CBF velocity reflect changes in CBF. Thus, estimation of transfer function between these 2 variables may identify frequencydependent properties of dynamic cerebral autoregulation.…”

mentioning

confidence: 75%

Autonomic Neural Control of Dynamic Cerebral Autoregulation in Humans

et al. 2002

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Background-The purpose of the present study was to determine the role of autonomic neural control of dynamic cerebral autoregulation in humans. Methods and Results-We measured arterial pressure and cerebral blood flow (CBF) velocity in 12 healthy subjects (aged 29Ϯ6 years) before and after ganglion blockade with trimethaphan. CBF velocity was measured in the middle cerebral artery using transcranial Doppler. The magnitude of spontaneous changes in mean blood pressure and CBF velocity were quantified by spectral analysis. The transfer function gain, phase, and coherence between these variables were estimated to quantify dynamic cerebral autoregulation. After ganglion blockade, systolic and pulse pressure decreased significantly by 13% and 26%, respectively. CBF velocity decreased by 6% (PϽ0.05). In the very low frequency range (0.02 to 0.07 Hz), mean blood pressure variability decreased significantly (by 82%), while CBF velocity variability persisted. Thus, transfer function gain increased by 81%. In addition, the phase lead of CBF velocity to arterial pressure diminished. These changes in transfer function gain and phase persisted despite restoration of arterial pressure by infusion of phenylephrine and normalization of mean blood pressure variability by oscillatory lower body negative pressure. Conclusions-These data suggest that dynamic cerebral autoregulation is altered by ganglion blockade. We speculate that autonomic neural control of the cerebral circulation is tonically active and likely plays a significant role in the regulation of beat-to

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Cerebral Arterial Diameters during Changes in Blood Pressure and Carbon Dioxide during Craniotomy

Cited by 258 publications

References 17 publications

Therapeutic Hypothermia Reduces Middle Cerebral Artery Flow Velocity in Patients with Severe Aneurysmal Subarachnoid Hemorrhage

Therapeutic Hypothermia Reduces Middle Cerebral Artery Flow Velocity in Patients with Severe Aneurysmal Subarachnoid Hemorrhage

Cerebrovascular responsiveness to steady-state changes in end-tidal CO₂ during passive heat stress

Autonomic Neural Control of Dynamic Cerebral Autoregulation in Humans

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