Assessment of middle cerebral artery diameter during hypocapnia and hypercapnia in humans using ultra-high-field MRI

2014 ◽  
Vol 117 (10) ◽  
pp. 1084-1089 ◽  
Author(s):  
Jasper Verbree ◽  
Anne-Sophie G. T. Bronzwaer ◽  
Eidrees Ghariq ◽  
Maarten J. Versluis ◽  
Mat J. A. P. Daemen ◽  
...  

In the evaluation of cerebrovascular CO2 reactivity measurements, it is often assumed that the diameter of the large intracranial arteries insonated by transcranial Doppler remains unaffected by changes in arterial CO2 partial pressure. However, the strong cerebral vasodilatory capacity of CO2 challenges this assumption, suggesting that there should be some changes in diameter, even if very small. Data from previous studies on effects of CO2 on cerebral artery diameter [middle cerebral artery (MCA)] have been inconsistent. In this study, we examined 10 healthy subjects (5 women, 5 men, age 21–30 yr). High-resolution (0.2 mm in-plane) MRI scans at 7 Tesla were used for direct observation of the MCA diameter during hypocapnia, −1 kPa (−7.5 mmHg), normocapnia, 0 kPa (0 mmHg), and two levels of hypercapnia, +1 and +2 kPa (7.5 and 15 mmHg), with respect to baseline. The vessel lumen was manually delineated by two independent observers. The results showed that the MCA diameter increased by 6.8 ± 2.9% in response to 2 kPa end-tidal Pco2 (PetCO2) above baseline. However, no significant changes in diameter were observed at the −1 kPa (−1.2 ± 2.4%), and +1 kPa (+1.4 ± 3.2%) levels relative to normocapnia. The nonlinear response of the MCA diameter to CO2 was fitted as a continuous calibration curve. Cerebral blood flow changes measured by transcranial Doppler could be corrected by this calibration curve using concomitant PetCO2 measurements. In conclusion, the MCA diameter remains constant during small deviations of the PetCO2 from normocapnia, but increases at higher PetCO2 values.

Author(s):  
Baraa K Al-Khazraji ◽  
Sagar Buch ◽  
Mason Kadem ◽  
Brad J Matushewski ◽  
Kambiz Norozi ◽  
...  

There is a need for improved understanding of how different cerebrovascular reactivity (CVR) protocols affect vascular cross-sectional area (CSA) when measures of vascular CSA are not feasible. In human participants, we delivered ~±4mmHg end-tidal partial pressure of CO2 (PETCO2) relative to baseline through controlled delivery, and measured changes in middle cerebral artery (MCA) cross-sectional area (CSA; 7 Tesla MRI), blood velocity (transcranial Doppler and Phase contrast MRI), and calculated CVR based on: a 3-minute steady-state (+4mmHg PETCO2) and a ramp (-3 to +4mmHg of PETCO2). We observed that 1) the MCA did not dilate during the ramp protocol (slope for CSA across time P>0.05; R2 = 0.006), but did dilate by ~7% during steady-state hypercapnia (P<0.05), and 2) MCA blood velocity CVR was not different between ramp and steady-state hypercapnia protocols (ramp: 3.8±1.7 vs. steady-state: 4.0±1.6 cm/s/mmHg), although calculated MCA blood flow CVR was ~40% greater during steady-state hypercapnia than during ramp (P<0.05), the discrepancy due to MCA CSA changes during steady-state hypercapnia. We propose that a ramp model, across a delta of -3 to +4mmHg PETCO2, may provide one alternative approach to collecting CVR measures in young adults with TCD when CSA measures are not feasible. Novelty • We optimized a magnetic resonance imaging sequence to measure dynamic middle cerebral artery (MCA) cross-sectional area (CSA) • A ramp model of hypercapnia elicited similar MCA blood velocity reactivity as the steady-state model while maintaining MCA CSA


2021 ◽  
Author(s):  
Baraa K. Al-Khazraji ◽  
Sagar Buch ◽  
Mason Kadem ◽  
Brad J. Matushewski ◽  
Kambiz Norozi ◽  
...  

AbstractThere is a need for improved understanding of how different cerebrovascular reactivity (CVR) protocols affect vascular cross-sectional area (CSA) when measures of vascular CSA are not feasible. In human participants, we delivered ~±4mmHg end-tidal partial pressure of CO2 (PETCO2) relative to baseline through controlled delivery, and measured changes in middle cerebral artery (MCA) cross-sectional area (CSA; magnetic resonance imaging (7 Tesla MRI)), blood velocity (transcranial Doppler and Phase contrast MRI), and calculated CVR based on steady-state versus a ramp protocol during two protocols: a 3-minute steady-state (+4mmHg PETCO2) and a ramp (delta of −3 to +4mmHg of PETCO2). We observed that 1) the MCA did not dilate during the ramp protocol, but did dilate during steady-state hypercapnia, and 2) MCA blood velocity CVR was similar between ramp and steady-state hypercapnia protocols, although calculated MCA blood flow CVR was greater during steady-state hypercapnia than during ramp, the discrepancy due to MCA CSA changes during steady-state hypercapnia. Due to the ability to achieve similar levels of MCA blood velocity CVR as steady-state hypercapnia, the lack of change in MCA cross-sectional area, and the minimal expected change in blood pressure, we propose that a ramp model, across a delta of ~−3 to +4mmHg PETCO2, may provide one alternative approach to collecting CVR measures in young adults with TCD when CSA measures are not feasible.


2003 ◽  
Vol 95 (1) ◽  
pp. 129-137 ◽  
Author(s):  
Kojiro Ide ◽  
Michael Eliasziw ◽  
Marc J. Poulin

This study examined the relationship between cerebral blood flow (CBF) and end-tidal Pco2 (PetCO2) in humans. We used transcranial Doppler ultrasound to determine middle cerebral artery peak blood velocity responses to 14 levels of PetCO2 in a range of 22 to 50 Torr with a constant end-tidal Po2 (100 Torr) in eight subjects. PetCO2 and end-tidal Po2 were controlled by using the technique of dynamic end-tidal forcing combined with controlled hyperventilation. Two protocols were conducted in which PetCO2 was changed by 2 Torr every 2 min from hypocapnia to hypercapnia ( protocol I) and vice-versa ( protocol D). Over the range of PetCO2 studied, the sensitivity of peak blood velocity to changes in PetCO2 (CBF-PetCO2 sensitivity) was nonlinear with a greater sensitivity in hypercapnia (4.7 and 4.0%/Torr, protocols I and D, respectively) compared with hypocapnia (2.5 and 2.2%/Torr). Furthermore, there was evidence of hysteresis in the CBF-PetCO2 sensitivity; for a given PetCO2, there was greater sensitivity during protocol I compared with protocol D. In conclusion, CBF-PetCO2 sensitivity varies depending on the level of PetCO2 and the protocol that is used. The mechanisms underlying these responses require further investigation.


1999 ◽  
Vol 91 (3) ◽  
pp. 677-677 ◽  
Author(s):  
Basil F. Matta ◽  
Karen J. Heath ◽  
Kate Tipping ◽  
Andrew C. Summors

Background The effect of volatile anesthetics on cerebral blood flow depends on the balance between the indirect vasoconstrictive action secondary to flow-metabolism coupling and the agent's intrinsic vasodilatory action. This study compared the direct cerebral vasodilatory actions of 0.5 and 1.5 minimum alveolar concentration (MAC) sevoflurane and isoflurane during an propofol-induced isoelectric electroencephalogram. Methods Twenty patients aged 20-62 yr with American Society of Anesthesiologists physical status I or II requiring general anesthesia for routine spinal surgery were recruited. In addition to routine monitoring, a transcranial Doppler ultrasound was used to measure blood flow velocity in the middle cerebral artery, and an electroencephalograph to measure brain electrical activity. Anesthesia was induced with propofol 2.5 mg/kg, fentanyl 2 micro/g/kg, and atracurium 0.5 mg/kg, and a propofol infusion was used to achieve electroencephalographic isoelectricity. End-tidal carbon dioxide, blood pressure, and temperature were maintained constant throughout the study period. Cerebral blood flow velocity, mean blood pressure, and heart rate were recorded after 20 min of isoelectric encephalogram. Patients were then assigned to receive either age-adjusted 0.5 MAC (0.8-1%) or 1.5 MAC (2.4-3%) end-tidal sevoflurane; or age-adjusted 0.5 MAC (0.5-0.7%) or 1.5 MAC (1.5-2%) end-tidal isoflurane. After 15 min of unchanged end-tidal concentration, the variables were measured again. The concentration of the inhalational agent was increased or decreased as appropriate, and all measurements were repeated again. All measurements were performed before the start of surgery. An infusion of 0.01% phenylephrine was used as necessary to maintain mean arterial pressure at baseline levels. Results Although both agents increased blood flow velocity in the middle cerebral artery at 0.5 and 1.5 MAC, this increase was significantly less during sevoflurane anesthesia (4+/-3 and 17+/-3% at 0.5 and 1.5 MAC sevoflurane; 19+/-3 and 72+/-9% at 0.5 and 1.5 MAC isoflurane [mean +/- SD]; P&lt;0.05). All patients required phenylephrine (100-300 microg) to maintain mean arterial pressure within 20% of baseline during 1.5 MAC anesthesia. Conclusions In common with other volatile anesthetic agents, sevoflurane has an intrinsic dose-dependent cerebral vasodilatory effect. However, this effect is less than that of isoflurane.


2020 ◽  
Vol 26 (6) ◽  
pp. 800-804
Author(s):  
Elena Elvira Soler ◽  
Blanca Serrano Serrano ◽  
Nicolás López Hernández ◽  
Natasha Guevara Dalrymple ◽  
Sarai Moliner Castellano ◽  
...  

We report the results of transcranial ultrasound monitoring in three patients with intracranial arterial stenosis of the middle cerebral artery treated with the only drug-eluting balloon certificated for intracranial use in highly symptomatic intracranial arterial stenosis, ELUTAX “3” (AR Baltic Medical). We performed transcranial Doppler ultrasounds 24 h, 72 h, 10 days, 15 days and 30 days after the angioplasty, thereby measuring mean flow velocity (MFV) in the maximum stenosis area in patients with symptomatic steno-occlusive disease of the middle cerebral artery treated with ELUTAX “3”. Two patients were treated during mechanical thrombectomy (MT) due to acute ischemic stroke and one patient was treated on elective basis due to symptomatic pre-occlusive stenosis, with recurrent transient ischemic attacks (TIAs) refractory to medical therapy. In Case 1, the first transcranial Doppler ultrasounds evidenced MFV of 348 cm/s, with progressive MFV reduction until 15 days post-treatment, with MFV of 177 cm/s. In Case 2, 24 h after angioplasty had an MFV of 258 cm/s, decreasing to 103 cm/s at 30 days. Case 3 had an MFV of 436 cm/s before angioplasty that immediately decreased after the procedure to 364 cm/s, with a final MFV of 260 cm/s at 30 days. We have recorded a progressive MFV reduction in intracranial arterial stenosis, with better outcomes in patients treated during MT. In our experience, the use of ELUTAX “3” for the treatment of symptomatic intracranial arterial stenosis achieves a progressive improvement of stenosis, evident in the first weeks, to a higher extent in cases of occlusive thrombosis. More studies are needed to provide more information about this device.


2003 ◽  
Vol 9 (1_suppl) ◽  
pp. 129-132
Author(s):  
T. Yamanome ◽  
M. Sasoh ◽  
Y. Kubo ◽  
Y. Nishikawa ◽  
H. Endoh ◽  
...  

For the treatment of 11 patients with hyperacute embolic occlusion of major cerebral arteries (ten with occlusion of middle cerebral artery and one with occlusion of basilar artery), TCD-enhanced thrombolysis (TCDET) was performed in combination with ultrasound irradiation, using diagnostic transcranial Doppler (TCD) (TC2-64B: 2MHz, 100mW/cm2, pulsed wave) (TCDET group), and the effectiveness of this procedure was compared with that of local intra-arterial fibrinolysis (LIF) in 45 patients with embolic occlusion of the middle cerebral artery (LIF group). Regarding dose of TPA, the LIF group used 1046.7 ± 607.8 units and the TCDET group 700.0 ± 431.3 units (p < 0.05). Regarding time technically required to attain recanalization, the LIF group required 68.2 minutes, and the TCDET group 28.6 minutes. A good outcome was noted in 60.8% of the LIF group and 64% of the TCDET group. Haemorrhagic transformation was observed in 7.8% of the LIF group and in 0% of the TCDET group. No complications due to TCD irradiation were observed in the TCDET group. These findings suggest that TCDET can be an effective method of achieving recanalization.


Sign in / Sign up

Export Citation Format

Share Document