Cerebral blood flow velocity underestimates cerebral blood flow during modest hypercapnia and hypocapnia

2014 ◽  
Vol 117 (10) ◽  
pp. 1090-1096 ◽  
Author(s):  
Nicole S. Coverdale ◽  
Joseph S. Gati ◽  
Oksana Opalevych ◽  
Amanda Perrotta ◽  
J. Kevin Shoemaker

To establish the accuracy of transcranial Doppler ultrasound (TCD) measures of middle cerebral artery (MCA) cerebral blood flow velocity (CBFV) as a surrogate of cerebral blood flow (CBF) during hypercapnia (HC) and hypocapnia (HO), we examined whether the cross-sectional area (CSA) of the MCA changed during HC or HO and whether TCD-based estimates of CBFV were equivalent to estimates from phase contrast (PC) magnetic resonance imaging. MCA CSA was measured from 3T magnetic resonance images during baseline, HO (hyperventilation at 30 breaths/min), and HC (6% carbon dioxide). PC and TCD measures of CBFV were measured during these protocols on separate days. CSA and TCD CBFV were used to calculate CBF. During HC, CSA increased from 5.6 ± 0.8 to 6.5 ± 1.0 mm2 ( P < 0.001, n = 13), while end-tidal carbon dioxide partial pressure (PetCO2) increased from 37 ± 3 to 46 ± 5 Torr ( P < 0.001). During HO, CSA decreased from 5.8 ± 0.9 to 5.3 ± 0.9 mm2 ( P < 0.001, n = 15), while PetCO2 decreased from 36 ± 4 to 23 ± 3 Torr ( P < 0.001). CBFVs during baseline, HO, and HC were compared between PC and TCD, and the intraclass correlation coefficient was 0.83 ( P < 0.001). The relative increase from baseline was 18 ± 8% greater ( P < 0.001) for CBF than TCD CBFV during HC, and the relative decrease of CBF during HO was 7 ± 4% greater than the change in TCD CBFV ( P < 0.001). These findings challenge the assumption that the CSA of the MCA does not change over modest changes in PetCO2.

2019 ◽  
Vol 126 (6) ◽  
pp. 1694-1700 ◽  
Author(s):  
M. Erin Moir ◽  
Stephen A. Klassen ◽  
Baraa K. Al-Khazraji ◽  
Emilie Woehrle ◽  
Sydney O. Smith ◽  
...  

Breath-hold divers (BHD) experience repeated bouts of severe hypoxia and hypercapnia with large increases in blood pressure. However, the impact of long-term breath-hold diving on cerebrovascular control remains poorly understood. The ability of cerebral blood vessels to respond rapidly to changes in blood pressure represents the property of dynamic autoregulation. The current investigation tested the hypothesis that breath-hold diving impairs dynamic autoregulation to a transient hypotensive stimulus. Seventeen BHD (3 women, 11 ± 9 yr of diving) and 15 healthy controls (2 women) completed two or three repeated sit-to-stand trials during spontaneous breathing and poikilocapnic conditions. Heart rate (HR), finger arterial blood pressure (BP), and cerebral blood flow velocity (BFV) from the right middle cerebral artery were measured continuously with three-lead electrocardiography, finger photoplethysmography, and transcranial Doppler ultrasonography, respectively. End-tidal carbon dioxide partial pressure was measured with a gas analyzer. Offline, an index of cerebrovascular resistance (CVRi) was calculated as the quotient of mean BP and BFV. The rate of the drop in CVRi relative to the change in BP provided the rate of regulation [RoR; (∆CVRi/∆T)/∆BP]. The BHD demonstrated slower RoR than controls ( P ≤ 0.001, d = 1.4). Underlying the reduced RoR in BHD was a longer time to reach nadir CVRi compared with controls ( P = 0.004, d = 1.1). In concert with the longer CVRi response, the time to reach peak BFV following standing was longer in BHD than controls ( P = 0.01, d = 0.9). The data suggest impaired dynamic autoregulatory mechanisms to hypotension in BHD. NEW & NOTEWORTHY Impairments in dynamic cerebral autoregulation to hypotension are associated with breath-hold diving. Although weakened autoregulation was observed acutely in this group during apneic stress, we are the first to report on chronic adaptations in cerebral autoregulation. Impaired vasomotor responses underlie the reduced rate of regulation, wherein breath-hold divers demonstrate a prolonged dilatory response to transient hypotension. The slower cerebral vasodilation produces a longer perturbation in cerebral blood flow velocity, increasing the risk of cerebral ischemia.


2016 ◽  
Vol 28 (4) ◽  
pp. 337-340 ◽  
Author(s):  
Brian P. Lemkuil ◽  
Brian T. Gierl ◽  
Piyush M. Patel ◽  
Matthew L. Pearn ◽  
Liem C. Nguyen ◽  
...  

2014 ◽  
Vol 103 (8) ◽  
pp. e334-e339 ◽  
Author(s):  
Shahab Noori ◽  
Michael Anderson ◽  
Sadaf Soleymani ◽  
Istvan Seri

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