Relationship between middle cerebral artery blood velocity and end-tidal PCO2 in the hypocapnic-hypercapnic range in humans

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.

2002 ◽  
Vol 80 (8) ◽  
pp. 819-827 ◽  
Author(s):  
Andrea Vovk ◽  
David A Cunningham ◽  
John M Kowalchuk ◽  
Donald H Paterson ◽  
James Duffin

This study characterized cerebral blood flow (CBF) responses in the middle cerebral artery to PCO2ranging from 30 to 60 mmHg (1 mmHg = 133.322 Pa) during hypoxia (50 mmHg) and hyperoxia (200 mmHg). Eight subjects (25 ± 3 years) underwent modified Read rebreathing tests in a background of constant hypoxia or hyperoxia. Mean cerebral blood velocity was measured using a transcranial Doppler ultrasound. Ventilation (VE), end-tidal PCO2 (PETCO2), and mean arterial blood pressure (MAP) data were also collected. CBF increased with rising PETCO2 at two rates, 1.63 ± 0.21 and 2.75 ± 0.27 cm·s–1·mmHg–1 (p < 0.05) during hypoxic and 1.69 ± 0.17 and 2.80 ± 0.14 cm·s–1·mmHg–1 (p < 0.05) during hyperoxic rebreathing. VE also increased at two rates (5.08 ± 0.67 and 10.89 ± 2.55 L·min–1·mmHg–1 and 3.31 ± 0.50 and 7.86 ± 1.43 L·min–1·mmHg–1) during hypoxic and hyperoxic rebreathing. MAP and PETCO2 increased linearly during both hypoxic and hyperoxic rebreathing. The breakpoint separating the two-component rise in CBF (42.92 ± 1.29 and 49.00 ± 1.56 mmHg CO2 during hypoxic and hyperoxic rebreathing) was likely not due to PCO2 or perfusion pressure, since PETCO2 and MAP increased linearly, but it may be related to VE, since both CBF and VE exhibited similar responses, suggesting that the two responses may be regulated by a common neural linkage. Key words: brain blood flow, middle cerebral artery, ventilation, mean arterial blood pressure.


2020 ◽  
Vol 319 (1) ◽  
pp. R33-R42
Author(s):  
Catherine L. Jarrett ◽  
Katherine L. Shields ◽  
Ryan M. Broxterman ◽  
Jay R. Hydren ◽  
Soung Hun Park ◽  
...  

Cerebral blood flow (CBF) is commonly inferred from blood velocity measurements in the middle cerebral artery (MCA), using nonimaging, transcranial Doppler ultrasound (TCD). However, both blood velocity and vessel diameter are critical components required to accurately determine blood flow, and there is mounting evidence that the MCA is vasoactive. Therefore, the aim of this study was to employ imaging TCD (ITCD), utilizing color flow images and pulse wave velocity, as a novel approach to measure both MCA diameter and blood velocity to accurately quantify changes in MCA blood flow. ITCD was performed at rest in 13 healthy participants (7 men/6 women; 28 ± 5 yr) with pharmaceutically induced vasodilation [nitroglycerin (NTG), 0.8 mg] and without (CON). Measurements were taken for 2 min before and for 5 min following NTG or sham delivery (CON). There was more than a fivefold, significant, fall in MCA blood velocity in response to NTG (∆−4.95 ± 4.6 cm/s) compared to negligible fluctuation in CON (∆−0.88 ± 4.7 cm/s) ( P < 0.001). MCA diameter increased significantly in response to NTG (∆0.09 ± 0.04 cm) compared with the basal variation in CON (∆0.00 ± 0.04 cm) ( P = 0.018). Interestingly, the product of the NTG-induced fall in MCA blood velocity and increase in diameter was a significant increase in MCA blood flow following NTG (∆144 ± 159 ml/min) compared with CON (∆−5 ± 130 ml/min) ( P = 0.005). These juxtaposed findings highlight the importance of measuring both MCA blood velocity and diameter when assessing CBF and document ITCD as a novel approach to achieve this goal.


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.


Cephalalgia ◽  
1990 ◽  
Vol 10 (2) ◽  
pp. 87-94 ◽  
Author(s):  
Arve Dahl ◽  
David Russell ◽  
Rolf Nyberg-Hansen ◽  
Kjell Rootwelt

Transcranial Doppler and rCBF examinations were carried out in 25 cluster headache patients. Spontaneous and glyceryl trinitrate (nitroglycerin) provoked attacks were accompanied by a bilateral decrease in middle cerebral artery blood flow velocities. This decrease was more pronounced on the symptomatic side but the difference did not reach statistical significance. Mean hemispheric blood flow and rCBF were within normal limits during provoked attacks and similar to those found when patients were attack-free. During cluster periods middle cerebral artery velocities were significantly higher on the symptomatic side. Glyceryl trinitrate caused a bilateral middle cerebral artery velocity decrease which was significantly greater on the symptomatic side. Attacks provoked by glyceryl trinitrate appeared to begin when the vasodilatory effect of this substance was receding.


2003 ◽  
Vol 94 (4) ◽  
pp. 1335-1344 ◽  
Author(s):  
Frank Pott ◽  
Johannes J. Van Lieshout ◽  
Kojiro Ide ◽  
Per Madsen ◽  
Niels H. Secher

Lifting of a heavy weight may lead to “blackout” and occasionally also to cerebral hemorrhage, indicating pronounced consequences for the blood flow through the brain. We hypothesized that especially strenuous respiratory straining (a Valsalva-like maneuver) associated with intense static exercise would lead to a precipitous rise in mean arterial and central venous pressures and, in turn, influence the middle cerebral artery blood velocity (MCA V mean) as a noninvasive indicator of changes in cerebral blood flow. In 10 healthy subjects, MCA V mean was evaluated in response to maximal static two-legged exercise performed either with a concomitantly performed Valsalva maneuver or with continued ventilation and also during a Valsalva maneuver without associated exercise ( n = 6). During static two-legged exercise, the largest rise for mean arterial pressure and MCA V meanwas established at the onset of exercise performed with a Valsalva-like maneuver (by 42 ± 5 mmHg and 31 ± 3% vs. 22 ± 6 mmHg and 25 ± 6% with continued ventilation; P < 0.05). Profound reductions in MCA V mean were observed both after exercise with continued ventilation (−29 ± 4% together with a reduction in the arterial CO2 tension by −5 ± 1 Torr) and during the maintained Valsalva maneuver (−21 ± 3% together with an elevation in central venous pressure to 40 ± 7 mmHg). Responses to performance of the Valsalva maneuver with and without exercise were similar, reflecting the deterministic importance of the Valsalva maneuver for the central and cerebral hemodynamic response to intense static exercise. Continued ventilation during intense static exercise may limit the initial rise in arterial pressure and may in turn reduce the risk of hemorrhage. On the other hand, blackout during and after intense static exercise may reflect a reduction in cerebral blood flow due to expiratory straining and/or hyperventilation.


Stroke ◽  
1991 ◽  
Vol 22 (1) ◽  
pp. 27-30 ◽  
Author(s):  
L M Brass ◽  
I Prohovnik ◽  
S G Pavlakis ◽  
D C DeVivo ◽  
S Piomelli ◽  
...  

Neurosurgery ◽  
2002 ◽  
Vol 51 (1) ◽  
pp. 30-43 ◽  
Author(s):  
Rod J. Oskouian ◽  
Neil A. Martin ◽  
Jae Hong Lee ◽  
Thomas C. Glenn ◽  
Donald Guthrie ◽  
...  

Abstract OBJECTIVE The goal of this study was to quantify the effects of endovascular therapy on vasospastic cerebral vessels. METHODS We reviewed the medical records for 387 patients with ruptured intracranial aneurysms who were treated at a single institution (University of California, Los Angeles) between May 1, 1993, and March 31, 2001. Patients who developed cerebral vasospasm and underwent cerebral arteriographic, transcranial Doppler ultrasonographic, and cerebral blood flow (CBF) studies before and after endovascular therapy for cerebral arterial spasm (vasospasm) were included in this study. RESULTS Forty-five patients fulfilled the aforementioned criteria and were treated with either papaverine infusion, papaverine infusion with angioplasty, or angioplasty alone. After balloon angioplasty (12 patients), CBF increased from 27.8 ± 2.8 ml/100 g/min to 28.4 ± 3.0 ml/100 g/min (P = 0.87); the middle cerebral artery blood flow velocity was 157.6 ± 9.4 cm/s and decreased to 76.3 ± 9.3 cm/s (P &lt; 0.05), with a mean increase in cerebral artery diameters of 24.4%. Papaverine infusion (20 patients) transiently increased the CBF from 27.5 ± 2.1 ml/100 g/min to 38.7 ± 2.8 ml/100 g/min (P &lt; 0.05) and decreased the middle cerebral artery blood flow velocity from 109.9 ± 9.1 cm/s to 82.8 ± 8.6 cm/s (P &lt; 0.05). There was a mean increase in vessel diameters of 30.1% after papaverine infusion. Combined treatment (13 patients) significantly increased the CBF from 33.3 ± 3.2 ml/100 g/min to 41.7 ± 2.8 ml/100 g/min (P &lt; 0.05) and decreased the transcranial Doppler velocities from 148.9 ± 12.7 cm/s to 111.4 ± 10.6 cm/s (P &lt; 0.05), with a mean increase in vessel diameters of 42.2%. CONCLUSION Balloon angioplasty increased proximal vessel diameters, whereas papaverine treatment effectively dilated distal cerebral vessels. In our small series, we observed no correlation between early clinical improvement or clinical outcomes and any of our quantitative or physiological data (CBF, transcranial Doppler velocities, or vessel diameters).


2002 ◽  
Vol 22 (9) ◽  
pp. 1124-1131 ◽  
Author(s):  
Christina Kruuse ◽  
Lars Lykke Thomsen ◽  
Torsten Bjørn Jacobsen ◽  
Jes Olesen

Cyclic nucleotides are important hemodynamic regulators in many tissues. Glyceryl trinitrate markedly dilates large cerebral arteries and increases cGMP. Here, the authors study the effect of sildenafil, a selective inhibitor of cGMP-hydrolyzing phosphodiesterase 5 on cerebral hemodynamics and headache induction. Ten healthy subjects were included in a double-blind, placebo-controlled crossover study where placebo or sildenafil 100 mg (highest therapeutic dose) were administered on two separate days. Blood velocity in the middle cerebral artery (Vmca) was recorded by transcranial Doppler, and regional cerebral blood flow in the perfusion area of the middle cerebral artery (rCBFmca) was measured using single photon emission computed tomography and 133xenon inhalation. Radial and temporal artery diameters were studied using high-frequency ultrasound. Blood pressure and heart rate were recorded repeatedly. Headache responses and tenderness of pericranial muscles were scored verbally. Sildenafil caused no significant changes in rCBFmca, Vmca, or in temporal or radial artery diameter, but heart rate increased and diastolic blood pressure decreased significantly compared to placebo. Despite the lack of cerebral arterial dilatation, sildenafil caused significantly more headache than placebo. The present results show that sildenafil 100 mg does not dilate cerebral or extracerebral arteries but nevertheless causes headache, which may be attributed to nonvascular mechanisms.


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