Middle cerebral artery blood velocity during intense static exercise is dominated by a Valsalva maneuver

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.

2000 ◽  
Vol 88 (5) ◽  
pp. 1545-1550 ◽  
Author(s):  
Frank Pott ◽  
Johannes J. van Lieshout ◽  
Kojiro Ide ◽  
Per Madsen ◽  
Niels H. Secher

Occasionally, lifting of a heavy weight leads to dizziness and even to fainting, suggesting that, especially in the standing position, expiratory straining compromises cerebral perfusion. In 10 subjects, the middle cerebral artery mean blood velocity ( V mean) was evaluated during a Valsalva maneuver (mouth pressure 40 mmHg for 15 s) both in the supine and in the standing position. During standing, cardiac output decreased by 16 ± 4 (SE) % ( P < 0.05), and at the level of the brain mean arterial pressure (MAP) decreased from 89 ± 2 to 78 ± 3 mmHg ( P < 0.05), as did V mean from 73 ± 4 to 62 ± 5 cm/s ( P < 0.05). In both postures, the Valsalva maneuver increased central venous pressure by ∼40 mmHg with a nadir in MAP and cardiac output that was most pronounced during standing (MAP: 65 ± 6 vs. 87 ± 3 mmHg; cardiac output: 37 ± 3 vs. 57 ± 4% of the resting value; P < 0.05). Also, V mean was lowest during the standing Valsalva maneuver (39 ± 5 vs. 47 ± 4 cm/s; P < 0.05). In healthy individuals, orthostasis induces an ∼15% reduction in middle cerebral artery V mean that is exaggerated by a Valsalva maneuver performed with 40-mmHg mouth pressure to ∼50% of supine rest.


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.


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

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.


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.


1995 ◽  
Vol 80 (1) ◽  
pp. 64-70 ◽  
Author(s):  
Andreas Weyland ◽  
Heidrun Stephan ◽  
Frank Grune ◽  
Wolfgang Weyland ◽  
Hans Sonntag

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