Middle cerebral artery blood velocity during a Valsalva maneuver in the standing position

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.

  • blood pressure
  • central venous pressure
  • cerebral autoregulation
  • cerebral blood flow
  • transcranial Doppler

lifting of a heavy weight may lead to a “blackout” (5), coughing may induce a syncope (15), and wind instrument players too may experience occasional fainting (3). These experiences suggest that, especially during standing, the expiratory strain of a Valsalva-like maneuver may critically reduce blood flow to the brain. A forced expiration against a closed glottis (a Valsalva maneuver) leads to a proportional elevation in the intrathoracic and central venous pressures (CVP), a marked reduction in cardiac output (CO), and characteristic changes in mean arterial pressure (MAP). Such hemodynamic alterations have consequences for the perfusion of the brain, as, even during a Valsalva maneuver performed in the supine position, the transcranial Doppler-determined middle cerebral artery (MCA) mean blood velocity (V mean) is reduced by ∼35% (29).

In healthy subjects, passive head-up tilt reduces MCAV mean (4, 12) and cerebral O2saturation (14). Presyncopal symptoms appear when MCAV mean is reduced by ∼50% (4, 12). These results indicate that, during standing, the downward shift in the distribution of the blood volume and the resulting decrease in CO may compromise cerebral perfusion. We hypothesized that, especially during standing, the hemodynamic changes associated with straining against a closed glottis would compromise blood supply to the brain. We evaluated the effects of a supine and an upright Valsalva maneuver on MCAV mean and determined CVP to assess the significance of the Valsalva-induced elevation in intrathoracic pressure on the cerebral perfusion pressure.


Subjects and experimental protocol.

Ten subjects [4 women and 6 men; age 25 (21–38) yr (median with range), weight 79 (50–90) kg, and height 183 (162–196) cm] participated in the study after giving informed consent to the protocol, as approved by the Ethics Committee of Copenhagen (KF 01–120/96). A mouthpiece was connected to a manometer, and the subjects were instructed to maintain an expiratory pressure of 40 mmHg for 15 s (28). A small leak in the tubing prevented the subjects from maintaining the pressure by closing the glottis, and care was taken to prevent deep breathing before and after the release of the strain. After instrumentation, the subjects were allowed to rest in the supine position for at least 30 min. After a test run, subjects rested for 5 min and performed three Valsalva maneuvers, each followed by 3 min of recovery. Subjects were then asked to stand up in a relaxed position, and, after 5 min, they performed three Valsalva maneuvers, each followed by 3 min of recovery.

Transcranial Doppler.

The proximal segment of the right MCA was insonated (Multidop X, DWL, Sipplingen, Germany) through the posterior temporal “window.” Once the optimal signal-to-noise ratio was obtained, the probe was covered with adhesive ultrasonic gel (Tensive, Parker Laboratories, Orange, NJ) that served for fixation to the skin. For further stabilization, a rubber band (DWL) was strapped around the head and the transducer. If necessary, tape was used to further fix the probe to the skin. Signal quality was evaluated during vigorous movement of the head, including bending forward and backward as well as shaking the head. By visual judgment of the Doppler signal, it was accepted when no interruptions or obvious artifacts of the spectral outline occurred.V mean was computed as the integral of maximal frequency shifts over one beat divided by the corresponding beat interval.

Cardiovascular monitoring.

Finger arterial pressure was measured with a Finapres model 5 (Netherlands Organization for Applied Scientific Research, Biomedical Instrumentation; TNO-BMI). The cuff was applied to the midphalanx of the middle finger of the dominant hand and placed at heart level. Beat-to-beat systolic and diastolic pressures, as well as MAP, were computed after analog-to-digital conversion at a sampling rate of 100 Hz. MAP was obtained as the integral of pressure over one beat divided by the corresponding beat interval. Heart rate (HR) was the inverse of the interbeat interval. A catheter (1.7 mm ID, 16 gauge) was placed in the superior caval vein through the basilic vein for CVP and central venous O2 saturation monitoring ( SvO2 ). CVP was recorded from a transducer (Bentley, Uden, The Netherlands) fastened to the subject in the midaxillary line at the level of the right atrium and connected to a monitor (8041, Simonsen & Weel, Copenhagen, Denmark). Stroke volume (SV) was obtained from the arterial pressure pulse wave by model flow analysis (FAST-mf/-cZ system, TNO, Amsterdam, The Netherlands). This method computes an aortic flow waveform by simulating a nonlinear, time-varying model of the aortic input impedance. The resulting CO correlates to a determination based on thermodilution (9). CO was the product of SV and HR and was expressed relative to control. The central blood volume was monitored by thoracic electrical impedance (TI) measured between skin electrodes employing 10 mA at 100 kHz (model 304 B, Minnesota Impedance Cardiograph, Sorcom, Minneapolis, MN). Two electrodes were positioned 5 cm above each other behind the right sternocleidomastoid muscle, and two other electrodes were placed at a similar distance in the left midaxillary line at the level of the xiphoid process. The outer electrodes served for current, whereas the inner pair recorded TI. An inverse correlation between TI and the central blood volume has been established during head-up tilt (20). Furthermore, during head-up tilt, TI is sensitive to changes in the distribution of technetium-labeled red cells (17) and also to the release of atrial natriuretic peptide from the right side of the heart (16, 21). We limited the use of TI as a marker of central blood volume to supine and standing baseline measurements. During the transition from normal breathing to strenuous expiratory straining, impedance would be expected to change independently of the central blood volume, as both an increase in electrode distance and the increased volume of air contained in the thorax would elevate TI.

Blood gases.

A 1.0-mm ID (19 gauge) catheter was placed in the brachial artery of the nondominant arm for arterial carbon dioxide tension ( PaCO2 ) and O2 saturation. For one Valsalva maneuver under each condition, blood samples were taken anaerobically in heparinized syringes (QS50, Radiometer, Copenhagen, Denmark) at rest, during the last seconds of the strain, and after ∼10 s of recovery. Samples were analyzed immediately by spectroscopy (OSM-3, ABL, Radiometer).

Data analysis.

Tracings of the variables were checked for artifacts and transformed to equidistantly resampled data at 2 Hz by polynomial interpolation, and for each subject the three runs were averaged as triggered by the onset of the increase in CVP. The circulatory response to the Valsalva maneuvers was divided into four phases (8, 25). A transient increase in MAP at the onset of the strain reflects transmission of the elevated intrathoracic pressure to the arterial tree (phase I) followed by a decrease in MAP, pulse pressure, and SV due to the reduced atrial filling (phase IIa) with partial recovery of MAP and HR toward the end of the strain (phase IIb). After release of the strain, MAP drops for 1–2 s as blood pools in the distended pulmonary vascular bed (phase III) followed by a pressure overshoot (phase IV) as an elevated CO is expelled against a constricted vascular bed.

Values are presented as means with standard error. The Friedman test was used to determine whether significant changes occurred with time or between circumstances, and such changes were located with Wilcoxon's matched-pair signed-rank test. To evaluate the significance of the Valsalva elevation in CVP for perfusion pressure to the brain, linear regression analysis was applied between MCA V meanand MAP, and between MCA V mean and the MAP-to-CVP difference (MAP-CVP). A P value of <0.05 was considered significant.


We observed a stable transcranial Doppler signal quality during the supine-to-standing transition, during standing, and also during the Valsalva maneuvers.

Supine Valsalva maneuver.

Table 1 lists the hemodynamic variables corresponding to each phase as defined from the changes in MAP. During straining, CVP increased immediately to 38 ± 4 mmHg and continued to increase toward the end of the strain (45 ± 4 mmHg). MAP demonstrated the characteristic changes with an increase in phase I (23 ± 4 mmHg) followed by a reduction close to baseline (phase IIa) and a subsequent recovery in phase IIb (22 ± 6 mmHg above baseline; Fig. 1). Inphase III, MAP dropped to the baseline level, which was followed by an overshoot in phase IV (19 ± 5 mmHg).

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Table 1.

Systemic and cerebral hemodynamic variables corresponding to 5 phases of the Valsalva maneuver

Fig. 1.

Systolic, mean, and diastolic middle cerebral artery (MCA) blood velocities (V MCA) and arterial blood pressures at the level of the MCA (ABP), central venous pressure (CVP), a cerebral perfusion pressure estimated from difference in mean arterial pressure (MAP) and CVP at the level of the brain (MAP-CVP), heart rate (HR), and changes in model flow stroke volume (ΔSV) and cardiac output (ΔCO) during a Valsalva maneuver (indicated by shaded bars) in the supine and standing positions. Values are means ± SE resampled on a 500-ms time scale (n = 10 subjects).

During the maneuver, CO decreased to 57 ± 4% of the baseline value until just before the release of the strain (Table 1, Fig. 1). SvO2 was not influenced significantly, whereas arterial O2 saturation became slightly elevated at the end of the maneuver and PaCO2 was reduced (Table 2).

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Table 2.

Arterial and central venous blood-gas variables during a Valsalva maneuver in the supine and standing position

Compared with MAP, MCA V mean reached the distinct phases of the Valsalva maneuver ∼0.5 s earlier. Peak changes in MCA V mean were a slight increase inphase I (+10 ± 2%; Table 1), a drop in phase II (−35 ± 4%), and an overshoot after the release of the strain (+40 ± 8%). Phase III could not be detected in MCAV mean.


In the standing position, TI increased from 40 ± 3 to 50 ± 3 Ω. CVP decreased (by 4 ± 2 mmHg), whereas MAP at heart level increased by 9 ± 2 mmHg, corresponding to a reduction at the level of the MCA by ∼10 mmHg (Fig. 1). SvO2 was lower (Table 2), and CO decreased by 16 ± 4% (Fig. 1), reflecting a lowered SV (−36 ± 3%) not fully compensated for by an increase in HR (by 21 ± 3 beats/min). Compared with supine rest, MCAV mean was reduced during standing (by 15 ± 5%). PaCO2 was only slightly reduced during standing (Table 2).

Upright Valsalva maneuver.

During straining, CVP increased immediately to 41 ± 3 mmHg and was not different from the CVP developed during the Valsalva maneuver in the supine position. Compared with the supine Valsalva maneuver, MAP changed more in phase IIa (−13 ± 4 mmHg below baseline), phase IIb (7 ± 5 mmHg above baseline), and phase III (−13 ± 4 mmHg below baseline), whereas increments were similar in phases I and IV. CO also decreased further during the standing Valsalva maneuver (to 37 ± 3% of the supine baseline value; Fig. 1) and reached the lowest value during phase IIa, reflecting a plateau in SV. Compared with the supine position, MCA V mean increased more inphase I (24 ± 4%) and dropped markedly in phase IIa (−47% from supine baseline). In contrast to the supine position, MCA V mean dropped in phase III(12 ± 4%), and the overshoot after the release of the strain (64 ± 11%) was higher. Peak changes in MCA V mean were not significantly different between the male and female subjects (Mann-Whitney test). None of the subjects fainted or became dizzy.

MCA Vmean and perfusion pressure.

The changes in MAP-CVP are shown in Fig. 1. For the supine Valsalva maneuver, the coefficient of determination (R 2) was larger for MCA V meanvs. MAP-CVP than for MCA V mean vs. MAP (Table3). During standing, in the individual subjects but not for the pooled data, R 2 tended to be higher for MCA V mean vs. MAP.

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Table 3.

Individual coefficients of determination (R2) for relation of MCA Vmean vs. MAP and MAP-CVP, respectively, during a standing and supine Valsalva maneuver


This study evaluated the influence of an upright Valsalva maneuver on the MCA V mean. In the standing position, MCAV mean was reduced ∼15%, and this reduction was exaggerated by a Valsalva maneuver to ∼50% of the value obtained during supine rest, whereas during a supine Valsalva maneuver the reduction in MCA V mean was by only ∼35%. These results indicate that, particularly in the upright posture, expiratory straining may critically compromise cerebral perfusion.

During standing, a drop in MCA V mean by ∼15% (2) may be in consequence of a decline in blood pressure at the level of the brain by ∼9 mmHg, but also the reduction in CO (∼16%) and PaCO2 (∼2 Torr) is likely to contribute. During orthostasis, the “CO2 reactivity” of brain circulation is not known, but it is similar for the supine and seated individual (2.9 vs. 2.6%/mmHg; Ref. 18), indicating that, during standing, PaCO2 accounts for ∼5% of the reduction in MCA V mean. Even at brain level, MAP was within the range normally associated with cerebral autoregulation, yet the lowered MAP may contribute to reduce cerebral perfusion (10). The importance of CO for the MCAV mean is demonstrated by an attenuated increase in MCA V mean during dynamic exercise after β-adrenergic blockade (a 12 vs. 22% increase) as the increase in CO is restricted ∼15% (11).

During the Valsalva maneuver, orthostasis affected MAP by causing a more pronounced drop below baseline in phase IIa and a blunted recovery in phase IIb. In the upright position, the smaller intrathoracic blood volume causes CO to become dependent on venous return and more so during the strain (27, 28). During the standing Valsalva maneuver, CO was as low as ∼40% of the value obtained during supine rest, reflecting a reduction in SV by ∼75%. Compared with the respective baseline values, an overshoot in SV and CO was pronounced only after the standing maneuver. Also, the increase in SvO2 during the upright Valsalva maneuver supports that CO did not adequately perfuse all parts of the body.

During the supine Valsalva maneuver, MCA V meanresembled the established pattern, i.e., it decreased with the onset of straining, recovered toward the end of the maneuver, and then demonstrated an overshoot (29). The distinct patterns of the arterial pressure, with its marked initial increase in phase I and sharp drop in phase III, were not reflected in MCAV mean, suggesting that CVP dominates the cerebral outflow pressure and, in turn, the perfusion pressure. In the supine position, we found a close relationship between MCAV mean and MAP-CVP (Fig. 1, Table 3). However, during standing, MCA V mean increased in phase I and dropped in phase III, more so than expected from the change in MAP-CVP. Furthermore, during standing, this initial increase in MCA V mean was larger than in the supine position, although the accompanying increase in MAP and CVP was similar. In an animal preparation, Kongstad and Grände (13) demonstrated that an increase in venous pressure has no influence on the tissue pressure for as long as the venous pressure is below the tissue pressure. Only when the venous pressure equals the tissue pressure does collapse of the outflow vein disappear and the two pressures increase in parallel. In the supine position, intracranial tissue pressure approximates CVP, and the Valsalva elevation in CVP would induce a parallel increase in the cerebral outflow pressure. In the standing position, the smaller influence of a 40-mmHg elevation in CVP for cerebral outflow pressure could reflect collapsed outflow veins (1). Such small deviation in the counterpressure is likely to become less important with further elevation of CVP.

PaCO2 decreased especially during the standing Valsalva maneuver. In contrast to breath holding without straining, a Valsalva maneuver is associated with a pronounced reduction in CO and, in turn, a reduced washout of CO2 from the tissue (19). The time constant for the MCAV mean response to a step decrease in end-tidal CO2 is ∼6 s, whereas the response to a step increase in CO2 takes ∼14 s (24). Thus during the Valsalva maneuver, PaCO2 may account for 10–15% of the reduction in MCA V mean, whereas it is unlikely to account for the overshoot after the maneuver.

The Valsalva maneuver also serves as a test for cerebral autoregulation, as demonstrated in patients with unilateral carotid stenosis and impaired cerebral autoregulation (29). In comparison with the healthy side, the rate of MCA V mean recovery inphase II vs. that of MAP is reduced, and the phase IVovershoot of MCA V mean is attenuated. During both the supine and the standing Valsalva maneuver, MCAV mean reached peak values earlier than MAP, and, inphase II, recovery of MCA V mean appeared to be similar. These findings could be taken to indicate maintained cerebral autoregulation during dynamic changes in MAP. On the other hand, MCA V mean was markedly reduced during standing, suggesting that, in orthostasis, concomitant changes in SV, CO, and also in PaCO2 render the Valsalva maneuver inappropriate for quantification of cerebral autoregulation.

Transcranial Doppler monitors blood velocity rather than volume flow, and changes in the diameter of the insonated vessel could modulate velocity independent of flow (7, 30). During craniotomy, Giller et al. (7) found the diameter of the large cerebral vessels unchanged with large changes in arterial pressure. Furthermore, as determined with magnetic resonance imaging in healthy individuals during hypocapnia, the MCA diameter remains stable, suggesting that the MCA is not involved in the regulation of cerebral vascular resistance (30).

Sympathetic activation is of potential importance for velocity in cerebral arteries because a reduction in diameter of the insonated artery would elevate velocity at an unchanged, or even reduced, volume flow. Evidence for MCA vasoconstriction was demonstrated during direct stimulation of the sympathetic trunk (31) and during maximal exercise, eliciting a 16-fold increase in plasma catecholamines (22) but not with the moderate increase in sympathetic nerve activity during, e.g., postexercise muscle ischemia (23). The Valsalva maneuver elicits large bursts of muscle sympathetic nerve activity duringphase II of straining when the MCA V mean is lowest, and sympathetic nerve activity drops to below baseline after the strain when MCA V mean is maximal (26), arguing against sympathetically mediated modulation of the MCA diameter.

Syncope is reported for weight-lifting exercise (5) when intrathoracic pressure increases up to 160 mmHg. The concomitant elevation in CVP protects the brain by counteracting the large increase in MAP, and the weight-lifters' blackout is ascribed to a critical reduction in cerebral perfusion due to preexercise hyperventilation (5). The occasional syncope that is observed during playing of wind instruments when mouth pressure may rise to >150 mmHg (6) is linked to cardiac arrhythmia, as frequently present during playing of the French horn (3). We suggest that, associated with intense expiratory strain, occasional fainting is related to the rise in CVP and, in turn, to a critical reduction in cerebral perfusion pressure.

In conclusion, in healthy individuals, orthostasis induces a reduction in MCA V mean that is exaggerated by the performance of a Valsalva maneuver to a level that may induce syncope. In contrast to the supine position during an upright Valsalva maneuver, cerebral perfusion pressure is dominated by the reduction in arterial inflow pressure and the contribution of CVP as outflow pressure is reduced.


We thank Karel Wesseling for valuable comments.


  • Address for reprint requests and other correspondence: F. Pott, Dept. of Anesthesia, Rigshospitalet 2041, Blegdamsvej 9, DK-2100 Copenhagen Ø, Denmark (E-mail: fpott{at}vip.cybercity.dk).

  • This study was supported by the Danish National Research Foundation (504–14), by the Danish Sports Research Council (1992–1–17), and by the Netherlands Heart Foundation (Grant 94.132).

  • The costs of publication of this article were defrayed in part by the payment of page charges. The article must therefore be hereby marked “advertisement” in accordance with 18 U.S.C. §1734 solely to indicate this fact.


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