Inspiratory resistance delays the reporting of symptoms with central hypovolemia: association with cerebral blood flow

2007 ◽  
Vol 293 (1) ◽  
pp. R243-R250 ◽  
Author(s):  
Caroline A. Rickards ◽  
Kathy L. Ryan ◽  
William H. Cooke ◽  
Keith G. Lurie ◽  
Victor A. Convertino

We tested the hypothesis that breathing through an inspiratory threshold device (ITD) during progressive central hypovolemia would protect cerebral perfusion and attenuate the reporting of presyncopal symptoms. Eight human subjects were exposed to lower-body negative pressure (LBNP) until the presence of symptoms while breathing through either an active ITD (−7 cmH2O impedance) or a sham ITD (0 cmH2O). Cerebral blood flow velocity (CBFV) was measured continuously via transcranial Doppler and analyzed in both time and frequency domains. Subjects were asked to report any subjective presyncopal symptoms (e.g., dizziness, nausea) at the conclusion of each LBNP exposure. Symptoms were coincident with physiological evidence of cardiovascular collapse (e.g., hypotension, bradycardia). Breathing on the active ITD increased LBNP tolerance time (mean ± SE) from 2,014 ± 106 s to 2,259 ± 138 s ( P = 0.006). We compared CBFV responses at the time of symptoms during the sham ITD trial with those at the same absolute time during the active ITD trial (when there were no symptoms). While there was no difference in mean CBFV at these time points (sham, 44 ± 4 cm/s vs. active, 47 ± 4; P = 0.587), total oscillations (sum of high- and low-frequency spectral power) of CBFV were higher ( P = 0.004) with the active ITD (45.6 ± 10.2 cm/s2) than the sham ITD (22.1 ± 5.4 cm/s2). We conclude that greater oscillations around the same absolute level of mean CBFV are induced by inspiratory resistance and may contribute to the delay in symptoms and cardiovascular collapse that accompany progressive central hypovolemia.

2003 ◽  
Vol 95 (4) ◽  
pp. 1439-1445 ◽  
Author(s):  
William H. Cooke ◽  
Guy L. Pellegrini ◽  
Olga A. Kovalenko

Complete ganglion blockade alters dynamic cerebral autoregulation, suggesting links between systemic autonomic traffic and regulation of cerebral blood flow velocity. We tested the hypothesis that acute head-down tilt, a physiological maneuver that decreases systemic sympathetic activity, would similarly disrupt normal dynamic cerebral autoregulation. We studied 10 healthy young subjects (5 men and 5 women; age 21 ± 0.88 yr, height 169 ± 3.1 cm, and weight 76 ± 6.1 kg). ECG, beat-by-beat arterial pressure, respiratory rate, end-tidal CO2 concentration, and middle cerebral blood flow velocity were recorded continuously while subjects breathed to a metronome. We recorded data during 5-min periods and averaged responses from three Valsalva maneuvers with subjects in both the supine and -10° head-down tilt positions (randomized). Controlled-breathing data were analyzed in the frequency domain with power spectral analysis. The magnitude of input-output relations were determined with cross-spectral techniques. Head-down tilt significantly reduced Valsalva phase IV systolic pressure overshoot from 36 ± 4.0 (supine position) to 25 ± 4.0 mmHg (head down) ( P = 0.03). Systolic arterial pressure spectral power at the low frequency decreased from 5.7 ± 1.6 (supine) to 4.4 ± 1.6 mmHg2 (head down) ( P = 0.02), and mean arterial pressure spectral power at the low frequency decreased from 3.3 ± 0.79 (supine) to 2.0 ± 0.38 mmHg2 (head down) ( P = 0.05). Head-down tilt did not affect cerebral blood flow velocity or the transfer function magnitude and phase angle between arterial pressure and cerebral blood flow velocity. Our results show that in healthy humans, mild physiological manipulation of autonomic activity with acute head-down tilt has no effect on the ability of the cerebral vasculature to regulate flow velocity.


2008 ◽  
Vol 79 (6) ◽  
pp. 557-564 ◽  
Author(s):  
Caroline A. Rickards ◽  
Kenneth D. Cohen ◽  
Lindsey L. Bergeron ◽  
Lubrina Burton ◽  
Prateek J. Khatri ◽  
...  

2018 ◽  
Vol 6 (4) ◽  
pp. e13594 ◽  
Author(s):  
Noud van Helmond ◽  
Blair D. Johnson ◽  
Walter W. Holbein ◽  
Humphrey G. Petersen-Jones ◽  
Ronée E. Harvey ◽  
...  

2001 ◽  
Vol 91 (5) ◽  
pp. 2199-2204 ◽  
Author(s):  
Sibrand Houtman ◽  
Jorge M. Serrador ◽  
Willy N. J. M. Colier ◽  
Derek W. Strijbos ◽  
Kevin Shoemaker ◽  
...  

Spinal cord-injured (SCI) individuals, having a sympathetic nervous system lesion, experience hypotension during sitting and standing. Surprisingly, they experience few syncopal events. This suggests adaptations in cerebrovascular regulation. Therefore, changes in systemic circulation, cerebral blood flow, and oxygenation in eight SCI individuals were compared with eight able-bodied (AB) individuals. Systemic circulation was manipulated by lower body negative pressure at several levels down to −60 mmHg. At each level, we measured steady-state blood pressure, changes in cerebral blood velocity with transcranial Doppler, and cerebral oxygenation using near-infrared spectroscopy. We found that mean arterial pressure decreased significantly in SCI but not in AB individuals, in accordance with the sympathetic impairment in the SCI group. Cerebral blood flow velocity decreased during orthostatic stress in both groups, but this decrease was significantly greater in SCI individuals. Cerebral oxygenation decreased in both groups, with a tendency to a greater decrease in SCI individuals. Thus present data do not support an advantageous mechanism during orthostatic stress in the cerebrovascular regulation of SCI individuals.


Author(s):  
Sole Lindvåg Lie ◽  
Jonny Hisdal ◽  
Lars Øivind Høiseth

Abstract Purpose Cerebral blood flow (CBF) needs to be precisely controlled to maintain brain functions. While previously believed to be autoregulated and near constant over a wide blood pressure range, CBF is now understood as more pressure passive. However, there are still questions regarding the integrated nature of CBF regulation and more specifically the role of cardiac output. Our aim was, therefore, to explore the effects of MAP and cardiac output on CBF in a combined model of reduced preload and increased afterload. Method 16 healthy volunteers were exposed to combinations of different levels of simultaneous lower body negative pressure and isometric hand grip. We measured blood velocity in the middle cerebral artery (MCAV) and internal carotid artery (ICAV) by Doppler ultrasound, and cerebral oxygen saturation (ScO2) by near-infrared spectroscopy, as surrogates for CBF. The effect of changes in MAP and cardiac output on CBF was estimated with mixed multiple regression. Result Both MAP and cardiac output had independent effects on MCAV, ICAV and ScO2. For ICAV and ScO2 there was also a statistically significant interaction effect between MAP and cardiac output. The estimated effect of a change of 10 mmHg in MAP on MCAV was 3.11 cm/s (95% CI 2.51–3.71, P < 0.001), and the effect of a change of 1 L/min in cardiac output was 3.41 cm/s (95% CI 2.82–4.00, P < 0.001). Conclusion The present study indicates that during reductions in cardiac output, both MAP and cardiac output have independent effects on CBF.


2015 ◽  
Vol 86 (8) ◽  
pp. 688-692 ◽  
Author(s):  
John J. Durocher ◽  
Jason R. Carter ◽  
William H. Cooke ◽  
Angelea H. Young ◽  
Morton H. Harwood

2017 ◽  
Vol 122 (4) ◽  
pp. 877-883 ◽  
Author(s):  
Anne-Sophie G. T. Bronzwaer ◽  
Jasper Verbree ◽  
Wim J. Stok ◽  
Mat J. A. P. Daemen ◽  
Mark A. van Buchem ◽  
...  

Lower-body negative pressure (LBNP) has been proposed as a MRI-compatible surrogate for orthostatic stress. Although the effects of LBNP on cerebral hemodynamic behavior have been considered to reflect those of orthostatic stress, a direct comparison with actual orthostasis is lacking. We assessed the effects of LBNP (−50 mmHg) vs. head-up tilt (HUT; at 70°) in 10 healthy subjects (5 female) on transcranial Doppler-determined cerebral blood flow velocity (CBF v) in the middle cerebral artery and cerebral perfusion pressure (CPP) as estimated from the blood pressure signal (finger plethysmography). CPP was maintained during LBNP but decreased after 2 min in response to HUT, leading to an ~15% difference in CPP between LBNP and HUT ( P ≤ 0.020). Mean CBF v initially decreased similarly in response to LBNP and for HUT, but, from minute 3 on, the decline became ~50% smaller ( P ≤ 0.029) during LBNP. The reduction in end-tidal Pco2 partial pressure (PetCO2) was comparable but with an earlier return toward baseline values in response to LBNP but not during HUT ( P = 0.008). We consider the larger decrease in CBF v during HUT vs. LBNP attributable to the pronounced reduction in PetCO2 and to gravitational influences on CPP, and this should be taken into account when applying LBNP as an MRI-compatible orthostatic stress modality. NEW & NOTEWORTHY Lower-body negative pressure (LBNP) has the potential to serve as a MRI-compatible surrogate of orthostatic stress but a comparison with actual orthostasis was lacking. This study showed that the pronounced reduction in end-tidal Pco2 together with gravitational effects on the brain circulation lead to a larger decline in cerebral blood flow velocity in response to head-up tilt than during lower-body negative pressure. This should be taken into account when employing lower-body negative pressure as MRI-compatible alternative to orthostatic stress.


2000 ◽  
Vol 278 (6) ◽  
pp. H1848-H1855 ◽  
Author(s):  
Rong Zhang ◽  
Julie H. Zuckerman ◽  
Benjamin D. Levine

To determine the dependence of cerebral blood flow (CBF) on arterial pressure over prolonged time periods, we measured beat-to-beat changes in mean CBF velocity in the middle cerebral artery (transcranial Doppler) and mean arterial pressure (Finapres) continuously for 2 h in six healthy subjects (5 men and 1 woman, 18–40 yr old) during supine rest. Fluctuations in velocity and pressure were quantified by the range [(peak − trough)/mean] and coefficients of variation (SD/mean) in the time domain and by spectral analysis in the frequency domain. Mean velocity and pressure over the 2-h recordings were 60 ± 7 cm/s and 83 ± 8 mmHg, associated with ranges of 77 ± 8 and 89 ± 10% and coefficients of variation of 9.3 ± 2.2 and 7.9 ± 2.3%, respectively. Spectral power of the velocity and pressure was predominantly distributed in the frequency range of 0.00014–0.1 Hz and increased inversely with frequency, indicating characteristics of an inverse power law (1/ f α). However, linear regression on a log-log scale revealed that the slope of spectral power of pressure and velocity was steeper in the high-frequency (0.02–0.5 Hz) than in the low-frequency range (0.002–0.02 Hz), suggesting different regulatory mechanisms in these two frequency ranges. Furthermore, the spectral slope of pressure was significantly steeper than that of velocity in the low-frequency range, consistent with the low transfer function gain and low coherence estimated at these frequencies. We conclude that 1) long-term fluctuations in CBF velocity are prominent and similar to those observed in arterial pressure, 2) spectral power of CBF velocity reveals characteristics of 1/ f α, and 3) cerebral attenuation of oscillations in CBF velocity in response to changes in pressure may be more effective at low than that at high frequencies, emphasizing the frequency dependence of cerebral autoregulation.


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