Coupling between arterial pressure, cerebral blood velocity, and cerebral tissue oxygenation with spontaneous and forced oscillations

Rickards, Caroline A.; Sprick, Justin D.; Colby, Hannah; Kay, Victoria; Tzeng, Yu‐Chieh

doi:10.1088/0967-3334/36/4/785

Cited by 15 publications

(10 citation statements)

References 40 publications

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“…Oscillatory patterns of arterial blood pressures, cerebral blood velocities and etCO 2 were determined using fast Fourier power spectral analysis, as previously described from our laboratory (Rickards, Sprick, Colby, Kay, & Tzeng, 2015). Data were made equidistant by interpolating linearly and resampling at 5 Hz.…”

Section: Discussionmentioning

confidence: 99%

Responses of cerebral blood velocity and tissue oxygenation to low‐frequency oscillations during simulated haemorrhagic stress in humans

Anderson

Sprick

Park

et al. 2019

Experimental Physiology

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New Findings What is the central question of this study?Do low‐frequency oscillations in arterial pressure and cerebral blood velocity protect cerebral blood velocity and oxygenation during central hypovolaemia? What is the main finding and its importance?Low‐frequency oscillations in arterial pressure and cerebral blood velocity attenuate reductions in cerebral oxygen saturation but do not protect absolute cerebral blood velocity during central hypovolaemia. This finding indicates the potential importance of haemodynamic oscillations in maintaining cerebral oxygenation and therefore viability of tissues during challenges to cerebral blood flow and oxygen delivery. Abstract Tolerance to both real and simulated haemorrhage varies between individuals. Exaggerated low‐frequency (∼0.1 Hz) oscillations in mean arterial pressure and brain blood flow [indexed via middle cerebral artery velocity (MCAv)] have been associated with improved tolerance to reduced central blood volume. The mechanism for this association has not been explored. We hypothesized that inducing low‐frequency oscillations in arterial pressure and cerebral blood velocity would attenuate reductions in cerebral blood velocity and oxygenation during simulated haemorrhage. Fourteen subjects (11 men and three women) were exposed to oscillatory (0.1 and 0.05 Hz) and non‐oscillatory (0 Hz) lower‐body negative pressure profiles with an average chamber pressure of −60 mmHg (randomized and counterbalanced order). Measurements included arterial pressure and stroke volume via finger photoplethysmography, MCAv via transcranial Doppler ultrasound, and cerebral oxygenation of the frontal lobe via near‐infrared spectroscopy. Tolerance was higher during the two oscillatory profiles compared with the 0 Hz profile (0.05 Hz, P = 0.04; 0.1 Hz, P = 0.09), accompanied by attenuated reductions in stroke volume (P < 0.001) and cerebral oxygenation of the frontal lobe (P ≤ 0.02). No differences were observed between profiles for reductions in mean arterial pressure (P = 0.17) and MCAv (P = 0.30). In partial support of our hypothesis, cerebral oxygenation, but not cerebral blood velocity, was protected during the oscillatory profiles. Interestingly, more subjects tolerated the oscillatory profiles compared with the static 0 Hz profile, despite similar arterial pressure responses. These findings emphasize the potential importance of haemodynamic oscillations in maintaining perfusion and oxygenation of cerebral tissues during haemorrhagic stress.

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Section: Discussionmentioning

confidence: 99%

Responses of cerebral blood velocity and tissue oxygenation to low‐frequency oscillations during simulated haemorrhagic stress in humans

Anderson

Sprick

Park

et al. 2019

Experimental Physiology

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“…In healthy adult volunteers, cerebral oxygenation measured by NIRS during hypovolemia has been studied experimentally by applying lower body negative pressure. 30,31 Literature on the effects of hypotension on NIRS oximetry measures in neonatal populations is limited. In preterm infants, mild short-term hypotensive episodes did not lower the cerebral oxygenation estimated by NIRS.…”

Section: Discussionmentioning

confidence: 99%

Quantifying cerebral hypoxia by near-infrared spectroscopy tissue oximetry: the role of arterial-to-venous blood volume ratio

et al. 2017

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"Quantifying cerebral hypoxia by near-infrared spectroscopy tissue oximetry: the role of arterial-tovenous blood volume ratio," J. Biomed. Opt. 22(2), 025001 (2017), doi: 10.1117/1.JBO.22.2.025001. Abstract. Tissue oxygenation estimated by near-infrared spectroscopy (NIRS) is a volume-weighted mean of the arterial and venous hemoglobin oxygenation. In vivo validation assumes a fixed arterial-tovenous volume-ratio (AV-ratio). Regulatory cerebro-vascular mechanisms may change the AV-ratio. We used hypotension to investigate the influence of blood volume distribution on cerebral NIRS in a newborn piglet model. Hypotension was induced gradually by inflating a balloon-catheter in the inferior vena cava and the regional tissue oxygenation from NIRS (rStO 2;NIRS ) was then compared to a reference (rStO 2;COX ) calculated from superior sagittal sinus and aortic blood sample co-oximetry with a fixed AV-ratio. Apparent changes in the AV-ratio and cerebral blood volume (CBV) were also calculated. The mean arterial blood pressure (MABP) range was 14 to 82 mmHg. PaCO 2 and SaO 2 were stable during measurements. rStO 2;NIRS mirrored only 25% (95% Cl: 21% to 28%, p < 0.001) of changes in rStO 2;COX . Calculated AVratio increased with decreasing MABP (slope: −0.007 · mmHg −1 , p < 0.001). NIRS estimates that CBV decreased with decreasing MABP (slope: 0.008 ml∕100 g∕mmHg, p < 0.001). Thus, cerebral NIRS oximetry responded poorly to changes in tissue oxygenation during hypotension induced by decreased preload. An increase in the AV-ratio during hypotension due to arterial vasodilation and, possibly, cerebral venous collapse may be a part of the explanation.

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“…To avoid this shortcoming, several methods of enhancing blood pressure (BP) oscillations have been used, from slow fixed-frequency breathing (Diehl et al 1995) to repeated squat-stand manoeuvres (Birch et al 1995) or thigh cuff deflation (Aaslid et al 2007). Oscillatory lower body pressure (LBP) is one such method that has proven to reliably and effectively elicit arterial pressure fluctuations to characterize cerebrovascular responses (Hamner et al 2004;Brothers et al 2009;Hamner & Tan, 2014;Rickards et al 2015;Merchant et al 2017).…”

Section: Introductionmentioning

confidence: 99%

Revisiting human cerebral blood flow responses to augmented blood pressure oscillations

Hamner

Ishibashi

Tan

2019

The Journal of Physiology

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Key points Cerebral autoregulation is most effective in buffering against pressure fluctuations slower than 0.03 Hz (∼30 s). This suggests that frequency bands for characterizing cerebral autoregulation should be redefined Low cross‐spectral coherence below 0.03 Hz highlights the limitations of transfer function approaches Haemodynamic changes induced by lower body pressure could not fully explain the differences in autoregulation estimated from spontaneous vs. augmented fluctuations, and thus, observations of spontaneous fluctuations should not be relied on whenever possible. Abstract There is currently little empirical basis for time scales that are considered to be most significant in cerebrovascular counter‐regulation of changes in arterial pressure. Although it is well established that cerebral autoregulation behaves as a ‘high‐pass’ filter, recommended frequency bands have been largely arbitrarily determined. To test effectiveness of cerebral autoregulation, we refined oscillatory lower body pressure (LBP) to augment resting pressure fluctuations below 0.1 Hz by a factor of two in 13 young male volunteers, and thoroughly characterized the time and frequency responses of cerebral autoregulation. We observed that despite a threefold increase in arterial pressure power <0.03 Hz with oscillatory LBP, there was no change in cerebral blood flow power, indicating near perfect counter‐regulation. By contrast, in the range 0.03–0.10 Hz, both cerebral blood flow and arterial pressure power more than doubled. Our data demonstrate that cerebral autoregulation is most effective in buffering against pressure fluctuations slower than 0.03 Hz (∼30 s). This suggests that frequency bands of interest should be redefined and recording length should be increased considerably to account for this. Furthermore, low cross‐spectral coherence below 0.03 Hz, even when pressure fluctuations were augmented, highlights the uncertainty in transfer function approaches and the need to either report precision or use non‐linear approaches. Finally, haemodynamic changes induced by LBP could not fully explain the differences in autoregulation estimated from spontaneous vs. augmented fluctuations, and thus, observations of spontaneous fluctuations should not be relied on whenever possible.

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Coupling between arterial pressure, cerebral blood velocity, and cerebral tissue oxygenation with spontaneous and forced oscillations

Cited by 15 publications

References 40 publications

Responses of cerebral blood velocity and tissue oxygenation to low‐frequency oscillations during simulated haemorrhagic stress in humans

Responses of cerebral blood velocity and tissue oxygenation to low‐frequency oscillations during simulated haemorrhagic stress in humans

Quantifying cerebral hypoxia by near-infrared spectroscopy tissue oximetry: the role of arterial-to-venous blood volume ratio

Revisiting human cerebral blood flow responses to augmented blood pressure oscillations

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