The role of cerebral oxygenation and regional cerebral blood flow on tolerance to central hypovolemia

Kay, Victoria; Rickards, Caroline A.

doi:10.1152/ajpregu.00367.2015

Cited by 39 publications

(50 citation statements)

References 46 publications

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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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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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“…9 Cerebral perfusion associated with high and low tolerance to hemorrhage An individual's tolerance to central hypovolemia during LBNP (simulated blood loss) largely reflects a reached ''threshold'' during a progressive reduction in cerebral blood flow and oxygenation. 10 A tracing of a continuous transcranial Doppler (TCD) measurement obtained from a Schiller et al The physiology of blood loss and shock 875 human subject undergoing progressive LBNP is presented in Figure 3(a). The TCD provides a measure of mean cerebral artery velocity (MCAv) which is progressively reduced as the subject's central blood volume decreases.…”

Section: Comparison Of Lbnp and Actual Hemorrhagementioning

confidence: 99%

The physiology of blood loss and shock: New insights from a human laboratory model of hemorrhage

Schiller

Howard

Convertino

2017

Exp Biol Med (Maywood)

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Hemorrhage is the leading cause of death in both civilian and military trauma. The work submitted in this review is important because it advances the understanding of mechanisms that contribute to the total integrated physiological compensations for inadequate tissue oxygenation (i.e. shock) that arise from hemorrhage. Unlike an animal model, we introduce the utilization of lower body negative pressure as a noninvasive model that allows for the study of progressive reductions in central blood volume similar to those reported during actual hemorrhage in conscious humans to the onset of hemodynamic decompensation (i.e. early phase of decompensatory shock), and is repeatable in the same subject. Understanding the fundamental underlying physiology of human hemorrhage helps to test paradigms of critical care medicine, and identify and develop novel clinical practices and technologies for advanced diagnostics and therapeutics in patients with life-threatening blood loss. AbstractThe ability to quickly diagnose hemorrhagic shock is critical for favorable patient outcomes. Therefore, it is important to understand the time course and involvement of the various physiological mechanisms that are active during volume loss and that have the ability to stave off hemodynamic collapse. This review provides new insights about the physiology that underlies blood loss and shock in humans through the development of a simulated model of hemorrhage using lower body negative pressure. In this review, we present controlled experimental results through utilization of the lower body negative pressure human hemorrhage model that provide novel insights on the integration of physiological mechanisms critical to the compensation for volume loss. We provide data obtained from more than 250 human experiments to classify human subjects into two distinct groups: those who have a high tolerance and can compensate well for reduced central blood volume (e.g. hemorrhage) and those with low tolerance with poor capacity to compensate.We include the conceptual introduction of arterial pressure and cerebral blood flow oscillations, reflexmediated autonomic and neuroendocrine responses, and respiration that function to protect adequate tissue oxygenation through adjustments in cardiac output and peripheral vascular resistance. Finally, unique time course data are presented that describe mechanistic events associated with the rapid onset of hemodynamic failure (i.e. decompensatory shock).

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“…Both blood loss and LBNP elicit similar responses in key haemodynamic parameters, including heart rate, stroke volume, cardiac output, arterial pressure and cerebral blood velocity (Hinojosa-Laborde et al, 2014;Johnson et al, 2014;. In studies using maximal LBNP to presyncope, it has been demonstrated that there is a continuum of tolerance among healthy human subjects (Kay & Rickards, 2016;Levine, Giller, Lane, Buckey, & Blomqvist, 1994;Lightfoot & Tsintgiras, 1995;Rickards, Ryan, Cooke, & Convertino, 2011), which has been attributed, in part, to protection of absolute blood flow (Levine et al, 1994;Lieshout, Wieling, Karemaker, & Secher, 2003) in either the anterior (Levine et al, 1994;Rickards et al, 2011) or the posterior circulation (Kay & Rickards, 2016) of the brain. In studies using maximal LBNP to presyncope, it has been demonstrated that there is a continuum of tolerance among healthy human subjects (Kay & Rickards, 2016;Levine, Giller, Lane, Buckey, & Blomqvist, 1994;Lightfoot & Tsintgiras, 1995;Rickards, Ryan, Cooke, & Convertino, 2011), which has been attributed, in part, to protection of absolute blood flow (Levine et al, 1994;Lieshout, Wieling, Karemaker, & Secher, 2003) in either the anterior (Levine et al, 1994;Rickards et al, 2011) or the posterior circulation (Kay & Rickards, 2016) of the brain.…”

Section: Introductionmentioning

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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The role of cerebral oxygenation and regional cerebral blood flow on tolerance to central hypovolemia

Cited by 39 publications

References 46 publications

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

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

The physiology of blood loss and shock: New insights from a human laboratory model of hemorrhage

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

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