Initial orthostatic hypotension is unrelated to orthostatic tolerance in healthy young subjects

2009 ◽  
Vol 107 (2) ◽  
pp. 506-517 ◽  
Author(s):  
Kate N. Thomas ◽  
James D. Cotter ◽  
Sean D. Galvin ◽  
Michael J. A. Williams ◽  
Chris K. Willie ◽  
...  
Keyword(s):  
Orthostatic Hypotension ◽  
Near Infrared ◽  
Cerebral Oxygenation ◽  
Lower Body Negative Pressure ◽  
Cerebral Vasoconstriction ◽  
Transient Nature ◽  
Head Up Tilt ◽  
Young Subjects ◽  
Initial Orthostatic Hypotension ◽  
End Tidal

The physiological challenge of standing upright is evidenced by temporary symptoms of light-headedness, dizziness, and nausea. It is not known, however, if initial orthostatic hypotension (IOH) and related symptoms associated with standing are related to the occurrence of syncope. Since IOH reflects immediate and temporary adjustments compared with the sustained adjustments during orthostatic stress, we anticipated that the severity of IOH would be unrelated to syncope. Following a standardized period of supine rest, healthy volunteers [ n = 46; 25 ± 5 yr old (mean ± SD)] were instructed to stand upright for 3 min, followed by 60° head-up tilt with lower-body negative pressure in 5-min increments of −10 mmHg, until presyncope. Beat-to-beat blood pressure (radial arterial or Finometer), middle cerebral artery blood velocity (MCAv), end-tidal Pco2, and cerebral oxygenation (near-infrared spectroscopy) were recorded continuously. At presyncope, although the reductions in mean arterial pressure, MCAv, and cerebral oxygenation were similar to those during IOH (40 ± 11 vs. 43 ± 12%; 36 ± 18 vs. 35 ± 13%; and 6 ± 5 vs. 4 ± 2%, respectively), the reduction in end-tidal CO2 was greater (−7 ± 6 vs. −4 ± 3 mmHg) and was related to the decline in MCAv ( R2 = 0.4; P < 0.05). While MCAv pulsatility was elevated with IOH, it was reduced at presyncope ( P < 0.05). The cardiorespiratory and cerebrovascular changes during IOH were unrelated to those at presyncope, and interestingly, there was no relationship between the hemodynamic changes and the incidence of subjective symptoms in either scenario. During IOH, the transient nature of physiological changes can be well tolerated; however, potentially mediated by a reduced MCAv pulsatility and greater degree of hypocapnic-induced cerebral vasoconstriction, when comparable changes are sustained, the development of syncope is imminent.

scholarly journals Cerebral vasoreactivity during hypercapnia is reset by augmented sympathetic influence

2011 ◽  
Vol 110 (2) ◽  
pp. 352-358 ◽  
Author(s):  
Peizhen Zhang ◽  
Guoyuan Huang ◽  
Xiangrong Shi
Keyword(s):  
Sympathetic Nerve ◽  
Sympathetic Nerve Activity ◽  
Near Infrared ◽  
Lower Body Negative Pressure ◽  
Transcranial Doppler Sonography ◽  
Nerve Activity ◽  
Hemodynamic Responses ◽  
Cerebral Hemodynamic ◽  
End Tidal ◽  
Cerebral Vasoreactivity

Sympathetic nerve activity influences cerebral blood flow, but it is unknown whether augmented sympathetic nerve activity resets cerebral vasoreactivity to hypercapnia. This study tested the hypothesis that cerebral vasodilation during hypercapnia is restrained by lower-body negative pressure (LBNP)-stimulated sympathoexcitation. Cerebral hemodynamic responses were assessed in nine healthy volunteers [age 25 yr (SD 3)] during rebreathing-induced increases in partial pressure of end-tidal CO2 (PetCO2) at rest and during LBNP. Cerebral hemodynamic responses were determined by changes in flow velocity of middle cerebral artery (MCAV) using transcranial Doppler sonography and in regional cerebral tissue oxygenation (ScO2) using near-infrared spectroscopy. PetCO2 values during rebreathing were similarly increased from 41.9 to 56.5 mmHg at rest and from 40.7 to 56.0 mmHg during LBNP of −15 Torr. However, the rates of increases in MCAV and in ScO2 per unit increase in PetCO2 (i.e., the slopes of MCAV/PetCO2 and ScO2/PetCO2) were significantly ( P ≤0.05) decreased from 2.62 ± 0.16 cm·s−1·mmHg−1 and 0.89 ± 0.10%/mmHg at rest to 1.68 ± 0.18 cm·s−1·mmHg−1 and 0.63 ± 0.07%/mmHg during LBNP. In conclusion, the sensitivity of cerebral vasoreactivity to hypercapnia, in terms of the rate of increases in MCAV and in ScO2, is diminished by LBNP-stimulated sympathoexcitation.

Accuracy of a Cerebral Oximeter in Healthy Volunteers under Conditions of Isocapnic Hypoxia 

1998 ◽  
Vol 88 (1) ◽  
pp. 58-65 ◽  
Author(s):  
Lindsey C. Henson ◽  
Carolyn Calalang ◽  
John A. Temp ◽  
Denham S. Ward
Keyword(s):  
Infrared Spectroscopy ◽  
Oxygen Saturation ◽  
Healthy Volunteers ◽  
Near Infrared Spectroscopy ◽  
Near Infrared ◽  
Cerebral Oxygenation ◽  
Jugular Bulb ◽  
Wide Range ◽  
Cerebral Oximeter ◽  
End Tidal

Background A cerebral oximeter measures oxygen saturation of brain tissue noninvasively by near infrared spectroscopy. The accuracy of a commercially available oximeter was tested in healthy volunteers by precisely controlling end-tidal oxygen (P[ET]O2) and carbon dioxide (P[ET]CO2) tensions to alter global cerebral oxygen saturation. Methods In 30 healthy volunteers, dynamic end-tidal forcing was used to produce step changes in P[ET]O2 resulting in arterial saturation ranging from approximately 70% to 100% under conditions of controlled normocapnia (each person's resting P[ET]CO2) or hypercapnia (resting plus 7-10 mmHg). Blood arterial (SaO2) and jugular bulb venous (S[jv]O2) saturations during each P(ET)O2 interval were determined by co-oximetry. The cerebral oximeter reading (rSO2) and an estimated jugular venous saturation (S[jv]O2), derived from a combination of SaO2 and rSO2, were compared with the measured S(jv)O2. Results The S(jv)O2 was significantly higher with hypercapnia than with normocapnia for the same SaO2. The rSO2 and S(jv)O2 were both highly correlated with S(jv)O2 for individual volunteers (mean r2 = 0.91 for each relation); however, the slopes and intercepts varied widely among volunteers. In three of them, the cerebral oximeter substantially underestimated the measured S(jv)O2. Conclusions During isocapnic hypoxia in healthy persons, cerebral oxygenation as estimated by near infrared spectroscopy precisely tracks changes in measured S(jv)O2 within individuals, but the relation exhibits a wide range of slopes and intercepts. Therefore the clinical utility of the device is limited to situations in which tracking trends in cerebral oxygenation would be acceptable.

scholarly journals Cerebral oxygenation and regional cerebral perfusion responses with resistance breathing during central hypovolemia

2017 ◽  
Vol 313 (2) ◽  
pp. R132-R139 ◽  
Author(s):  
Victoria L. Kay ◽  
Justin D. Sprick ◽  
Caroline A. Rickards
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Cerebral Artery ◽  
Cerebral Circulation ◽  
Near Infrared ◽  
Cerebral Oxygenation ◽  
Lower Body Negative Pressure ◽  
Transcranial Doppler Ultrasound ◽  
Cerebral Blood Velocity ◽  
Posterior Cerebral Circulation

Resistance breathing improves tolerance to central hypovolemia induced by lower body negative pressure (LBNP), but this is not related to protection of anterior cerebral blood flow [indexed by mean middle cerebral artery velocity (MCAv)]. We hypothesized that inspiratory resistance breathing improves tolerance to central hypovolemia by maintaining cerebral oxygenation (ScO2), and protecting cerebral blood flow in the posterior cerebral circulation [indexed by posterior cerebral artery velocity (PCAv)]. Eight subjects (4 male/4 female) completed two experimental sessions of a presyncopal-limited LBNP protocol (3 mmHg/min onset rate) with and without (Control) resistance breathing via an impedance threshold device (ITD). ScO2 (via near-infrared spectroscopy), MCAv and PCAv (both via transcranial Doppler ultrasound), and arterial pressure (via finger photoplethysmography) were measured continuously. Hemodynamic responses were analyzed between the Control and ITD condition at baseline (T1) and the time representing 10 s before presyncope in the Control condition (T2). While breathing on the ITD increased LBNP tolerance from 1,506 ± 75 s to 1,704 ± 88 s ( P = 0.003), both mean MCAv and mean PCAv were similar between conditions at T2 ( P ≥ 0.46), and decreased by the same magnitude with and without ITD breathing ( P ≥ 0.53). ScO2 also decreased by ~9% with or without ITD breathing at T2 ( P = 0.97), and there were also no differences in deoxygenated (dHb) or oxygenated hemoglobin (HbO2) between conditions at T2 ( P ≥ 0.43). There was no evidence that protection of regional cerebral blood velocity (i.e., anterior or posterior cerebral circulation) nor cerebral oxygen extraction played a key role in the determination of tolerance to central hypovolemia with resistance breathing.

Investigation of the cerebral haemoglobin and cytochrome signals using near infrared spectroscopy during head up tilt in patients with orthostatic hypotension

2005 ◽  
Vol 25 (1_suppl) ◽  
pp. S571-S571
Author(s):  
Martin Tisdall ◽  
Ilias Tachtsidis ◽  
Katharine Bleasdale-Barr ◽  
Chris J Mathias ◽  
Dave T Delpy ◽  
...  
Keyword(s):  
Infrared Spectroscopy ◽  
Orthostatic Hypotension ◽  
Near Infrared Spectroscopy ◽  
Near Infrared ◽  
Head Up Tilt

Initial orthostatic hypotension and cerebral blood flow regulation: effect of α1-adrenoreceptor activity

2013 ◽  
Vol 304 (2) ◽  
pp. R147-R154 ◽  
Author(s):  
Nia C. S. Lewis ◽  
Philip N. Ainslie ◽  
Greg Atkinson ◽  
Helen Jones ◽  
Emily J. M. Grant ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Orthostatic Hypotension ◽  
Relative Difference ◽  
Cerebral Hypoperfusion ◽  
Adrenergic Blockade ◽  
Absolute Level ◽  
Arterial Blood ◽  
Placebo Trial ◽  
Initial Orthostatic Hypotension ◽  
End Tidal

We examined the hypothesis that α1-adrenergic blockade would lead to an inability to correct initial orthostatic hypotension (IOH) and cerebral hypoperfusion, leading to symptoms of presyncope. Twelve normotensive humans (aged 25 ± 1 yr; means ± SE) attempted to complete a 3-min upright stand, 90 min after the administration of either α1-blockade (prazosin, 1 mg/20 kg body wt) or placebo. Continuous beat-to-beat measurements of middle cerebral artery velocity (MCAv; Doppler), blood pressure (finometer), heart rate, and end-tidal Pco2were obtained. Compared with placebo, the α1-blockade reduced resting mean arterial blood pressure (MAP) (−15%; P < 0.01); MCAv remained unaltered ( P ≥ 0.28). Upon standing, although the absolute level of MAP was lower following α1-blockade (39 ± 10 mmHg vs. 51 ± 14 mmHg), the relative difference in IOH was negligible in both trials (mean difference in MAP: 2 ± 2 mmHg; P = 0.50). Compared with the placebo trial, the declines in MCAv and PetCO2during IOH were greater in the α1-blockade trial by 12 ± 4 cm/s and 4.4 ± 1.3 mmHg, respectively ( P ≤ 0.01). Standing tolerance was markedly reduced in the α1-blockade trial (75 ± 17 s vs. 180 ± 0 s; P < 0.001). In summary, while IOH was little affected by α1-blockade, the associated decline in MCAv was greater in the blockade condition. Unlike in the placebo trial, the extent of IOH and cerebral hypoperfusion failed to recover toward baseline in the α1-blockade trial leading to presyncope. Although the development of IOH is not influenced by the α1-adrenergic receptor pathway, this pathway is critical in the recovery from IOH to prevent cerebral hypoperfusion and ultimately syncope.

scholarly journals The cerebrovascular response to lower-body negative pressure vs. head-up tilt

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 ◽  
...  
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Negative Pressure ◽  
Cerebral Blood Flow Velocity ◽  
Lower Body Negative Pressure ◽  
Orthostatic Stress ◽  
Lower Body ◽  
Head Up Tilt ◽  
End Tidal ◽  
Pronounced Reduction

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.

scholarly journals Near-Infrared Spectroscopy for the Evaluation of Anesthetic Depth

2015 ◽  
Vol 2015 ◽  
pp. 1-11 ◽  
Author(s):  
Gabriela Hernandez-Meza ◽  
Meltem Izzetoglu ◽  
Mary Osbakken ◽  
Michael Green ◽  
Kurtulus Izzetoglu
Keyword(s):  
Infrared Spectroscopy ◽  
Near Infrared Spectroscopy ◽  
Near Infrared ◽  
Cerebral Oxygenation ◽  
Standard Of Care ◽  
Functional Near Infrared Spectroscopy ◽  
Gold Standard Method ◽  
Anesthetic Drugs ◽  
Sedation Monitoring ◽  
End Tidal

The standard-of-care guidelines published by the American Society of Anesthesiologists (ASA) recommend monitoring of pulse oximetry, blood pressure, heart rate, and end tidal CO2during the use of anesthesia and sedation. This information can help to identify adverse events that may occur during procedures. However, these parameters are not specific to the effects of anesthetics or sedatives, and therefore they offer little, to no, real time information regarding the effects of those agents and do not give the clinician the lead-time necessary to prevent patient “awareness.” Since no “gold-standard” method is available to continuously, reliably, and effectively monitor the effects of sedatives and anesthetics, such a method is greatly needed. Investigation of the use of functional near-infrared spectroscopy (fNIRS) as a method for anesthesia or sedation monitoring and for the assessment of the effects of various anesthetic drugs on cerebral oxygenation has started to be conducted. The objective of this paper is to provide a thorough review of the currently available published scientific studies regarding the use of fNIRS in the fields of anesthesia and sedation monitoring, comment on their findings, and discuss the future work required for the translation of this technology to the clinical setting.

Cerebral hypoperfusion during hypoxic exercise following two different hypoxic exposures: independence from changes in dynamic autoregulation and reactivity

2008 ◽  
Vol 295 (5) ◽  
pp. R1613-R1622 ◽  
Author(s):  
Philip N. Ainslie ◽  
Michael Hamlin ◽  
John Hellemans ◽  
Peter Rasmussen ◽  
Shigehiko Ogoh
Keyword(s):  
Near Infrared ◽  
Cerebral Oxygenation ◽  
Function Analysis ◽  
Low Frequency ◽  
Cerebrovascular Reactivity ◽  
Cerebral Hypoperfusion ◽  
Cerebrovascular Function ◽  
Transfer Function Analysis ◽  
End Tidal ◽  
Hypoxic Exercise

We examined the effects of exposure to 10–12 days intermittent hypercapnia [IHC: 5:5-min hypercapnia (inspired fraction of CO2 0.05)-to-normoxia for 90 min ( n = 10)], intermittent hypoxia [IH: 5:5-min hypoxia-to-normoxia for 90 min ( n = 11)] or 12 days of continuous hypoxia [CH: 1,560 m ( n = 7)], or both IH followed by CH on cardiorespiratory and cerebrovascular function during steady-state cycling exercise with and without hypoxia (inspired fraction of oxygen, 0.14). Cerebrovascular reactivity to CO2 was also monitored. During all procedures, ventilation, end-tidal gases, blood pressure, muscle and cerebral oxygenation (near-infrared spectroscopy), and middle cerebral artery blood flow velocity (MCAv) were measured continuously. Dynamic cerebral autoregulation (CA) was assessed using transfer-function analysis. Hypoxic exercise resulted in increases in ventilation, hypocapnia, heart rate, and cardiac output when compared with normoxic exercise ( P < 0.05); these responses were unchanged following IHC but were elevated following the IH and CH exposure ( P < 0.05) with no between-intervention differences. Following IH and/or CH exposure, the greater hypocapnia during hypoxic exercise provoked a decrease in MCAv ( P < 0.05 vs. preexposure) that was related to lowered cerebral oxygenation ( r = 0.54; P < 0.05). Following any intervention, during hypoxic exercise, the apparent impairment in CA, reflected in lowered low-frequency phase between MCAv and BP, and MCAv-CO2 reactivity, were unaltered. Conversely, during hypoxic exercise following both IH and/or CH, there was less of a decrease in muscle oxygenation ( P < 0.05 vs. preexposure). Thus IH or CH induces some adaptation at the muscle level and lowers MCAv and cerebral oxygenation during hypoxic exercise, potentially mediated by the greater hypocapnia, rather than a compromise in CA or MCAv reactivity.

scholarly journals A Comparison of the Hamamatsu NIRO 500 and the INVOS 3100 Near-Infrared Spectrophotometers

1998 ◽  
Vol 26 (5) ◽  
pp. 548-557 ◽  
Author(s):  
C. D. Gomersall ◽  
P. L. Leung ◽  
T. Gin ◽  
G. M. Joynt ◽  
R. J. Young ◽  
...  
Keyword(s):  
Oxygen Saturation ◽  
Near Infrared ◽  
Cerebral Oxygenation ◽  
Haemoglobin Concentration ◽  
Carbon Dioxide Tension ◽  
Cerebral Oxygen Saturation ◽  
Cerebral Oxygen ◽  
Infrared Spectrophotometer ◽  
Total Haemoglobin ◽  
End Tidal

Near-infrared spectroscopy is a technique used for non-invasive measurement of cerebral oxygenation and a number of commercial devices are currently available for use. We compared measurements of cerebral oxygenation made with two near-infrared spectrophotometers—the Somanetics Invos 3100 cerebral oximeter and the Hamamatsu NIRO-500 near-infrared spectrophotometer. Hypoxia was induced in six healthy male volunteers with and without occlusion of scalp blood flow. Oxygen saturation, end-tidal carbon dioxide tension, regional cerebral oxygen saturation, change in regional cerebral oxyhaemoglobin concentration and change in regional cerebral total haemoglobin concentration were measured. The INVOS 3100 displays cerebral oxygen saturation directly. The NIRO-500 displays change in total haemoglobin concentration and oxyhaemoglobin concentration, and the cerebral oxygen saturation was calculated offline. Statistical analysis disproved the assumption that the INVOS 3100 and the NIRO-500 were measuring the same changes in cerebral oxygenation. Neither machine can be confirmed for reliability against a gold standard and operational difficulties mean that neither can be recommended for routine clinical use.

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