Influence of moderate and profound hyperventilation on cerebral blood flow, oxygenation and metabolism

Clausen, Tobias; Scharf, A.; Menzel, M.; Soukup, Jens; Holz, Carsten; Rieger, Andreas; Hanisch, Frank; Bráth, Endre; Németh, Norbert; Miko, Iren; Vajkoczy, Peter; Radke, J.; Henze, Dirk

doi:10.1016/j.brainres.2004.05.099

Cited by 33 publications

(21 citation statements)

References 41 publications

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“…Consistent with this point, HV-induced CBF decreases measured in awake male (34% (Raichle et al, 1970)) and nonanesthetized goats (38% (Albrecht et al, 1987)) are much less than that measured in anesthetized dogs (60%, (Raichle et al, 1970)). This point is supported by a recent study which used a 1 h anesthesia baseline before a HV challenge (20 to 30 mm Hg) in pigs (Clausen et al, 2004). Results demonstrated severe CBF decreases (B55%) in two of nine animals during the first 30 mins HV period, to 30 mm Hg, and three of nine animals (B75%) during the second 30 mins HV period (to 20 mm Hg), reaching the conclusion that HV cannot be considered safe.…”

Section: Discussionsupporting

confidence: 62%

Brain Changes to Hypocapnia Using Rapidly Interleaved Phosphorus-Proton Magnetic Resonance Spectroscopy at 4 T

Friedman

Jensen

Frederick

et al. 2006

J Cereb Blood Flow Metab

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Substantial controversy persists in the literature concerning the physiologic consequences hypocapnia, or low partial pressure of carbon dioxide (PaCO 2 ). Invasive animal studies have demonstrated large pH increases ( > 0.25 U), phosphocreatine (PCr) decreases ( > 30%), and adenosine triphosphate (ATP) decreases ( > 10%) after hyperventilation (HV) (20 mm Hg PaCO 2 ). However, using magnetic resonance spectroscopy, HV studies in awake humans have demonstrated only small pH changes (B0.05 U) and no changes in PCr or ATP. It remains important to ascertain whether this failure to detect PCr changes in human studies reflects a true absence of changes, or a limitation in data fidelity. The present study used a rapidly interleaved phosphorus-proton spectroscopy acquisition from large samples at high magnetic field (4 T), to measure pH, PCr, inorganic phosphate, b-ATP, and lactate changes with high temporal and signal sensitivity. Five of six subjects had usable data. During 20 mins HV, PaCO 2 reached a minimum at 16 mins (17 mm Hg); however, the maximum pH change ( + 0.047) peaked earlier (14 mins). Maximal lactate increases were measured at 15 mins. By 10 mins, maximum changes were observed for PCr (À3.4%) and inorganic phosphate ( + 6.4%). No changes in b-ATP were observed. The peak in pH, despite continued decreases in PaCO 2 , suggests active buffering during HV. These data, and the small magnitude of early PCr and inorganic phosphate changes, do not support substantial energy compromise during HV. Other mitigating factors, such as anesthesia-induced deregulation of the cerebrovasculature, might have contributed to the exaggerated metabolic changes observed in previous animal investigations.

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Section: Discussionsupporting

confidence: 62%

Brain Changes to Hypocapnia Using Rapidly Interleaved Phosphorus-Proton Magnetic Resonance Spectroscopy at 4 T

Friedman

Jensen

Frederick

et al. 2006

J Cereb Blood Flow Metab

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“…CBF of the right frontal lobe subcortical white matter was measured continuously with a thermal diffusion intraparenchymal probe (Hemedex, Cambridge, MA) inserted 1 cm anterior to the microdialysis probe 16,17 .…”

Section: Neuromonitoringmentioning

confidence: 99%

Differing Effects when Using Phenylephrine and Norepinephrine To Augment Cerebral Blood Flow after Traumatic Brain Injury in the Immature Brain

Friess

Bruins

Kilbaugh

et al. 2015

Journal of Neurotrauma

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Low cerebral blood flow (CBF) states have been demonstrated in children early after traumatic brain injury (TBI), and have been correlated with poorer outcomes. Cerebral perfusion pressure (CPP) support following severe TBI is commonly implemented to correct cerebral hypoperfusion, but the efficacy of various vasopressors has not been determined. Sixteen 4-week-old female swine underwent nonimpact inertial brain injury in the sagittal plane. Intraparenchymal monitors were placed to measure intracranial pressure (ICP), CBF, brain tissue oxygen tension (PbtO2), and cerebral microdialysis 30 min to 6 h post-injury. One hour after injury, animals were randomized to receive either phenylephrine (PE) or norepinephrine (NE) infusions titrated to a CPP>70 mm Hg for 5 h. Animals were euthanized 6 h post-TBI, and brains were fixed and stained to assess regions of cell and axonal injury. After initiation of CPP augmentation with NE or PE infusions, there were no differences in ICP between the groups or over time. Animals receiving NE had higher PbtO2 than those receiving PE (29.6±10.2 vs. 19.6±6.4 torr at 6 h post-injury, p<0.05). CBF increased similarly in both the NE and PE groups. CPP support with PE resulted in a greater reduction in metabolic crisis than with NE (lactate/pyruvate ratio 16.7±2.4 vs. 42.7±10.2 at 6 h post-injury, p<0.05). Augmentation of CPP to 70 mm Hg with PE resulted in significantly smaller cell injury volumes at 6 h post-injury than CPP support with NE (0.4% vs. 1.4%, p<0.05). Despite similar increases in CBF, CPP support with NE resulted in greater brain tissue oxygenation and hypoxic-ischemic injury than CPP support with PE. Future clinical studies comparing the effectiveness of various vasopressors for CPP support are warranted.

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“…All have used surrogate endpoints such as jugular venous oxygen saturation or metabolic imaging of the brain. [10][11][12][13] There is reasonable consistency among these studies that hyperventilation can adversely alter the measured parameters and may increase the areas of potentially ischemic brain. Presumably, this is due to arterial constriction, not only resulting in a reduction of ICP but also producing ischemia at the same time.…”

Section: Hyperventilation For Neurocritical Carementioning

confidence: 87%

“…Toutes ces études ont eu recours à des critères de substitution tels que la saturation en oxygène de la veine jugulaire ou l'imagerie métabolique du cerveau. [10][11][12][13] Une certaine cohérence existe entre ces études, soutenant que l'hyperventilation peut modifier de façon nuisible les paramètres mesurés et pourrait augmenter les zones potentiellement ischémiques du cerveau. Il est possible que cela soit dû à une constriction artérielle, provoquant non seulement une réduction de la PIC mais aussi une ischémie dans le même temps.…”

Section: L'hyperventilation Dans Les Soins Intensifs Neurologiquesunclassified

L’hyperventilation: un vent néfaste qui souffle parfois favorablement

Gelb

Chan

2008

Can J Anesth/J Can Anesth

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H yperventilation has been an integral part of the management of neurosurgical patients for the past 50 years. It has been so emblematic that a blindfolded individual could easily identify a neurosurgical operating room by the sound of the hard working ventilator. However, the routine use of hyperventilation has been re-evaluated with the emergence of evidence that it could be harmful.The first description of the benefits of hyperventilation in neuroanesthesia was published in 1957. 1 In the report, Furness reviewed the outcomes of 72 patients receiving "adequate ventilation" with a fixed ventilatory frequency of 20 breaths·min -1 during craniotomy. Although there was no formal assessment of the operating conditions and no measurement of arterial carbon dioxide tension (PaCO 2 ), "gradually the neurosurgeons were completely convinced" that hyperventilation produced better conditions compared with their previous experience using spontaneous ventilation. The report neglected to distinguish among the roles of hypocapnia, mechanical ventilation vs spontaneous breathing, and the contribution of muscle relaxation. 2,3 These latter were the subject of much debate and some research over the next decade. Neurophysiology of hyperventilationHyperventilation increases cerebral perivascular pH, resulting in cerebral arterial vasoconstriction and the decrease in cerebral blood flow (CBF) and cerebral blood volume (CBV). The CBV response to hyperventilation is blunted when compared to that of CBF. In general, for every mmHg decrease in PaCO 2 , there is a 1% decrease in CBV and a 2-3% decrease in CBF. 4 It is the reduction in CBV associated with hyperventilation that explains the decrease in intracranial pressure (ICP). 4,5 This response gradually normalizes over 12-24 hr. If hyperventilation is extended beyond this period, a restoration to normal PaCO 2 values may result in hyperemia and elevated ICP. Hyperventilation for neurocritical careGiven its favourable effect on ICP in experimental circumstances, aggressive hyperventilation was seen as a cheap, easy, and reversible treatment for patients with intracranial hypertension. Other perceived benefits included a redistribution of CBF to ischemic regions of the brain and the reversal of acidosis in the brain and cerebrospinal fluid (CSF). 4 Despite these claims, good outcome studies demonstrating a clear benefit of hyperventilation in the operating room or the neurocritical care unit were lacking. Indeed, studies using ICP as a surrogate endpoint often reported variable responses after hyperventilation in critically ill patients. 6,7 We believe this may be attributed to the heterogeneity of the human diseases as opposed to the controlled environment in the laboratory.The enthusiasm for hyperventilation therapy came to a sudden halt when almost 17 years ago Muizelaar et al. 8 reported the deleterious effect of prolonged hyperventilation in brain injured patients. A total of 113 patients with severe head injury were randomized to receive hyperventilation (PaCO 2 , 24-28 mmHg), h...

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Influence of moderate and profound hyperventilation on cerebral blood flow, oxygenation and metabolism

Cited by 33 publications

References 41 publications

Brain Changes to Hypocapnia Using Rapidly Interleaved Phosphorus-Proton Magnetic Resonance Spectroscopy at 4 T

Brain Changes to Hypocapnia Using Rapidly Interleaved Phosphorus-Proton Magnetic Resonance Spectroscopy at 4 T

Differing Effects when Using Phenylephrine and Norepinephrine To Augment Cerebral Blood Flow after Traumatic Brain Injury in the Immature Brain

L’hyperventilation: un vent néfaste qui souffle parfois favorablement

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