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PubMed1992

The hyperventilation provocation test in panic disorder.

Forty-eight patients with DSM-III-R Panic Disorder underwent a hyperventilation provocation Test (HVPT). Twenty-four patients rated the symptoms induced during the HVPT as similar to those occurring during panic attacks in daily life. Contrary to the classical hyperventilation model of panic, no differences were found in respiratory physiology between recognizers and non-recognizers before and during voluntary hyperventilation. Moreover, recognizers and non-recognizers reported comparable levels of panic and hyperventilation symptoms and state anxiety during panic attacks in daily life. Ten of the recognizers also had a panic attack during the HVPT, independent of any differential CO2 alterations. Compared to non-panickers, panickers obtained higher scores for agoraphobia and depression. On the basis of these results, it is concluded that recognizers or panickers do not show a tendency towards hyperventilation, but that reports of severe panic and hyperventilation symptoms are more closely related to the level of anxiety. These results are more consistent with the cognitive model of panic, which emphasizes the patient's tendency to interpret somatic symptoms catastrophically.

Adult↗

PubMed1995

Voluntary hyperventilation: the influence of duration and depth on the development of symptoms.

Hyperventilation is considered an important factor in the development of somatic symptoms or even panic attacks, though its role has recently been disputed. Arguments are often based on findings from the so-called Hyperventilation Provocation Test (HVPT), which is a procedure consisting of voluntarily overbreathing. The HVPT has been widely used for diagnosing Hyperventilation Syndrome and for experimentally eliciting panic attacks. Almost no attention, however, has been paid to standardizing the test and determining critical values with respect to depth and duration of hyperventilation. In the present study, symptom development was examined in 16 healthy subjects who underwent four HVPTs that differed in depth of hyperventilation (end-tidal PCO2 < 2.4 kPa or < 1.9 kPa), as well as duration of hyperventilation (2 or 5 min). Both depth and duration appeared to have an independent effect on the development of symptoms. In the 5-min condition, symptoms appeared mainly within the first 3 min. To be sure that the HVPT is long enough and deep enough to elicit symptoms in most people, a minimum duration of 3 min is advised, with end-tidal PCO2 decreasing to at least 1.9 kPa or dropping well over 50% of baseline.

Adult↗

PubMed1989

Significance of hyperventilation-induced ST segment depression in patients with coronary artery disease.

To investigate the significance of hyperventilation-induced ST segment depression, 329 consecutive patients with angina and documented coronary artery disease who underwent hyperventilation and exercise tests during pharmacologic washout were studied. The hyperventilation test induced ST segment depression in 79 patients. In 36 of these 79 patients, the electrocardiographic changes occurred early during overbreathing (Group I), whereas in 26 they occurred late during recovery (Group II). Seventeen patients developed ST segment depression both during over-breathing and during recovery (Group III). Group I patients had a higher frequency of history of angina during exercise, multivessel disease and lower tolerance to exercise as compared with patients in Group II. In Group I, the rate-pressure product at the time to onset of ST depression during overbreathing was similar to that during exercise (152 +/- 24 versus 148 +/- 42; p = NS), whereas in Group II the rate-pressure product at the time to onset of ST depression during recovery was comparable with that under control conditions (104 +/- 30 versus 98 +/- 27; p = NS) and far less than that required to produce ischemia during exercise (104 +/- 30 versus 201 +/- 56; p less than 0.0011). In nine Group III patients, the acute administration of propranolol prevented the early hyperventilation-induced ST segment depression, whereas nifedipine abolished the delayed hyperventilation-induced ST segment depression. These findings suggest that early hyperventilation-induced ST segment depression is due to increased oxygen demand in patients with poor coronary reserve and may be prevented by beta-adrenergic blockers, which are useful for lowering oxygen consumption.(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗

PubMed1995

Response of human epileptic temporal lobe cortical blood flow to hyperventilation.

Bilateral long-term surface cortical cerebral blood flow (CBF) and electrocorticographic (ECoG) monitoring were performed in eight patients with complex partial seizures. In each patient, the epileptic temporal lobe was localized using ictal ECoG. Mean seizure interval (frequency-1) off anticonvulsant medication, a clinical measure of epileptogenicity, was 1.0 +/- 0.3 h (range: 0.4 to 2.5 h). During 13 interictal hyperventilation periods, 3.6 +/- 0.6 min in duration, the mean decrease in epileptic and nonepileptic temporal cortical CBF was 13.7 +/- 2.3 versus 6.4 +/- 1.9 ml/(100 g min) (t = 2.230, d.f. = 16, P < 0.05), representing 20.9% and 10.8% reduction from baseline CBF during hyperventilation, respectively. Seizure interval decreased (i.e. frequency increased) with increasing magnitude of seizure focus CBF reduction during hyperventilation. Seizure interval was significantly correlated with epileptic temporal lobe CBF decrease during hyperventilation (R = 0.763, d.f. = 5, P < 0.05). The data suggest that, compared to nonepileptic brain, epileptic temporal lobe is particularly prone to hypoperfusion during hyperventilation. Epileptogenicity is a function of this seizure focus susceptibility to ischemia. The finding of abnormal seizure focus autoregulation during hyperventilation has implication for epileptic focus localization with cerebral blood flow analysis.

Adolescent↗

PubMed2006

The effect of hyperventilation on strength-duration properties in diabetic polyneuropathy.

OBJECTIVE: Hyperventilation and ischaemia increase axonal excitability by changing Na+ conductance in healthy subjects. However, the changes in excitability during and after ischaemia in diabetic patients are less than in healthy controls. This is known as ischaemic resistance. In this study, we investigated the effects of hyperventilation for 20 min on strength-duration time constant (SDTC) of motor axons of the median nerve of diabetic patients with polyneuropathy to determine whether diabetics are less affected by hyperventilation, a form of resistance similar to the ischaemic resistance of diabetics. METHODS: The SDTC of 14 diabetic patients with polyneuropathy and 10 healthy volunteers were measured following stimulation of right median nerve at the wrist prior to and after hyperventilation for 20 min. RESULTS: There was a significant increase in the SDTC in control subjects, but no significant change in the SDTC for patients with diabetic polyneuropathy. The score of the clinical response (paraesthesiae and carpopedal spasm) to hyperventilation of controls was also significantly greater in the controls than the patients. CONCLUSION: Hyperventilation for 20 min has little influence on SDTC in patients with diabetic polyneuropathy. SIGNIFICANCE: The 'resistance' of diabetic nerve is not confined to ischaemia but involves other manoeuvres that can alter axonal excitability.

Action Potentials↗

PubMed2004

Central neurogenic hyperventilation in a conscious child associated with glioblastoma multiforme.

Central neurogenic hyperventilation refers to progressive tachypnea leading to hypocarbia and respiratory alkalosis caused by cortical disorders, initially reported in comatose patients with mainly pontine infarction. Central neurogenic hyperventilation in conscious patients is even rarer, numbering around 30 reported cases including seven children, mainly associated with infiltrative gliomas and lymphomas of the brainstem and pons. We report the evolution of central neurogenic hyperventilation in a conscious child associated with an infiltrative glioblastoma multiforme diagnosed 1 year before admission. He presented with progressive tachypnea and dyspnea of 1 week duration. On examination he was fully alert and aware of his respiratory disorder. Respiratory rate was 56 breaths per minute using accessory respiratory muscles. Hyperventilation was unchanged during sleep. Arterial blood gases disclosed marked hypocarbia: Pco(2) of 8 mm Hg resulting in severe respiratory alkalosis at pH of 7.8. Central neurogenic hyperventilation was therefore suggested after exclusion of other respiratory or cardiac disorders. The exaggerated tachypnea persisted along with respiratory alkalosis. Over a period of 2 months his overall state markedly deteriorated; he lapsed into coma, and finally succumbed after involvement of medullary cardiovascular centers. Although extremely rare in the pediatric age group, central neurogenic hyperventilation should be suspected in any alert child presenting with unexplained increasing tachypnea and hypocarbia leading to respiratory alkalosis. The evolution of such a disorder may be an alarming sign of ensuing deterioration in patients with tumors of the brainstem and medulla before cardiovascular derangement.

Alkalosis, Respiratory↗

PubMed2001

Hyperventilation challenge test in panic disorder and depression with panic attacks.

Our aim was to determine whether panic disorder (PD) patients, major depressive patients without panic attacks (MD) and major depressive patients with panic attacks (MDP) respond similarly to hyperventilation challenge tests. We randomly selected 35 PD patients, 33 MDP patients, 27 MD patients and 30 normal volunteers with no family history of anxiety or mood disorder. The patients had not been treated with psychotropic drugs for at least 1 week. They were induced to hyperventilate (30 breaths/min) for 4 min, and anxiety was assessed before and after the test. A total of 16 (45.7%) PD patients, 12 (36.4%) MDP patients, four (11.1%) MD patients, and two (6.7%) normal volunteers had a panic attack after hyperventilating. The PD and MDP patients were significantly more responsive to hyperventilation than the MD patients and the normal volunteers. The MD patients had a significantly lower heart-rate response to the test than all the other groups. There is growing evidence that PD patients are more sensitive to the vasoconstrictive effects on basilar arterial blood flow caused by hyperventilation-induced hypocapnia than are comparison subjects. Our data suggest that there is an association between panic attacks and hyperreactivity to an acute hyperventilation challenge test.

Adult↗

PubMed2003

Differential sensitivity of the three ASI factors in predicting panic disorder patients' subjective and behavioral response to hyperventilation challenge.

The overall aim of the present investigation was to examine the association between the subscales of the ASI and emotional responding to voluntary hyperventilation challenge in a panic disorder population. Based on findings from [J. Abnorm. Psychol. 110 (2001) 372.], we predicted that the AS-Physical Concerns subscale would best predict the fear response to hyperventilation. We also examined the relative contribution of each of the three ASI subscales in predicting behavioral tolerance to hyperventilation. Participants (N = 192) meeting DSM-IV criteria for panic disorder with or without agoraphobia completed the Anxiety Sensitivity Index (ASI) and underwent a voluntary hyperventilation challenge. Consistent with prediction, the AS-Physical subscale significantly predicted subjective fear during the hyperventilation challenge (12% of variance accounted for); whereas only the AS-Social subscale accounted for significant variance (4%) in patients' behavioral tolerance to the hyperventilation challenge.

Adult↗

PubMedDate not supplied

Anxiety sensitivity and response to hyperventilation challenge: physiologic arousal, interoceptive acuity, and subjective distress.

Twenty-four female undergraduates, 12 high on anxiety sensitivity and 12 low on anxiety sensitivity, were subjected to a hyperventilation challenge task. Physiologic and subjective measures of arousal and distress were obtained before, during, and after the hyperventilation challenge. Alternating between the eight 15-second intervals of hyperventilation, participants engaged in a heartbeat-tracking task for eight 10-second intervals to assess interoceptive acuity. Although the hyperventilation challenge produced phase main effects for physiologic arousal, and group and time main effects for subjective distress, there were no significant interaction effects. Results revealed no significant interoceptive acuity differences across the low and high anxiety sensitivity groups. However, subjective ratings of physiological sensations during hyperventilation were significantly greater for the high anxiety sensitivity group. Hierarchical multiple regression analyses revealed that anxiety sensitivity accounted for additional variance beyond trait anxiety in explaining subjective ratings of arousal and distress in this nonclinical sample in response to a hyperventilation challenge.

Adult↗

PubMed2001

The relation between hyperventilation and pediatric syncope.

OBJECTIVE: The objective was to evaluate prospectively the role of hyperventilation in the development of neurocardiogenic syncope in children during head-upright tilt testing (HUTT). STUDY DESIGN: Tilt testing was performed in 34 children (mean age 10.6 years) with clinical suspicion of syncope. Respiratory rate and end-tidal carbon dioxide pressure were continuously monitored during HUTT. RESULTS: Tilt test was negative in 12 cases; 3 (25%) patients of this group exhibited hyperventilation any time during the test. In the remaining 22 cases the HUTT was positive, and 15 (68.2%) patients of this group exhibited hyperventilation at the onset of clinical symptoms and during syncope. In the positive HUTT group, the mean time elapsed from the tilt to the onset of syncope and the mean time elapsed from the onset of clinical symptoms to syncope (latency time) were significantly longer for patients who hyperventilated than for those who did not hyperventilate, (21.8 vs 11.5 minutes) (P =.002) and (78 vs 51 seconds) (P =.04), respectively. CONCLUSIONS: Spontaneous hyperventilation could play a relevant role in the pathophysiology of pediatric neurocardiogenic syncope, and it could point out a specific subtype of response to orthostatic stress in susceptible patients. We suggest the inclusion of capnography in tilt-test protocols could improve the assessment of syncope in children.

Adolescent↗

PubMed1992

Retraction brain ischaemia: mannitol plus nimodipine preserves both cerebral blood flow and evoked potentials during normoventilation and hyperventilation.

In our miniature swine model simulating operating room brain retraction, we investigated the effects of mannitol plus nimodipine on cerebral blood flow (CBF) and evoked potentials (EP) ipsilateral and contralateral to retraction, in comparison with either agent alone, during both normoventilation and hyperventilation. We here report results in 27 animals with intravenous mannitol (2 g kg-1 over 15 min) and/or nimodipine (1 microgram kg-1 min-1 constant infusion). Mannitol plus nimodipine was superior both to controls and to either mannitol alone or nimodipine alone in preserving EP amplitude ipsilateral to retraction during both normoventilation and hyperventilation. Mannitol alone was effective in normoventilation at preserving EP, while nimodipine alone was effective in hyperventilation. No significant asymmetries in CBF or EP were seen with mannitol plus nimodipine in either normoventilation or hyperventilation. By five minutes postretraction CBF had returned to preretraction values for all groups, and EP amplitude had returned also except for hyperventilated controls. In this model of brain retraction, mannitol plus nimodipine is superior to either agent alone in maintaining both CBF and EP when normoventilation and hyperventilation are employed. The results are discussed in terms of the possible mechanisms for the different and complementary effects of mannitol and nimodipine.

Animals↗

PubMed1993

Hyperventilation-echocardiography test for the diagnosis of myocardial ischaemia at rest.

The purpose of this study was to assess the feasibility, safety, specificity and sensitivity of the hyperventilation test performed under echocardiographic monitoring for the provocation of vasospastic ischaemia. Hyperventilation (approximately 30 cycles.min-1 for 5 min) was performed in 104 hospitalized patients, referred for pain typical of angina at rest, under 2-D echocardiographic and 12-lead electrocardiographic monitoring. All the tests were completed and no significant side effect was observed. In-hospital documentation of spontaneous myocardial ischaemia and/or ergonovine-induced ischaemia was achieved in 38 patients (group I). A positive hyperventilation-echocardiography test (occurrence of new transient asynergies or worsening of basal ones) was obtained in 32/38 patients. Among the group I patients, only 23 had diagnostic ST-T changes and only 16 experienced chest pain during the hyperventilation-echo test. Of the 66 patients without evidence of myocardial ischaemia at rest (negative ECG monitoring during hospitalization and/or negative ergonovine maleate-echo test)--Group II, none showed echocardiographic changes, seven presented ST-T changes and six complained of typical chest pain during the test. Thus, in relation to in-hospital documentation of myocardial ischaemia at rest, both spontaneous and/or ergonovine-induced episodes, the hyperventilation-echo test showed a specificity of 100%, a sensitivity of 84%, a positive predictive value of 100% and a negative predictive value of 92%. In conclusion, hyperventilation performed under echocardiographic monitoring is feasible and safe; it can be proposed as a screening test to unmask vasospastic myocardial ischaemia in patients with angina at rest, in whom documentation of spontaneous episodes is not available.

Adult↗

PubMed2002

The effects of sustained hyperventilation on regional cerebral blood volume in thiopental-anesthetized rats.

UNLABELLED: Sustained hyperventilation has a time-limited effect on cerebrovascular dynamics. We investigated whether this effect was similar among brain regions by measuring regional cerebral blood volume (CBV) with steady-state susceptibility contrast magnetic resonance imaging during 3 h of hyperventilation. Regional CBV was determined in nine thiopental-anesthetized, mechanically-ventilated rats every 30 min in the dorsoparietal neocortex, the corpus striatum, and the cerebellum. The corpus striatum was the only brain region showing a stable reduction in CBV during the hypocapnic episode (PaCO(2), 24 +/- 3 mm Hg). In contrast, neocortex and, to a lesser extent, cerebellum exhibited a progressive return toward normal values despite continued hypocapnia. No evidence of a rebound in CBV was found on return to normal ventilation in the three brain regions. We conclude that sustained hyperventilation can lead to an uneven change in the reduction of CBV, possibly because of differences of brain vessels in their sensitivity to extracellular pH. Our results in neocortex confirm the transient effect of sustained hyperventilation on cerebral hemodynamics. IMPLICATIONS: Sustained hyperventilation has a transient effect in decreasing cerebral blood volume (CBV). Using susceptibility contrast magnetic resonance imaging in thiopental-anesthetized rats, we found differences between brain regions in their transient CBV response to sustained hyperventilation.

Anesthesia↗

PubMed1975

Physiologic effects of hyperventilation and phlebotomy in baboons: systemic and cerebral oxygen extraction.

Eighteen anesthetized baboons were studied to determine the effects of passive hyperventilation and phlebotomy on oxygen transport. After 1 hour of hyperventilation a significant increase in the red cell affinity for oxygen occurred in vivo. This was not associated with any significant changes in cardiac output, oxygen consumption, or in lactic acid production. There was a 40% decrease in cerebral blood flow, a 10 mm Hg decrease in the pulmonary artery Po2 level, and a 17 mm Hg decrease in the jugular venous Po2 level. After 1 hour of hyperventilation, the plasma inorganic phosphorus level decreased significantly, the red cell ATP level decreased slightly, and the red cell 2. 3 DPG level increased significantly, indicating that inorganic phosphorus had been removed from the blood during hyperventilation. Passive hyperventilation was maintained, and the baboons were bled 32% of their red cell volume. The blood volume was partially restored with nonbuffered isotonic saline. One hour after the phlebotomy and volume restoration (2 hours of hyperventilation) there were no changes in oxygen consumption, cardiac output, cerebral blood flow, or blood lactate levels, but the pulmonary artery Po2 level was decreased by 15 mm Hg, and the jugular venous Po2 level was decreased by 20 mm Hg. Systemic oxygen consumption was not affected by the significant decrease in pulmonary artery Po2.

Animals↗

PubMed2002

Effect of hyperventilation on cerebral blood flow in traumatic head injury: clinical relevance and monitoring correlates.

OBJECTIVE: To investigate the effect of hyperventilation on cerebral blood flow in traumatic brain injury. DESIGN: A prospective interventional study. SETTING: A specialist neurocritical care unit. PATIENTS: Fourteen healthy volunteers and 33 patients within 7 days of closed head injury. INTERVENTIONS: All subjects underwent positron emission tomography imaging of cerebral blood flow. In patients, PaCO2 was reduced from 36 +/- 1 to 29 +/- 1 torr (4.8 +/- 0.1 to 3.9 +/- 0.1 kPa) and measurements repeated. Jugular venous saturation (SjvO2 ) and arteriovenous oxygen content differences (AVDO2 ) were monitored in 25 patients and values related to positron emission tomography variables. MEASUREMENTS AND MAIN RESULTS: The volumes of critically hypoperfused and hyperperfused brain (HypoBV and HyperBV, in milliliters) were calculated based on thresholds of 10 and 55 mL.100g(-1).min(-1), respectively. Whereas baseline HypoBV was significantly higher in patients ( p<.05), baseline HyperBV was similar to values in healthy volunteers. Hyperventilation resulted in increases in cerebral perfusion pressure (p <.0001) and reductions in intracranial pressure (p <.001), whereas SjvO2 (>50%) and AVDO2 (<9 mL/mL) did not exceed global ischemic thresholds. However, despite these beneficial effects, hyperventilation shifted the cerebral blood flow distribution curve toward the hypoperfused range, with a decrease in global cerebral blood flow (31 +/- 1 to 23 +/- 1 mL.100g(-1).min(-1); p<.0001) and an increase in HypoBV (22 [1-141] to 51 [2-428] mL; p<.0001). Hyperventilation-induced increases in HypoBV were apparently nonlinear, with a threshold value between 34 and 38 torr (4.5-5 kPa). CONCLUSIONS: Hyperventilation increases the volume of severely hypoperfused tissue within the injured brain, despite improvements in cerebral perfusion pressure and intracranial pressure. Significant hyperperfusion is uncommon, even at a time when conventional clinical management includes a role for modest hyperventilation. These reductions in regional cerebral perfusion are not associated with ischemia, as defined by global monitors of oxygenation, but may represent regions of potentially ischemic brain tissue.

Adolescent↗

PubMed2000

Cerebral oxygenation during hemorrhagic shock: perils of hyperventilation and the therapeutic potential of hypoventilation.

OBJECTIVES: Prophylactic hyperventilation of patients with head injuries worsens outcome, presumably by exacerbating tissue hypoxia. Oxygen tension in brain tissue (PbrO2) provides a direct measurement of cerebral metabolic substrate delivery and varies with changing end-tidal carbon dioxide tension (ETCO2) and mean arterial pressure. However, the effects of hyperventilation and hypoventilation on PbrO2 during hemorrhagic shock are not known. The aim of this study was to examine the effects of alteration in ventilation on PbrO2 in hemorrhaged swine. METHODS: Clark-type polarographic probes were inserted into the brain tissue of seven swine to measure PbrO2 directly. To examine the effects of alterations in ventilation on hemorrhage-induced hypotension, swine were hemorrhaged to 50% estimated blood volume and PbrO2 was monitored during hyperventilation (RR = 30) and hypoventilation (RR = 4). RESULTS: After the 50% hemorrhage, PbrO2 declined rapidly from 39.8 +/- 4.6 mm Hg to 11.4 +/- 2.2 mm Hg. Hyperventilation resulted in a further 56% mean decrease in PbrO2. Hypoventilation produced a 166% mean increase in PbrO2. These changes were significant (p = 0.001) for absolute and percentage differences from baseline. CONCLUSION: During hemorrhage, alterations in ventilation significantly changed PbrO2: hyperventilation increased brain-tissue hypoxia whereas hypoventilation alleviated it. This finding suggests that hyperventilation has deleterious effects on brain oxygenation in patients with hemorrhagic shock and those with head trauma. Conversely, hypoventilation with resultant hypercapnia may actually help resolve hemorrhagic shock-induced cerebral hypoxia.

Animals↗

PubMed2002

Hyperventilation in traumatic brain injury patients: inconsistency between consensus guidelines and clinical practice.

BACKGROUND: This study assessed patients with traumatic brain injury (TBI) to determine whether prehospital and community hospital providers employed hyperventilation therapy inconsistent with consensus recommendation against its routine use. METHODS: This prospective analysis of 37 intubated TBI patients without herniation, undergoing helicopter transport to an urban Level I center, entailed flight crews' noting of assisted ventilation rate (AVR) and end-tidal carbon dioxide (ETCO2) upon their arrival at trauma scenes or community hospitals. A priori-set levels of AVR and ETCO2 were used to assess frequency of guideline-inconsistent hyperventilation, and Fisher's exact and Kruskal-Wallis tests assessed association between guideline-inconsistent hyperventilation and manual vs. mechanical ventilation mode. RESULTS: Inappropriately high AVR and low ETCO2 were seen in 60% and 70% of patients, respectively. Manual ventilation was associated with guideline-inconsistent hyperventilation assessed by AVR (p = 0.038) and ETCO2 (p = 0.022). CONCLUSION: Prehospital and community hospital hyperventilation practices are not consistent with consensus recommendations for limitation of hyperventilation therapy.

Adolescent↗

PubMed2007

Hyperventilation following head injury: effect on ischemic burden and cerebral oxidative metabolism.

OBJECTIVE: To determine whether hyperventilation exacerbates cerebral ischemia and compromises oxygen metabolism (CMRO2) following closed head injury. DESIGN: A prospective interventional study. SETTING: A specialist neurocritical care unit. PATIENTS: Ten healthy volunteers and 30 patients within 10 days of closed head injury. INTERVENTIONS: Subjects underwent oxygen-15 positron emission tomography imaging of cerebral blood flow, cerebral blood volume, CMRO2, and oxygen extraction fraction. In patients, positron emission tomography studies, somatosensory evoked potentials, and jugular venous saturation (SjO2) measurements were obtained at Paco2 levels of 36+/-3 and 29+/-2 torr. MEASUREMENTS AND MAIN RESULTS: We estimated the volume of ischemic brain and examined the efficiency of coupling between oxygen delivery and utilization using the sd of the oxygen extraction fraction distribution. We correlated CMRO2 to cerebral electrophysiology and examined the effects of hyperventilation on the amplitude of the cortical somatosensory evoked potential response. Patients showed higher ischemic brain volume than controls (17+/-22 vs. 2+/-3 mL; p<or=.05), with worse matching of oxygen delivery to demand (p<.001). Hyperventilation consistently reduced cerebral blood flow (p<.001) and resulted in increases in oxygen extraction fraction and ischemic brain volume (17+/-22 vs. 88+/-66 mL; p<.0001), which were undetected by SjO2 monitoring. Mean CMRO2 was slightly increased following hyperventilation, but responses were extremely variable, with 28% of patients demonstrating a decrease in CMRO2 that exceeded 95% prediction intervals for zero change in one or more regions. CMRO2 correlated with cerebral electrophysiology, and cortical somatosensory evoked potential amplitudes were significantly increased by hyperventilation. CONCLUSIONS: The acute cerebral blood flow reduction and increase in CMRO2 secondary to hyperventilation represent physiologic challenges to the traumatized brain. These challenges exhaust physiologic reserves in a proportion of brain regions in many subjects and compromise oxidative metabolism. Such ischemia is underestimated by common bedside monitoring tools and may represent a significant mechanism of avoidable neuronal injury following head trauma.

Adolescent↗