Transient deoxyhemoglobin formation as a contrast for perfusion MRI studies in patients with brain tumors: a feasibility study.

Background: Transient hypoxia-induced deoxyhemoglobin (dOHb) has recently been shown to represent a comparable contrast to gadolinium-based contrast agents for generating resting perfusion measures in healthy subjects. Here, we investigate the feasibility of translating this non-invasive approach to patients with brain tumors. Methods: A computer-controlled gas blender was used to induce transient precise isocapnic lung hypoxia and thereby transient arterial dOHb during echo-planar-imaging acquisition in a cohort of patients with different types of brain tumors (n = 9). We calculated relative cerebral blood volume (rCBV), cerebral blood flow (rCBF), and mean transit time (MTT) using a standard model-based analysis. The transient hypoxia induced-dOHb MRI perfusion maps were compared to available clinical DSC-MRI. Results: Transient hypoxia induced-dOHb based maps of resting perfusion displayed perfusion patterns consistent with underlying tumor histology and showed high spatial coherence to gadolinium-based DSC MR perfusion maps. Conclusion: Non-invasive transient hypoxia induced-dOHb was well-tolerated in patients with different types of brain tumors, and the generated rCBV, rCBF and MTT maps appear in good agreement with perfusion maps generated with gadolinium-based DSC MR perfusion.

A dual-center validation of the PIRAMD scoring system for assessing the severity of ischemic Moyamoya disease.

Background: Prior Infarcts, Reactivity, and Angiography in Moyamoya Disease (PIRAMD) is a recently proposed imaging-based scoring system that incorporates the severity of disease and its impact on parenchymal hemodynamics in order to better support clinical management and evaluate response to intervention. In particular, PIRAMD may have merit in identifying symptomatic patients that may benefit most from revascularization. Our aim was to validate the PIRAMD scoring system. Methods: Patients with ischemic Moyamoya disease, who underwent catheter angiographic [modified Suzuki Score (mSS) and collateralization status], morphological MRI and a parenchymal hemodynamic evaluation with blood oxygenation-level dependent cerebrovascular reactivity (BOLD-CVR) at two transatlantic centers, were retrospectively included. The primary outcome was the presence of neurological symptoms. The diagnostic capacity of each PIRAMD feature alone was evaluated, as well as combined and the inter-institutional differences of each parameter were evaluated. Results: Seventy-two hemispheres of 38 patients were considered for analysis, of which 39 (54%) were classified as symptomatic. The presence of a prior infarct had the highest odds ratio [odds ratio (OR) =24; 95% CI: 6.7-87.2] for having neurological symptoms, followed by impaired CVR (OR =17; 95% CI: 5-62). No inter-institutional differences in the odds ratios or area under the curve (AUC) were found for any study parameter. The PIRAMD score had an AUC of 0.88 (95% CI: 0.80-0.96) with a similar AUC for the PIRAMD grading score. Conclusions: Our multicentric validation of the recently published PIRAMD scoring system was highly effective in rating the severity of ischemic Moyamoya disease with excellent inter-institutional agreement. Future studies should investigate the prognostic value of this novel imaging-based score in symptomatic patients with Moyamoya disease.

The Choroid Plexus as an Alternative Locus for the Identification of the Arterial Input Function for Calculating Cerebral Perfusion Metrics Using MRI.

BACKGROUND AND PURPOSE: MR imaging-based cerebral perfusion metrics can be obtained by tracing the passage of a bolus of contrast through the microvasculature of the brain parenchyma. Thus, the temporal signal pattern of the contrast agent is typically measured over a large artery such as the MCA to generate the arterial input function. The largest intracranial arteries in the brain may not always be suitable for selecting the arterial input function due to skull base susceptibility artifacts or reduced size from steno-occlusive disease. Therefore, a suitable alternative arterial input function window would be useful. The choroid plexus is a highly vascular tissue composed essentially of arterialized blood vessels and acellular stroma with low metabolic requirements relative to its blood flow and may be a suitable alternative to identify the arterial input function. MATERIALS AND METHODS: We studied 8 healthy participants and 7 patients with gliomas who were administered a bolus of gadolinium. We selected an arterial input function from both the left and right M1 segments of the MCA and both lateral ventricles of the choroid plexus for each participant. We compared the changes in the T2* signal and the calculated resting perfusion metrics using the arterial input functions selected from the MCA and choroid plexus. RESULTS: We found no systematic difference between resting perfusion metrics in GM and WM when calculated using an arterial input function from the MCA or choroid plexus in the same participant. CONCLUSIONS: The choroid plexus provides an alternative location from which an arterial input function may be sampled when a suitable measure over an MCA is not available.

The value of a shorter-delay arterial spin labeling protocol for detecting cerebrovascular impairment.

BACKGROUND: The aim of this study was to determine the relationship between blood oxygen level dependent (BOLD) cerebrovascular reactivity (CVR) and cerebral blood flow (CBF) obtained from arterial spin labeling (ASL) using different post labeling delays (PLD). METHODS: Forty-two patients with steno-occlusive diseases and impaired CVR were divided into two groups, one scanned with a 1.5-second (1.5-s) and the other with a 2.5-second (2.5-s) PLD ASL protocol. For all patients, a region of interest (ROI) was drawn around the CVR impairment. This affected ROI was then left-right flipped across the brain midline to obtain the control ROI. For both groups, the difference in grey matter CVR between affected and control ROI was first tested to confirm significance. The average grey matter CBF of affected and control ROIs were then compared. The same analysis method was used to compare affected and control hemispheres. RESULTS: In both groups of 1.5-s and 2.5-s PLD, CVR values in the affected ROI (-0.049±0.055 and -0.042±0.074%/mmHg, respectively) were significantly lower compared to that in the control ROI (0.152±0.054 and 0.152±0.053%/mmHg, respectively, P<0.0001). In the group with the 1.5-s PLD, CBF in the affected ROI (37.62±11.37 mL/100 g/min) was significantly lower compared to CBF in the control ROI (44.13±11.58 mL/100 g/min, P<0.05). However, in the group with the 2.5-s PLD, no significant differences could be seen between CBF in the affected ROI (40.50±14.82 mL/100 g/min) and CBF in the control ROI (39.68±12.49 mL/100 g/min, P=0.73). In the hemisphere-based analysis, CBF was significantly lower in the affected side than in the control side for the group with the 1.5-s PLD (P<0.05) when CVR was impaired (P<0.0001), but not for the group with the 2.5-s PLD (P=0.49). CONCLUSIONS: In conclusion, our study reveals and highlights the value of a shorter-PLD ASL protocol, which is able to reflect CVR impairment. At the same time, we offer a better understanding of the relationship between BOLD CVR and CBF obtained from ASL.

Effects of Hypercapnia on Myocardial Blood Flow in Healthy Human Subjects.

Elevation of the end-tidal partial pressure of CO2 (PETco2) increases cerebral and myocardial blood flow (MBF), suggesting that it may be a suitable alternative to pharmacologic stress or exercise for myocardial perfusion imaging. The purpose of this study was to document the pharmacodynamics of CO2 for MBF using prospective end-tidal targeting to precisely control arterial Pco2 and PET to measure the outcome variable, MBF. Methods: Ten healthy men underwent serial 82Rb PET/CT imaging. Imaging was performed at rest and during 6-min hypercapnic plateaus (baseline; PETco2 at 50, 55, and 60 mm Hg; repeat of PETco2 at 60 mm Hg; and repeat of baseline). MBF was measured using 82Rb injected 3 min after the beginning of hypercapnia and a 1-tissue-compartment model with flow-dependent extraction correction. Results were compared with those obtained during an adenosine stress test (140 µg/kg/min). Results: Baseline PETco2 was 38.9 ± 0.8 (mean ± SD) mm Hg (range, 35-43 mm Hg). All PETco2 targets were sustained, with SDs of less than 1.5 mm Hg. Heart rate, systolic blood pressure, rate × pressure product, and respiratory frequency increased with progressive hypercapnia. MBF increased significantly at each level of hypercapnia to 1.92-fold over baseline (0.86 ± 0.24 vs. 0.45 ± 0.08 mL/min/g; P = 0.002) at a PETco2 of 60 mm Hg. MBF after the administration of adenosine was significantly greater than that with the maximal hypercapnic stimulus (2.00 vs. 0.86 mL/min/g; P < 0.0001). Conclusion: To our knowledge, this study is the first to assess the response of MBF to different levels of hypercapnia in healthy humans with PET. MBF increased with increasing levels of hypercapnia; MBF at a PETco2 of 60 mm Hg was double that at baseline.

A Novel Stress-Diathesis Model to Predict Risk of Post-operative Delirium: Implications for Intra-operative Management.

Introduction: Risk assessment for post-operative delirium (POD) is poorly developed. Improved metrics could greatly facilitate peri-operative care as costs associated with POD are staggering. In this preliminary study, we develop a novel stress-diathesis model based on comprehensive pre-operative psychiatric and neuropsychological testing, a blood oxygenation level-dependent (BOLD) magnetic resonance imaging (MRI) carbon dioxide (CO2) stress test, and high fidelity measures of intra-operative parameters that may interact facilitating POD. Methods: The study was approved by the ethics board at the University of Manitoba and registered at clinicaltrials.gov as NCT02126215. Twelve patients were studied. Pre-operative psychiatric symptom measures and neuropsychological testing preceded MRI featuring a BOLD MRI CO2 stress test whereby BOLD scans were conducted while exposing participants to a rigorously controlled CO2 stimulus. During surgery the patient had hemodynamics and end-tidal gases downloaded at 0.5 hz. Post-operatively, the presence of POD and POD severity was comprehensively assessed using the Confusion Assessment Measure -Severity (CAM-S) scoring instrument on days 0 (surgery) through post-operative day 5, and patients were followed up at least 1 month post-operatively. Results: Six of 12 patients had no evidence of POD (non-POD). Three patients had POD and 3 had clinically significant confusional states (referred as subthreshold POD; ST-POD) (score ≥ 5/19 on the CAM-S). Average severity for delirium was 1.3 in the non-POD group, 3.2 in ST-POD, and 6.1 in POD (F-statistic = 15.4, p < 0.001). Depressive symptoms, and cognitive measures of semantic fluency and executive functioning/processing speed were significantly associated with POD. Second level analysis revealed an increased inverse BOLD responsiveness to CO2 pre-operatively in ST-POD and marked increase in the POD groups when compared to the non-POD group. An association was also noted for the patient population to manifest leucoaraiosis as assessed with advanced neuroimaging techniques. Results provide preliminary support for the interacting of diatheses (vulnerabilities) and intra-operative stressors on the POD phenotype. Conclusions: The stress-diathesis model has the potential to aid in risk assessment for POD. Based on these initial findings, we make some recommendations for intra-operative management for patients at risk of POD.

Arterial CO2 as a Potent Coronary Vasodilator: A Preclinical PET/MR Validation Study with Implications for Cardiac Stress Testing.

Myocardial blood flow (MBF) is the critical determinant of cardiac function. However, its response to increases in partial pressure of arterial CO2 (PaCO2), particularly with respect to adenosine, is not well characterized because of challenges in blood gas control and limited availability of validated approaches to ascertain MBF in vivo. Methods: By prospectively and independently controlling PaCO2 and combining it with 13N-ammonia PET measurements, we investigated whether a physiologically tolerable hypercapnic stimulus (∼25 mm Hg increase in PaCO2) can increase MBF to that observed with adenosine in 3 groups of canines: without coronary stenosis, subjected to non-flow-limiting coronary stenosis, and after preadministration of caffeine. The extent of effect on MBF due to hypercapnia was compared with adenosine. Results: In the absence of stenosis, mean MBF under hypercapnia was 2.1 ± 0.9 mL/min/g and adenosine was 2.2 ± 1.1 mL/min/g; these were significantly higher than at rest (0.9 ± 0.5 mL/min/g, P < 0.05) and were not different from each other (P = 0.30). Under left-anterior descending coronary stenosis, MBF increased in response to hypercapnia and adenosine (P < 0.05, all territories), but the effect was significantly lower than in the left-anterior descending coronary territory (with hypercapnia and adenosine; both P < 0.05). Mean perfusion defect volumes measured with adenosine and hypercapnia were significantly correlated (R = 0.85) and were not different (P = 0.12). After preadministration of caffeine, a known inhibitor of adenosine, resting MBF decreased; and hypercapnia increased MBF but not adenosine (P < 0.05). Conclusion: Arterial blood CO2 tension when increased by 25 mm Hg can induce MBF to the same level as a standard dose of adenosine. Prospectively targeted arterial CO2 has the capability to evolve as an alternative to current pharmacologic vasodilators used for cardiac stress testing.

Sequential gas delivery provides precise control of alveolar gas exchange.

Of the factors determining blood gases, only alveolar ventilation (VA) is amenable to manipulation. However, current physiology text books neither describe how breath-by-breath VA can be measured, nor how it can be precisely controlled in spontaneously breathing subjects. And such control must be effected independent of minute ventilation (VE) and the pattern of breathing. Control of VA requires the deliberate partition of inhaled gas between the alveoli and the anatomical deadspace. This distribution is accomplished by sequential gas delivery (SGD): each breath consists of a chosen volume of 'fresh' gas followed by previously exhaled gas. Control of VA through SGD is a simple, inexpensive, yet powerful tool with many applications. Here we describe how to implement SGD, how it precisely controls VA, and consequently how it controls arterial blood gases.

Assessment of myocardial reactivity to controlled hypercapnia with free-breathing T2-prepared cardiac blood oxygen level-dependent MR imaging.

PURPOSE: To examine whether controlled and tolerable levels of hypercapnia may be an alternative to adenosine, a routinely used coronary vasodilator, in healthy human subjects and animals. MATERIALS AND METHODS: Human studies were approved by the institutional review board and were HIPAA compliant. Eighteen subjects had end-tidal partial pressure of carbon dioxide (PetCO2) increased by 10 mm Hg, and myocardial perfusion was monitored with myocardial blood oxygen level-dependent (BOLD) magnetic resonance (MR) imaging. Animal studies were approved by the institutional animal care and use committee. Anesthetized canines with (n = 7) and without (n = 7) induced stenosis of the left anterior descending artery (LAD) underwent vasodilator challenges with hypercapnia and adenosine. LAD coronary blood flow velocity and free-breathing myocardial BOLD MR responses were measured at each intervention. Appropriate statistical tests were performed to evaluate measured quantitative changes in all parameters of interest in response to changes in partial pressure of carbon dioxide. RESULTS: Changes in myocardial BOLD MR signal were equivalent to reported changes with adenosine (11.2% ± 10.6 [hypercapnia, 10 mm Hg] vs 12% ± 12.3 [adenosine]; P = .75). In intact canines, there was a sigmoidal relationship between BOLD MR response and PetCO2 with most of the response occurring over a 10 mm Hg span. BOLD MR (17% ± 14 [hypercapnia] vs 14% ± 24 [adenosine]; P = .80) and coronary blood flow velocity (21% ± 16 [hypercapnia] vs 26% ± 27 [adenosine]; P > .99) responses were similar to that of adenosine infusion. BOLD MR signal changes in canines with LAD stenosis during hypercapnia and adenosine infusion were not different (1% ± 4 [hypercapnia] vs 6% ± 4 [adenosine]; P = .12). CONCLUSION: Free-breathing T2-prepared myocardial BOLD MR imaging showed that hypercapnia of 10 mm Hg may provide a cardiac hyperemic stimulus similar to adenosine.

Quantitative assessment of pulmonary aspiration: A novel porcine model.

OBJECTIVES: Pulmonary aspiration is a common cause of ventilator-associated pneumonia in the intensive care setting. Current bench and animal models of aspiration are based on the qualitative assessments. The purpose of the present study was to develop a porcine model for the real-time quantitative assessment of aspiration. METHODS: Five sus scrofa piglets were anaesthetized and underwent placement of a pH probe through the endotracheal tube so that the distal tip of the probe resided at the carina. The pH probe was sutured to the posterior tracheal wall via an open approach and the position of the probe tip was verified by flexible endoscopy. 10 mL of acidic solution (pH = 2.7) was delivered through a catheter attached to the outside of the endotracheal tube so that the solution remained between the endotracheal tube and trachea proximal to the inflated endotracheal tube cuff. The pH probe was connected to a pH metre, a multifunctional data acquisition device with an analogue output signal measuring the voltage generated, and a computer for analysis. Leakage of fluid past the endotracheal tube cuff (aspiration) was therefore continuously assessed quantitatively by detecting voltage changes over a period of time. RESULTS: The mean voltage of the tracheal mucosa at the beginning of the experiment (maximum voltage) was 916.6 mV ± 24.5 mV (range 891.0-945.7 mV). There was a slight drop in voltage at the end of the 2 h period to 840.8 ± 22.6 mV (range = 812.3-867.3 mV). After deflation of the endotracheal tube cuff, the mean voltage dropped to 497.3 mV ± 24.8 mV (range 435.7-567.1 mV) with a mean drop in voltage of 419.3 mV ± 32.6 mV (range 368.9-455.3 mV). CONCLUSIONS: This porcine model allows for the continuous quantitative assessment of aspiration over time. Such a model may be of value for the evaluation of techniques for reducing aspiration.

Impact of extracranial-intracranial bypass on cerebrovascular reactivity and clinical outcome in patients with symptomatic moyamoya vasculopathy.

BACKGROUND AND PURPOSE: The purpose of this study was to evaluate in symptomatic moyamoya patients the effect of surgical revascularization on impaired cerebrovascular reactivity (CVR) and its relationship to clinical outcome. METHODS: Brain revascularization was performed using a direct superficial temporal artery to middle cerebral artery bypass or indirect encephalo-dural-arterial synangiosis. CVR was measured pre- and 3 months postoperatively using blood oxygen level-dependent MRI during iso-oxic hypercapnic changes in end-tidal carbon dioxide. Outcomes were assessed by MRI, clinical examination, and modified Rankin Scale scores. RESULTS: Fifty-five hemispheres were revascularized in 39 patients (superficial temporal artery to middle cerebral artery in 47, encephalo-dural-arterial synangiosis in 8). Surgery reversed CVR impairment in 52 hemispheres (94.5%) and in 36 of 39 patients (92.3%; Fisher exact test, P<0.001), and this was predictive of a patent extracranial-intracranial bypass. New, clinically silent perioperative hemorrhages, cortical foci of ischemia, or new white matter T2 hyperintensities were detected after 11 surgeries (20%), but no new lesions arose after 3 postoperative months. One patient had a clinical perioperative stroke (1.8%). In clinical follow-up, 37 of 39 patients (95%) had stable or improved modified Rankin Scale scores and 2 patients (5.1%) worsened. No patients with patent bypasses or CVR improvements exhibited new clinical symptoms, but failure of CVR improvement corresponded to a poorer long-term outcome (Fisher exact test, P<0.001). CONCLUSIONS: Cerebral revascularization surgery is a safe and effective treatment for reversing preoperative CVR defects and may prevent recurrence of preoperative symptoms. Moreover, CVR measurements may be useful in long-term follow-up and for predicting bypass patency.

Surgical revascularization reverses cerebral cortical thinning in patients with severe cerebrovascular steno-occlusive disease.

BACKGROUND AND PURPOSE: Chronic deficiencies in regional blood flow lead to cerebral cortical thinning without evidence of gross tissue loss at the same time as potentially negatively impacting on neurological and cognitive performance. This is most pronounced in patients with severe occlusive cerebrovascular disease in whom affected brain areas exhibit "steal physiology," a paradoxical reduction of cerebral blood flow in response to a global vasodilatory stimulus intended to increase blood flow. We tested whether surgical brain revascularization that eliminates steal physiology can reverse cortical thinning. METHODS: We identified 29 patients from our database who had undergone brain revascularization with pre- and postoperative studies of cerebrovascular reactivity using blood oxygen(ation) level-dependent MRI and whose preoperative study exhibited steal physiology without MRI-evident structural abnormalities. Cortical thickness in regions corresponding to steal physiology, and where applicable corresponding areas in the normal hemisphere, were measured using Freesurfer software. RESULTS: At an average of 11 months after surgery, cortical thickness increased in every successfully revascularized hemisphere (n=30). Mean cortical thickness in the revascularized regions increased by 5.1% (from 2.40 ± 0.03 to 2.53 ± 0.03; P<0.0001). CONCLUSIONS: Successful regional revascularization and reversal of steal physiology is followed by restoration of cortical thickness.

Feasibility and precision of cerebral blood flow and cerebrovascular reactivity MRI measurements using a computer-controlled gas delivery system in an anesthetised juvenile animal model.

PURPOSE: To demonstrate the feasibility and repeatability of cerebrovascular reactivity (CVR) imaging using a controlled CO(2) challenge in mechanically ventilated juvenile pigs. MATERIALS AND METHODS: Precise end-tidal partial pressure CO(2) (PETCO(2)) control was achieved via a computer-controlled model-driven prospective end-tidal targeting (MPET) system integrated with mechanical ventilation using a custom-built secondary breathing circuit. Test-retest blood-oxygen level dependent (BOLD) CVR images were collected in nine juvenile pigs by quantifying the BOLD response to iso-oxic square-wave PETCO(2) changes. For comparison, test-retest baseline arterial spin labeling (ASL) cerebral blood flow (CBF) images were collected. Repeatability was quantified using the intra-class correlation coefficient (ICC) and coefficient of variation (CV). RESULTS: The repeatability of the PETCO(2) (CV < 2%) step changes resulted in BOLD CVR ICC > 0.94 and CV < 6% for cortical brain regions, which was similar to ASL CBF repeatability (ICC > 0.96 and CV < 4%). CONCLUSION: This study demonstrates the feasibility and precision of CVR imaging with an MPET CO(2) challenge in mechanically ventilated subjects using an animal model. Translation of this method into clinical imaging protocols may enable CVR imaging in young children with cerebrovascular disease who require general anesthesia.

Isocapnic hyperpnoea shortens postanesthetic care unit stay after isoflurane anesthesia.

BACKGROUND: We conducted a prospective controlled clinical trial of the effect of isocapnic hyperpnoea (IH) on the times-to-recovery milestones in the operating room (OR) and postanesthetic care unit (PACU) after 1.5 to 3 hours of isoflurane anesthesia. METHODS: Thirty ASA grade I-III patients undergoing elective gynecological surgery were randomized at the end of surgery to either IH or the conventional recovery (control). Six patients with duration of anesthesia of <90 minutes were excluded from the analysis. The anesthesia protocol included propofol, fentanyl, morphine, rocuronium, and isoflurane in air/O(2). Unpaired t tests and analyses of variance were used to test for differences in times-to-recovery indicators between the two groups. RESULTS: The durations of anesthesia in IH and control groups were 140.8 + or - 32.7 and 142 + or - 55.6 minutes, respectively (P = 0.99). The time to extubation was much shorter in the IH group than in the control group (6.6 + or - 1.6 (SD) vs. 13. 6 + or - 3.9 minutes, respectively; P < 0.01). The IH group also had shorter times to eye opening (5.8 + or - 1.3 vs. 13.7 + or - 4.5 minutes; P < 0.01), eligibility for leaving the OR (8.0 + or - 1.7 vs. 17.4 + or - 6.1 minutes; P < 0.01), and eligibility for PACU discharge (74.0 + or - 16.5 vs. 94.5 + or - 14.7 minutes; P < 0.01). There were no differences in other indicators of recovery. CONCLUSION: IH accelerates recovery after 1.5 to 3 hours of isoflurane anesthesia and shortens OR and PACU stay.

BOLD-MRI cerebrovascular reactivity findings in cocaine-induced cerebral vasculitis.

BACKGROUND: An 18-year-old woman presented to a regional stroke center with dysphasia and right hemiparesis 2 days after consuming alcohol and inhaling cannabis and -- for the first time -- cocaine. INVESTIGATIONS: Physical examination, blood tests for inflammatory markers, vasculitis and toxicology screen, echocardiography, electrocardiography, CT scanning, brain MRI, magnetic resonance angiography, magnetic resonance vessel wall imaging, catheter angiography, and correlation of blood oxygen level-dependent (BOLD)-MRI signal intensity with changes in end-tidal partial pressure of carbon dioxide. DIAGNOSIS: Cocaine-induced cerebral vasculitis. MANAGEMENT: No specific therapy was initiated. The patient's vital signs and neurological status were monitored during her admission. Follow-up medical imaging was performed after the patient's discharge from hospital.

Accelerated recovery from sevoflurane anesthesia with isocapnic hyperpnoea.

BACKGROUND: Isocapnic hyperpnoea (IH) reduces recovery time from isoflurane anesthesia in animals and humans. We studied the effect of IH on the emergence profile of sevoflurane-anesthetized patients by comparing postoperative recovery variables in patients administered IH (IH group) to those recovered in the customary fashion (control group). METHODS: We enrolled 30 ASA I-III patients undergoing elective gynecological surgery. Induction and maintenance of anesthesia were standardized with a protocol consisting of fentanyl, propofol, rocuronium, and sevoflurane in air/O2. Patients were randomly assigned to control (C) or IH groups at the end of the surgery. We recorded time intervals from discontinuing sevoflurane to recovery milestones. RESULTS: Time to tracheal extubation was much shorter in the IH group compared with group C (6.2 +/- 2.1 vs 12.3 +/- 3.8 min, respectively, P < 0.01). The IH group also had shorter times to initiation of spontaneous ventilation (4.2 +/- 1.7 vs 6.5 +/- 3.8 min, P = 0.047), eye opening (5.5 +/- 1.4 vs 13.3 +/- 4.4 min, P < 0.01), bispectral index value >75 (3.9 +/- 1.1 vs 8.8 +/- 3.7 min, P < 0.01), leaving operating room (7.7 +/- 2.0 vs 15.3 +/- 3.4 min, P < 0.01), and eligibility for postanesthetic care unit discharge (67.2 +/- 19.3 vs 90.6 +/- 20.0 min, P < 0.01). CONCLUSION: IH accelerates recovery from sevoflurane anesthesia and shortens operating room and postanesthetic care unit stay.

Vagal nerve activity contributes to improve the efficiency of pulmonary gas exchange in hypoxic humans.

The aim of this study was to test our hypothesis that both phasic cardiac vagal activity and tonic pulmonary vagal activity, estimated as respiratory sinus arrhythmia (RSA) and anatomical dead space volume, respectively, contribute to improve the efficiency of pulmonary gas exchange in humans. We examined the effect of blocking vagal nerve activity with atropine on pulmonary gas exchange. Ten healthy volunteers inhaled hypoxic gas with constant tidal volume and respiratory frequency through a respiratory circuit with a respiratory analyser. Arterial partial pressure of O(2) (P(aO(2))) and arterial oxygen saturation (S(pO(2))) were measured, and alveolar-to-arterial P(O(2)) difference (D(A-aO(2))) was calculated. Anatomical dead space (V(D,an)), alveolar dead space (V(D,alv)) and the ratio of physiological dead space to tidal volume (V(D,phys)/V(T)) were measured. Electrocardiogram was recorded, and the amplitude of R-R interval variability in the high-frequency component (RRIHF) was utilized as an index of RSA magnitude. These parameters of pulmonary function were measured before and after administration of atropine (0.02 mg kg(-1)). Decreased RRIHF (P < 0.01) was accompanied by decreases in P(aO(2)) and S(pO(2)) (P < 0.05 and P < 0.01, respectively) and an increase in D(A-aO(2)) (P < 0.05). Anatomical dead space, V(D,alv) and V(D,phys)/V(T) increased (P < 0.01, P < 0.05 and P < 0.01, respectively) after atropine administration. The blockade of the vagal nerve with atropine resulted in an increase in V(D,an) and V(D,alv) and a deterioration of pulmonary oxygenation, accompanied by attenuation of RSA. Our findings suggest that both phasic cardiac and tonic pulmonary vagal nerve activity contribute to improve the efficiency of pulmonary gas exchange in hypoxic conscious humans.

Efficiency of oxygen administration: sequential gas delivery versus "flow into a cone" methods.

OBJECTIVE: Fio2 values of a new oxygen mask that exploits efficiencies afforded by sequential gas delivery (SGD) were compared to those of a nonrebreathing mask (NRM) and a Venturi oxygen mask. DESIGN: Prospective, single-blinded, randomized study. SETTING: Laboratory study. SUBJECTS: Eight healthy male volunteers. INTERVENTIONS: Volunteers breathed through each of the masks at various minute ventilations (VE). Oxygen flows were 2, 4, and 8 L/min to the SGD mask but only 8 L/min to the other masks. MEASUREMENTS AND MAIN RESULTS: Net FIO2 was calculated from end-tidal fractional concentrations of oxygen and CO2 with the alveolar gas equation. Only the SGD mask at an oxygen flow of 8 L/min consistently provided both FIO2>0.95 (at resting VE) and higher FIO2 than the other masks at all VE. The SGD mask delivered FIO2 comparable to other masks at only a fraction of the oxygen flow and was characterized by a consistent relation between FIO2 and oxygen flow for a given VE. CONCLUSION: We conclude that SGD can be exploited to provide FIO2>0.95 with oxygen flows as low as 8 L/min, as well as accurate and efficient dosing of oxygen even in the presence of hyperpnea.

Calculation of O2 consumption during low-flow anesthesia from tidal gas concentrations, flowmeter, and minute ventilation.

We present the principles of a new method to calculate O2 consumption (V*O2) during low-flow anesthesia with a circle circuit when the source gas flows, end-tidal O2 concentrations and patient inspired minute ventilation are known. This method was tested in a model with simulated O2 uptake and CO2 production. The difference between calculated V*O2 and simulated V*O2 was 0.01 +/- 0.02 L/min. A similar approach can be used to calculate uptake of inhaled anesthetics. At present, with this method, the limiting factor in precision of measurement of V*O2 and uptake of anesthetic is the precision of measurement of gas flow and gas concentration (especially O2 concentration in end-tidal gas, FETO2) available in clinical anesthetic units.