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Moderate hyperventilation during intravenous anesthesia increases net cerebral lactate efflux.
Grüne, F, Kazmaier, S, Sonntag, H, Stolker, RJ, Weyland, A
Anesthesiology. 2014;(2):335-42
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Abstract
BACKGROUND Hyperventilation is known to decrease cerebral blood flow (CBF) and to impair cerebral metabolism, but the threshold in patients undergoing intravenous anesthesia is unknown. The authors hypothesized that reduced CBF associated with moderate hyperventilation might impair cerebral aerobic metabolism in patients undergoing intravenous anesthesia. METHODS Thirty male patients scheduled for coronary surgery were included in a prospective, controlled crossover trial. Measurements were performed under fentanyl-midazolam anesthesia in a randomized sequence aiming at partial pressures of carbon dioxide of 30 and 50 mmHg. Endpoints were CBF, blood flow velocity in the middle cerebral artery, and cerebral metabolic rates for oxygen, glucose, and lactate. Global CBF was measured using a modified Kety-Schmidt technique with argon as inert gas tracer. CBF velocity of the middle cerebral artery was recorded by transcranial Doppler sonography. Data were presented as mean (SD). Two-sided paired t tests and one-way ANOVA for repeated measures were used for statistical analysis. RESULTS Moderate hyperventilation significantly decreased CBF by 60%, blood flow velocity by 41%, cerebral oxygen delivery by 58%, and partial pressure of oxygen of the jugular venous bulb by 45%. Cerebral metabolic rates for oxygen and glucose remained unchanged; however, net cerebral lactate efflux significantly increased from -0.38 (2.18) to -2.41(2.43) µmol min 100 g. CONCLUSIONS Moderate hyperventilation, when compared with moderate hypoventilation, in patients with cardiovascular disease undergoing intravenous anesthesia increased net cerebral lactate efflux and markedly reduced CBF and partial pressure of oxygen of the jugular venous bulb, suggesting partial impairment of cerebral aerobic metabolism at clinically relevant levels of hypocapnia.
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Preventing cerebral oedema in acute liver failure: the case for quadruple-H therapy.
Warrillow, SJ, Bellomo, R
Anaesthesia and intensive care. 2014;(1):78-88
Abstract
Severe cerebral oedema is a life-threatening complication of acute liver failure. Hyperammonaemia and cerebral hyperaemia are major contributing factors. A multimodal approach, which incorporates hyperventilation, haemodiafiltration, hypernatraemia and hypothermia (quadruple-H therapy), may prevent or attenuate severe cerebral oedema. This approach is readily administered by critical care clinicians and is likely to be more effective than the use of single therapies. Targeting of PaCO2 in the mild hyperventilation range, as seen in acute liver failure patients before intubation, aims to minimise hyperaemic cerebral oedema. Haemodiafiltration aims to achieve the rapid control of elevated blood ammonia concentrations by its removal and to reduce production via the lowering of core temperature. The administration of concentrated saline increases serum tonicity and further reduces cerebral swelling. In addition, the pathologically increased cerebral blood-flow is further attenuated by therapeutic hypothermia. The combination of all four treatments in a multimodal approach may be a safe and effective means of attenuating or treating the cerebral oedema of acute liver failure and preventing death from neurological complications.
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An examination of the relation between traumatic event exposure and panic-relevant biological challenge responding among adolescents.
Hawks, E, Blumenthal, H, Feldner, MT, Leen-Feldner, EW, Jones, R
Behavior therapy. 2011;(3):427-38
Abstract
The current study uniquely extended research that has linked traumatic event exposure to panic-spectrum problems among adolescents. It was hypothesized that among 127 adolescents (age range: 10 to 17 years; M = 14.63, SD = 2.24), those who endorsed a history of traumatic event exposure would evidence significantly greater anxious and fearful reactivity to a well-established 3-min voluntary hyperventilation procedure compared to nonexposed individuals. Results were consistent with hypotheses, suggesting traumatic event exposure is associated with anxious and fearful reactivity to abrupt increases in bodily arousal among adolescents. Moreover, consistent with hypotheses, anxiety sensitivity significantly mediated the relations between traumatic event exposure and both self-reported panic symptoms and panic symptoms elicited by the challenge. Future prospective research is now needed to better understand temporal relations between traumatic event exposure and indices of panic and related vulnerability.
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Effect of sodium cromoglycate on mast cell mediators during hyperpnea in athletes.
Kippelen, P, Larsson, J, Anderson, SD, Brannan, JD, Dahlén, B, Dahlén, SE
Medicine and science in sports and exercise. 2010;(10):1853-60
Abstract
INTRODUCTION The role of mast cells in the airway response to exercise and the benefit of sodium cromoglycate (SCG) in athletes are unclear. PURPOSE The purpose of this study was to clarify the role of mast cell mediators in the airway response to exercise in athletes and to investigate the effect of SCG. METHODS Eleven athletes with exercise-induced bronchoconstriction (EIB+) and 11 without (EIB-) performed a eucapnic voluntary hyperpnea (EVH) test (a surrogate for exercise) 10 min after inhalation of a placebo or 40 mg of the mast cell stabilizing agent sodium cromoglycate. The urinary concentrations of 9a,11β-PGF2 (a metabolite of PGD2 and a marker of mast cell activation) and leukotriene E4 (LTE4) were measured by enzyme immunoassay 60 min before and for 90 min after the challenge. RESULTS In the EIB+ group, the maximum fall in forced expiratory volume in 1 s (FEV1) of 20.3% ± 3% on placebo was reduced to 11.5% ± 1.9% after SCG (P = 0.003). There was an increase in the urinary excretion of 9α,11β-PGF2 on the placebo day after EVH in both groups (P < 0.05) that was abolished by SCG. In the EIB+ group, there was also an increase of urinary LTE4 on the placebo day that was abolished by SCG, whereas the urinary excretion of LTE4 was inconsistent in the EIB- group. CONCLUSIONS The results support mast cell activation with release of bronchoconstrictive mediators after hyperpnea in athletes with and without EIB and inhibition by SCG. The degree of airway responsiveness to the specific mediator released is likely to determine whether or not bronchoconstriction will occur after EVH.
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Is lactic acidosis a cause of exercise induced hyperventilation at the respiratory compensation point?
Meyer, T, Faude, O, Scharhag, J, Urhausen, A, Kindermann, W
British journal of sports medicine. 2004;(5):622-5
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Abstract
OBJECTIVES The respiratory compensation point (RCP) marks the onset of hyperventilation ("respiratory compensation") during incremental exercise. Its physiological meaning has not yet been definitely determined, but the most common explanation is a failure of the body's buffering mechanisms which leads to metabolic (lactic) acidosis. It was intended to test this experimentally. METHODS During a first ramp-like exercise test on a cycle ergometer, RCP (range: 2.51-3.73 l x min(-1) oxygen uptake) was determined from gas exchange measurements in five healthy subjects (age 26-42; body mass index (BMI) 20.7-23.9 kg x m(-2); Vo(2peak) 51.3-62.1 ml x min(-1) x kg(-1)). On the basis of simultaneous determinations of blood pH and base excess, the necessary amount of bicarbonate to completely buffer the metabolic acidosis was calculated. This quantity was administered intravenously in small doses during a second, otherwise identical, exercise test. RESULTS In each subject sufficient compensation for the acidosis, that is, a pH value constantly above 7.37, was attained during the second test. A delay but no disappearance of the hyperventilation was present in all participants when compared with the first test. RCP occurred on average at a significantly (p = 0.043) higher oxygen uptake (+0.15 l x min(-1)) compared with the first test. CONCLUSIONS For the first time it was directly demonstrated that exercise induced lactic acidosis is causally involved in the hyperventilation which starts at RCP. However, it does not represent the only additional stimulus of ventilation during intense exercise. Muscle afferents and other sensory inputs from exercising muscles are alternative triggering mechanisms.
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Effects of hydration and hyperventilation on cortical complexity.
Müller, V, Birbaumer, N, Preissl, H, Braun, C, Mayer-Kress, G, Lang, F
Experimental brain research. 2003;(3):341-55
Abstract
The effects of hydration and hyperventilation on cortical complexity were investigated in a sample of 19 healthy volunteers in a double-blind placebo design using magnetoencephalographic recordings. The subjects were asked to abstain from the intake of liquids 18 h before the study. Spontaneous magnetoencephalograms (MEG) were recorded before and after drinking 750 ml water (WAT group: nine subjects) or saline solution (SAL group: ten subjects) with eyes closed and open and during hyperventilation (HV) with eyes open. The MEG data were analysed using both linear (spectral power) and non-linear (pointwise dimension and largest Lyapunov exponent) algorithms. The prediction that intake of water, because of induced cell swelling, will lead to an increased synchronization and a decreased complexity of the spontaneous MEG during hyperventilation was confirmed. Hyperventilation following the drinking condition produced an increase in all power spectra with a stronger increase of delta and theta power after drinking of water. This synchronization of spontaneous MEG is accompanied by a general significant decrease of cortical complexity, especially after water drinking. Moreover, cortical complexity was inversely related to delta and theta power and partly also to alpha power. The SAL and WAT groups showed different relations between alpha power and dimensional complexity during HV: whereas in the SAL group the correlations between these measures became more negative during HV, they reversed in the WAT group to become positive. The synchronizing effect of hyperventilation, leading to a decrease of cortical complexity, is related in the SAL group to delta, theta and alpha power, whereas in the WAT group only delta and theta activity contribute to a reduction of cortical complexity.
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Effects of hyperventilation on fast goal-directed limb movements in spinocerebellar ataxia type 6.
Manto, MU
European journal of neurology. 2001;(5):401-6
Abstract
It has been shown previously that hyperventilation modifies the features of the nystagmus in cerebellar patients (Walker and Zee, 1999). It has been hypothesized that hyperventilation influences the oculomotor control through a metabolic effect on cerebellar calcium channels, which play a critical role in the firing behaviour of neuronal populations in the cerebellum. This hypothesis has been tested here by analysing fast goal-directed limb movements before and after hyperventilation in spinocerebellar ataxia type 6 (SCA-6), a disease associated with a polyglutamine expansion in the alpha 1-A voltage-dependent calcium channel. Cerebellar hypermetria associated with fast distal single-joint movements was found to be increased following hyperventilation in patients presenting SCA-6 but remained unchanged in patients with idiopathic late-onset cerebellar degeneration (ILOCA). This is a new provocative test to enhance distal dysmetria in SCA-6. The present results strengthen the hypothesis of Walker and Zee. It is suggested that hyperventilation enhances the defective calcium transfers in SCA-6, resulting in an impairment of the calcium influx in particular into Purkinje cells involved in the control of fast goal-directed voluntary movements.
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Diuretic effect of hypoxia, hypocapnia, and hyperpnea in humans: relation to hormones and O(2) chemosensitivity.
Hildebrandt, W, Ottenbacher, A, Schuster, M, Swenson, ER, Bärtsch, P
Journal of applied physiology (Bethesda, Md. : 1985). 2000;(2):599-610
Abstract
We studied the contributions of hypoxemia, hypocapnia, and hyperpnea to the acute hypoxic diuretic response (HDR) in humans and evaluated the role of peripheral O(2) chemosensitivity and renal hormones in HDR. Thirteen healthy male subjects (age 19-38 yr) were examined after sodium equilibration (intake: 120 mmol/day) during 90 min of normoxia (NO), poikilocapnic hypoxia (PH), and isocapnic hypoxia (IH) (days 1-3, random order, double blind), as well as normoxic voluntary hyperpnea (HP; day 4), matching ventilation during IH. O(2) saturation during PH and IH was kept equal to a mean level measured between 30 and 90 min of breathing 12% O(2) in a pretest. Urine flow during PH and IH (1.81 +/- 0.92 and 1.94 +/- 1.03 ml/min, respectively) but not during HP (1.64 +/- 0.96 ml/min) significantly exceeded that during NO (control, 1.38 +/- 0.71 ml/min). Urine flow increases vs. each test day's baseline were significant with PH, IH, and HP. Differences in glomerular filtration rate, fractional sodium clearance, urodilatin, systemic blood pressure, or leg venous compliance were excluded as factors of HDR. However, slight increases in plasma and urinary endothelin-1 and epinephrine with PH and IH could play a role. In conclusion, the early HDR in humans is mainly due to hypoxia and hypocapnia. It occurs without natriuresis and is unrelated to O(2) chemosensitivity (hypoxic ventilatory response).