过度换气对脑电压缩谱阵图的影响

目的：研究对过度换气（ＨＶ）对常规脑电图的压缩谱阵（ＣＳＡ）的影响。方法：对３０例正常人常规ＨＶ前、中、后各１ｍｉｎ的脑电图进行ＣＳＡ分析。结果：ＨＶ前枕区主频谱峰较额区为快，波幅较高。ＨＶ中谱阵主峰解体、增强、减弱或不变，整个主峰频率有左移倾向，年龄越小改变越明显。结论：ＣＳＡ能充分地实时显示常规ＨＶ前后脑电功率变化的特点，并有新的发现     

75例颞叶癫癎患者动态EEG与过度换气EEG癎样放电规律探讨

目的：了解睡眠EEG与过度换气EEG的痢样放电规律。方法：评估75例颞叶癫痫患者动态EEG与过度换气EEG的痫样放电特点。结果：过度换气EEG痫样放电检出率明显低于浅睡期EEG，差异具有极显著意义（P〈0．01）；但与清醒期和深睡期EEG痫样放电检出率比较差异无显著意义（P〉0．05）。结论：颞叶癫痫患者浅睡期EEG痫样放电率明显高于过度换气EEG，对颞叶癫痫患者进行睡眠EEG检测，有助于提高痫样放电的检出率。     

经颅多普勒监测下过度通气治疗重型颅脑损伤患者的临床研究

目的探讨经颅多普勒（TCD）监测下调整过度通气治疗策略对重症颅脑损伤（sTBI）患者的疗效。 方法将59例sTBI患者分为对照组（30例）和实验组（29例）,对照组采用过度通气治疗,实验组在对照组基础上,根据TCD监测的脑血管痉挛（CVS）程度调整通气治疗策略。监测两组患者治疗前后大脑中动脉（MCA）的平均血流速度（Vm）,并计算治疗前后的平均血流速度变化值（ΔVm）。同时,将两组sTBI患者分为无CVS组（Vm<120 cm/s）、轻度CVS组（120 ≤ Vm<140 cm/s）、中重度CVS组（Vm ≥ 140 cm/s）,对各亚组间的ΔVm进行比较。采用格拉斯哥结局量表（GOS）对两组患者治疗6个月后的疗效进行评估。 结果实验组患者ΔVm显著高于对照组患者[22.0（13.0,39.5）cm/s vs. 10.0（7.0,26.3）cm/s,H = 2.527,P = 0.012]。对照组和实验组不同CVS程度患者间ΔVm比较,差异有统计学意义（H = 20.276,P = 0.001）;实验组中,轻度CVS组及中重度CVS组均显著高于无CVS组[23.0（21.5,41.0）、40.0（22.5,52.0）、13.0（9.8,18.0）cm/s],且中重度CVS组更高（P均<0.05）;且对于中重度CVS患者,实验组的ΔVm明显较对照组增加[40.0（22.5,52.0）cm/s vs. 9.0（8.0,31.0）cm/s,P<0.05]。治疗6个月后实验组GOS评分整体优于对照组（u = 2.059,P = 0.045）。 结论根据TCD监测结果调整过度通气治疗策略有利于缓解CVS,改善sTBI患者的疗效。     

Seguridad en procedimientos dermatológicos: anafilaxia,reacción vasovagal e hiperventilación

This article, part of a the series on safety in dermatologic procedures, covers the diagnosis, prevention, management, and treatment of 3 situations or conditions. The first condition we address is anaphylaxis, an uncommon but severe and potentially fatal reaction that must be recognized quickly so that urgent management coordinated with an anesthesiologist can commence. The second is the vasovagal reaction, which is the most common complication in dermatologic surgery. This event, which occurs in 1 out of every 160 procedures, usually follows a benign course and resolves on its own. However, in patients susceptible to vasovagal reactions, syncope may lead to asystole and cardiac arrest. The third is acute hyperventilation syndrome, which is an anomalous anxiety-related increase in breathing rate beyond metabolic requirements. Brief practical recommendations for managing all 3 events are included.     

Influence of a twofold voluntary hyperventilation on visually evoked cortical potentials and human pupillogram

We studied the direct and aftereffects of twofold hyperventilation (HV) on pattern reversing VEPs and pupillograms (PGs) of 19 healthy volunteers. The VEP-N₈₀ and P₁₀₀ latencies increased during HV. Both peak times were maintained for a longer period, up to 20 minutes after HV-2 ended. In addition, the PG-latency time during HV and the PG-construction time during and after HV were increased. The results indicated a temporary delay of neural afferent transmission in the visual system during and after HV. A similar delay of the nervous transmission appeared in the efferent part of the system regulating the pupillary movements after HV ended. The observed changes of the VEP and PG parameters most probably resulted from the hypocapnia cased by HV and its effect on the brain vessels, although other explanations for the changes of the VEP- and PG-parameters may have been possible.     

Absence Seizure with Generalized Rhythmic Delta Activity

In seven children, 5-11 years old, who presented with spells of staring or unresponsiveness, hyperventilation reproduced clinical spells that were accompanied on the EEG by generalized, rhythmic, delta activity. The discharges were usually of abrupt onset, extremely high amplitude, recurrent, and prolonged. One spontaneous staring spell, not provoked by hyperventilation, was also accompanied by generalized rhythmic delta activity. All patients had improvement or complete control of their spells and abolition of the EEG changes with ethosuximide or valproate. Delta activity during hyperventilation in children may not always be benign and may be associated with clinical absence seizures.     

Hyperventilation or Hypoglycaemia?

Two women with insulin-treated diabetes who presented with hyperventilation in the setting of generalized anxiety disorder and panic disorder, respectively, are reported. The symptoms of hyperventilation and hypoglycaemia proved indistinguishable even after successful treatment with a behavioural approach including explanation, breathing retraining, and relaxation. With diabetic patients a cognitive strategy is complicated by conditioning to think in terms of diabetic control and an inability to safely reattribute symptoms to faulty breathing habit because of the risk of ignoring hypoglycaemia.     

Altered Responsiveness During Hyperventilation-Induced EEG Slowing: A Non-Epileptic Phenomenon in Normal Children

Summary: The relation between hyperventilation (HV)-induced high-amplitude rhythmical slowing (HIHARS) and altered responsiveness without generalized spike and wave activity has not been clearly defined. To test whether altered responsiveness is a nonspecific physiologic response rather than a symptom of generalized epilepsy, we assessed verbal recall ability and motor response testing in 12 healthy nonepileptic children (mean age 9.6 years). Both tasks were administered as a baseline before HV, during HV but before onset of EEG slowing, and during HIHARS. Verbal recall and motor responsiveness remained unchanged during baseline and HV before onset of slowing. During HIHARS, all children exhibited impaired verbal recall (p<0·005) and 8 of 12 failed to respond to repeated auditory clicks (p < 0·005). Our findings indicate that in a normal setting, responsiveness may be impaired during HV in healthy nonepileptic children.     

Pulmonary gas exchange does not worsen during repeat exercise in women

The purposes were to determine (1) if repeat exercise worsens pulmonary gas exchange in women, and, (2) if the level of pulmonary edema obtained in these same women is related to the gas exchange impairment during exercise. Fourteen women (27 +/- 4 yrs; maximal oxygen uptake = 3.12 +/- 0.42 L/min) with minimal arterial PO2 (PaO2) ranging from 76 to 104 mmHg with a maximal alveolar-arterial PO2 difference (AaDO2) ranging from 7 to 35 mmHg performed three bouts of near-maximal exercise on a cycle ergometer (236 +/- 27 W) for 5 min each with 10 min of rest between sets. Cardiorespiratory parameters and oxygenation were measured at rest, throughout exercise and recovery. Chest radiographs were obtained before and 30 min after the interval training session (see Respir Physiol Neurobiol, 153 (2006) 181-190). Repeat exercise did not affect pulmonary gas exchange between sets 1 and 3 (change in PaO2 = 3 +/- 2 mmHg; change in AaDO2 = 1 +/- 2 mmHg P > 0.05). Arterial PCO2 decreased by 4 +/- 2 mmHg (P < 0.05) between sets 1 and 2, which did not reduce further in set 3. The level of PaO2 or AaDO2 was not related to the change in edema score or the post-exercise edema score (P > 0.05). In conclusion, pulmonary gas exchange is not worsened in women during interval training despite the mild edema triggered by exercise.