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Objective: The objective of this study was to observe the effects of various clinical factors on the activation and appearance of epileptiform abnormalities (EAs) in routine electroencephalography (rEEG) by different provocation methods., Methods: This observational study involved a review of 136 patients presented for EEG recording due to various indications and their EEG showing EAs during various provocation methods., Results: Generalized spike-wave discharges (GSWDs) were the most frequent activated epileptiform pattern observed in, 81 (59.1%) recordings. This pattern was seen mainly in females 49 (P = 0.00), in patients with generalized seizures 48 (P = 0.00), in prolonged EEG records 3 (P = 0.03), and in both genetic 35 (P = 0.00) and lesional epilepsies 21 (P = 0.00). Focal sharp waves with bilateral synchrony (FSWSBS) were the most activated ictal pattern (P = 0.00). Ictal EAs after hyperventilation (HV) (P = 0.03) and intermittent photic stimulation (IPS) (P = 0.01) were mainly observed in patients with uncontrolled seizures (P = 0.00), and immune-mediated epilepsy (P = 0.02). Females sex (odds ratio [OR]: 1.33, confidence interval [CI]: 0.6-2.6; P = 0.25), bilateral tonic-clonic seizures (OR: 1.17, CI: 0.5-2.4; P = 0.31) and lesional epilepsies (OR: 1.45, CI: 0.7-2.9; P = 0.20) had risk of activation of EAs by provocation methods; however this risk was not statistically significant. While sleep deprivation (SD) (OR: 6.33, CI: 2.2-18.2; P = 0.00), nonrapid eye movement sleep (NREM) (OR: 2.41, CI: 1.0-5.4; P = 0.00), and prolong EEG recording (OR: 1.91, CI: 0.9-3.9; P = 0.04) were leading to a statistically significant risk of activation and appearances of EAs due to provocation., Conclusion: Different provocation methods can activate and augment the variety of EEG patterns of diverse clinical significance. Detection of activated ictal EAs is dependent on various patient factors, including seizure control, and the provocation method applied. Further larger prospective cohort studies with adequate sample sizes are warranted., (Copyright © 2024 Copyright: © 2024 Annals of African Medicine.)

Introduction: Chronic dyspnoea that remains unexplained after resting pulmonary function and cardiovascular testing is a common problem in clinical practice. The aim of this study was to determine the utility of cardiopulmonary exercise testing (CPET) in the diagnosis of unexplained dyspnoea., Methods: This retrospective single-centre study included consecutive patients with dyspnoea who had normal resting cardiopulmonary examinations (including chest X-ray, electrocardiography, pulmonary function tests [PFTs], and cardiac ultrasound). CPET was performed using a cycle ergometer with analysis of blood gases. The results were interpreted as being most likely due to one of the six pathophysiological mechanisms shown below. Consensus required agreement between at least three of the authors., Results: Of the 194 patients included (median age 53 years, sex-ratio (M:F) 0.83, mean body mass index 27.3±5.36kg/m 2 ), 32% of the test profiles were compatible with deconditioning, 20% with inappropriate hyperventilation (without gas exchange abnormalities), 18% with disorders of gas exchange, 13% with sub-maximal CPET, 9% with cardiovascular anomalies, and 8% with normal CPET. Of the patients with gas exchange abnormalities, the most common causes were bronchiectasis (6), emphysema (6), recent pneumonia (2), and diffuse interstitial pneumonitis (2). Ten of the patients with cardiovascular abnormalities had chronotropic insufficiencies, 5 had excessive tension responses, and 3 had disorders of rhythm or repolarisation., Conclusions: CPET may greatly facilitate the diagnosis of unexplained dyspnoea. More than 50% of the dyspnoea cases examined here were due to deconditioning or hyperventilation syndrome and would benefit from a simple pulmonary rehabilitation program., (Copyright © 2019 SPLF. Published by Elsevier Masson SAS. All rights reserved.)

Clinical and functional assessment of the vestibular nerve is fundamental in demonstrating vestibular signs and searching for associated otological and neurological signs. This may help orient topographic diagnosis toward central or peripheral syndrome and etiologic diagnosis.

The hyperventilation syndrome is a disease affecting children as well as adults. It predominates in female and may be debilitating. It is frequently associated with anxiety. The diagnosis, that is unfortunately often belated, is a diagnosis of exclusion and relies on the anamnesis, various non specific signs, on the Nijmegens score and on a hyperventilation provocation test. A specialized treatment allows, in most cases, a good control of ventilation and the disappearance of symptoms.

Hyperventilation syndrome is frequent in adults. There are only very few and very ancient publications in children. Diagnosis is sometimes difficult, because the symptoms often mimic those of organic diseases. Hyperventilation syndrome and organic diseases, especially asthma, often coincide. Intensive efforts should be made to diagnose hyperventilation syndrome at an early stage because this will prevent stigmatization and fixation of symptoms and disease, and also prevent children from undergoing unnecessary medical examinations and therapies. The authors review the literature about hyperventilation syndrome in children.

Purpose: The effectiveness of a voluntary hypoventilation technique was assessed in two rehabilitation centers in patients with hyperventilation syndrome., Methods: In the first center, 55 patients participated in an open program determining themselves the frequency and number of their consultations. In the second center 158 patients participated in a 10-week program that imposed five 60-min sessions., Results: In the first center, the patients participated in 4.8 30-min sessions over a 6.1 week period. Their cardinal complaints had declined by 48% (range 14% to 67% depending on the type of complaint) at the end of the program. In the second center the patients experienced an improvement in their comfort of life (less sleep disorders, fatigability, symptoms of severe hypocapnia), increasingly so with each new session, those having completed the program reaching a 62% improvement., Discussion: Due to the strong correlation observed between the clinical improvement (with a longer interval between acute episodes) and the quality of patient participation the beneficial effect of these voluntary hypoventilation rehabilitation programs cannot be attributed solely to the psychological effect of patient care.

The notion of respiratory behaviour is grounded, among other approaches, on studies of neuronal mechanisms of voluntary breathing, clinical data, conditioning experiments and respiratory sensations. The interactions between cortical centres of voluntary breathing and respiratory neurones in the brain stem are poorly understood: voluntary control operates through the direct action of corticomotor centres on respiratory motoneurones; however these cortical structures may directly act on bulbopontine centres, and therefore indirectly on respiratory motoneurones. Recordings in animals of brain stem neuronal activity, brain imaging in humans, and transcortical stimulation of the diaphragm in humans and in animal models support either one or the other hypothesis. The mutual independence of the automatic and the voluntary controls of breathing appears in patients with impaired bulbopontine automatism and operational voluntary control (Central Congenital Hypoventilation Syndrome), and in patients with the reverse impairment (locked-in syndrome). Finally, recent studies in humans and animals show that classical conditioning affects respiratory control and sensations.

During pregnancy, changes in the thoracic configuration subsequent to progressive increase in the abdominal volume have a moderate effect on respiratory function. The cephalic displacement of the diaphragm reduces the expiratory reserve volume and the residual volume. The main consequence is an increase in the closing volume of the airways due to the fact that the lower residual functional capacity occurs during the tidal volume. The increase in the closing volume decreases the ventilation of the adjacent alveolar areas which could explain an increased heterogenicity of the ventilation-perfusion ratios. Increased tidal volume is almost always observed during pregnancy and is the cause of hyperventilation and a major increase in alveolar ventilation which can reach 70% of the post partum value. This hyperventilation is probably due to increased chemosensitivity of the CO2 respiratory centers induced by the hyperprogesteronism observed during pregnancy.

Objective: To assess in children with a transcranial Doppler the effect on cerebral blood flow velocities of desflurane, whose cerebral vasodilator effects have been studied in animals and in adults with intracranial lesions., Study Design: Prospective clinical study., Patients: Ten healthy children, mean age: 3.4 yr, ASA physical class 1, undergoing minor urologic surgery, were included in this study., Method: Induction was obtained with atropine 10 micrograms.kg-1, fentanyl 3 micrograms.kg-1 and propofol 3 mg.kg-1. Endotracheal intubation was facilitated by atracurium 0.3 mg.kg-1. Mechanical ventilation, with a 50% air/oxygen mixture was adjusted to achieve an end-tidal CO2 (PETCO2) level of 38 +/- 2 mmHg. Monitoring included measurement of mean arterial blood pressure (MAP), heart rate, PETCO2, SpO2 and end-tidal desflurane concentrations (FETDes). Mean blood flow velocities (Vmean) were measured in the middle cerebral artery using a bi-directional 2 MHz TCD system (EME-TC 2000 S). A first TCD measurement followed intubation (T1). Thereafter, desflurane was adjusted to 1 MAC. Six other TCDs were recorded each minute until FETDes reached the inspired fraction (T2-T7). Thereafter, CO2 reactivity was assessed with a hypocapnia test, induced by hyperventilation. Measures were done at T8 (PETCO2: 33 +/- 1 mmHg), T9 (PETCO2: 29 +/- 1 mmHg), and T10 (initial PETCO2: 38 +/- 1 mmHg). All these measurements were made before starting surgery. Analysis of variance (ANOVA) was used to analyse the data (P < 0.05 was considered as significant)., Results: The Vmean and heart rate increased significantly with increasing concentrations of desflurane (Vmean from 68 +/- 27 to 106 +/- 30 cm.s-1 and heart rate from 109 +/- 17 to 136 +/- 15 b.min-1 between T1 and T7). During hypocapnia, Vmean decreased to 68 +/- 23 cm.s-1 at T9, and returned to normal values with PETCO2 at 38 mmHg at T10. SpO2 remained unchanged. Mean arterial pressure was stable from T1 to T7, but decreased significantly at T9 and T10., Conclusion: Desflurane elicits a dose-dependent increase in cerebral blood flow velocities and heart rate, but does not change mean arterial pressure, suggesting that its cerebrovascular action is independent of its systemic vascular action. CO2 reactivity is maintained at one MAC. The results in children are similar to those seen in adults.

Atypical clinical and/or EEG presentation may complicate the diagnosis of juvenile myoclonic epilepsy (JME). To assess the sensitivity of a standard EEG recording, we retrospectively evaluated the EEG performed at their first referral in 56 consecutive JME patients first seen between 1986 and 1992 (26 M, 30 F, aged 12-53, mean 24.4, with onset of JME at age 10-33, mean 14.3). The diagnosis had been made in none of these patients prior to referral, and was often confirmed only during follow-up. A 20-minute standard EEG was recorded, including hyperventilation (HV) and intermittent light stimulation (ILS). This EEG was normal in 15 cases (27%), showing aspecific or misleading changes in 11 cases (20%) and typical changes in only 30 cases (54%). The baseline EEG was normal in 25 (45%), atypical in 11 (20%), and typical for JME in only 20 (35%). HV and ILS yielded 37 and 39 normal, 10 and 7 aspecific and 9 and 10 specific findings, respectively. A single standard EEG without activation may thus be inconclusive or misleading for the diagnosis of JME in more than 50% of newly referred patients.

Hyperventilation syndrome is a frequent, but poorly understood clinical entity. The clinical expression is a rich combination of respiratory, cardiac and neurological signs which can simulate various organic diseases. Hypocapnia remains the primum movens for most authors although the relationship with psychiatric situations, in particular in anxious patients, is increasingly emphasized. The diagnosis is currently based on the elimination of diseases associated with hyperventilation, then on Nijmegen's questionnaire and is confirmed by the reproduction of the same clinical picture in a voluntary hyperventilation test. Respiratory function tests offer little information. Treatment is based on combining rehabilitation therapy focused on the diaphragm and on relaxation. Specialized care may be needed in psychiatric patients.

This study compares three non-pharmacological approaches to the chronic hyperventilation syndrome (CHS). Eighteen subjects were evaluated at the start of the study then one and 6 months after having received in a random fashion one of the following treatments: group I (teaching approach of one hour on the respiratory physiology of the CHS and on breathing techniques; n = 5); group II (same approach as in group I with breathing retraining of 8 sessions; n = 8); group III (same as group II with the addition of a modified Jacobson's progressive relaxation; n = 5). Whereas all three groups had a similar symptomatic score at the beginning of the study (although subjects of group III had in general higher scores and were symptomatic for a longer period), our results show that all subjects improved after 4 weeks, those in group II showing the greatest improvement (p < 0.05). This confirms the relevance of applied and repeated pedagogy in approaching subjects with the CHS.

135 sportsmen and women, 55 girls, 80 boys, aged from 7 to 30 years, from various sports, who complained of bad tolerance of exertion were examined with an exercise test and isocapnic spontaneous hyperventilation. 61, about 45%, during a hyperventilation test had a fall of V.E.M.S. greater than or equal to 20%, showing bronchial hyperreactivity. After three tests, this fall index was greater than or equal to 50%. 68% of the positive responses were seen in boys and 2/3 of the subjects with a positive response were atopics. No other argument could be maintained from the questioning or clinical history to predict the positive or negative character of the hyperventilation (age, sporting level, symptoms, previous asthma or asthmatic, allergy). H.S.V.I. of the chests of a sporting population that complains of exertion intolerance, therefore allows verification of an H.R.B. assessment of its severity and to follow evolution after treatment.

Despite current discussions promoting physical and sports activities in asthmatics, no studies have yet been done on the possible pathophysiological justifications for rehabilitation by sports programs. Consequently asthmatics are retrained in an empirical fashion and the assessment of these programs is subjective. The aim of this article is thus to review the different studies concerning the adjustment of asthmatics to muscular exercise and to deduce from these what could or should be the pathophysiological objectives of reconditioning protocols. The principal ideas which emerge from this study derive from three fundamental facts: 1) the training of asthmatics should be based on an individual approach since clinical severity leads to very unequal adaptations during muscular exercise; 2) it is advisable to strive against the declining physical fitness of the asthmatics, which is responsible for the accelerated functional deterioration, disturbances of psychomotor development and an increased risk of exercise-induce asthma; 3) the decrease of excessive exercise hyperventilation is, from the evidence, the greatest priority among the pathophysiological objectives, because hyperventilation is a principal cause implicated in the disturbance of cardiovascular adjustments to effort by heart-lung interaction.

At present, the administration of bicarbonate for metabolic acidosis has become controversial with regard to the indications and the modalities of treatment. Scientific evidence of the therapeutic value of bicarbonate is still lacking. In the opposite, there is a strong evidence of its adverse effects, such a paradoxical acidosis, sodium load and over all a worsening of haemodynamic status. Other therapeutic measures are limited. They include the administration of Carbicarb which does not increase the CO2 content, haemodialysis with bicarbonate and/or hyperventilation. As for every therapeutic action, the treatment must rely on an interpretation of the pathophysiological mechanism, resulting in the definition of therapeutic goals. The amendment of acidosis is not always a therapeutic priority. In ketoacidosis for instance, the depth of acidosis is mainly related to the degree of dehydration, the treatment of which results in a normalization of pH.

The malnutrition may exert deleterious effects on every constituent of the respiratory system: respiratory drive, respiratory muscles and pulmonary parenchyma. The occurrence of malnutrition in patients with chronic obstructive pulmonary disease (COPD) is associated with a poor prognosis. However the relationships between nutritional status and ventilatory function remain poorly defined. The malnutrition of COPD patients results mainly from a hypermetabolic state. In undernourished COPD patients, nutritional repletion has been reported to improve the performance of respiratory muscles. In COPD patients with acute respiratory failure, a hypercaloric nutrition may induce ventilatory complications that result mainly from an excessive CO2 production. The use of a lipid-enriched diet has been recently proposed in these patients to facilitate weaning from ventilatory support.

1 We have studied the unit activity of 88 pulmonary stretch receptors (RPI) in the vagus nerve of the cat by using the single fibre technique. 2 In spite of a 38% decrease in tidal volume, the discharge frequency of RPI is statistically unchanged during polypnea, However, RPI are recruited earlier, but their discharge overlaps expiration. 3 Individual influences of tidal volume, temperature, and FACO2 on RPI activities are tested. During polypnea, the excitatory influences of hyperthermia and hypocapnia act against the depressing action of tidal volume reduction: RPI are still active. 4 During polypnea, respiratory rhythm and tidal volume are unchanged after bivagotomy. RPI activity seems functionally insignificant. This result suggests that the thermally induced respiratory response is mediated by structures in the upper brain stem (probably the preoptic anterior hypothalamus) and is not dependent on the integrity of the vagus nerve.

Liver diseases are frequently associated with pulmonary complications and acid-base disorders, alterations which are frequently overlooked and thus undiagnosed in these patients. Among the respiratory abnormalities, mention should be made of the numerous functional and anatomic alterations responsible for arterial desaturation, the frequent chronic hyperventilation and the rare plexiform pulmonary hypertension. Acid-base disorders, especially respiratory alkalosis and metabolic alkalosis, are common. These conditions have a number of therapeutic implications since some of them play an important role in the pathophysiology of hepatic encephalopathy. The complications and their specific diagnostic features are reviewed and some therapeutic proposals are made.

The incidence of age on the frequency of post-hyperventilation apnea was studied in two randomly chosen distinct populations. The hyperpnea and ventilatory response were recorded during a standard E.E.G. tracing in 1 060 subjects by a thermistor and in 100 other subjects by pneumotachography and capnography. Post-hyperventilation frequency was determined for the two populations taken overall and then for subjects under and over 60 years of age. The results were compared with demographic data (sex, excess bodyweight coefficient, illness), and experimental conditions (alertness, recording technique). In the second population the mean ventilation per minute rate was calculated during a reference rest period and two successive hyperventilation tests. The frequency of post-hyperventilation apnea is higher before 60 years of age in the absence of variations in alertness and/or associated supramedullary lesions. Ventilatory response under 60 years of age is seen as a prolonged phase of hypoventilation. After 60 years of age, in the absence of apnea, ventilation returns immediately to its reference value, while in the presence of apnea the hypoventilatory phase observed is of brief duration and delayed. These results are discussed and compared to those in the published literature.

Adequate electromyographic method are available in order to record the electrical activity of the vertebral (oesophageal surface electrodes) and the right or left costal (concentric needle electrodes) parts of the diaphragm and in order to stabilize the EMG's base line (rejection of the electrical movement's artefacts by means of RC filters). The electromyographic patterns of the agonistic and antagonistic activity of the diaphragm in normal subjects have been clearly defined in different circumstances such as quiet ventilation and hyperventilation. Disturbances of the ventilatory diaphragmatic activity have been demonstrated by electromyography in different diseases: broncho-pneumopathies; supraspinal disorders, myopathies. In normal subjects, global motor responses of the diaphragm to the electrical stimulation of each phrenic nerve can be easily recorded with surface electrodes located in the oesophageal hiatus or placed over the lower intercostal spaces. The phrenic nerve conduction times was measured in 30 normal adults. The average value of this parameter was 7,5 +/- 0,53 msec for excitation on the right side and 8,2 +/- 0,71 on the left. The measurement of the phrenic nerve conduction time seems to provide a sensitive index of involvement of the nerve in diaphragmatic dyskinesias. Prolongation of conduction time was demonstrated in phrenic lesions of various aetiologies such as: peripheral polyneuropathies, traumatic sequelae, mediastinal tumors, phrenic neuritis or idiopathic diaphragmatic paresis. Electrical phrenic stimulation and prostigmin have permitted to establish the diagnosis of myasthenic bloc of the phrenodiaphragmatic transmission.

CO2 is a potent cerebral vasodilator which induces major changes in cerebral blood flow and volume. Acute hypocapnia decreases cerebral blood volume; thus the intracranial pressure can be reduced rapidly, thereby improving cerebral hemodynamics. Hypocapnia, rapidly achieved by controlled hyperventilation, is therefore a valid treatment in cerebral resuscitation, especially when associated with elevated intracranial pressure. However, the effect of hypocapnia is short and unusually does not exceed a few hours. Consequently the indications for prolonged hyperventilation are very limited, if they exist at all. Intracranial pressure and cerebral blood flow changes induced by PEEP are still controversial.

During exercises at constant workload, the hyperlactatemia threshold (continuous lactate production during the whole exercise) (48% VO2 max) and the hyperventilation threshold (57% VO2 max) are not simultaneous. This finding demonstrates that the hyperventilation threshold could not be regarded as an "anaerobic threshold".

Using a spectrometer for the study of exhaled gases and a monitor of transcutaneous oxygen pressure, our purpose has been to quantify our ideas about physiological apneas in the conscious voluntary adults. We compared the apneas, concerning the duration and the induced fall of peripheric oxygen pressure, after normoventilations in air and in oxygen, then after hyperventilations in air and in oxygen. These experiences confirm the tiny interest of previous normoventilation in oxygen compared with in air, the danger of hypoxemia by previous hyperventilation in air and the possibility of prolonged but safe apnea after hyperventilations in oxygen, that we can advocate in the induction of anaesthesia for some circumstances.

Gaseous carbon dioxide was used to produce experimental pulmonary embolism in anaesthetized rats, the vagal nerves of which were either intact or severed. 1. Within seconds following intravenous CO2 injection, pulmonary hypertension, moderate systemic hypotension and bradycardia occurred. After a short hyperventilation period, intact rats showed a brief and transient apnea. Vagotomy suppresses (1) apnea presumably by interruption of reflexes from J pulmonary receptors (Paintal, 1967) and (2) bradycardia by the same token or by suppression of a reflex from auricular origin (Thorén, 1976). 2. Following that initial phase, the events were totally dependent on the right ventricular ability to overcome the pulmonary vascular resistance. If it failed, left and right pressures fell and a secondary apnea followed systemic hypotension. Vagotomy had no effect at this stage. Only half of all animals showed these features. 3. Pulmonary hypertension and hyperventilation lasted twenty minutes at least in intact rats, while vagotomized ones showed an evolution toward acute pulmonary oedema and death. 4. With the same amount of CO2/kg, the dogs of Verstappen et al. (1977) showed only minimal cardio-vascular alterations. The mode of effective embolization in the two species was probably different, as a function of the respective circulation times. But this geometrical point of view is not the only one to be considered: in rats, the rise of pulmonary arterial blood pressure remains even when mechanical obstruction by bubbles has dissipated and a local prolonged vasospasm could be advocated. 5. Acute pulmonary oedema rapidly occurring in vagotomized rats seems to be related to the hyperinflation (very large tidal volume) as also seen in this species with other intensive respiratory drives.

After summarizing the phenomena of respiratory physiology involved in the hyperpnea test, the author studies the quantitative relation between the drop in PECO2 (pressure of CO2 in expired air) and changes in the EEG during hyperpnea. Normal subjects are divided into two groups of a hundred (6 to 19 1/2 years of age; 20 to 59 1/2 years of age). The PECO2 at rest is higher among the young subjects than among the adults, and its decline during hyperpnea is sharper. Thus, children show discrete respiratory acidosis in comparison with adults. The EEG of normal adults is practically unchanged during hyperpnea whereas, in the young group, moderate changes in the profile were observed in 45 out of 100 cases (classified empirically as normal). The PECO2 reaches a lower level in subjects showing EEG changes than in those showing none. All the reported differences are statistically significant (p less than 0.01). The probability of hyperpnea modifying the EEG profile becomes progressively less with age, and may be related to the reduced production of CO2 in older subjects. Epileptic subjects (primary generalized epilepsy) produce more CO2 than normal subjects during the hyperpnea test. The statistical data reported in the study show the importance of the size of the drop in ventilatory CO2 in the determination of EEG changes. The rest of hyperpnea in EEG can therefore be validly interpreted only if capnographic variations are measured. A standard quantitative hyperpnea test of this type should be devised, with specification of the hypocapnia level to be achieved.

The effects of isocapnic hyperventilation (A) and normoventilation (B) on PaCO2, PaO2 and A-aDO2 were compared in 102 patients undergoing elective surgery, randomized into two comparable groups A and B. Cases for thoracic, high abdominal and intracranial surgery were excluded, as well as patients with clinically evident pulmonary pathology. A volumetric ventilator was used in association with three different breathing systems (A: Bain system and circle system without CO2 absorption; B: circle system with CO2 absorption). The groups were comparable, except for percentage of overweight: 75% in group A and 56% in group B. Overweight was defined as weight above the mean ideal weight of 100%, and obesity as a weight above 120% the mean ideal weight. Blood gases were sampled 1) preoperatively, 2) 15 min and 3) 60 min after the beginning of mechanical ventilation, 4) postoperatively, 90 min after extubation, without supplemental oxygen. The preoperative mean PaO2 values were 79 +/- 11.4 mmHg (A) and 82.5 +/- 13.2 mmHg (B); the PaCO2 were 37.2 +/- 3.7 mmHg (A) and 37.2 +/- 3.8 mmHg (B). During surgery, PaO2 was distinctly higher (p less than 0.01) in group A than in group B (on average 15-20 mmHg higher), indicating the favourable effect of great tidal volumes on gas exchange. Correspondingly, the A-aDO2 was less increased in group A than in group B (p less than 0.01). At 15 min, 33% of the patients were hypocapnic (PaCO2 less than 35 mmHg): one case in group A and three in group B could be classed as severe hypocapnia (PaCO2 = 25-30 mmHg).(ABSTRACT TRUNCATED AT 250 WORDS)

In rats anesthetized by pentobarbital, hyperoxia, induced by inhalation of 100% O2 for 5 minutes, provokes transient bradycardia and long lasting systemic arterial hypertension. Pure oxygen initially depresses ventilation for 3 minutes. Blockade of alpha 1 adrenergic receptors does not suppress arterial hypertension, which appears to be due to a direct vasoconstriction.

In this article, Charles Vaille maintains that for the past two decades there has been a renewed outbreak of substance abuse with inhalants among youth throughout the world. He asserts that this phenomenon can no longer be considered as limited to a few isolated incidents. The volatile substances are common place, inexpensive, and unlike other drugs, legal; they are subject to neither international nor national controls. The specificity of addicts to inhalants renders prevention very difficult. Vaille discusses this point after describing the following two types of inhalant addiction: 1. Inhalation of gas fumes: two examples of youths inhaling fumes are cited followed by a description of ways in which inhaling or "sniffing" is performed. Vaille then presents the short-term effects of the "high", both psychological and physical. He then proceeds to disclose the harmful long-term effects concluding that addiction due to inhaling fumes seems to be developed throughout Europe. 2. Forced hyperventilation: a detailed description of how the "game" of forced hyperventilation is played is followed by a discussion of its effects on health. In discussing regulatory measures, Vaille maintains that a country's first effort at preventing substance abuse is to limit and modify the existence of such substances. After describing the various means attempted, he concludes that these effects will always result in an elusive prevention, due to the extraordinary number of inhalant substances as well as the enticing aspect of the "forbidden fruit". Regulatory measures offer an answer to those seeking a clear conscience rather than attempting to get at the root of the problem.(ABSTRACT TRUNCATED AT 250 WORDS)

Seven healthy male subjects underwent a treadmill incremental work test in control conditions and during an intravenous epinephrine infusion (10 micrograms/min). At all exercise intensities, epinephrine increased heart rate, ventilation, respiratory quotient and plasma lactate levels without significant changes in oxygen consumption. Under epinephrine infusion, the "anaerobic threshold", considered as the critical intensity at which ventilation began to increase non linearly with oxygen consumption, appeared at a lower intensity and for a higher plasma lactate level than in control conditions. We conclude that the hyperventilation threshold does not necessarily reflect a muscular hypoxia. It could be due to an effect of catecholamines on peripheral chemoreceptors, maybe by alpha-adrenergic vasoconstriction in the carotid bodies.

The appearance of an asthmatic crisis in the minutes following physical exercise is common in symptomatic asthma. Exercise induced asthma (EIA) is linked to hyperventilation; voluntary isocapnic hyperventilation is capable of triggering a crisis. It is well established at present that EIA and post-hyperventilation asthma (HIA) are triggered by a rise in heat and water loss by the airways, which is inherent in hyperventilation. The respective role of water loss and cooling the airways are uncertain but one tends to think at the present time that the primary stimulus is the variation in osmolality of the liquid lining the epithelium. However, a relationship between the quantity of energy dissipated in the airways and the severity of EIA or HIA exists, although it is less tight than was once thought. This is perhaps not surprising, as the intermediary mechanisms connecting the stimulus to the response of the airways are poorly understood. All in all physical exercise and isocapnic hyperventilation of dry air and possibly cold air are useful and equivalent non-specific bronchial provocation tests, if only the ventilation and physical properties of the inhaled air are the same. Hyperventilation lends itself better than exercise to establishing dose-effect curves linking bronchial response to minute ventilation. Recommendations concerning the interruption of drugs, the measurement of the response and the assessment of the results are the same as with other non specific bronchial provocation tests with irritant substances or pharmacological agents.

Nineteen normal subjects with no past history of hearing or balance impairment have undergone an electronystagmogram (E.N.G.), according to the usual technique in our laboratory. About one month or more after this first test, they underwent a second E.N.G. but this time with periods of hyperventilation distributed at certain precise moments of the test. Our analyses have not demonstrated that hyperventilation causes nystagmus or enhances in preexisting nystagmus in normal subjects, although the changes in the positional test were close to being significant.