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The label 'chronic fatigue syndrome' (CFS) has persisted for many years because of the lack of knowledge of the aetiological agents and the disease process. In view of more recent research and clinical experience that strongly point to widespread inflammation and multisystemic neuropathology, it is more appropriate and correct to use the term 'myalgic encephalomyelitis' (ME) because it indicates an underlying pathophysiology. It is also consistent with the neurological classification of ME in the World Health Organization's International Classification of Diseases (ICD G93.3). Consequently, an International Consensus Panel consisting of clinicians, researchers, teaching faculty and an independent patient advocate was formed with the purpose of developing criteria based on current knowledge. Thirteen countries and a wide range of specialties were represented. Collectively, members have approximately 400 years of both clinical and teaching experience, authored hundreds of peer-reviewed publications, diagnosed or treated approximately 50 000 patients with ME, and several members coauthored previous criteria. The expertise and experience of the panel members as well as PubMed and other medical sources were utilized in a progression of suggestions/drafts/reviews/revisions. The authors, free of any sponsoring organization, achieved 100% consensus through a Delphi-type process. The scope of this paper is limited to criteria of ME and their application. Accordingly, the criteria reflect the complex symptomatology. Operational notes enhance clarity and specificity by providing guidance in the expression and interpretation of symptoms. Clinical and research application guidelines promote optimal recognition of ME by primary physicians and other healthcare providers, improve the consistency of diagnoses in adult and paediatric patients internationally and facilitate clearer identification of patients for research studies.

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BACKGROUND: Evidence is growing that sleep problems in adolescents are significant impediments to learning and negatively affect behaviour, attainment of social competence and quality of life. The objectives of the study were to determine the level of sleepiness among students in high school, to identify factors to explain it, and to determine the association between sleepiness and performance in both academic and extracurricular activities METHODS: A cross-sectional survey of 2201 high school students in the Hamilton Wentworth District School Board and the Near North District School Board in Ontario was conducted in 1998/9. A similar survey was done three years later involving 1034 students in the Grand Erie District School Board in the same Province. The Epworth Sleepiness Scale (ESS) was used to measure sleepiness and we also assessed the reliability of this tool for this population. Descriptive analysis of the cohort and information on various measures of performance and demographic data were included. Regression analysis, using the generalised estimating equation (GEE), was utilized to investigate factors associated with risk of sleepiness (ESS>10). RESULTS: Seventy per cent of the students had less than 8.5 hours weeknight sleep. Bedtime habits such as a consistent bedtime routine, staying up late or drinking caffeinated beverages before bed were statistically significantly associated with ESS, as were weeknight sleep quantity and gender. As ESS increased there was an increase in the proportion of students who felt their grades had dropped because of sleepiness, were late for school, were often extremely sleepy at school, and were involved in fewer extracurricular activities. These performance measures were statistically significantly associated with ESS. Twenty-three percent of the students felt their grades had dropped because of sleepiness. Most students (58-68%) reported that they were "really sleepy" between 8 and 10 A.M. CONCLUSION: Sleep deprivation and excessive daytime sleepiness were common in two samples of Ontario high school students and were associated with a decrease in academic achievement and extracurricular activity. There is a need to increase awareness of this problem in the education and health communities and to translate knowledge already available to strategies to address it.

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PURPOSE: To evaluate the efficacy of inhaled nitric oxide (iNO) on oxygenation, shunt, and pulmonary vascular resistance index (PVRI) in severely hypoxemic, ventilated patients. METHODS: In a two-period double-blind crossover design, 14 critically ill, hypoxemic, ventilated patients were randomized to receive iNO 10 ppm in 100% oxygen or no iNO in 100% oxygen for 30 min followed by a 30-min washout period and then crossed over to the other intervention. Responders to iNO then received iNO, which was increased from 5 ppm to 25 ppm in 5 ppm increments. Severity of illness scores and cardiorespiratory variables were measured. RESULTS: Nitric oxide decreased shunt (P=0.002) and PVRI (P=0.033) and increased oxygenation (P=0.011) although the latter two were not statistically significant after adjustment for multiple comparisons. Treatment by period interactions were observed. CONCLUSION: Our findings suggest that iNO improves oxygenation to a clinically significant extent in critically ill patients who are severely hypoxemic.

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PURPOSE: Continuous lateral rotational therapy (CLRT) <40 degrees is a method of altering the position of the ventilated patient to help clear secretions from the lung. CLRT has not been shown to reduce the incidence of atelectasis or pneumonia but potentially offers a way to maximize positional drainage in these patients without producing adverse effects. Treatment intervention, bracketed by two (nonrotational) control periods. The purpose of this study was to determine if CLRT alters mucus transport in critically ill, intubated patients in the intensive care unit of a teaching hospital. MATERIALS AND METHODS: Thirteen critically ill, but stable, mechanically ventilated patients, mean age 74 years, were enrolled. They were placed supine on a Biodyne bed (KCI, San Antonio, Texas) and pressures in the cushions adjusted to patient's weight. A radiolabeled aerosol was delivered by bagging for 2 to 3 minutes and repeated measurements of lung radioactivity were obtained by imaging of the thorax over the following 3 hours. A 90-minute period of rotation of the bed, 30 degrees to either side was preceded and followed by two 45-minute control periods during which the patient remained supine and stationary on the bed. Coughs and suctions were recorded and blood gases obtained pre and post study. RESULTS: (1) The mucous clearance was slower than that reported in normal subjects and in ambulatory patients with COPD; (2) there was a slight, but not significant, increase in clearance during CLRT; (3) clearance reverted to pre-oscillation levels following therapy. Lack of significant effect may be attributed to too shallow an angle for rotation or too short an intervention period. CONCLUSION: Positional drainage effected by short duration CLRT did not appear to stimulate significant mucous removal from the lung in critically ill patients but also did not cause any adverse effects.

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To determine whether nocturnal periodic breathing (PB) at altitude is due primarily to unstable control of ventilation or the inability to maintain stable sleep states, we performed visual and computer analyses of the electroencephalographic and respiratory records of healthy volunteers at simulated altitudes of 4572, 6100 and 7620 m. Transient arousals were associated with < 52% of the apneas identified; thus, the PB cycle was not always associated with transient arousal. Following the termination of oxygen breathing, the reinitiation of PB was not dependent on the occurrence of arousal as the primary event. The transition from apnea to breathing preceded the appearance of arousal by approximately 1 to 4 sec. Ventilatory drive in the breaths immediately following arousal was significantly larger than corresponding control breaths, matched for SaO2. Our findings suggest that altitude-induced PB is unlikely to result from primary fluctuations in state. Arousals promote the development of PB with apnea and help to sustain these episodes, but are not necessary for their initiation.

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Frequent sleep disturbances and desaturation during sleep are common at high altitude, but few data are available from the highest altitudes at which humans are known to sleep. Because sleep fragmentation at low altitude may impair mental function and oxygen deprivation produces lasting central nervous system abnormalities, a better understanding of the severity of sleep disturbances and oxygen desaturation at extreme altitudes is important. The purpose of this study was to determine the severity of sleep disturbance and the extent of arterial oxygen desaturation at extreme simulated altitude. Out of eight healthy male subject volunteers who started, five aged 27.2 +/- 1.5 yr completed the study during 6 weeks of progressive hypobaric hypoxia in a decompression chamber. The men were studied at barometric pressures of 760, 429, 347, 282 mm Hg and following return to 760 mm Hg. All demonstrated frequent nighttime awakenings (37.2 awakenings per subject per night at 282 mm Hg, decreasing significantly to 14.8 on return to sea level, p less than 0.05). Total sleep time decreased from 337 +/- 30 min at 760 mm Hg to 167 +/- 44 min at 282 mm Hg (p less than 0.01). Rapid eye movement (REM) sleep decreased from 17.9% +/- 6.0% of sleep time at sea level to 4.0% +/- 3.3% at 282 mm Hg (p less than 0.01). Sleep continuity as reflected by brief arousals increased from 22 +/- 6 arousals per hour of sleep at sea level to 161 +/- 66 arousals per hour at 282 mm Hg (p less than 0.01). All subjects showed arterial oxygen desaturation proportional to the altitude. The average oxygen saturation (SaO2) was 79% +/- 3% at 429 mm Hg, 66% +/- 6% at 347 mm Hg, and 52% +/- 2% at 282 mm Hg. Sleep stage had only a minimal effect on SaO2 at any altitude. SaO2 was negatively correlated with brief sleep arousals, r = -0.72, p less than 0.01. All subjects demonstrated periodic breathing with apneas throughout much of the night at 347 and 282 mm Hg. These data indicate that sleep quality progressively worsens as SaO2 decreases despite lack of progressive changes in sleep stages at altitude. This study extends previous information on the severity of desaturation during sleep, and suggests that improvements in oxygenation might prove beneficial in restoring consolidated sleep, possibly even improving daytime performance.

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To obtain data on oxygen use among hospital inpatients criteria for instituting, monitoring, and stopping oxygen therapy were formulated. The records of 90 consecutive patients who had been started on oxygen therapy outside the critical care areas of a university hospital were then examined. By the criteria, 79% of patients were deemed to have required oxygen therapy, 14.5% had been adequately monitored, and only 12% had had therapy terminated on the basis of appropriate physiological measurements. Prospective studies are required to validate monitoring recommendations and establish their cost-benefit ratio in terms of patient comfort and health-care costs.

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This study was performed to determine the roles of increased intrathoracic blood volume and increased vagal tone in the changes in lung volume and nitrogen washout produced by saline infusion. In the first study, measurements of TLC, VC, FRC, ERV, and slope of phase III nitrogen washout (delta N2) were made on 8 subjects before, during, and after inflation of the leg compartments of medical anti-shock trousers (MAST). In the second study, 13 volunteers were infused intravenously with warm saline (30 ml/kg) for 30 min. Repeat measurements were made approximately 20 and 40 min after infusion. Each subject then received intravenously 0.03 mg/kg atropine, and measurements were repeated. In 7 of these subjects, a third study was performed in which the atropine was injected before saline infusion. Inflation of the MAST (see figures 5 and 6) caused a 1.9% decrease in VC, 5.3% decrease in FRC, and no change in delta N2. Saline infusion caused decreases in TLC, VC, and FRC (4.0, 3.1, and 10.1%, respectively) and a 15.0% increase in delta N2. Atropine reversed the change in delta N2 after saline infusion and prevented these changes when given prior to saline. Atropine had no effect on lung volumes whether given before or after saline infusion. We speculate from our data that saline infusion has 2 effects on the lung. One is a simple displacement of air by increased intravascular volume producing the reduction in lung volumes. The second is an increase in small airways resistance that is mediated by vagal reflex and blocked with atropine.

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The study compares two popular forms of written tests; the multiple choice test (MCQ) and the Modified Essay Question (MEQ). Two factors were varied in the experiment: the format of the questions (multiple choice, directed free response, or open-ended free response) and the context of the questions (in a patient problem or in random sequence). Six problems were developed in each version, and administered to a total of 36 medical students at three educational levels using a Latin-square design. The results showed a significant effect of each factor in the design, amounting to a difference of 8.7% between MCQ and directed free response, 4.2% between directed and open-ended free response and 4.3% between problem and random context. However, the correlation of scores based on content across the formats approached unity after correction for attenuation. A process score, based on the style and presentation in the undirected format, correlated more strongly with the free-response questions. The results suggest that, although the MCQ and MEQ may assess different skills, there is a very strong relationship between content scores derived from the two formats. The free response formats may present the opportunity for assessment of other factors related to presentation if scoring procedures are modified. Finally, the effect of randomizing questions is a deterioration of performance when compared to placing questions in the problem context.

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We have studied the effect of long-term digoxin on exercise performance in 15 patients with pulmonary heart disease due to severe chronic airflow obstruction (FEV1/VC ratio 29 +/- 6%: mean +/- SD). Digoxin (0.25 mg/day) was given for 8 weeks in a randomized, double-blind crossover, placebo-controlled trial. All patients were ambulatory and had clinical features of right ventricular dysfunction but no clinical evidence of left ventricular dysfunction. Assessments included progressive and steady-state exercise, pulmonary function studies and evaluation of right and left ventricular function. In all patients the right ventricular ejection fraction was reduced; in 4 patients the left ventricular ejection fraction was also reduced. In patients whose left ventricular ejection fraction was initially abnormal, 8 weeks of digoxin increased left ventricular ejection fraction to normal. In spite of the improvement in resting ventricular function, exercise performance, the cardiopulmonary response to exercise, pulmonary function and general health status did not improve. We conclude that in patients with pulmonary heart disease: 1) digoxin improves ventricular function only if left ventricular function is reduced, and 2) despite the improvement in ventricular function digoxin does not improve pulmonary function, cardiopulmonary response to exercise or general feeling of well being.

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In a randomized, controlled trial, ten patients with pulmonary heart disease due to severe chronic airflow obstruction were stratified into two groups: group 1 had clinical features of congestive heart failure during respiratory failure and were regularly receiving diuretics; group 2 had no such clinical features and were not receiving diuretics. In group 1, when placebo was substituted for diuretics, pulmonary edema developed in three patients; exercise performance and ventricular function of the remaining two patients deteriorated. In group 2, there was no difference in exercise tolerance or ventricular function between placebo and diuretic therapy. The clinical deterioration in group 1 was related to abnormal left ventricular function. Thus, diuretics benefit only patients who have clinical features of congestive heart failure. In patients with isolated abnormal right ventricular function, diuretics may be harmful.

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The acute effects of intravenously administered hydralazine on pulmonary hemodynamics and ejection radionuclide angiography were evaluated in 9 patients with chronic airflow obstruction (forced expiratory volume in one second, 1.2 +/- 0.8 L, mean +/- SD), pulmonary hypertension (mean pulmonary artery pressure (PAP), 29 +/- 13 mmHg), and sleep hypoxemia (maximal sleep desaturation, 20 +/- 16%). The effect of hydralazine was measured during both normoxia and hypoxia and compared with the effect of hyperoxia. Hydralazine increased cardiac index from 3.7 +/- 0.2 to 4.5 +/- 0.8 L/min/m2 (mean +/- SE, p less than 0.05, n = 9), but there were no significant changes in PAP (29 +/- 4 to 32 +/- 4 mmHg), mean pulmonary vascular resistance index (PVRI) (390 +/- 80 to 360 +/- 80 dyn.s.cm.-5.m2), mean right ventricular stroke work index (12.7 +/- 2.7 to 15.0 +/- 2.2 g.m/m2), and mean pulmonary capillary wedge pressure (12 +/- 1 to 12 +/- 2 mmHg). Mean right ventricular ejection fraction and mean right ventricular end diastolic volume also were not changed after treatment with hydralazine. Hyperoxia was used to assess the reversibility of pulmonary hypertension and to compare this with hydralazine. Hyperoxia increased arterial oxygen saturation (SaO2) from 91 +/- 1 to 96 +/- 1% and decreased the cardiac index from 3.8 +/- 0.1 to 3.1 +/- 0.2 L/min/m2 (p less than 0.02, n = 6) but, as with hydralazine, there was no significant change in PAP (28 +/- 6 to 25 +/- 6 mmHg) and PVRI (350 +/- 120 to 360 +/- 80 dyn.s.cm-5).m2).(ABSTRACT TRUNCATED AT 250 WORDS)

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Almitrine, a peripheral chemoreceptor agonist, was given intravenously in a dose of 0.5 mg/kg/h for 2 h in a randomized double-blind manner with placebo, to 11 patients with severe chronic air-flow obstruction and hypoxemia (SaO2 less than 90%). There was no significant placebo effect. Maximal respiratory effect occurred at the end of the almitrine infusion with an increase in ventilation from 8.2 + 0.9 to 11.6 + 1.5 L/min (mean +/- SEM), and improvements in SaO2 from 83 +/- 3 to 90 +/- 2%, in PaO2 from 48 +/- 2 to 55 +/- 3 mmHg, and in PaCO2 from 54 + 3 to 47 +/- 4 mmHg. Venous admixture was reduced from 38 +/- 4% to 22 +/- 3%. In 4 patients, blood gas values substantially improved, but there was no change in total ventilation for ventilatory pattern. This study of acute effects showed that almitrine improved arterial PO2 and PCO2 in patients with chronic air-flow obstruction both by increasing ventilation and by improving ventilation-perfusion relationships.

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In this study we examined the effect of a 15% increase in extracellular fluid volume on lung density, lung volumes, nitrogen washout, chest radiographs and computerized tomographic (CT) scans of the thorax in 5 volunteers. The objective of the study was to determine the sensitivity of these techniques in detecting small changes in lung water. Lung density was measured by a gamma ray Compton scatter technique and with an Ohio nuclear delta 2020 CT scanner. We measured or derived functional residual capacity, residual volume (RV), vital capacity (VC), and total lung capacity by helium dilution. Single-breath nitrogen washout was used to measure closing volume and the slope of phase III nitrogen washout (delta N2). Chest radiographs were taken in the posteroanterior and lateral projections. With the CT scanner we obtained slices 1 cm thick through the bases of the lungs and at 6 and 12 cm up from the bases. All these measurements were made before and 20 to 90 min after the intravenous infusion of 30 ml/kg body weight of warm saline over a period of 20 min. The most striking findings were a 24% increase in delta N2, a 14% increase in RV, and a 4.5% decrease in VC. Chest radiographs and the CT scans showed an increase in the size of the azygos veins. There was no change in Compton scatter density or the CT numbers. These results suggest that (1) tests of small airway function, such as RV and delta N2, are more sensitive than radiographic techniques to small increases in lung water, (2) there is some protection of the lung to increases in extracellular fluid volume.

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Developments of the past decade have greatly improved the likelihood that patients can control their asthma. Inhaled medications are basic to a regimen that may include bronchodilators only, or bronchodilators along with cromoglycate and steroid to the extent required to achieve and maintain control. The regimen is modified for the individual and designed to control symptoms while avoiding an overdose of any one agent and overuse of inhaled bronchodilators (a sign of their lessening effectiveness). The regimen outlined emphasizes controlling asthma day to day and providing effective intervention early to prevent attacks from becoming severe.

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A pocket calculator program is described which facilitates rapid evaluation of pulmonary function at rest and during exercise. It embodies the Fick Principle applied to carbon dioxide; mixed venous carbon dioxide tension is measured by rebreathing, obviating the need for central venous or pulmonary artery catheterisation. The program is in two parts, Gas Phase and Blood Phase, which may be used separately. The variables calculated include tidal volume, CO2 production, oxygen consumption, respiratory quotient, alveolar ventilation and dead space: tidal volume ratio (Gas Phase); bicarbonate concentration, base excess, veno-arterial CO2 content difference, cardiac output, mixed venous oxygen saturation and pulmonary venous admixture (Blood Phase). Use of the program enables these variables to be calculated rapidly and accurately. Accuracy is improved by the application of equations which correct for alveolar-to-blood tension differences, effects of differing hemoglobin concentrations, arterial oxygen saturations and acid-base abnormalities; these calculations are otherwise very lengthy, time consuming and prone to error. The program allows simple noninvasive measurements to be applied to patients with a wide variety of metabolic, cardiac and pulmonary abnormalities in rest and exercise.

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