Period Of Hyperventilation Research Articles

Subjective symptoms and cardiac reactivity to brief hyperventilation in individuals with high anxiety sensitivity

Cognitive models maintain that panic attacks may be initiated by fear resulting from the interpretation of somatic sensations as personally threatening or harmful. Similarly, several researchers have proposed that the enhanced response of panickers to biological challenge may result from the fear of induced anxiety sensations rather than from direct stimulation of aberrant biochemical systems. The present study examined the effects of both panic history and fear of anxiety sensations on subjective and cardiac responses to biological challenge. Eighty nonclinical subjects were chosen on the basis of level of anxiety sensitivity and history of previous panic attacks. High and low anxiety-sensitive panickers and nonpanickers (four groups of 20 subjects) were subjected to a 90 sec period of voluntary hyperventilation, during which heart rate was assessed. Regardless of panic history, total symptom scores did not differ between high and low anxiety-sensitive subjects at baseline or pre-hyperventilation, but did differ at post-hyperventilation. There were, however, no significant differences in post-hyperventilation measures of heart rate. The apparent mismatch of subjective and physiological responsivity to the challenge in high anxiety-sensitive individuals (i.e. more severe symptom self-reports in the absence of increased cardiac activation) provides support for the hypothesis that high anxiety sensitivity is associated with an enhanced tendency to panic in response to biological challenge.

Sleep in the harp seal (Pagophilus groenlandica). Comparison of sleep on land and in water.

Four young harp seals (aged three to five months) were implanted with electrodes for recording electrocorticograms (ECoG) of the two hemispheres, and electrocardiogram, electroculogram, and electromyogram of the neck muscles. In all the seals ECoG slow waves developed simultaneously in both hemispheres, irrespective of whether they slept on land, on the water surface or submerged. Slow-wave sleep (SWS) was present in animals on the water surface and submerged, while paradoxical sleep (PS) occurred only when the animals were submerged. Breathing in SWS could be both regular (pauses less than twenty seconds) and intermittent (pauses lasting up to three minutes alternating with hyperventilation periods). All the PS episodes occurred during single respiratory pauses and ended by waking while the seal ascended to the water surface to breathe. Flipper movements were sometimes observed in SWS, but never in PS. The ability of harp seals to cease respiration during sleep and to sleep under water could be an adaptation to living conditons in the freezing seas.

Sleep in the harp seal (Pagophilus groenlandica). Peculiarities of sleep in pups during the first month of their lives.

Two white-coated (ten day-old) and two grey-spotted (one month-old) pups of the harp seal were implanted with electrodes for recording the electrocorticograms of the two hemispheres, electrocardiogram, electrooculogram and electromyogram of the neck muscles. In all individuals ECoG slow waves always developed synchronously in both hemispheres. When white and grey pups were recorded on the snow, the amount of active wakefulness was, respectively, 21.1% (s.e. 11.8%) and 29.9% (s.e. 0.2%) of total recording time, quiet wakefulness = 27.1% (s.e. 4.4%) and 38.2% (s.e. 6.6%), drowsiness = 7.7% (s.e. 0.5%) and 2.07% (s.e. 0.9%), light slow-wave sleep (SWS) = 15.1% (s.e. 3.2%) and 13.0% (s.e. 2.4%), deep SWS = 21.2% (s.e. 2.4%) and 13.8% (s.e. 3.8%), paradoxical sleep (PS) = 8.0% (s.e. 1.4%) and 7.4% (s.e. 1.1%). PS always followed SWS and was fragmented. Respiration was very rare and irregular in PS and a considerable part of PS episodes occurred within a single respiratory pause. During SWS all pups displayed respiratory pauses of up to three minutes, alternating with hyperventilation periods. Heart rate was lowest in PS. Peculiarities of sleep and the pace of sleep pattern development during the first month in seals may be adaptive to the cold environment and ice field drifting in their habitat.

The energetic cost of agonistic behaviour in the velvet swimming crab, Necora (= Liocarcinus) puber (L.)

Abstract. Realistic predictions from game theory about how animals should behave in a variety of competitive situations require knowledge of the costs associated with alternative strategies. In this study, the energetic cost of agonistic behaviour in velvet swimming crabs was investigated. There was a linear relationship between the rate of oxygen consumption and the rate of beating of the ventilatory pumps (the scaphognathites) and there was no evidence of significant anaerobic energy production during agonistic interactions. Energy expenditure by the crabs should therefore have been closely related to their oxygen consumption and scaphognathite activity. An irregular pattern of scaphognathite activity was recorded during agonistic behaviour, incorporating periods of extreme hyperventilation as well as cessation of scaphognathite activity. Maximum scaphognathite rates were among the highest reported for a range of similar decapod crustaceans. During agonistic behaviour, the respiratory activity of the interactants was related both to the degree of escalation and to the duration of the interaction. Recovery was prolonged in some cases. The estimate of total energetic cost included respiratory activity during the recovery phase and was correlated with interaction content and duration for losers only. However, there was no significant difference between the estimates of energy expenditure of winners and losers. As injuries are rare, energy expenditure may account for a large proportion of the total cost of contest behaviour in this crab.

The effect of respiratory alkalosis on oxygen consumption in anesthetized patients

Study Objective: To investigate whether hyperventilation significantly altered oxygen consumption in anesthetized and paralyzed patients undergoing surgery. Design: Open crossover trial with 1 hour of hyperventilation preceded and followed by 1 hour of normoventilation. Setting: University medical center. Patients: Eight patients (five men and three women) undergoing lengthy orthopedic surgery with general anesthesia and muscle paralysis. Interventions: After baseline normoventilationfor 1 hour (Period 1), the anesthetized patients were hyperventilated to an arterial carbon dioxide tension (PaCO 2) of 20 to 25 mmHg for 1 hour (Period 2). Patients then experienced another hour of normoventilation (Period 5). Measurements and Main Results: Hemodynamic variables, electrocardiography, temperature, end-tidal partial pressure of CO 2 (P ETCO 2), oxygen consumption (VO 2), carbon dioxide production, and minute ventilation were continuously followed throughout the study, and arterial blood gases were drawn at the beginning and end of each study period. During the period of hyperventilation, pH was significantly higher and P. ETCO 2 and (PaCO 2) significantly lower compared with the periods of normoventilation. (VO 2), was significantly increased during hyperventilation compared with the periods of normoventilation. Hemodynamic variables and temperature were similar in the three study periods. Conclusions: In anesthetized paralyzed patients, there is an increase in whole-body (VO 2), with hypocapnic alkalosis.

Nasal flow-resistive responses to challenge with cold dry air.

Recent studies have suggested that the inhalation of cold air through the nose is associated with the subsequent release of mediators of immediate hypersensitivity. To determine if mucosal surface heat and water loss influence the nasal functional response to cold air, we measured nasal resistance by posterior rhinomanometry before and 1, 5, and 10 min after a 4-min period of isocapnic hyperventilation (30 l/min) through the nose in nine healthy subjects (5 males, 4 females; aged 25-39 yr) while they inhaled air at 0 degrees C. During the challenge period, the subjects breathed either in and out of the nose or in through the nose and out through the mouth. No changes in nasal resistance developed when subjects breathed exclusively through the nose; however, when subjects breathed in through the nose and out through the mouth, nasal resistance was increased 200% at 1 min (P less than 0.01) after the challenge and returned to baseline values by 10 min after cessation of the challenge. These data indicate that nasal functional responses to cold dry air are dependent on the pattern of the ventilatory challenge. If the heat given up from the nasal mucosa to the incoming air is not recovered during expiration (as is the case with inspiration through the nose and expiration through the mouth), nasal obstruction will occur. Hyperpnea of cold air, per se, does not influence nasal resistance.

Cardiovascular changes associated with obstructive sleep apnea syndrome

Five men free of lung or cardiovascular diseases and with severe obstructive sleep apnea participated in a study on the impact of sleep states on cardiovascular variables during sleep apneas. A total of 128 obstructive apneas [72 from stage 2 non-rapid-eye-movement (NREM) sleep and 56 from rapid-eye-movement (REM) sleep] were analyzed. Each apnea was comprised of an obstructive period (OP) followed by a hyperventilation period, which was normally associated with an arousal. Heart rate (HR), stroke volume (SV), cardiac output (CO) (determined with an electrical impedance system), radial artery blood pressures (BP), esophageal pressure nadir, and arterial O2 saturation during each OP and hyperventilation period were calculated for NREM and REM sleep. During stage 2 NREM sleep, the lowest HR always occurred during the first third of the OP, and the highest was always seen during the last third. In contrast, during REM sleep the lowest HR was always noted during the last third of the OP. There was an inverse correlation when the percentage of change in HR over the percentage of change in SV during an OP was considered. The HR and SV changes during NREM sleep allowed maintenance of a near-stable CO during OPs. During REM sleep, absence of a compensatory change in SV led to a significant drop in CO. Systolic, diastolic, and mean BP always increased during the studied OPs.(ABSTRACT TRUNCATED AT 250 WORDS)

Changes in the QT Interval During Obstructive Sleep Apnea

Abnormalities of ventricular repolarization are associated with life-threatening ventricular arrhythmias. The effects of obstructive sleep apnea on the QT interval were evaluated in 12 male patients with obstructive sleep apnea syndrome (OSAS) who had no evidence of underlying cardiac, pulmonary or central nervous system disease. Seventy episodes of OSAS during nonrapid eye movement (NREM) sleep were randomly selected for analysis of RR and QT intervals. Differences in the QT interval, corrected QT interval (QTc) and RR interval just before the onset of apnea, at the end of apnea and during the postapnea hyperventilation period were compared. As expected, the RR interval prolonged considerably during OSAS (1,499 +/- 128 msec) compared to quiet sleep (1,019 +/- 131 msec, p less than 0.002) and decreased during the postapnea hyperventilation period (969 +/- 152 msec, p less than 0.002). The QT interval was prolonged at the onset of apnea (482 +/- 34 msec) compared to the active awake state (421 +/- 10 msec, p less than 0.01). Further prolongation of the QT interval was observed during OSAS (528 +/- 64 msec, p less than 0.002). The QT interval shortened abruptly during the postapnea hyperventilation period (435 +/- 34 msec, p less than 0.002). The QTc was also prolonged during the onset of apnea (482 +/- 34 msec) and shortened significantly during apnea (435 +/- 34 msec, p less than 0.002) and during the postapnea hyperventilation period (423 +/- 39 msec). Significant variations of the RR interval, QT and QTc intervals were not observed during episodes of NREM sleep after initiation of effective therapy in six patients.(ABSTRACT TRUNCATED AT 250 WORDS)

Quantification of sleep disordered breathing by computerized analysis of oximetry, heart rate and snoring

Intermittent snoring and cyclic oscillations of heart rate and oxyhaemoglobin saturation (Sao2) are characteristic features of the obstructive sleep apnoea syndrome (OSAS). Thus, overnight recordings of laryngeal sounds and heart rate by a portable device (MESAM) and of Sao2 by oximetry are applicable to screen outpatients for the presence of OSAS. Computerized analysis for time intervals of constant heart rate and intervals between snoring sounds is used by MESAM to quantify respiratory disturbances during sleep. Rapid increases in Sao2 during the postapnoeic hyperventilation period together with the number of desaturations are used by a new software for quantitative analysis of oximetry. To elucidate reliability of results from automatically scored MESAM and oximetry recordings, we compared the four computer calculated respiratory disturbance indices from heart rate (RDIH), snoring (RDIS), resaturations (RDIR) and desaturations (RDID) with the apnoea plus hypopnoea index (AHI) from simultaneously performed polysomnography. The study population consisted of 53 snorers with an AHI of 19.0 +/- 2.6 (median +/- SEM; range 0.7-87.8). Whereas both RDI's from MESAM correlated rather weakly with the AHI from polysomnography (RDIH: r = 0.32, p less than 0.05; RDIS: r = 0.33, p less than 0.05), this correlation was much better for the RDI's from oximetry (RDIR: r = 0.951, RDID: r = 0.93; p much less than 0.0001). Accepting a plus/minus 30 percent difference from the AHI, the RDIR classified 77% of patients correctly, the RDID 62%, the RDIS 32% and the RDIH 23%. In conclusion, results from computerized analysis of oximetry for desaturations and rapid resaturations correlate more closely with polysomnography than those from automatic scoring of MESAM recordings.

Non-invasive pulmonary blood flow measurement by means of CO2 analysis of expiratory gases

Two different methods of CO2-derived non-invasive assessment of the pulmonary blood flow were evaluated. The principle of the formula, as proposed by Gedeon et al., is based on a rapid change in arterial CO2 content and subsequent changes in endtidal PCO2 and CO2 elimination. Both methods were compared to thermodilution cardiac output in 44 postoperative patients after CABG. The first method consisted of a short period of hyperventilation followed by hypoventilation. Comparison with the thermodilution cardiac output showed a low correlation coefficient: using a measured arterial--end-tidal PCO2 difference (E) r = 0.397 was found. Entering a fixed E of 0.53 kPa resulted in r = 0.454. These disappointing figures may be explained by procedural mistakes. The second method, based on partial rebreathing by means of adding an additional dead space of 220 ml for 30-45 s, correlated very well with the thermodilution findings. Correlation coefficients of r = 0.925 (measured E) and r = 0.925 (fixed E) were found. Considering the simplicity of the method, the additional dead space approach seems to be an easy and reliable way to determine pulmonary blood flow.

Magnesium Deficiency in the Cause of the Sudden Infant Death Syndrome: An Updated Hypothesis

This is a hypothesis that the sudden infant death syndrome (SIDS, crib death) results from a relative magnesium (Mg) deficiency in respect to calcium in a stressed, young infant. Multiparity in the very young, poor mother living under stressful urban conditions favors the development of maternal and fetal magnesium deficiency. The prematurely born infant has reduced magnesium stores and may have respiratory distress at birth, requiring diuretics and respiratory stimulants that provoke increased urinary loss of magnesium. The relative calcium excess in a stressed infant results in platelet aggregation chiefly in the pulmonary microvasculature with massive release of thromboxane A2 (TXA2), catecholamines and other mediators of shock. TXA2 causes apnea and sudden death by promoting constriction of pulmonary and coronary vessels, bronchoconstriction, and further platelet aggregation. These effects normally are counterbalanced by prostacyclin, PGI2, which is synthesized in the vascular endothelium. PGI2 production is curtailed by shock and by endothelial injury imposed by tobacco and cocaine smoke and polluted urban air. TXA2 is essentially unopposed. Death may be instantaneous or may follow a period of hyperventilation, resulting in well-expanded lungs. The infant's increased physical activity, increased permeability of blood vessels, relative thrombocytopenia, and a brief spike of hypertension from TXA2 and catecholamines released from platelets contribute to the development of intrathoracic petechiae. A coagulopathy develops, and blood remains fluid. Anaerobic metabolism and magnesium deficiency reduce ATP production. The exhausted infant dies. Death occurs between 2 and 4 months of age, when protection from magnesium, glucocorticoids, and PGI2 are reduced and when testosterone, which favors platelet aggregation, is increased in males. Biochemically proving magnesium deficiency is difficult in the infant postmortem. A prospective therapeutic trial of magnesium can be recommended.

Mechanism for increase in tracheobronchial blood flow induced by hyperventilation of dry air in dogs

To test whether the consistent increase in tracheal and bronchial blood flow observed in dogs during hyperventilation of dry air might be the result of release of mediators such as vasodilatory prostaglandins or neuropeptides, we studied two groups of anesthetized mechanically ventilated dogs. Group 1 (n = 6) was hyperventilated for four 30-min periods with 1) warm humid air (38-40 degrees C, 100% relative humidity), 2) warm dry air (38-40 degrees C, 0% relative humidity), 3) warm humid air, and 4) warm dry air. After period 2, a loading dose of indomethacin (4 mg/kg iv) was given over 15 min followed by a constant infusion (4 mg.kg-1.h-1). Group 2 (n = 10) was hyperventilated for four 15- to 20-min periods by use of the protocol described above. After period 3 (group 2a) or period 2 (group 2b), topical 4% lidocaine hydrochloride solution was instilled into the trachea and main stem bronchi. Five minutes before the end of each period of hyperventilation, cardiac output and vascular pressures were measured. To determine airway blood flow, differently labeled radioactive microspheres were injected into the left atrium. After the last measurements, dogs were killed and the lungs excised. Blood flow to the trachea, main stem bronchi, and parenchyma (group 1 only) was calculated. Results showed that hyperventilation of dry air produced a significant increase in blood flow to the trachea and bronchi (period 2). In group 1, this increase was attenuated (P less than 0.02) after administration of indomethacin.(ABSTRACT TRUNCATED AT 250 WORDS)

Respiratory responses after prolonged periods of voluntary hyperventilation in normal man

Respiratory responses after prolonged periods of voluntary hyperventilation in normal man

Airway blood flow response to eucapnic dry air hyperventilation in sheep.

Eucapnic hyperventilation, breathing dry air, produces a two- to fivefold increase in airway blood flow in the dog. To determine whether airway blood flow responds similarly in the sheep we studied 16 anesthetized sheep. Seven sheep (1-7) were subjected to two 30-min periods of eucapnic hyperventilation breathing 1) warm humid air [100% relative humidity (rh)] followed by 2) warm dry air [0% rh] at 40 breaths/min. To determine whether there was a dose-response effect on blood flow of increasing levels of hyperventilation of dry air, another nine sheep (8-16) were subjected to four 30-min periods of eucapnic hyperventilation breathing warm humid O2 followed by warm dry O2 at 20 or 40 breaths/min in random sequence. Five minutes before the end of each period of hyperventilation, hemodynamics, blood gases, and tracheal mucosal temperature were measured, and tracheal and bronchial blood flows were determined by injection of 15- or 50-micron-diam radiolabeled microspheres. After the last measurements had been made, all sheep were killed, and the lungs and trachea were removed for determination of blood flow to trachea, bronchi, and parenchyma. In sheep 1-7, warm dry air hyperventilation at 40 breaths/min produced an increase in blood flow to trachea (7.6 +/- 3.5 to 17.0 +/- 6.2 ml/min, P less than 0.05) and bronchi (9.0 +/- 5.4 to 18.2 +/- 8.2 ml/min, P less than 0.05) but not to the parenchyma. When blood flow was compared with the two ventilatory rates (sheep 8-16), tracheal blood flow increased (9.1 +/- 3.3 to 18.2 +/- 6.1 ml/min, P less than 0.05) at a rate of 40 breaths/min but not at 20 breaths/min.(ABSTRACT TRUNCATED AT 250 WORDS)

The hyperventilation syndrome in panic disorder, agoraphobia and generalized anxiety disorder

The symptom complex of panic disorder and generalized anxiety disorder suggests an etiological role for hyperventilation. The present study investigates the overlap between DSM-III-R panic disorder, panic disorder with agoraphobia and generalized anxiety disorder with hyperventilation syndrome (HVS). The anxiety disorder diagnoses were based on a structured interview, and HVS determined by the so-called hyperventilation provocation test (a brief period of voluntary hyperventilation with recognition of symptoms). The overlap rates with HVS were: 48% for panic disorder, 83% for panic disorder with agoraphobia and 82% for generalized anxiety disorder. However, a pilot study on transcutaneous monitoring of carbon dioxide tension leads us to question the validity of the voluntary hyperventilation method that we used to determine HVS-status. It is unclear whether hyperventilation plays an important role in panic and general anxiety, as our overlap findings suggest. For patients who recognize the symptoms induced by voluntary hyperventilation, the hyperventilation provocation procedure provides a therapeutic means of exposure to feared bodily sensations.

Pial arteriolar vessel diameter and CO2 reactivity during prolonged hyperventilation in the rabbit.

Hyperventilation reduces intracranial pressure (ICP) acutely through vasoconstriction, but its long-term effect on vessel diameter is unknown. In seven rabbits with a cranial window implanted 3 weeks earlier, the effect of prolonged hyperventilation on vessel diameter was studied. Anesthesia was maintained for 54 hours with a pentobarbital drip (1 mg/kg/hr). The pH, CO2, and HCO3- levels were measured in arterial blood and cisterna magna cerebrospinal fluid (CSF). The diameter of 31 pial arterioles was measured with an image splitter. After baseline measurements, pCO2 was reduced from 38 to 25 mm Hg and allowed to return to 38 mm Hg for 10 minutes every 4 hours. There was an initial vasoconstriction of 13%, which progressively diminished by 3% every 4 hours. Thus, by the 20th hour, vessel diameters at a pCO2 of 25 mm Hg had returned to slightly above baseline values obtained at a pCO2 of 38 mm Hg. The temporary return of pCO2 to 38 mm Hg every 4 hours caused vasodilation: 12% at 4 hours, gradually increasing to 16% at 52 hours. Thus, at 52 hours, the vessel diameters were 105% of baseline at a pCO2 of 25 mm Hg and increased to 122% at a pCO2 of 38 mm Hg. Arterial pH had returned to baseline at 20 hours, and CSF pH had returned at 24 hours. Bicarbonate in blood and CSF remained decreased throughout the experiments. In three control experiments during which normocapnia was maintained, vessel diameter and pH and bicarbonate levels remained unaltered over the same period. The CO2 reactivity, tested by brief periods of hyperventilation every 4 hours, also did not change. These results indicate that hyperventilation is effective in reducing cerebral blood volume for less than 24 hours and that it should be used only during actual ICP elevations. If used preventively, its effect may have worn off by the time ICP starts to rise for other reasons, and further decreases in pCO2 cannot be obtained. Moreover, the reduction in buffer capacity with lower bicarbonate renders the vessels more sensitive to changes in PaCO2. This could lead to more pronounced elevations in ICP during transient rises in PaCO2, such as during endotracheal suctioning in head-injured patients.

The effect on airway function of inspired air conditions after isocapnic hyperventilation with dry air

The magnitude of postexercise or posthyperventilation bronchoconstriction in patients with asthma is related to the temperature and the water content of the inspired air during the exercise or hyperventilation period. Recent studies have suggested that the inspired air conditions during recovery from exercise may also be important in determining the magnitude of postexercise airway narrowing. In the present study, normal subjects (n = 8) and patients with asthma (n = 12) were studied on separate days. On day 1 the subjects performed isocapnic hyperventilation with warm dry air and recovered breathing warm dry air. On the second day, an identical warm dry air challenge was administered, but recovery occurred while they were breathing warm humid air. There was no significant bronchoconstriction in the normal subjects, irrespective of the inspired air conditions during recovery. The patients with asthma showed greater bronchoconstriction during recovery in warm, humid air (maximal decrease in FEV 1 31% ± 17%) than in dry air (maximal decrease in FEV 1 19% ± 20%; p < 0.05). These results suggest that the inspired air condition during recovery from isocapnic hyperventilation of dry air is also a determinant of the magnitude of the bronchoconstrictor response.

Time-course of blood acid-base state during arousal from hibernation in the European hamster.

1. Arterial blood was sampled at 15 min-intervals in European hamsters Cricetus cricetus fitted with indwelling catheters, from deep hibernation to full arousal. Temperature-corrected pH and PCO2, respectively pH* and P*CO2, were directly measured at 37 degrees C. 2. Deep hibernation corresponded to a respiratory acidosis: pH* = 7.01 +/- 0.01 (mean +/- SE), P*CO2 = 160 +/- 4 Torr (n = 9 animals). 3. Three periods could be distinguished in the arousal: (i) a period of hyperventilation (28 +/- 5 min), in which P*CO2 was reduced to 79 +/- 4 Torr, while cheek pouch temperature increased only by 0.9 +/- 0.2 degrees C; (ii) a period of metabolic acidification by lactate accumulation (84 +/- 6 min), corresponding to the period of peak thermogenesis; (iii) a progressive return to euthermic conditions (104 +/- 10 min), by simultaneous respiratory and metabolic alkalinization. 4. Over 60% of the blood CO2 stores accumulated at the beginning of the hibernation bout were released by hyperventilation during the first period, prior to the full development of thermogenesis. This is in agreement with the hypothesis of an inhibitory role of the respiratory acidosis in hibernation.

Can eucapnic hyperventilation prolong a subsequent breath-hold?

Previous studies have shown that, upon breaking a maximal breath-hold (BH), reinhalation of the expired gas allows an additional period of breath-holding. This indicates that mere ventilatory movements can diminish the urge to breathe. We sought to determine if vigorous ventilations, performed immediately prior to a maximal BH and in such a way that CO 2 stores are not changed, can prolong a subsequent BH. Maximal BHs were accomplished with and without a preceding period of hyperventilation. The gas breathed during hyperventilation was air with 4.37% CO 2, or oxygen containing either 0.04% CO 2 (hypocapnic hyperventilation) or 4.37% CO 2 (eucapnic hyperventilation). During hyperventilation, expired minute volume and frequency were clamped at 60L/min and 30 breaths/min, respectively. End-tidal and transcutaneous CO 2 tensions were monitored. Eucapnic hyperventilation did not prolong maximal BHs. Therefore, the ventilatory movements of hyperventilation do not appear to affect the duration of a subsequent maximal BH if these movements are not accompanied by changes in CO 2 stores.

Cold air challenge in children with asthma.

A study was designed to determine the sensitivity and specificity of a cold air bronchial provocation test. A total of 18 children with asthma (mean age 12 years) and 18 normal children (mean age 14 years) were studied. The cold air challenge consisted of a 4 min period of isocapnic hyperventilation of subfreezing air (mean temperature -15 degrees C). In-Induced response in forced expiratory volume in 1 sec (FEV1) expressed as a percentage of predicted normal values was obtained at 4, 6, and 8 min post-challenge. The average response to the cold air was a 27% decrease of FEV1 in asthmatics, which was significantly different from that of the normal children, who showed no statistically significant drop. In both the asthmatic and normal groups, the maximal drop in FEV1 had occurred by the time measurements 4 min post-challenge had been made. At that time, the smallest overlap was observed between normal and asthmatic children. This suggests that the fourth minute post-challenge can be chosen as a cut-off time to distinguish normal from asthmatic children. Considering a decrease of FEV1 greater than 10% as a positive test, the sensitivity of the cold air challenge was 95% and the specificity was 89%.