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Study objectives: To determine whether there is any difference in diagnostic, therapeutic, and outcome efficacy between protocols utilizing daily ( ie , routine) chest radiographs (CXRs) and those utilizing clinically indicated ( ie , nonroutine) CXRs in mechanically ventilated patients. Design: Prospective, randomized, observational study. Setting: A 20-bed medical ICU at a university hospital. Patients: Adult patients who had been receiving mechanical ventilation for > 48 h. Interventions: None. Measurements and results: Ninety-four patients who had been intubated for at least 48 h were randomized to receive either routine or nonroutine CXRs and were observed until extubation or death. The percentage of CXRs with new findings was significantly larger in the nonroutine CXR group (53.1%; 120 CXRs) compared to that in the routine CXR group (33.4%; 98 CXRs; odds ratio [OR], 1.59; 95% confidence interval [CI], 1.16 to 2.18; p=0.004). The number of CXRs with new findings that resulted in interventions was significantly larger in the nonroutine CXR group (26.5%; 60 CXRs) compared to that in the routine CXR group (13.3%; 39 CXRs; OR, 2.0; 95% CI, 1.29 to 3.08; p=0.002). There was no difference in the mean duration of mechanical ventilation (routine CXR arm, 7.93 days; nonroutine CXR arm, 6.76 days; p=0.2606), length of ICU stay (routine CXR arm, 11.93 days; nonroutine CXR arm, 9.55 days; p=0.1936), and total length of hospital stay (routine CXR arm, 19.34 days; nonroutine CXR arm, 16.45 days; p=0.2199) between the two groups. Although patients in the nonroutine arm of the study received fewer CXRs, adverse outcomes ( eg , length of mechanical ventilation, length of hospital stay, length of ICU stay, and mortality) did not increase (p = 0.818). Using the number of CXRs per patient as a surrogate, there was a statistically significant cost savings and decreased radiation exposure in the nonroutine CXR group. Conclusions: For mechanically ventilated patients, a strategy calling for daily routine CXRs compared to CXRs obtained based on clinical indications alone was not associated with reduced ICU or hospital length of stay or with reduced mortality.

Mechanical vibration of the chest wall can reduce dyspnea. It is unclear which sensations of respiratory discomfort are modulated by vibration (work/effort, air hunger, tightness). We performed two experiments to test whether vibration modifies air hunger: Experiment 1-eight adults performed six breath holds and rated their uncomfortable 'urge to breathe.' Vibration was applied separately at four chest-wall and two control sites, using two amplitudes. Breath-hold duration and ratings were unchanged by vibration at any site or amplitude. Experiment 2-nine adults were mechanically ventilated (mean 8.73 L/min) at constant hypercapnia (mean 48 mmHg) to produce mild to moderate ratings of air hunger (mean 37% of scale) with minimal respiratory muscle work. Vibration at 2nd or 3rd intercostal spaces during either inspiration or expiration did not change air hunger compared to triceps vibration. These experiments demonstrated that vibration does not relieve air hunger; we postulate that the effect of vibration is specific to the form of dyspnea.

The cost of graduate medical education in the United States is subsidized by the federal government through direct and indirect Medicare payments. These payments are intended to cover the portion of resident salaries, teaching expenses, and indirect hospital costs associated with the academic mission attributable to the care of Medicare beneficiaries, using a complex allocation formula. However, there are other program expenses associated with medical education that are not reimbursed by Medicare and still significantly affect the competitiveness and quality of the educational programs. Although most educators recognize the amount of extra work and money required to run high-quality training programs, there are few analyses demonstrating the actual amount and effect of these extra expenditures on graduate medical education.1-4 Programs often spend significant amounts on recruitment efforts, including interviews, travel reimbursements, and orientation days. They purchase resource education materials for residents, such as books, simulation training, digital resources, association and membership dues, and in-service examinations to support their education. For scientific meetings and events, they often pay for travel and lodging expenses, program application fees and food; graduation ceremonies, awards, and certificates add to the expenses of running a program. Other items purchased for trainee support include laboratory coats, office supplies, computer hardware and software, parking, meal cards, and pagers. As fiscal pressures intensify for academic medical centers and associated faculty practice plans, it is essential to identify the magnitude and distribution of these “hidden costs” of residency training. As part of a strategic review of education and budgets, the 8 core Accreditation Council for Graduate Medical Education (ACGME) residency programs (comprising 461 trainees) at an academic medical center reported all nonsalary costs of training residents. The programs were asked to identify the costs by category of expenditure (using the 4 categories noted above) and the source of the funding: hospital cost center, physician practice plan, or special funds (eg, philanthropy, grants). The total annual hidden costs for resident education at that institution were $1,865,016. Approximately 70% ($1,315,693) was paid by the physician practice plan; 25% ($462,202) by the hospital; and 5% ($87,121) from special funds. The average annual cost per resident was $4439 (range, $1500 to $9417 among programs). By category, the average annual per resident costs were Educational materials $1423 (32.1%); Trainee support $1299 (29.3%); Meetings and events $1191 (26.8%); and Recruitment $525 (11.8%). See the figure. One limitation of this analysis was that we relied on our program directors to define the costs and the category under which they would best be classified. Departmental budgets were not audited independent of those reports. The figures obtained were from 2006 (as part of a baseline analysis for ongoing institutional efforts to support residency training programs) so may not be accurate for 2012 conditions (they likely underestimate current costs). The figures reported are for a single institution only. While it is probable that similar conditions exist elsewhere, further study is warranted to investigate the effect of these costs on hospitals and academic practices as the cost containment elements of health care reform reduce clinical margins and jeopardize the cross-subsidization of education that has been prevalent for many years. With more than 109 000 ACGME-accredited residents currently in training, even if this analysis is off by an order of magnitude, it still represents a cost of tens of millions of dollars per year in the United States alone.5

Asthma evokes several uncomfortable sensations including increased "effort to breathe" and chest "tightness." We have tested the hypotheses that "effort" and "tightness" are due to perception of increased work performed by the respiratory muscles. Bronchoconstriction was induced by inhaled methacholine in 15 subjects with mild asthma (FEV(1)/FVC baseline = 81.9% +/- 5.8; bronchoconstriction = 64.0% +/- 8.6). To relieve the work of breathing, and thereby minimize activation of respiratory muscle afferents and motor command, subjects were mechanically ventilated. Subjects separately rated effort to breathe and tightness during mechanical ventilation and during spontaneous breathing. Bronchoconstriction produced elevated end-expiratory lung volume (279 +/- 62 ml); in a control study, end-expiratory lung volume was increased equally in the absence of bronchoconstriction by increasing end-expiratory pressure. During bronchoconstriction, ratings of effort were greater during spontaneous breathing than during mechanical ventilation (p < 0.05). Ratings of tightness were unchanged by the absence of respiratory muscle activity (p = 0.12). Hyperinflation alone did not produce tightness or effort. We conclude that tightness is not related to the increase in respiratory work during bronchoconstriction.

Dyspnea is a cardinal symptom of asthma and may arise from several pathophysiological mechanisms, including pulmonary hyperinflation, stimulation of vagal receptors, and, rarely, chemoreceptor stimulation. The language that patients use to describe their breathlessness may provide important clues about the physiology underlying symptoms in a particular patient. Several physiological derangements may contribute to dyspnea in a given individual. The variability in the severity of breathlessness for any given degree of airflow obstruction may relate to differences in the relative importance of these physiological changes and/or to a range of perceptual abilities in asthmatic patients. One hypothesis that is under current investigation is that defective perception of asthma symptoms may lead to undertreatment and the potential for greater morbidity and mortality from asthma.

Vibration of the thoracic surface has been shown to modify the drive to breathe and the sensation of dyspnea. It has been suggested that respiratory muscle afferents generate these effects. The possibility that the consequences of chest-wall vibration also involve intra-pulmonary afferents led us to investigate whether such vibration reaches the airways. Two vibratory stimuli were independently applied to four chest-wall sites and two control sites on eight healthy subjects. During separate breath holds, the vibrator was held on each site while subjects periodically opened and closed the pharynx. Airway pressure (P(AW)) was measured at the mouth. Spectral analysis of P(AW) showed pressure oscillations occurred at the same frequency as that of the vibrators when the pharynx was open; oscillation amplitude was vastly reduced when the pharynx was closed. Oscillation amplitude was also significantly larger during vibration at greater amplitude. These data demonstrate that vibration over the chest-wall vibrates the lung and could potentially excite intrapulmonary receptors.

To test the hypothesis that patients perceive the same quality of dyspnea during mild bronchoconstriction and external resistive loads, we studied subjects with asthma under two conditions: (1) during methacholine bronchoprovocation to mimic the bronchospasm of mild asthma and (2) while breathing on a circuit to which was added a range of external resistors to mimic the mechanical load of mild asthma. During each of these stimuli, respiratory variables, overall dyspnea intensity on a modified Borg scale, and the qualitative descriptors of breathlessness from a 19-item questionnaire were assessed. The "chest tightness" and "constriction" responses were significantly more frequent in the methacholine trials as compared with the external load trials (p0.0001). The "chest tightness" or "constriction" response was chosen during 92% of the 26 trials of methacholine bronchoconstriction compared with 3% of the 72 trials of breathing against the external resistors. Changes in functional residual capacity were not significantly different between the two conditions. We conclude that in mild asthma, the sensation of chest tightness is distinct from the sensation of work and effort and is not attributable to the mechanical load imposed on the respiratory system.

In a Dutch birth cohort study published in this issue of the Journal, children had an increased risk of bronchial hyperresponsiveness or dyspnea at age 8 years if they had a high body mass index (BMI) at 6 to 7 years of age with or without increased BMI at an earlier age. Taking advantage of the longitudinal nature of their study of 3,756 children, the authors also report the encouraging finding that children who had a high BMI at a young age but whose BMI returned to normal did not have increased risk either of bronchial hyperresponsiveness or dyspnea. As always, extrapolation from an observational study to early-life interventions should be done cautiously. It is not known whether children whose BMI decreases without any known deliberate intervention are the subset of children who might benefit from BMI screening or from weight-reduction programs. Programs for screening and early intervention in obesity abound, but further prospective evaluation of their success in reducing weight and obesity-associated respiratory symptoms is needed. But what does overweight-associated dyspnea signify in the children from this birth cohort, and is dyspnea a symptom of asthma, as the investigators suggest? Mouse model data suggest that obesity can lead to bronchial hyperresponsiveness. Airway narrowing can occur through obesity-associated lung and tidal volume reduction, low-grade systemic inflammation, or obesity-related changes in adipose-derived hormones, including leptin and adiponectin. Nevertheless, studies of adults in which data suggest that asthma might be overdiagnosed in obese adults with dyspnea are accumulating. Misdiagnosis of asthma can result in inappropriate prescription of short-acting bronchodilators or corticosteroids in persons who are short of breath for obesity-related dyspnea that does not represent reversible airway obstruction. In a study of 16,171 participants ( 17 years of age) from the Third National Health and Nutrition Examination Survey, the highest BMI quintile (ie, the most obese participants) was associated with the greatest risk of self-reported asthma, bronchodilator use, and dyspnea with exertion (odds ratio, 2.66; 95% CI, 2.35-3.00). The highest BMI quintile, however, had the lowest risk for significant airflow

Background Laboratory-induced dyspnea (breathing discomfort) in healthy subjects is widely used to study perceptual mechanisms, yet the relationship between laboratory-induced dyspnea in healthy volunteers and spontaneous dyspnea in patients with chronic lung disease is not well established. We compared affective responses to dyspnea 1) in COPD patients vs. healthy volunteers (HV) undergoing the same laboratory stimulus; 2) in COPD during laboratory dyspnea vs. during activities of daily living (ADL). Methods We induced moderate and high dyspnea levels in 13 COPD patients and 12 HV by increasing end-tidal CO2 (PETCO2) during restricted ventilation, evoking air hunger. We used the multidimensional dyspnea profile (MDP) to measure intensity of sensory qualities (e.g., air hunger (AH) and work/effort (W/E)) as well as immediate discomfort (A1) and secondary emotions (A2). Ten of the COPD subjects also completed the MDP outside the laboratory following dyspnea evoked by ADL. Results COPD patients and HV reported similar levels of immediate discomfort relative to sensory intensity. COPD patients and HV reported anxiety and frustration during laboratory-induced dyspnea; variation among individuals far outweighed the small differences between subject groups. COPD patients reported similar intensities of sensory qualities, discomfort, and emotions during ADL vs. during moderate laboratory dyspnea. Patients with COPD described limiting ADL to avoid greater dyspnea. Conclusions In this pilot study, we found no evidence that a history of COPD alters the affective response to laboratory-induced dyspnea, and no difference in affective response between dyspnea evoked by this laboratory model and dyspnea evoked by ADL.

The purposes of this study were: to examine the decriptors of breathlessness chosen by a large sample of patients with cardiorespiratory disease; to determine test-retest reliability of a patient's selection of the descriptors; and to assess whether a patient's recall of the experience of breathlessness is the same as that provoked by physical activity. Questionnaire data were collected at an initial visit for patients who complained of breathlessness and at a second visit in a subgroup of patients. A total of 218 patients who sought medical care for difficulty breathing due to one of seven different conditions were recruited from an outpatient pulmonary disease clinic at a university medical center. Patients selected statements that described qualities of breathlessness from a 15-item questionnaire and completed pulmonary function tests. At a subsequent visit (4 to 15 d later) a subgroup of 16 patients with chronic obstructive pulmonary disease (COPD) repeated the questionnaire at rest (to assess reliability) and after walking in a hallway to provoke a moderate intensity of breathlessness (to compare recall with direct experiences). The relationship among descriptors was evaluated by cluster analysis. The "work/effort" cluster was common for all diagnoses. Each condition was characterized by more than one cluster except COPD. Each diagnosis was associated with a unique set of dusters (e.g., asthma with "work/effort" and "tight," interstitial lung disease with "work/effort" and "rapid" breathing). Percent agreement for all descriptors selected at Visits 1 and 2 (recall) was 79% (r = 0.82; p = 0.001). Percent agreement at Visit 2 between descriptors for recall and for breathlessness provoked by walking was 68% (r = 0.69; p = 0.004). We conclude that patients with different cardiorespiratory conditions experience distinct qualities of breathlessness. Patients' recall of their sensations of breathlessness is reliable and comparable to dyspnea with walking. Employing a questionnaire containing descriptors of breathlessness may help to establish a specific diagnosis and to identify mechanisms whereby a specific intervention relieves dyspnea.

Explicit teaching of humanism is a goal of education reform, but specific strategies to do so are limited. The authors developed a longitudinal third-year medical student curriculum combining reflective and academic writing with literary reading and reflection to i) improve writing skills, ii) enhance scholarly activities, and iii) foster humanism in patient care. From 2005-2007, 24 third year Harvard Medical School (HMS) participated in a writing program at this hospital. All students completed pre/post surveys and qualitative assessments of the writing program. Students felt better-equipped to access resources (P=0.03), conduct a literature review (P

The act of breathing diminishes the discomfort associated with hypercapnia and breath-holding. To investigate the mechanisms involved in this effect, we studied the effect of tidal volume (V T ) on CO 2 -evoked air hunger in 5 high-level quadriplegic subjects whose ventilatory capacity was negligible, and who lacked sensory information from the chest wall. Subjects were ventilated at constant frequency with a hyperoxic gas mixture, and end-tidal P CO 2 was maintained at a constant but elevated level. V T was varied between the subjects' normal V T and a smaller V T . Subjects used a category scale to rate their respiratory discomfort or ‘air hunger’ at 30–40 sec intervals. In 4 of 5 subjects there was a strong inverse relationship between breath size and air hunger ratings. The quality of the sensation associated with reduced V T was nearly identical to that previously experienced with CO 2 alone. We conclude that afferent information from the lungs and upper airways is sufficient to modify the sensation of air hunger.

Obstructive apneas occur infrequently during Stage 3-4 NREM sleep (SWS), even in patients with severe obstructive sleep apnea. To investigate whether upper airway (UA) dilator muscle activity preferentially increases during SWS as a partial explanation for this phenomenon, we measured phasic electromyogram activity of the genioglossus muscle (EMGgg) during continuous Stage 2 NREM sleep and SWS in 5 healthy males. Subjects were studied supine during a complete cycle of nocturnal NREM sleep after partial sleep deprivation. EMGgg was measured with perorally inserted bipolar electrodes, and quantified as peak phasic inspiratory activity during all continuous epochs of NREM sleep. We found EMGgg to be increased during SWS relative to stage 2 sleep by a mean of 58% among all subjects (P = 0.02); neither end-tidal PCO2 nor inspired minute ventilation varied between these sleep stages. Upper airway resistance, measured in 3 of the subjects on a separate study night, was not different between SWS and Stage 2 sleep. We speculate that the increase in phasic EMGgg during SWS in our normal subjects may reflect a mechanism whereby UA patency tends to be preserved during this stage.

In patients with obstructive sleep apnea (OSA), substantial elevations of systemic blood pressure (BP) and depressions of oxyhemoglobin saturation (SaO2) accompany apnea termination. The causes of the BP elevations, which contribute significantly to nocturnal hypertension in OSA, have not been defined precisely. To assess the relative contribution of arterial hypoxemia, we observed mean arterial pressure (MAP) changes following obstructive apneas in 11 OSA patients during non-rapid-eye-movement (NREM) sleep and then under three experimental conditions: 1) apnea with O2 supplementation; 2) hypoxemia (SaO2 80%) without apnea; and 3) arousal from sleep with neither hypoxemia nor apnea. We found that apneas recorded during O2 supplementation (SaO2 nadir 93.6% +/- 2.4; mean +/- SD) in six subjects were associated with equivalent postapneic MAP elevations compared with unsupplemented apneas (SaO2 nadir 79-82%): 18.8 +/- 7.1 vs. 21.3 +/- 9.2 mmHg (mean change MAP +/- SD); in the absence of respiratory and sleep disruption in eight subjects, hypoxemia was not associated with the BP elevations observed following apneas: -5.4 +/- 19 vs. 19.1 +/- 7.8 mmHg (P less than 0.01); and in five subjects, auditory arousal alone was associated with MAP elevation similar to that observed following apneas: 24.0 +/- 8.1 vs. 22.0 +/- 6.9 mmHg. We conclude that in NREM sleep postapneic BP elevations are not primarily attributable to arterial hypoxemia. Other factors associated with apnea termination, including arousal from sleep, reinflation of the lungs, and changes of intrathoracic pressure, may be responsible for these elevations.

Dyspnea--an unpleasant or uncomfortable awareness of breathing or need to breathe--is a common symptom of patients with cardiopulmonary disease. Although often thought of as a single symptom, dyspnea probably subsumes many sensations. Experimental conditions used to induce dyspnea are characterized by discrete groups or clusters of descriptive phrases. Similarly, as the language of dyspnea is refined further, different disease states may be distinguishable by the nuances of breathlessness described by patients. Evidence is gathering that the sensations of dyspnea are modified by information from a variety of receptors throughout the respiratory system. The sense of effort, although still important in the breathlessness associated with mechanical loads, is insufficient to explain the dyspnea arising from a number of experimental and clinical conditions. As our understanding of the interactions between effort and afferent information from the respiratory system grows, new therapeutic interventions to alleviate dyspnea are likely to follow.

Patients with breathlessness commonly describe subjective relief when seated near an open window or in front of a fan. Previous studies suggest that a flow of air or application of cold solutions to the face, nasal mucosa, or pharynx may alter ventilation. We hypothesized that a flow of cold air directed against the cheek would reduce the sensation of breathlessness associated with loaded breathing. Sixteen subjects breathed on a device with an inspiratory resistive load (63 cm H2O/L/s) while PCO2 was maintained at 55 torr for 5 min. All studies were performed 4 times with each subject, twice with cold air directed against the cheek (4 degrees to 10 degrees C, 4 km/h) and twice with no flow on the subject. Subjects were asked to rate their breathlessness using a modified Borg scale. Cold air directed on the face reduced breathlessness induced by an inspiratory resistive load and hypercapnia (6.2 +/- 1.7 Borg scale units with no flow, 5.1 +/- 1.7 with cold air; p less than 0.002) without causing a significant reduction in ventilation. This effect was not observed when cold air was directed to the leg and does not appear to be associated with a reduction in the ventilatory response to hypercapnia or with initiation of the diving reflex. We conclude that cold air directed against the cheek significantly reduces dyspnea associated with the combination of hypercapnia and an inspiratory resistive load.

Both nasal obstruction and nasal anesthesia result in disordered breathing during sleep in humans, and bypassing the nasal route during tidal breathing in experimental animals produces decreased electromyographic activity of upper airway (UA) dilating muscles. To investigate UA responses to breathing route in normal awake humans, we studied eight healthy males (ages 21–38 yr) during successive trials of voluntary nose breathing (N), voluntary mouth breathing (M), and mouth breathing with nose occluded (MO). We measured genioglossus electromyographic activity (EMGgg) with perorally inserted bipolar electrodes, alae nasi (EMGan) and diaphragm EMG activity (EMGdi) with surface electrodes, and minute ventilation (VE) with a pneumotachograph. Mean phasic inspiratory EMG activity of both UA muscles was significantly greater during N than during M or MO, even when a 2.5-cmH2O.l-1.s inspiratory resistance was added to MO (P less than 0.01). In contrast, neither EMGdi nor VE was consistently affected by breathing route. EMGgg during N was significantly decreased after selective topical nasal anesthesia (P less than 0.002); a decrease in EMGan did not achieve statistical significance. These data suggest that peak UA dilating muscle activity may be modulated by superficial receptors in the nasal mucosa sensitive to airflow.

1. To investigate whether changes in Paco2 can be detected independently of the CO2-induced changes in pulmonary ventilation, we tested five normal subjects for the ability to distinguish different levels of end-tidal Pco2 (PETco2) while holding minute ventilation constant. 2. Helped by a visual feedback system, the subjects maintained a constant ventilation targeted at a level that was higher than that dictated by the chemical drive at PETco2 = 50 mmHg (6.7 kPa). End-tidal Pco2 was held at 40 mmHg (5.3 kPa) during the first 2 min of each test trial ('control period'); then, for 4 min ('test period'), PETco2 was either elevated to 50 mmHg or kept at 40 mmHg. Twelve runs were performed by each subject. 3. In 24 out of the total 30 trials (80%) in which PETco2 was raised during the test period to 50 mmHg, the subjects detected the changes. There was one false positive result (3%), when PETco2 kept at 40 mmHg during the test period was reported as different from control. In four out of the five subjects the ability to detect the change in PETco2 from 40 to 50 mmHg was statistically significant. 4. We conclude that increases in PETco2 can be detected independently of changes in the absolute level of ventilation.

Various theories about the genesis of dyspnea have often assumed that the sensation is similar from patient to patient and is generated by a single underlying mechanism. To investigate whether breathlessness induced in normal volunteers by different stimuli represents one or more than one sensation, we studied 30 subjects in whom breathlessness was induced by each of 8 different stimuli: breath-holding, CO2 inhalation, inhalation of CO2, with ventilation voluntarily targeted below the level dictated by chemical drive, breathing with a resistive load, breathing with an elastic load, voluntary elevation of functional residual capacity, voluntary limitation of tidal volume, and exercise. For each stimulus, subjects were asked to choose description of their sensation(s) of breathlessness from a questionnaire listing 19 descriptors. The responses from this questionnaire were evaluated using cluster analysis to search for relationships among descriptors and to identify natural groupings. We found that distinct groups of descriptors emerged, i.e., subjects could distinguish different sensations of breathlessness. In addition, we found an association between certain descriptor groups and stimuli. We conclude that the term breathlessness may encompass multiple sensations, and, therefore, may not be explainable by a single physiologic mechanism.

We studied the effect of oral monosodium glutamate (MSG) on airways function in 12 subjects with a history of chronic stable asthma in a double-blind, randomized, crossover protocol. Subjects ingested either 25 mg/kg of MSG or sodium chloride (equimolar to MSG) following a 6-hour fast. Spirometry [forced expiratory volume in 1 second (FEV1) and forced vital capacity] was performed before administration of the test substances and for a minimum of 4 hours thereafter. At no time during the observation period was the mean change in FEV1 more negative following MSG than following placebo. MSG is unlikely to be a contributing factor in bouts of broncho-spasm in subjects with asthma, and routine avoidance of MSG by individuals with asthma need not be advised.

Suppression of ventilation by tasks such as talking may produce breathlessness in normal individuals under conditions when a strong respiratory drive exists, e.g., during exercise, and in patients with severe lung disease. To investigate the nature of breathlessness produced by a dissociation between ventilation and chemical drive, we studied ten naive normal subjects who breathed at various levels of ventilation while end-tidal PCO2 (PETCO2) was held at 55 mm Hg. After a 10-min equilibration period of free breathing at PETCO2 = 55 mm Hg, subjects used a visual target to adjust ventilation to five different levels ranging from 50% below to 50% above the chemically driven ventilation (CDV). Ratings of breathlessness were made on a visual analogue scale relative to the intensity of breathlessness experience at CDV. As ventilation was targeted to levels below CDV, all subjects became increasingly breathless; the response was more variable when ventilation was targeted to levels above CDV. Overall, the relationship between ventilation and breathlessness was described by a hyperbolic function, for which the coefficient of determination (R2) was 0.92. Ventilation was suppressed below CDV without recruitment of antagonistic muscles during inspiration. The intensity of breathlessness was not correlated with measures of respiratory effort. We conclude that suppressed ventilation is a useful model for the study of breathlessness not fully explained by measures of respiratory effort and we speculate that the dissociation between chemical drive and afferent signals produced by motion of the lung and chest wall is important in modulating the sensation of breathlessness.