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Nurses routinely assess pain in hospitalized patients; similar assessment of dyspnea is increasing. Most nurses start with a yes–no question when assessing pain or dyspnea; many record “no” as a zero rating, skipping the rating scale. We tested the hypothesis that recording “no” answers as “zero” fails to detect the symptoms that would have been detected with a rating scale. Nurses asked 60 patients yes–no questions about the presence of dyspnea and pain, then asked patients to rate the symptoms using a 0–10 scale. All “yes” answers were followed by a concordant rating (i.e., greater than zero). More than 25% of “no” answers were followed by a discordant rating (> zero). Documenting “no” as “zero” missed information potentially useful in care planning; patients who rate dyspnea above zero are at greater risk of adverse outcomes. This information can also provide opportunity to start a discussion with patients who may benefit from symptom management.

Dyspnea is an uncomfortable sensation with the potential to cause psychological trauma. Patients presenting with acute respiratory failure, particularly when tidal volume is restricted during mechanical ventilation, may experience the most distressing form of dyspnea known as air hunger. Air hunger activates brain pathways known to be involved in posttraumatic stress disorder (PTSD), anxiety, and depression. These conditions are considered part of the post-intensive care syndrome. These sequelae may be even more prevalent among patients with ARDS. Low tidal volume, a mainstay of modern therapy for ARDS, is difficult to avoid and is likely to cause air hunger despite sedation. Adjunctive neuromuscular blockade does not prevent or relieve air hunger, but it does prevent the patient from communicating discomfort to caregivers. Consequently, paralysis may also contribute to the development of PTSD. Although research has identified post-ARDS PTSD as a cause for concern, and investigators have taken steps to quantify the burden of disease, there is little information to guide mechanical ventilation strategies designed to reduce its occurrence. We suggest such efforts will be more successful if they are directed at the known mechanisms of air hunger. Investigation of the antidyspnea effects of sedative and analgesic drugs commonly used in the ICU and their impact on post-ARDS PTSD symptoms is a logical next step. Although in practice we often accept negative consequences of life-saving therapies as unavoidable, we must understand the negative sequelae of our therapies and work to minimize them under our primary directive to "first, do no harm" to patients.

Background Dyspnea (breathing discomfort) is commonly experienced by critically ill patients and at this time is not routinely assessed and documented. Intensive care unit nurses at the study institution recently instituted routine assessment and documentation of dyspnea in all patients able to report using a numeric scale ranging from 0 to 10. Objective To assess nurses’ perceptions of the utility of routine dyspnea measurement, patients’ comprehension of assessment questions, and the impact on nursing practice and to gather nurses’ suggestions for improvement. Methods Data were obtained from interviews with intensive care unit nurses in small focus groups and an anonymous online survey randomly distributed to nurses representing all intensive care units. Results Intensive care unit nurses affirmed the importance of routine dyspnea assessment and documentation. Before implementing the measurement tool, nurses often assessed for breathing discomfort in patients by using observed signs. Most nurses agreed that routine assessment can be used to predict patients’ outcomes and improve patient-centered care. Nurses found the assessment tool easy to use and reported that it did not interfere with workflow. Nurses felt that patients were able to provide meaningful ratings of dyspnea, similar to ratings of pain, and often used patients’ ratings in conjunction with observed physical signs to optimize patient care. Conclusion Our study shows that nurses understand the importance of routine dyspnea assessment and that the addition of a simple patient report scale can improve care delivery and does not add to the burden of work-flow.

Aerosol furosemide may be an option to treat refractory dyspnea, though doses, methods of delivery, and outcomes have been variable. We hypothesized that controlled delivery of high dose aerosol furosemide would reduce variability of dyspnea relief in patients with underlying pulmonary disease. Seventeen patients with chronic exertional dyspnea were recruited. Patients rated recently recalled breathing discomfort on a numerical rating scale (NRS) and the multidimensional dyspnea profile (MDP). They then performed graded exercise using an arm-ergometer. The NRS was completed following each exercise grade, and the MDP was repeated after a pre-defined dyspnea threshold was reached. During separate visits, patients received either aerosol saline or 80 mg of aerosol furosemide in a randomized, double-blind, crossover design. After treatment, graded exercise to the pre-treatment level was repeated, followed by completion of the NRS and MDP. Treatment effect was defined as the difference between pre- and post-treatment NRS at end exercise, expressed in absolute terms as % Full Scale. “Responders” were defined as those showing treatment effect ≥ 20% of full scale. Final analysis included 15 patients. Neither treatment produced a statistically significant change in NRS and there was no significant difference between treatments (p = 0.45). There were four “responders” and one patient whose dyspnea worsened with furosemide; two patients were responders with saline, of whom one also responded to furosemide. No adverse events were reported. High dose controlled delivery aerosol furosemide was not statistically different from saline placebo at reducing exercise-induced dyspnea. However, a clinically meaningful improvement was noted in some patients.

The sensation that develops as a long breath hold continues is what this article is about. We term this sensation of an urge to breathe "air hunger." Air hunger, a primal sensation, alerts us to a failure to meet an urgent homeostatic need maintaining gas exchange. Anxiety, frustration, and fear evoked by air hunger motivate behavioral actions to address the failure. The unpleasantness and emotional consequences of air hunger make it the most debilitating component of clinical dyspnea, a symptom associated with respiratory, cardiovascular, and metabolic diseases. In most clinical populations studied, air hunger is the predominant form of dyspnea (colloquially, shortness of breath). Most experimental subjects can reliably quantify air hunger using rating scales, that is, there is a consistent relationship between stimulus and rating. Stimuli that increase air hunger include hypercapnia, hypoxia, exercise, and acidosis; tidal expansion of the lungs reduces air hunger. Thus, the defining experimental paradigm to evoke air hunger is to elevate the drive to breathe while mechanically restricting ventilation. Functional brain imaging studies have shown that air hunger activates the insular cortex (an integration center for perceptions related to homeostasis, including pain, food hunger, and thirst), as well as limbic structures involved with anxiety and fear. Although much has been learned about air hunger in the past few decades, much remains to be discovered, such as an accepted method to quantify air hunger in nonhuman animals, fundamental questions about neural mechanisms, and adequate and safe methods to mitigate air hunger in clinical situations. © 2021 American Physiological Society. Compr Physiol 11:1449-1483, 2021.

The clinical presentation of COVID‐19 due to infection with SARS‐CoV‐2 is highly variable with the majority of patients having mild symptoms while others develop severe respiratory failure. The reason for this variability is unclear but is in critical need of investigation. Some COVID‐19 patients have been labelled with ‘happy hypoxia’, in which patient complaints of dyspnoea and observable signs of respiratory distress are reported to be absent. Based on ongoing debate, we highlight key respiratory and neurological components that could underlie variation in the presentation of silent hypoxaemia and define priorities for subsequent investigation.

Dyspnea is an uncomfortable sensation with the potential to cause psychological trauma. Patients presenting with acute respiratory failure, particularly when tidal volume is restricted during mechanical ventilation, may experience the most distressing form of dyspnea known as air hunger. Air hunger activates brain pathways known to be involved in posttraumatic stress disorder (PTSD), anxiety, and depression. These conditions are considered part of the post-intensive care syndrome. These sequelae may be even more prevalent among patients with ARDS. Low tidal volume, a mainstay of modern therapy for ARDS, is difficult to avoid and is likely to cause air hunger despite sedation. Adjunctive neuromuscular blockade does not prevent or relieve air hunger, but it does prevent the patient from communicating discomfort to caregivers. Consequently, paralysis may also contribute to the development of PTSD. Although research has identified post-ARDS PTSD as a cause for concern, and investigators have taken steps to quantify the burden of disease, there is little information to guide mechanical ventilation strategies designed to reduce its occurrence. We suggest such efforts will be more successful if they are directed at the known mechanisms of air hunger. Investigation of the antidyspnea effects of sedative and analgesic drugs commonly used in the ICU and their impact on post-ARDS PTSD symptoms is a logical next step. Although in practice we often accept negative consequences of life-saving therapies as unavoidable, we must understand the negative sequelae of our therapies and work to minimize them under our primary directive to "first, do no harm" to patients.

As many as one in 10 patients experience dyspnoea at hospital admission but the relationship between dyspnoea and patient outcomes is unknown. We sought to determine whether dyspnoea on admission predicts outcomes.We conducted a retrospective cohort study in a single, academic medical centre. We analysed 67 362 consecutive hospital admissions with available data on dyspnoea, pain and outcomes. As part of the Initial Patient Assessment by nurses, patients rated “breathing discomfort” using a 0 to 10 scale (10=“unbearable”). Patients reported dyspnoea at the time of admission and recalled dyspnoea experienced in the 24 h prior to admission. Outcomes included in-hospital mortality, 2-year mortality, length of stay, need for rapid response system activation, transfer to the intensive care unit, discharge to extended care, and 7- and 30-day all-cause readmission to the same institution.Patients who reported any dyspnoea were at an increased risk of death during that hospital stay; the greater the dyspnoea, the greater the risk of death (dyspnoea 0: 0.8% in-hospital mortality; dyspnoea 1–3: 2.5% in-hospital mortality; dyspnoea ≥4: 3.7% in-hospital mortality; pWe found that dyspnoea of any rating was associated with an increased risk of death. Dyspnoea ratings can be rapidly collected by nursing staff, which may allow for better monitoring or interventions that could reduce mortality and morbidity.

In the ‘placebo arm’ of a recent study, we found that aerosol saline (sham treatment) produced substantial relief of laboratory-induced dyspnea (Breathing discomfort—BD) in nearly half the subjects. The sham intervention included a physiological change, and instructions to subjects could have produced expectation of dyspnea relief. In the present study, we attempted to discover whether the response to sham aerosol was driven by behavioral or physiological aspects of the intervention. Dyspnea (air hunger) was evoked by constraining tidal volume during graded hypercapnia. We measured $${\text{PET}}_{{{\text{CO}}_{ 2} }}$$ versus BD relationship before and after aerosol saline. To minimize subjects’ expectations of dyspnea relief, participants were clearly instructed that we would only deliver saline aerosol. In Protocol 1, we delivered aerosol saline with a ventilator (mimicking our prior study); in Protocol 2, we delivered aerosol without a ventilator. Administration of aerosol saline had little effect on BD in this group of subjects with one exception: one subject experienced appreciable reduction in BD in Protocol 1. This treatment effect was less in Protocol 2. The two most likely explanations are (a) that procedures surrounding ventilator administration of aerosol produced a psychological placebo treatment effect even though the subject knew a drug was not given; (b) there were behavioral changes in breathing undetected by our measurements of respiratory flow and volume that altered the subjects comfort. When the expectation of treatment effect is minimized, a significant reduction in dyspnea in response to saline placebo is uncommon but not impossible.

Because dyspnoea is seldom experienced by healthy people, it can be hard for clinicians and researchers to comprehend the patient’s experience. We collected patients’ descriptions of dyspnoea in their own words during a parent study in which 156 hospitalised patients completed a quantitative multidimensional dyspnoea questionnaire. These volunteered comments describe the severity and wide range of experiences associated with dyspnoea and its impacts on a patients’ life. They provide insights not conveyed by structured rating scales. We organised these comments into the most prominent themes, which included sensory experiences, emotional responses, self-blame and precipitating events. Patients often mentioned air hunger (‘Not being able to get air is the worst thing that could ever happen to you.’), anxiety, and fear (‘Scared. I thought the world was going to end, like in a box.’). Their value in patient care is suggested by one subject’s comment: ‘They should have doctors experience these symptoms, especially dyspnoea, so they understand what patients are going through.’ Patients’ own words can help to bridge this gap of understanding.

International audience; Aerosolized furosemide has been shown to relieve dyspnea; nevertheless, all published studies have shown great variability in response. This dyspnea relief is thought to result from the stimulation of slowly adapting pulmonary stretch receptors simulating larger tidal volume. We hypothesized that better control over aerosol administration would produce more consistent dyspnea relief; we used a clinical ventilator to control inspiratory flow and tidal volume. Twelve healthy volunteers inhaled furosemide (40mg) or placebo in a double blind, randomized, crossover study. Breathing Discomfort was induced by hypercapnia during constrained ventilation before and after treatment. Both treatments reduced breathing discomfort by 20% full scale. Effectiveness of aerosol furosemide treatment was weakly correlated with larger tidal volume. Response to inhaled furosemide was inversely correlated to furosemide blood level, suggesting that variation among subjects in the fate of deposited drug may determine effectiveness. We conclude that control of aerosol delivery conditions does not improve consistency of treatment effect; we cannot, however, rule out placebo effect.

Published studies have shown great variability in response when aerosolized furosemide has been tested as a palliative treatment for dyspnea. We hypothesized that a higher furosemide dose with controlled aerosol administration would produce consistent dyspnea relief. We optimized deposition by controlling inspiratory flow (300–500 ml/s) and tidal volume (15% predicted vital capacity) while delivering 3.4 micron aerosol from either saline or 80 mg of furosemide. We induced dyspnea in healthy subjects by varying inspired PCO2 while restricting minute ventilation. Subjects rated “Breathing Discomfort” on a Visual Analog Scale (BDVAS, 100% Full Scale ≡ intolerable). At the PETCO2 producing 60% BDVAS pre-treatment, furosemide produced a clinically meaningful reduction of BDVAS (i.e., > 20%FS) in 5/11 subjects; saline reduced dyspnea in 3/11 subjects; neither treatment worsened dyspnea in any subject. Furosemide and saline treatment effects were not statistically different. There were no significant adverse events. Higher furosemide dose and controlled delivery did not improve consistency of treatment effect compared with prior studies.

Several studies have mapped brain regions associated with acute dyspnea perception. However, the time-course of brain activity during sustained dyspnea is unknown. Our objective was to determine the time-course of neural activity when dyspnea is sustained. Eight healthy subjects underwent brain blood oxygen level dependent functional magnetic imaging (BOLD-fMRI) during mechanical ventilation with constant mild hypercapnia (~45 mmHg). Subjects rated dyspnea (air hunger) via visual analog scale (VAS). Tidal volume (VT) was alternated every 90 seconds between high VT (0.96±0.23 L) that provided respiratory comfort (12±6% full scale) and low VT (0.48±0.08 L) which evoked air hunger (56±11% full scale). BOLD signal was extracted from a priori brain regions and combined with VAS data to determine air hunger related neural time-course. Air hunger onset was associated with BOLD signal increases that followed two distinct temporal profiles within sub-regions of the anterior insula, anterior cingulate and prefrontal cortices (cortico-limbic circuitry): (1) fast, BOLD signal peak 40 seconds. BOLD signal during air hunger offset followed fast and slow temporal profiles symmetrical, but inverse (signal decreases) to the time-courses of air hunger onset. We conclude that differential cortico-limbic circuit elements have unique contributions to dyspnea sensation over time. We suggest that previously unidentified sub-regions are responsible for either the acute awareness or maintenance of dyspnea. These data enhance interpretation of previous studies and inform hypotheses for future dyspnea research.

Intensive care unit (ICU) patients are exposed to many sources of discomfort. Although increasing attention is being given to the detection and treatment of pain, very little is given to the detection and treatment of dyspnea (defined as "breathing discomfort").Published information on the prevalence, mechanisms, and potential negative impacts of dyspnea in mechanically ventilated patients are reviewed. The most appropriate tools to detect and quantify dyspnea in ICU patients are also assessed.Growing evidence suggests that dyspnea is a frequent issue in mechanically ventilated ICU patients, is highly associated with anxiety and pain, and is improved in many patients by altering the ventilator settings.Future studies are needed to better delineate the impact of dyspnea in the ICU and to define diagnostic, monitoring and therapeutic protocols.

Rationale: Opioids are commonly used to relieve dyspnea, but clinical data are mixed and practice varies widely. Objectives: Evaluate the effect of morphine on dyspnea and ventilatory drive under well-controlled laboratory conditions. Methods: Six healthy volunteers received morphine (0.07 mg/kg) and placebo intravenously on separate days (randomized, blinded). We measured two responses to a CO2 stimulus: (1) perceptual response (breathing discomfort; described by subjects as “air hunger”) induced by increasing partial pressure of end-tidal carbon dioxide (PetCO2) during restricted ventilation, measured with a visual analog scale (range, “neutral” to “intolerable”); and (2) ventilatory response, measured in separate trials during unrestricted breathing. Measurements and Main Results: We determined the PetCO2 that produced a 60% breathing discomfort rating in each subject before morphine (median, 8.5 mm Hg above resting PetCO2). At the same PetCO2 after morphine administration, median breathing discomfort was reduced by 65% of its pretreatment value; P < 0.001. Ventilation fell 28% at the same PetCO2; P < 0.01. The effect of morphine on breathing discomfort was not significantly correlated with the effect on ventilatory response. Placebo had no effect. Conclusions: (1) A moderate morphine dose produced substantial relief of laboratory dyspnea, with a smaller reduction of ventilation. (2) In contrast to an earlier laboratory model of breathing effort, this laboratory model of air hunger established a highly significant treatment effect consistent in magnitude with clinical studies of opioids. Laboratory studies require fewer subjects and enable physiological measurements that are difficult to make in a clinical setting. Within-subject comparison of the response to carefully controlled laboratory stimuli can be an efficient means to optimize treatments before clinical trials.

Context Dyspnea is an uncomfortable and distressing sensation experienced by hospitalized patients. Objectives There is no large-scale study of the prevalence and intensity of patient-reported dyspnea at the time of admission to the hospital. Methods Between March 2014 and September 2016, we conducted a prospective cohort study among all consecutive hospitalized patients at a single tertiary care center in Boston, MA. During the first 12 hours of admission to medical-surgical and obstetric units, nurses at our institution routinely collect a patient's 1) current level of dyspnea on a 0–10 scale with 10 anchored at "unbearable," 2) worst dyspnea in the past 24 hours before arrival at the hospital on the same 0–10 scale, and 3) activities that were associated with dyspnea before admission. The prevalence of dyspnea was identified, and tests of difference were performed across patient characteristics. Results We analyzed 67,362 patients, 12% of whom were obstetric patients. Fifty percent of patients were admitted to a medical-surgical unit after treatment in the emergency department. Among all noncritically ill inpatients, 16% of patients experienced dyspnea in the 24 hours before the admission. Twenty-three percent of patients admitted through the emergency department reported any dyspnea in the past 24 hours. Eleven percent experienced some current dyspnea when interviewed within 12 hours of admission with 4% of patients experiencing dyspnea that was rated 4 or greater. Dyspnea of 4 or more was present in 43% of patients admitted with respiratory diagnoses and 25% of patients with cardiovascular diagnoses. After multivariable adjustment for severity of illness and patient comorbidities, patients admitted on the weekend or during the overnight nursing shift were more likely to report dyspnea on admission. Conclusion Dyspnea is a common symptom among all hospitalized patients. Routine documentation of dyspnea is feasible in a large tertiary care center.

High-quality research is needed to improve quality of life for people with chronic refractory breathlessness in COPD. The joint American Thoracic Society (ATS)/European Respiratory Society (ERS) statement “An official American Thoracic Society/European Respiratory Society statement: research questions in COPD” by Celli et al. [1] is a timely summary of the current evidence and the questions that arise directly from where that evidence reaches its limits. Such documents are crucial in framing research strategies for researchers and research funders.

Effective management of dyspnea in chronic obstructive pulmonary disease (COPD) requires a clearer understanding of its underlying mechanisms. This roundtable reviews what is currently known about the neurophysiology of dyspnea with the aim of applying this knowledge to the clinical setting. Dyspnea is not a single sensation, having multiple qualitative descriptors. Primary sources of dyspnea include: (1) inputs from multiple somatic proprioceptive and bronchopulmonary afferents, and (2) centrally generated signals related to inspiratory motor command output or effort. Respiratory disruption that causes a mismatch between medullary respiratory motor discharge and peripheral mechanosensor afferent feedback gives rise to a distressing urge to breathe which is independent of muscular effort. Recent brain imaging studies have shown increased limbic system activation in response to various dyspneogenic stimuli and emphasize the affective dimension of this symptom. All of these mechanisms are likely instrumental in exertional dyspnea causation in COPD. Increased central motor drive (and effort) is required to increase ventilation during activity because the inspiratory muscles become acutely overloaded and functionally weakened. Abnormal dynamic ventilatory mechanics and excessive chemostimulation during exercise also result in a widening disparity between escalating central neural drive and restricted thoracic volume displacement. This neuromechanical uncoupling may form the basis for the distressing sensation of unsatisfied inspiration. Interventions that alleviate dyspnea in COPD do so by improving ventilatory mechanics, reducing central neural drive, or both-thereby partially restoring neuromechanical coupling of the respiratory system. Self-management strategies address the affective aspect of dyspnea and are essential to successful treatment.

BACKGROUND:Dyspnea (breathing discomfort) can be as powerfully aversive as pain, yet is not routinely assessed and documented in the clinical environment. Routine identification and documentation of dyspnea is the first step to improved symptom management and it may also identify patients at risk of negative clinical outcomes. OBJECTIVE:To estimate the prevalence of dyspnea and of dyspnea-associated risk among hospitalized patients. DESIGN:Two pilot prospective cohort studies. SETTING:Single academic medical center. PATIENTS:Consecutive patients admitted to four inpatient units: cardiology, hematology/oncology, medicine, and bariatric surgery. MEASUREMENTS:In Study 1, nurses documented current and recent patient-reported dyspnea at the time of the Initial Patient Assessment in 581 inpatients. In Study 2, nurses documented current dyspnea at least once every nursing shift in 367 patients. We describe the prevalence of burdensome dyspnea, and compare it to pain. We also compared dyspnea ratings with a composite of adverse outcomes: 1) receipt of care from the hospital's rapid response system, 2) transfer to the intensive care unit, or 3) death in hospital. We defined burdensome dyspnea as a rating of 4 or more on a 10-point scale. RESULTS:Prevalence of burdensome current dyspnea upon admission (Study 1) was 13% (77 of 581, 95% CI 11%-16%). Prevalence of burdensome dyspnea at some time during the hospitalization (Study 2) was 16% (57 of 367, 95% CI 12%-20%). Dyspnea was associated with higher odds of a negative outcome. CONCLUSIONS:In two pilot studies, we identified a significant symptom burden of dyspnea in hospitalized patients. Patients reporting dyspnea may benefit from a more careful focus on symptom management and may represent a population at greater risk for negative outcomes.

© W. S. Maney & Son Ltd 2015. Breathlessness remains a challenging symptom, common to a multitude of malignant and non-malignant diseases, for which there are limited effective therapies once disease control is optimized. The American Thoracic Society (ATS) statement on dyspnoea reports that: (i) progress in dyspnoea management has not matched progress in elucidating underlying mechanisms; (ii) there is a critical need for interdisciplinary translational research to connect dyspnoea mechanisms with treatments; and (iii) there is a need to validate dyspnoea measures as patient-reported outcomes for clinical trials. Research into the many dimensions of breathlessness and its significance to patients and their carers has increased in recent years. This meeting is convened yearly to bring together researchers across various disciplines including respiratory medicine, anaesthetics, medical humanities, engineering, and palliative care, t further understanding of the symptom, discuss new techniques and advances in research, and pave the way forward for future studies and interventions. The presentations generated much vibrant discussion amongst the multidisciplinary attendees and highlighted areas where care for breathless patients could be improved. This is a positive time for breathlessness research, with several ATS research priorities being addressed and it is clear that further studies and ensuing interventions are on the horizon.

Mouthpieces and masks change breathing, and distract the subject. Accepted non-invasive methods avoid this problem, inductive plethysmographs and respiratory magnetometers, but are expensive and unusable in magnetic resonance imaging (MRI) scanners. Because changes in ventilation affect arterial gases, and thus cerebral blood flow, measurement of breathing is desirable during many functional MRI studies. Using an old principle, we constructed an inexpensive, non-invasive device unaffected by magnetic fields. We adapted a simple calibration method to reduce error and make the method accessible to more users. 'Pneumobelts' consist of flexible corrugated silicon tubes worn around the rib cage (RC) and the abdomen (AB). Changes in RC and AB are determined from pressure changes within the 'pneumobelts'. Estimates of tidal volume are generated from the sum of the RC and AB changes. We empirically determined the appropriate RC weighting as 1.3:1 (RC:AB). Volume estimation was tested (n = 9) in different body positions and during different breathing maneuvers. The weighted sum of the two signals gave an accurate estimate of tidal volume with tidal volumes less than 1200 ml (mean error = 6-7%). Breaths over 1900 ml produced larger errors (mean error = 11-16%). Our results are generalizable to any linear circumference measuring device.

Study objectives: We sought to improve speech in tracheostomized individuals receiving positivepressure ventilation. Such individuals often speak with short phrases, long pauses, and have problems with loudness and voice quality. Subjects: We studied 15 adults with spinal cord injuries or neuromuscular diseases receiving long-term ventilation. Interventions: The ventilator was adjusted using lengthened inspiratory time (TI), positive end-expiratory pressure (PEEP), and combinations thereof. Results: When TI was lengthened (by 8 to 35% of the ventilator cycle), speaking time increased by 19% and pause time decreased by 12%. When PEEP was added (5 to 10 cm H2O), speaking time was 25% longer and obligatory pauses were 21% shorter. When lengthened TI and PEEP were combined (with or without reduced tidal volume), their effects were additive, increasing speaking time by 55% and decreasing pause time by 36%. The combined intervention improved speech timing, loudness, voice quality, and articulation. Individual differences in subject response to the interventions were substantial in some cases. We also tested high PEEP (15 cm H2O) in three subjects and found speech to be essentially identical to that produced with a one-way valve. Conclusions: These simple interventions markedly improve ventilator-supported speech and are safe, at least when used on a short-term basis. High PEEP is a safer alternative than a one-way valve. (CHEST 2003; 124:1512–1521)

Air hunger (uncomfortable urge to breathe) is a component of dyspnea (shortness of breath). Three human H215O positron emission tomography (PET) studies have identified activation of phylogenetically ancient structures in limbic and paralimbic regions during dyspnea. Other studies have shown activation of these structures during other sensations that alert the organism to urgent homeostatic imbalance: pain, thirst, and hunger for food. We employed blood oxygen level dependent (BOLD) functional magnetic resonance imaging (fMRI) to examine activation during air hunger. fMRI conferred several advantages over PET: enhanced signal-to-noise, greater spatial resolution, and lack of ionizing radiation, enabling a greater number of trials in each subject. Six healthy men and women were mechanically ventilated at 12–14 breaths/min. The primary experiment was conducted at mean end-tidal Pco2of 41 Torr. Moderate to severe air hunger was evoked during 42-s epochs of lower tidal volume (mean = 0.75 L). Subjects described the sensation as “like breath-hold,” “urge to breathe,” and “starved for air.” In the baseline condition, air hunger was consistently relieved by epochs of higher tidal volume (mean = 1.47 L). A control experiment in the same subjects under a background of mild hypocapnia (mean end-tidal PCO2= 33 Torr) employed similar tidal volumes but did not evoke air hunger, controlling for stimulus variables not related to dyspnea. During each experiment, we maintained constant end-tidal Pco2and PO2to avoid systematic changes in global cerebral blood flow. Whole-brain images were acquired every 5 s (T2*, 56 slices, voxel resolution 3 × 3 × 3 mm). Activations associated with air hunger were determined using voxel-based interaction analysis of covariance that compared data between primary and control experiments (SPM99). We detected activations not seen in the earlier PET study using a similar air hunger stimulus ( Banzett et al. 2000 ). Limbic and paralimbic loci activated in the present study were within anterior insula (seen in all 3 published studies of dyspnea), anterior cingulate, operculum, cerebellum, amygdala, thalamus, and basal ganglia. Elements of frontoparietal attentional networks were also identified. The consistency of anterior insular activation across subjects in this study and across published studies suggests that the insula is essential to dyspnea perception, although present data suggest that the insula acts in concert with a larger neural network.

Two men with high cervical spinal cord injuries and phrenic nerve pacers were studied with and without an elastic binder around the abdomen. Speech improved with the binder, as determined by listener preference ratings provided by 10 judges and by the subjects themselves. Improvement was substantial in one subject and slight in the other. The subject with the greater improvement exhibited higher peak tracheal pressure, higher sound pressure level, and longer utterance duration with the binder in place. Speech improvement was attributed primarily to augmentation of tidal volume associated with the use of the binder. An abdominal binder can be an effective intervention to improve speech in certain individuals with spinal cord injuries and phrenic nerve pacers. Speech may be further improved by using behavioral strategies, such as neck muscle activation, glossopharyngeal breathing, and pharyngeal or buccal speech production.

We directly compared convergent, discriminant and concurrent validity of the Dyspnoea-12 (D-12) and Multidimensional Dyspnoea Profile (MDP) in people with chronic obstructive pulmonary disease.Breathlessness measures (D-12, MDP, visual analogue scales and descriptors) were completed for two focal periods (daily life and end of walk test). Instrument structure (D-12 and MDP item grouping) was assessed with factor analysis. Differences between airflow severity stage and focal periods (ANOVA, t-test and Chi-squared test), associations between D-12 and MDP (r, r

Dyspnoea is defined as “breathing discomfort” [1]. The paper by GrOnseth et al. [2] in this issue of European Respiratory Journal ( ERJ ) reports the prevalence of dyspnoea in 15 countries throughout the world. There are few studies of dyspnoea in the general population available, so this added information is welcome. The overall prevalence of dyspnoea in their study population was 27%, which is not far out of line with several other studies dating from 1964 to the present [3–5]. Some studies, based on review of medical records, have reported much lower prevalence [6]. However, patients may neglect to report dyspnoea to their clinician because they think it does not reach a sufficient level of importance, or clinicians may fail to record what their patients say. Requiring patients to scale their symptoms can result in more uniform reporting, because the patient does not have to decide how much is reportable, it takes very little time and it facilitates uniform documentation. Busy clinicians may ask “is dyspnoea worth documenting?” One powerful argument for routine assessment is the need to reduce suffering, as with pain. A second argument is the emerging predictive value of dyspnoea in forecasting medical needs. In addition to being prevalent, “dyspnoea” is a powerfully aversive sensation [7] and patients deserve adequate management of this symptom, as passionately argued by Currow et al. [8]. Effective interventions exist and should be used [9–11]; assessing dyspnoea is the first step in managing it. Dyspnoea is frequently overlooked despite its prevalence and the severity of distress it causes [12]. For example, despite having had dyspnoea for months a majority of advanced cancer patients had not received any treatment for it [ …

There is growing awareness that dyspnoea, like pain, is a multidimensional experience, but measurement instruments have not kept pace. The Multidimensional Dyspnea Profile (MDP) assesses overall breathing discomfort, sensory qualities, and emotional responses in laboratory and clinical settings. Here we provide the MDP, review published evidence regarding its measurement properties and discuss its use and interpretation. The MDP assesses dyspnoea during a specific time or a particular activity (focus period) and is designed to examine individual items that are theoretically aligned with separate mechanisms. In contrast, other multidimensional dyspnoea scales assess recalled recent dyspnoea over a period of days using aggregate scores. Previous psychophysical and psychometric studies using the MDP show that: 1) subjects exposed to different laboratory stimuli could discriminate between air hunger and work/effort sensation, and found air hunger more unpleasant; 2) the MDP immediate unpleasantness scale (A1) was convergent with common dyspnoea scales; 3) in emergency department patients, two domains were distinguished (immediate perception, emotional response); 4) test–retest reliability over hours was high; 5) the instrument responded to opioid treatment of experimental dyspnoea and to clinical improvement; 6) convergent validity with common instruments was good; and 7) items responded differently from one another as predicted for multiple dimensions., The Multidimensional Dyspnea Profile provides a unified, reliable instrument for both clinical and laboratory research http://ow.ly/Ix8ic

Vagus nerve stimulation is used to reduce the frequency and intensity of seizures in patients with epilepsy. In the present study four such patients were studied while awake. We analyzed the physiological responses to vagus nerve stimulation over a broad range of tolerable stimulus parameters to identify vagal A-fiber threshold and to induce respiratory responses typical of C-fiber activation. A-fiber threshold was determined by increasing stimulation current until laryngeal motor A-fibers were excited (frequency=30 Hz). With A-fiber threshold established, C-fiber excitation was attempted with physiologically appropriate stimulus parameters (low frequency and high amplitude). Results: A-fiber thresholds were established in all patients, threshold currents ranged between 0.5 and 1.5 mA. Stimulation at lower frequency (2–10 Hz) and higher amplitudes (2.75–3.75 mA) did not produce cardiorespiratory effects consistent with C-fiber activation. It is possible that such effects were not observed because vagal C-fibers were not excited, because C-fiber effects were masked by the ‘wakeful drive’ to breathe, or because epilepsy or the associated therapy had altered central processing of the vagal afferent inputs.

Dyspnea in patients could arise from both an urge to breathe and increased effort of breathing. Two qualitatively different sensations, "air hunger" and "respiratory work and effort," arising from different afferent sources are hypothesized. In the laboratory, breathing below the spontaneous level may produce an uncomfortable sensation of air hunger, and breathing above it a sensation of work or effort. Measurement of a single sensory dimension cannot distinguish these as separate sensations; we therefore measured two sensory dimensions and attempted to vary them independently. In five normal subjects we obtained simultaneous ratings of air hunger and of work and effort while independently varying PCO(2) or the level of targeted voluntary breathing. We found a difference in response to the two stimulus dimensions: air hunger ratings changed more steeply when PCO(2) was altered and ventilation was constant; work or effort ratings changed more steeply when ventilation was altered and PCO(2) was constant. We conclude that "air hunger" is qualitatively different from "work and effort" and arises from different afferent sources.

Breathing sensations of AIR HUNGER, WORK and EFFORT may depend on projections of central motor discharge (corollary discharge) to the forebrain. Source of motor drive (brainstem or cortex) may determine what is perceived. To test the effect of changing motor discharge at constant ventilation, we induced partial neuromuscular blockade during hypercapnic hyperpnea (31 + or - 9 L min(-1); PET(CO(2))=49 + or - 2 Torr) and during matched volitional hyperpnea (34 + or - 5 L min(-1); PET(CO(2))=41 + or - 1 Torr). Decline of vital capacity was similar between conditions (39%). Ventilation was unchanged with paralysis, indicating increased respiratory motor drive to maintain hyperpnea. Sensations were rated on a seven point ordinal scale. Median EFFORT and WORK increased 3-3.5 points with paralysis during both forms of hyperpnea (P0.02, Wilcoxon signed rank). Median AIR HUNGER increased 2.5 points with paralysis during hypercapnic (P0.02) but not during volitional hyperpnea. Data suggests that EFFORT and WORK arise from motor cortex activity (subjects reported engaging volitional control when paralyzed even during hypercapnia) and suggests that AIR HUNGER arises from medullary motor activity.

We studied physiological and sensory effects of left cervical vagal stimulation in six adult patients receiving this stimulation as adjunctive therapy for intractable epilepsy. Stimulus strength varied among subjects from 0.1 to 2.1 microCoulomb (microC) per pulse, delivered in trains of 30-45 s at frequencies from 20 to 30 Hz; these stimulation parameters were standard in a North American study. The stimulation produced no systematic changes in ECG, arterial pressure, breathing frequency tidal volume or end-expiratory volume. Five subjects experienced hoarseness during stimulation. Three subjects with high stimulus strength (0.9-2.1 microC) recalled shortness of breath during stimulation when exercising; these sensations were seldom present during stimulation at rest. No subjects reported the thoracic burning sensation or cough previously reported with chemical stimulation of pulmonary C fibers. Four of six subjects (all those receiving stimuli at or above 0.6 microC) experienced a substantial reduction in monthly seizure occurrence at the settings used in our studies. Although animal models of epilepsy suggest that C fibers are the most important fibers mediating the anti-seizure effect of vagal stimulation, our present findings suggest that the therapeutic stimulus activated A fibers (evidenced by laryngeal effects) but was not strong enough to activate B or C fibers.

Breathlessness arises from increased medullary respiratory center activity projecting to the forebrain (respiratory corollary discharge hypothesis). Subjects with congenital central hypoventilation syndrome (CCHS) lack the normal hyperpnea and breathlessness during hypercapnia. The corollary discharge hypothesis predicts that if CCHS subjects have normal hyperpnea during exercise, they will experience normal breathlessness during exercise. To test this, we studied four CCHS subjects and six matched controls during an exhausting constant-load cycling test requiring substantial anaerobiosis. CCHS subjects rated significantly less breathlessness at the end of the test than controls, but ventilation (index of respiratory corollary discharge) was also somewhat lower in CCHS (not significant). In both groups, breathlessness increased disproportionately more than ventilation towards the end of exercise. These data failed to disprove the corollary discharge hypothesis of breathlessness, but do suggest that the relationship between ventilation and breathlessness is non-linear and/or that projections of chemoreceptor afferents to the forebrain (presumed lacking in CCHS) is one source of breathlessness in normals.

Competition between airflow requirements for speaking and gas exchange occurs in ventilator-dependent tracheotomized subjects who can `steal' air from alveolar ventilation during the ventilator's inflation phase to produce sound. We wondered whether these subjects adopted strategies to minimize hypoventilation when speaking, particularly when ventilatory drive and respiratory discomfort are increased by hypercapnia. We recorded speech and ventilatory and speaking volumes in five ventilated subjects during reading and extemporaneous speech. All subjects spoke during the ventilator's inflation (and expiratory) phase, losing approximately 15% of their inspired tidal volume. During induced hypercapnia (15 mmHg increase in P et CO 2 ) which caused shortness of breath, all subjects could still speak adequately. Two subjects `adapted' to hypercapnia by reducing the air used for speaking during inflation. In contrast, one subject reacted, as normal subjects do, by increasing the airflow per syllable (a mal-adaptive strategy in ventilated subjects). These changes were modest despite the strong hypercapnic stimulus.

We administered lidocaine aerosol intratracheal anesthesia to a ventilator-dependent, tracheostomized C1-C2 tetraplegie subject to determine its effect on her ability to detect small changes in tidal volume. A psychophysical test of volume detection was given before and immediately after a 20 percent lidocaine aerosol was delivered through the subject’s cuffed tracheostomy tube. On each of three occasions, she reliably (p

We tested whether subjects could detect and localize inflation confined to a single lung lobe. A balloon-sealed catheter was placed into a lobar bronchus of unsedated subjects via fiberoptic bronchoscopy. Topical anesthesia (lidocaine) was used to suppress cough and irritation associated with inflation of the sealing balloon. Small (45–60 ml) or large (100–240 ml) stimulus volumes were insufflated via the catheter. In a forced-choice protocol, subjects were readily able to detect large inflations and correctly identify the side on which the stimulus was given, but small inflations were at the threshold of detection and were not correctly localized. Additional lidocaine applied to the bronchus in two subjects did not degrade detection. Circumstantial evidence suggests that the sensation arose in the lung. We conclude that this technique is feasible for the study of pulmonary perception.

Six subjects who were tracheostomized and chronically ventilator-supported because of neuromuscular disease or injury were studied to determine if their speech could be improved. Using subjects' own portable ventilators, adjustments were made that reduced inspiratory flow and added positive end-expiratory pressure (PEEP). These adjustments resulted in increases in speaking time per ventilator cycle, increases in number of syllables produced per cycle, and decreases in peak tracheal pressure. Improvements in speech were perceptible to listeners in 3 of the 6 subjects. Listeners preferred speech produced under the ventilator-adjusted condition primarily because the quantity of speech produced per ventilator cycle increased, loudness fluctuation decreased, and voice quality improved. The only subject who showed no perceptible benefit from the adjustments had a substantial air leak around her tracheostomy tube. Importantly, gas exchange was not compromised in any of the subjects. We believe that adjustments such as prolonging inspiration and adding PEEP, when implemented in collaboration with appropriate health-care professionals, represent a simple, inexpensive, and safe intervention for improving speech in certain ventilator-supported individuals.

Dyspnea assessment is valuable in diagnosis, prognosis, symptom management, and targeted intervention, and in the allotment and management of patient care resources. The assessment of dyspnea, like that of pain, depends on patient self-report. Expert consensus panels have called for dyspnea to be measured quantitatively and documented on a routine basis, as is the practice with pain. But little information is available on how to measure and record dyspnea ratings systematically. Consequently, the prevalence of dyspnea in hospital settings may be greater than is generally recognized, and dyspnea may be insufficiently managed. This article describes a pilot study that sought to test the feasibility of measuring dyspnea as part of the initial patient assessment performed by nurses within several inpatient units of a large urban hospital.

Hypercapnia produces an uncomfortable urge to breathe (‘air hunger’), which is alleviated by increasing breathing. It has been postulated that awake humans control breathing partly to minimize these sensations; such behavioral control presumably involves the forebrain. To test this postulate, we compared the ventilatory response to hypercapnia when the subject breathed spontaneously to the response when the subject used forebrain commands to control ventilation—on the basis of minimizing air hunger (achieved with subject-controlled positive pressure ventilation). In six healthy adults during hypercapnia (46 mmHg), spontaneous ventilation significantly exceeded, by 17%, the level of (mechanical) ventilation needed to alleviate air hunger. This suggests that spontaneous breathing is not behaviorally controlled to minimize discomfort. Alternatively, mechanical ventilation confers an additional relief of air hunger beyond that provided by spontaneous breathing. Since mechanical ventilation (with reduced respiratory muscle contraction) was more effective than spontaneous breathing in relieving air hunger, our results also suggest afferents that signal the degree of respiratory muscle contraction do not contribute to air hunger relief.

Hypercapnia evokes an uncomfortable sensation, termed 'air hunger'. We examined the relationship between PETCO2 and ratings of air hunger intensity under three conditions in 16 subjects: 1) mechanical ventilation with hyperoxic gas mixtures at fixed frequency and tidal volume (twice resting ventilation), 2) the same mechanical ventilation, but with hypoxic gas mixture, 3) spontaneous breathing with hyperoxic gas mixture. In each case, PETCO2 was varied randomly among several levels, each held for 5 min. During hyperoxic mechanical ventilation, the mean threshold for air hunger sensation was 43 Torr, i.e., 4 Torr above resting PETCO2; intolerable air hunger was evoked by 50 Torr. The threshold and tolerable levels of PETCO2 varied among individuals, but were not well correlated with their ventilatory responses to CO2. Hypoxia (PETO2 60-75 Torr) shifted the PETCO2 at both threshold and tolerance down by only 2 Torr. Breathing greatly reduced the air hunger experienced at any given PETCO2 (threshold increased 5 Torr, and sensitivity decreased 50%).

We present a simple and reliable method to calibrate respiratory magnetometers and Respitrace to infer respiratory volume changes. As in earlier methods, we assume two degrees of freedom in the chest wall and that volume displacement depends linearly on surface motion at the rib cage and abdomen. Because the area of the rib cage is larger, a given motion of its surface produces a greater lung volume change; therefore, the rib cage motion signal is given a larger gain before the two signals are added to estimate volume. In contrast to earlier methods, we use a “standard ratio” to weight relative gains of the rib cage and abdominal signals for all subjects rather than determining a gain ratio for each individual subject. Our procedure does not require subjects to perform the sometimes difficult isovolume maneuvers used in the calibration method of Konno and Mead (J. Appl. Physiol. 22: 407–422, 1967), does not require statistical computation used in the multiple-breath linear regression method, and does not produce the occasional substantial errors in gain ratio that may occur with the other methods. When magnetometers are used, the standard ratio is 4:1 (rib cage-to-abdomen); when Respitrace is used, the standard ratio is 2:1. In 11 subjects, calibration with standard ratios was as accurate as the isovolume and linear regression techniques. Accuracy during normal breathing was nearly always within 10% (median 2%), but occasional large errors occurred with both instruments.

Background Most measures of dyspnea assess a single aspect (intensity or distress) of the symptom. We developed the Multidimensional Dyspnea Profile (MDP) to measure qualities and intensities of the sensory dimension and components of the affective dimension. The MDP is not indexed to a particular activity and can be applied at rest, during exertion, or during clinical care. We report on the development and testing of the MDP in patients with a variety of acute and chronic cardiopulmonary conditions. Methods One hundred fifty-one adults admitted to the ED with breathing symptoms completed the MDP three times in the ED, twice at least 1 h apart (T1, T2), and near discharge from the ED (T3). Measures were repeated in 68 patients twice in a follow-up session 4 to 6 weeks later (T4-T5). The ED sample was 56% men with a mean age of 53 ± 15 years; the follow-up sample was similar. Results Factor analysis resulted in a two-factor solution with a total explained variance of 63%, 74%, and 72% at T1, T2, and T3, respectively. One domain related to primary sensory qualities and immediate unpleasantness, and the second encompassed emotional response. For the two domains, Cronbach α ranged from 0.82 to 0.95, and the intraclass correlation coefficient ranged from 0.91 to 0.98. Repeated-measures analysis was significant for change (T1, T3, T4), showing responsiveness to change in MDP domains with treatment (F[2,66] = 19.67, P > .001). Conclusions These analyses support the reliability, validity, and responsiveness to clinical change of the MDP with two domains in an acute care and follow-up setting.

Study Objective: To describe the subjective experience and the physiologic effects of endotracheal intubation and complete neuromuscular block in unsedated humans. Setting: Metropolitan V.A. Hospital. Patients: 4 healthy, unsedated volunteers. Interventions: Subjects' tracheas were incubated using topical anesthesia, then subjects were completely paralyzed with vecuronium and mechanically ventilated at various endtidal partial pressure of carbon dioxide (P ET CO 2 ) levels, all without sedation. Measurements and Main Results: Heart rate (HR), blood pressure, oxygen saturation by pulse oximeter (SpO 2 ), and P ET CO 2 were measured. Sul bjects' verbatim descriptions of their experiences and answers to systematic questions were recorded after the experiments. All subjects reported that tracheal intubation was a very unpleasant experience. None of the subjects found paralysis itself to be distressing, and it did not affect mention. Subjects felt breathless when P ET CO 2 was even slightlyelevated. HR was increased by intubation, but not by paralysis. All subjects reported sore throat, muscle aches, fever, and fatigue lasting up to 24 hours after the experiment. One subject experienced nausea and vomiting. Another subject experienced a sore throat that persisted for weeks due to a vocal cord ulcer, which resolved spontaneously. All subjects' SPO 2 levels after the experiment were below their pre-experiment baselines. Conclusions: Our findings suggest that paralysis of healthy, knowledgeable, and psychologically well-prepared subjects for experimental purposes is feasible but may result in unpleasant, self-limiting after effects. Further, we conclude that, in any case of awake paralysis, close attention should be paid to arterial PCO 2 , adequate sedation and analgesia, minimization of pain during procedures, psychological support, and maintenance of communication when possible.