Treatment of Acute Dyspnea with Morphine to Avert Respiratory Failure.
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ABSTRACT:
SUBMITTER: Soffler MI
PROVIDER: S-EPMC6276783 | biostudies-literature | 2017 Apr
REPOSITORIES: biostudies-literature
Publications
Treatment of Acute Dyspnea with Morphine to Avert Respiratory Failure.
Soffler Morgan I MI Rose Alexandra A Hayes Margaret M MM Banzett Robert R Schwartzstein Richard M RM
Annals of the American Thoracic Society 20170401 4
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Project description:BackgroundMorphine relieves dyspnea in various clinical circumstances. Whether or not this applies to patients admitted to intensive care units (ICUs) for acute respiratory failure (ARF) is unknown. We evaluated the efficacy and safety of low-dose morphine on dyspnea in patients admitted to the ICU for ARF.MethodsIn this single-center, double-blind, phase 2, randomized, controlled trial, we assigned non-intubated adults admitted to the ICU for ARF with severe dyspnea, defined by a visual analog scale for dyspnea (dyspnea-VAS) from zero (no dyspnea) to 100 mm (worst imaginable dyspnea) ≥40 mm, to receive a low dose of Morphine Hydrochloride (intravenous titration followed by subcutaneous relay) or Placebo. All patients received standard therapy, including etiological treatment and non-invasive respiratory support.ResultsTwenty-two patients were randomized, 11 in each group. The average dyspnea (median [interquartile range]) over 24 hours did not significantly differ between the two groups (40 [25 - 43] mm in the Morphine group vs. 40 [36 - 49] mm in the Placebo group, p=0.411). Dyspnea-VAS was lower in the Morphine group than in the Placebo group at the end of intravenous titration (30 [11 - 30] vs. 35 [30 - 44], p=0.044) and four hours later (18 [10 - 29] vs. 50 [30 - 60], p=0.043). The cumulative probability of intubation was higher in the Morphine group than in the Placebo group (p=0.046) CONCLUSION: In this phase 2 pilot trial, morphine did not improve 24-hour average dyspnea in adult patients with ARF, even though it had a statistically significant immediate effect. Of concern, Morphine use was associated with a higher intubation rate.Trial registrationThe protocol was declared on the ClinicalTrial.gov database (no. NCT04358133) and was published in September 2022.
| S-EPMC11251226 | biostudies-literature
Project description:BackgroundDyspnea is common and severe in intensive care unit (ICU) patients managed for acute respiratory failure. Dyspnea appears to be associated with impaired prognosis and neuropsychological sequels. Pain and dyspnea share many similarities and previous studies have shown the benefit of morphine on dyspnea in patients with end-stage onco-hematological disease and severe heart or respiratory disease. In these populations, morphine administration was safe. Here, we hypothesize that low-dose opioids may help to reduce dyspnea in patients admitted to the ICU for acute respiratory failure. The primary objective of the trial is to determine whether the administration of low-dose titrated opioids, compared to placebo, in patients admitted to the ICU for acute respiratory failure with severe dyspnea decreases the mean 24-h intensity of dyspnea score.MethodsIn this single-center double-blind randomized controlled trial with 2 parallel arms, we plan to include 22 patients (aged 18-75 years) on spontaneous ventilation with either non-invasive ventilation, high flow oxygen therapy or standard oxygen therapy admitted to the ICU for acute respiratory failure with severe dyspnea. They will be assigned after randomization with a 1:1 allocation ratio to receive in experimental arm administration of low-dose titrated morphine hydrochloride for 24 h consisting in an intravenous titration relayed subcutaneously according to a predefined protocol, or a placebo (0.9% NaCl) administered according to the same protocol in the control arm. The primary endpoint is the mean 24-h dyspnea score assessed by a visual analog scale of dyspnea.DiscussionTo our knowledge, this study is the first to evaluate the benefit of opioids on dyspnea in ICU patients admitted for acute respiratory failure.Trial registrationClinicalTrials.gov NCT04358133 . Registered on 24 April 2020.
| S-EPMC9523987 | biostudies-literature
Project description:INTRODUCTION AND OBJECTIVES:Dyspnea is the most common symptom among hospitalized patients with heart failure (HF) but besides dyspnea questionnaires (which reflect the subjective patient sensation and are not fully validated in HF) there are no measurable physiological variables providing objective assessment of dyspnea in a setting of acute HF patients. Studies performed in respiratory patients suggest that the measurement of electromyographic (EMG) activity of the respiratory muscles with surface electrodes correlates well with dyspnea. Our aim was to test the hypothesis that respiratory muscles EMG activity is a potential marker of dyspnea severity in acute HF patients. METHODS:Prospective and descriptive pilot study carried out in 25 adult patients admitted for acute HF. Measurements were carried out with a cardio-respiratory portable polygraph including EMG surface electrodes for measuring the activity of main (diaphragm) and accessory (scalene and pectoralis minor) respiratory muscles. Dyspnea sensation was assessed by means of the Likert 5 questionnaire. Data were recorded during 3 min of spontaneous breathing and after breathing at maximum effort for several cycles for normalizing data. An index to quantify the activity of each respiratory muscle was computed. This assessment was carried out within the first 24 h of admission, and at day 2 and 5. RESULTS:Dyspnea score decreased along the three measured days. Diaphragm and scalene EMG index showed a positive and significant direct relationship with dyspnea score (p<0.001 and p = 0.003 respectively) whereas pectoralis minor muscle did not. CONCLUSION:In our pilot study, diaphragm and scalene EMG activity was associated with increasing severity of dyspnea. Surface respiratory EMG could be a useful objective tool to improve assessment of dyspnea in acute HF patients.
| S-EPMC7190138 | biostudies-literature
Project description: Not available
| S-EPMC8019335 | biostudies-literature
Project description:RationaleOpioids are commonly used to relieve dyspnea, but clinical data are mixed and practice varies widely.ObjectivesEvaluate the effect of morphine on dyspnea and ventilatory drive under well-controlled laboratory conditions.MethodsSix healthy volunteers received morphine (0.07 mg/kg) and placebo intravenously on separate days (randomized, blinded). We measured two responses to a CO(2) stimulus: (1) perceptual response (breathing discomfort; described by subjects as "air hunger") induced by increasing partial pressure of end-tidal carbon dioxide (Pet(CO2)) 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 resultsWe determined the Pet(CO2) that produced a 60% breathing discomfort rating in each subject before morphine (median, 8.5 mm Hg above resting Pet(CO2)). At the same Pet(CO2) after morphine administration, median breathing discomfort was reduced by 65% of its pretreatment value; P < 0.001. Ventilation fell 28% at the same Pet(CO2); 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.
| S-EPMC3208656 | biostudies-literature
Project description:BackgroundThe acute heart failure (AHF) Syndromes International Working Group proposed that dyspnea be assessed under standardized, incrementally provocative maneuvers and called for studies to assess the feasibility of this approach. We sought to assess the feasibility and statistical characteristics of a novel provocative dyspnea severity score (pDS) versus the traditional dyspnea visual analog scale (DVAS) in an AHF trial.MethodsAt enrollment, 24, 48 and 72hours, 230 ROSE-AHF patients completed a DVAS. Dyspnea was then assessed with 5-point Likert dyspnea scales administered during 4 stages (A: upright-with O2, B: upright-without O2, C: supine-without O2 and D: exercise-without O2). Patients with moderate or less dyspnea were eligible for the next stage.ResultsAt enrollment, oxygen withdrawal and supine provocation were highly feasible (≥97%), provoking more severe dyspnea (≥1 Likert point) in 24% and 42% of eligible patients, respectively. Exercise provocation had low feasibility with 38% of eligible patients unable to exercise due to factors other than dyspnea. A pDS was constructed from Likert scales during the 3 feasible assessment conditions (A-C). Relative to DVAS, the distribution of the pDS was more skewed with a high "ceiling effect" at enrollment (23%) limiting sensitivity to change. Change in pDS was not related to decongestion or 60-day outcomes.ConclusionsAlthough oxygen withdrawal and supine provocation are feasible and elicit more severe dyspnea, exercise provocation had unacceptable feasibility in this AHF cohort. The statistical characteristics of a pDS based on feasible provocation measures do not support its potential as a robust dyspnea assessment tool in AHF.
| S-EPMC4748181 | biostudies-literature
Project description:BackgroundAcute respiratory distress syndrome (ARDS) is a life-threatening condition resulting from acute pulmonary inflammation. However, no specific treatment for ARDS has yet been developed. Previous findings suggest that lung injuries related to ARDS could be regulated by endocan (Esm-1). The aim of this study was to evaluate the potential efficiency of endocan in the treatment of ARDS.MethodsWe first compared the features of acute pulmonary inflammation and the severity of hypoxemia in a tracheal LPS-induced acute lung injury (ALI) model performed in knockout (Esm1-/-) and wild type (WT) littermate C57Bl/6 mice. Next, we assessed the effects of a continuous infusion of glycosylated murine endocan in our ALI model in Esm1-/- mice.ResultsIn our ALI model, we report higher alveolar leukocytes (p < 0.001), neutrophils (p < 0.001), and MPO (p < 0.001), and lower blood oxygenation (p < 0.001) in Esm1-/- mice compared to WT mice. Continuous delivery of glycosylated murine endocan after LPS-induced ALI resulted in decreased alveolar leukocytes (p = 0.012) and neutrophils (p = 0.012), higher blood oxygenation levels (p < 0.001), and reduced histological lung injury (p = 0.04), compared to mice treated with PBS.ConclusionsEndocan appears to be an effective treatment in an ARDS-like model in C57Bl/6 mice.
| S-EPMC9857156 | biostudies-literature
Project description:ObjectivesDespite decades of research, the acute respiratory distress syndrome remains associated with significant morbidity and mortality. This Concise Definitive Review provides a practical and evidence-based summary of treatments in addition to low tidal volume ventilation and their role in the management of severe respiratory failure in acute respiratory distress syndrome.Data sourcesWe searched the PubMed database for clinical trials, observational studies, and review articles describing treatment adjuncts in acute respiratory distress syndrome patients, including high positive end-expiratory pressure strategies, recruitment maneuvers, high-frequency oscillatory ventilation, neuromuscular blockade, prone positioning, inhaled pulmonary vasodilators, extracorporeal membrane oxygenation, glucocorticoids, and renal replacement therapy.Study selection and data extractionResults were reviewed by the primary author in depth. Disputed findings and conclusions were then reviewed with the other authors until consensus was achieved.Data synthesisSevere respiratory failure in acute respiratory distress syndrome may present with refractory hypoxemia, severe respiratory acidosis, or elevated plateau airway pressures despite lung-protective ventilation according to acute respiratory distress syndrome Network protocol. For severe hypoxemia, first-line treatment adjuncts include high positive end-expiratory pressure strategies, recruitment maneuvers, neuromuscular blockade, and prone positioning. For refractory acidosis, we recommend initial modest liberalization of tidal volumes, followed by neuromuscular blockade and prone positioning. For elevated plateau airway pressures, we suggest first decreasing tidal volumes, followed by neuromuscular blockade, modification of positive end-expiratory pressure, and prone positioning. Therapies such as inhaled pulmonary vasodilators, glucocorticoids, and renal replacement therapy have significantly less evidence in favor of their use and should be considered second line. Extracorporeal membrane oxygenation may be life-saving in selected patients with severe acute respiratory distress syndrome but should be used only when other alternatives have been applied.ConclusionsSevere respiratory failure in acute respiratory distress syndrome often necessitates the use of treatment adjuncts. Evidence-based application of these therapies in acute respiratory distress syndrome remains a significant challenge. However, a rational stepwise approach with frequent monitoring for improvement or harm can be achieved.
| S-EPMC6277052 | biostudies-literature
Project description:Acute respiratory failure occurs in up to half of patients with haematological malignancies and 15% of those with solid tumours or solid organ transplantation. Mortality remains high. Factors associated with mortality include a need for invasive mechanical ventilation, organ dysfunction, older age, frailty or poor performance status, delayed intensive care unit admission, and acute respiratory failure due to an invasive fungal infection or unknown cause. In addition to appropriate antibacterial therapy, initial clinical management aims to restore oxygenation and predict the most probable cause based on variables related to the underlying disease, acute respiratory failure characteristics, and radiographic findings. The cause of acute respiratory failure must then be confirmed using the most efficient, least invasive, and safest diagnostic tests. In patients with acute respiratory failure of undetermined cause, a standardised diagnostic investigation should be done immediately at admission before deciding whether to perform more invasive diagnostic procedures or to start empirical treatments. Collaborative and multidisciplinary clinical and research networks are crucial to improve our understanding of disease pathogenesis and causation and to develop less invasive diagnostic strategies and more targeted treatment options.
| S-EPMC7185453 | biostudies-literature
Project description: Not available
| S-EPMC8143984 | biostudies-literature