American journal of respiratory and critical care medicine最新文献

Rationale: No systematic investigation into dyspnea in patients receiving prolonged ventilation (>21 days) after recovering from critical-illness has been published.

Objectives: To determine magnitude, nature and pathophysiological basis of dyspnea during an unassisted-breathing trial in prolonged-ventilation patients.

Methods: Dyspnea intensity and descriptor selection were investigated in 27 prolonged-ventilation patients during a 60-min unassisted-breathing trial. Pressure-time product (PTP), respiratory mechanics, and transcutaneous PCO₂ (PtcCO₂) were also measured.

Measurements and main results: Of 10 patients who reported dyspnea during assist-control ventilation, 9 (90.0%) selected "Not getting enough air" to characterize dyspnea. Tidal-volume setting was lower in dyspneic than non-dyspneic patients: 480.0 versus 559.4 ml (p<0.046). During the unassisted-breathing trial (n=26), patients developed increases in dyspnea (p<0.01) and PtcCO2 (p<0.01), but no change in minute ventilation. Dyspnea score was strongly linked to PtcCO2 (p<0.012) and airway resistance (p<0.013) but not respiratory work (although PTP was almost 3 times higher than normal). At 60 min into the trial, 83.3% of patients selected "Not getting enough air" on its own or in combination with "Too much effort" to describe discomfort whereas only 16.7% selected "Too much effort" on its own (p<0.001). Across the dyspnea spectrum, patients chose "Not getting enough air" overwhelmingly over other descriptor options (p<0.001).

Conclusions: Patients developed increases in dyspnea and PtcCO₂ but unchanged minute ventilation and work of breathing during an unassisted-breathing trial; patients selected air-hunger descriptors overwhelmingly over excessive effort; the observations support the belief that air hunger results from heightened respiratory-center stimulation combined with incapacity to increase minute ventilation.

Rationale: High flow therapy reduces dyspnea in acute respiratory failure but the underlying mechanisms are not fully elucidated.

Objectives: To compare dyspnea, airway occlusion pressure (P_0.1) and inspiratory work with and without nasal high flow (NHF, FiO₂ 21%, temperature 31°C) in intubated patients under pressure support ventilation and during a spontaneous breathing trial (SBT).

Methods: Dyspnea (numerical rating scale, NRS and Mechanical Ventilation - Respiratory Distress Observational Scale, MV-RDOS), P_0.1, esophageal pressure, respiratory muscles EMG, arterial blood gas were compared in intubated patients on pressure support ventilation presenting a dyspnea-NRS > 3 during two sequences: 1) pressure support ventilation with NHF at 0 L/min followed by 30, 50 and 60 L/min (the last three were randomized) and 2) a SBT with NHF at 0 and 50 L/min (randomized).

Measurements and main results: Twenty patients were included. During pressure support ventilation, as compared to dyspnea-NRS that was 5 (4 - 6) at NHF 0 L/min, dyspnea-NRS was 3 (2 - 6) and 3 (2 - 5) at NHF 30L/min and NHF 50L/min, respectively (p<0.05). However, there was no change in MV-RDOS, P_0.1, esophageal pressure, respiratory muscles EMG and gas exchange. During the SBT, at NHF 50 L/min, dyspnea-NRS and P_0.1 were lower than during the SBT at NHF 0 L/min (p<0.01 and p=0.04 respectively) whereas MV-RDOS, esophageal pressure, respiratory muscles EMG did not change as compared to SBT with NHF 0 L/min.

Conclusions: In orally intubated patients, nasal high flow was associated with lower dyspnea and lower respiratory drive without affecting the inspiratory work.

Rationale: Unrecognised coronary artery disease (CAD) may contribute to adverse outcomes in chronic obstructive pulmonary disease (COPD). Improved identification of at-risk groups could inform better preventative care. We aimed to evaluate the burden and relationships of radiologically detectable CAD in COPD, establish frequency of occult disease, and examine potential cardiovascular screening methods.

Methods: Using CT coronary angiogram (CTCA), we prospectively evaluated CAD in 50 patients with COPD compared to age, sex-matched controls. In those with COPD, the relationship of CAD to cardiac symptoms (chest pain, dyspnoea), functional capacity (six-minute walk), exacerbations and inflammation was assessed. The performance of screening tests (cardiovascular risk scores, biomarkers and CT thorax-derived coronary artery calcium score (CACS-Tx)) were evaluated using receiver operator curves.

Results: CAD was present in 88% of patients with COPD (42% had obstructive (≥50% stenosis of any vessel) and 28% severe obstructive (≥70%) disease). Rates of obstructive (OR 3·1 (95%CI 1·1-8·9) P=0·037) and severe obstructive CAD (OR 10·1(95%CI 1·9-52·7) P=0·006) were higher in COPD than controls. In the COPD group, those with CAD had greater functional impairments but not dyspnoea scores, and 75% reported no chest pain or prior IHD. CAD was more extensive in those with increased systemic inflammation (fibrinogen, c-reactive protein, leucocyte, and neutrophil count), bronchial wall thickening, and sputum bacterial growth but bore no relation to exacerbation frequency. CACS-Tx was an effective screening tool, with an area under the curve for CAD of 0·98 (95%CI 0·95-1·00) and obstructive CAD of 0·89 (95%CI 0·79-1·00).

Conclusions: CTCA-detected CAD is common in patients with COPD, correlating poorly with symptoms and risk scores. Radiological screening, using CT thorax, might improve detection and outcomes in this patient group.

Chronic obstructive pulmonary disease (COPD) is a heterogenous lung condition characterized by progressive airflow obstruction. Despite advancements in diagnosis and treatment, the disease burden remains high; although clinical trials have shown improvements in outcomes such as exacerbations, quality of life, and lung function, improvement may not be attainable for many patients. For patients who do experience improvement, it is challenging to set management goals given the progressive nature of COPD. We therefore propose disease stability as an appropriate and attainable treatment goal. Other disease areas have developed definitions of no disease activity or remission, which provide relevant information for defining and achieving stability for patients with COPD. Disease stability builds on related concepts already defined in COPD such as clinical control and clinically important deterioration. Current components that could form part of a disease stability definition include exacerbations, health status (including quality of life and symptoms) and lung function. Considerations should be given to intervals over which stability is defined and assessed, appropriate thresholds, and defining a composite. Ensuring a holistic approach, objective measurements and harmonious, clear communication between patients and physicians can further support establishing disease stability. Here we propose a preliminary definition of disease stability, informed by existing research in COPD. Further research will be needed to validate the framework for use in clinical and research settings. Exploring disease stability as a goal, however, is an opportunity to develop and validate an attainable treatment target to advance the standard of care for patients with COPD.