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Hl Dept of Biological & Medical Sciences
Background. Inhaled furosemide offers a potentially novel treatment for dyspnoea, which may reflect modulation of pulmonary stretch receptor feedback to the brain. Specificity of relief is unclear because different neural pathways may account for different components of clinical dyspnoea. Our objective was to evaluate if inhaled furosemide relieves the air hunger component (uncomfortable urge to breathe) but not the sense of breathing work/effort of dyspnoea. Methods. A randomised, double blind, placebo-controlled crossover trial in 16 healthy volunteers studied in a university research laboratory. Each participant received 3 mist inhalations (either 40 mg furosemide or 4 ml saline) separated by 30–60 min on 2 test days. Each participant was randomised to mist order ‘furosemide-saline-furosemide’ (n- = 8) or ‘saline-furosemide-saline’ (n = 8) on both days. One day involved hypercapnic air hunger tests (mean ± SD PCO2 = 50 ± 3.7 mmHg; constrained ventilation = 9 ± 1.5 L/min), the other involved work/effort tests with targeted ventilation (17 ± 3.1 L/min) and external resistive load (20cmH2O/L/s). Primary outcome was ratings of air hunger or work/effort every 15 s on a visual analogue scale. During saline inhalations, 1.5 mg furosemide was infused intravenously to match the expected systemic absorption from the lungs when furosemide is inhaled. Corresponding infusions of saline during furosemide inhalations maintained procedural blinding. Average visual analogue scale ratings (%full scale) during the last minute of air hunger or work/effort stimuli were analysed using Linear Mixed Methods. Results. Data from all 16 participants were analysed. Inhaled furosemide relative to inhaled saline significantly improved visual analogues scale ratings of air hunger (Least Squares Mean ± SE − 9.7 ± 2%; p = 0.0015) but not work/effort (+ 1.6 ± 2%; p = 0.903). There were no significant adverse events. Conclusions. Inhaled furosemide was effective at relieving laboratory induced air hunger but not work/effort in healthy adults; this is consistent with the notion that modulation of pulmonary stretch receptor feedback by inhaled furosemide leads to dyspnoea relief that is specific to air hunger, the most unpleasant quality of dyspnoea.
Objective. The study aimed to evaluate the impact of a multidisciplinary inpatient heart failure team (HFT) on treatment, hospital readmissions and mortality of patients with decompensated heart failure (HF). Methods A retrospective service evaluation was undertaken in a UK tertiary centre university hospital comparing 196 patients admitted with HF in the 6 months prior to the introduction of the HFT (pre-HFT) with all 211 patients seen by the HFT (post-HFT) during its first operational year. Results. There were no significant differences in patient baseline characteristics between the groups. Inpatient mortality (22% pre-HFT vs 6% post-HFT; p<0.0001) and 1-year mortality (43% pre-HFT vs 27% post-HFT; p=0.001) were significantly lower in the post-HFT cohort. Post-HFT patients were significantly more likely to be discharged on loop diuretics (84% vs 98%; p=<0.0001), ACE inhibitors (65% vs 76%; p=0.02), ACE inhibitors and/or angiotensin receptor blockers (83% vs 91%; p=0.02), and mineralocorticoid receptor antagonists (44% vs 68%; p<0.0001) pre-HFT versus post-HFT, respectively. There was no difference in discharge prescription rates of betablockers (59% pre-HFT vs 63% post-HFT; p=0.45). The mean length of stay (17±19 days pre-HFT vs 19±18 days post-HFT; p=0.06), 1-year all-cause readmission rates (46% pre-HFT vs 47% post-HFT; p=0.82) and HF readmission rates (28% pre-HFT vs 20% post-HFT; p=0.09) were not different between the groups. Conclusions. The introduction of a specialist inpatient HFT was associated with improved patient outcome. Inpatient and 1-year mortality were significantly reduced. Improved use of evidence-based drug therapies, more intensive diuretic use and multidisciplinary care may contribute to these differences in outcome.