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Karl Swedberg, Relaxing from dyspnoea, European Heart Journal, Volume 35, Issue 16, 21 April 2014, Pages 1017–1018, https://doi.org/10.1093/eurheartj/eht567
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Extract
This editorial refers to ‘Serelaxin in acute heart failure patients with preserved left ventricular ejection fraction: results from the RELAX-AHF trial’†, by G. Filipatos et al., on page 1041
Breathing differs from other vital functions in that it is regulated not only by automatic centres located in the brainstem but also by voluntary signals initiated in the cortex.1 Dyspnoea is the most prevalent symptom in heart failure and it is experienced in different ways and reported with several qualitative expressions. It seems as though dyspnoea associated with heart failure is different from the dyspnoea associated with pulmonary disease and is felt as being more suffocating than in other conditions.1,2
The pathophysiology behind dyspnoea is complex and incompletely understood. The mechanisms include haemodynamic, pulmonary, muscular, and factors in the central nervous system.1,3,4 The most simplistic approach in heart failure is that dyspnoea is a direct expression of elevated pulmonary intracapillary pressures and the ensuing increased intrapulmonary water.5