The following is a summary of “Excess ventilation and exertional dyspnoea in heart failure and pulmonary hypertension” published in the November 2022 issue of Respiratory by Neder et al.
Exertional dyspnoea often results from alveolar hyperventilation and/or increased physiological dead space (excess ventilation), both of which occur when ventilation rates exceed metabolic needs. Patients with pulmonary arterial hypertension (PAH), chronic thromboembolic pulmonary hypertension (CTEPH), and heart failure (HF) with reduced (HFrEF) or preserved (HFpEF) ejection fraction has been found to benefit greatly from the use of supplemental ventilation (CTEPH).
In this article, researchers give the attending physician the tools they need to do 2 things: understand the underlying causes of their patients’ breathlessness and justify therapeutically reducing their patients’ breathing rates. Alveolar hyperventilation occurs in HFrEF, PAH, and small-vessel, distal CTEPH due to increased neurochemical afferent stimulation and (mostly chemo-) receptor sensitivity caused by decreased bulk oxygen transport. Their excessive breathing can be reduced with therapies that enhance central haemodynamics and/or minimize chemosensitivity. However, the combination of high filling pressures in HFpEF and decreased lung perfusion resulting in ventilation/perfusion mismatch in proximal CTEPH increases physiological dead space.
As a result, bigger reductions in excess ventilation have been linked to lowering pulmonary capillary pressures and manually unclogging larger pulmonary veins (pulmonary endarterectomy and balloon pulmonary angioplasty). Regardless of the illness, getting regular exercise has powerful therapeutic effects. Some of the terrible effects of these common disorders may be lessened if pressing issues about the connection between excess ventilation and exertional dyspnoea, and the moderating role of pharmacological and nonpharmacological therapies, are finally answered.