Faculty Opinions recommendation of Commentary on "Mechanism of augmented exercise hyperpnea in chronic heart failure and dead space loading" by Poon and Tin.

Author(s):  
James Duffin
2021 ◽  
Vol 30 (159) ◽  
pp. 200141
Author(s):  
Piergiuseppe Agostoni ◽  
Susanna Sciomer ◽  
Pietro Palermo ◽  
Mauro Contini ◽  
Beatrice Pezzuto ◽  
...  

In chronic heart failure, minute ventilation (V′E) for a given carbon dioxide production (V′CO2) might be abnormally high during exercise due to increased dead space ventilation, lung stiffness, chemo- and metaboreflex sensitivity, early metabolic acidosis and abnormal pulmonary haemodynamics. The V′Eversus V′CO2 relationship, analysed either as ratio or as slope, enables us to evaluate the causes and entity of the V′E/perfusion mismatch. Moreover, the V′E axis intercept, i.e. when V′CO2 is extrapolated to 0, embeds information on exercise-induced dead space changes, while the analysis of end-tidal and arterial CO2 pressures provides knowledge about reflex activities. The V′Eversus V′CO2 relationship has a relevant prognostic power either alone or, better, when included within prognostic scores. The V′Eversus V′CO2 slope is reported as an absolute number with a recognised cut-off prognostic value of 35, except for specific diseases such as hypertrophic cardiomyopathy and idiopathic cardiomyopathy, where a lower cut-off has been suggested. However, nowadays, it is more appropriate to report V′Eversus V′CO2 slope as percentage of the predicted value, due to age and gender interferences. Relevant attention is needed in V′Eversus V′CO2 analysis in the presence of heart failure comorbidities. Finally, V′Eversus V′CO2 abnormalities are relevant targets for treatment in heart failure.


2002 ◽  
Vol 92 (4) ◽  
pp. 1409-1416 ◽  
Author(s):  
Piergiuseppe Agostoni ◽  
Riccardo Pellegrino ◽  
Cristina Conca ◽  
Joseph R. Rodarte ◽  
Vito Brusasco

The changes in breathing pattern and lung mechanics in response to incremental exercise were compared in 14 subjects with chronic heart failure and 15 normal subjects. In chronic heart failure subjects, exercise hyperpnea was achieved by increasing breathing frequency more than tidal volume. The rate of increase in breathing frequency with carbon dioxide output was inversely correlated ( r = −0.61, P< 0.05) with dynamic lung compliance measured at rest, but not with static lung compliance either at rest or at maximum exercise. Although decrease in expiratory flow reserve near functional residual capacity in chronic heart failure occurred earlier with exercise than in the normal subjects ( P < 0.01), it was not correlated with changes in breathing pattern or occurrence of tachypnea. Tachypnea was achieved in chronic heart failure subjects with an increase in duty cycle because of a greater than normal decrease in expiratory time with exercise. We conclude that in chronic heart failure preexisting increase in lung stiffness plays a significant role in causing tachypnea during exercise. The results of the present study do not support the hypothesis that dynamic compression of the airways downstream from the flow-limiting segment occurring during exercise contributes to hyperpnea.


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