Causes of breathing inefficiency during exercise in heart failure

Abstract

Background: Patients with heart failure (HF) develop abnormal pulmonary gas exchange; specifically, they have abnormal ventilation relative to metabolic demand (ventilatory efficiency/minute ventilation in relation to carbon dioxide production [V(E)/VCO₂]) during exercise. The purpose of this investigation was to examine the factors that underlie the abnormal breathing efficiency in this population.

Methods and results: Fourteen controls and 33 moderate-severe HF patients, ages 52 ± 12 and 54 ± 8 years, respectively, performed submaximal exercise (∼65% of maximum) on a cycle ergometer. Gas exchange and blood gas measurements were made at rest and during exercise. Submaximal exercise data were used to quantify the influence of hyperventilation (PaCO₂) and dead space ventilation (V(D)) on V(E)/VCO₂. The V(E)/VCO₂ relationship was lower in controls (30 ± 4) than HF (45 ± 9, P < .01). This was the result of hyperventilation (lower PaCO₂) and higher V(D)/V(T) that contributed 40% and 47%, respectively, to the increased V(E)/VCO₂ (P < .01). The elevated V(D)/V(T) in the HF patients was the result of a tachypneic breathing pattern (lower V(T), 1086 ± 366 versus 2003 ± 504 mL, P < .01) in the presence of a normal V(D) (11.5 ± 4.0 versus 11.9 ± 5.7 L/min, P = .095).

Conclusions: The abnormal ventilation in relation to metabolic demand in HF patients during exercise was due primarily to alterations in breathing pattern (reduced V(T)) and excessive hyperventilation.

Copyright © 2010 Elsevier Inc. All rights reserved.

Figures

Figure 1

The relationship between VE/VCO2 slope and VE/VCO2 ratio at submaximal exercise.

Figure 2

Individual (open) and group mean (black) data for VE/VCO2 ratio in normal (circle) and HF (triangle) patients at submaximal exercise. * Significant difference between control and HF group (p<0.01).

Figure 3

Relationships of PaCO2, VD/VT, and VE/VCO2. Graph A and B are models of the effects of changing PaCO2 and VD/VT on VE/VCO2 in normal controls (○ individual data, ● group mean) and HF patients (△ individual data, ▲ group mean). Grey lines are isopleths of VD/VT (A) and PaCO2 (B); black lines are trend lines for control and HF data. Graph C quantifies the relative contribution of PaCO2 (black), VD/VT (stripes) and VCO2 (dots) to the increased VE/VCO2 seen in HF group. * Significant difference between control and HF groups (p<0.01).

Figure 3

Relationships of PaCO2, VD/VT, and VE/VCO2. Graph A and B are models of the effects of changing PaCO2 and VD/VT on VE/VCO2 in normal controls (○ individual data, ● group mean) and HF patients (△ individual data, ▲ group mean). Grey lines are isopleths of VD/VT (A) and PaCO2 (B); black lines are trend lines for control and HF data. Graph C quantifies the relative contribution of PaCO2 (black), VD/VT (stripes) and VCO2 (dots) to the increased VE/VCO2 seen in HF group. * Significant difference between control and HF groups (p<0.01).

Figure 4

The contribution of VD and VA to minute ventilation in the control and HF groups at rest and submaximal exercise. * Significant difference between control and HF groups (p<0.01).

Figure 5

Differences in breathing pattern in normal (circle) and HF (triangle) patients from rest (black) to submaximal exercise (open). Grey lines are isopleths of VT; black lines demonstrate the change in breathing pattern with exercise in each group.

Figure 6

The effect of alterations in VT (black line) and BF (grey line), when maintaining a constant VE of 31 L/min at a given dead space (isopleths), on VD/VT. HF data is presented for VT (▲ HF-VT) and BF (■ HF-BF). This group had a dead space of ~400ml and a VD/VT of ~0.4. In this model when VT (△ VT*2) was doubled to a more normal value (~2200ml), to maintain the same VE i.e. 31 L/min, BF (□ BF/2) was reduced by half. If dead space remained the same (400ml) VD/VT would be reduced by half to 0.2.