During exercise patients with chronic left heart failure ventilate more than normal individuals at the same workload; the ratio of minute ventilation to minute production of carbon dioxide (VE/VCO2) is increased. The relation between increased VE/VCO2, severity of heart failure, and exercise capacity has not been defined. VE/VCO2 was measured in 47 patients with chronic left heart failure (New York Heart Association grades II and III) and in 1009 healthy controls. Exercise capacity was assessed by peak oxygen consumption (VO2max) during progressive exercise. In the controls VO2max ranged from 25 to 93 ml/kg/min; VE/VCO2 was 17-36 and did not correlate with VO2max. In chronic left heart failure the VO2max ranged from 9 to 29 ml/kg/min; VE/VCO2 was 22-42 and correlated strongly with VO2max. End tidal carbon dioxide and respiratory rate at peak exercise were similar in the controls and patients with chronic left heart failure. The increase in VE/VCO2 on exercise in chronic left heart failure indicates increased physiological dead space, presumably caused by a ventilation-perfusion mismatch. In the controls and patients with chronic left heart failure the relation of VE/VCO2 to VO2max was curvilinear with a threshold of VO2max below which VE/VCO2 started to rise above the normal range. This point of inflection may be explained by the existence of a critical level of cardiac function necessary to perfuse adequately all lung zones on exercise.

Abnormal patterns of diastolic ventricular filling are well recognized in chronic heart failure, but their relationship to the severity of heart failure is not known. The present study evaluates the relationship of diastolic filling indices to the severity of heart failure and to exercise capacity. In 40 patients with chronic heart failure secondary to ischaemic left ventricular impairment, exercise capacity was measured as peak oxygen consumption (VO2max) by progressive treadmill exercise. Left ventricular function was assessed by M-mode and Doppler echocardiographic indices. Peak aortic velocity correlated weakly with VO2max (R = +0.38, P less than 0.05). VO2max did not correlate with other systolic indices, including mean aortic acceleration, time to peak velocity, or isovolumic contraction time. VO2max correlated with the mitral inflow E/A ratio (R = -0.57, P less than 0.005) and with the Doppler estimate of isovolumic relaxation time (R = -0.48, P less than 0.01). Two distinct patterns of diastolic filling were observed: subjects with mild-to-moderate heart failure (NYHA grade II, VO2max 15-20 ml.kg-1.min-1) had abnormally low E/A ratios and long isovolumic relaxation times, whereas those with severe heart failure (NYHA grade III-IV, VO2max less than 12 ml.kg-1.min-1) had abnormally high E/A ratios and short isovolumic relaxation times. Different patterns of abnormal diastolic filling with different degrees of severity of heart failure may explain some of the previous controversy as to the prevalence of abnormal diastolic function in chronic heart failure. Exercise capacity in chronic heart failure appears more closely related to abnormalities of diastolic filling pattern than to indices of systolic function.

Bronchoconstriction is seen at rest in patients with chronic heart failure, and may contribute towards exercise limitation. To investigate the effect of bronchodilator agents on exercise capacity, 10 patients (mean age 60 years, range 39-72) in New York Heart Association class II and III heart failure, underwent symptom-limited maximal exercise testing after inhalation of nebulized salbutamol (5 mg), ipratropium bromide (500 micrograms) or placebo delivered on separate days in a randomized, double-blinded study. There was an increase in forced expiratory volume in one second from pre-treatment to after nebulizer, 2.28 +/- 0.20 to 2.38 +/- 0.19 l (P < 0.05) with salbutamol, and 2.27 +/- 0.21 to 2.37 +/- 0.21 l (P < 0.05) with ipratropium bromide. There was an increase in maximal oxygen consumption after salbutamol 17.9 +/- 1.3 ml.kg-1.min-1 (P < 0.05) and ipratropium bromide 17.0 +/- 1.4 ml.kg-1.min-1 (P < 0.05), compared with placebo 16.3 +/- 1.4 ml.kg-1.min +/- 1. Peak minute ventilation during exercise also increased after salbutamol 52.8 +/- 4.5 l.min-1 (P < 0.05), compared with placebo 46.1 +/- 3.1 l.min-1. The small but significant increase in exercise capacity in chronic heart failure following bronchodilator agents implies that a degree of bronchoconstriction is present in these patients and contributes to exercise limitation.

Overnight studies were performed in 10 patients with severe chronic left heart failure (New York Heart Association grades III and IV) without pulmonary disease and in eight controls. Transcutaneous oxygen (Po2) and carbon dioxide tensions (Pco2) and oxygen saturation were measured and the electrocardiogram was recorded. During sleep mean oxygen saturation fell to 92-7% (minimum 86-1%) from 95-1% when awake. During the night oxygen saturation was below 95% for 62% of the time, below 90% for 6% of the time, and below 85% for 1% of the time. In four patients there were oxygen desaturation dips (a fall of > 4% in oxygen saturation from a stable baseline that lasted > 30 s) with concurrent increases in Pco2. Two patients had bradycardia during the dips: in one there was non-sustained ventricular tachycardia during the dips and in the other there was ST depression (> 0-1 mV at 80 ms after the J point) during a dip. In the controls the fall in mean oxygen saturation from 9514% when they were awake to 9414% when they were asleep was less than the fall in patients with heart failure and there were no desaturation dips or arrhythmias.Thus patients with severe heart failure had episodes of oxygen desaturation during sleep, some of which were associated with arrhythmia. Such episodes may be related to the increased risk of sudden death in chronic heart failure.

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