In healthy normal individuals (n = 69), coronary patients with myocardial ischaemia (n = 27) and patients with chronic heart failure (CHF, n = 33), four widely applied methods to determine ventilatory threshold (VT) were analysed: V-slope, ventilatory equivalent for O2 (EqO2), gas exchange ratio (R) and end-tidal partial pressure of oxygen. Lactate threshold [LAT, log lactate vs log oxygen uptake (VO2)] was also determined. Analysis focused on rate of success of threshold determination, comparability of threshold methods, reproducibility and interobserver variability. Cycle ergometry protocols with ramp-like mode and graded steady-state mode used in exercise testing were considered separately. In healthy normal individuals and coronary patients with myocardial ischaemia, at least three VT could be determined during ramp-like mode and two VT during graded steady-state mode, 82% of the time. For CHF patients, the rate of successful determination of VT was lower. Compared to LAT, VO2 at VT was significantly higher using R and EqO2 methods of VT determination in healthy normal subjects (P < 0.01), and significantly higher when using all four methods in coronary patients (P < 0.01 or P < 0.05, respectively). No difference was observed between VO2 at VT and LAT in CHF patients. In healthy normal individuals, day-to-day reproducibility of VT and LAT was high (error of a single determination from duplicate determinations was between 3.9% and 6.2% corresponding to a VO2 of 52.2 and 89.2 ml.min-1). Interobserver variability was low (error between 0.3% and 5% corresponding to a VO2 of 9.8 and 68 ml.min-1). In CHF patients, interobserver variability was moderately greater (error between 4.6% and 8.2%, corresponding to a VO2 of 35.1 and 62.4 ml.min-1). To optimize threshold determination, standardized procedures are suggested.
This study compares hemodynamic, metabolic, and gas exchange responses, catecholamine levels, and symptoms in 35 male patients with chronic heart failure (CHF) ([mean +/- SD] age 53 +/- 11 yr; ejection fraction 24 +/- 11%) during three differently graded exercise test protocols. On three consecutive days patients performed cycle ergometry supine, with prolonged steps (prol BE) and right heart catheterization, ramplike cycle ergometry sitting (ramp BE), and ramplike treadmill walking (TMW). As in routine clinical practice, the prol BE was terminated when pathologic central hemodynamics and/or increased symptomology occurred, and ramp BE and TMW due to increased symptomology and/or physician's decision. During prol BE at ventilatory threshold (VT) the VO2 (8.6 +/- 1.8 ml.kg-1.min-1) was lower than during ramp BE (9.3 +/- 2.1 ml.kg-1.min-1) (P < 0.017) and TMW (11.8 +/- 2.3 ml.kg-1.min-1) (P < 0.0001). Prol BE, ramp BE, and TMW also differed significantly with respect to ventilation (22 +/- 7 l.min-1; 26 +/- 6 l/min-1; 29 +/- 7 l.min-1; P < 0.01) and heart rate (100 +/- 15 beats.min-1; 103 +/- 18 beats.min-1; 110 +/- 16 beats.min-1; P < 0.017). No differences were found in lactate levels, catecholamine levels, and ratings of leg fatigue and dyspnea. At test termination, the peak VO2 during prol BE (100.8 +/- 3.3 ml.kg-1.min-1) was lower than during ramp BE (13.3 +/- 4.1 ml.kg-1.min-1) (P < 0.0001) and TMW (14.7 +/- 3.4 ml.kg-1.min-1) (P < 0.0001). Peak norepinephrine value during ramp BE (4.531 +/- 2.788 nmol.l-1) was higher than during prol BE (3.707 +/- 2.262 nmol.l-1) (P < 0.001). Among the three tests, no significant differences were found for peak values of heart rate, lactate, and ratings of dyspnea. Although the VO2.kg-1 at VT was significantly higher during ramp BE and TMW compared to prol BE (P < 0.001), the values expressed as a percent of peak VO2.kg-1 were significantly lower (70 +/- 4%; 72 +/- 6%; 79 +/- 3%; P < 0.017). A systematic effect on aerobic capacity with reduced peak values during ramp BE and TMW was demonstrated when test termination was based primarily on pathological findings of central hemodynamics from prol BE.
In view of the frequent follow-up evaluations of patients with severe chronic heart failure, the purpose of this study was to assess whether noninvasive gas exchange parameters from cardiopulmonary exercise testing (CPX), measured at ventilatory threshold (VT), are related to invasively measured peak diastolic pulmonary artery pressure (dPAP) and peak cardiac output (CO). 23 males with severe chronic heart failure underwent CPX on a bicycle ergometer (supine; steps of 25 W/5 min) during right heart catheterization. dPAP and/or CO increased significantly from rest to VT (18 ±10-9 30 ±10 mm Hg, p < 0.01; 4.8 ± 1.4 -9 6.4 ± 2.3 liters/min, p< 0.05), but did not from VT to peak exercise (33 ± 10 mm Hg; 7.3 ± 2.5 liters/min). Data indicated severely deteriorated hemodynamics at rest and during exercise. Oxygen uptake (VO2) increased from rest (270 ± 45 ml/min) to VT (650 ± 135 ml/min at 27 ± 7 W) to peak exercise (829 ± 183 ml/min at 39 ± 23 W). VO2 data were normal for a given workload. From all CPX data at VT, only 02 pulse correlated with peak dPAP (r = -0.58; p < 0.05). Peak CO correlated with O2 pulse (r = -0.49), VO2 (r = 0.46), ventilatory equivalent for O2 (r = -0.43) and tidal volume (r = 0.43), measured at VT (p < 0.05 for all parameters). Variance of peak dPAP and peak CO could only be explained by O2 pulse at VT (58 and 49%, respectively). Noninvasive cardiopulmonary data at VT did not give sufficient information about peak dPAP and peak CO in patients with severe chronic heart failure using a steady-state protocol. This indicates that early ventilatory threshold should not be considered indicative of reduced CO due to skeletal muscle underperfusion in heart failure patients.
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