Cardiopulmonary exercise testing (CPX) is a useful clinical tool for evaluating the severity of disease and the limitations of activities of daily life in cardiac patients. 9 As described by the Fick's equation, O2 uptake (V O2) is the product of cardiac output and the arteriovenous O2 difference. Among the parameters obtained from CPX, the peak V O2 is traditionally considered as the gold standard for identifying patients with a poor prognosis and selecting candidates for cardiac transplantation. 10 The slope of the increase in ventilation (V E) to the increase in CO2 output (V CO2) (V E-V CO2 slope) is also an established index reflecting cardiopulmonary dysfunction during exercise. 9 scillatory breathing, alternating between hyperpnea and hypopnea during sleep and commonly referred to as central sleep apnea or Cheyne-Stokes respiration, has long been recognized in cardiac patients. An instability of the ventilatory control system, 1 long circulation time, 2-4 high sensitivity of ventilation to changes in CO2, 5 a decrease in the PaCO2 regulatory set point, 5,6 or fluctuations in the pulmonary blood flow 7,8 have been proposed as possible mechanisms underlying this abnormal breathing. A similar breathing pattern has also been recognized during waking hours in cardiac patients, especially those with heart failure. The mechanisms underlying oscillatory breathing while awake are assumed to overlap, at least in part, with those of central sleep apnea. However, reports on the mechanisms of oscillatory breathing while awake are limited. The relation between the magnitude of oscillatory breathing while awake and the severity of heart failure has not Relation Between Oscillatory Breathing and Cardiopulmonary Function During Exercise in Cardiac PatientsJo Kato, MD; Akira Koike, MD; Masayo Hoshimoto-Iwamoto, PhD; Osamu Nagayama, BSc; Koji Sakurada; Akira Sato, MD; Takeshi Yamashita, MD; Karlman Wasserman, MD, PhD; Kazutaka Aonuma, MD Background: Oscillatory breathing, alternating between hyperpnea and hypopnea, has been recognized in cardiac patients, especially in those with heart failure. We evaluated whether the cycle length and amplitude of oscillatory breathing correlate with impaired cardiopulmonary function during exercise.

n resting conditions, complex compensatory mechanisms are believed to adequately regulate blood flow to vital organs, especially to the brain. During exercise, however, the O2 demand of exercising muscles surges to levels 10-15 times higher than that in the resting condition. The blood flow to the exercising muscles increases tremendously to meet this sudden surge in O2 demand, thereby leading to a relative hypoperfusion of other organs. Our group recently studied cerebral oxygenation during exercise using near-infrared spectroscopy (NIRS) in patients with left ventricular dysfunction. 1 We found, as a result, that nearly half of the patients exhibited decreases in the cerebral oxyhemoglobin (O2Hb) during exercise, and that the decrease was more prominent in patients with a lower left ventricular ejection fraction (LVEF). 1 In these patients, cerebral O2Hb, a parameter that initially remained constant at lower work rates during incremental exercise, began to decrease at higher work rates. 1,2 The decrease in cerebral O2Hb presumably reflected a cerebral hypoxia during exercise resulting from impaired O2 transport to the brain.While risk stratification of chronic heart disease had been primarily based on resting hemodynamic measurements, cardiopulmonary exercise testing (CPX) has now become indispensable in singling out those patients with a poor prognosis. Among the parameters obtained from CPX, the peak O2 uptake (V • O2) is considered a gold standard for identifying patients with a poor prognosis and selecting candidates for cardiac transplantation. 3 The ratio of the increase in ventilation (V • E) to the increase in CO2 output (V • CO2) during exercise (V • E/V • CO2 slope) and the ratio of the increase in V• O2 to the increase in work rate (ΔV • O2/ΔWR) are also independent prognostic markers in cardiac patients. 4 In 1999, Lee et al reported that cerebral metabolism measured by magnetic resonance spectroscopy is abnormally deranged in patients with heart failure. 5 They also found that this abnormality is an independent predictor of mortality in these patients. 6 The cerebral metabolic abnormality is assumed to be due to overall and/or local disturbances of cerebral blood flow, that is, impaired cerebral oxygenation. 5 The impaired cerebral oxygenation can be detected by the non-invasive measurement of cerebral O2Hb using NIRS, and the detection might be more sensitive during exercise in which the O2 demand by exercising muscles increases tremendously, rather than measurements taken at rest. If the cerebral metabolic abnormality resulting from decreased cerebral O2 transport is related to prognosis, the decrease in cerebral O2Hb during exercise must also influence the prognosis.In the present study, we sought to establish a prognostic value of decreased cerebral O2Hb during exercise in cardiac patients. We selected patients with coronary artery disease, and compared the prognostic power of cerebral O2Hb during exercise with those of established respiratory gas indexes obtained from CPX, as cerebral oxygena...

We compared the prognostic power of end-tidal CO 2 pressure (PETCO 2 ) during exercise, an index of arterial CO 2 pressure, with those of established respiratory gas indexes during exercise testing in patients with left ventricular dysfunction. Seventy-eight consecutive patients with a left ventricular ejection fraction (LVEF) B40% were enrolled in the study. All the patients performed a symptom-limited incremental exercise test with respiratory gas measurements. PETCO 2 at peak exercise, peak O 2 uptake ( _ VO 2 ), the ratio of the increase in ventilation to the increase in CO 2 output ( _ VE/ _ VCO 2 slope), and the ratio of the increase in _ VO 2 to the increase in work rate (D _ VO 2 / DWR) were measured. PETCO 2 at peak exercise was significantly correlated with peak _ VO 2 , _ VE/ _ VCO 2 slope and D _ VO 2 /DWR. During a prospective follow-up period of 992 ± 570 days, 14 cardiac deaths occurred. As compared to survivors, non-survivors had a significantly lower LVEF, lower PETCO 2 at peak exercise, lower peak _ VO 2 , lower D _ VO 2 /DWR and a higher _ VE/ _ VCO 2 slope. Among these indexes, only PETCO 2 at peak exercise was found to be an independent predictor for cardiac death. PETCO 2 at peak exercise is useful in predicting poor prognosis in patients with left ventricular systolic dysfunction.

Circulation Journal Official Journal of the Japanese Circulation Society http://www. j-circ.or.jp n resting normal subjects at sealevel, alveolar PO2 and PCO2 are approximately 100 mmHg and 40 mmHg, respectively. In patients with pulmonary vascular occlusive disease, there is regional hypoperfusion relative to ventilation. This is reflected in an increased physiological dead space ventilation, due to an uneven ventilation -perfusion (V/Q) relationship, that is, high V/Q mismatch. Consequently, endtidal PCO2 (PETCO2) is reduced and end-tidal PO2 (PETO2) is increased. 1 Patients with left ventricular (LV) dysfunction also have high V/Q mismatch because of reduced pulmonary blood flow despite adequate ventilation. 2,3 Thus, in these patients, PETO2 must be higher and PETCO2 must be lower, according to the severity of LV dysfunction.In the present study, we hypothesized that in patients with LV dysfunction, PETO2 and PETCO2 measured during exercise may be better correlated with the severity of the cardiopulmonary dysfunction than that at rest. In order to test this hypothesis, we measured PETCO2 and PETO2 both at rest, at anaerobic threshold (AT) and at peak exercise. We then correlated these variables with indices of cardiopulmonary function during exercise, 4 in patients with LV dysfunction. Methods SubjectsThe subjects were 38 consecutive cardiac patients who performed exercise testing with respiratory gas analysis at the Cardiovascular Institute between January 2007 and December Background: The aim of the present study was to compare the end-tidal O2 pressure (PETO2) to end-tidal CO2 pressure (PETCO2) in cardiac patients during rest and during 2 states of exercise: at anaerobic threshold (AT) and at peak. The purpose was to see which metabolic state, PETO2 or PETCO2, best correlated with exercise limitation. I

Abstract:Incremental exercise testing to a symptom-limited maximum has been used to measure the ratio of the increase in ventilation (V . E) to the increase in CO 2 output (V . CO 2 ) during exercise (V . E/V . CO 2 slope), a valuable index reflecting the severity of the ventilation-perfusion mismatch in heart failure. Here we studied whether this same value for the slope of V . E/V . CO 2 could be determined from a short constant work-rate exercise test of moderate intensity. Twenty-three patients with a previous myocardial infarction underwent moderate-intensity (69 ± 15 W) constant work-rate exercise for 6 min and an incremental work-rate exercise test to the max. The V . E/V . CO 2 slope was calculated from the incremental exercise test from the start of increasing the work-rate to the ventilatory compensation point.The V . E/V . CO 2 slope was similarly calculated from the start of constant work-rate exercise until the 4th minute, when V . E and V . CO 2 changed minimally. The V . E/V . CO 2 slope determined from incremental exercise was 33.8 ± 5.9, ranging from 20.9 to 42.8. The slope obtained from constant work-rate exercise was 32.9 ± 5.7. The V . E/V . CO 2 slopes obtained from the two exercise tests did not differ significantly. The slope obtained from constant work-rate exercise was significantly positively correlated with the slope obtained from the incremental exercise ( r = 0.84, p < 0.0001). The V . E/V . CO 2 slope can be determined from constant work-rate exercise at a moderate intensity. This indicates that the relationship between ventilation and CO 2 output is consistent and independent of the mode of exercise testing.

The overshoot in oxygen uptake (VO2 overshoot) during recovery from maximal exercise is thought to reflect an overshoot in cardiac output. We investigated whether this phenomenon is related to cardiopulmonary function during exercise in cardiac patients. A total of 201 consecutive patients with previous myocardial infarction underwent cardiopulmonary exercise testing (CPX). An apparent VO2 overshoot during the recovery from CPX (6.5+/-8.1% increase relative to the peak VO2) was observed in ten patients. A comparison of patients with the VO2 overshoot to those without the VO2 overshoot revealed that the former had a significantly lower left ventricular ejection fraction (40.1+/-19.1 vs. 55. 2+/-14.9%, respectively, p = 0.002) and larger left ventricular diastolic and systolic dimensions. Patients with the VO2 overshoot also had a significantly lower peak VO2 (13.1+/-6.1 vs. 18.1+/-4.5 ml/min/kg, p < 0.001), lower DeltaVO2/DeltaWR (work rate) (6.6+/-3.8 vs. 9.5+/-1.7 mL/min/W, p < 0.0001), and a higher E (minute ventilation)/VCO2 (carbon dioxide output) slope (45.0+/-18.6 vs. 32.6+/-6.6, p < 0.0001) than those without the overshoot. A VO2 overshoot during recovery from maximal exercise was found in 5% of patients with previous myocardial infarction. This condition, which suggests a transient mismatch between cardiac contractility and afterload reduction, was found to be related to impaired cardiopulmonary function during exercise.