Cardiac Output Response to Exercise in Chronic Cardiac Failure Patients

Abstract

SummaryThe purpose of this study was to investigate the precise pattern of stroke volume (SV) response during exercise in patients with chronic heart failure (CHF) compared with age-matched controls. Fourteen patients with CHF and 7 controls performed symptom-limited bicycle exercise testing with respiratory gas exchange measurement. Patients were classified into group A (n = 7) with peak V ・ O 2 ≥18.0 mL/kg/minute and group B (n = 7) with peak V ・ O 2 < 18.0 mL/kg/ minute. SV and cardiac output (CO) were continuously measured during exercise using a novel thoracic impedance method (Physioflow). CO and SV were lower in the group B patients than those in controls at peak exercise [CO: 11.3 ± 1.0 (SE) versus 15.6 ± 0.9 L/minute, P < 0.05, SV: 89 ± 6 versus 110 ± 6 mL, P < 0.05]. SV reached its peak levels during submaximal exercise and remained close to the peak value until peak exercise in 6 of 7 group B patients (86%). On the other hand, it progressively increased until peak exercise in 6 of 7 controls (86%) and 5 of 7 group A patients (71%). In all subjects, CO at peak exercise was more closely correlated with SV at peak exercise (r = 0.86, P < 0.001) than with peak heart rate (r = 0.69, P < 0.001). CHF patients with impaired exercise capacity had attenuated increment of CO during exercise, and SV reached its peak levels during submaximal exercise. (Int Heart J 2012; 53: 293-298) Key words: Stroke volume, Exercise capacity, Left ventricular function, Cardiopulmonary exercise testing, Impedance method P atients with chronic heart failure (CHF) show exercise intolerance, and their peak oxygen uptake (peak V ・ O 2 ) is reduced compared to healthy individuals of the same age.1,2) Because oxygen uptake (V ・ O 2 ) is the product of cardiac output (CO) and the arterio-venous oxygen content difference [C(a-v)O 2 ], a decrease in peak V ・ O 2 may be due to a decrease in either CO and/or C(a-v)O 2 at peak exercise. The CO response of patients with CHF during exercise is attenuated compared to that in normals. [3][4][5] Thus, in patients with CHF, the heart can not generate a CO that is sufficient to meet the metabolic demands of the tissues during exercise. Since CO is the multiplication of stroke volume (SV) and heart rate (HR), a decrease in CO may be due to either that in SV and/or HR at peak exercise. However, because patients with CHF often have chronotropic incompetence, the mechanism of the decrease in CO at peak exercise has not been fully studied.Because V ・ O 2 is the product of CO and C(a-v)O 2 , and because C(a-v)O 2 primarily reflects the capacity of O 2 uptake in the working muscles, the CO during exercise is a better indicator of cardiac function than peak V ・ O 2 . It has been also shown that the CO during exercise is a prognostic indicator in patients with CHF.6,7) Sullivan, et al 5) demonstrated that SV and CO both during submaximal and maximal exercise are low in patients with CHF. Magnusson, et al 8) also reported that the CO increase during submaximal exercise was attenuated in patients with CHF...

Relationship between non‐invasive haemodynamic responses and cardiopulmonary exercise testing in patients with coronary artery disease

“…Previous studies using non‐invasive estimates of cardiac haemodynamics showed strong associations between CO and VO 2 at peak exercise ( r = 0·81 Fukuda et al ., ; r = 0·72 Myers et al ., ) in heart failure patients. Differences in the strength of the correlations reported in previous investigations and what was found in the current study may be the result of the characteristics of the chronic disease population assessed.…”

Relationship between chronotropic incompetence and β-blockers based on changes in chronotropic response during cardiopulmonary exercise testing

“…Witte et al supported the concept that chronotropy is not a major factor in determining exercise capacity in patients with CHF [19], suggesting that HR limitation is unlikely to be the cause, but rather the consequence, of exercise intolerance in CHF patients [21]. Fukuda et al demonstrated that CHF patients with impaired exercise capacity had attenuated increments in cardiac output during exercise [22].…”

Assessment of Transthyretin Combined With Mini Nutritional Assessment on Admission Provides Useful Prognostic Information in Patients With Acute Decompensated Heart Failure

“…Evidence of cardiac rehabilitation has been shown in patients with heart disease. [10][11][12][13] However, there is little evidence of nutritional management in HF patients and the most appropriate nutritional assessment has not yet been established.…”