Exercise In Congestive Heart Failure Research Articles

PENGALAMAN PERAWAT MELAKUKAN LATIHAN AKTIFITAS FISIK PADA PASIEN CONGESTIVE HEART FAILURE

People with congestive heart failure (CHF) need a comprehensive rehabilitative program to restore physical abilities post-attacks and prevent re-attacks. Physical exercise in congestive heart failure (CHF) patients is aimed at optimizing the physical capacity of the body, providing counseling to patients and families in preventing worsening and helping patients to return to physical activity as before congestive heart failure (CHF). This study aims to explore in depth the experience of nurses doing physical exercise exercises in congetive heart failure patients. The research design used is descriptive phenomenology. Participants in this study amounted to 6 participants selected by purposive sampling technique. The data collected were in-depth interviews completed with field notes and then made in verbatim and analyzed using Colaizzi's approach. The research results found four themes, namely: the implementation of physical exercise exercise congestive heart failure patient is not optimal; increased knowledge of nurses and patients; the need for support from the hospital; and expectations for the exercise of physical activity. The results showed that things that could affect physical exercise activity in congestive heart failure patients were standard operating procedures, nurse knowledge, hospital support; and expectations for the exercise of physical activity. This study provides an understanding of the nurse's understanding of physical activity exercises so that nurses are able to provide appropriate nursing care.Keywords: experience, physical activity exercise, congetive heart failure

Atrial Fibrillation Is Associated with Decreased Cardiac Sympathetic Response to Isometric Exercise in CHF in Comparison to Sinus Rhythm

The presence of atrial fibrillation (AF) in congestive heart failure (CHF) is accompanied by increased mortality, although the exact mechanism is unclear. In previous studies, we have demonstrated cardiac baroreceptor abnormalities in association with AF and CHF. In this study, we sought to examine the effect of cardiac rhythm on the cardiac sympathetic response to exercise in CHF. In 13 CHF patients (six AF, seven SR, left ventricular ejection fraction 31 +/- 2%, age 61 +/- 1 years), we measured the hemodynamic and cardiac sympathetic response isometric handgrip (IHG) exercise. At baseline the groups were well matched. Baseline hemodynamics and cardiac sympathetic activity did not significantly differ between the cohorts. In response to IHG exercise, both groups demonstrated significant hemodynamic responses. In conjunction, the sinus rhythm (SR) group demonstrated a significant increase in cardiac sympathetic response to exercise (P = 0.04) while in contrast the AF group did not (P = 0.6). In this study, we demonstrate for the first time that the combination of AF and CHF is accompanied by a marked attenuation of the cardiac sympathetic response to acute hemodynamic stress. This implies AF is associated with a further impairment of baroreceptor response in CHF compared to SR. These findings present possible insights to the associated increased mortality and pathogenesis of AF with CHF.

Sympathetic nerve responses to muscle contraction and stretch in ischemic heart failure

Congestive heart failure (CHF) induces abnormal regulation of peripheral blood flow during exercise. Previous studies have suggested that a reflex from contracting muscle is disordered in this disease. However, there has been very little investigation of the muscle reflex regulating sympathetic outflows in CHF. Myocardial infarction (MI) was induced by the coronary artery ligation in rats. Echocardiography was performed to determine fractional shortening (FS), an index of the left ventricular function. We examined renal and lumbar sympathetic nerve activities (RSNA and LSNA, respectively) during 1-min repetitive (1- to 4-s stimulation to relaxation) contraction or stretch of the triceps surae muscles. During these interventions, the RSNA and LSNA responded synchronously as tension was developed. The RSNA and LSNA responses to contraction were significantly greater in MI rats (n = 13) with FS <30% than in control animals (n = 13) with FS >40% (RSNA: +49 +/- 7 vs. +19 +/- 4 a.u., P < 0.01; LSNA: +28 +/- 7 vs. +8 +/- 2 a.u., P < 0.01) at the same tension development. Stretch also increased the RSNA and LSNA to a larger degree in MI (n = 13) than in control animals (n = 13) (RSNA: +36 +/- 6 vs. +19 +/- 3 a.u., P < 0.05; LSNA: +24 +/- 3 vs. +9 +/- 2 a.u., P < 0.01). The data demonstrate that CHF exaggerates sympathetic nerve responses to muscle contraction as well as stretch. We suggest that muscle afferent-mediated sympathetic outflows contribute to the abnormal regulation of peripheral blood flow seen during exercise in CHF.

Effect of K + ATP Channel and Adenosine Receptor Blockade During Rest and Exercise in Congestive Heart Failure

K(+)(ATP) channels are important metabolic regulators of coronary blood flow (CBF) that are activated in the setting of reduced levels of ATP or perfusion pressure. In the normal heart, blockade of K(+)(ATP) channels results in a approximately 20% reduction in resting CBF but does not impair the increase in CBF that occurs during exercise. In contrast, adenosine receptor blockade fails to alter CBF or myocardial oxygen consumption (MVO(2)) in the normal heart but contributes to the increase in CBF during exercise when vascular K(+)(ATP) channels are blocked. Congestive heart failure (CHF) is associated with a decrease in CBF that is matched to a decrease in MVO(2) suggesting downregulation of myocardial energy utilization. Because myocardial ATP levels and coronary perfusion pressure are reduced in CHF, this study was undertaken to examine the role of K(+)(ATP) channels and adenosine in dogs with pacing-induced CHF. Myocardial blood flow (MBF) and MVO(2) were measured during rest and treadmill exercise before and after K(+)(ATP) channel blockade with glibenclamide (50 microg/kg/min ic) or adenosine receptor blockade with 8-phenyltheophylline (8-PT; 5 mg/kg iv). Inhibition of K(+)(ATP) channels resulted in a decrease in CBF and MVO(2) at rest and during exercise without a change in the relationship between CBF and MVO(2). In contrast, adenosine receptor blockade caused a significant increase in CBF that occurred secondary to an increase of MVO(2). These findings demonstrate that coronary K(+)(ATP) channel activity contribute to the regulation of resting MBF in CHF, and that endogenous adenosine may act to inhibit MVO(2) in the failing heart.

REBUTTAL FROM DRS. MIDDLEKAUFF AND SINOWAY

POINT-COUNTERPOINTREBUTTAL FROM DRS. MIDDLEKAUFF AND SINOWAYPublished Online:01 Jan 2007https://doi.org/10.1152/japplphysiol.00994b.2006MoreSectionsPDF (39 KB)Download PDF ToolsExport citationAdd to favoritesGet permissionsTrack citations ShareShare onFacebookTwitterLinkedInWeChat In the portion of the debate, Piepoli and Coats did an outstanding job reviewing the large body of work compiled by their group over the last decade or so. This body of work suggests that reflexes emanating from skeletal muscle play an important role in evoking increases in ventilation as well as sympathoconstrictor signals during exercise in congestive heart failure (HF). The authors' work suggests that peripheral limitations play an important role in determining exercise limitation seen in HF. However, it would have been informative for the readers of the Journal of Applied Physiology if the authors had dealt directly with the issue at hand, namely “whether heightened mechanoreceptor or metaboreceptor responses explain the exaggerated reflex responses seen with exercise in HF.” In limiting their review to a discussion of their impressive body of work they presented no discussion as to why the controversy exists and why Piepoli and Coats and Middlekauff and Sinoway should be afforded the opportunity to debate this issue in the first place. For our part (Middlekauff and Sinoway), we think that the debate is real and is important. We should note that we as well as the protagonists in this debate believe that peripheral issues are crucial determinants of symptomatology during exercise in HF.Speaking for our side, we were turned on to the issue of the role in the “periphery” in HF by the classic work of Zelis et al. (2) and later by LeJemtel and colleagues (1). The work cited in our review as well as that by Piepoli and Coats differed from that of Zelis et al. and LeJemtel et al. in that we assign a greater importance to the sympathetic constrictor influences seen than to the impaired vasodilatory capacity described by Zelis et al. and LeJemtel et al. Where we and our protagonists in this debate differ is that we believe that the heightened reflex responses seen in HF are due to the stimulation of afferents that are mechanically sensitive and not metabosensitive. In fact, the work we describe in our original review suggests that metabo responses are in fact attenuated. We describe a series of experiments over a 15-yr period from a number of different laboratories that are consistent with this hypothesis. These studies span the continuum of hypothesis-driven clinical investigation to studies using a decerebrate rat model of HF. We believe the experiments presented and the line of debate presented by us is systematic and compelling. We congratulate our adversaries on their important contributions to this body or work and only wish they had presented a compelling series of hypotheses on which we could further the discussion and enhance the rate at which we learn about this important reflex system.REFERENCES1 LeJemtel TH, Maskin CS, Lucido D, Chadwick BJ. Failure to augment maximal limb blood flow in response to one-leg versus two-leg exercise in patients with severe heart failure. Circulation 74: 245–251, 1986.Crossref | PubMed | ISI | Google Scholar2 Zelis R. The contribution of local factors to the elevated venous tone of congestive heart failure. J Clin Invest 54: 219–224, 1974.Crossref | ISI | Google Scholar Download PDF Previous Back to Top Next FiguresReferencesRelatedInformationCited ByRenal vasoconstriction is augmented during exercise in patients with peripheral arterial disease7 November 2013 | Physiological Reports, Vol. 1, No. 6 More from this issue > Volume 102Issue 1January 2007Pages 496-496 Copyright & PermissionsCopyright © 2007 the American Physiological Societyhttps://doi.org/10.1152/japplphysiol.00994b.2006History Published online 1 January 2007 Published in print 1 January 2007 Metrics

Sympathetic responses to exercise in myocardial infarction rats: a role of central command

In congestive heart failure (CHF), exaggerated sympathetic activation is observed during exercise, which elicits excess peripheral vasoconstriction. The mechanisms causing this abnormality are not fully understood. Central command is a central neural process that induces parallel activation of motor and cardiovascular systems. This study was undertaken to determine whether central command serves as a mechanism that contributes to the exaggerated sympathetic response to exercise in CHF. In decerebrated rats, renal and lumbar sympathetic nerve responses (RSNA and LSNA, respectively) to 30 s of fictive locomotion were examined. The fictive locomotion was induced by electrical stimulation of the mesencephalic locomotor region (MLR). The study was performed in control animals (fractional shortening > 40%) and animals with myocardial infarctions (MI; fractional shortening < 30%). With low stimulation of the MLR (current intensity = 20 microA), the sympathetic responses were not significantly different in the control (RSNA: +18 +/- 4%; LSNA: +3 +/- 2%) and MI rats (RSNA: +16 +/- 5%; LSNA: +8 +/- 3%). With intense stimulation of the MLR (50 microA), the responses were significantly greater in MI rats (RSNA: +127 +/- 15%; LSNA: +57 +/- 10%) than in the control rats (RSNA: +62 +/- 5%; LSNA: +21 +/- 6%). In this study, the data demonstrate that RSNA and LSNA responses to intense stimulation of the MLR are exaggerated in MI rats. We suggest that intense activation of central command may play a role in evoking exaggerated sympathetic activation and inducing excessive peripheral vasoconstriction during exercise in CHF.

Respostas cardiopulmonares ao exercício em pacientes com insuficiência cardíaca congestiva de diferentes faixas etárias

This paper aims at comparing cardiorespiratory functional capacity during exercise--represented by indicators of functional limitation, maximal oxygen uptake (VO2max), and anaerobic threshold--plus cardiopulmonary responses to maximal exercise in congestive heart failure (CHF) patients belonging to different age groups. Fifty-four CHF patients, stratified by age group, were evaluated as follows: group I--30 to 39 years (n = 12); group II--40 to 49 years (n = 18); group III--50 to 59 years (n = 17); and group IV--60 years and above (n = 7). All patients underwent maximal cardiopulmonary exercise testing (CPET) on treadmills. A single-factor analysis of variance (ANOVA) was performed to compare different age groups. No significant differences were found in maximal oxygen uptake and anaerobic threshold among the age groups, nor in maximal values for carbon dioxide production, oxygen pulse, respiratory exchange ratio, pulmonary ventilation, and ventilatory equivalents for oxygen and carbon dioxide. These findings suggest that cardiorespiratory functional capacity during exercise in patients with CHF, as well as cardiopulmonary variables at maximal exercise, may be similarly affected by the heart disease in all studied age groups.

Heart rate response to graded exercise correlates with aerobic and ventilatory capacity in patients with heart failure

Autonomic dysfunction and reduced exercise tolerance are typical features of patients with congestive heart failure (CHF). Baro-chemoreflex balance and organ response may have a common role in conditioning exercise tolerance, ventilation, and chronotropic competence in patients with CHF. We tested the hypothesis that there is a relationship between functional capacity and chronotropic competence to exercise in CHF. In all, 48 stable outpatients with CHF (age 65 +/- 10 years, 41 men, NYHA class 2.1 +/- 0, ejection fraction 31 +/- 7%, peak VO2 16 +/- 4 ml/kg/min) performed cardiopulmonary exercise testing (CPX). Heart rate (HR) response to exercise was assessed by the chronotropic index (CRI). The CRI was calculated by the following formula: CRI = peak HR - rest HR/220 - age - rest HR x 100 (normal value > 80%). The relationship of CRI to peak oxygen consumption (VO2) and ventilation/carbon dioxide production (VE/VCO2) ratio was examined. A group of 33 healthy controls underwent CPX as well. The CRI correlated directly with peak VO2 (r = 0.638, p < 0.001) and inversely with VE/VCO2 (r = -0.492, p < 0.001) in patients with CHF. A CRI < 78% identified patients with CHF and a peak VO2 < 20 ml/kg/min, area under the receiver operating curve (AUROC): 0.76, 95% confidence interval (CI) 0.60-0.92. A CRI < 74% predicted exercise hyperventilation in CHF (AUROC: 0.71 for VE/VCO2 > 30, 95% CI 0.53-0.88). The CRI was not significantly related either to peak VO2 or to VE/VCO2 in the control group. In patients with mild to moderate CHF, CRI correlates with functional capacity. This relationship adds new data on pathophysiologic grounds and supports the routine incorporation of CRI into CPX interpretation.

Muscle metaboreflex is blunted with reduced vascular resistance response of nonexercised limb in patients with chronic heart failure

Background Exercise-mediated muscle metaboreflex (MMR) activates the sympathetic nervous system afferently and may play an important role in the reduction in blood flow in nonexercised limb, thus enhancing exercised skeletal muscle blood flow (ie, normal regional blood flow redistribution during exercise). However, few data are available to describe the relationship between MMR and peripheral vascular control during exercise in congestive heart failure (CHF). The aim of this study was to determine whether MMR is impaired in CHF, and, if so, whether MMR is related to clinical severity of CHF and to changes in nonexercised limb vascular resistance in CHF. Methods and results Eleven CHF patients and 9 healthy age- and gender-matched controls were examined. All subjects performed a rhythmic handgrip exercise test at 50% of maximal voluntary contraction for 3 minutes on 2 occasions with and without postexercise upper arm regional circulatory occlusion (RCO/non-RCO). Changes in systolic blood pressure were measured and plotted against protocol time for both RCO and non-RCO. The area under each curve was estimated, and the calculating difference in the area between RCO and non-RCO was regarded as MMR. In addition, changes in calf vascular resistance were measured continuously by plethysmography after the handgrip test and the area differences between the RCO and non-RCO data was taken to represent MMR-provoked resistance changes in the nonexercised limb. During the handgrip exercise, systolic blood pressure increased similarly on the 2 occasions for both groups. MMR was significantly lower in CHF patients than in controls (68.2 ± 23.1 versus 160.4 ± 29.6 arbitrary units; P < .05). Decrease in MMR activity was related to clinical severity of CHF (controls, 160.4 ± 29.6; New York Heart Association class II, 87.6 ± 29.8; New York Heart Association class III, 34.3 ± 34.8 arbitrary units; P < .05). The increase in calf vascular resistance between RCO and non-RCO protocols in the control group was significant (+146.5 ± 38.0 arbitrary units; P < .05), whereas the difference in the CHF group was not significant (−72.9 ± 126.9 arbitrary units; not significant). Conclusions Exercise-induced MMR control in mild to moderate CHF is impaired in association with a blunted increase in nonexercised limb vascular resistance. This suggests that blunted MMR activity impairs regional blood flow redistribution and may contribute in part to exercise intolerance in this disorder.

P2752 Comparative efficacy of digoxin, bisoprolol and their combination to control ventricular response at rest and during exercise in congestive heart failure and atrial fibrillation

P2752 Comparative efficacy of digoxin, bisoprolol and their combination to control ventricular response at rest and during exercise in congestive heart failure and atrial fibrillation

Chronotropic incompetence response to exercise in congestive heart failure, relationship with the cardiac autonomic status.

In chronic congestive heart failure (CHF), attenuated heart rate response to exercise, a manifestation of chronotropic incompetence (CI), contributes to limiting exercise capacity. The present study was thus conducted to evaluate the respective role of chronic attenuation of cardiac vagal tone associated with depressed baroreflex sensitivity or affected cardiac sympathetic responsiveness in CHF patients with CI. Spontaneous cardiac baroreflex sensitivity (BRS) assessed by sequence method and spectral- and time-domain analysis of heart rate variability (HRV) were analysed in 21 chronic CHF patients. All patients performed a symptom-limited exercise test with measurement of gas exchange. Chronic incompetence which was defined as failure to achieve > or =80% of the heart rate reserve (%HRR) given by (HRpeak - HRrest)/(predictive maximal heart rate - HRrest) was observed in 14 (66%) patients. There was no significant difference in age, heart rate, peak oxygen uptake or left ventricular ejection fraction between the patients with and without CI. Although there was no significant difference in BRS, low frequency power of HRV in normalized units (LFnu) and SDNN were significantly lower in CI patients. Percentage of HRR correlated significantly with LFnu on 15 min (r=0.64, P<0.005) and, with LFnu on 24 h (r=0.52, P<0.01), SDNN (r=0.48, P=0.03) and SDANN (r=0.48, P=0.03), but not BRS (r=0.04, P=NS). Autonomic nervous system derangement is a complex process in CHF. The role of basal depressed cardiac sympathetic tone seems to contribute more closely than depressed baroreflex sensitivity to the impaired heart rate response to exercise frequently observed in CHF patients.

Synergistic efficacy of enalapril and losartan on exercise performance and oxygen consumption at peak exercise in congestive heart failure

Oxygen consumption at peak exercise (peak VO 2) is a strong independent predictor of the outcome in congestive heart failure (CHF). Renin-angiotensin system inhibition with either ACE or AT 1 receptor blockers is effective on peak VO 2. We evaluated whether mechanisms are similar for the 2 categories of drugs and whether their combination is able to produce a synergistic effect. Twenty CHF patients were randomized to receive, in a double-blind fashion, placebo + placebo (P+P), enalapril (20 mg/day) + placebo (E+P), losartan (50 mg/day) + placebo (L+P), and enalapril + losartan (E+L) or the same preparations in a reverse order, each for 8 weeks. Two patients did not complete the trial. Pulmonary function, cardiopulmonary exercise test, plasma neurohormones, and quality of life were assessed at the end of each treatment. Compared with P+P, E+P, and L+P similarly (16% and 15%, respectively) and significantly (p <0.01) augmented peak VO 2. Enalapril improved lung function (reduced slope of ventilation vs carbon dioxide production and dead space to tidal volume ratio, and increased alveolar membrane conductance and tidal volume). Losartan likely activated the exercising muscle perfusion (raised ΔVO 2/Δwork rate, which is a measure of aerobic work efficiency). In combination, they further increased peak VO 2, 10% from E+P (p <0.05) and 11% from L+P (p <0.05). Compared with run-in, E+P and L+P significantly reduced plasma norepinephrine by 70 ± 14 pg/ml and 100 ± 16 pg/ml and aldosterone by 1.6 ± 0.7 ng/dl and 1.6 ± 0.8 ng/dl. These changes were significantly greater when the drugs were combined (140 ± 20 pg/ml for norepinephrine, and 5.6 ± 0.9 ng/dl for aldosterone). Quality-of-life score did not improve significantly at each treatment step. Thus, lorsartan and enalapril similarly increased peak VO 2 in CHF patients, but mediators of this effect were, at least in part, different therapeutic targets that may be synergistic when the 2 drugs are combined.

Skeletal muscle lactate accumulation and creatine phosphate depletion during heavy exercise in congestive heart failure. Cause of limited exercise capacity?

To study the mechanisms of limited exercise capacity and skeletal muscle energy production in male patients with congestive heart failure. Muscle biopsy study. Skeletal muscle metabolic response to maximal bicycle exercise was studied in 10 patients with chronic congestive heart failure (ejection fraction 0.22 +/- 0.05; peak oxygen consumption, VO2 15.1 +/- 4.9 ml.min-1.kg-1) and in nine healthy subjects (peak VO2 33.5 +/- 6.7 ml.min-1.kg-1). Activities of skeletal muscle enzymes were measured from the vastus lateralis muscle of 48 patients (ejection fraction 0.24 +/- 0.06, peak VO2 17.4 +/- 5.4 ml.min-1.kg-1) and 36 healthy subjects (peak VO2 38.3 +/- 8.4 ml.min-1.kg-1). Although blood lactate levels were lower in patients than in healthy subjects (2.2 +/- 0.3 vs 5.2 +/- 0.6 mmol.l-1; P < 0.001) at peak exercise (96 +/- 11 W for patients and 273 +/- 14 W for controls), skeletal muscle lactate was similarly elevated (25.6 +/- 3.2 vs 22.7 +/- 2.7 mmol.kg-1) and creatine phosphate was equally depressed (P < 0.02) to low levels (7.0 +/- 1.9 vs 6.7 +/- 0.9 mmol.kg-1). The muscle ATP decreased by 21% (P < 0.05) and 8% (P < 0.01) in the patients and controls, respectively. Activities of rate limiting enzymes of the citric acid cycle (alpha-ketoglutarate dehydrogenase) and oxidation of free fatty acids (carnitine palmitoyltransferase II) were 48% and 21% lower than in controls, but the mean phosphofructokinase activity was unchanged in congestive heart failure. It seems that the main limiting factor of exercise performance during heavy exercise is the same in congestive heart failure and healthy subjects, a high rate of skeletal muscle lactate accumulation and high-energy phosphate depletion. In congestive heart failure, the low activity of aerobic enzymes is likely to impair energy production and lead to lactate acidosis at low workloads.

Ventilatory drive during exercise in congestive heart failure

Background: Continuous increases in the ventilatory equivalent for carbon dioxide (the ratio of minute ventilation to carbon dioxide production, an index of ventilatory drive) during exercise in patients with congestive heart failure would suggest that factors other than carbon dioxide excessively stimulate ventilation during exercise, and may be an important factor in exercise-related dyspnea and fatigue in these patients. Methods and Results: Eighty-five patients with congestive heart failure and 17 normal control subjects underwent symptom-limited exercise testing with gas-exchange analysis. Patients were divided into four functional classes (A–D, Weber's classification) based on peak exercise oxygen consumption. In all heart failure patient groups and in control subjects the ventilatory equivalent for carbon dioxide decreased ( P < .005, class D; P < .0001, all other groups) from rest to anaerobic threshold. Three isolated patients showed a continuous increase in ventilatory drive during exercise (mean peak oxygen consumption 13.7 mL/kg/ min). In the lowest functional class (D) the ventilatory equivalent for carbon dioxide was greater than in all other groups at rest, at anaerobic threshold, and at peak exercise ( P < .01). Conclusions: In all heart failure groups and in normal control subjects ventilatory drive, as determined by the ventilatory equivalent for carbon dioxide, decreases during exercise. Continuous increases in ventilatory drive during exercise are infrequently seen, suggesting that factors other than carbon dioxide production do not excessively stimulate ventilation in heart failure patients during exercise.

Nitric oxide inhalation reduces pulmonary tidal volume during exercise in severe chronic heart failure

Multiple mechanisms have been proposed to explain the hyperventilation and the limited exercise capacity in congestive heart failure (CHF) including increased intrapulmonary pressures, total pulmonary resistance, and airway abnormalities. We investigated the hypothesis that inhalation of nitric oxide could influence the maximum exercise capacity and excessive ventilatory response to exercise in CHF. Fifteen patients in CHF (mean age 48 ± 12 years) underwent a control and a nitric oxide inhalation progressive treadmill exercise test with 30 ppm. We determined the maximum oxygen consumptiom (peak VO 2 ), CO 2 production (VCO 2 ), minute pulmonary ventilation (VE), respiratory rate, tidal volume (VT), ventilatory equivalent for oxygen (VE/VO 2 ), ventilatory equivalent for carbon dioxide (VE/VCO 2 ), estimated physiologic dead space/tidal volume ratio (VD/VT), VE/VCO 2 slope, heart rate, systemic arterial pressure, VE/exercise time slope, and VT/exercise time slope during every incremental exercise. Mean maximum exercise values of heart rate, systolic systemic arterial pressure, diastolic systemic arterial pressure, VD/VT, respiratory rate, peak VO 2 , VO 2 /heart rate, VE/CO 2 , and maximum exercise time were unchanged by inhalation of nitric oxide. There was a strong trend toward reduction of VE/VO 2 from 53 ± 15 to 47 ± 12 ( p = 0.051) and in maximum VE from 58 ± 21 to 48 ± 17 L × min -1 ( p = 0.059). Maximum VT decreased from 1639 ± 556 to 1406 ± 479 ml ( p = 0.04). The VE/VCO 2 slope was reduced from 43 ± 12 to 35 ± 8 ( p = 0.018). Two patients had signs of pulmonary congestion during peak exercise or the recovery period with inhalation of nitric oxide. The VE/exercise time slope and VT/exercise time slope during incremental exercise were reduced by inhalation of nitric oxide, demonstrating a statistically significant minor increase in VE and VT. Inhalation of nitric oxide attenuated the excessive increase in VT response to exercise in CHF. The l -arginine-nitric oxide pathway may be involved in mechanisms contributing to hyperventilation during exercise in CHF. (Am Heart J 1997;134:737-44.)

Transient Fall in Oxygen Intake During Exercise in Congestive Heart Failure

We report four cases in which oxygen intake abruptly decreased during a graded exercise test. In all these cases, there was an acute event (arrhythmia, mitral regurgitation) that had very likely resulted in a decrease in cardiac output. These studies provide new evidence of oxygen intake dependence on oxygen transport, even in nonsteady-state situations.

Exercise in Congestive Heart Failure 478

Exercise in Congestive Heart Failure 478

Influence of digitalis on left ventricular functional response to exercise in congestive heart failure

This was a double-blind, placebo-controlled, crossover study designed to determine the influence of digitalis treatment on left ventricular (LV) response to physical exercise in patients with congestive heart failure (CHF). In 10 patients with CHF (ejection fraction 29 ± 2%), LV function was assessed during upright bicycle exercise using an ambulatory radionuclide detector for continuous noninvasive monitoring of cardiac function. Exercise was performed during control conditions and after a 3-week treatment with digoxin (0.25 mg/day orally) or placebo. Ten normal volunteers matched for sex and age constituted the control group. In normals, exercise ejection fraction and end-diastolic volume increased (both p < 0.001), while end-systolic volume decreased progressively (p < 0.001). In control conditions, patients with CHF had a sharp increase in heart rate during exercise, while ejection fraction did not change; both end-diastolic and end-systolic volumes increased significantly (both p < 0.001) during exercise. During digoxin treatment, heart rate response to exercise recorded in patients with CHF was comparable to that recorded in normal subjects. In addition, a significant increase in ejection fraction during exercise was detected (p < 0.001), and the increase in end-systolic volume was significantly smaller than that observed in control conditions (p < 0.05). When patients received placebo, the responses of LV function to exercise were comparable to those observed in control conditions. These findings demonstrate that digitalis has a favorable influence on LV functional adaptation to exercise in CHF.

Comparison of metabolic, ventilatory, and neurohumoral responses during light forearm isometric exercise and isotonic exercise in congestive heart failure

Maximal treadmill exercise responses were compared with light forearm isometric exercise responses in patients with chronic, stable heart failure (n = 14), and normal sedentary controls (n = 11). Isometric exercise was performed to exhaustion with 25% of maximal voluntary contraction. Gas-exchange analysis was used to determine oxygen consumption (VO 2), carbon dioxide production (VCO 2), and minute ventilation (VE) during exercise. Significant correlations were observed in normal controls, but not in patients with heart failure, between peak isotonic exercise and peak isometric exercise for VO 2 (r = 0.75, p = 0.001) and VCO 2 (r = 0.67, p < 0.03), and between submaximal isotonic exercise (50% of peak) and peak isometric exercise for VO 2 (r = 0.75, p = 0.007), VCO 2 (r = 0.67, p = 0.02), and VE (r = 0.71, p = 0.01). At 90 seconds after isometric exercise in both groups, significant correlations t < 0.05) were observed with peak isotonic exercise VE (r = 0.62 normals, and r = 0.63 heart failure). Plasma norepinephrine increased significantly (p < 0.01) after both isotonic and isometric exercise in patients with heart failure, although peak values were greater with isotonic than with isometric exercise (p = 0.01). Plasma atrial natriuretic peptide and renin activity did not change with either isotonic or isometric exercise. In conclusion, maximal isotonic exercise responses are not predictive of peak isometric VO 2 or VCO 2 in patients with heart failure. However, VE during maximal isotonic exercise predicts postisometric exercise ventilation in both normals and patients with heart failure; this may determine the extent of dyspnea that patients with heart failure experience with isometric activities of daily living.

Prognostic value of plasma catecholamines, plasma renin activity, and plasma atrial natriuretic peptide at rest and during exercise in congestive heart failure: Comparison with clinical evaluation, ejection fraction, and exercise capacity

Survival in congestive heart failure is related to plasma catecholamines and atrial natriuretic peptide at rest, but the prognostic importance of changes during exercise is unknown. The aim of this study was to evaluate the prognostic value of catecholamines and atrial natriuretic peptide at rest and during maximal exercise in congestive heart failure, and to compare it to clinical and exercise test variables and left ventricular ejection fraction. One hundred ninety consecutive patients (136 men and 54 women; median age, 66 years; range, 42–75 years) with clinically stable congestive heart failure were included. Sixteen patients were in New York Heart Association class I, 87 in class II, 83 in class III, and 4 in class IV. Left ventricular ejection fraction was 0.30 (range, 0.06-0.74). Total survival after 1 year was 79%, after 2 years, it was 68%. Prognostic variables at univariate analysis were: plasma noradrenaline at rest ( P < .0001), plasma adrenaline at rest ( P = .049), and atrial natriuretic peptide at rest ( P = .016). During exercise, plasma catecholamines and plasma atrial natriuretic peptide increased significantly; the change, however, was not related to survival. Six variables carried significant, independent prognostic information in a multivariate analysis: left ventricular ejection fraction ( P = .03), plasma noradrenaline at rest ( P = .009), New York Heart Association class III + IV ( P = .005), increase in heart rate during exercise ≤ 35 min −1 ( P < .0001), serum creatinine > 121 umol/L ( P = .004), and serum urea > 7.6 mmol/L ( P = .007). Patients with congestive heart failure have a poor survival despite intensive medical treatment. Plasma catecholamines and plasma atrial natriuretic peptide are elevated at rest and rises further during exercise; the increase, however, is not related to mortality. Plasma noradrenaline at rest contributes with further prognostic information despite knowledge of clinical and exercise variables and was the only neurohormonal variable with independent, significant prognostic information on survival.