scholarly journals Exercise intolerance in comorbid COPD and heart failure: the role of impaired aerobic function

2019 ◽  
Vol 53 (4) ◽  
pp. 1802386 ◽  
Author(s):  
Alcides Rocha ◽  
Flavio F. Arbex ◽  
Priscila A. Sperandio ◽  
Frederico Mancuso ◽  
Mathieu Marillier ◽  
...  
Keyword(s):  
Heart Failure ◽  
Cardiac Output ◽  
Systolic Heart Failure ◽  
Treatment Strategies ◽  
Symptom Burden ◽  
Cardiopulmonary Exercise Test ◽  
Forced Expiratory Volume ◽  
Exercise Intolerance ◽  
Chronic Obstructive ◽  
Aerobic Function

Impaired aerobic function is a potential mechanism of exercise intolerance in patients with combined cardiorespiratory disease. We investigated the pathophysiological and sensory consequences of a low change in oxygen uptake (ΔV′O2)/change in work rate (ΔWR) relationship during incremental exercise in patients with coexisting chronic obstructive pulmonary disease (COPD) and systolic heart failure (HF).After clinical stabilisation, 51 COPD–HF patients performed an incremental cardiopulmonary exercise test to symptom limitation. Cardiac output was non-invasively measured (impedance cardiography) in a subset of patients (n=18).27 patients presented with ΔV′O2/ΔWR below the lower limit of normal. Despite similar forced expiratory volume in 1 s and ejection fraction, the low ΔV′O2/ΔWR group showed higher end-diastolic volume, lower inspiratory capacity and lower transfer factor compared to their counterparts (p<0.05). Peak WR and peakV′O2were ∼15% and ∼30% lower, respectively, in the former group: those findings were associated with greater symptom burden in daily life and at a given exercise intensity (leg discomfort and dyspnoea). The low ΔV′O2/ΔWR group presented with other evidences of impaired aerobic function (sluggishV′O2kinetics, earlier anaerobic threshold) and cardiocirculatory performance (lower oxygen pulse, lower stroke volume and cardiac output) (p<0.05). Despite similar exertional hypoxaemia, they showed worse ventilatory inefficiency and higher operating lung volumes, which led to greater mechanical inspiratory constraints (p<0.05).Impaired aerobic function due to negative cardiopulmonary–muscular interactions is an important determinant of exercise intolerance in patients with COPD–HF. Treatment strategies to improve oxygen delivery to and/or utilisation by the peripheral muscles might prove particularly beneficial to these patients.

Clinical Characterization of Nursing Facility Residents With Chronic Obstructive Pulmonary Disease

2021 ◽  
Vol 36 (5) ◽  
pp. 248-257
Author(s):  
H. Edward Davidson ◽  
Peter Radlowski ◽  
Lisa Han ◽  
Theresa I. Shireman ◽  
Carole Dembek ◽  
...  
Keyword(s):  
Chronic Obstructive Pulmonary Disease ◽  
Pulmonary Disease ◽  
Clinical Characteristics ◽  
Symptom Burden ◽  
Forced Expiratory Volume ◽  
Chronic Obstructive ◽  
Nursing Facility ◽  
Data Set ◽  
Obstructive Pulmonary Disease ◽  
Medication Delivery

OBJECTIVE AND DESIGN: To describe clinical characteristics, medication use, and low peak inspiratory flow rate (PIFR) (< 60 L/min) prevalence in nursing facility residents with chronic obstructive pulmonary disease (COPD). PATIENTS AND SETTING: Residents 60 years of age and older with a COPD diagnosis and≥ 6 months' nursing facility residence, were enrolled between December 2017 and February 2019 from 26 geographically varied United States nursing facilities. OUTCOME MEASURES: Data, extracted from residents' charts, included demographic/clinical characteristics, COPD-related medications, exacerbations and hospitalizations within the past 6 months, and functional status from the most recent Minimum Data Set. At enrollment, residents completed the modified Medical Research Council (mMRC) Dyspnea Scale and COPD Assessment Test (CAT™). Spirometry and PIFR were also assessed. RESULTS: Residents' (N = 179) mean age was 78.0 ± 10.6 years, 63.7% were female, and 57.0% had low PIFR. Most prevalent comorbidities were hypertension (79.9%), depression (49.2%), and heart failure (41.9%). The average forced expiratory volume in 1 second (FEV11) % predicted was 45.9% ± 20.9%. On the CAT, 78.2% scored≥ 10 and on the mMRC Dyspnea Scale, 74.1% scored≥ 2, indicating most residents had high COPD symptom burden. Only 49.2% were receiving a scheduled long-acting bronchodilator (LABD). Among those with low PIFR prescribed a LABD, > 80% used dry powder inhalers for medication delivery. CONCLUSION: This study highlights underutilization of scheduled LABD therapy in nursing facility residents with COPD. Low PIFR was prevalent in residents while the majority used suboptimal medication delivery devices. The findings highlight opportunities for improving management and outcomes for nursing facility residents with COPD.

scholarly journals Cardiopulmonary Exercise Test in heart failure: A Sine qua non

2020 ◽  
Vol 9 (2) ◽  
pp. 1-8 ◽  
Author(s):  
Stefanos Sakellaropoulos ◽  
Dimitra Lekaditi ◽  
Stefano Svab
Keyword(s):  
Heart Failure ◽  
Exercise Test ◽  
Exercise Physiology ◽  
Cardiopulmonary Exercise Testing ◽  
Critical Evaluation ◽  
Research Area ◽  
Cardiopulmonary Exercise Test ◽  
Exercise Intolerance ◽  
Reduced Ejection Fraction ◽  
Cardiopulmonary Exercise

A robust literature, over the last years, supports the indication of cardiopulmonary exercise testing (CPET) in patients with cardiovascular diseases. Understanding exercise physiology is a crucial component of the critical evaluation of exercise intolerance. Shortness of breath and exercise limitation is often treated with an improper focus, partly because the pathophysiology is not well understood in the frame of the diagnostic spectrum of each subspecialty. A vital field and research area have been cardiopulmonary exercise test in heart failure with preserved/reduced ejection fraction, evaluation of heart failure patients as candidates for LVAD-Implantation, as well as for LVAD-Explantation and ultimately for heart transplantation. All the CPET variables provide synergistic prognostic discrimination. However, Peak VO2 serves as the most critical parameter for risk stratification and prediction of survival rate.

Cardiac and Non-Cardiac Determinants of Exercise Capacity in Chronic Kidney Disease

2021 ◽  
pp. ASN.2020091319
Author(s):  
Shanmugakumar Chinnappa ◽  
Nigel Lewis ◽  
Omer Baldo ◽  
Ming-Chieh Shih ◽  
Yu-Kang Tu ◽  
...  
Keyword(s):  
Heart Failure ◽  
Cardiac Output ◽  
Exercise Capacity ◽  
Significant Role ◽  
Exercise Physiology ◽  
Cardiopulmonary Exercise Test ◽  
Information Criteria ◽  
Healthy Controls ◽  
Cross Sectional ◽  
Patients With Heart Failure

Background Impaired exercise capacity is a significant symptom of CKD and is associated with poor survival. Furthermore, there is a growing interest in applying exercise as a diagnostic tool or as therapy in CKD. However, an in-depth understanding of exercise physiology in CKD is still lacking. Methods To evaluate the role of cardiac (central) and noncardiac (peripheral) determinants of exercise capacity in CKD, we conducted a cross-sectional study of 70 male CKD patients (stages 2-5) without diabetes or cardiac disease, 35 healthy controls, and 25 patients with heart failure. An integrated cardiopulmonary exercise test using a CO2 rebreathing technique was used to measure peak O2 consumption (VO2peak) and peak cardiac output simultaneously, and to calculate peak peripheral O2 extraction [C(a-v)O2], the peripheral determinant (the ability of exercising skeletal muscles to extract oxygen). We performed multiple regression analysis and used Bayesian information criteria (BIC) changes to quantitatively assess the individual contribution of central and peripheral factors. Results Compared with healthy controls, in patients with CKD, the VO2peak was impaired proportionate to its severity. Peak cardiac output was the predominant determinant of VO2peak in healthy controls and patients with heart failure, whereas C(a-v)O2 played a more significant role in determining VO2peak in CKD (β=0.68, P<0.001) compared with cardiac output (β=0.63, P<0.001). In addition, the magnitude of BIC reduction was greater for C(a v)O2 compared with cardiac output (BIC, 298.72 versus 287.68) in CKD. Conclusions In CKD, both peak cardiac output and peak C(a-v)O2 are independent predictors of VO2peak, and the more significant role played by peak C(a-v)O2 highlights the importance of noncardiac factors in determining exercise capacity in CKD.

Role of Diastole in Left Ventricular Function, II: Diagnosis and Treatment

2004 ◽  
Vol 13 (6) ◽  
pp. 453-466 ◽  
Author(s):  
Shannan K. Hamlin ◽  
Penelope S. Villars ◽  
Joseph T. Kanusky ◽  
Andrew D. Shaw
Keyword(s):  
Heart Failure ◽  
Diastolic Dysfunction ◽  
Left Atrial ◽  
Diastolic Heart Failure ◽  
Systolic Heart Failure ◽  
Clinical Signs ◽  
Left Ventricular ◽  
Exercise Intolerance ◽  
Radiographic Findings ◽  
Ventricular Compliance

Left ventricular diastolic dysfunction plays an important role in congestive heart failure. Although once thought to be lower, the mortality of diastolic heart failure may be as high as that of systolic heart failure. Diastolic heart failure is a clinical syndrome characterized by signs and symptoms of heart failure with preserved ejection fraction (0.50) and abnormal diastolic function. One of the earliest indications of diastolic heart failure is exercise intolerance followed by fatigue and, possibly, chest pain. Other clinical signs may include distended neck veins, atrial arrhythmias, and the presence of third and fourth heart sounds. Diastolic dysfunction is difficult to differentiate from systolic dysfunction on the basis of history, physical examination, and electrocardiographic and chest radiographic findings. Therefore, objective diagnostic testing with cardiac catheterization, Doppler echocardiography, and possibly measurement of serum levels of B-type natriuretic peptide is often required. Three stages of diastolic dysfunction are recognized. Stage I is characterized by reduced left ventricular filling in early diastole with normal left ventricular and left atrial pressures and normal compliance. Stage II or pseudonormalization is characterized by a normal Doppler echocardiographic transmitral flow pattern because of an opposing increase in left atrial pressures. This normalization pattern is a concern because marked diastolic dysfunction can easily be missed. Stage III, the final, most severe stage, is characterized by severe restrictive diastolic filling with a marked decrease in left ventricular compliance. Pharmacological therapy is tailored to the cause and type of diastolic dysfunction.

P2625Pathophysiology of diaphragm involvement in systolic heart failure: insights from diaphragm ultrasound and phrenic nerve stimulation studies

2019 ◽  
Vol 40 (Supplement_1) ◽  
Author(s):  
J Spiesshoefer ◽  
I T Tuleta ◽  
A G Giannoni ◽  
M B Boentert
Keyword(s):  
Heart Failure ◽  
Phrenic Nerve ◽  
Systolic Heart Failure ◽  
Exercise Intolerance ◽  
Design Data ◽  
Diaphragm Function ◽  
Phrenic Nerves ◽  
And Gender ◽  
The Right ◽  
Conductive Properties

Abstract Background Diaphragm ultrasound allows for assessment of both diaphragm excursion and thickness. Cervical and cortical magnetic stimulation (CEMS and COMS) with recording of the diaphragmatic compound motor action potential (CMAP) is diagnostically useful to evaluate the conductive properties of the inspiratory pathway. Systolic heart failure (HF) is characterized by a loss of systolic pump function. Diaphragm weakness in HF has been reported to potentially contribute to exercise intolerance Methods 14 patients with systolic HF (11 men, 3 women; 64±12 years, NYHA 2±0.9, LVEF 36.1±5.6%) and 12 healthy controls matched for age and gender (4 men, 8 women; 56±8 years) underwent spirometric lung function testing and assessment of diaphragm excursion (during tidal breathing, TB, voluntary sniff, VS and deep breathing, DB) and thickness of the right hemidiaphragm by ultrasound. COMS and CEMS of the phrenic nerves with simultaneous bilateral recording of the diaphragm CMAP using surface electrodes was performed in 9 patients. Results Compared to controls, HF patients showed reduced forced vital capacity (75.46±18.05% vs. 107.62±17.13%, p<0.05). Diaphragm excursion amplitude was significantly reduced in HF patients (4.29±1.35 cm vs. 7.34±2.10 cm, p<0.05). Diaphragm contractility was impaired too, as reflected by the diaphragm thickening ratio (DTR; 2.01±0.46 vs. 2.53±0.74, p<0.05). Diaphragm CMAP following COMS and CEMS of the phrenic nerves revealed normal latencies in HF patients compared to controls (COMS Latency; 19.05±2.37 msec vs. 18.97±3.59 msec, p= n. s.). Conclusions Diaphragm involvement in systolic HF is reflected by reduced FVC and impaired ultrasound parameters of diaphragm function. Diaphragmatic pathology is likely to be myopathic because magnetic phrenic nerve conduction studies show no abnormalities. Diaphragm ultrasound may be useful as a diagnostic tool for assessment of diaphragm function in systolic HF. Acknowledgement/Funding This study was supported by Sanofi-Genzyme, Neu-Isenburg, Germany. The funders had no role in study design, data collection and analysis, preparation.

Mechanical cardiopulmonary interactions during exercise in health and disease

2020 ◽  
Vol 128 (5) ◽  
pp. 1271-1279 ◽  
Author(s):  
William S. Cheyne ◽  
Megan I. Harper ◽  
Jinelle C. Gelinas ◽  
John P. Sasso ◽  
Neil D. Eves
Keyword(s):  
Heart Failure ◽  
Exercise Intolerance ◽  
Chronic Obstructive ◽  
Pulmonary Hemodynamics ◽  
Obstructive Pulmonary Disease ◽  
Healthy Humans ◽  
Significant Research ◽  
Clinical Consequences ◽  
Cardiopulmonary Interaction ◽  
Ventricular Filling

The heart and lungs are anatomically coupled through the pulmonary circulation and coexist within the sealed thoracic cavity, making the function of these systems highly interdependent. Understanding of the complex mechanical interactions between cardiac and pulmonary systems has evolved over the last century to appreciate that changes in respiratory mechanics significantly impact pulmonary hemodynamics and ventricular filling and ejection. Furthermore, given that the left and right heart share a common septum and are surrounded by the nondistensible pericardium, direct ventricular interaction is an important mediator of both diastolic and systolic performance. Although it is generally considered that cardiopulmonary interaction in healthy individuals at rest minimally affects hemodynamics, the significance during exercise is less clear. Adverse heart-lung interaction in respiratory disease is of growing interest as it may contribute to the pathogenesis of comorbid cardiovascular dysfunction and exercise intolerance in these patients. Similarly, heart failure represents a pathological uncoupling of the cardiovascular and pulmonary systems, whereby cardiac function may be impaired by the normal ventilatory response to exercise. Despite significant research contributions to this complex area, the mechanisms of cardiopulmonary interaction in the intact human and the clinical consequences of adverse interactions in common respiratory and cardiovascular diseases, particularly during exercise, remain incompletely understood. The purpose of this review is to present the key physiological principles of cardiopulmonary interaction as they pertain to resting and exercising hemodynamics in healthy humans and the clinical implications of adverse cardiopulmonary interaction during exercise in chronic obstructive pulmonary disease (COPD), pulmonary hypertension, and heart failure.

P6325Gas exchange improvements during exercise correlate with hemodynamic changes in heart failure patients with a left ventricular assist device

2019 ◽  
Vol 40 (Supplement_1) ◽  
Author(s):  
K Seuthe ◽  
M Morosin ◽  
H Smail ◽  
F Gerhardt ◽  
A Simon ◽  
...  
Keyword(s):  
Heart Failure ◽  
Cardiac Output ◽  
Cardiopulmonary Exercise Test ◽  
Left Ventricular ◽  
Peak Oxygen Consumption ◽  
Ventricular Assist ◽  
Heart Failure Patients ◽  
Left Ventricular Assist

Abstract Background The implantation of left ventricular assist devices (LVAD) has established its role in therapy for patients with end stage heart failure. Benefits in survival as well as an improved quality of life, compared to optimized medical therapy (OMT) alone, has been proven. There are limited data in the literature on the metabolic changes during exercise in LVAD patients, and in most studies no increase in peak oxygen consumption on cardiopulmonary exercise test (CPET) could be shown early after surgery. However, recent data suggests an improvement in peak oxygen uptake (VO2) as a late effect after rehabilitation. To further investigate these findings we sought to analyse CPET data from patients before LVAD implantation as well as in the early and late follow up in correlation with hemodynamic changes at these times. Methods We collected and retrospectively analysed data of heart failure patients who had undergone LVAD implantation, and in whom a right heart catheterization, a cardiopulmonary exercise test and an echocardiography had been performed at time before, as well as 6 Months and 12 months after LVAD implantation, respectively. Results Data of 43 patients implanted with an LVAD between 2011 and 2017 were analysed. There was significant improvement in cardiac output (3,2 vs 4,3 L/min, p<0,001) and VE/VCO2 slope (46 vs 38, p=0,001) 6 months after LVAD implant as well as a significant reduction in PCWP (26 vs 11 mmHg, p<0,001), PAP mean (40 vs 22 mmHg, p<0,001), RA mean (12 vs 8 mmHg, p=0,002) and PVR (4,2 vs 2,5 WU, p<0,001). However, there was no significant increase in peak VO2 after 6 months. 12 months after LVAD implantation there were no further significant changes in cardiac output, intracardiac pressures or VE/VCO2 slope, which all remained similar to the 6 months follow up. However, at that point, a significant increase in peak VO2 was seen, compared to baseline (1060 vs 1410ml/min, p=0,001) and to 6 months after surgery (Figure 1). Conclusion Cardiac output increases in heart failure patients early after LVAD implantation. Consequently, permanent ventricular off loading results in the reduction of intracardiac pressures and improvement in the VE/VCO2 slope 6 months after surgery. However, a significant rise in peak oxygen consumption could only be noted 12 months after surgery, suggesting either a delayed long-term effect of improved hemodynamics or other causes such as enhanced mobility or training due to improved quality of life.

scholarly journals Pulmonary Hypertension and Chronic Obstructive Pulmonary Disease: When Is It Out of Proportion?

2013 ◽  
Vol 12 (3) ◽  
pp. 122-126
Author(s):  
Sonja Bartolome
Keyword(s):  
Heart Failure ◽  
Chronic Obstructive Pulmonary Disease ◽  
Pulmonary Hypertension ◽  
Pulmonary Disease ◽  
Diastolic Heart Failure ◽  
Hypoxic Pulmonary Vasoconstriction ◽  
Systolic Heart Failure ◽  
Chronic Obstructive ◽  
Obstructive Pulmonary Disease ◽  
Obstructive Sleep

Patients with chronic obstructive pulmonary disease (COPD) often present with mild pulmonary hypertension (PH). This finding has been attributed to hypoxic pulmonary vasoconstriction. However, a small proportion of COPD patients will present with moderate or severe elevations in their pulmonary artery pressure (PAP), and these patients appear to have worsened symptoms and survival when compared to patients with milder elevations in PAP. The diagnosis of PH in COPD may be difficult, due to inaccuracies in the echocardiographic estimates of PAP in these patients. Additionally, many patients with COPD will also have comorbid conditions such as diastolic heart failure, systolic heart failure, or obstructive sleep apnea, which may cause increased pulmonary pressures through other mechanisms. Clinical trials investigating the effect of PH-specific therapy for patients with PH and COPD have been small, with mixed results. A careful evaluation for other causes of PH and hemodynamic evaluation will help guide medical therapy for this group of patients.

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