Lung Function and Exercise Gas Exchange in Chronic Heart Failure

Wasserman, Karlman; Zhang, Yongyu; Gitt, Anselm K.; Belardinelli, Romualdo; Koike, Atsushi; Lubarsky, Laura; Agostoni, Piergiuseppe

doi:10.1161/01.cir.96.7.2221

Cited by 367 publications

(311 citation statements)

References 27 publications

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“…Major pathogenetic bases for lung stiffening are interstitial lung congestion and heart to lung pathological interaction because of cardiomegaly, vascular engorgement, increased alveolar surface tension, unequal ventilation and activation of contractile elements of the vascular wall [17]. The combination of these factors leads to the development of a typical restrictive lung pattern [18,19]. According to Wasserman, the lung restriction may occur as a function of haemodynamic derangement, suggesting a pathogenetic role of an increased wasted ventilation with those patients with higher VE/VCO 2 slope exhibiting the higher dead space to tidal volume ratio and a premature increase in respiratory rate as a compensatory mechanism.…”

Section: Airways Function Abnormalitiesmentioning

confidence: 99%

Exercise intolerance in chronic heart failure: mechanisms and therapies. Part I

Piepoli

Guazzi

Boriani

et al. 2010

European Journal of Cardiovascular Prevention & Rehabilitat

113

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Muscular fatigue and dyspnoea on exertion are among the most common symptoms in chronic heart failure; however their origin is still poorly understood. Several studies have shown that cardiac dysfunction alone cannot fully explain their origin, but the contribution of the multiorgan failure present in this syndrome must be highlighted. In this study, divided in two parts (see part II: pp. 643-648), we aimed to summarize the existing evidence and the most controversial aspects of the complex interplay of different factors involved in symptom generation. In this first part of the review, six key factors are revised: the heart, the lung, the skeletal muscle, the hormonal changes, the O 2 delivery to the periphery, the endothelium. In the second part, the role of the excitatory reflexes and the cardiac cachexia will be presented, and finally, the potential therapeutic implications are discussed. We believe that a better knowledge of the pathophysiology of this syndrome may contribute to the management of the patients and to the improvement in their stress tolerance and quality of life.

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Section: Airways Function Abnormalitiesmentioning

confidence: 99%

Exercise intolerance in chronic heart failure: mechanisms and therapies. Part I

Piepoli

Guazzi

Boriani

et al. 2010

European Journal of Cardiovascular Prevention & Rehabilitat

113

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“…In patients with left ventricular dysfunction, the failure of pulmonary blood flow (cardiac output) to increase appropriately during exercise aggravates the V/Q mismatch (high ventilation/perfusion) and the pulmonary dead space, leading to a greater arterialend-tidal PCO 2 difference. This greater difference attributes to the lower PETCO 2 and becomes much greater with the increasing severity of heart failure [4,7,20]. Also during exercise, patients with heart failure have a lower PaCO 2 as compared to healthy subjects because of their lactic acidosis-induced hyperventilation [21].…”

Section: Parameters Obtained From Cardiopulmonary Exercise Testingmentioning

confidence: 99%

“…It has been demonstrated that PETCO 2 becomes low in pulmonary vascular occlusive disease because of a lack of perfusion of ventilated lungs [5,6]. It has also been shown that cardiac patients have an abnormally low PETCO 2 during exercise, in accordance with a decreased peak _ VO 2 [4,7,8]. In patients with previous myocardial infraction, it has been noted that physical training increases PETCO 2 not at rest, but during exercise, in accordance with an improved response of cardiac output during exercise [9].…”

Section: Introductionmentioning

confidence: 99%

Prognostic value of end-tidal CO2 pressure during exercise in patients with left ventricular dysfunction

et al. 2008

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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.

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“…1,2 HF is one of the leading cause of death worldwide, with more than 20 million people affected. The overall prevalence of HF in the adult population in developed countries is 2%.…”

Section: Introductionmentioning

confidence: 99%

“…HF prevalence follows an exponential pattern, rising with age, and it affects 6e10% of people over the age of 65 years. 2 The cardinal symptoms of HF are fatigue and shortness of breath. 3,4 The origin of dyspnea in HF is probably multifactorial.…”

Section: Introductionmentioning

confidence: 99%

Study the mechanical pulmonary changes in patients with congestive heart failure (CHF) by impulse oscillometry

Nourizadeh¹,

Ghelich²,

Amin

et al. 2013

Journal of Cardiovascular Disease Research

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a b s t r a c tBackground: Heart failure is one of the most leading cause of death worldwide, but the mechanical characteristics of the pulmonary system in these patients have not been studied enough. The aim of this study was to measure mechanical pulmonary changes in patients with congestive heart failure (CHF) by using impulse oscillometry (IOS), which can obtain data by simpler means and independently from respiratory muscle strength. Materials and methods:We assessed 24 CHF patients and 24 controls by spirometry and IOS using the Jaeger IOS system. IOS measures central and peripheral airway resistances (R20, R5) and central and peripheral reactances (X20, X5) using sound waves with different frequencies, which superimposed on the patients respiratory tidal volume and then records reflects. P value < 0.05 was taken to be significant. Results: The mean age of patients and controls was 61 AE 10 and 57 AE 7 years, respectively. The mean ejection fraction (EF) was 37 AE 17% for patients and 55 AE 7% for controls. Patients had a lower X5 (À0.20 AE 0.13 vs À0.13 AE 0.07; P < 0.05), forced expiratory volume in 1 second (FEV1; 2.26 AE 0.68 vs 3.09 AE 0.82: P < 0.01 L/min), and forced vital capacity (FVC; 2.55 AE 0.86 vs 3.32 AE 0.87; P < 0.05) compared to the controls. They also had elevated R5: 0.37 AE 0.21 vs 0.27 AE 0.09; P < 0.06). X5 was correlated with spirometric abnormalities (P < 0.05) and was lower in patients than in controls. Conclusion: X5 was lower and R5 was higher in patients than in controls. CHF patients can be assessed by IOS more comfortable than by spirometry. IOS can reliably measure peripheral airway resistance in this group of patients.

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Lung Function and Exercise Gas Exchange in Chronic Heart Failure

Cited by 367 publications

References 27 publications

Exercise intolerance in chronic heart failure: mechanisms and therapies. Part I

Exercise intolerance in chronic heart failure: mechanisms and therapies. Part I

Prognostic value of end-tidal CO2 pressure during exercise in patients with left ventricular dysfunction

Study the mechanical pulmonary changes in patients with congestive heart failure (CHF) by impulse oscillometry

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