Inspiratory muscle weakness and dyspnea in chronic heart failure.

Dyspnea is a common, disabling symptom in chronic heart failure, yet the underlying mechanisms remain unknown. The respiratory muscle pump is composed of skeletal muscles whose strength directly influences the pump's performance. Respiratory muscle weakness is important in the dyspnea experienced by some patients with pulmonary disease; however, the role of the respiratory muscle pump in the dyspnea of chronic heart failure has not previously been examined. To assess respiratory muscle strength and its relation to dyspnea during daily activity, we measured maximum inspiratory and expiratory mouth pressures as indices of respiratory muscle strength and the baseline dyspnea index in nine stable, chronic cardiac pump failure patients who had no evidence of primary lung disease, and in nine age- and sex-matched healthy control subjects. The chronic heart failure patients, when compared with their matched control subjects, had reduced inspiratory and expiratory muscle strength, and both inspiratory and expiratory muscle strength were significantly correlated with dyspnea during daily activity (r2 = 0.80, p = 0.001 and r2 = 0.45, p = 0.05, respectively). Inspiratory muscle strength accounted for all of the variance in dyspnea that was correlated with respiratory muscle strength when the relative contributions of inspiratory and expiratory muscle strength were examined. There was no correlation between lung volumes or spirometry and dyspnea in the heart failure patients. These findings indicate that patients with stable chronic heart failure have inspiratory and expiratory muscle weakness and further suggest that the respiratory muscle pump significantly contributes to the dyspnea during the activities of daily living.     

Inspiratory muscle endurance in patients with chronic heart failure.

OBJECTIVE: To assess the significance of changes in respiratory muscle endurance in relation to respiratory and limb muscle strength in patients with mild to moderate chronic heart failure using a threshold loading technique. SUBJECTS: 20 patients with chronic heart failure (17 male) aged 63.8 (SD 7.4) years and 10 healthy men aged 63.1 (5.6) years. Heart failure severity was New York Heart Association (NYHA) grade II (n = 11) and NYHA grade III/IV (n = 9). METHODS: Respiratory muscle strength was measured from mouth pressures during maximum inspiratory effort (MIP) at functional residual capacity (FRC) and limb muscle strength was measured using a hand grip dynamometer. Inspiratory muscle endurance was measured using a threshold loading technique. The total endurance duration, the maximum threshold pressure achieved (P-Max), and the inspiratory load (% ratio of P-Max/MIP) were recorded in all subjects. RESULTS: Inspiratory muscles were weaker in patients with heart failure than in the controls [MIP 53.6 (16.5) v 70.9 (20.2) cm H2O, P < 0.05]. Hand grip strength was similar in both subject groups [31.6 (SD) v 36.1 (15.9) dynes]. Total endurance duration was significantly reduced in the patient group [494 (223) v 996 (267) s, P < 0.01], as was the maximal threshold pressure achieved [P-Max 18.5 (6.4) v 30.7 (6.6) cm H2O, P < 0.01]. When expressed as a percentage of MIP, P-Max was also lower in the patients [35.2 (11.8) v 44.8 (11.4)%, P < 0.05]. There was no significant correlation between any measure of endurance and limb muscle strength. CONCLUSIONS: Respiratory muscle endurance is reduced in patients with chronic heart failure. These changes probably reflect a generalised skeletal myopathy and provide further evidence of respiratory muscle dysfunction in patients with this disease. Respiratory muscle endurance needs now to be related to symptoms and the effects of treatment and respiratory muscle training should also be explored.     

Do hemodynamic indices correlate with maximum exercise capacity and oxygen consumption in chronic congestive heart failure?

The mechanism of exercise intolerance in chronic congestive heart failure remains unclear. We correlated resting haemodynamic variables with the peak exercise capacity and maximum oxygen consumption (VO2 max) in patients with congestive heart failure in 27 studies on treadmill exercise testing using the modified Bruce protocol. VO2 max was measured using breath by breath expiratory gas analysis. The patients were in severe congestive heart failure (NYHA class II and III, pulmonary artery wedge pressure 23 +/- 2 mmHg, cardiac index 2.4 +/- 0.21 l/min/m2). VO2 max was 23 +/- 2 ml/kg/min. Fatigue was the commonest symptom limiting the exercise. None of the hemodynamic variables correlated well with VO2 max. [right atrial pressure (r = 0.08), pulmonary artery pressure (r = 0.05), pulmonary artery wedge pressure (r = 0.08), aortic pressure (r = -0.3) & cardiac index (r = 0.29)]. Both uni- and multi-variate analysis failed to show any relation between VO2 max and resting hemodynamic variables. We conclude that unlike the acute heart failure syndromes, resting hemodynamic variables do not correlate with exercise capacity in patients with chronic congestive heart failure. The abnormal resting haemodynamics do not limit exercise in these patients. Peripheral mechanisms may thus be more important.     

Diaphragm strength in chronic heart failure.

Reduced respiratory muscle strength has been reported in chronic heart failure (CHF) in several studies. The data supporting this conclusion come almost exclusively from static inspiratory and expiratory mouth pressure maneuvers (MIP, MEP), which many subjects find difficult to perform. We therefore performed a study using measurements that are less dependent on patient aptitude and also provide specific data on diaphragm strength. In 20 male patients and 15 control subjects we measured MIP and MEP as well as esophageal and transdiaphragmatic pressure during maximal sniffs (Sn Pes, Sn Pdi) and cervical magnetic phrenic nerve stimulation (Tw Pdi). In a subgroup the response to paired phrenic nerve stimulation (pTw Pdi) at interpulse intervals from 10 to 200 ms (5 to 100 Hz) was also determined. As expected, MIP was significantly reduced in the CHF group (CHF, 69.5 cm H(2)O; control, 96.7 cm H(2)O; p = 0.01), but differences were much less marked for Sn Pes (CHF, 95.2 cm H(2)O; control, 104.8 cm H(2)O; p = 0.20) and MEP (CHF, 109.1 cm H(2)O; control, 135.7 cm H(2)O; p = 0.09). Diaphragm strength was significantly reduced (Sn Pdi: CHF, 123.8 cm H(2)O; control 143.5 cm H(2)O; p = 0.04. Tw Pdi: CHF, 21.4 cm H(2)O; control, 28.5 cm H(2)O; p = 0.0005). Paired phrenic nerve stimulation suggested a trend to increased twitch summation at 5 to 20 Hz in CHF, although this did not reach significance. We conclude that mild reduction in diaphragm strength occurs in CHF, possibly because of an increased proportion of slow fibers, but overall strength of the respiratory muscles remains well preserved.     

Inspiratory muscle strength in asthma

Augmentation of inspiratory muscle strength (Pimax) represents an adaptive response to airway obstruction. We explore the possibility that respiratory muscle weakness may herald hospital admission during acute bronchospasm. The Pimax measured 81 +/- 25 percent of a predicted value in 20 patients with acute bronchospasm (forced expiratory volume in one second, 36 +/- 17 percent predicted). Pimax was related to both hyperinflation (functional residual capacity, as percent predicted) and body weight (subjects were 122 +/- 29 percent ideal body weight), but not to the degree of airway obstruction per se. Furthermore, measurements of axial (craniocaudal) motion of the rib cage and asynchrony of rib cage and abdominal motions during tidal breathing did not correlate with either the degree of air flow obstruction or Pimax. We conclude that little if any respiratory muscle weakness occurs with bronchospasm. Furthermore, Pimax does not correlate with the degree of airway obstruction and does not explain abnormalities of rib cage and abdominal motion associated with asthma.     

Dependence of oxygen consumption on oxygen delivery in patients with chronic congestive heart failure

We previously have shown that in patients with adult respiratory distress syndrome (ARDS) oxygen consumption (VO2) is linearly related to oxygen delivery (DO2) below a threshold DO2 of 21 ml/min/kg. To evaluate this relationship in chronic congestive heart failure (CHF), we studied eight patients with chronic CHF at baseline and during treatment with nitroglycerin. The resting DO2 and VO2 were 10.7 +/- 2.3 ml/min/kg and 3.8 +/- 0.87 ml/min/kg, respectively. In our eight patients, we found a significant relationship between changes in VO2 and in DO2 (delta VO2 = 0.16 + 0.34 X delta DO2, r = 0.84, n = 29). There was no significant relationship between DO2 and mixed venous oxygen tension (PvO2, r = 0.16), nor was there a significant relationship between cardiac output (Qt) and PvO2 (r = 0.21). We conclude that in patients with chronic CHF, changes in VO2 appear to be dependent on changes in DO2. This may represent an adaptive tissue response to chronically reduced systemic oxygen transport.     

Inspiratory muscle relaxation rate slows during exhaustive treadmill walking in patients with chronic heart failure

Exercise intolerance is a feature of chronic heart failure (CHF). We hypothesized that excessive loading of the respiratory muscle pump might contribute to exertional breathlessness. One marker of excessive muscle-loading is slowing of maximum relaxation rate (MRR) and, therefore, to test our hypothesis, we investigated the effect of exhaustive treadmill walking on inspiratory muscle MRR in patients with CHF. We studied eight stable patients with mild-moderate CHF walking on a treadmill until termination because of severe dyspnea. Inspiratory muscle MRR was determined from esophageal pressure (Pes) change during submaximal sniffs (Sn) before and immediately after exercise to a mean (SD) minute ventilation of 77 () L/min. For comparison, nine healthy subjects performed a similar protocol; exercise was terminated either by severe dyspnea or when minute ventilation reached 100 L/min. There were no significant differences in terms of heart rate, respiratory rate, tidal volume, or inspiratory duty cycle at cessation of exercise. The mean slowing of Sn Pes MRR in the first minute after termination of exercise in the CHF group was 22.4% and in the normal control group it was 2.8% (p < 0.01). Our data show that slowing of inspiratory muscle relaxation rate occurs in patients with CHF walking to severe breathlessness. We conclude that severe loading of the inspiratory muscles is a feature of exertional dyspnea in CHF.     

Inspiratory muscle training in patients with heart failure and inspiratory muscle weakness: a randomized trial.

OBJECTIVES: This study sought to evaluate the effects of inspiratory muscle training in inspiratory muscle strength, as well as in functional capacity, ventilatory responses to exercise, recovery oxygen uptake kinetics, and quality of life in patients with chronic heart failure (CHF) and inspiratory muscle weakness. BACKGROUND: Patients with CHF may have reduced strength and endurance in inspiratory muscles, which may contribute to exercise intolerance and is associated with a poor prognosis. METHODS: Thirty-two patients with CHF and weakness of inspiratory muscles (maximal inspiratory pressure [Pi(max)] <70% of predicted) were randomly assigned to a 12-week program of inspiratory muscle training (IMT, 16 patients) or to a placebo-inspiratory muscle training (P-IMT, 16 patients). The following measures were obtained before and after the program: Pi(max) at rest and 10 min after maximal exercise; peak oxygen uptake, circulatory power, ventilatory oscillations, and oxygen kinetics during early recovery (VO2/t-slope); 6-min walk test; and quality of life scores. RESULTS: The IMT resulted in a 115% increment Pi(max), 17% increase in peak oxygen uptake, and 19% increase in the 6-min walk distance. Likewise, circulatory power increased and ventilatory oscillations were reduced. The VO2/t-slope was improved during the recovery period, and quality of life scores improved. CONCLUSIONS: In patients with CHF and inspiratory muscle weakness, IMT results in marked improvement in inspiratory muscle strength, as well as improvement in functional capacity, ventilatory response to exercise, recovery oxygen uptake kinetics, and quality of life.     

Effect of exercise therapy on oxygen consumption in patients with chronic heart failure

The effect of exercise training on delta Vo2/delta WR was studied in 12 patients(11 men, one woman, mean age 62 +/- 9 yr)with chronic heart failure(old myocardial infarction, dilated cardiomyopathy, patients after coronary arterial bypass graft surgery and patients after aortic valve replacement). Cardiopulmonary exercise testing was performed to decide the exercise tolerance and assess the delta Vo2/delta WR. Patients underwent physical training at the anaerobic threshold for 3 months. Cardiopulmonary exercise testing was performed after the second week and after the third month. The anaerobic threshold increased at the third month compared with before exercise testing and the second week(p < 0.05, respectively) (before exercise testing: 13.6 +/- 2.0 ml/min/kg, the second week: 14.7 +/- 2.5 ml/min/kg, the third month: 16.2 +/- 2.1 ml/min/kg). The delta Vo2/delta WR increased at the second week compared with before exercise testing(before exercise testing: 8.9 +/- 1.9 ml/min/W, the second week: 10.6 +/- 1.9 ml/min/W, p < 0.05), but significantly decreased at the third month compared with the second week(the third month: 9.4 +/- 1.7 ml/min/W, p < 0.05). Serial increase of the anaerobic threshold and the peak Vo2/heart rate suggests that the exercise tolerance and cardiac function of the patients improved significantly. The increase of the delta Vo2/delta WR after the first 2 weeks seemed to depend on the luxury blood supply to both working and non-working muscles. The decrease of delta Vo2/delta WR at the third month may be due to the redistribution of the blood flow to the working muscles.     

Combining the ventilatory response to exercise and peak oxygen consumption is no better than peak oxygen consumption alone in predicting mortality in chronic heart failure

BACKGROUND: A low peak oxygen uptake (pVO(2)) and steep VE/VCO(2) slope are independently associated with a worse prognosis in patients with chronic heart failure (CHF). We wished to confirm whether combining these variables as a ratio would lead to a more accurate predictor of prognosis than using either alone. METHODS: 388 CHF patients completed a treadmill-based cardiopulmonary exercise test (CPET) to volitional exhaustion using a modified Bruce protocol. RESULTS: 212 CHF patients completed the CPET with a peak RER >or= 1.0. Of these, 48 patients died and one was transplanted during follow-up. In surviving patients, the median follow-up period was 42 months (IQR 34-49 months). The ratio VE/VCO(2) slope/pVO(2) was calculated for each individual and its ability to predict outcome compared with other variables. The Cox multivariable survival analysis showed that pVO(2) was the strongest independent predictor of mortality in CHF patients. CONCLUSION: Our study shows that the composite variable VE/VCO(2) slope/pVO(2) is a less effective prognosticator than pVO(2) alone in patients with CHF.     

Respiratory muscle strength in congestive heart failure

In experimental animals, conditions which drastically decrease cardiac output may reduce the strength and endurance of respiratory muscles leading to hypercapnic respiratory failure. Because patients with chronic CHF have reduced cardiac output and vital capacity (FVC), we measured PImax and PEmax and maximal handgrip force in 16 patients with CHF and 18 AMNs. The patients with CHF had a mean left ventricular ejection fraction of 26 +/- 7 percent. Maximal respiratory pressures were significantly reduced; group mean values (+/- SD) for PImax at FRC were 41.4 +/- 5.6 cm H2O (CHF) and 102.1 +/- 27.4 cm H2O (AMN) (p less than 0.001), with PImax values in five patients with CHF as low as 20 to 30 cm H2O. In most patients, PEmax was comparably reduced. Handgrip force was less dramatically reduced, suggesting selective respiratory muscle weakness. Possible explanations include reduction in respiratory muscle blood flow or generalized muscular atrophy and weakness related to cardiac cachexia.     

Fragility is a key determinant of survival in heart failure patients

Background

Heart failure (HF) is a chronic condition with poor prognosis, and has a high prevalence among older adults. Due to older age, fragility is often present among HF patients. However, even young HF patients show a high degree of fragility. The effect of fragility on long-term prognosis in HF patients, irrespective of age, remains unexplored. The aim of this study was to assess the influence of fragility on long-term prognosis in outpatients with HF.

Methods and results

At least one abnormal evaluation among four standardized geriatric scales was used to identify fragility. Predefined criteria for such scales were: Barthel Index, < 90; OARS scale, < 10 in women and < 6 in men; Pfeiffer Test, > 3 (± 1, depending on educational grade); and ≥ 1 positive response for depression on the abbreviated Geriatric Depression Scale (GDS). We assessed 1314 consecutive HF outpatients (27.8% women, mean age years 66.7 ± 12.4 years with different etiologies. Fragility was detected in 581 (44.2%) patients. 626 deaths occurred during follow-up; the median follow-up was 3.6 years [P₂₅–P₇₅: 1.8–6.7] for the total cohort, and 4.9 years [P₂₅–P₇₅: 2.5–8.4] for living patients. Fragility and its components were significantly associated with decreased survival by univariate analysis. In a comprehensive multivariable Cox regression analysis, fragility remained independently associated with survival in the entire cohort, and in age and left ventricular ejection fraction subgroups.

Conclusion

Fragility is a key determinant of survival in ambulatory patients with HF across all age strata.     

Inspiratory muscle strength and endurance in patients with chronic obstructive pulmonary disease

The maximal inspiratory pressure (MIP) and the sustainable inspiratory maximal pressure (SIPm) in 79 patients with chronic obstructive pulmonary disease (COPD) which were divided into the mild group (MG) and the mid-severe group (MSG) were measured. The results showed that MIP and SIPm were significantly lower in MSG than the prediction and in MG, the inspiratory fatigue in MSG was taken place in lower load and shorter time. We considered: MIP and SIPm fallen significantly in COPD patients might play a very important role in developing patients' respiratory failure.     

Alterations of skeletal muscle in chronic heart failure.

BACKGROUND. The present study was designed to define the prevalence and characteristics of skeletal muscle alterations in patients with chronic heart failure (CHF) and their relation to exercise capacity. METHODS AND RESULTS. The ultrastructure of skeletal muscle was analyzed by ultrastructural morphometry in 57 patients with CHF and 18 healthy controls. The volume density of mitochondria (Vvm) and the surface density (Svmc) of mitochondrial cristae were evaluated as a structural correlate of oxidative capacity of skeletal muscle. Vvm and Svmc were reduced by approximately 20% in patients with severe CHF irrespective of age and etiology. The cytochrome oxidase activity in mitochondria as determined by cytochemistry and subsequent morphometry in a subset of patients (n = 10) was significantly decreased in heart failure (p less than 0.01). The capillary length density of skeletal muscle was reduced in CHF (n = 12, p less than 0.05), and the fiber type distribution was shifted to type II fibers (n = 15, p less than 0.05). Vvm and Svmc were significantly related to peak exercise VO2 (r = 0.56, p less than 0.001, n = 60) and to VO2 at anaerobic threshold (r = 0.535, p less than 0.0001, n = 60). In 16 patients with severe heart failure, Vvm was inversely related to the duration of heart failure (r = 0.545, p less than 0.03). In 11 patients who underwent repeat biopsies after 4 months, a correlation was observed between the change in Vvm and the change in peak exercise VO2 (r = 0.89, p less than 0.001). CONCLUSIONS. These findings indicate that patients with CHF develop significant ultrastructural abnormalities of skeletal muscle reflecting a depressed oxidative capacity of working muscle. It appears that these alterations of skeletal muscle contribute to the decreased exercise capacity of these patients but are, in principle, reversible by an effective treatment regimen.