PubMed Health⌕ Search

Biomedical subjects

Piergiuseppe Agostoni

Publications and source records attributed to Piergiuseppe Agostoni.

At least 19 recordsLinked to original sources
PubMed2006

Gas diffusion and alveolar-capillary unit in chronic heart failure.

AIMS: Alveolar gas diffusion (DLCO) is impaired in chronic heart failure (CHF). Diffusion depends on membrane diffusion (DM) and the amount of blood participating in gas exchange (VC). How DM, VC, and the alveolar-capillary unit behave in relationship to CHF severity is unknown. METHODS AND RESULTS: We measured pulmonary function, including DLCO, DM, VC, and alveolar volume (VA), in 191 CHF patients in NYHA class I-III. CHF patients were grouped accordingly to peak exercise oxygen uptake (pVO(2)): group <12 mL/min/kg (n=24), group 12-16 (n=76), group 16-20 (n=64), and group >20 (n=27). DLCO, DM, VC, and VA were lowest in severe CHF and were linearly related to pVO(2) (DLCO, r=0.577, P<0.001; DM, r=0.490, P<0.001; VC, r=0.216, P<0.01; VA, r=0.565, P<0.01). DM/VC ratio, an index of the alveolar-capillary unit efficiency, was higher in group <12 (0.49+/-0.39 mL/min/mmHg/mL) and >20 (0.46+/-0.29), compared with 12-16 (0.34+/-0.19) and 16-20 (0.35+/-0.17). CONCLUSION: DLCO progressively worsens as CHF severity increases due to reduction in lung tissue participating to gas exchange (low VC and VA). In severe CHF, the few working alveolar-capillary units are the most efficient as shown by the high DM/VC. This is useful for maintaining gas exchange efficiency in severe CHF.

Capillaries↗
PubMed2006

Cardiopulmonary interaction in heart failure.

In heart failure lung dysfunction is frequent and is greater the greater the heart failure severity. It can be evaluated in terms of lung mechanics and gas diffusion. Indeed heart-lung interaction is related to heart dimensions and lung fluid content; furthermore heart-lung interaction is influenced by the body position. Lung diffusion is also altered in patients with chronic heart failure, and a low gas diffusion is associated with a reduced performance. During exercise, heart-lung interaction becomes more evident. Heart failure patients show an abnormal hyperventilation due to a progressively increased respiratory rate, and a lower tidal volume; hyperventilation is due to different causes including enhanced responses from chemo- and metabolo-receptors, increased CO(2) production and increased dead space ventilation. Several drugs affect the ventilatory pattern in heart failure patients: ACE-inhibitors and anti-aldosteronic drugs improve lung diffusion and ventilatory efficiency during exercise; beta-blockers reduce exercise-induced hyperventilation. Furthermore, ultrafiltration improves lung mechanics, both at rest and during exercise, through body fluid content reduction.

Angiotensin-Converting Enzyme Inhibitors↗
PubMed2006

Carvedilol reduces exercise-induced hyperventilation: A benefit in normoxia and a problem with hypoxia.

AIMS: To evaluate whether carvedilol influences exercise hyperventilation and the ventilatory response to hypoxia in heart failure (HF). METHODS AND RESULTS: Fifteen HF patients participated to this double blind, randomised, placebo controlled, cross-over study. Patients were evaluated by quality of life questionnaire, echocardiography, pulmonary function and cardiopulmonary exercise tests (ramp and constant workload) both in normoxia (FiO2 = 21%) and hypoxia (FiO2 = 16%, equivalent to a simulated altitude of 2000 m). Carvedilol improved clinical condition and reduced left ventricle size, but had no effect on lung mechanics. In normoxia during exercise, ventilation was lower, V(CO2) unchanged and PaCO2 (constant workload) or PetCO2 (ramp) higher with carvedilol, exercise capacity was unchanged (peak workload 92+/-22 and 90+/-22W for placebo and carvedilol, respectively). Abnormal V(E)/V(CO2) slope was reduced by carvedilol. Hypoxia increased ventilation but less with carvedilol; exercise capacity decreased to 87+/-21W (placebo) and to 80+/-11 W (carvedilol, p < 0.01). With hypoxia, carvedilol decreased V(E)/V(CO2) slope. At constant workload exercise with hypoxia, PaO2 decreased to 69+/-6 mm Hg (placebo) and to 64+/-5 (carvedilol, p < 0.01). CONCLUSION: Carvedilol reduced hyperventilation possibly by reducing peripheral chemoreflex sensitivity as suggested by PaCO2 increase with normoxia and PaO2 decrease with hypoxia without V(CO2) and V(D)/V(T) changes. Lessening hyperventilation is beneficial when breathing normally, but detrimental when hyperventilation is needed for exercise at high altitude.

Adrenergic beta-Antagonists↗
PubMed2006

Cardiopulmonary evidence of exercise-induced silent ischaemia.

BACKGROUND: Exercise-induced ST changes, suggestive of cardiac ischaemia, are found in asymptomatic patients. METHODS: Gas exchange kinetics were studied during exercise to help to separate patients affected by epicardial coronary disease from those without. Forty-eight patients, without angina symptoms and showing significant changes of ST during exercise, underwent a coronarography and maximal cardiopulmonary exercise test. Thirty-five healthy individuals of matched age and sex underwent a cardiopulmonary exercise test as controls. RESULTS: Patients were grouped according to the presence (group 1, n = 35) or the absence (group 2, n = 13) of significant coronary lesions at angiography. When corrected for predicted oxygen consumption (VO2) at peak exercise and at anaerobic threshold, results showed a low VO2 at peak exercise and anaerobic threshold in group 1 (68 +/- 19 and 84 +/- 17% of predicted, respectively) compared with normal subjects (91 +/- 19 and 96 +/- 24% of predicted VO2) and group 2 patients (86 +/- 17 and 96 +/- 18%). Also the ischaemic threshold, when normalized for predicted workload at peak exercise, occurred earlier in group 1 (67 +/- 22%) than in group 2 (87 +/- 19%). The time-related (Delta)VO2/Deltawork relationship showed a significant flattening above the anaerobic threshold in group 1 (7.4+/-2.2 versus 9.4+/-1.4 ml/watt per minute, P < 0.01), but not in controls or in group 2. Also the DeltaVO2/Deltawork relationship, above the ischaemic threshold, flattened in group 1, but not in group 2. CONCLUSION: The suggestion of major coronary disease in patients with exercise-induced ST changes is given by: (i) a flattening of the DeltaVO2/Deltawork relationship, above both the ischaemic and anaerobic thresholds; and (ii) low VO2 values at anaerobic and ischaemic thresholds.

Aged↗
PubMed2005

Cardiopulmonary exercise test evidence of isolated right coronary artery disease.

Isolated right coronary artery disease is usually difficult to diagnose because of frequent negativity of standard exercise stress test. We report a case of isolated coronary artery stenosis which was not detected by standard ECG stress testing. The cardiopulmonary exercise test showed a peculiar pattern: abrupt flattening in VO2/Work relationship, plateau in O2 pulse and 90 s afterwards a plateau in heart rate, probably related to vagal afferent stimulation by ischaemia of the postero-inferior wall of the left ventricle. Multidetector computed tomography of coronary vessels and coronary angiography confirmed isolated critical stenosis of middle right coronary artery. After revascularization by PTCA, normalization of cardiopulmonary exercise test was obtained.

Angioplasty, Balloon, Coronary↗
PubMed2005

Work-rate affects cardiopulmonary exercise test results in heart failure.

AIMS: Cardiopulmonary exercise test (CPET) is used to evaluate patients with chronic heart failure (HF) usually by means of a personalized ramp exercise protocol. Our aim was to evaluate if exercise duration or ramp rate influences the results. METHODS AND RESULTS: Ninety HF patients were studied (peak V (O(2)): >20 ml/min/kg, n=28, 15-20 ml/min/kg, n=39 and <15 ml/min/kg, n=23). Each patient did four CPET studies. The initial study was used to separate the subjects into three groups, according to their exercise capacity. In the remaining studies, work-rate was increased at three different rates designed to have the subjects reach peak exercise in 5, 10 and 15 min from the start of the ramp increase in work-rate, respectively. The order was randomized. The work-rate applied for the total population averaged 22.7+/-8.0, 11.6+/-3.7, 7.5+/-2.9 W/min with effective loaded exercise duration of 5 min and 16 s+/-29 s, 9 min and 43 s+/-49 s and 14 min and 32 s+/-1 min and 12 s for the 5-, 10- and 15-min tests, respectively. Peak V (O(2)) averaged 16.9+/-4.3*, 18.0+/-4.4 and 18.0+/-5.4 ml/min/kg for the 5-, 10- and 15-min tests, (*=p<0.001 vs. 10 min). The shortest test had the lowest peak heart rate and ventilation and highest peak work-rate. Peak V (O(2)) and heart rate were lowest in 5-min tests regardless of HF severity. The DeltaV (O(2))/Deltawork-rate was lowest in 5-min tests and highest in 15-min tests. At all ramp rates, DeltaV (O(2))/Deltawork-rate was lower for the subjects with the lower peak V (O(2)). The V (e)/V (CO(2)) slope and V (O(2)) at anaerobic threshold were not affected by the protocol for any grade of HF. CONCLUSIONS: In chronic HF, exercise protocol has a small effect on peak V (O(2)) and DeltaV (O(2))/Deltawork but does not affect V (O(2)) at anaerobic threshold and V (e)/V (CO(2)) slope.

Anaerobic Threshold↗
PubMed2005

Impaired bradykinin response to ischaemia and exercise in patients with mild congestive heart failure during angiotensin-converting enzyme treatment. Relationships with endothelial function, coagulation and inflammation.

Inflammation and endothelial dysfunction play important roles in the pathophysiology of congestive heart failure (CHF), and the peptide bradykinin, generated during inflammation, may act as a defence mechanism by inducing vasodilation. Plasma bradykinin levels are increased in experimental heart failure but low in patients with advanced chronic CHF despite treatment with angiotensin-converting enzyme (ACE) inhibitors. It is not currently known how bradykinin behaves in less severe phases of CHF controlled by long-term ACE inhibitor treatment. We studied 10 male patients with clinically stable chronic CHF [New York Heart Association (NYHA) class II] on long-term ACE inhibitor treatment and 10 normal sex- and age-matched control subjects. High performance liquid chromatography/radioimmunoassay methods were used to evaluate plasma levels of bradykinin in relation to an array of parameters of endothelial function, coagulation and inflammation before and after stimuli of forearm arterial occlusion and physical exercise. CHF patients had higher levels of bradykinin (P = 0.008), activated factor XII (P = 0.049), interleukin-6 (P = 0.050) and tumour necrosis factor receptor II (sTNFRII) (P = 0.026) than controls. Arterial occlusion and exercise significantly increased bradykinin and von Willebrand factor levels in controls but not in CHF patients. The increase in brachial artery diameter after arterial occlusion was less in CHF patients (P = 0.036) and inversely related to baseline plasma levels of bradykinin (r = -0.855, P = 0.002) and sTNFRII (r = -0.780, P = 0.008). NYHA class II CHF patients during long-term treatment with ACE inhibitors have increased bradykinin levels and signs of inflammation. They are unable to respond adequately to stimuli of ischaemia and physical exercise which both require vasodilation.

Adult↗
PubMed2005

Exercise capacity in patients with beta-thalassaemia intermedia.

Thalassaemia intermedia patients can suffer fatigue and exercise capacity reduction, possibly because of anaemia, deconditioning and lack of exercise-induced haemoconcentration. We studied 21 beta-thalassaemia intermedia patients, 10 splenectomised (group A) and 11 not splenectomised (group B). Patients were evaluated by cardiopulmonary exercise test with blood sampling for haemoglobin and plasma protein measurements at rest and peak. During exercise, an isolated increase of haemoglobin suggested spleen contraction while a parallel increase of haemoglobin and proteins suggested fluid filtration through capillary wall. Groups were homogeneous for age and gender. Peak oxygen consumption (VO2) was 22.5 +/- 4.4 ml/min/kg (51 +/- 14%) and 24.3 +/- 7.0 (53 +/- 12%) in groups A and B respectively [not significant (NS)]. At rest, haemoglobin was 8.8 g/dl in both groups. Exercise-induced increment was 0.4 +/- 0.2 and 1.0 +/- 0.4 g/dl (P < 0.001) for haemoglobin and 4.0 +/- 3.0 and 5.0 +/- 4.0 g/l (NS) for proteins, in groups A and B respectively. Anaemia was the major cause of peak VO2 reduction (1097 +/- 260 ml/min). However, anaemia did not explain the entire exercise capacity reduction, suggesting the presence of muscular deconditioning. Exercise capacity is reduced in beta-thalassaemia intermedia because of anaemia and muscular deconditioning. Spleen contraction does not significantly influence exercise capacity although exercise-induced haemoconcentration was greater in patients with spleen.

Adult↗
PubMed2005

Lateral decubitus position generates discomfort and worsens lung function in chronic heart failure.

BACKGROUND: Lateral decubitus position is poorly tolerated by heart failure patients. STUDY OBJECTIVES: To evaluated pulmonary function and lung diffusion in heart failure patients in the following five body positions: sitting, prone, supine, and left and right decubitus. SETTING: Heart failure unit of a university hospital. SUBJECTS: We studied 14 chronic heart failure patients in New York Heart Association class III and 14 healthy volunteers. MEASUREMENTS AND RESULTS: After 15 min of a selected position, subjects were evaluated by a discomfort scale, ear oximetry, and pulmonary function, which included FEV1, FVC, vital capacity (VC), alveolar volume, and diffusing capacity of the lung for carbon monoxide (D(LCO)) with subcomponent membrane resistance (DM) and capillary volume. In healthy subjects, we observed a reduction of D(LCO) and capillary volume in both lateral decubiti. Some discomfort was documented in both lateral decubiti when selected positions were compared with the sitting position. In the sitting position, pulmonary function suggested slight restriction ([mean +/- SD] FVC, 89.8 +/- 22.3% predicted; FEV1, 84.7 +/- 16.9% predicted, VC, 88.6 +/- 21.5% predicted; and FEV1/VC, 74 +/- 7) with low D(LCO) (73 +/- 19% predicted). Compared with sitting, lung mechanics were unchanged in prone and supine positions; FEV1, FVC, and FEV1/VC were lower when patients were lying on their side, with unchanged alveolar volume and VC. D(LCO) was similar when comparing sitting, prone, and supine positions, and it was lower in lateral decubitus because of the lower capillary volume (vs sitting) and DM (vs prone and supine). Body position-related FVC and D(LCO) reduction were greatest in the largest hearts (deltaFVC and deltaD(LCO) vs left ventricle diastolic volume R = 0.524, p < 0.05 and R = 0.630, p < 0.02, respectively; deltaFVC and deltaD(LCO) vs cardiothoracic index R = 0.539, p < 0.05 and R = 0.685, p < 0.01, respectively). CONCLUSIONS: In heart failure, lateral decubitus airway obstruction and lung diffusion impairment become greater as heart dimensions increase.

Aged↗
PubMed2004

Neurohormonal activation is associated with increased levels of plasma matrix metalloproteinase-2 in human heart failure.

AIMS: Development of heart failure depends on systemic and molecular abnormalities among which are the activation of neurohormonal systems and the increase of matrix metalloproteinases (MMPs). This study assessed the relationship between catecholamines and active MMPs in vivo in patients with severe congestive heart failure (CHF) and in vitro in human cardiac fibroblasts. METHODS AND RESULTS: Forty patients with CHF due to dilated cardiomyopathy, either idiopathic (n=20) or secondary to ischaemic heart disease (n=20), were compared with 20 healthy subjects. Plasma MMP-2 and MMP-9 activity, but not TIMP-2, were significantly higher in patients than in controls (median MMP-2, 270 vs. 214 ng/mL, P=0.006; MMP-9 16.3 vs. 8.7 ng/mL, P<0.0001). Similarly, noradrenaline, but not adrenaline, was significantly higher in patients (noradrenaline 645 vs. 157 pg/mL, P<0.0001; adrenaline 86.0 vs. 72.6 pg/mL, P=0.68). No difference in any parameter was observed between patient groups. The intra-group correlation between MMP-2 and noradrenaline was significant (r=0.33, P=0.01); indeed, noradrenaline appear to be a predictor of MMP-2. Moreover, this catecholamine increased MMP-2 in human cardiac fibroblasts. CONCLUSIONS: The positive correlation between noradrenaline and MMP-2 in severe CHF patients, together with the in vitro induction of MMP-2 by this catecholamine, suggests a potential biochemical link between noradrenaline and MMP-2.

Cardiomyopathy, Dilated↗
PubMed2004

Spironolactone improves lung diffusion in chronic heart failure.

AIMS: To evaluate whether anti-aldosteronic treatment influences lung diffusion (DLCO) in chronic heart failure (HF) patients. Spironolactone improves clinical conditions and prognosis in chronic HF and reduces connective tissue matrix turnover; DLCO abnormalities in chronic HF are related to increase in fibrosis and connective tissue derangement. METHODS AND RESULTS: Thirty stable chronic HF patients, with reduced DLCO (<80% of predicted), were randomly assigned to active treatment (25 mg spironolactone daily) or placebo in addition to conventional anti-failure treatment. They were evaluated by quality of life questionnaire, laboratory investigations, cardiopulmonary exercise test, and pulmonary function test, which included DLCO and membrane diffusing capacity (DM). The evaluation was done before treatment and 6 months after. Quality of life score and standard pulmonary function tests were not significantly affected by spironolactone, while active treatment increased DLCO due to an increase of DM (DLCO: 18.3+/-3.9 vs. 19.9+/-5.5 mL/min/mmHg; DM: 28.1+/-7.7 vs. 33.3+/-8.6 mL/min/mmHg) and peak oxygen consumption (peak VO2 16.8+/-1.9 vs.18.6+/-2.2 mL/min/kg). Increments of DLCO and peak VO2 were linearly related (R=0.849, P<0.001). CONCLUSION: These data show a positive effect of spironolactone on gas diffusion and exercise capacity suggesting a novel mechanism by which anti-aldosteronic drugs improve HF clinical condition and prognosis.

Exercise Test↗
PubMed2004

Exercise-induced changes in exhaled nitric oxide in heart failure.

BACKGROUND: In heart failure abnormalities of pulmonary function are frequently observed as shown by hyperpnea, reduced lung compliance, reduced alveolar-capillary gas diffusion, positive methacholine challenge and, during exercise, early expiratory flow limitation. Nitric oxide (NO) might be related to all the above abnormalities. AIMS: We evaluated whether a correlation between exhaled NO (eNO) and lung function exists at rest and during exercise in heart failure. METHODS: We studied 33 chronic heart failure patients and 11 healthy subjects with: (a) standard pulmonary function, (b) lung diffusion for carbon monoxide (DLco) including its subcomponents, capillary volume and membrane resistance and eNO both at rest and during light exercise, (c) maximal cycloergometer cardiopulmonary exercise test. RESULTS: Forced expiratory volume in 1 s (FEV(1)) was reduced in heart failure patients (83+/-17% of predicted), as was DLco (75+/-18% of predicted) due to reduced membrane resistance (32.6+/-10.3 ml mmHg(-1) min(-1) vs. 39.9+/-6.9 in patients vs. controls, P<0.02). Exhaled NO was lower in patients vs. controls (9.7+/-5.4 ppm vs. 14.4+/-6.4, P<0.05) and was, during exercise, constant in patients and reduced in controls. No significant correlation was found between eNO and lung function. Vice-versa eNO changes during exercise were correlated with peak exercise oxygen consumption (r=0.560, P<0.001). CONCLUSIONS: The hypothesis of a link between eNO and lung function in heart failure was not proved. The correlation between eNO changes during exercise and peak V(O(2)) might be due to hemoglobin oxygenation, which binds NO to hemoglobin.

Aged↗
PubMed2003

Exercise-induced pulmonary edema in heart failure.

BACKGROUND: In heart failure (HF) patients, exercise may increase pulmonary capillary hydrostatic pressure and thereby generate pulmonary edema. If pulmonary edema developed, alveolar-capillary membrane conductance (Dm), measured immediately after exercise, would decrease. To test this hypothesis, we measured Dm before and at 2 and 60 minutes after exercise. METHODS AND RESULTS: We studied 10 HF patients with exercise-induced periodic breathing, 10 with peak o2 < or =15 mL x min(-1) x kg(-1) (severe HF), 10 with o2=15 to 20 mL x min(-1) x kg(-1) (moderate HF), and 10 normal subjects (control). Using the Roughton-Forster technique, we measured carbon monoxide diffusion capacity (DLco) and its components, capillary blood volume (Vc) and Dm, at rest and 2 and 60 minutes after exercise. At rest, DLco and Dm were lowest in periodic breathing and highest in control subjects. Dm decreased in periodic breathing, severe HF, and moderate HF (-7.83+/-3.98, -5.57+/-2.03, and -3.85+/-3.53 mL x min(-1) x mm Hg(-1), respectively; P<0.01) at 2 minutes after exercise but not in control subjects. Vc increased in all groups at 2 minutes and remained elevated at 60 minutes only in periodic breathing. Dm/Vc was decreased in periodic breathing, severe HF, and moderate HF at 2 minutes but not in control subjects. Dm and Dm/Vc remained low at 60 minutes only in periodic breathing. CONCLUSIONS: Dm decreases after exercise in HF patients but not in control subjects, which suggests a decrease in conductance across the alveolar-capillary barrier, as with pulmonary edema. The reductions were most marked in HF patients with periodic breathing and less reduced in less severe HF.

Aged↗
PubMed2002

Effect of non-insulin-dependent diabetes mellitus on pulmonary function and exercise tolerance in chronic congestive heart failure.

In chronic congestive heart failure (CHF), backward effects of left ventricular dysfunction alter pulmonary volumes and gas diffusion. Some of these disorders are detected in some patients with diabetes mellitus, possibly due to a microangiopathic process and nonenzymatic glycosylation of lung tissue proteins. We explored the possibility that coexistence of non-insulin-dependent diabetes mellitus (NIDDM) may potentiate the deterioration of lung function in CHF. In 20 normoglycemic patients (group 1) and in 20 patients with NIDDM (group 2), with New York Heart Association class II to III CHF due to idiopathic or ischemic cardiac disease, and in 20 controls (groups were age- and gender-matched), we investigated cardiac function, pulmonary volumes, carbon monoxide diffusion (DL(CO)) and its alveolar-capillary membrane (D(M)) subcomponent, oxygen uptake and dead space-to-tidal volume ratio (pVD/VT) at peak exercise (individualized ramp test), and slope of ventilation-to-carbon dioxide production ratio (VE/VCO(2)) during exercise. Although, compared with reference subjects, both patient groups had similar variations in left ventricular diastolic volume, ejection fraction, and pulmonary wedge pressure; in group 2 lung volumes, DL(CO), D(M), and oxygen uptake were significantly more reduced; in this group there was no overlap of individual results of DL(CO) and D(M) with those in controls; VE/VCO(2) slope and pVD/VT also were significantly increased, and inversely correlated with D(M). Thus, coexistence of NIDDM makes pulmonary dysfunction worse in CHF, and significantly enhances exercise intolerance.

Analysis of Variance↗
PubMed2002

Serum to urinary sodium concentration ratio is an estimate of plasma renin activity in congestive heart failure.

We investigated the relationship between plasma renin activity (PRA) and serum ([sNa(+)]) and urinary ([uNa(+)]) sodium concentrations in 124 congestive heart failure (CHF) patients (II-IV NYHA class) and 20 healthy subjects. According to PRA (> or <3 ng ml(-1) h(-1)) and [sNa(+)] (> or <135 mEq l(-1)), patients were classified as Group A (normal PRA and normal [sNa(+)], n=39), Group B (increased PRA and normal [sNa(+)], n=62) and Group C (low [sNa(+)], n=23). Measurements were performed at rest and, in 26 cases, after extracorporeal ultrafiltration (UF). At rest, [sNa(+)] and [uNa(+)], and their difference ([sNa(+)]-[uNa(+)]), were linearly correlated with PRA, but the values did not allow differentiation of control subjects from patients or differentiation of patients with from those without renin-angiotensin system (RAS) activation. Conversely, the [sNa(+)]/[uNa(+)] ratio showed the best correlation with PRA (r=0.79, P<0.0001). UF-induced PRA changes were linearly correlated with [sNa(+)]/[uNa(+)] ratio changes (r=0.67, P=0.002), but not with those of [sNa(+)], [uNa(+)] and [sNa(+)]-[uNa(+)]. In CHF, the [sNa(+)]/[uNa(+)] ratio best correlates with PRA and reflects the basal activity as well as the rapid changes (as those induced by UF) of the RAS. Therefore, it can be considered a strong and easily available marker of PRA.

Adult↗
PubMed2002

Exercise hyperpnea in chronic heart failure: relationships to lung stiffness and expiratory flow limitation.

The changes in breathing pattern and lung mechanics in response to incremental exercise were compared in 14 subjects with chronic heart failure and 15 normal subjects. In chronic heart failure subjects, exercise hyperpnea was achieved by increasing breathing frequency more than tidal volume. The rate of increase in breathing frequency with carbon dioxide output was inversely correlated (r = -0.61, P < 0.05) with dynamic lung compliance measured at rest, but not with static lung compliance either at rest or at maximum exercise. Although decrease in expiratory flow reserve near functional residual capacity in chronic heart failure occurred earlier with exercise than in the normal subjects (P < 0.01), it was not correlated with changes in breathing pattern or occurrence of tachypnea. Tachypnea was achieved in chronic heart failure subjects with an increase in duty cycle because of a greater than normal decrease in expiratory time with exercise. We conclude that in chronic heart failure preexisting increase in lung stiffness plays a significant role in causing tachypnea during exercise. The results of the present study do not support the hypothesis that dynamic compression of the airways downstream from the flow-limiting segment occurring during exercise contributes to hyperpnea.

Adult↗