Biomedical subjects

Loredana Stendardi

Publications and source records attributed to Loredana Stendardi.

9 recordsLinked to original sources

PubMed2006

Respiratory muscle energetics during exercise in healthy subjects and patients with COPD.

The energy expenditure required by the respiratory muscles during exercise is a function of their work rate, cost of breathing, and efficiency. During exercise, ventilatory requirements increase further exacerbating the potential imbalance between inspiratory muscle load and capacity. High level of exercise intensity in conjunction with contracting respiratory muscles is the reason for respiratory muscle fatigue in healthy subjects. Available evidence would suggest that fatigue of the diaphragm and other respiratory muscles is an important mechanism involved in redistribution of blood flow. Reflex mechanisms of sympathoexcitation are triggered in fatigued diaphragm during heavy exercise when cardiac output is not sufficient to adequately meet the high metabolic requirements of both respiratory and limb musculature. It is very likely that local changes in locomotor muscle blood flow may occur during exhaustive endurance exercise and that changes may have important effect on O2 transport to the working locomotor muscles and, therefore, on their fatigability. In a condition when the respiratory muscles receive their share of blood flow at the expense of limb locomotor muscles, minimizing mechanical work of breathing and therefore its metabolic cost allows a greater amount of cardiac output to be available to be delivered to working limb muscles. Malfunction in any of the multiple components responsible for circulatory flow and O2 delivery will limit the blood supply therefore inhibiting the supply of O2 and the energy substrate to the contracting muscles. Studies are needed to overcome these limitations.

Energy Metabolism↗

PubMed2006

Dyspnea and asthma.

PURPOSE OF REVIEW: Dyspnea--the perception of respiratory discomfort--is a primary symptom of asthma. This review examines possible ways to link mechanisms, measurement and treatment that will increase our understanding of this condition. RECENT FINDINGS: Functional neuroimaging methods have proven to be powerful tools that serve as advanced models of sensor motor brain function. Studies examining functional neuroimaging methods have revealed activation of distinct brain areas associated with increased dyspnea. Pulmonary hyperinflation has been proposed to influence the perception of dyspnea. The association of hyperinflation with minor levels of bronchoconstriction reflects the partition of the sensory effect of airway narrowing per se from that of the attendant elastic loading of the inspiratory muscles. There is evidence to suggest, however, that hyperinflation does not play an important role in the pathogenesis of exercise dyspnea as it does during induced bronchoconstriction. Decreased levels of perception of airway obstruction may be a risk factor associated with life-threatening asthma. A poor perceiver may be vulnerable to further hypoxia-induced suppression of respiratory sensation. Monitoring the response to bronchodilator therapy with formoterol and salbutamol in patients with acute or chronic asthma has resulted in significantly faster improvement in dyspnea, within 2 min. SUMMARY: Regardless of the factors involved, much variability in dyspnea scores remains unexplained. Quantitative and qualitative assessment of the perception of dyspnea, symptom measurement and quality of life complement physiological measurements and contribute to our understanding of dyspnea in asthma.

Airway Resistance↗

PubMed2006

Is there a link between the qualitative descriptors and the quantitative perception of dyspnea in asthma?

BACKGROUND: There is no obvious link between qualitative descriptors and overall intensity of dyspnea during bronchoconstriction in patients with asthma. AIMS: To determine whether qualitative and quantitative perception of methacholine-induced bronchoconstriction independently contribute to characterizing clinically stable asthma. MATERIAL AND METHODS: We assessed changes in inspiratory capacity, and quantitative (by Borg scale) and qualitative (by a panel of eight dyspnea descriptors) sensations of dyspnea at 20 to 30% fall in FEV(1) during methacholine inhalation in 49 asthmatics. Furthermore, we calculated the level of perception of bronchoconstriction at 20% fall in FEV(1) (PB(20)). RESULTS: Descriptors selected by patients during methacholine inhalation allowed us to define three language subgroups: (1) chest tightness (subgroup A, n = 21); (2) work/effort (subgroup B, n = 7); and (3) both descriptors (subgroup C, n = 13). Eight of the 49 patients (subgroup D) were not able to make a clear-cut distinction among descriptors. The subgroups exhibited similar function at baseline and during methacholine inhalation. Most importantly, patients selected chest tightness to a greater extent (42.85%), and work/effort (14.3%) and both descriptors (26.5%) to a lesser extent at the lowest level of bronchoconstriction (FEV(1) fall < 10%) as at 20% fall in FEV(1). Thirty-two patients were normoperceivers (PB(20) > or = 1.4 to < 5 arbitrary units [au]), 7 patients were hyperperceivers (PB(20) > or = 5 au), and 10 patients were hypoperceivers (PB(20) < 1.4 au). Language subgroups were equally distributed across the perceiver subgroups. CONCLUSIONS: In patients with clinically stable asthma, PB(20) and language of dyspnea independently contribute to defining the condition of the disease. However, the possibility that this independence may be due to a beta-error should be taken into account.

Administration, Inhalation↗

PubMed2005

Pathophysiology of exercise dyspnea in healthy subjects and in patients with chronic obstructive pulmonary disease (COPD).

In patients with a number of cardio-respiratory disorders, breathlessness is the most common symptom limiting exercise capacity. Increased respiratory effort is frequently the chosen descriptor cluster both in normal subjects and in patients with chronic obstructive pulmonary disease (COPD) during exercise. The body of evidence indicates that dyspnea may be due to a central perception of an overall increase in central respiratory motor output directed preferentially to the rib cage muscles. On the other hand, the disparity between respiratory motor output and mechanical response of the system is also thought to play an important role in the increased perception of exercise in patients. The expiratory muscles also contribute to exercise dyspnea: a decrease in Borg scores is related to a decrease in end-expiratory lung volume and to a decrease in end-expiratory gastric pressure at isowork after lung volume reduction surgery. Changes in respiratory mechanics and intrathoracic pressure surrounding the heart can reduce cardiac output by affecting the return of blood to the heart from the periphery, or by interfering with the ability of the heart to eject blood into the peripheral circulation. Change in arterial blood gas content may affect breathlessness via direct or indirect effects. Old and more recent data have demonstrated that hypercapnia makes an independent contribution to breathlessness. In hypercapnic COPD patients an increase in PaCO2 seems to be the most important stimulus overriding all other inputs for dyspnea. Hypoxia may act indirectly by increasing ventilation (VE), and directly, independent of change in VE. Finally, chemical (metabolic) ventilatory stimuli do not have a specific effect on breathlessness other than via their stimulation of VE. We conclude that exercise provides a stimulus contributing to dyspnea, which can be applied to many diseases.

Dyspnea↗

PubMed2005

Dyspnea and leg effort during exercise.

Dyspnea and leg effort are the major symptoms limiting exercise in healthy subjects and in patients with a variety of respiratory disorders. Quantitative measurement of both symptoms may be obtained by category scales such as VAS and Borg, with the latter being widely used. Furthermore, descriptor clusters of dyspnea help to assess some of the reasons for stopping exercise. The intensity of dyspnea and leg effort are similar in different disease states; this symmetry suggests that the limiting discomfort is a function of the intensity of increased motor drive to peripheral and respiratory muscles. An alternative explanation for the factors which limit exercise is that the subjects stop exercise volitionally when the discomfort associated with continuing exercise exceeds that which they are willing to tolerate. Muscle strength contributes to the intensity of dyspnea and leg effort at a given power output: the greater the muscle force, the lower the symptom. Symptoms also correlate with intensity and duration of a task by a power function in such a way that when minimizing the intensity of a given muscular task by prolonging the duration of activity, the symptom is drastically reduced. Skeletal muscle fatigue may be a factor limiting exercise tolerance both in healthy subjects and in patients with cardiorespiratory disorders. In conclusion, symptom measurement complements physiological measurements, both being essential to a comprehensive understanding of exercise tolerance.

Bicycling↗

PubMed2005

Arm exercise and hyperinflation in patients with COPD: effect of arm training.

BACKGROUND: Unlike studies on leg exercise, reports on the regulation of dynamic hyperinflation during arm exercise are scanty. We ascertained the following in patients with COPD: (1) whether and to what extent upper-limb exercise results in dynamic hyperinflation, and (2) the mechanism whereby an arm-training program (ATP) reduces arm effort and dyspnea. PATIENTS: Twelve patients with moderate-to-severe COPD were tested during incremental, symptom-limited arm exercise after a non-intervention control period (pre-ATP) and after ATP. METHODS: Exercise testing (1-min increments of 5 W) was performed using an arm ergometer. Oxygen uptake (V(O2)), carbon dioxide output, minute ventilation (Ve), tidal volume, and respiratory rate (RR) were measured continuously during the tests. Inspiratory capacity (IC), exercise dyspnea, and arm effort using a Borg scale were assessed at each step of exercise. RESULTS: Arm exercise resulted in a significant decrease in IC and significant positive relationships of IC with an increase in V(O2) and exercise dyspnea and arm effort. The results of ATP were as follows: (1) a significant increase in exercise capacity (p < 0.001); (2) no change in the relationships of exercise dyspnea and arm effort with Ve and IC, and of IC with V(O2); (3) at a standardized work rate, Ve, exercise dyspnea, and arm effort significantly decreased, while the decrease in IC was significantly less (p < 0.01) than before the ATP; the decrease in Ve was accomplished primarily by a decrease in RR; and (4) at standardized Ve, exercise dyspnea and arm effort decreased significantly. CONCLUSIONS: Arm exercise results in the association of dynamic hyperinflation, exercise dyspnea, and arm effort in COPD patients. An ATP increases arm endurance, modulates dynamic hyperinflation, and reduces symptoms.

Aged↗

PubMed2003

Overall contribution of chest wall hyperinflation to breathlessness in asthma.

BACKGROUND: Studies suggest that the increased volume of both abdominal and rib cage compartments of the chest wall contribute to dyspnea during methacholine-induced airway narrowing. MATERIAL: Eight male patients with asthma aged 34 +/- 13 years (mean +/- SD) before and during methacholine challenge. METHODS: The volume of the chest wall (Vcw), volume of the abdomen (Vab), and volume of the rib cage (Vrc) were measured by using a three-dimensional optoelectronic plethysmography. RESULTS: During methacholine challenge, the increase in end-expiratory Vcw (Vcw,ee) [0.55 +/- 0.23 L, p < 0.001] was due to increased Vrc (0.37 +/- 0.20 L, p < 0.01) and, to a lesser extent, Vab (0.18 +/- 0.10 L, p < 0.005). Linear univariate regression analysis showed that changes in dyspnea (Borg scale) with the highest methacholine dose correlated with both DeltaFEV(1) and DeltaVcw,ee. Multiple regression analysis with the Borg score as dependent variable and all other ventilatory indexes as independent variables showed that DeltaVcw,ee and DeltaFEV(1) were the only significant contributors to the Borg score. Taken together Vcw,ee and FEV(1) explained 56% of variance in the Borg score (r(2) = 0.56), although Vcw,ee explained 48% of it. CONCLUSIONS: During methacholine challenge in patients with asthma, the overall increase in Vcw,ee is a better predictor of dyspnea that the reduction in FEV(1).

Adult↗

PubMed2002

Dissociation between respiratory effort and dyspnoea in a subset of patients with stroke.

Dyspnoea is not a prominent complaint of resting patients with recent hemispheric stroke (RHS). We hypothesized that, in patients with RHS presenting abnormalities in respiratory mechanics, increased respiratory motor output could translate into an increased perception of dyspnoea. We studied eight wheelchair-bound patients with RHS (mean age 62.4 years), previously evaluated by computerized tomography scanning, and a control group of normal subjects, matched for age and sex. We assessed routine spirometry, inspiratory and expiratory muscle pressures, breathing pattern and dyspnoea using a modified Borg scale. In six patients, we also measured oesophageal pressure during the maximal sniff manoeuvre and tidal inspiratory swing, and mechanical characteristics of the lung in terms of dynamic elastance during both quiet breathing and a hypercapnic/hyperoxic rebreathing test. During room air breathing, ventilation and tidal volume were similar in patients and controls, while tidal inspiratory swings of oesophageal pressure, an index of inspiratory motor output, were greater in patients ( P =0.005). Patients also exhibited a greater dynamic elastance ( P =0.013). During rebreathing, dynamic elastance remained higher ( P =0.01) and a greater than normal inspiratory motor output was found ( P =0.03). Responses of ventilation and tidal volume to carbon dioxide tension were normal, and in all patients but one a lower Borg score for the unit change in carbon dioxide tension and ventilation was found. In conclusion, a higher than normal inspiratory motor output was unexpectedly associated with a blunted perception of dyspnoea in this subset of RHS patients. This is likely to be due to the modulation of the integration process of respiratory sensation.

Adult↗

PubMedDate not supplied

Respiratory muscles and dyspnea in obese nonsmoking subjects.

To our knowledge no data have been reported on the contribution to acute increase in dyspnea by the respiratory muscles in obese nonsmoking subjects. To better focus on this topic, we studied seven obese subjects and an age-matched normal control group, assessing baseline pulmonary function, breathing pattern, esophageal pressure (Pes), and gastric (Pga) and transdiaphragmatic (Pdi) pressures. Pes was also recorded during a sniff maneuver (Pessn). During a hypercapnic rebreathing test we recorded inspiratory swing in Pes (Pessw), expiratory changes in Pga, and inspiratory swings in Pdi (Pdisw). Change in inspiratory capacity was considered the mirror image of end-expiratory lung volume (EELV). Dyspnea was assessed by a modified Borg scale. Under control conditions, patients exhibited a reduced expiratory reserve volume and intrinsic positive end-expiratory pressure (PEEPi). At the end of hypercapnic stimulation, compared with controls our obese subjects exhibited greater respiratory frequency (Rf), shorter expiratory time, greater Pessw, and lower Pdisw. Increases in EELV and PEEPi were found in the obese subjects but not in controls. Changes in Borg correlated with changes in PETCO2, VE, Pessw (%Pessn), and Pdisw to a greater extent in patients than in controls. Stepwise regression analysis indicated the amount of variability in Borg that was predicted by both Pdisw (r2 = 0.31, p < 0.0004), and Pessw (%Pessn) (r2 = 0.09, p < 0.005) in controls, and by Pessw (%Pessn) (r2 = 0.40, p < 0.00001) in obese subjects. We conclude that the rib cage muscles contributed to dyspnea to a greater extent in this subset of obese subjects.

Adult↗