Muscle kinematics for minimal work of breathing.
(25/966)
A mathematical model was analyzed to obtain a quantitative and testable representation of the long-standing hypothesis that the respiratory muscles drive the chest wall along the trajectory for which the work of breathing is minimal. The respiratory system was modeled as a linear elastic system that can be expanded either by pressure applied at the airway opening (passive inflation) or by active forces in respiratory muscles (active inflation). The work of active expansion was calculated, and the distribution of muscle forces that produces a given lung expansion with minimal work was computed. The calculated expression for muscle force is complicated, but the corresponding kinematics of muscle shortening is simple: active inspiratory muscles shorten more during active inflation than during passive inflation, and the ratio of active to passive shortening is the same for all active muscles. In addition, the ratio of the minimal work done by respiratory muscles during active inflation to work required for passive inflation is the same as the ratio of active to passive muscle shortening. The minimal-work hypothesis was tested by measurement of the passive and active shortening of the internal intercostal muscles in the parasternal region of two interspaces in five supine anesthetized dogs. Fractional changes in muscle length were measured by sonomicrometry during passive inflation, during quiet breathing, and during forceful inspiratory efforts against a closed airway. Active muscle shortening during quiet breathing was, on average, 70% greater than passive shortening, but it was only weakly correlated with passive shortening. Active shortening inferred from the data for more forceful inspiratory efforts was approximately 40% greater than passive shortening and was highly correlated with passive shortening. These data support the hypothesis that, during forceful inspiratory efforts, muscle activation is coordinated so as to expand the chest wall with minimal work. (+info)
Influence of respiratory muscle work on VO(2) and leg blood flow during submaximal exercise.
(26/966)
The work of breathing (W(b)) normally incurred during maximal exercise not only requires substantial cardiac output and O(2) consumption (VO(2)) but also causes vasoconstriction in locomotor muscles and compromises leg blood flow (Q(leg)). We wondered whether the W(b) normally incurred during submaximal exercise would also reduce Q(leg). Therefore, we investigated the effects of changing the W(b) on Q(leg) via thermodilution in 10 healthy trained male cyclists [maximal VO(2) (VO(2 max)) = 59 +/- 9 ml. kg(-1). min(-1)] during repeated bouts of cycle exercise at work rates corresponding to 50 and 75% of VO(2 max). Inspiratory muscle work was 1) reduced 40 +/- 6% via a proportional-assist ventilator, 2) not manipulated (control), or 3) increased 61 +/- 8% by addition of inspiratory resistive loads. Increasing the W(b) during submaximal exercise caused VO(2) to increase; decreasing the W(b) was associated with lower VO(2) (DeltaVO(2) = 0.12 and 0.21 l/min at 50 and 75% of VO(2 max), respectively, for approximately 100% change in W(b)). There were no significant changes in leg vascular resistance (LVR), norepinephrine spillover, arterial pressure, or Q(leg) when W(b) was reduced or increased. Why are LVR, norepinephrine spillover, and Q(leg) influenced by the W(b) at maximal but not submaximal exercise? We postulate that at submaximal work rates and ventilation rates the normal W(b) required makes insufficient demands for VO(2) and cardiac output to require any cardiovascular adjustment and is too small to activate sympathetic vasoconstrictor efferent output. Furthermore, even a 50-70% increase in W(b) during submaximal exercise, as might be encountered in conditions where ventilation rates and/or inspiratory flow resistive forces are higher than normal, also does not elicit changes in LVR or Q(leg). (+info)
Does the cellular bronchoalveolar lavage fluid profile reflect the severity of sarcoidosis?
(27/966)
The aim of this study was to assess whether the cellular bronchoalveolar lavage fluid (BALF) profile, particularly the number of polymorphonuclear neutrophils (PMNs), is associated with disease severity of sarcoidosis and its usefulness in determining remission. Twenty-six nonsmoking outpatients with sarcoidosis were included in this study. The patients were divided into two subgroups according to the absolute number of PMNs in BALF: < or =0.2x10(4) cells x mL(-1) (group 1; n = 15) and >0.2x10(4) cells x mL(-1) (group 2; n = 11). The radiographic stage, high-resolution computed tomography (HRCT) findings, 67Ga lung uptake as well as lung function tests differed significantly between group 1 and 2. Follow-up revealed that 14 (93.3%) patients of group 1 compared to four (36.4%) of group 2 recovered spontaneously without the help of corticosteroids. In contrast, no differences were found in the number of lymphocytes in BALF nor in the serum angiotensin converting enzyme (sACE) level between both groups. The number of PMNs, the transfer factor of the lungs for carbon monoxide (TL,CO), the forced expiratory volume in one second (FEV1) and one of the HRCT subscores discriminated between patients with different disease progression. Of these parameters the PMNs appeared to be the only one which differentiated patients who demonstrated remission and those who deteriorated. In conclusion, these results indicate that the number of polymorphonuclear neutrophils in bronchoalveolar lavage fluid distinguish between sarcoidosis patients who demonstrated remission and those having a more severe course of the disease. Whether polymorphonuclear neutrophils may be considered as markers of disease activity and/or prognosis in sarcoidosis needs further investigation. (+info)
Heart failure-related myopathy. Clinical and pathophysiological insights.
(28/966)
AIMS: To evaluate the relationship of skeletal and respiratory muscular dysfunction with the degree of clinical severity, cardiac impairment and exercise intolerance in patients with chronic heart failure. METHODS AND RESULTS: Ninety-one patients (age 52.7+/-8 years) on standard therapy and in a stable clinical condition with normal nutritional status underwent evaluation of (1) clinical severity and metabolic status (NYHA class, weight, albuminaemia, natraemia, cortisol, insulin, neurohormones), (2) cardiac function (Echo, right heart catheterization), (3) exercise tolerance (peak VO(2)), (4) dynamic isokinetic forces of the quadriceps and hamstring (Cybex method), and respiratory muscle strength (maximal inspiratory and expiratory pressures). Fifty patients had a peak VO(2)<14 ml x kg(-1) x min(-1)(10.6+/-2) and 41 had values >/=14 (18.3+/-4). In the former group, leg and respiratory strength were significantly lower (extensors: 80+/-24 vs 100.9+/-22 Nm; flexors: 48.5+/-24 vs 75.3+/-22, both P<0.001; maximal expiratory pressure: 85.5+/-30 vs 104.8+/-31, P<0.01). Muscular strength was not related to indices of clinical severity, metabolic status, neurohormones or to the degree of systolic/diastolic cardiac function, but it was related to weight and age. Multivariate analysis of the peak VO(2)with clinical, haemodynamic and peripheral indicators showed weight (beta= 0.32, P = 0.007), muscular strength (beta= 0.32, P = 0.01) and NYHA class (beta= 0.31, P = 0.001) as the only independent predictors. The joint adjusted R(2)value was 0.48 (P<0.001). CONCLUSION: Muscular dysfunction is part of the syndrome of heart failure. Together with symptom perception, it predicts nearly half of the variation in exercise tolerance. (+info)
Inhaled and systemic corticosteroid therapies: Do they contribute to inspiratory muscle weakness in asthma?
(29/966)
BACKGROUND: Patients with asthma incur the risk of steroid-induced myopathy, which is a well-known side effect of treatment with corticosteroids. However, the adverse effect of long-term steroid treatment on respiratory muscle function remains controversial. OBJECTIVE: We aimed to evaluate the effects of long-term moderate dose of systemic corticosteroids and high-dose inhaled beclomethasone on maximal inspiratory and expiratory pressures (PImax and PEmax, respectively) in two groups of asthmatic patients exhibiting comparable levels of hyperinflation. METHODS: Twelve steroid-dependent asthmatic patients requiring 10-20 mg/day of prednisone-equivalent corticosteroids for an average of 9.83 +/- (SD) 9.86 years; 14 subjects with moderate to severe asthma who have used inhaled beclomethasone for at least 1 year at a daily dose higher than 1,000 microg and 15 healthy controls were included to the study. RESULTS: No significant difference in pulmonary function tests and arterial blood gases appeared between two asthmatic groups with different treatment modalities. PImax as an absolute value was significantly lower in steroid-dependent asthmatics than in patients treated with inhaled beclomethasone and controls (p < 0.01). %PImax was also lower in steroid-dependent asthmatics than in control groups (p < 0.01). A significant correlation was found between %PImax and hyperinflation assessed by %RV, %FRC, %FRC/TLC (p < 0.05) in all asthmatic patients. CONCLUSIONS: We believe that hyperinflation plays a major role in inspiratory muscle dysfunction in asthma, but the finding of significantly decreased PImax values in steroid-dependent asthmatics when compared with patients on high-dose inhaled beclomethasone with a comparable level of hyperinflation points to a deleterious effect of long-term, moderate-dose systemic corticosteroid but not high-dose beclomethasone on inspiratory muscle function in asthmatics. (+info)
Role of respiratory motor output in within-breath modulation of muscle sympathetic nerve activity in humans.
(30/966)
We measured muscle sympathetic nerve activity (MSNA, peroneal microneurography) in 5 healthy humans under conditions of matched tidal volume, breathing frequency, and end-tidal CO(2), but varying respiratory motor output as follows: (1) passive positive pressure mechanical ventilation, (2) voluntary hyperventilation, (3) assisted mechanical ventilation that required the subject to generate -2.5 cm H(2)O to trigger each positive pressure breath, and (4) added inspiratory resistance. Spectral analyses showed marked respiratory periodicities in MSNA; however, the amplitude of the peak power was not changed with changing inspiratory effort. Time domain analyses showed that maximum MSNA always occurred at end expiration (25% to 30% of total activity) and minimum activity at end inspiration (2% to 3% of total activity), and the amplitude of the variation was not different among conditions despite marked changes in respiratory motor output. Furthermore, qualitative changes in intrathoracic pressure were without influence on the respiratory modulation of MSNA. In all conditions, within-breath changes in MSNA were inversely related to small changes in diastolic pressure (1 to 3 mm Hg), suggesting that respiratory rhythmicity in MSNA was secondary to loading/unloading of carotid sinus baroreceptors. Furthermore, at any given diastolic pressure, within-breath MSNA varied inversely with lung volume, demonstrating an additional influence of lung inflation feedback on sympathetic discharge. Our data provide evidence against a significant effect of respiratory motor output on the within-breath modulation of MSNA and suggest that feedback from baroreceptors and pulmonary stretch receptors are the dominant determinants of the respiratory modulation of MSNA in the intact human. (+info)
Chest wall kinematics and respiratory muscle action in walking healthy humans.
(31/966)
We studied chest wall kinematics and respiratory muscle action in five untrained healthy men walking on a motor-driven treadmill at 2 and 4 miles/h with constant grade (0%). The chest wall volume (Vcw), assessed by using the ELITE system, was modeled as the sum of the volumes of the lung-apposed rib cage (Vrc,p), diaphragm-apposed rib cage (Vrc,a), and abdomen (Vab). Esophageal and gastric pressures were measured simultaneously. Velocity of shortening (V(di)) and power [Wdi = diaphragm pressure (Pdi) x V(di)] of the diaphragm were also calculated. During walking, the progressive increase in end-inspiratory Vcw (P < 0.05) resulted from an increase in end-inspiratory Vrc,p and Vrc,a (P < 0.01). The progressive decrease (P < 0.05) in end-expiratory Vcw was entirely due to the decrease in end-expiratory Vab (P < 0.01). The increase in Vrc,a was proportionally slightly greater than the increase in Vrc,p, consistent with minimal rib cage distortion (2.5 +/- 0.2% at 4 miles/h). The Vcw end-inspiratory increase and end-expiratory decrease were accounted for by inspiratory rib cage (RCM,i) and abdominal (ABM) muscle action, respectively. The pressure developed by RCM,i and ABM and Pdi progressively increased (P < 0.05) from rest to the highest workload. The increase in V(di), more than the increase in the change in Pdi, accounted for the increase in Wdi. In conclusion, we found that, in walking healthy humans, the increase in ventilatory demand was met by the recruitment of the inspiratory and expiratory reserve volume. ABM action accounted for the expiratory reserve volume recruitment. We have also shown that the diaphragm acts mainly as a flow generator. The rib cage distortion, although measurable, is minimized by the coordinated action of respiratory muscles. (+info)
Proximal diabetic neuropathy presenting with respiratory weakness.
(32/966)
A patient is described with proximal diabetic neuropathy presenting with respiratory weakness. A 50 year old man developed progressive shortness of breath over 2 months. He also had weakness of hip flexion. Phrenic nerve responses were absent, and spontaneous activity was seen in the intercostal and lumbar paraspinal muscles with long duration neurogenic MUPs and reduced recruitment in the diaphragm. Without treatment, the patient began to improve with resolution of his proximal leg weakness and breathing difficulties. Proximal diabetic neuropathy is another cause of neuromuscular respiratory weakness. (+info)