Noninvasive measurement of the tension-time index in children with neuromuscular disease

2003 ◽  
Vol 95 (3) ◽  
pp. 931-937 ◽  
Author(s):  
Laura T. Mulreany ◽  
Daniel J. Weiner ◽  
Joseph M. McDonough ◽  
Howard B. Panitch ◽  
Julian L. Allen

Respiratory muscle weakness is common in children with neuromuscular disease (NMD). We hypothesized that weakness puts them at risk for respiratory muscle fatigue, a harbinger of chronic respiratory failure. We therefore measured a noninvasive index of respiratory muscle fatigue, the tension-time index of the respiratory muscles (TTmus), in 11 children with NMD and 13 control subjects. Spirometric flow rates and maximal inspiratory pressure were significantly lower in the NMD group than in controls (43 ± 23 vs. 99 ± 21 cmH2O, P < 0.001). The mean TTmus was significantly higher in the NMD group than in controls (0.205 ± 0.117 vs. 0.054 ± 0.021, P < 0.001). The increase in TTmus was primarily due to an increase in the ratio of average mean inspiratory pressure to maximal inspiratory pressure, indicating decreased respiratory muscle strength reserve. We found a significant correlation between TTmus and the residual volume-to-total lung capacity ratio ( r = 0.504, P = 0.03) and a negative correlation between TTmus and forced expiratory volume in 1 s ( r = -0.704, P < 0.001). In conclusion, children with NMD are prone to respiratory muscle fatigue. TTmus may be useful in assessing tolerance during weaning from mechanical ventilation, identifying impending respiratory failure, and aiding in the decision to institute therapies.

1981 ◽  
Vol 60 (4) ◽  
pp. 463-466 ◽  
Author(s):  
S. C. Gandevia ◽  
K. J. Killian ◽  
E. J. M. Campbell

1. Eight subjects maintained maximal inspiratory pressure as long as possible. The subjects accurately judged the pressure developed, but considered that the sense of effort or motor command increased progressively during the contraction as fatigue developed. 2. A reference inspiratory load was overestimated after maximal inspiratory contractions. 3. These findings are consistent with the hypothesis that awareness of the motor command or effort contributes to the estimation of respiratory loads.


1994 ◽  
Vol 77 (1) ◽  
pp. 236-244 ◽  
Author(s):  
J. Yanos ◽  
M. J. Patti ◽  
A. S. Banner

The cause of respiratory arrest in acute asthma is not known. By its nature, respiratory arrest is difficult to study clinically. The possible causes of respiratory arrest include cardiovascular dysfunction, respiratory muscle fatigue, and central respiratory failure. We used a dog model of respiratory arrest in acute bronchoconstriction that examined the effects of hypoxemia and intrinsic loading in an attempt to establish the mechanism. Our hypothesis was that, in a setting of hypoxemia and intrinsic loading similar to human fatal asthma, respiratory arrest is caused by a central respiratory failure, more specifically, failure of the central rhythm generator. We studied 18 dogs divided into 1) an intrinsically loaded group, 2) a hypoxemic group, and 3) both a loaded and a hypoxemic group. Intrinsic loading was induced with methacholine combined with selective beta 2-blockade, and the hypoxemia was controlled by varying inspired O2 fraction. Respiratory arrest occurred only in animals with both hypoxemia and intrinsic loading. We found no evidence of hemodynamic instability or respiratory muscle fatigue. Instead, there was an abrupt cessation of ventilation while the intensity of the central neural output was maintained. Our results are consistent with a failure of the central rhythm generator as the causal agent in respiratory arrest.


1977 ◽  
Vol 53 (5) ◽  
pp. 419-422 ◽  
Author(s):  
P. T. Macklem ◽  
C. S. Roussos

1. The question whether respiratory muscle fatigue ever causes respiratory failure is over 40 years old, but we still have no definitive answer to this question. Skeletal muscle fatigue occurs when the rate of energy consumption of themu scle is greater than the energy supplied, so that energy stores are utilized and eventually become depleted. 2. Five factors which are important in the development of muscle fatigue (a, the tension developed by the muscle; b, the maximum tension the muscle can develop; c, the energy stored within the muscle; d, the energy supplied to the muscle; e, the efficiency of the muscle). These can be affected in many diseases, so disposing to fatigue, thus respiratory muscle fatigue is likely to be a common occurrence. 3. Respiratory muscle fatigue can in principle easily be diagnosed at the bedside by application of a simple electromyographic technique used to detect fatigue in other skeletal muscles.


CHEST Journal ◽  
1990 ◽  
Vol 97 (3) ◽  
pp. 97S ◽  
Author(s):  
T.K. Aldrich ◽  
D.J. Prezant ◽  
J.P. Karpel ◽  
A.S. Multz ◽  
J.M. Hendlen

1989 ◽  
Vol 15 (S1) ◽  
pp. S17-S20 ◽  
Author(s):  
M. Aubier

2017 ◽  
Vol 27 (80) ◽  
pp. 65-75 ◽  
Author(s):  
Katarzyna Kucia ◽  
Ewa Dybińska ◽  
Tomasz Białkowski ◽  
Tomasz Pałka

INTRODUCTION The lifeguard is the person in charge of safety in water environments. After a rescue, it is possible that he has to execute a CPR. The European Resuscitation Council (ERC) as well as theAmerican Heart Association are currently encouraging a quality CPR performance. The lifeguard may be obliged to carry out a CPR during a long period of time as the response of the Emergency Medical Service takes 5–8 min on average and it can even reach 20 min. The normal respiratory muscle effort at maximal swimming intensity requires a significant fraction of cardiac output and causes leg blood flow to fall. The main objective of this paper was to determine respiratory muscle fatigue (RMF) level in swimming with different intensity on quality and efficiency rescu action in the water. MATERIAL AND METHODS The study involved eleven lifeguards male (9) and female (2); age: (24.25±1.5); body height( 176,27±7,88) and body mass (75.81±11,01)form University School of Physical Education, Cracow. Two tests were conducted: the first test involved the execution of 5 min of CPR (rested), and the second one in performing water rescue and subsequent CPR (exhausted) for 5 minutes. The quality of the CPR at rest and at fatigue condition was compared. The recording instrument was the Ambu Defib Trainer W (Wireless).The time and precision of the simulated water rescue was also registered. Two spirometry tests were performed the first test was set before swimming and the second after (exhausted). Maximal respiratory pressures (PImax, PEmax) were evaluated before and directly after swimming in different intensity.The quality of the respiratory muscle fatigue at rest and at fatigue condition was compared. The recording instrument was portable MicroLoop spirometer. RESULTS After e simulated water rescue significantly increase parameters such as: ventilation minute volume rested (3,06±22,10) exhausted (4,23 ±22,10. P < .001); ventilation rate rested (3.60±34.80) exhausted (4,80 ±34.80. P < .001); and stomach inflation rested (2,0±20,47) exhausted (5.80 ±20.47. P < .001). The greatest variation in the results of the respiratory muscle fatigue both before and after swimming with different intensity was observed only in two parameters: maximal ventilation index (MVV) and peak exhaust flow (PEF). CONCLUSIONS The accumulated fatigue during a simulated water rescue performed by lifeguards reduces the quality of compression depth and pause between compressions. The following respiratory parameters were found to have the strongest effect on the swimming: during maximum exercise intensity and FEV 1 (-0.77) rested and FEV 1 (-0.57) exhausted and FVC (-0.79) rested and FVC (-0.70) exhausted.


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