1.1.1

The inspiratory muscles

As expiration ends, persisting air entrapment in a patient’s lungs creates positive end – expiratory pressure. This pressure compels the diaphragm at the beginning of its labors to carry out a major inspiratory effort in order to generate an inspiratory flow sufficing first to vanquish the positive pressure, and then to create the negative pressure that will provoke a flow of air into the lungs .

A large proportion of the energy that would normally be supplied by the diaphragm is expended in this laborious effort, which diminishes the volume of the respiratory reserve that can no longer easily meet the respiratory demand manifested during the patient’s struggles . His labors lead to the arrival of thoraco-pulmonary distension along with a tendency towards a flattening of diaphragmatic muscle fibers placing them in mechanically unfavorable conditions. More particularly, the diaphragmatic cupolas are lowered and flattened. As their contractile fibers are shortened, they become functionally insufficient. As a result, the inspiratory action of the diaphragm is weakened, and the accessory inspiratory muscles are solicited .

In order to adapt to these modifications, the diaphragm undergoes a diminishment in the number and length of its sarcomeres so as to recreate a more workable length-tension relationship at the level of the previously mentioned fibers . The strength produced by the new length is equal to that which had been produced by the old length. The peak inspiratory flow rate (PIFR) may thereby be conserved in many patients. On the other hand, ventilation takes place at a threshold level likely to lead to muscle fatigue. Type IIA diaphragmatic muscle fibers, which are less prone to fatigue, will tend to grow . The diaphragm’s aerobic capacities will likewise grow through increased capillarisation and more mitochondria .

As the disease evolves, the new length-tension relationship no longer allows the diaphragm to generate optimal strength when it contracts. As it labors, it approaches its maximum shortening capacity; as a result, its workload increases, as does its oxygen consumption, which becomes six times as great as that observed in normal subjects . As the disease worsens, it can no longer meet the heightened demand for oxygen, which is likewise augmented by the solicitation of accessory respiratory muscles , which appears to conserve their strength and endurance. All told, these different modifications of ventilatory mechanics lead to lowered inspiratory efficiency .

This evolution justifies today’s consensus according to which the decompensation undergone by the CPOD patient is largely due to muscle fatigue in the diaphragm and among the other respiratory muscles .

1.1.2

The expiratory muscles

Even though the abdominal muscles in humans appear to conserve their strength, their endurance is likely to diminish .

1.1.3

Flow-volume curve

The obstructive syndrome is accompanied by reduced respiratory flow even though volume remains the same or is only slightly modified. FEV1, the Tiffeneau ratio (FEV1/forced vital capacity) and the peak expiratory flow rate (PEFR) are all diminished.

Due to the pathological conditions, the smaller bronchi are partially obstructed. The flow-volume curve or loop is typically concave towards the top, and its shape translates the normal expiratory velocity of the air in the large respiratory airways, and the reduced velocity in the smaller airways, which is due to their being partially obstructed ( Fig. 1 ).

Flow-volume curve. On the left: a normal flow-volume curve ; on the right: flow-volume curve of a chronic obstructive pulmonary disease (CPOD) subject. We may note the concave curve typical of COPD translating the normal expiratory velocity of the air to be found in the large respiratory airways, and the reduced velocity in the smaller airways, which is due to their being partially obstructed.

Source: O’Donnell, 2008 .

Disease evolution is marked by increasing obstruction of the lower and smaller respiratory airways and by the irreversibility of the process .

Early therapeutic intervention during the Gold I and Gold II stages ( Table 1 ) is likely to be relatively efficient with regard to FEV1 decrease and quality of life, but relatively inefficient in terms of survival ( Fig. 2 ).

Assessment criteria of the natural history of chronic obstructive pulmonary disease (CPOD) according to the stage: early therapeutic intervention will be more efficient with regard to FEV1 decrease and quality of life. Improvement with regard to FEV1 decrease, improved quality of life, improved survival rate.

Source: Dusser, 2008 .

Later therapeutic intervention (Gold II and Gold III stages), once the obstruction would appear to be less reversible, will have more limited therapeutic efficiency, particularly with regard to FEV1 decrease. On the other hand, it may have a more pronounced effect on exacerbations and mortality. At these stages of disease evolution, comorbidities weigh heavily, and a global, integrated approach is consequently justified .

1.1.4

Rehabilitative care

From the standpoint of a rehabilitation technician, appropriate treatment of the respiratory symptoms linked with COPD (or with exacerbation of the latter) includes:

• •
  

  bronchial decluttering meant to clear the airways;

  
  
• •
  

  diaphragmatic rehabilitation (solicitation of the physiological diaphragmatic contraction) aimed at improved stamina;

  
  
• •
  

  reinforcing of the lower limb muscles so as to limit functional deconditioning;

  
  
• •
  

  psychological support and therapeutic education.

Weakened respiratory muscles and/or altered diaphragmatic mechanics may render the respiratory difficulty a key element in the clinical picture. Dyspnea and intolerance to physical exertion further worsen the quality of life .

While it appears that targeted training of the inspiratory muscles with specific loading (hand-held devices) may significantly augment their strength and endurance , the effects of this type of training on the other parameters have yet to be assessed. This situation has led us to implement a protocol aimed at reinforcing the respiratory muscles in conjunction with the application of bronchial decluttering techniques (accelerated expiratory flow and diaphragmatic rehabilitation). We have attempted to assess its effects as concerns:

• •
  

  increased functional capacities of these muscles;

  
  
• •
  

  mechanically improved diaphragmatic conditions;

  
  
• •
  

  increased capacity for physical exertion.

Our hypothesis is that this type of training will facilitate:

• •
  

  improved functioning of internal mechanics through ameliorated elastic behavior of the lungs;

  
  
• •
  

  increased chest expansion through heightened enablement of the respiratory muscles;

  
  
• •
  

  improved mechanical performance of the diaphragm;

  
  
• •
  

  diminished dyspnea;

  
  
• •
  

  improvement pertaining to the quality of life signs listed in Saint-George’s respiratory questionnaire (SGRQ).

Our hypothesis is that these improvements would be greater than those objectified when bronchial decluttering and diaphragmatic rehabilitation techniques are applied alone.

1.2.1

Population

Our prospective study was carried out over a period of 7 months. The subjects were selected subsequent to a survey conducted in a population of active and passive smokers and ex-smokers. Spirometric tests were proposed to patients presenting with clinical signs of COPD (coughing, dyspnea, expectorations) so as to validate or invalidate the clinical picture. The patients diagnosed as “COPD subjects” were divided into four different groups by assigning them, in the order of consultation and one by one, to groups 1 through 4. Patients were selected in accordance with the following inclusion criteria:

• •
  

  cooperating COPD subjects;

  
  
• •
  

  diagnosed clinically and through spirometric measurement (grades I and II in the Gold classification);

  
  
• •
  

  presenting with 50% < FEV1 < 80% of predicted or theoretical value in the spirometric test;

  
  
• •
  

  presenting with an improvement < 15% of the FEV1 following use of bronchodilators;

  
  
• •
  

  from 45 to 75 years of age;

  
  
• •
  

  of either sex.

Inclusion criteria were:

• •
  

  heart failure or associated cardiac pathology;

  
  
• •
  

  previous pulmonary or cardiac surgery;

  
  
• •
  

  patient depending on oxygen therapy or undergoing cortisone treatment;

  
  
• •
  

  associated neuromuscular pathologies.

The groups participating in the study were defined as follows ( Fig. 3 ):

• •
  

  group 1 (inspiratory);

  
  
• •
  

  group 2 (expiratory);

  
  
• •
  

  group 3 (inspiratory and expiratory);

  
  
• •
  

  group 4 (controls).

Distribution of the different groups according to the rehabilitation program applied.

• •
  

  Population: 40 COPD subjects.

  
  
• •
  

  Experimental groups; control group.

  
  
• •
  

  Group 1, 10 COPD subjects, respiratory physiotherapy and inspiratory muscle exercise (Threshold ^® IMT).

  
  
• •
  

  Group 2, 10 COPD subjects, respiratory physiotherapy and expiratory muscle exercise (Threshold ^® PEP).

  
  
• •
  

  Group 3, 10 COPD subjects, respiratory physiotherapy and inspiratory and expiratory muscle exercise (Threshold ^® IMT and PEP).

  
  
• •
  

  Group 4, 10 COPD subjects, respiratory physiotherapy.

Our variables comprised:

• •
  

  FEV1, PEFR and peak instantaneous inspiratory flow rate (PIIFR) evaluated by spirometric measurement;

  
  
• •
  

  quality of life signs evaluated by SGRQ and its secondary criteria (symptoms, repercussions on physical activity, impact on daily life);

  
  
• •
  

  the distance covered during the 6-minute walking test;

  
  
• •
  

  heart rate (HR) at rest, evaluated by a blood pressure monitor;

  
  
• •
  

  dyspnea evaluated by the Sadoul scale;

  
  
• •
  

  lower limb fatigue evaluated by the Visual Analog Fatigue Scale (VAFS);

  
  
• •
  

  costo-diaphragmatic recess evaluated by frontal chest radiograph;

  
  
• •
  

  strength developed by the inspiratory and expiratory muscles through Threshold ^® measurement of maximum inspiratory (Ip _max ) and expiratory (Ep _max ) pressure.

1.2.2

Protocols

Sixteen rehabilitation sessions were carried out by each patient at a frequency of two sessions a week over the course of 8 weeks. The 1st and the 16th sessions were reserved for application of the different measurements and evaluations.

1.2.2.2

Measurement apparatuses

The EasyOne™ spirometer measures the flow of air entering into and exiting out of the patient’s lungs.

The Threshold ^® IMT ( Fig. 5 ) is a tool helping to train the inspiratory muscles with a pressure load representing a fraction of the patient’s Ip _max .

Threshold ^® IMT.

The Threshold ^® PEP ( Fig. 6 ) is a tool used in expiratory rehabilitation by positive expiratory pressure, and it is equipped with a one-way valve functioning independently from the patient’s respiratory flow.

Threshold ^® PEP.

Pressure is adjustable and ranges from 4 cm H ₂ O to 20 cm H ₂ O. When the strength of the expiratory muscles is measured, it becomes possible to calculate Ep _max .

The heart rate monitor automatically displays a heart rate reading.

The VAFS allows the patient to self-evaluate the fatigue experienced at the level of the lower limbs on a scale graded from 0 (no tiredness) to 10 (intolerable tiredness necessitating rest).

The SGRQ allows for assessment of the quality of life parameters.

The Sadoul scale classifies patients in terms of the stages of their pathology, which are graded from 0 (no dyspnea) to 4 (dyspnea accompanying even the slightest effort).

A simple goniometer with plastic arms enabled us to measure the costo-diaphragmatic recess on the frontal lung X-ray taken during maximal inspiration.

1.3.1

Synoptic patient data

Forty COPD subjects participated in this study. The participants were women (52.5%, n = 21) and men (47.5%, n = 19). Their average age was 60.38 ± 8.02 years (45, 75). Twenty-seven subjects (70%) were smokers, eight subjects (20%) had stopped smoking over the past 6 months, and five subjects (8%) were non-smokers. The Body Mass Index (BMI) of these patients was 28.3 ± 3.11 kg/m ² [22.2, 36.7].

1.3.2

Spirometric measurements

Table 2 shows significant FEV1 and PEFR improvement in group 1 alone. In none of our four groups was the PIFR modified.

1.3.3

Quality of life

Table 3 shows significant improvement in the overall score pertaining to quality of life (symptoms experienced, repercussions on physical activity, impact on daily life) in the four groups constituting our population.

1.3.4

Functional capacities and fatigue

Table 4 details the results gathered during the 6-minute walking test (walking distance, heart rate, dyspnea and inspiratory muscle fatigue). It objectifies significant improvement in the dyspnea and lower limb fatigue scores in the four groups constituting our population. Only in group 1, however, did walking distance and heart rate significantly improve.

1.3.5

The costo-diaphragmatic recess X-ray

In none of our four groups did we detect any modification of the lower left costo-diaphragmatic recess; this finding underscores how difficult it is to detect modified positioning of the diaphragm.

1.3.6

Respiratory pressures

Table 5 shows that the only significant improvements of the parameters pertaining to respiratory pressures were registered in groups 1 and 3 with regard to Ip _max alone.

1.4.1

Spirometric volumes

Table 6 recapitulates the different individual and mean measurements carried out in our patients and allows us to draw attention to some of the points we consider important.

1.4.2

Saint-George’s respiratory questionnaire (SGRQ)

At the end of the rehabilitation program, significant improvement with regard to the quality of life parameters (patient satisfaction, functional capacities in daily life and heightened autonomy) was observed in all of our groups, particularly group 1.

These improvements have been mentioned by Wijkstra et al. following a home rehabilitation program, and also by Lacasse and Mota et al. .

1.4.3

The 6-minute walking test

At the end of the rehabilitation program, significant improvement with regard to the 6-minute walking test was observed in the four groups. It was observed for all the test parameters in group 1, but only for dyspnea and inspiratory muscle fatigue in the other groups.

Our results are in agreement with those reported by Redelmeier et al. , Weiner et al. , Derom et al. , Crowe et al. , as well as Perez and Guenard .

1.4.4

The lower costo-diaphragmatic recess

At the end of the rehabilitation program, measurements of the lower left costo-diaphragmatic angle had not been statistically modified; had such modification occurred, our hypothesis pertaining to modifications of the morphology of the diaphragm might have been corroborated. No significant difference in radiographic measurement before and after rehabilitation has been reported in COPD subjects.

1.4.5

Maximal respiratory pressures

At the end of the rehabilitation program, significant improvement in measured Ip _max was observed in the 1st and the 3rd groups. No modification was undergone by Ep _max .

The results of our study are in accordance with the data to be found in the literature. Specific and customized training employing Threshold ^® IMT significantly improves Ip _max and inspiratory muscle strength. As a result, Threshold ^® IMT has been used in the retraining of COPD patients (Gold 1). Similar results have been noted in several other studies in which it has been observed that inspiratory muscle exercise utilizing this tool, in the framework of a program progressing from 30% to 60% of the patient’s Ip _max , effectively complements the pulmonary rehabilitation program followed by the COPD patient.

In our study, the Ep _max measurements carried out before and after rehabilitation in group 2 (training targeting the expiratory muscles) and group 3 (training targeting both the inspiratory and the expiratory muscles) underwent no modification, notwithstanding use of a Threshold ^® PEP specifically targeting the expiratory muscles. The absence of change may be due to the fact that the maximum pressure provided by the apparatus (21 cm H ₂ O) is similar to the figures recorded in our patients (18 and 18.5 cm H ₂ O).

1.4.6

The limits of this study

One of the shortcomings of our work consisted in the fact that all of the evaluations were carried out and that all of the rehabilitation techniques were implemented by the same physiotherapist. The presence of another person performing evaluations of these patients might have been more suitable in order to avoid any possible personal influence with regard to the results of the assessments, especially in measurement of dyspnea and in the terms of the SGRQ parameters.

The relatively low population was due to the exigencies entailed by the limited time frame of our study. This population would subsequently grow as we recruited more subjects for the different groups.

2.1.1

Muscles inspiratoires

À la fin de l’expiration, il persiste au niveau des poumons du patient un piégeage d’un certain volume d’air créant une pression positive résiduelle. Cette pression impose, de la part du diaphragme au début de son travail, un effort inspiratoire important pour générer un débit inspiratoire suffisant lui permettant, tout d’abord, de vaincre la pression positive avant de pouvoir créer une pression négative qui provoquera l’appel de l’air dans les poumons .

Une partie importante de l’énergie qui pourrait être fournie par le diaphragme est utilisée pour cette lutte. Cela diminue le volume de réserve inspiratoire qui pourrait répondre à la demande respiratoire lors de l’effort du patient . Ce travail provoque l’installation d’une distension thoraco-pulmonaire et une tendance à l’aplatissement des fibres musculaires diaphragmatiques qui les place dans des conditions mécaniquement défavorables. Les coupoles du diaphragme deviennent abaissées et aplaties. Elles seront placées dans une situation d’insuffisance fonctionnelle par raccourcissement de leurs fibres contractiles. De ce fait, l’action inspiratoire du diaphragme se réduit ce qui provoque une sollicitation des muscles inspirateurs accessoires .

Le diaphragme, pour s’adapter à ces modifications, va diminuer le nombre et la longueur des sarcomères pour recréer un meilleur rapport tension-longueur au niveau de ces fibres . La force produite par cette nouvelle longueur est égale à celle produite par l’ancienne longueur. Le DIP serait préservée chez un bon nombre des patients. En revanche, la ventilation se fait aux alentours des seuils de charges susceptibles de conduire à une fatigue musculaire. Les fibres musculaires diaphragmatiques de type IIA, moins fatigables, vont augmenter . Ses capacités aérobies seront également majorées par augmentation de sa capilarisation et du nombre de ses mitochondries .

Avec l’évolution, la nouvelle relation tension-longueur ne lui permet plus de générer des forces optimales lors de sa contraction. Il travaille proche de ses capacités maximales de raccourcissement. Cela a pour conséquence une augmentation de son travail, et donc de sa consommation de l’oxygène, atteignant cinq fois les valeurs observées chez les sujets normaux . Il ne peut plus répondre à une demande accrue de la consommation d’oxygène lorsque la maladie s’aggrave. La demande en oxygène est également augmentée par la sollicitation des muscles respiratoires accessoires . Ses derniers semblent conserver leurs forces et leurs endurances. L’ensemble de ses modifications de la mécanique ventilatoire induisent une réduction de l’efficacité inspiratoire .

Ainsi, se trouve justifié le consensus actuel qui ramène la décompensation du patient BPCO à une fatigue musculaire du diaphragme et des autres muscles respiratoires .

2.1.2

Muscles expiratoires

Chez l’Homme, bien que la force des muscles abdominaux semble être conservée, leur endurance serait diminuée .

2.1.3

Courbe débit–volume

Le syndrome obstructif s’accompagne d’une réduction des débits respiratoires alors que les volumes sont peu ou pas modifiés. Le VEMS et le rapport de Tiffeneau (VEMS/capacité vitale fonctionnelle) ainsi que le débit expiratoire de pointe (DEP) sont diminués.

Les petites bronches sont partiellement obstruées à cause des conditions pathologiques. La courbe de débit–volume est typiquement concave vers le haut ce qui traduit la normalité de la vitesse de l’expiration de l’air qui se trouve dans les grosses voies respiratoires et la réduction de celle des petites voies qui est du à leurs obstructions partielles ( Fig. 1 ).

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