Introduction
The respiratory system is accountable for providing oxygen to the body since energy is required for life on day to day basis. Oxygen is required to obtain energy from the food that is consumed. We breathe in air that is rich in oxygen (Miller et al, 2005). Oxygen is needed to burn down the food we eat to release energy. The energy that is released from food is used for body functions and all these functions need energy. To get the energy, oxygen must be present. In the absence of oxygen, the cells will die, so we breathe to get oxygen to keep alive (Lands et al, 1993). Most people do not take note when they are exposing themselves to harmful smells, they are not aware of the repercussions of inhaling those unwanted particles in the lungs (Sharp et al, 2009). When breathing in, various things happen. One the bow-shaped diaphragm contracts thus becoming flat(Norvell and Berger, 2008). The other one is the ribcage which is moved upwards by the ribs. Both these occurrences increase the volume of the lungs. This forces the lungs to suck in the air. This process is referred to as inspiration or inhalation (Norvell and Berger, 2008). There is always a low concentration of oxygen in the air we consume compared to very high carbon dioxide.
On the other hand, when breathing out, several events take place. The flat diaphragm relaxes and becomes bow-shaped again and the rib-cage moves downwards and inwards (Askanazi et al, 2004). These incidences normally make the lungs expel air due to the decreasing volume in the lungs. The ribs are curved bones at the side of the chest that form the chest cavity or the ribcage (Matsui and Grubb, 2006). They protect the organs inside the ribcage. The body requires oxygen to succeed in processing the entire chemical that constantly goes on in the body.
The respiratory system gets oxygen from the air and passes it to the blood which then transports it to the entire body (Decramer et al, 2008). When the body works, it releases some chemicals that may be harmful to it. For instance, when the body burns food in the presence of oxygen to give energy, carbon dioxide is released as waste material. Breathing is automatic (Corey and Farewell, 2006). We do not think whether to breathe in or out. All the same, several diseases can infect the gaseous exchange system and these are respiration. They however interfere with breathing and cause a lot of discomforts and even death if not dealt with early enough (Baraldi, 2003). They normally occur due to the quality of the air we breathe in which may either be polluted or contaminated with micro-organism which causes the disease. For instance, acute asthma is characterized by difficulty in breathing due to spasms in the smooth muscles in the wall of the bronchioles. The bronchioles narrow causing difficulty in breathing out. There is also over secretion of thick mucus substance (Wood, 2007). This infection advances and can be harmful to patients.
What are the mechanisms contributing to pulmonary hyperinflation?
Pulmonary hyperinflation affects persons with chronic problems such as the blocking of the pulmonary thus causing asthma to the patient (Boucher, 2004). This is an abnormal enlargement in functional remains capacity, thus lung quantity towards the last part of tidal termination. It’s almost widespread in people suffering suggestive disseminated airway impediment (Boucher, 2004). Hyperinflation which is a condition on or after an ordinary chest radiograph indicates an increase in entire lung capacity (Worlitzsch and Tarran, 2002). The reduction quantity of the respiratory system becomes greater in patients with persistent airway disease due to changes in the expandable properties in the walls of the chest and the lungs (Voisin and Prefaut, 2005).
To add to this, an unpredictable amount of active hyperinflation may well be present. However, it has been noted that hyperinflation progresses with age. This is a consequence due to the commencement of inspiration before lung capacity has fallen to the relaxation capacity of the respiratory system (Gilmartin and Gibson, 2007). This is commonly present at the break where patients who are reasonable to cruel airway hindrance but normally amplify more on doing exercise, by this means boosting the mechanical weight lying on to the aspiratory muscles, therefore, reducing their mechanical benefit (Chmiel and Davis, 2003).
The key proven consequences as well as associations of hyperinflation comprise of deformation of chest wall movement, damaged aspiratory muscle task, more oxygen rate of inhalation, a bigger chance of hypercapnia, damaged workout presentation, in addition to greater brutality to breathlessness (Wine, 2007). This indicates a sure improvement following behavior with a bronchodilator might be appropriate, some way in reducing overexcited rise (Pickles et al, 2005).
Chan and Gonda (2004) noted that “the apparent favorable effects of pulmonary hyperinflation on lung technicalities such as an enhanced airway patency and lung resilient recoil are certainly overwhelmed by the harmful effects on the pressure producing capacity of the respiratory muscles”. The systems underlying pulmonary hyperinflation and also pathophysiological consequences do not diverge from those portrayed in impulsively breathing patients (Chan and Gonda, 2004). During a severe attack of asthma, the residual capacity can rise because of gas trapping caused by premature airway shutting down, while the failure of the lung elastic withdrawal displaces the pressure volume and diminishes the work of breathing.
The pressures generated by the respiratory muscles always overcome lung recoil and its patency (Oliver and Wallis, 2005). However, the displacement of the respiratory system always increases the ventilator capacity hence pushing the rest of the system to a higher and flat part of the pressure-volume area or curve (Oliver and Wallis, 2005). This process leads to an increased expansion of the chest and also a systematical increase in the expiratory pressure which is combined with dynamic hyperinflation (Button and Boucher, 2006). Chronic pulmonary diseases, for instance, chronic obstructive pulmonary disease have often been seen as potential precautions.
Hyperinflation is often accompanied by a decreased mechanical benefit of the inspiratory muscles and consequently a maximum static inspiratory pressure (Bethesda, 2003). The lungs are elastic muscles and can therefore expand to take in air or compress to expel air, they are spongy and this is because they are made of very many air sacs called alveoli. This organ normally holds the air (Hoo et al, 2004). They are covered by blood vessels to allow for the movement of air into and out of the blood. While breathing expiration exhalation and inspirational inhalation normally takes place. In inspiration, external inter-coastal muscles relax the ribs are pulled upward and outside the diaphragm down thus causing it to flatten. The volume of the chest cavity increases as the pressure reduces. The air is then forced into the lungs from the outside (Liechti-Gallati, 2004a). When exhalation and inhalation are taking place the ribs expand and contract thus pulling the diaphragm up and down due to contraction of muscles. (Hoo et al, 2004). The diaphragm muscles relax and assume a normal shape. As a result of the relaxation of these muscles, pressure levels in the lungs are increased hence leading to a decrease in chest volumes (Beardsmore, 2005). The air is forced outside the lungs via the air passage then into the atmosphere. During air movement in the human body it is fast moistened, then filtered, and finally heated. The filtering is accompanied using hair cilia in the nostrils mucus found in the tracheal system also helps in the filtering of air by trapping dust particles and bacteria (Edwards, 2000).
Adverse effects of pulmonary hyperinflation on the inspiratory muscles
Interpulmonary allocation of the transformation in pleural pressure while breathing is yet to be known (Lindblad, 2003). The windpipe commonly known as the (trachea) is the pipe that leads air from the nose into the lungs. It has tiny hairs inside it that move about to sweep out dust particles and mucus, which is then coughed out (Roumeliotis and Levison, 2001). The trachea has rings around it to ensure that it stays open all the time to avoid suffocation. At its lowest end, it divides into two tubes called bronchi (bronchus in singular) each of which leads into one of the lungs (Decramer, 2005). Epiglottis is a small finger-like membrane that takes care of the trachea (Wallis and Stocks, 2004). The unwanted materials are blocked from entering the lung through the bends which are thereon the windpipe. As soon as the lung is inflated acutely, the capability of the diaphragm which produces pressure, in particular, pleural pressure is damaged since the muscle during reduction is shorter and produces less force (Fitz-Simmons and Stallings, 2000). The enlargement of the muscles in the radius of curvature can cause the lungs to produce low pressure when the volumes of the lungs are high (Stern, 1997). As quoted by Stern (1997), “Lung inflation similarly weakens the pressure-producing capacity of the inspiratory intercostal muscles, both the parasternal intercostals and the external intercostals” (Liechti-Gallati, 2000b).
On the contrary, the diaphragm, this difficult effect is mainly associated with the positioning and movement of the ribs in the human body, but not the muscle capacity to produce force (Rosenstein and Cutting, 2003). During the collective creation of the two sets of muscles, the change is more than when isolated diaphragm foundation; this increases the weight on the diaphragm decreases the shortening of the muscle, and enlarges muscle force (Meister, 2004). In addition, the establishment of the diaphragm slows down the cranial dislodgment of the inactive diaphragm that appears when there are isolated intercostals hence strengthening and increasing the respiratory result of the intercostals (Passy et al, 2001). As a result, of these changes which occur during collective diaphragm-intercostals commencement of the same is greater than the total sum of the power produced during split muscle opening (Tim’s, 2005). This synergic contact developed is certainly important in lung enlargement and lung volumes, either on the unilateral basis or bilateral circumstances which put excessive pressure on pumps directed to inspiratory muscles.
Researchers have shown that the Force produced by a thin muscle collection during isometric tightening is also known to differ with the function of the muscle length. The span of the muscle bunch is increased and the functional energy enlarges steadily until an upper limit is attained and after this, it goes down to the normal span: this length which is more or the same as the original length is called optimal length (Laird and Ware, (2007).
The mechanical action of individual accessory muscles
In inspiration, external inter-coastal muscles relax the ribs pulled upwards and outwards the diaphragm thus causing it to flatten (Kraemer, 2004). When the patient breaths out air are forced out of the lungs hence increasing the pressure of the chest, in this condition the pressure in the lungs is reduced. (Green, 1990). Oxygen diffuses out of the blood capillaries from where it is breathed out during expiration. Alveolar ventilation usually relies on the respiratory muscles. Alveolar ventilation is used to reduce the mechanical force or weight and also decrease the airflow hence managing the geometry modification in the thorax. Gloss pharyngeal is breathing where a couple of gulp with the lips and tongue is normally regarded as (Green, 1990). The pharynx is found between the mouth and the air pipe, this part has respiratory and gastrointestinal zones. A pharynx is also known as the voice and it is a tube that is conical in shape. The pharynx contains ligaments that are bound to the walls of the cartilage that move chest muscles up and down (Poulton, 2003). Technology has come up with an apparatus for qualifying the air breathed through in the body. Currently, there has been an increase in artificial pulmonary ventilation due to the modernization of medical support. Patients who are dependent on ventilators most of the time have a lot of fear, that the apparatus can accidentally get disconnected from the ventilator (Craig, 2003).
There is always a variance between patients who have breathing problems due to injuries on the spinal cord with those who have poliomyelitis (Kraemer, 2006a). Variety muscles of respiration help in both inspiration and expiration, which require changes in the pressure within the thoracic cavity (Demizio and Coates, 2002). To attain this process, respiratory muscles change the size and dimension of the thorax. Normally tidal air occurs when a certain amount of air is inhaled or exhaled during a regular process by a normal human being (Woo, 2002). However, it has been noted that there exist several factors affecting the rate of breathing in these patients making this condition deteriorate (Rommens and Markiewicz, 2004). For instance the state of the body, the rate is higher when the body engages in physical activity (Knoop et al, 2003). Young people are more active as several growth processes are occurring in their bodies, therefore there is a higher oxygen demand, and hence the rate of breathing increases. An increase in temperature enhances the breathing rate because it generally increases the rate of metabolic reactions in the body hence more blood supply or oxygen becomes necessary (Kraemer and Meister, 2009). When one is emotionally affected, the temperature tends to rise due to the hormone adrenaline which increases metabolic activities.
To ensure that the patients who breathe through ventilators have a long and productive cough, doctors allow them to develop a better vital capability. This capability enables the patients to breathe freely without the assistance of the ventilator (Nesbitt, 1975). This is a cough that expels mucus or sputum from the respiratory tract to clear tracheal secretion.
Expiratory muscle recruitment
During breathing or respiration, the muscles in the chest and the diaphragm normally contract and expand thus pulling and pushing the ribs up and down (Fisherman, 2004). A dome shape is formed when the breathing process is taking place in the patient’s chest, thereby increasing the volume of air that is forced out of the lungs hence decreasing air in the chest cavity (Corey et al, 1992). The filtering is accomplished using hair cilia. Mucus which is found in the nose normally traps bacteria and dust particles, hence filtering the air. It is more shocking to note that there is a scarcity of data linked to expiratory muscles to help solve this problem (Kraemer and Schoni, 2006). The muscles are engaged in patients at some point experimentally stimulated bronchoconstriction even though inhalation adjacent to expiratory resistance and towards the end of the expiration causes a passive commencement of the upcoming inspiration. The devices in which the airflow restriction is conveyed by expiratory muscle enrollment are not clarified (Trowbridge, 2008). Expiratory muscle reduction during cessation can be a nonspecific ordinary factor of the reaction towards the respiratory system to the enlarged respiratory motivation. Abdominal force employment during expiration permits maintenance of diaphragm muscle filament length and the strength producing ability of the diaphragm at the commencement of inspiratory muscle tightening, regardless of lung hyperinflation (Schellauf, 2001).Whereas a minimum inspiratory muscle limitation is usually featured to hyperinflation putting the inspiratory muscles at an automatic drawback. Expiratory muscle limitation is an attribute of a comprehensive myopathy found in these patients (Laird et al, 2004).
On top of losing strength, it was later shown that the survival of the expiratory muscles is diminishing (Crameri, 2006). This drop-off is normally related to the brutal airflow impediment together with the decline of the force of other muscle groupings, signifying that damaged expiratory muscle survival has the same fundamental source as the comprehensive failure of strength (Gallati, 2004b). The diminishing expiratory muscle presentation contributes to condensed exercise patience and reduced worth of life in patients’ (Knowles, 1997). Also, expiratory muscle limitation is connected with failure to cough well. The expiratory muscles have been particularly skilled in quite a several settings. Such training is liable to improve expiratory muscle potency, and to progress cough value is strictly disabled various sclerosis patients, to recover the awareness of dyspnea in children with neuromuscular disease, also minimize the feeling of respiratory attempt during exercise in vigorous subjects (Kraemer, 2009b).
Non-specifically instructed with normocapnic hyperpnea, the potency of the expiratory influence was increased, with a positive effect on exercise routine and eminence of life. On the other hand, the enhancement of the expiratory muscle power was not precise, as the inspiratory muscle survival also improved, making it hard to conclude (Gallati, 2005c). The total volume that the lung can accommodate is known as lung capacity. It is noted to be 5500ml for an adult male and 4000ml for an adult female. Inspiratory reserved volume refers to the volume of air in the lungs after a forced inhalation in association with tidal volume (Levison, 2001). If after normal respiration we force an extra amount of air out by contracting abdominal and thoracic muscles, this volume of air is the expiratory reserve volume. The air which is inhaled after a deep breath is known as residual air volume and it is not important in the gaseous exchange. However, residual volume increases with lungs infection (Gallati, 2003a).
References
Askanazi, J. et al. (2004) Nutrition and the respiratory system: Crit Care Med, 10(3):163-172.
Baraldi, E. (2003) Flow limitation in infants with bronchopulmonary dysplasia and respiratory function at school age: Lancet, 361(9359):753-754.
Beardsmore, C.S. (2005) Lung function from infancy to school age in cystic fibrosis: Arch Dis Child, 73(6):519-523.
Bethesda, M.D. (2003) Cystic Fibrosis Foundation National Patient Registry In Annual Data Report Cystic: Fibrosis Foundation; New York..
Bisgaard, H. (2004) Serial lung function and responsiveness in cystic fibrosis during early childhood: Am J Respir Crit Care Med, (11):1209-1216.
Boucher, R.C. (2004) New concepts of the pathogenesis of cystic fibrosis lung disease. Eur Respir J 23 (1):146-158. Mall M, Grubb BR, Harkema JR, O’Neal WK, Boucher.
Button,B and Boucher, R.C (2006) Regulation of normal and cystic fibrosis airway surface liquid volume by phasic shear stress. Annu Rev Physiol, 68:543-561.
Chan, H.K. and Gonda, I. (2004) Mucociliary clearance in patients with cystic fibrosis and in normal subjects: Am J Respir Crit Care Med, 150(1):66-71.
Chmiel, J.F and Davis P.B. (2003) State of the Art: Why do the lungs of patients with cystic fibrosis become infected and why can’t they clear the infection? Respir Res 4(1):8.
Corey, M. and Farewell, V. (2006) Determinants of mortality from cystic fibrosis. Pediatr Pulmonol.
Corey, M. et al. (1992) Prediction of mortality in patients with cystic fibrosis: N Engl J Med, 326(18):1187-1191.
Craig, R.F. (2003) Longitudinal study of childhood wheezy bronchitis and asthma: outcome at age 42. Bmj, 326(7386):422-423.
Crameri, R. (2006) Effect of allergic bronchopulmonary aspergillosis on lung function in children with cystic fibrosis. Am J Respir Crit Care Med, 174(11):1211- 1220.
Decramer, M. (2005) Hyperinflation and respiratory muscle interaction: Eur Respir J 10(4): 934-941.
Decramer, M. et al. (2008) Effects of acute hyperinflation on chest wall mechanics in human beings. J Appl Physiol, 63(4):1493-1498.
Demizio, D. and Coates, A.L. (2002) Lung recoil and the determination of airflow limitation in cystic fibrosis and asthma: Pediatr Pulmonol, 15(1):13-18.
Edwards, L.J. (2000) Modern statistical techniques for the analysis of longitudinal data in biomedical research: Pediatr Pulmonol, 30(4):330-344.
Fisherman, W.S. (2004) Guide for the Uniform Data Set for Medical Rehabilitation: Including the Functional Independence Measure, Version 5. Buffalo, NY: UB Foundation Activities.
Fitz-Simmons, S. and Stallings, V.A. (2000) Longitudinal relationship among growth, nutritional status, and pulmonary function in children with cystic fibrosis: analysis of the Cystic Fibrosis Foundation National CF Patient Registry: J Pediatr, 137(3):374-380.
Gallati, S. (2003a) Genetics of cystic fibrosis. In Cystic fibrosis and bronchiectasis: Volume 24. Edited by: Lynch JP: New York, NY: Thieme Medical Publishers, Inc; 629-637.
Gallati, S. (2004b) The role of common single-nucleotide polymorphisms Hum Mutat, 24(2):120-129.
Gallati, S. (2005c) Ventilation inhomogeneities in relation to standard lung function in patients with cystic fibrosis. Am J Respir Crit Care Med, 171(4):371-378.
Gilmartin, J.J. and Gibson, G.J. (2007) Abnormalities of chest wall motion in patients with chronic airflow obstruction. Thorax, 39(4):264-271.
Green, M. (1990) Respiratory muscle functions in cystic fibrosis. Thorax, 45(10):750- 752.
Hoo, A.F. et al. (2004) the evolution of airway function in early childhood following clinical diagnosis of cystic fibrosis. Am J Respir Crit Care Med, 169(8):928- 933.
Knoop, C. et al (2003) Function and bulk of respiratory and limb muscles in patients with cystic fibrosis: Am J Respir Crit Care Med, 168(8):989-994.
Knowles, M. (1997) longitudinal analysis of pulmonary function decline in patients with cystic fibrosis. J Pediatr, 131(6):809-814.
Kraemer, R. (2004) Early detection of lung function abnormalities in infants with cystic fibrosis. J R Soc Med, 82 (Suppl 16):21-25.
Kraemer, R. (2006a) Two buffer PAGE system-based SSCP/HD analysis: Eur J Hum Genet, 7(5):590-598.
Kraemer, R. (2009b) Antipseudomonal therapy in cystic fibrosis: aztreonam and amikacin versus ceftazidime and amikacin. Eur J Clin Microbiol Infect Dis , 8(10):858-865.
Kraemer, R. and Meister, B. (2009) Fast real-time moment-ratio analysis of multibreath nitrogen washout in children. J Appl Physiol, 59(4):1137-1144.
Kraemer, R. and Schoni, M.H. (2006) Ventilatory inequalities, pulmonary function and blood oxygenation. Respiration, 57(5):318-324.
Laird, N.M. and Ware, J.H. (2007) Random-effects models for longitudinal data. Biometrics, 38(4):963-974.
Laird, N.M. et al. (2004) Longitudinal studies with continuous responses. Stat Methods Med Res, 1(3):225-247.
Lands, L.C. et al. (1993) Respiratory and peripheral muscle function in cystic fibrosis. Am Rev Respir Dis, 147(4):865-869.
Levison, H. (2001) Maximal inspiratory and expiratory pressures are reduced in hyperinflated, malnourished, young adult male patients with cystic fibrosis. Am Rev Respir Dis, 132(4):766-769.
Liechti-Gallati, S, (2004a) Genotype-phenotype association in infants with cystic fibrosis at the time of diagnosis: Pediatr Res, 44(6):920-926.
Liechti-Gallati, S. (2000b) Buccal cell DNA analysis in premature and term neonates: s Eur J Pediatr, 159(1–2):99-102.
Lindblad, A. (2003) Method for assessment of volume of trapped gas in infants during multiple-breath inert gas washout. Pediatr Pulmonol, 35(1):42-49.
Matsui, H. and Grubb, B.R. (2006) Evidence for periciliary liquid layer depletion, not abnormal ion composition, in the pathogenesis of cystic fibrosis airways disease.1005-1015.
Meister, B. (2004) intrapulmonary gas distribution in healthy children: Respir Physiol, 65(2):127-137.
Miller, S. et al. (2005) Cystic fibrosis: N Engl J Med Pub med Abstract Publisher full Text.
Nesbitt, C.J (1975) Survival patterns in cyctic fibrosis. J Chronic Dis, 28(11–12):609- 622.
Norvell, T.M and Berger, M. (2008) Bronchoalveolar lavage findings in cystic fibrosis patients with stable, clinically mild lung disease suggest ongoing infection and inflammation. Am J Respir Crit Care Med. Pub-Med: 150(2):448-454.
Oliver, C. and Wallis, C. (2005) Multiple-breath washout as a marker of lung disease in preschool children with cystic fibrosis: Am J Respir Crit Care Med, 171(3):249-256.
Passy P.E. et al. (2001) Tracheostomy and Ventilator Speaking Valves Instruction Booklet: Irvine, Calif: Passy-Muir Inc.
Pickles, R.J. et al. (2005) Normal and cystic fibrosis airway surface liquid homeostasis. The effects of phasic shear stress and viral infections: J Biol Chem, 280(42):35751-35759.
Poulton, R. (2003) A longitudinal, population-based, cohort study of childhood asthma followed to adulthood. N Engl J Med, 349(15):1414-1422.
Rommens, J. and Markiewicz, D. (2004) The relation between genotype and phenotype in cystic fibrosis – analysis of the most common mutation (delta F508). N Engl J Med, 323(22):1517-1522.
Rosenstein, B.J and Cutting, G.R. (2003) The diagnosis of cystic fibrosis: a consensus statement. Cystic Fibrosis Foundation Consensus Panel: J Pediatr, 132(4):589-595.
Roumeliotis, D. and Levison, H. (2001) the effects of chronic airflow limitation, increased dead space, and the pattern of ventilation on gas exchange during maximal exercise in advanced cystic fibrosis. Am Rev Respir Dis, 138(6):1524-1531.
Schellauf, H.P. (2001) Combined body plethysmographic, spirometric and flow volume reference values for male and female children. Eur J Pediatr , 160(5):300-306.
Sharp, J.T. et al (2009): Thoracoabdominal motion in chronic obstructive pulmonary disease. Am Rev Respir Dis.
Stern, R.C. (1997) The diag nosis of cystic fibrosis. N Engl J Med, 336(7):487-491.
Suan, G. (2006) Lung function in infants with cystic fibrosis: Thorax, 43(7):545-551.
Tim’s, P. (2005).Lung function in children and adolescents: Basel, Switzerland: Karger.
Trowbridge, F.L. (2008) Development of normalized curves for the international growth reference: historical and technical considerations. Am J Clin Nutr, 46(5):736-748.
Valsecchi, M.G. (2002) Epidemiology and survival analysis of cystic fibrosis in an area of intense neonatal screening over 30 years: Am J Epidemiol, 156(5):397-401.
Voisin, M. and Prefaut, C. (2005) Determinants of the tension-time index of inspiratory muscles in children with cystic fibrosis: Pediatr Pulmonol , 23(5):336-343.
Wallis, C.E and Stocks, J. (2004) Multiple breath inert gas washout as a measure of ventilation distribution in children with cystic fibrosis: Thorax, 59(12):1068- 1073.
Wine, J.J. (2007) the genesis of cystic fibrosis lung disease.J Clin Invest, 103(3):309-312.
Woo, M.S. (2002) Clinical findings and lung pathology in children with cystic fibrosis. Am J Respir Crit Care Med, 165(8):1172-1175.
Wood, R. (2007) In Cystic fibrosis. Edited by: Taussig LM. New York: Thieme- Stratton; 1984:434-460.
Worlitzsch, D. and Tarran, R. (2002) Effects of reduced mucus oxygen concentration in airway Pseudomonas infections of cystic fibrosis patients: J Clin Invest 109(3): 317-325.