AUSTRAlIAN PHYSIOTHeRAPY

Bredge McCarren

Hyperinflation is a compensatory mechanism which occurs in response toincreased resistanee of the airways. Hyperinflation allows for an increase in minute ventilation and improves the efficiency of the inspiratory intercostals. However, there are detrimental effects on the function of the diaphragm and the accessory muscles,which increasethe work of breathing. The physiotherapist'sinitalgoal is to enhance theaction of the respi ratory muscIes andnot to select strategies thatwiHinterfere with this compensatory mechanism. Oncethe underlying problem is stabilised, the physiotherapist may then use strategies which assist with the reversal of the problem. [McCarren 8: Dynamic pulmonaryhyperinflation. Australian Journal of Physiotherapy 38:175179,1992]

Key words: Respiratory mechanics; Lung diseases, Obstructive; Physical Therapy

BMc Carren BSc, GradDipPhty, is a lecturer in the Faculty of Health Sciences, University of Sydney Correspondence: .BredgeMcCarren, School of Physiotherapy, Faculty of Health Sciences, University of Sydney, East Street, Lidcombe, New South Wales, 2141

ORIGINAL ARTICLE

Dynamic pulmonary hyperinflation

O

yn.a.mic pu.1m.onary hYP ...erinflation is one of the main reasons that patients with obstructive lung disease are breathless (Killian and Campbell 1983). Dynamic hyperinflation is a compensatory mechanism which results in an increase in the end expiratory lung volume above the predicted functional residual capacity (FRC) (Gottfried et al 1986). It is important that physiotherapists recognise the mechanisms and effects of dynamic hyperinflation·ventilation. This knowledge will assist physiotherapists to develop appropriate management programs, which support and optimise the·actions ofthe respiratory muscles inmain~aining effective ventilation, whilst the medical treatment of the underlying cause takes effect. Hyperinflation is recognised clinically bya number ofindications. Observation shows that the patient has a typical barrel shaped chest. Chest xray confirms this, as the lung fields are larger and blacker than normal,the diaphragm is flatter and the rib alignment iSIDore horizontal than the normal chest wall and lung. The breathing pattern also is very characteristic. The typical upper ·chest breathing pattern with recruitment of the accessory muscles predominates, with very little movement ofthe lower chest walL Static lung function tests demonstrate that FRC, residual volume (RV) and total lung capacity (TLC) are all increased (West 1987). Dynamic hyperinflation is a compensatory mechanism of the respiratory system which occurs in response to an increase in resistance in the airways (Gottfriedet a11986,

Macklem 1984). Patients with airflow limitation dynamically hyperinflate their chests to maintain adequate minute ventilation when they are experiencing an acute inflammatory response within the airways or·when they are exercising. The mechanism which triggers this phenomenon is similar in both situations. \Vhen the airways narrow asa result of bronchoconstriction, inflammation or decreased elastic recoil, the expiratory flow decreases and expiration increases in time. The patient will maintain minute ventilation by increasing the respiratory rate. Expiratory time decreases, thereby decreasing the time available to exhale to FRC prior to the next inspiration (Gottfried et al 1986). Also, active expiration increases pleural pressure. The dynamic increase in pleural pressure compresses the narrowed or floppy airways which further decreases airflow and leads to gas trapping (Macklem 1984). The FRC increases and dynamic hyperinflation of the chest wall ensues. During exercise, the patient with chronic airflow limitation also must increase their respiratory rate to maintain the .required .minute ventilation. The resultant dynamic hyperinflation occurs through a similar pathophysiological mechanism. The effects of dynamic hyperinflation are both advantageous and disadvantageous . The overall advantage of dynamic hyperinflation is the capacity to improve ventilation. Hyperinflation of the chest walland of the underlying lungtissue distends the narrowed

OR IGI N ALAR TIC L E AUSTRAlIAN

~HYSIOTHtRA~Y

from Page 115

airways, decreases resistance (Macklem 1984) and maintains ventilation. Patients who already generate maximum expiratory flow rates in tidal breathing also achieve a further·benefit from hyperinflation. The flow-volume curve of the chronic airflow limited patient (see Figure 1) illustrates that as a consequence ofhyperinflation, the tidal volume curve moves towards TLC (Derenneet al 1988). An increase in tidal volume as well as an improved ability to increase expiratory flow rates enables the patient to increase their minute ventilation. The main disadvantage of dynamic hyperinflation is the altered mechanics of the respiratory muscles. With dynamic hyperinflation, the pressure generating ability of the respiratory muscles is decreased and the recruitment pattern changes. The act of respiration then becomes more expensive in terms of energy consumption (Fleury et aI1987). The muscle most affected by hyperinflation is the diaphragm (Decramer et al 1986, Decramerand De Troyer 1984), which is the main inspiratory muscle. During dynamic hyperinflation the diaphragm flattens and descends in the thoracic cage. This causes shortening of the diaphragm and decreases its ability to generate tension because of the length tension relationship (see Figure 2) (Grassino etal1978). The diaphragm becomes less efficient in moving the thoracic cage and contributing to ventilation. However the long term adaption of absorption ofsarcomeres in the diaphragm has been shown to occur in emphysematous hamsters with stable hyperinflation (Farkas and Roussos 1983). The absorption of sarcomeres moves the length tension curve to the left and restores the.optimal relationship (Farkas and Roussos 1983). This compensation may also occur inpatients with stable chronic airflow limitation (CAL) (Similowskiet aI1991). In addition, the shortening of the diaphragm changes the geometry of the costal and crural portions of the muscle. Normally these muscles lie in parallel (Macklemet·aI1983).

Flow

Volume

TlC

RV

figure 1.

Maximum flow-volume curve of the normal(right line curve) and the airflow limited patient(left line curve).The dotted curve is the tidal flow-volume curve and the dashed curve is thecompensatoryhyperinflated curve acbieved during exercise oracula

exacerbation of the airflow limited patient.

Hyperinflation places them in series, reducing the tension able to be developed (Macklem 1984, Macklem et aI1983). It has been proposed that the effect of hyperinflation on the power generating ability of the diaphragm is related to Laplace's law (Celli 1989). Thislaw states that pressure (P) is related to the tangential tension (T)over the radius (r) ofthe dome (P=T/r).Thus as the radius of the dome of the diaphragm in the hyperinflated lung increases towards infinity, the pressure generated by the .diaphragm theoretically.decreases. ·The relative importance ofthis factor in the contribution to the mechanical disadvantage of the diaphragm is unclear, as· this muscle .acts more as a flat topped table than a dome (Braunet aI1982). As CAL progresses and the degree of hyperinflation increases, the action of the diaphragm changes. The diaphragm is believed to act as a flxator in the patient with CAL with severe hyperinflation (Macklem et al 1983) and ventilation is achieved by the action of the intercostal and accessory

muscles. This implies that the major action of the diaphragm is to prevent the transmission of the negative pleural pressure to the abdomen, thus avoiding suction of the diaphragm into the thorax. In more severe hyperinflation the diaphragm may even become expiratory in action as demonstrated by Hoover's sign inward movement ofthe lower portion of the ribcage during inspiration. This phenomenon is due to the re-alignment of the diaphragm fibres. The contraction of the diaphragm exerts an!nward force on the chest wall, which becomes expiratory inaction (Zocchi etal 1987). Hyperinflation also alters the action of the intercostal muscles. In·the normal thoracic cage during tidal breathing, the main action of the intercostals is to prevent the paradoxical inward motion of the intercostal spaces (De Troyer and Estenne 1984). The concentric action of the inspiratory intercostals during respiration is to move the ribs ,closer together. However, whether the action is inspiratory or expiratory depends on the compliance or

AUSTRAliAN PHYSIOTHERAPY

o RIG I N A1

A RTI ClE

c

o (J')

c ~

Length (em) o Normal

• Hyperi nflated

Figure 2. The length-tension curve of the normal diaphragm and the chronic hyperinflated

diaphragm.

impedance ·of the chest wall (DeTroyer et al 1985) which alters with lung volume. At low lung volumes the thoracic cage is less· resistant or less stiff to the upward movement of the ribs, so the action of the intercostal muscles tends to be inspiratory. At high lung volumes (ie TLC) the chest wall is more resistant or more stiff to a further upward movement, and so demonstrates.low compliance to inspiratory actions. At TLC the chest wall is more compliant to the downward movement and the action of the intercostals becomes expiratory as there is a high compliance of the soft tissues to expiration. 'As many dynamically hyperinflated patients' FRC is high, the action qf the contracting intercostal muscles maybe expiratory. A number of researchers have proposed that patients with CAL use the intercostal.muscles in preference to the accessory muscles (Decramer 1989, Martin et at 1980, Martinez etal 1990, Sanchez et al 1984). Sanchez and associates (1984) noted that the level of metabolic enzymes in the intercostals increased with an.increasing degree of airway obstruction and related pulmonary hyperinflation. Researchers have also demonstrated that the parasternal intercostal muscles

reach optimal length at TLC and are therefore more able to contribute effectively to inspiration (Farkas etal 1985, Jianget al 1989). The accessory muscles also have altered mechanics and action as a result of dynamic hyperinflation. Little is known about the inspiratory.accessory muscles and the effects of hyperinflation. Studies have shown, however, that with increasing lung volume the tension generated by these muscles decreases (Danon et a11979). The expiratory accessory muscles, namely theahdominals, are recruited by some hyperinf1ated patients to assist the inspiratory muscles. Doddet al (1984) demonstrated that, while exercising, some patients with CAL used the abdominal release mechanism to decrease the work of the diaphragm while maintaining its output. The mechanism responsible involves the abdominal muscles contracting at the end of expiration, pushing the abdominal contents up against the diaphragm and improving its lengthtension relationship. Just prior to inspiration there isa sudden release of the abdominal pressure and the diaphragm is sucked down passively, causing an increase in lung volume. Grassino and co-workers (1981) found that the elastic energy.stored by the

abdominals acting as inspiratory agonists during expiration, may be responsible for an inspiratory volume of 500m1.Somepatients,while dynamically hyperinflated, may use the abdominal release mechanism thereby changing the recruitment pattern of the respiratory muscles. The improvements in dt:;creasing resistance .and improving ventilation are crucial to patients in respiratory failure. Dynamic hyperinflation adds a mechanical advantage through the development of the optimal length of the parasternal intercostal muscles and the passive descent of the diaphragm via use of the abdominal release mechanism in somepatierits. The mechanical disadvantage to the diaphragm and the accessory muscles and the changed action of the respiratory muscles leads to an increase in the work of breathing in patients with dynamic hyperinflation (Fleury et aI1987).

Clinical implications The issue for physiotherapists to remember when treating dynamically hyperinflated patients is that it is important not to alter the compensatory mechanisms associated with· maintaining the necessary hyperinflation. The increase in FRC, the related use of the accessory muscles and the abdominal release mechanism are vital, as they enable the patient to minimise the underlying problem of resistance.and enhance the patient's ability to maintain the required minute ventilation (Macklem, 1984). The goal of the physiotherapist is to assist the patient in maintaining the increase in ventilation efficiently.and effectively until the underlying problem is reversed. The reversal of the primary respiratory problem, the increased resistance to airflow, is the main strategy of medical management, usually with the use of pharmacological agents (Sherman et al 1991). The physiotherapist also may decrease resistance by assisting with the removal of excessive secretions (Cochraneet a1 1977, Webberet a11986). However,

ORIGINAL ARTie l E

from Page 111

the therapist initially aims to decrease the unnecessary demand on the respiratory system and relieve the distress ofthe patient, until the drugs become effective. Once the demand on the respiratory muscles is decreased, the removal of excessive secretions as well as other treatment strategies maybe used with maximum effectiveness. Strategies which decrease dyspnoea and the·work of the respiratory muscles can either assist the respiratory muscles and increase their mechanical output without increasing the oxygen demand or decrease any unnecessary oxygen requirements of the rest of the body. This will bring about a resultant decrease in the demand on the respiratory system and the work of breathing will diminish. Positioning is a good example ofa physiotherapeutic strategy that uses both principles (Reid and Loveridge 1983).

Positioning Physiotherapists use positioning to improve the function of the inspiratory muscles. In the dynamically hyperinflated patient it is often noted that some patients adopt the lean forward position, with the arms supported and stabilised. In this position the function of the diaphragm improves (O'Neill and McCarthy 1983), and its tension increases with a decrease in neural drive (Druz and Sharp 1982). It is proposed that the diaphragm length is also improved in the lean forward position. Patients report thatthis position relieves their dyspnoea (Druz and Sharp 1982). Positioning is therefore used to improve mechanical output. In addition, passively supporting the shoulder.girdle decreases the tonic activity of the inspiratory accessory muscles (Dmz and Sharp 1982). Therapists can also decrease postural muscular activity by supporting the trunk and lower limbs with appropriate supported positioning. Positioning is also used to decrease oxygen consumption by eliminating unnecessary muscular activity.

Relaxation Another means of eliminating unnecessary muscular .activity is through relaxation. It is very stressful to be gasping for breath. Enhancing the coping mechanisms helps to decrease oxygen demand (Harris 1984) which then decreases the load on the respiratory system. The relaxation techniques used by therapists are a matter of personal preference, however it is probably beneficial to avoid relaxation strategies which centre around deep breathing, as this will interfere with the patient's preferred breathing pattern and may focus the patient on their problem.

Continuous positive airway pressure Continuous positive airway pressure (CPAP) is becoming a popular mechanical means of decreasing the cost ofbreathing in patients with CAL (Gherini et aI1979). It is proposed that continuous positive pressure supports and splints thenarrowed.and floppy airways through inspiration and expiration (Gherini etaI1979). This support indirectly takes over the role of the respiratory muscles -in maintaining thehyperinflated chest wall (Petrof et aI1990). A decrease in the oxygen requirements of the respiratory muscles follows. Thismay rest the respiratory muscles and prevent fatigue and ensuing failure (Petrofet aI1990).However, it is important to recognise that if the mechanical pressure applied by CPAP becomes greater than intrinsic positive end expiratory pressure (PEEP), further dynamic hyperinflation will occur and the deleterious effects of high intrathoracic pressures will follow (Gmm and Chauncey 1988).

Nasal intermittent positive pressureventHation Nasal intermittent positive pressure ventilation (NIPPV) is being investigated as a means ofassisting these dynamically hyperinflated patients in maintaining ventilation while in acute respiratory failure (Bott etal 1991, Elliot et al 1990). Itis believed that the assisted ventilation

AUSTRAlIAN PHYSIOTHERAry

rests the respiratory muscles· and enables them to cope with the increased resistive load until medical interventions are effective in reversing the problem. NIPPV reverses the hypercapnia and the hypoxia which occurs in those patients in respiratory failure (Bott et aI1991). Hypercapnia (Juanet a11984) and hypoxia (Esau 1989,]ardim eta11981) have been shown to induce fatigue and decrease the contractility of the respiratory muscles. NIPPV rests and improves the. contractility of the respiratory muscles (Ellisetal 1987).

Conclusion Physiotherapy has an important part to play in assisting patients with hyperinflated lung and chest wall. ·The many strategies that are available aim to decrease the work of the inspiratory muscles or to improve their function. It is important to realise that hyperinflation is a physiological compensation to increased resistance within the airways. .Therefore, interference with .the adopted breathing pattern will reduce the effectiveness of the patient's coping strategies. Once the demand of ventilation on the respiratory system is decreased, the respiratory muscles can then be more effective with more strenuous physiotherapy strategies designed to reverse the respiratory problem.

References Bott j, CarrollM, .Conway JH, HitchcockRA, BrownAl\f, GodfreyRC, Bowcott]M, Elliot MW, KeiltySE, Ward EM, WedzichaJAand Moxham] (1991): The effect of nasal intennittent positive pressure ventilation on acute exacerbations of chronic obstructive puhnonarydisease (COPD).American Review ofRespiratory Diseases 143:A472. Braun NMT, AroraNS and Rochester DF (1982): Force-length relationship of the normal human diaphragm.JournalofAppliedPhysiology 53:405-12.

Celli BR (1989): Clinical and physiological evaluation of respiratory muscle function. Clinics ofChest Medicine 10:199-214. CochraneGM, Webber BAand Clarke SW(1977): Effects of sputum on lung function. British MedicalJournal 2:1181-83. Danon J, Druz WS, Goldberg NBand Sharp]T (1979): Function of the isolated paced diaphragm and the cervical accessory muscles

AUSTRAlIAN PHYSIOTHERAPY

ORIGINAL ART.IC1E

inClquadriplegics. American Review of Respiratory Diseases 119:909-19. Decramer M (1989): Effects of hyperinflation on the respiratory muscles. European Respiratory Journal 2:299-302. DecramerMand De Troyer A (1984): Respiratory changesin parastemalintercostallength.Journal ofAppliedPhysiology.Respiration, Environment and Exercise Physiology 57:1254-60. Decramer M, Jiang TX, ReidMB, Kelly S, MacklemPT and Demedts M (1986): Relationship between diaphragm length and abdominal dimensions. Journal of Applied Physiology 61:1815-20. DerenneJP, FleuryBandParienteR (1988): Acute respiratory failure of chronic obstructive pulmonary disease. American Review of Respiratory Diseases .138:1006-13. :De TroyerAand EstenneM(1984): Co-ordination betweenrihcage muscles andthediaphraghm during quietbreathing in humans. Journal of Applied Physiology. Respiration,Environment and Exercise Physiology 57:899-906. De Troyer A, Kelly S, MacklemPTandZin WA (1985): Mechanics of intercostal space and actions of external and internal intercostal muscles. Journal of Clinical Investigation 75:850-7. Dodd DS, Brancastiano TP and Engel LA(1984): Chest wall mechanics during exercise in patients with severe chronic air-flow obstruction. American Review of Respiratory Diseases 129:3l..38. Druz WS and Sharp JT (1982): Electrical and mechanical activity of the diaphragm accompanyingbody position change in severe COPD.American Review ofRespiratory Diseases 125:275-80. Elliot MW, StevenMH, PhillipsGDand Braithwaite M (1990): Non-invasive mechanical ventilation for acute respiratory failure. British MedicalJournal 300:358-60. Ellis ER,ByePTP, BruderenJW and SullivanCE (1987): Treatmentofrespiratory failure during sleep in patients with neuromuscular disease. American Review ofRespiratory Diseases 135: 148-52. Esau SA (1989): Hypoxia, hypercapnic acidosis decreases tension and increasesfatigue in the hamster diaphragm muscle in vitro. American Review ofRespiratory Diseases 139: 1410-17. FarkasGA, Decramer M, Rochester DF and De Troyer A (1985): Contractile properties of intercostal ·muscles and their functional significance. Journal of Applied Physiology 59:528 ~35. Farkas GA and Roussos C (1983): Diaphragm in emphysematous hamsters: Sarcomere adaptability. Journal of Applied Physiology 54:1635-40. FleuryB, Murciano D, Talamo C, Aubier M, ParienteR and Milic-EmiliJ (1987): Workof breathingin patients with chronic obstructive pulmonary disease inacute respiratory failure. American Review of Respiratory Diseases 131:822-7.

Gherini S, Peters RMand Virgilo RW (1979): Mechanical work on the lungs and the work of breathing with positive . end-expiratory pressure and continous positive airway pressure. Chest 76:251-6. GottfriedSB, Rossi A and Milic-Emili] (1986): Dynamichyperinflation, intrinsic PEEP and the mechanically ventilated patient. Intensive and Critical Care Digest 5:30...33. Grassino AE,DurenneJP, Almirall J, Milic-Emili J and Whitelaw WA(1981): Configuration of the chest wall and occlusion pressures in awake man. Journal of Applied Physiology 33:134-42. Grassino AE, Goldman MD, Mead] and Sears TA (1978): Mechanics ofthe human diaphragm during voluntary contraction. Journal of Applied Physiology 44:829-39. GrumCM and Chauncey JB (1988):Convential mechanicalventilation. ClinicsofChestMedicine 9:37-46. Harris JS (1984):Stressors and stress in critical care. Critical Care Nurse: 84-97. KillianK] and Campbell E]M (1983): Dyspnoea. In Roussos C and Macklem PT (Eds): Lung Biology in Health and Disease. The Thorax. Part B.New York: Marcel Dekker Inc., 787828. ]ardim], FarkasG, PrefaultC, Thomas D, Macklem PT and Roussos CH (1981): The failing inspiratory muscles under normoxic and hypoxic conditions. American Review of Respiratory Diseases 124:274-79. Jiang TX, DeScheppen K,Demedts M and Decramer M (1989): Effects of acute mechanical hyperinflation onthe effectiveness ofthe parasternal intercostals.American Review ofRespiratory Diseases 139:522-28 ] uanG,Calverley P, Talamo G, Schnader] and Roussos C(1984): Effectofcarbon dioxide on diaphragmatic function in human beings. The New EnglandJournal ofMedicine 310:874-9. Ma~klem PT (1984): Hyperinflation. American Review ofRespiratory Diseases 129: 1-2. Macklem PT,MacklemDM and De Troyer A (1983): A model of inspiratory muscle mechanics. Journal of Applied Physiology. Respiration, EnvironmentandExercise Physiology 55:547-57. Martin], PowellE, ShoreS, Emrich] and Engel LA (1980): Therole ofrespiratory musclesin the hyperinflation of hronchialasthma. American Review of Respiratory Diseases 121:441-7. MartinezF], Couser]I and Celli BR (1990): Factors influencing ventilatory· muscle recruitment in patients with chronic airflow obstruction. American Review of Respiratory Diseases 142:276-82. o'Neill Sand McCarthy DS (1983): Postural relief of dyspnoea in· severe chronic airflow limitation: relationship to respiratory muscle strength. Thorax 38: .595-600. Petrof B], Legare M, Goldberg P,Milic-Emili] and GottfriedSB (1990): Continuous positive airway pressure reduces work of breathing

and dyspnoea during. weaning from mechanical ventilationinchronic obstructive pulmonary disease. American Review of Respiratory Diseases 144:281-89. Reid WD and LoveridgeBM(1983): Physiotherapy management of patients with chronic obstructive airways disease. Physiotherapy Canada 35:183-95. Sanchez], BastienC, Medrano G, Riquet M and Durenne JP (1984): Metabolic enzymatic activities in the diaphragm of normal men and patients with moderate chronic obstructive pulmonary disease. Bulletin Europeende Physiopathologie Respiratoire 20:535-40. Sherman CB, Osmanski]P and Hudson LD (1991): Acute .exacerbation ·in COPD patients.In Cherniack NS (Ed.): Chronic Obstructive Pulmonary Disease. Toronto: WE Saunders, pp.443-56. SimilowskiT, Van S,GauthierAP, Macklem PT and Bellemare F (1991 ):Contraetileproperties of the human diaphragm during chronic hyperinflation. The New England Journal of Medicine 325:917-23. Webber BA, Hofmeyer ]L,MorganMDLand Hodson ME (1986): Effects of· postural drainage, incorporating the forced expiratory technique, on pulmonary function in cystic fibrosis. Bntish Journal ofDiseases ofthe Chest 80:353-9. WestJB (1987): Obstructive Diseases. Pulmonary Pathophsiology -"- the essentials. Baltimore: Williams and Wilkins, pp. 59-81. Zoechi L, Garzaniti N, Newman S and Macklem PT (1987): Effect of hyperinflation and equalization of abdominal pressure on diaphragma tic action. Journal of Applied Physiology 62:1655-64.