Musculos Respiratorios e Sua Relacao Com Cirurgias Toracias e Abdominais

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1999;54;458-465ThoraxN M Siafakas, I Mitrouska, D Bouros and D Georgopoulos

Surgery and the respiratory muscles

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Surgery and the respiratory muscles

N M Siafakas, I Mitrouska, D Bouros, D Georgopoulos

Respiratory muscles are the only skeletal mus-cles vital to life. Surgical procedures can aVectthe respiratory muscles by a number of patho-physiological mechanisms including thoraco-abdominal mechanics, reflexes, neuromechani-cal coupling, and loss of muscular integrity.Impairment of respiratory muscle functionafter surgery may lead to postoperative compli-cations such as hypoventilation, hypoxia, atel-ectasis, and infections, some of which may belife threatening. In this paper we review surgerythat impairs the function of the respiratorymusclesnamely cardiac, thoracic, and upperabdominal surgery. Therapeutic interventionsor protective measures for respiratory musclesduring or after each type of surgery are alsobriefly addressed. Lung transplantation and

lung volume reduction surgery are discussed,since both have been shown to improve thefunction of respiratory muscles, and possiblepathophysiological mechanisms are reviewed.The preoperative assessment of respiratorymuscle function is also considered. Further-more, when postoperative pulmonary compli-cations occur it is worth considering whetherthe cause could be dysfunction of the respira-tory muscles and thus a proper assessment oftheir function is needed.

Function of the respiratory musclesThe most important function of the respiratorymuscles is breathing since they are the motor

arm of the respiratory system. Breathing, a life-long task, is borne mainly by the inspiratorymuscles, especially the diaphragm. The otherinspiratory muscles contribute little to quietbreathing but are recruited when higher levelsof ventilation are required, such as in exerciseand obstructive or restrictive lung disease. Theexpiratory muscles are not usually used duringbreathing except at high levels of ventilatoryeVort. A second function of the respiratorymuscles is to perform explosive manoeuvressuch as coughing and vomiting. The respira-tory muscles also have a role as stabilisers of thethorax and abdomen since they take part in theformation of the thoracic and abdominal walls.

Respiratory muscle function depends on thefunction of the respiratory centres, the spinalmotor neurons, the peripheral nerves, and theirneuromuscular junctions.14

Surgery may aVect respiratory muscle func-tion by a number of diVerent mechanisms. Forexample, a surgical incision of the chest orabdominal wall aVects the integrity of the res-piratory muscles and thus directly aVects theirfunction. In addition, anaesthesia uses pharma-cological agents such as neuromuscular block-ers which aVect the contraction of respiratorymuscles, sometimes for a considerable timeafter the end of the operation. Furthermore,

surgery or pharmacological agents such as

sedatives which aVect the neural structures of

the respiratory muscles will influence their per-

formance.

It is well known that dysfunction of the respi-

ratory muscles due to surgery may lead to a

reduction in the vital capacity (VC) and tidal

volume (VT), total lung capacity (TLC) and,

thus, insuYcient cough. This may cause

atelectasis in the basal lung segments and a

decrease in functional residual capacity (FRC)

which, in turn, aVects the gas exchange proper-

ties of the lung by increasing the ventilation/

perfusion (V~/Q~ ) mismatch.58 The situation may

be further aggravated by hypoventilation due to

several factors including sedation, pain, and

increased mechanical load. As a result, hypoxia

may ensue with a detrimental eVect on the con-dition of the patient. In addition, atelectasis may

be a risk factor for pulmonary infections9 which

have significant morbidity and mortality in this

patient population. In severe cases these conse-

quences of respiratory muscle impairment maylead to respiratory failure and death. 7

However, surgery may also improve the

function of the respiratory muscles. Indeed,recent surgical proceduresparticularly forsevere chronic obstructive pulmonary

diseasehave, among other beneficial eVects, afavourable influence on respiratory musclefunction.10 11

In this review surgery that impairs the func-

tion of respiratory muscles is first discussed,and then surgery that is beneficial to respira-tory muscle function. Practical therapeutic

approaches are considered in each case. Preop-erative assessment of respiratory muscle func-tion and postoperative recommendations are

also addressed.

Methodological aspectsMany of the studies that have been reviewedused volitional tests such as maximum inspira-

tory pressure (MIP) or maximum expiratorypressure (MEP) to investigate the eVect of sur-gery on respiratory muscle function. These

tests are easy to perform but may be aVected bypain or by the personality or motivation of thepatient, and sedatives such as pethidine could

also influence the results. In addition,the termsrespiratory muscle impairment, failure ofrespiratory muscle contractility, and respira-

tory muscle dysfunction have been usedindiscriminantly and this is often confusing.However, even with these limitations and criti-

cisms of the methodologies used, the mainmessagethat surgery aVects the function ofrespiratory muscles, either negatively or

positivelyis still valid.

Thorax 1999;54:458465458

Department of

Thoracic Medicine

N M SiafakasI MitrouskaD Bouros

Intensive Care Unit

D Georgopoulos

University of Crete

Medical School, 71110

Heraklion, Crete,

Greece

Correspondence to:

Professor N M Siafakas.

Received 13 August 1998

Returned to author

15 October 1998

Revised manuscript received

14 December 1998

Accepted for publication

21 December 1998

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Surgery that impairs respiratory musclefunctionIt has been shown that significant volumedisplacements between thoracic and abdomi-nal cavities occur during surgery simply bychanging posture (supine) and by the adminis-tration of general anaesthesia (fig 1).58 Thesevolume changes aVect the curvature of the dia-phragm (Laplaces law) and move it from itsresting length/tension position. As a result, itseYciency as a pressure generator changes.

The main pathophysiological mechanismsby which surgery has a detrimental eVect onrespiratory muscles are listed in table 1.

CARDIAC SURGERY

Diaphragmatic impairment due to phrenicnerve dysfunction is a well recognised compli-cation of heart surgery.1218 It has a negative

impact on the patients overall outcome and,depending on the pulmonary reserve of thepatient, prolongs ventilatory support anddelays discharge from the ICU or hospital. Theincidence of diaphragmatic dysfunction inpatients undergoing cardiac surgery variesfrom 10% to 85% according to the electro-physiological, radiological or other techniquesused for its detection,1921 and is similar inadults, children and infants.22 23

Although several factors have been impli-cated in phrenic nerve dysfunction aftercardiac surgery, most of the cases are either dueto cold injury or direct damage to thenerve.14 18 24 25 Other possible causes include

disruption of the blood supply or stretching ofthe nerve. Dissection of the left internal mam-mary artery as a conduit for aortocoronarybypass may be associated with significant

impairment in perfusion and function of the

left phrenic nerve26 leading to unilateral

diaphragmatic dysfunction. Direct damage to

the phrenic nerve by electrocautery during the

preparation of the internal mammary artery

may also occur.26

Unilateral damage of the phrenic nerve is

usually of little clinical significance in patients

with normal pulmonary function27 but this may

not be the case in patients with borderline res-

piratory function. On the other hand, bilateral

phrenic nerve injury carries significant morbid-

ity and necessitates, at least initially, mechani-

cal ventilatory support. Fortunately, bilateral

phrenic injury is relatively uncommon, occur-

ring in approximately 2% of cases.18 Hypoven-

tilation due to phrenic nerve dysfunction may

be considerably exaggerated during REM sleep

when the activity of other respiratory muscles is

reduced.28 However, the importance of this has

not been established.

Cold induced injury to the phrenic nerve due

to the use of ice slush to protect the

myocardium was first reported in 1964 by

Scannell.

29

Since then several investigators havereached similar conclusions.12 18 24 30 The eVect

of temperature on phrenic nerve and diaphrag-

matic function during cardiac surgery has been

investigated by Mills et al24 who concluded that

diaphragmatic function was aVected even by

mild hypothermia. The incidence of phrenic

nerve dysfunction after topical use of ice slush

has been reported to be in the range of

2573%.18 24 29 31 32 Recovery of the diaphragm

after cold injury may vary from 30 days to two

years.13 In a recent prospective study of the risk

factors for phrenic nerve dysfunction in 63

patients undergoing cardiac surgery Dimopou-

louet al18 reported that 21% of patients showed

electrophysiologically abnormal nerve func-tion. Among the potential risk factorsthe use of

ice slush for myocardial preservation was the

only independent factor related to phrenic

nerve dysfunction with an eightfold higher

incidence.18 On the other hand, the use of a

cooling jacket to prevent direct contact of the

phrenic nerve with the ice significantly de-

creased diaphragmatic dysfunction after car-

diac surgery. Indeed, Bonchek et al33 reported

no phrenic nerve injury in 750 patients in

whom a cooling jacket was used. The use of

cold normal saline solution has been reported

to protect the myocardium adequately without

adversely aVecting the phrenic nerve,34 but this

was not confirmed by Dimopoulou et al.18

The type of surgical incision has also been

shown to aVect respiratory muscle function,

with sternotomy being reported to impair

respiratory muscle function less than lateral

thoracotomy.35 Preoperative prophylactic in-

spiratory muscle training has been found to

reduce postoperative pulmonary complications

in patients undergoing coronary artery bypass

surgery.36 In addition, uncontrolled studies

have indicated that the use of a rocking bed to

treat diaphragmatic dysfunction after cardiac

surgery may be beneficial.25 37

Figure 1 Rib cage (RC), abdominal (ABD) and diaphragmatic (D) volume andposition changes under general anaesthesia. Dashed line represents the awake endexpiratory position of the diaphragm and shaded area the diaphragmatic movements duringanaesthesia (diaphragmatic shift = 500 ml). The total eVect is reduction in functionalresidual capacity (FRC= 450 ml), central blood volume (CBV= 300 ml), redistributionand increase in peripheral blood volume (PBL= +100 ml). Modified from Froese andBryan5 and Hedenstierna et al.6

D

PBV

RC ABD

CBV

Table 1 Pathophysiological mechanisms impairing function of respiratory muscles aftersurgery

EVect on neural control of respiratory muscles (e.g. phrenicotomy)EVect on integrity of respiratory muscles by the surgical incisionReflex mechanisms (phrenic nerve inhibition)Change in the length/tension relationship (change in FRC)Change in the thoracoabdominal mechanics (e.g. reduction of rib cage compliance)Anaesthesia (pharmacological agents/loads) and postoperative painSpecific surgical procedures (e.g. cooling during open heart surgery)Surgery on organs aVecting respiratory muscle function (e.g. parathyroidectomy)

Surgery and the respiratory muscles 459



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THORACIC SURGERY

Respiratory muscle function after thoracic sur-gery may be aVected directly by damage to themuscle itself or to the nerves as a consequenceof the incision, or indirectly as a result ofchanges in the mechanics of the respiratorysystem. Distortion of chest wall configurationmay reduce the chest wall compliance andincrease the work of breathing leading to adecrease in the mechanical eYciency of the

respiratory muscles.38 The eYciency of the res-piratory muscles may be further reduced by adecrease in lung compliance due to atelectasis.Theoretically, the eVective respiratory musclemass may be reduced by mechanical restrictionof motion or by muscle deconditioning aftermajor surgery, thereby further impairing therespiratory muscle response to an imposedload. This, however, needs to be investigated inmore detail.

In patients with borderline respiratory mus-cle function the increased work of breathing,mainly due to the decrease in chest wallcompliance after thoracotomy, carries consid-erable morbidity and mortality.3841 It has been

shown that lung resection (segmentectomy,lobectomy, pneumonectomy), particularly inpatients over 70 years of age, decreases MIPand MEP.41 This decrease may last for at leastfour weeks after the operation. Even rightsleeve resection has been reported to causeparalysis of the hemidiaphragm requiringplication.42 In addition, Maeda et al observedan increase in intercostal/accessory musclerecruitment after thoracotomy and pulmonaryresection and interpreted this as indicating dia-phragmatic dysfunction.39

It seems that the chest wall damage duringthoracotomy may play a crucial part in thedecrease in respiratory muscle strength. In-deed, a smaller decrease in MIP and MEP was

observed in patients undergoing thoracoscopyand video assisted thoracic surgery (VATS).41

In an animal model diaphragmatic functionwas evaluated using sonomanometers afterVATS or thoracotomy. The shortening fractionof the diaphragm decreases after both proce-dures but it recovers faster after VATS.43 Simi-lar results were reported in humans.44 Theseresults indicate that the changes in chest wallsecondary to the incision used is one of thedeterminants of respiratory muscle functionafter thoracic surgery. Postoperative pain andthe diVerent doses of sedatives and analgesicsmay aVect the results of volitional tests andcould be an alternative explanation for the dif-

ferences seen between thoracotomy andthoracoscopy.4446 Further clarification of thesefindings is needed.

However, it is of interest to note that thoracicepidural anaesthesia does not prevent respira-tory muscle dysfunction. Fratacci et al moni-tored diaphragmatic function after thora-cotomy by implanting one pair of sono-micrometric crystals and two electromyo-graphic electrodes on the costal diaphragm ofsix patients undergoing an elective pulmonaryresection.46 A marked reduction in activediaphragmatic shortening was seen after thora-cotomy which was not reversed by thoracic

epidural anaesthesia, despite an improvementin other indices of respiratory function. Theinterpretation of these results, however, iscomplicated by the possibility that thoracicepidural anaesthesia may influence eVerenttraYc to some inspiratory and expiratory mus-cles. The eVect of intercostal block on lungfunction after thoracotomy is reported to beminimal.45

Preoperative respiratory muscle training may

prevent postoperative pulmonary complica-tions by increasing both inspiratory andexpiratory muscle strength in patients under-going thoracic surgery.47 However, the eVect ofrespiratory muscle training on sustained venti-lation and maximal oxygen consumption (V~O2)is limited.40

ABDOMINAL SURGERY

It is well documented that the function of therespiratory muscles is aVected during and afterabdominal surgery. It has been suggested thatrespiratory muscle dysfunction may be respon-sible for a number of pulmonary complicationsincluding atelectasis and pneumonia. The side

of the operation, as well as the type, are themost important factors aVecting the respira-tory muscles.

Indeed, it has been shown that the incidenceof significant respiratory muscle dysfunctionafter lower abdominal surgery is very low(25%) while that of upper abdominal surgerymay approach 2040%.4851 As early as 1910Pasteur described the influence of the site ofoperation on the frequency of postoperativepulmonary complications. He suggested thatdiaphragmatic weakness may be the cause ofthese complications. In 1933 it was shown byBeecher54 55 that upper abdominal surgery isassociated with decreased lung volumes andadoption of a rapid shallow pattern of breath-

ing. These findings are similar to that encoun-tered in patients with neuromuscular diseases,suggesting that respiratory muscle dysfunctionmay play a significant role in this breathingpattern. This has been supported by thedecrease in maximum inspiratory, transdia-phragmatic, and expiratory muscle pressuresobserved after upper abdominal surgery in sev-eral studies.48 50 5658 This decrease is sustainedfor 48 hours after surgery59 60 and may persistfor a week,59 gradually returning to normal.Furthermore, a shift to predominantly rib cagebreathingas shown by an increase in the ratioof oesophageal to gastric pressure swings(Poes/Pga) or by the abdominal to rib cage

excursions (fig 2)indicates that the intercos-tal inspiratory muscles are more active.8 48 56

This is because the diaphragm is the musclethat is mainly aVected during upper abdominalsurgery. The mechanism that underlies thereduction in diaphragmatic strength and theshift to predominantly rib cage breathing is notfully understood. Although anaesthesia andpain may be responsible for dysfunction of therespiratory muscles, studies in animals andhumans support the hypothesis that an inhibi-tory reflex generated during the surgical proce-dure is the major mechanism. This reflex inhi-bition of the phrenic nerve output has been

460 Siafakas, Mitrouska,Bouros,et al



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postulated to be elicited by the manipulation ofthe gallbladder and other splanchnicorgans.48 61

Dysfunction of the respiratory muscles isgreatly reduced when upper abdominal surgeryis performed with laparoscopy rather than openlaparotomy.61 Rovina et al assessed respiratory

muscle strength after laparoscopic cholecystec-tomy and compared it with that after electivecholecystectomy. 61 They observed that, al-though MIP decreased in both groups aftersurgery, the decrease was significantly greaterin patients who had undergone open surgery,and MEP was also significantly lower in thesepatients. The authors postulated that thepredominant mechanism for the observeddiVerence in the global respiratory musclestrength was greater reflex inhibition of respira-tory muscles in patients who underwent opensurgery. However, the diVerence seen in MEPcould be due to the intact abdominal wall dur-ing laparoscopic surgery. The lower MEP maynot permit the patient undergoing opensurgery to reach the same residual volumepostoperatively as those undergoing laparo-scopic surgery, and this may contribute to alower value of MIP. Similar results have beenreported by other investigators after laparo-scopic cholecystectomy59 6266 and gastroplastyvia laparotomy.67 68 In addition, it has beenspeculated that opiates enhance this postopera-tive inhibitory reflex mechanism.49 Recently, anumber of drugs and physical manoeuvreshave been tested in order to reverse this inhibi-tion. Jansen et al69 showed that doxapram, aprimary stimulant of respiration (central),reduced the incidence of postoperative pulmo-

nary complications and increased oxygenationafter upper abdominal surgery. In addition,Siafakaset al60 showed in a double blind studythat aminophylline had a protective eVect onrespiratory muscle function against phrenicnerve inhibition after upper abdominal surgery.Finally, physical manoeuvres such as intermit-tent positive pressure breathing, incentivespirometry, and deep breathing exercises havebeen shown to prevent, to some extent, pulmo-

nary complications after abdominalsurgery.50 70 71

Although these findings are limited to a fewupper abdominal surgical procedures, it islikely that, as far as the eVects of surgery on thefunction of respiratory muscles is concerned,similar results would be obtained in other typesof upper abdominal operations including livertransplantation. For instance, McAlister et al72

reported a 38% incidence of right hemidi-aphragm paralysis due to direct injury (crashinjury) of the right phrenic nerve followingorthotopic liver transplantation. This dysfunc-tion did not have a serious eVect on theoutcome of the surgery. In addition, it has been

reported in young children with diaphragmaticnerve paralysis due to liver transplantation thatdiaphragmatic plication may have a favourableimpact.73

Surgery that improves respiratorymuscle functionHyperinflation is a common feature in patientswith severe chronic obstructive pulmonary dis-ease (COPD) and has significant adverseeVects on inspiratory muscle function (fig 3).Static hyperinflation aVects respiratory mus-cles by causing them to operate at anunfavourable position on their length-tensioncurve and by flattening the curvature of thediaphragm. According to Laplaces law, thecurvature of the diaphragm is an importantdeterminant of its ability to produce pressure.Thus, transdiaphragmatic pressure is smallerwhen the diaphragm is flattened than when it iscurved. In addition, hyperinflation shortens themuscle fibres of the diaphragm and probablyimpairs its blood supply74 while decreasing thezone of apposition and causing a medial orien-tation of the diaphragmatic fibres (fig 3).

It is obvious that, if hyperinflation can bereduced by surgery, the function of the respira-tory muscles, in particular the diaphragm,could be improved. Two types of operations

3

0

1

2

8

ABDAP(mm)

RCAP(mm)

0 2 4 6

3

2

4

5

1

Figure 2 Plots of theanteroposterior diameter ofthe abdomen (ABDAP)versus the diameter of therib cage (RC

AP) in patients

undergoing cholecystectomy.Each loop represents a tidalbreath. 1 = preoperative(control), 2 = 24 hours, 3= 68 hours,4 = 24 hours,5 = 48 hours postoperative.Breathing is shifted from

predominantly abdominal

(1) to rib cage (2 and 3)and back again toabdominal (4 and 5).

Modified from Ford et al.48

Figure 3 Summary of detrimental eVects of hyperinflation on respirator y muscle function. Modified from Tobin.74

Zone ofapposition

Ribs

Normal Hyperinflation

Thoracic cage elasticrecoil directed inwards

Shortenedmuscle fibres

?Impaired blood supply

Horizontal ribs

Decreaseddiaphragmatic

curvature

Decreased zoneof apposition

Medial orientation ofdiaphragmatic fibres




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reduce hyperinflationnamely, lung trans-plantation and LVRS.

LUNG TRANSPLANTATION

In patients with COPD lung transplantationhas been shown to be associated with changesin respiratory muscle function. In 1992 Wil-liams et al 75 reported that MIP increasedsignificantly three months and one year afterdouble lung transplantation. Although this

finding was not discussed by the authors, itmay be due to the improvement in the generalcondition of the patients (better motivation,improved nutrition, respiratory muscle recon-ditioning, improved blood gas tensions). How-ever, subsequent studies have indicated thatreduction of hyperinflation may play a pivotalrole. Wanke and coworkers76 measured the sniffdiaphragmatic pressure (sniV Pdi) at diVerentvolumes and analysed the relation between Pdiand lung volumes in patients with end stageCOPD and in those undergoing single or dou-ble lung transplantation. In addition, they usedphrenic nerve stimulation at FRC. Lung trans-plantation caused a reduction in lung volume

and, as a consequence, sniV

Pdi in thesepatients was higher than in the patients withCOPD at all volumes analysed. However, sniVPdi at comparable intrathoracic gas volumeswas not reduced in the patients with COPDwhen compared with those who underwentlung transplantation. Thus, the increase in Pdiwas due to the fact that the diaphragm wasplaced in a more favourable position for press-ure generation after lung transplantation. Thisstudy indicates that changes in mechanicalfeedback (force-length relationship of inspira-tory muscles) as a result of lung transplantationin patients with COPD may be the majordeterminant of the increase in diaphragmaticpressure. It also suggests that chronic static

hyperinflation does not cause major functionalalterations of the muscle fibres of thediaphragm.76

Although diaphragmatic strength is in-creased after lung transplantation in patientswith severe COPD, the neural drive to thismuscle is significantly reduced. Brath et alassessed the neural drive to the diaphragmusing the diaphragmatic electromyographicactivity (EMGdi) during fatiguing inspiratorythreshold loading manoeuvres in patients whohad undergone single or double lungtransplantation.77 Compared with those whohad not undergone lung transplantation, theyobserved a decrease in the EMG activation of

the diaphragm which was also evident on thenon-transplanted side in recipients of singlelung transplants. Despite the reduced EMGactivation, the endurance of inspiratory mus-cles was well preserved.The authors postulatedthat the reduced neural activation was due tothe better position of the diaphragm for gener-ating pressure. Although the diaphragmaticEMG may not always be proportional to theneural drive to the diaphragm, these results arein agreement with animal and human studieswhich have shown that the eVerent drive to thediaphragm is well adjusted to account forchanges in diaphragmatic mechanical

eYciency.7881 It follows that, in addition to dia-phragmatic strength, neuromechanical feed-back mechanisms may also modify someaspects of the control of breathing. Finally, thedecrease in central drive may contribute to thereduction in the sense of dyspnoea during ven-tilatory stress in activities of everyday liferesulting in an improvement in the quality oflife for these transplanted patients.11

It is worth pointing out that, even if the MIP

and MEP are improved after heart-lung trans-plantation, they are still smaller than predictedvalues.82 This reduction cannot be solelyattributed to the surgical procedure. Severalpreoperative and postoperative factors may beresponsible for the decreased strength of therespiratory muscles. Deconditioning may playa significant role since rehabilitation pro-grammes, including both inspiratory and ex-piratory muscle training, invariably increaserespiratory muscle strength.83 84 These studies,however, do not exclude learning or motiva-tional eVects on the increase in respiratorymuscle strength measured by MIP and MEP.

The eVect of lung or lung-heart transplanta-

tion in patients with diseases other than COPDhas not been well studied. Persistent hyperin-flation has been reported after heart-lungtransplantation for cystic fibrosis,85 possiblydue to the chest wall configuration. The changein the shape of the rib cage may represent astructural adaptation in response to chronichyperinflation acquired during growth85 since,unlike COPD, cystic fibrosis is a disease ofchildhood and adolescence.

LUNG VOLUME REDUCTION SURGERY

Lung volume reduction surgery (LVRS) in-cludes relatively new surgical techniques de-signed to alleviate symptoms of severe COPDmainly due to emphysema. It involves removal

of part of the diseased lung tissue (usually theupper lobe) and most patients respond by areduction in dyspnoea and improvement inexercise tolerance and quality of life.10 8689 Ithas been shown that successful LVRS improvesrespiratory muscle function.9095 Three monthsafter surgery the maximal transdiaphragmaticpressure (Pdimax) and twitch transdiaphrag-matic response to phrenic nerve stimulation areincreased. A recent study by Criner et alfounda significant correlation between the increase inmaximum transdiaphragmatic pressure andthe reduction in FRC (trapped gas) afterLVRS.95 However, other investigators haveshown that these increases are greater than

those that could be explained by a decrease inlung volume or by placing the diaphragm in amore favourable position on the length-tensioncurve. The change in mechanical feedback istherefore not the only mechanism underlyingthe improvement in respiratory muscle func-tion observed after LVRS. Factors that mightcontribute to this disproportionate increase inPdimax include a learning eVect, a decrease indyspnoea, an improvement in inspiratory mus-cle perfusion, and inspiratory muscle re-conditioning. The learning eVect appears to beretained for less than one week,96 making thisfactor an unlikely explanation for the increase




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in Pdimax. A decrease in dyspnoea due to a

reduction in respiratory muscle load couldcause better cooperation during the perform-ance of the Pdimax manoeuvre by favouringgreater diaphragmatic recruitment. However,the significant increase in the twitch transdia-phragmatic pressure response to phrenic nervestimulation oVersfirm evidence for the eVect ofLVRS on diaphragmatic contractility, leavingthe increase in perfusion and muscle recondi-tioning as possible mechanisms for the im-provement seen in inspiratory musclefunction.91 Indeed, if LVRS improves rightventricular function, the resulting improve-ment in inspiratory muscle perfusion mayenhance muscle strength.97 98 This improve-

ment may also be explained by better condi-tioning because of the ability of the patient toundertake more exercise due to improvementsin pulmonary mechanics, skeletal musclecapacity, and cardiovascular function.99

It has been shown that the tidal breathingratio of Pga/Pdi increases after LVRS.91 100

This increase could be due to an increase in thediaphragmatic contribution to tidal breathingor, when expiratory muscles contract, to adecrease in the recruitment of the expiratorymuscles.27 Data from patients following LVRSsupport the first possibility since an earlyinspiratory fall in Pga, which indicates relaxa-tion of expiratory muscles, is not a commonfinding in these patients.91 100 The increased

contribution of the diaphragm during tidalbreathing may be responsible for the reductionin recruitment of the muscles of the rib cageafter surgery. Furthermore, the increasedeYciency of the diaphragm as a pressuregenerator may cause the considerable reduc-tion in respiratory drive observed after LVRS.It therefore seems that LVRS increases theneuromechanical coupling of the diaphragm byseveral mechanisms.91 This increase, combinedwith the de-recruitment of rib cage muscles, assuggested by the change in the Pga/Pdiratio, may account for the decrease in dyspnoeaat rest and the increased exercise tolerance.91

Recent studies have shown that LVRS has no

eV

ect on the static mechanical properties of thechest wall101 and reinforce the improvement inpulmonary elastic recoil.102 However, furtherstudies are needed to clarify these issues.

SURGERY FOR OBESITY

Weight lost following gastroplasty for morbidobesity is associated with improvement in lungvolumes and respiratory muscle function.103

Clinical applicationsPREOPERATIVE

Although respiratory muscles are impairedafter most throracoabdominal surgical proce-

dures, little attention is paid to preoperativeassessment of their function. Spirometric tests,lung volumes (VC, FRC, RV), and measure-ments of MIP and MEP are simple tests forassessing respiratory muscle function. Table 2summarises the clinical conditions in whichpreoperative assessment of respiratory musclefunction is indicated. A normal VC without asignificant fall (80 cm H2O indicate adequate respira-tory muscle strength and suYcient cough.104

However, we should note that MIP and MEPare volitional tests and thus require coopera-tion of the patients. It follows that, althoughhigh values of MIP and MEP exclude muscleweakness, the reverse is not true. Indeed, lowvalues of MIP and MEP may be due topatients cooperation. The easiest test designedto evaluate inspiratory muscle strength is thesniV nasal inspiratory pressure, a naturalmanoeuvre which many patients find easier toperform.105 A sniVnasal inspiratory pressure of>70 cm H2O indicates almost normal inspira-

tory muscle strength.

104

The sniV

test can bealso performed using an oesophageal or gastriccatheter to obtain either the sniVoesophagealpressure (sniVPoes) or the sniV transdiaphrag-matic pressure (sniVPdi).106 It has been shownthat these tests have a better reproducibilityand a narrower normal range than the sniVnasal inspiratory pressure.106 If the patient isconsidered to be at a high risk of developingrespiratory muscle dysfunction after surgerywith borderline lung function, more advancedmethodology using one of the followingnon-volitional tests might be needed to evalu-ate the function of the respiratory musclesaccurately: (1) electrical or magnetic stimula-tion of the phrenic nerve and measurement of

the EMG signal, the nerve conduction time,and the twitch Pdi107 108; (2) measurement oftwitch mouth pressure after magnetic stimula-tion of the phrenic nerve109 110 which has theadvantage of being non-invasive (but in pa-tients with COPD mouth pressure does notaccurately reflect inspiratory muscle pressureand this must be taken into account111); (3)measurement of gastric pressure during cough-ing to evaluate expiratory muscle strength,although normal values have yet to be formallydescribed.

In addition, during the preoperative periodrespiratory physicians should discuss with thesurgical team the best incision to use (ster-

notomy versus lateral thoracotomy), the use ofless intensive surgery (laparoscopic or thoraco-scopic), protection of the phrenic nerve(jacket), and should supervise respiratory mus-cle training.36 47

POSTOPERATIVE

During the postoperative period and depend-ing on the type of surgery performed, deepbreathing exercises, incentive spirometric test-ing, or positive pressure breathing may be usedto prevent complications.50 70 71 In the presenceof postoperative complications physiciansshould be aware that respiratory muscle

Table 2 Medical disorders for which preoperative assessment of respiratory muscle functionis needed

Patients with borderline lung function, with or without hyperinflation (COPD, asthma)Severe obesityDeformities of thoracic cage (e.g. kyphoscoliosis)Neuromuscular disordersPoor nutritional states (e.g. malignancies)Chronic glucocorticosteroid therapyEndocrine disorders (e.g. thyroid diseases)




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dysfunction could be the cause and thefunction of the respiratory muscles should beassessed. Finally, aminophylline or doxaprammay be given to minimise phrenic nerve inhibi-tion when pulmonary complications occurafter upper abdominal surgery.60 69

ConclusionSurgery may aVect the function of respiratorymuscles in a number of ways. Some types of

surgical procedure adversely influence respira-tory muscle function while others have afavourable eVect. Changes in respiratory mus-cle function may be due to a direct eVect of thesurgical procedure on the respiratory musclesor their neural control, or to indirect mecha-nisms. Several complications associated withrespiratory muscle dysfunction caused bysurgery may increase the morbidity andmortality to a considerable extent. The physi-cian dealing with these patients should beaware of the detrimental eVects of surgery onrespiratory muscles and take the appropriatemeasures to reduce the magnitude and compli-cation of respiratory muscle dysfunction. On

the other hand, diV

erent surgical procedures,particularly lung transplantation and lung vol-ume reduction surgery, are unequivocally asso-ciated with improved respiratory muscle func-tion. This improvement may be due to severalfactors related directly or indirectly to the res-piratory muscles.

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Musculos Respiratorios e Sua Relacao Com Cirurgias Toracias e Abdominais

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