Obesity and the lung: 3? Obesity, respiration and intensive care

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1 1 Pulmonary and Critial Care and Sleep Mediine Divisions, Brigham and Women s Hospital, Harvard Medial Shool, Boston, Massahusetts, USA; 2 West Australian Sleep Disorders Researh Institute, Department of Pulmonary Physiology, Sir Charles Gairdner Hospital, Nedlands, Western Australia, Australia Correspondene to: Dr A Malhotra, Pulmonary and Critial Care and Sleep Mediine Divisions, Brigham and Women s Hospital, Harvard Medial Shool, 75 Franis Street, Boston, MA 02115, USA; amalhotra1@partners.org Reeived 4 November 2007 Aepted 11 Marh 2008 Obesity and the lung: 3? Obesity, respiration and intensive are A Malhotra, 1 D Hillman 2 ABSTRACT Obesity is a major problem from a publi health perspetive and a diffiult pratial matter for intensivists. The obesity pandemi has required treating liniians to develop an appreiation of the substantial pathophysiologial effets of obesity on the various organ systems. The important physiologial onepts are illustrated by fousing on obstrutive sleep apnoea, obesity hypoventilation syndrome, abdominal ompartment syndrome and ventilatory management of the obese patient with aute respiratory distress syndrome. The obesity pandemi has led to an inreased appreiation of the speial needs of severely overweight patients. Obesity presents major pathophysiologial and tehnial issues, partiularly when patients are ritially ill. 1 3 Problems in obese patients in the intensive are unit (ICU) may inlude diffiulties with airway maintenane, disordered ventilation and gas exhange, impaired irulation and altered drug pharmaokinetis. Proedures are more hallenging, whether nonoperative (eg, airway intubation, vasular aess, neural bloks, urinary atheterisation) or operative. Safe transport, repositioning, image aquisition and mobilisation an be major hallenges requiring areful planning and exeution. The problems of obesity are ompounded by its ommon omorbidities whih inlude hypertension, asthma, 4 5 hyperlipidaemia and type 2 diabetes mellitus whih further inrease patient risk. 6 Of the many effets of obesity on various organ systems (fig 1), we have hosen to fous on the following four obesity-related syndromes ommonly enountered in the ICU that illustrate the diverse effets and multiple mehanisms through whih obesity inreases morbidity and ompliates management: 7 obstrutive sleep apnoea (OSA), a ontext in whih to disuss airway management; obesity hypoventilation syndrome with onsideration of ventilation and gas exhange abnormalities; abdominal ompartment syndrome and the role of obesity in intra-abdominal hypertension; and aute respiratory distress syndrome in obese subjets with disussion of the ompliating role of obesity in the management of severe parenhymal lung disorders. OBESITY AND OBSTRUCTIVE SLEEP APNOEA OSA is a ommon ondition 8 haraterised by reurrent episodes of upper airway obstrution during sleep, whih are assoiated with arterial Review series oxygen desaturation and repetitive arousals resulting in disrupted sleep and exessive daytime sleepiness OSA predisposes to a variety of problems inluding systemi hypertension 11 and vasular disease, diabetes, 14 metaboli syndrome, 15 depression, gastro-oesophageal reflux and aident risk. OSA is important in ICU pratie as it is a linial indiator of a diffiult airway and an ompliate perioperative management inreasing the risk of ICU admission, ontribute to the evolution of respiratory failure and result in failed extubation following mehanial ventilation. The diffiult airway The anatomial problems that ontribute to OSA may ontribute to diffiult intubation with parameters suh as the Mallampati sore being helpful to haraterise these. The speifi diffiulties that obesity poses for intubation (box 1) relate to limited mouth opening and nek mobility 23 ompounded by diffiulties in maintaining airway pateny prior to suessful intubation. Furthermore, obesity-related dereases in funtional residual apaity partiularly when reumbent result in lower oxygen stores and impaired gas exhange beause of ateletasis in dependent lung zones. Hene, time in apnoea before arterial oxygen desaturation ours is redued 26 and the prospets of a an t intubate, an t ventilate senario are ompounded by the minimal time available to resolve the airway issue. Furthermore, both obesity and OSA predispose to gastro-oesophageal reflux, inreasing the risk of pulmonary aspiration while the airway remains unproteted. A preise definition of the risk of diffiult intubation in morbid obesity and OSA has not been undertaken, but is likely to be high as both onditions are assoiated with upper airway narrowing Some have argued that morbid obesity alone is not ommonly assoiated with intubation diffiulty 30 given proper patient positioning. However, the risk is likely to inrease where other indiators of diffiult intubation are also present inluding mandibular retrusion, limited mouth opening and poor nek extension. The presene of OSA may be an additional indiator of risk of diffiult intubation in obese patients. 21 Without these additional features it appears reasonable to undertake rapid sequene endotraheal intubation with preoxygenation, use of short-ating neuromusular relaxants and rioid pressure under experiened supervision and with equipment for diffiult intubation available (eg, bougies/introduers). Where additional anatomial Thorax: first published as /thx on 26 September Downloaded from on 14 Otober 2018 by guest. Proteted by opyright. Thorax 2008;63: doi: /thx

2 Figure 1 Obesity-related ompliations. features indiating diffiult intubation are present, problems may be irumvented by undertaking awake fibreopti-assisted intubation. 31 Airway management problems are not onfined to these matters. Traheostomy is more problemati in morbidly obese patients beause of aess, diffiulty identifying landmarks and inreased distane from skin to trahea ompliating orret tube plaement. 32 Hene, even reating a rash airway where endotraheal intubation has proved impossible or onverting from prolonged endotraheal intubation to traheostomy is diffiult. Furthermore, extubation may be problemati in obese patients with OSA where the onsious state is ompromised, 33 either through illness or the effet of sedative drugs, and extreme aution needs to be exerised before extubation in suh irumstanes. Following extubation, ontinuous positive airway pressure (CPAP) or non-invasive ventilation (NIV) must be available for high-risk patients, inluding those with OSA, for use during sleep or sedation 34 (see setion on OSA and failed extubation below). A list of the potential fators ompliating endotraheal intubation in obesity is shown in box 2. Perioperative management of patients with obesity and OSA While there is some inonsisteny in findings regarding the effets of obesity on postoperative morbidity in non-ardia patients, there is substantial evidene to suggest that it is assoiated with an inreased inidene of wound infetions and breakdown, 37 venous thromboembolism 38 and adverse ardia events, 39 partiularly where severe. The risk of admission to the ICU inreases as does the risk of prolonged ventilation, length of ICU stay and mortality in the ICU, partiularly in the surgial ICU 40 or with extreme obesity (body mass index (BMI) >40 kg/m 2 ). Following ardia surgery, prolonged ventilation is more ommon in patients in this high weight range, as are longer lengths of stay in hospital. 41 In the early postoperative period the risk of hypoxaemia and/ or upper airway obstrution is inreased. 42 This early postoperative period is a time of partiular vulnerability beause of the residual effets of anaestheti, paralyti and analgesi drugs, all predisposing to upper airway obstrution and depressing arousal responses whih protet against asphyxia. Not surprisingly, patients with OSA appear to be vulnerable during this period. While data on postoperative risk in OSA are sparse and some suggest few problems for outpatient surgery at least, 43 ompliations are more apparent when the immediate perioperative period is examined, partiularly following upper airway surgery and espeially in hildren. 44 This finding presumably reflets the ompounding influenes of drug effets and surgially-indued oedema 45 on an anatomially small upper airway. The data regarding perioperative risk for patients with OSA following major surgery are also sparse, but a ase-ontrol study of postoperative morbidity following hip or knee arthroplasty demonstrated a substantial inrease in the inidene of serious ompliations requiring emergeny interventions, ICU admissions and length of stay. 46 Patients with a ombination of morbid obesity and OSA may be at partiular risk of postoperative pulmonary ompliations, but there are few published data to define this risk. Suh onstraints have limited the development of pratie guidelines for the perioperative management of patients with OSA 47 and the reent guidelines were largely based on expert opinion. 48 Beause of the vulnerability of patients with OSA in the perioperative period, the following priniples should be onsidered: efforts to identify OSA preoperatively; use of CPAP therapy perioperatively; use of regional rather than general anaesthesia if possible; areful reversal of neuromusular blokade; awake extubation following general anaesthesia; use of regional analgesi tehniques rather than sedating systemi analgesis; use of the lateral rather than supine posture; and extended lose monitoring in the postoperative period. Many of the priniples, along with bed head elevation, appear appliable to the management of obese patients whether or not they have OSA. CPAP therapy is arguably underused in the perioperative period in the management of obese patients, partiularly but not onfined to those with OSA. 49 Its advantages inlude both pneumati splinting of the upper airway and reruitment of ateletati lung. CPAP is well tolerated by patients familiar with it but may be a hallenge in CPAP-naïve patients. Other less ertain strategies to seure airway pateny, suh as use of the lateral posture and a Thorax: first published as /thx on 26 September Downloaded from on 14 Otober 2018 by guest. Proteted by opyright. 926 Thorax 2008;63: doi: /thx

3 Box 1 Effet of obesity on physiologial parameters q Intra-abdominal pressure: abdominal ompartment syndrome an ause renal, hepati failure and viseral nerosis. q Intraranial pressure: assoiated with raised intra-abdominal and pleural pressures. q Central venous pressure: inreased by high intra-abdominal and pleural pressures. q Pulmonary artery olusion pressure: inreased by high intraabdominal and pleural pressures. q Pulmonary artery pressure: mild to moderate elevations may result from obstrutive sleep apnoea alone. Q Total lung apaity. Q Vital apaity. Q Funtional residual apaity: ateletasis and redued oxygen stores inrease propensity for desaturation. q Pleural pressure: reflets hest wall ompression. Q Respiratory system ompliane: stiffer respiratory system likely from lung and hest wall ontribution. q Airway resistane: risk of asthma and airway losure. Q Hyperapni ventilatory response: ontributes to obesity hypoventilation syndrome. q Upper airway resistane: ontributes to diffiult airway and sleep apnoea. nasopharyngeal airway, may be neessary in CPAP-intolerant patients. Suessful appliation of positive pressure in the ase of postoperative upper airway obstrution obviates the need for reintubation in some patients. OSA, obesity and respiratory failure While most patients with OSA alone do not develop daytime hyperapnia, when other fators that weaken or mehanially load the respiratory musles or impair gas exhange suh as severe obesity (see setion on Obesity hypoventilation syndrome below) 50 or hroni obstrutive pulmonary disease (COPD) are present, OSA an ontribute to respiratory failure. The term overlap syndrome 51 was introdued to desribe the assoiation of OSA and COPD and the apaity of OSA to exaerbate disturbanes in ventilation and gas exhange in patients with COPD. In general, respiratory failure during wakefulness is assoiated with sleep-related hypoxaemia and hyperapnia in both COPD and obesity. 52 These assoiations are important to intensivists as failure to onsider OSA and its ontribution to respiratory failure will exaerbate diffiulties in weaning patients from ventilatory support, prolong length of stay, inrease morbidity and, in survivors, lead to reurrent hospital admissions. The possibility of OSA should be onsidered in patients with reurrent respiratory failure unexplained by degree of impairment of ventilatory apaity during wakefulness. Study of ventilation during sleep will define the problem and determine the most appropriate form of treatment: CPAP in the ase of predominant upper airway obstrution and NIV where there is a major entral (nonobstrutive) hypoventilatory omponent. 50 Suh treatments must be titrated to optimise gas exhange during sleep, as the degree of adequay of this is an important determinant of magnitude of improvement in wakeful respiratory funtion. 53 OSA, obesity and failed extubation Upper airway pateny is determined by a balane between fores that narrow the airway and those that dilate it. Patients Box 2 Potential fators ompliating endotraheal intubation in obesity Anatomially diffiult airway. Rapid desaturation due to redued funtional residual apaity. Drug distribution and metabolism. Underlying ardiomyopathy. Underlying pulmonary hypertension. Diabetes mellitus affeting autonomi reflexes. Diffiult rash airway inluding riothyroidotomy or traheostomy. Diffiult vasular aess. Aspiration risk. with OSA have narrow airways and require disproportionate ativation of pharyngeal musles during wakefulness to maintain pateny. 54 Ativation is driven by a ombination of influenes inluding the wakeful state itself, ventilatory drive and reflex ativation initiated by upper airway mehanoreeptors that respond to intraluminal negative pressure developed during inspiration. 9 If the patient is obtunded, there is redued drive to the upper airway musles from these soures. The presene of an endotraheal tube may blunt upper airway reflexes. 55 This ombination of irumstanes may lead to postextubation upper airway obstrution in patients with narrow upper airways suh as those with obesity and/or OSA. In support of this onept, several authors have noted that attempts to fast trak extubation after ardia surgery and abdominal aneurysm reonstrution 58 are less suessful in obese patients. The use of non-invasive positive pressure ventilation applied immediately after extubation appears a useful strategy to allow suessful weaning and extubation in diffiult to wean patients 59 or to prevent re-intubation in highrisk patients. Beause end-expiratory lung volume an affet upper airway pateny, some also advoate the reverse Trendelenburg position after extubation to maximise lung volume and thus pharyngeal pateny. 60 OSA and ardia funtion Both obesity and OSA have been assoiated with impairment in left ventriular funtion. The mehanisms underlying obesityrelated ardiomyopathy are unlear. However, some authors have suggested that OSA may ontribute through ateholamine-mediated mehanisms (similar to oaine-indued or phaeohromoytoma-assoiated ardiomyopathy). 61 Inreases in pulmonary artery pressures (PAP) are debated in OSA. Although marked inreases in PAP are unommon from OSA alone, OSA may ause mild to moderate inreases in PAP. 62 Inreased PAP indued by OSA is generally reversible with CPAP treatment. These patients have marked hypoxi vasoreativity with substantial inreases in PAP ourring during mild hypoxaemia. We have ared for patients in the ICU with underlying OSA who develop marked inreases in PAP in the setting of mild hypoxaemia (eg, seondary to pneumonia). OSA ombined with parenhymal lung disease or other daytime blood gas abnormalities (suh as obesity hypoventilation syndrome, OHS) have been assoiated with severe pulmonary hypertension and or pulmonale in some ases. Severe inreases in PAP an our during sleep (espeially REM sleep) if the OSA remains untreated. The haemodynami management of obese patients with OSA requires onsideration of these findings. Thorax: first published as /thx on 26 September Downloaded from on 14 Otober 2018 by guest. Proteted by opyright. Thorax 2008;63: doi: /thx

4 OBESITY HYPOVENTILATION SYNDROME (OHS) The ombination of obesity (BMI.30 kg/m 2 ) and hyperapnia (arterial arbon dioxide tension (PaCO 2 ).45 mm Hg (6 kpa)) during wakefulness in the absene of other known auses of alveolar hypoventilation defines the obesity hypoventilation syndrome. 50 In severely obese (BMI >35 kg/m 2 ) hospitalised patients, up to 31% have hyperapnia with no other ause for it, with the prevalene of OHS inreasing with inreasing BMI. 63 There are several ontributing mehanisms inluding: exessive loading of respiratory musles by the mass of entrally deposited fat; disordered gas exhange, partiularly when reumbent, beause of ateletasis in dependent lung zones; obesity-related upper airway narrowing; and disordered ventilatory ontrol. Sleep is a vulnerable period beause of diminished drive to respiratory musles and periods of entral (non-obstrutive) hypoventilation with assoiated hypoxaemia and hyperapnia may often last many minutes before eventual arousal. 9 Up to 90% of patients with OHS have a ombination of entral hypoventilation and OSA with onomitant effets on ventilation and gas exhange. 66 The degree of daytime hyperapnia appears to be diretly related to the degree of sleep-disordered breathing, 52 orretion of whih results in ontrol of wakeful ventilatory failure when off ventilatory support. 67 This may be ahieved with CPAP in ases of OSA, but NIV is often required to augment arbon dioxide elimination where there is a entral omponent. 68 NIV allows inspiratory and expiratory pressure to be independently adjusted with end expiratory pressure to maintain pharyngeal pateny (and reruit ateletati lung, analogous to positive end expiratory pressure (PEEP)) and inspiratory pressure support to ontrol entral hypoventilation (analogous to pressure support). In some ases NIV may be neessary initially but onversion to (less expensive) CPAP may be feasible one the respiratory failure is ontrolled. 69 While the possibility of OHS should be atively onsidered in severely obese patients in the outpatient setting, intensivists frequently diagnose this problem during respiratory and right heart failure. 70 There may be a history of snoring and sleepiness from disturbed sleep seondary to sleep-disordered breathing. Intensivists must appreiate the pivotal role of sleep-related hypoventilation to avoid diffiulty weaning these patients from ventilatory support and to prevent reurrent respiratory and right heart failure. In patients with OSA, extubation an be onsidered one ventilatory apaity during wakefulness is adequate; however, ongoing NIV may be required during sleep. 71 Studies of ventilation during sleep help to define the problem and are preferably undertaken before patients require hospitalisation. Although the thresholds of severity of sleep-related hypoventilation, independent of daytime respiratory failure, requiring intervention with NIV remain to be defined, more than 1 2% of total sleep time spent below an oxygen saturation of 85% (equivalent arterial oxygen tension (PaO 2 ) of approximately 55 mm Hg (7.3 kpa)) provides an independent justifiation for this treatment. Subsequent studies of ventilation during sleep on treatment allow a deision about the requirement for and the type (CPAP or NIV) of ongoing treatment. Thus, OHS is an important syndrome in the ICU. OBESITY AND ABDOMINAL COMPARTMENT SYNDROME The abdominal ompartment syndrome (ACS) has been reognised relatively reently in medial patients in the ICU. 72 Trauma surgeons had previously observed that trauma patients who developed anuria frequently improved following deompressive laparotomy. More reent studies have suggested that important inreases in intra-abdominal pressure (IAP) an also our in up to 20% of medial patients in the ICU. Although a variety of proesses may ontribute to raised IAP inluding asites, ileus and intraperitoneal haemorrhage, the best preditor of ACS in multivariate analysis is BMI. 73 Thus, obesity represents a major risk fator for ACS in ritially ill patients. The pathogenesis of ACS reflets the fat that the abdomen an behave like a losed spae. 73 Under normal onditions IAP is relatively low (lose to atmospheri pressure). With deposition of fat and aumulation of fluid during onditions of apillary leak, gradual inreases in IAP an our. With suffiient inreases in IAP, ritial blood vessels an be ompressed leading to ishaemia of abdominal organs. For example, inreased IAP an lead to renal failure ostensibly through ompression of renal venules. Involvement of other organs suh as the liver, with hepati nerosis, has also been reported. Inreased IAP an also affet ardiopulmonary physiology as it an be transmitted to the intrathorai ompartment, yielding inreases in intrapleural pressure. The degree of transmission of abdominal pressure to the pleural spae depends on the tension developed in the diaphragm, refleted in transdiaphragmati pressure. Beause the diaphragm an remodel with hroni inreases in IAP, medial onditions suh as obesity and hroni asites tend to have a greater influene on pleural pressure than aute onditions suh as intraperitoneal haemorrhage. With regard to inreases in pleural pressure, several points deserve emphasis. First, some have debated whether negative transpulmonary pressure (pleural pressure in exess of airway opening pressure) is physiologially possible. 74 Several mehanisms explain how inreased pleural pressures an be sustained inluding the development of regional ateletasis, airway losure and/or expiratory flow limitation. Seond, there are apparent measurement artefats whih an our in the setting of inreased pleural pressures. For example, intravasular pressures whih are generally measured referened to atmosphere an appear unexpetedly high in patients with inreased IAP; that is, a high entral venous pressure or left Figure 2 Impat of experimental manipulations in pigs of intraabdominal pressure (IAP) on entral venous pressure (CVP), pleural pressure and intraranial pressure (ICP). Note that resusitation does not improve the intraranial pressure but release of the IAP (abdominal deompression) does lower ICP onsiderably. Failure to reognise inreases in IAP ould therefore ontribute to mistreatment or poor outome. Reprodued with permission from Citerio and Berra. 97 Thorax: first published as /thx on 26 September Downloaded from on 14 Otober 2018 by guest. Proteted by opyright. 928 Thorax 2008;63: doi: /thx

5 ventriular end diastoli (wedge) pressure ould be observed in the setting of hypovolaemia if the ardia hambers are being externally ompressed. Third, real haemodynami effets of inreased pleural pressure an our sine, for example, right atrial ompression an limit venous return from extrathorai strutures inluding the head. Thus, ACS has been assoiated with pseudotumor erebri as well as inreases in intraranial pressure in trauma patients. 75 Internists are often alarmed by neurosurgial reommendations to perform deompressive laparotomy to address intraranial hypertension. However, this strategy is effetive in some ases (fig 2). Optimal patient are therefore requires an understanding of IAP hanges on patient physiology and measurements. The diagnosis of ACS requires a high linial index of suspiion beause physial examination is frequently misleading in making this diagnosis. 73 A number of methods have been used to estimate IAP inluding measurement of intragastri pressure, ommon ilia venous pressure, intraperitoneal pressure (via a paraentesis needle) and bladder pressure (via a Foley atheter). The Foley atheter tehnique is reasonably well validated and has a relatively low risk. A needle is inserted into the side port of the Foley atheter and this atheter is transdued using the monitoring equipment for the entral venous pressure. The tehnique requires that ml of fluid is present in the bladder sine an empty bladder may not reflet IAP whereas an overfilled bladder may reate a reoil pressure aross the bladder wall whih again does not reflet the pressure throughout the abdominal avity. Raising the bag of urine and observing the height of the standing olumn of urine as a manometer an provide an approximation of the IAP. Thus, estimation of the IAP an be straightforward if the liniian suspets ACS. The treatment of ACS is somewhat more hallenging. If reversible pathology is present, the underlying ause should learly be addressed. Large volume paraentesis an be helpful in ases of massive asites. The authors have observed ases of omplete reversal of renal failure following paraentesis in patients with irrhosis who had been inorretly diagnosed with hepatorenal syndrome, a ondition assoiated with a very high mortality. Use of the reverse Trendelenburg position an help to redue pressure on retroperitoneal strutures. Gastri deompression, treatment of ileus and feal disempation an all be helpful in lowering IAP. Although deompressive laparotomy is onsidered the most definitive treatment, this proedure omes with obvious risk so surgeons are often relutant to perform this proedure for suh patients. OBESITY AND ACUTE RESPIRATORY DISTRESS SYNDROME (ARDS) When total respiratory ompliane is onsidered in obese patients, the effets of obesity on the hest wall must be separated from the effets attributable to dereased lung ompliane, as seen in aute lung injury (ALI) and aute respiratory distress syndrome (ARDS). This distintion has major impliations for the appliation of mehanial ventilation in obese patients. Three important physiologial onepts are ritial to the seletion of mehanial ventilator settings in suh patients. First, the transpulmonary pressure (pressure differene between airway opening and pleural spae) is the distending pressure aross the lung and must be distinguished from transthorai pressure (differene between pleural and ambient atmospheri) whih is the distending pressure aross the hest wall. Airway pressures applied during mehanial ventilation reflet the sum of these lung and hest wall omponents. In experiments designed to distinguish the effets of high inflation pressures using manipulations suh as asting of the hest wall, it has learly been shown that it is exessive transpulmonary pressure that leads to damage of the lung, a phenomenon referred to as ventilator-indued lung injury. 78 The transpulmonary pressure is the ritial variable determining risk of lung injury sine marked inreases in airway pressure may be observed with minimal lung streth and injury when the hest wall is restrited, refleted in raised pleural pressure. Obese patients an frequently be safely ventilated with relatively high applied pressures sine transpulmonary pressures are quite low in this setting. 79 Seond, the reruitability of the lung whih refers to the ability to open ollapsed units of the lung must be onsidered. Collapse of alveoli an our due to inreases in surfae tension (eg, from surfatant dysfuntion) or from raised pleural pressures that effetively ompress lung units leading to their ollapse. 80 Suh units an sometimes be reruited (reopened) if the applied pressures are suffiient to overome the opening pressure. Obese patients frequently develop onsiderable ateletasis, partiularly in the posterior dependent lung zones. 24 Third, parenhymal heterogeneity is important. This refers to the onept that high shear fores an our in the lung, partiularly at juntions of normal and abnormal lung. Classi physiology studies have estimated effetive pressures in exess of 100 m H 2 O at juntions of normal and abnormal lung, even when applied pressures are below the generally reommended eiling of 30 m H 2 O. 81 Thus, many liniians attempt to ahieve parenhymal homogeneity (eg, by the use of reruitment manoeuvres to open ollapsed alveoli 82 ) and thereby minimise shear fores within the ventilated lung. Beause obese patients frequently have onsiderable ateletasis, they would be predited to have parenhymal heterogeneity even without well-established lung injury. With these physiologial priniples in mind, mehanial ventilator settings an be onsidered. One hallenge is that most liniians do not routinely measure pleural pressure and therefore transpulmonary pressure is not known at the bedside in most ases. The liniian is therefore often in a situation of having to surmise or infer what pleural pressures are prevailing in a given patient. The failure to fully aount for the hest wall effets on airway pressures may lead to inappropriate therapy, suh as undertitration of PEEP. We have frequently used PEEP values of m H 2 O in obese patients to maintain oxygenation and parenhymal homogeneity. In patients with ALI/ARDS, randomised trials have shown a benefit on mortality with the appliation of 6 ml/kg tidal volume ompared with 12 ml/kg. One point of major emphasis is that 6 ml/kg must be alulated on the basis of ideal body weight rather than atual measured body weight. The reason for this is that, when a patient gains weight, the lung does not hange in size appreiably and therefore an individual whose weight inreases from 70 kg to 140 kg should reeive 420 ml tidal volume (rather than 840 ml). Exessive tidal volumes may be applied to patients beause this important onept is overlooked. Beause the number of alveoli partiipating in gas exhange is diffiult to predit at the bedside, there is no easy way to tell the proportion of lung partiipating in eah tidal inflation. Thus, a volume targeted approah ould lead to regional overdistension even when applied pressures are below the reommended 30 m H 2 O threshold. 85 On the other hand, pressure targeted approahes ould lead to marked inreases in tidal volume, partiularly in spontaneously breathing patients. Suh patients an generate large transpulmonary pressures that Thorax: first published as /thx on 26 September Downloaded from on 14 Otober 2018 by guest. Proteted by opyright. Thorax 2008;63: doi: /thx

6 may not be obvious to the liniian at the bedside. We believe that a satisfatory low-streth result an be obtained using either volume or pressure targeted strategies, provided adjustments are made during serial bedside assessments. Regardless of how it is ahieved, lung streth should be minimised in patients with ALI/ARDS to prevent worsening lung injury. A few points relative to ALI/ARDS are noteworthy in obese patients. Suh patients often have marked inreases in pleural pressure and therefore we believe that the reommended eiling in airway pressure of 30 m H 2 O an be safely exeeded in suh patients. 74 In some ases heavy sedation and/or paralysis are required to keep suh patients below this limit. In addition, when PEEP requirements are high, only very small tidal volumes an be delivered if end-inspiratory plateau pressures are kept below 30 m H 2 O. In suh ases we would favour allowing inflation pressures to exeed 30 m H 2 O, reognising that transpulmonary pressures and therefore lung distension often remain minimal in suh ases. Permissive hyperapnia allowing arbon dioxide values to inrease and ph to fall an also be used in suh ases based on strong experimental evidene, although linial evidene is still evolving. 87 Open lung protetive ventilation remains ontroversial sine most (but not all) of the linial trials have shown no outome benefit to this approah The onept relies on the issue of parenhymal homogeneity suh that efforts to open ollapsed alveoli and then maintain their pateny using high PEEP ould be benefiial. In this setting, low peak distending pressures are provided yielding permissive hyperapnia. The intervention, as employed by Amato et al, 90 therefore requires reruitment manoeuvres, high PEEP, low tidal volume and permissive hyperapnia. High frequeny osillation tehniques have been advoated by some authors to ahieve this goal Ongoing trials are examining the role of open lung protetive ventilation although the existing data are equivoal at best. CONCLUSIONS In all these ommonly enountered linial senarios obesity magnifies patient risk, by predisposing to the underlying ondition, ontributing to the assoiated pathophysiologial derangements and ompliating management from a tehnial and logistial point of view. Regrettably, the problem of morbid obesity is flourishing and an inreasing proportion of patients in the ICU suffer from its pervasive effets, adding to its status as the one of the greatest hallenges to the health of ommunities in the developed world. The reent demonstration of improved long-term outome following bariatri surgery provides some soure for optimism, but is likely to further inrease the burden of ritially ill obese patients due to rare but serious perioperative ompliations. 96 Thus, pratitioners must be aware of these important issues relevant to this speial population. Funding: AM is funded by National Institutes of Health RO1-HL73146, SCOR P50 HL and AG and an Established Investigator Award from the Amerian Heart Assoiation and has reeived onsulting and/or researh funding from Respironis, Cephalon, Restore Medial, Apnex Medial, Itamar Medial, Novartis, Inspiration Medial, NMT Medial and Pfizer. DH is supported by National Health and Medial Researh Counil grants and and an Australian Researh Counil Disovery Grant and has reeived onsulting and/or researh funding from ResMed and Inspiration Medial. Competing interests: None. REFERENCES 1. MTigue K, Larson JC, Valoski A, et al. 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