Crit Care Clin 24 (2008) 517531Sleep and Mechanical Ventilation

Aylin Ozsancak, MD, Carolyn DAmbrosio, MD,Erik Garpestad, MD, Greg Schumaker, MD,

Nicholas S. Hill, MD*Division of Pulmonary, Critical Care and Sleep Medicine, Tufts Medical Center,

750 Washington Street #257, Boston, MA 02111, USA

The critical care environment is a harsh one for sleep. Patients with crit-ical illness have normal or low total sleep time, but sleep architecture isseverely altered. The circadian rhythm is disrupted, with patients spendingas much time sleeping during the day as at night. Consolidation is lost,stages 1 and sometimes 2 become more prominent, and stages 3 and 4and rapid eye movement (REM) are severely diminished. Arousals andawakenings are frequent and contribute to severe fragmentation. Sleepquantity may be preserved, but quality is lacking. Many factors are thoughtto contribute to poor quality sleep in the intensive care unit (ICU). Tradi-tionally, noise has been considered a major factor in sleep disruption,although more recent studies suggest that it is responsible for only a minorityof disruptions. Other reasons for disruption of sleep include patient care (eg,the need to check vital signs or draw blood), eects of medications that cansuppress REM or slow wave sleep, release of cytokines and endocrinologiceects, and the toxic eects of infection on neurologic function.

Increasingly in recent years, investigators have focused on the role of theventilator itself in disrupting sleep, by way of pain and discomfort related tointubation and suctioning and dyssynchrony between the patient and venti-lator (Box 1). In the following sections, we briey review relevant aspects ofnormal and abnormal sleep and the control of breathing and discuss evi-dence that suggests that mechanical ventilation and its modes contributeto sleep fragmentation. We also consider how long-term mechanicalDr Hill is funded by Eli Lilly Distinguished Scholarship in Critical Care of the Chest

Foundation and Respironics.

* Corresponding author.

E-mail address: nhill@tufts-nemc.org (N.S. Hill).

0749-0704/08/$ - see front matter 2008 Elsevier Inc. All rights reserved.doi:10.1016/j.ccc.2008.03.002 criticalcare.theclinics.com

A healthy adults sleep architecture normally consists of approximately80% non-REM and 20% REM stages. Non-REM sleep is further subdi-vided into three stages (N1, N2, and N3) [1], with stage N1 occurring atventilation aects sleep in patients with chronic respiratory failure duringinvasive and noninvasive ventilation (NIV).

Normal and abnormal sleep

Box 1. Contributors to sleep disruption in the intensive care unit

Ventilator mode and other settings (eg, respiratory rate,tidal volume)

Patient-ventilator dyssynchronyDiscomfort, pain, or anxiety caused by endotracheal tube,ventilator or acute illness

Air leakage during NIVSedation and other medication (eg, analgesics, vasopressors,corticosteroids)

Patient care activities (eg, vital signs, suctioning, positioning)Severity of critical illness (eg, sepsis, multiorgan dysfunction)Noise (eg, conversations, alarms)Light

518 OZSANCAK et alsleep onset for a few minutes. Because it is the transitional stage betweensleep and wakefulness, stage N1 commonly increases when sleep is severelyfragmented, with patients repeatedly awakening and falling back tosleep. Stage N2, characterized by K-complexes and sleep spindles, alsomay increase in the face of fragmentation. Stage N3 is high-voltage(O 75 mV), slow wave (0.52 Hz) sleep. More recent nomenclaturehas combined what were formerly called stages 3 and 4 into just stageN3, but for the purposes of this article we use the older nomenclature,because most of the studies have used the older Rechtschaen and Kalesterminology [2].

REM sleep is characterized by episodic bursts of rapid eye movements,low chin muscle tone, irregularities in respiration and heart rate, muscle ato-nia (except for the diaphragm and ocular muscles), and emergence ofdreams. Non-REM and REM sleep alternate nearly every 90 to 110 minutesthroughout the night such that slow wave sleep and REM sleep occur pre-dominantly in the rst and last third of the night, respectively [3]. REM andstage N3 are essential for normal restorative sleep, but the latter isconsidered the most restorative stage.

Arousals are abrupt shifts of the electroencephalogram frequency thatlast 3 or more seconds and are associated with a lightening of sleep by at

above the waking PCO2 leading to transient apnea in some individuals until

it rises to the sleeping eupnoeic threshold (Fig. 1). This apnea may arousethe individual and contribute to periodic breathing and lead to hyperventi-lation and subsequent hypocapnia, which may reinitiate the process as theindividual falls back to sleep. These arousals also may simply cause awak-enings. As sleep progresses to the latter part of stage 2 and slow wave sleep(stages 3 and 4), the periodic breathing disappears, and breathingbecomes more regular. Consequently, any condition that leads to anleast one stage. Awakenings refer to abrupt shifts to full wakefulness. Awak-enings and arousals lead to sleep fragmentation, and their frequent occurrencediminishes the proportion of REM and slow wave sleep, largely because thereis too little consolidated sleep in the lighter stages to attain them. Severefragmentation leads to poor quality sleep, with excessive sleepiness andcognitive impairment. If sleep deprivation is severe, delirium, immunesuppression, protein catabolism, and respiratory depression can ensue [4].

Control of breathing during normal sleep

During wakefulness, chemoreceptor inputs (from the carotid body forhypoxia and hypercapnia and from the medullary chemoreceptor for hyper-capnia) and aerent inputs from chest wall receptors (such as Hering-Breuerreex) control ventilation. The behavioral control system (ie, inuence ofdaily activities such as eating, talking, coughing, or sneezing on ventilation)and cortical inputs also can override the chemical and mechanical stimuli[5,6]. During sleep, however, the latter two controllers become quiescentso that the chemoreceptor and respiratory reex feedback systems becomethe primary controllers of breathing.

At sleep onset, the apneic PaCO2 threshold (ie, below which apnea oc-curs) rises to a level within 1 to 2 mm Hg of the normal awake eupnoeicthreshold (ie, the PaCO2 at which apnea is terminated by reinitiation ofbreathing) and 2 to 5 mm Hg below sleeping eupnoeic threshold [7]. Partlyas a consequence of these sleep-induced changes in apneic and eupnoeicthresholds, the transition from wakefulness to sleep causes breathinginstability. Upper airway and respiratory muscle tone diminish, leading toa decrease in tidal volume. This decrease, combined with a decline inrespiratory drive that slightly lowers respiratory rate, decreases minute ven-tilation [8] and leads to an increase in PaCO2 by approximately 2 to 3 mm Hg(and 23 mm Hg higher during REM sleep) [9,10], a reduction in PaO2 by 3to 10 mm Hg, and a reduction in oxygen saturation by 0% to 2% [8,11,12].

Although there is considerable variability within individuals, breathingoften becomes arrhythmic at sleep onset, with the apneic threshold rising

519SLEEP AND MECHANICAL VENTILATIONincrease in the frequency of transitional stage sleep (eg, a stay in a criticalcare unit) also leads to more vulnerability to periodic breathing and centralapneas and subsequently to more arousals, which are the main contributorsto fragmented sleep.

(mmHg)Sleep during mechanical ventilation in the acute care setting

Assessment of sleep in the intensive care unit

Monitoring of sleep in the ICU is challenging. Polysomnography (PSG)is the gold standard for determining the quantity and quality of sleep but isexpensive and time consuming. Sedation, analgesia, acute illness, and elec-trical interference may alter the electroencephalogram (EEG) tracing,

VE

(l/mi

n)10

5

40

30

10 20 30 Time (sec)Awake Sleep Onset NREM Sleep stages

Fig. 1. Schematic changes in apneic and eupnoeic thresholds of PaCO2 (top), and minute venti-

lation (VE) (bottom) during sleep onset. The apneic threshold (dashed line) rises with sleep

onset, precipitating apnea until the PaCO2 rises above it, leading to a resumption of breathing

during Non-REM sleep.PaCO2520 OZSANCAK et alrendering the interpretation inaccurate. Alternative methods, such as actig-raphy or the bispectral index, have their own advantages and disadvantages[13,14]. Actigraphy is a simple, easy method used mainly in outpatients tomeasure patient movement as an index of sleep. This approach has severelimitations in the ICU, however, because motion is hampered in manypatients by restraints and sedation. The bispectral index is derived frommultiple analyses of the raw electroencephalogram, including power andbispectral, which are further subjected to multivariate analysis. The valueobtained correlates well with the depth of anesthesia in normal volunteersbut has not been validated in the ICU setting [14].

Subjective assessments of sleep have been attempted, including patientself-assessment based on recall and nurse assessment. Patient assessmentis unreliable because of sedation, delirium/dementia, or recall bias, andnurse assessment tends to overestimate sleep because of the diculty in dif-ferentiating between sedation and actual sleep [15].

Sleep in the intensive care unit

Severe sleep abnormalities in the ICU have been known for decades, hav-ing been rst reported in 1985 among a small series of patients in a surgicalunit who slept less than 2 hours per night during the rst 2 nights after

haveared

with night [16,18,20,24].

The reasons for the fragmented sleep are undoubtedly multifactorial

(see Box 1). Noise levels in the ICU range from 50 to 80 dBdas loud asa factorydand noise levels have long been thought to be responsible formuch of the sleep disruption. Several studies have found that although noiseis an important factor, it is responsible for only a minority of the disrup-tions. Freedman and colleagues [25] found that patients rated human inter-ventions and diagnostic tests as disruptive as noise. In a study by this groupthat monitored noise and EEG tracings in ICU patients for 24 to 48 hours,only 11.5% of arousals and 17% of awakenings were attributable to noise[16]. In a similar study, Gabor and colleagues [18] found that 7.1% and20.9% of arousals and awakenings were attributable to patient careactivities and environmental noise, respectively, accounting for less than30% of total sleep disruptions. Other factors are responsible for most sleepdisruptions in most patients, and one of these factors may be mechanicalventilation.

Sleep during invasive mechanical ventilation

Several studies have examined sleep during invasive mechanical ventila-tion but have been unable to distinguish between disrupted sleep relatedto the ventilator per se as opposed to that related to the ICU environment.In a study based on questionnaires lled out by patients on the day of theirdischarge from the ICU, ventilated patients rated themselves as signicantlysleepier than nonventilated patients [25]. No association was established be-tween a patients ventilator status and perceived sleep disruptions by nursecare activities, noise/light, or sleep quality, however. Although this ndingmay suggest that poor sleep quality and disrupted sleep are related to theICU environment and not to the ventilator, the limitations of a question-solidated sleep occurring throughout the 24-hour cycle. Some studiesrecorded a higher percentage of sleep during the waking hours compsurgery and had virtually no stage 3 or 4 sleep [15]. Subsequent studies haveshown that total sleep times vary enormously among individuals, from 1.7to 19.4 hours per 24 hours in one study [16]. Sleep in the ICU is oftenseverely fragmented. Arousals and awakenings have been reported to occurbetween 22 and 79 times per hour [17,18], respectively, far in excess of thenormal. The quantity of REM sleep is markedly reduced, ranging from11% to none [1517,1923] compared with the normal of 20% to 25%,and slow wave sleep is severely reduced. In some patients, atypical sleeppatterns on EEG may reect medications or the severity of illness, such assepsis [20]. The circadian rhythm is also severely disrupted, with noncon-

521SLEEP AND MECHANICAL VENTILATIONnaire based on patient recall preclude rm conclusions.Studies that have examined PSG in mechanically ventilated patients

in the ICU have observed the same kinds of sleep fragmentation and alter-ation of sleep architecture as in patients in the ICU generally: increased

fragmentation, highly variable total sleep time, increased percentage ofstage 1 (and sometimes 2) sleep, and reduced REM and slow wave sleep[1524,26,27]. Circadian rhythm is often lost, and the need for sedation,analgesia, and frequent suctioning contributes to polysomnographic abnor-malities. A study that monitored PSG for 24 to 48 hours in 22 patients in theICU, 20 of whom were receiving mechanical ventilation, found that totalsleep time was normal at an average of 8.8 hours per patient but was com-prised of a mean of 41 sleep periods that averaged 15 minutes each dispersedthroughout the 24-hour monitoring period (Fig. 2) [16]. There were no sig-nicant correlations among age, gender, APACHE III score, or length ofICU stay and the day-versus-night distribution of sleep or arousal index.Whether this severe sleep fragmentation has adverse eects on weaning orsubsequent outcomes is unknown.

Eect of ventilator mode

Several more recent studies have examined the possibility that the venti-lator mode itself might contribute to sleep arousals during mechanical

522 OZSANCAK et alFig. 2. Disrupted and dispersion of sleep over a 24-hour monitoring period in ve subjects in anventilation [17,2123]. Parthasarathy and Tobin [17] hypothesized that pres-sure support ventilation would cause more central apneas than assist controlventilation because it has no backup rate and might hyperventilate patients(and lower PaCO2 below the apneic threshold) during sleep. Setting assistcontrol and pressure support adjusted to deliver 8 mL/kg during wakeful-ness, patients received at least 2 hours each of assist control, pressureICU. Black areas represent episodes of sleep; white areas represent wakefulness. (FromFreedman

NS, Gazendam J, Levan L, et al. Abnormal sleep/wake cycles and the eect of environmental

noise on sleep disruption in the intensive care unit. Am J Respir Crit Care Med 2001;163:

453; with permission.)

support, and pressure support with added dead space in random order dur-ing a single night. The authors conrmed their hypothesis, observing morecentral apneas and worse sleep fragmentation (79 versus 54 arousals andawakenings per hour [P ! .05]) with pressure support than with assistcontrol. They also found that the added dead space (which raised PaCO2)eliminated most of the central apneas and sleep disruption in the pressuresupport group (Fig. 3), which was consistent with the hypothesis that over-ventilation leading to hypocapnea during sleep was responsible for theworse sleep fragmentation. Six of the 11 patients in the study had congestiveheart failure, however, which may have predisposed them to the develop-ment of central apneas.

One speculation that derives from the study by Parthasarathy and Tobin[17] is that lower dose pressure support would eliminate the central apneasand improve sleep quality. Toublanc and colleagues [22] used a pressuresupport of only 6 cm H2Odjust enough to overcome the added breathingwork attributable to the endotracheal tube. In a single night crossover trial,

523SLEEP AND MECHANICAL VENTILATIONFig. 3. Upper panel shows that 6 of 11 mechanically ventilated patients developed apneas dur-

ing pressure support (PS; closed circles) as compared with none during assist control ventilation(AC; open triangles). Lower panel shows that the addition of dead space virtually eliminated the

apneas during pressure support (open circles). Individual and group mean values are shown.

(From Parthasarathy S, Tobin MJ. Eect of ventilator mode on sleep quality in critically ill

patients. Am J Respir Crit Care Med 2002;166:1425; with permission.)

they compared low-dose pressure support to assist control set at 10 mL/kgor enough to suppress spontaneous breathing. They found that althoughcentral apneas were not a problem with low-dose pressure support, assistcontrol was still preferable; it was associated with better sleep quality, in-cluding greater proportions of stages 1 and 2 sleep early on and more stages3 and 4 sleep during the latter part of the night. The authors concluded thatto optimize sleep quality, patients should be rested with assist control ven-tilation at night while undergoing daytime weaning trials. They did not testan intermediate level of pressure support, however, which might haveavoided overventilation and still unloaded the breathing muscles.

Bosma and colleagues [21] hypothesized that a mode that has the poten-tial to enhance patient-ventilator synchrony, proportional assist ventilation(PAV), would also improve sleep quality compared with pressure support.

524 OZSANCAK et alPAV targets instantaneous inspiratory ow and can respond to increasedpatient eort by increasing delivered pressure and ow, depending on thespecic ow and volume assist settings and proportional assist selected[28,29]. Esophageal and gastric balloons were inserted so that ventilator set-tings could be adjusted to achieve equivalent reductions in breathing workwith both modes. Thirteen patients were crossed over in random order toreceive PAV or pressure support on consecutive days. Patients had fewerincidences of auto-triggering, failed triggering, double-triggering, or delayedcycling with PAV, which was also associated with fewer arousals (Fig. 4)and consequently more slow wave and REM sleep. The authors concludedthat by optimizing patient-ventilator synchrony compared with pressuresupport, PAV improved quality of sleep.

More recently, Alexopoulou and colleagues [23] compared PAV topressure support in patients manifesting good patient-ventilator synchrony.PAV is an upgraded PAV mode that automatically adjusts inspiratory and

Fig. 4. Linear regression analysis correlates the number of patient-ventilator asynchronies per

hour with the number of arousals per hour. By optimizing patient-ventilator synchrony, PAV(lled circles) was associated with less asynchrony and fewer arousals than pressure support

(open circles). (From Bosma K, Ferreyra G, Ambrogio C, et al. Patient-ventilator interaction

and sleep in mechanically ventilated patients: pressure support versus proportional assist

ventilation. Crit Care Med 2007;35:1053; with permission.)

expiratory assist settings by calculating resistance and elastance using300-msec pause maneuvers after random breaths, obviating the needfor insertion of esophageal and gastric balloons, but the authors aimed toascertain whether the brief pause maneuvers disrupted sleep. They foundthat although PAV was associated with enhanced sleep eciency com-

voidoverventilation, or the assist-control mode can be used during sleep so that

525SLEEP AND MECHANICAL VENTILATIONthe backup rate eliminates the central apneas.

Sleep during noninvasive ventilation

NIV, which is the provision of mechanical ventilation without requiringan articial airway, usually via a full face or nasal mask, has been usedincreasingly in critical care units internationally to treat respiratory failuremainly caused by chronic obstructive pulmonary disease exacerbations orcongestive heart failure [30,31]. As such, most applications of NIV lastbetween hours and a few days [32], so most patients wean o before sleepdeprivation is likely to become severe. Many patients with respiratory fail-ure are at risk for sleep deprivation when they are admitted to a hospital,however, and even a few more days of poor sleep could be deleterious, sosleep during acute applications of NIV is of interest. As of yet, no studieshave been published describing sleep during NIV, although the expectationis that its administration in the critical care environment would be

Box 2. Strategies to optimize sleep qualityduring mechanical ventilation

Rest with assist control mode overnighttially improve sleep in the ICU (Box 2), ventilator modes can be set to apared with pressure support in sedated patients, there were no other dier-ences in sleep quality for sedated and nonsedated patients. The authors alsofound that at high levels of assist, both modes induced periodic breathing.Although this study did not replicate the advantages of PAV over pressuresupport observed by Bosma and colleagues [21], the exclusion of patientswho manifestes dyssynchrony on pressure support might have eliminatedthe chance of making such an observation.

In summary, these studies demonstrate that the ventilator mode and spe-cic ventilator settings can contribute to irregular breathing patterns andsleep fragmentation. In spontaneous breathing modes such as pressuresupport or PAV, excessively high settings can predispose to central apneasby means of overventilation and suppression of the drive to breathe as theapneic threshold rises with sleep onset. To avoid this problem and poten-Avoid overventilation with spontaneous breathing modes(pressure support or PAV)

Use modes that optimize synchrony (PAV)

associated with the same severe sleep fragmentation observed in other crit-ically ill patients. Our preliminary investigation of four patients using NIVin ICUs monitored with PSG for 24 hours supports this expectation; pa-tients had a marked increase in the frequency of arousals and a paucity ofslow wave or REM sleep (representative hypnogram in Fig. 5). One patientwith pneumonia, whose sleep was disrupted by frequent arousals related tocough, had no REM or slow wave sleep whatsoever and required intubationapproximately 6 hours after completion of the PSG. The question ofwhether severe sleep disruption predicts NIV failure cannot be answeredfrom our data but may be a topic for a later investigation.

Sleep during mechanical ventilation in the long-term setting

Sleep during long-term invasive mechanical ventilation

In recent years, patients who fail to wean from invasive mechanical ven-tilation within a couple of weeks have been undergoing earlier tracheostomy

526 OZSANCAK et alFig. 5. Fragmented sleep pattern of a patient using NIV in the ICU (using oxygen with nasal

cannula for the rst 5 hours). Upper panel shows sleep stages (label to left), middle panel

indicates arousals with vertical marks, and black horizontal bars show that bilevel pressuresthan in the past [3335]. If suciently stable, these patients are then trans-ferred to postacute care or long-term acute care hospitals, where they con-tinue on mechanical ventilation and undergo more gradual weaning as theirmedical condition stabilizes and they gain strength in response to physicaltherapy [36]. A substantial portion of these patients (up to 50%) dies whilein long-term acute care [37]. Most of the survivors (70%) wean and undergodecannulation. Some patients who fail to wean are able to return home ifwere 12 cm H2O inspiratory and 5 cm H2O continuously after the rst 5 hours, except for a brief

interruption after 9AM. Sleep consisted of mainly stage 1 and 2 with a brief period of stage 3.

The total number of arousals and awakenings was 23/hour. (Aylin Ozsancak and colleagues,

Unpublished data.)

pira-mity

[40,41]. In these studies, NPPV was applied just nocturnally using the

nasal route. Used in this way, the greater convenience and portability ofNPPV compared with body ventilators and its ability to avoid upper air-way obstruction led to a rapid switch, so that by the early 1990s, NPPVwas seen as the ventilatory mode of rst choice for patients with chronicrespiratory failuredpreferred even to tracheostomy ventilation. Initialstudies on sleep in these patients using withdrawal for periods of timeaveraging a week demonstrated that compared with nights when patientsdid not use it, nasal NPPV mitigated sleep-related hypoventilation, whichimproved nocturnal oxygenation and prevented deterioration in daytimegas exchange [42]. PSG demonstrated fewer arousals (65 versus 114)when patients used NPPV, although the percentage of REM sleep wasunaected [43].tion (NPPV) was reported as an eective way to stabilize chronic restory failure caused by neuromuscular disease or chest wall deforthey have the capability and requisite resources. Others remain hospitalizedin long-term acute care or are transferred to a skilled nursing facility.

Little is known about sleep of long-term mechanically ventilated patientsin a long-term acute care setting or at home. It is reasonable to expect thatas the acute illness subsides, fewer interruptions for tests or vital signs arenecessary, and the environment becomes less noisy, sleep quality wouldimprove. It is expected that sleep fragmentation would diminish, slowwave and REM sleep would return, and circadian rhythm would be re-stored, but this has not been established. It also would be expected that sleepquality at home would approach normal in long-term ventilator users, whomight be supported for up to several decades, depending on their age atinitiation and cause of respiratory failure.

Sleep during long-term noninvasive ventilation

Various dierent approaches to NIV have been used in the past [38].During the polio epidemics, so-called body ventilators, including negativepressure ventilators such as iron lungs, provided mechanical ventilatoryassistance long-term to thousands of aicted individuals. These machinesare rarely used any longer, however, partly because of their lack of portabil-ity but also because studies during the early 1990s demonstrated that theyexacerbated or even induced obstructive sleep apnea because the negativepressure was not triggered by the patient, which predisposed the patientto upper airway collapse caused by asynchrony between upper airway sti-ening and ventilator action [39].

Beginning during the mid-1980s, noninvasive positive pressure ventila-

527SLEEP AND MECHANICAL VENTILATIONSubsequent PSG in a small cohort of long-term users of NPPV withrestrictive thoracic disease demonstrated the frequent occurrence of oralair leaks during nasal NPPV, which occurred during most sleep [44] andfor all breaths during slow wave sleep. In some patients, these air leaks

wasce.ma-

nometry by seeking an inspiratory pressure that reduced the transdiaph-

ragmatic pressure swing by more than 40% but less than 80% and toavoid any positive deection in esophageal pressure at the onset of expi-ration. Extrinsic positive end-expiratory pressure was set at 80% of theintrinsic positive end-expiratory pressure measured during spontaneousbreathing. The authors found that sleep eciency (80.6% versus71.7%), arousal index (16 versus 29.9 events/h), percentage of REM(17.3% versus 9.1%), and ineective trigger eorts were improved byphysiologic as opposed to usual pressure support (all P ! .05). Thesendings demonstrated that the settings for pressure support inuencesleep quality, but they do not establish that manometry is necessary toachieve optimal settings. No single usual way to set pressure supporthas been agreed upon for patients with chronic respiratory failure causedby neuromuscular disease. The usual approach used by Fanfulla andcolleagues [46] was aggressive and arrived at inspiratory and expiratorybined with an extrinsic positive end-expiratory pressure level that progressively increased in each patient, according to his or her toleranPhysiologic pressure support was set using esophageal and gastricwere associated with frequent arousals and diminished the quality of sleep.In a later study, Teschler and colleagues [45] eliminated the mouth leaks bytaping the mouths of patients using nasal NPPV and demonstrated a reduc-tion in the frequency of arousals.

NPPV for chronic respiratory failure caused by restrictive thoracic disor-ders greatly improves nocturnal gas exchange, which is associated witha marked reduction in the frequency of arousals compared with no ventila-tory assistance at all. Because of the innate leakiness of the NIV system,however, mouth leaks can contribute to more arousals than would be thecase if leaks could be eliminated. Some patients seem to accommodate tothe leaks and have relatively few arousals related to them, and others mayrespond to strategies aimed at reducing them. Taping of the mouth is prob-ably not practical in the long-term, but switching to an oronasal mask maybe helpful in some patients.

Eect of ventilator settings on sleep during long-term noninvasivepositive pressure ventilation

Fanfulla and colleagues [46] examined the eect of two dierent waysof setting pressure support on sleep quality in nine patients with neuro-muscular disease who had been established on long-term NPPV. Pressuresupport was set in the usual manner, which was the maximal toleratedinspiratory pressure that reduced the awake PaCO2 by more than 5% com-

528 OZSANCAK et alpressures in some patients that were considerably higher than thosedetermined physiologically. Other authorities prefer determination ofpressures in a sleep laboratory, with pressures selected to minimizerespiratory events [47], and still others favor a gentler approach that

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Sleep and Mechanical VentilationNormal and abnormal sleepControl of breathing during normal sleepSleep during mechanical ventilation in the acute care settingAssessment of sleep in the intensive care unitSleep in the intensive care unitSleep during invasive mechanical ventilationEffect of ventilator modeSleep during noninvasive ventilation

Sleep during mechanical ventilation in the long-term settingSleep during long-term invasive mechanical ventilationSleep during long-term noninvasive ventilationEffect of ventilator settings on sleep during long-term noninvasive positive pressure ventilation

SummaryReferences