preoxygenation and prevention of desaturation during ... · pdf fileairway/review article...

AIRWAY/REVIEW ARTICLE

Preoxygenation and Prevention of Desaturation DuringEmergency Airway Management

Scott D. Weingart, MD, Richard M. Levitan, MD

From the Division of Emergency Critical Care, Department of Emergency Medicine, Mount Sinai School of Medicine, New York, NY (Weingart); andthe Department of Emergency Medicine, Thomas Jefferson University Hospital, Philadelphia, PA (Levitan).

Patients requiring emergency airway management are at great risk of hypoxemic hypoxia because of primary lungpathology, high metabolic demands, anemia, insufficient respiratory drive, and inability to protect their airwayagainst aspiration. Tracheal intubation is often required before the complete information needed to assess therisk of periprocedural hypoxia is acquired, such as an arterial blood gas level, hemoglobin value, or even a chestradiograph. This article reviews preoxygenation and peri-intubation oxygenation techniques to minimize the risk ofcritical hypoxia and introduces a risk-stratification approach to emergency tracheal intubation. Techniquesreviewed include positioning, preoxygenation and denitrogenation, positive end expiratory pressure devices, andpassive apneic oxygenation. [Ann Emerg Med. 2011;xx:xxx.]

0196-0644/$-see front matterCopyright © 2011 by the American College of Emergency Physicians.doi:10.1016/j.annemergmed.2011.10.002

alaoaw

pmcabpm

baoawptad

twaas

INTRODUCTIONMaintaining hemoglobin saturation during airway

management is critical to patient safety. Desaturation to below70% puts patients at risk for dysrhythmia, hemodynamicdecompensation, hypoxic brain injury, and death.1,2 Thechallenge for emergency physicians is to secure a tracheal tuberapidly without critical hypoxia or aspiration. In patientswithout pulmonary pathology, adequate hemoglobin, or lowmetabolic demands and an initial pulse oximetry reading of100% on room air, there is a low risk of desaturation afteradequate preoxygenation. Conversely, in a septic patient withmultilobar pneumonia who is already hypoxemic (oxygensaturation �90%) despite 100% oxygen at high flow, there isan immediate risk of critical tissue hypoxia during trachealintubation.

This article reviews preoxygenation and peri-intubationoxygenation techniques to minimize the risk of hypoxemiaduring emergency tracheal intubation of adult patients. Itintroduces a risk-stratification approach based on initial pulseoximetry level in response to oxygen administration andprovides recommendations about specific techniques based onperiprocedural risk. Techniques reviewed include positioning,preoxygenation and denitrogenation, use of positive pressuredevices to increase mean airway pressure, and passive apneicoxygenation during tracheal intubation efforts.

WHAT IS THE RATIONALE FOR PROVIDINGPREOXYGENATION BEFORE TRACHEALINTUBATION?

Preoxygenation allows a safety buffer during periods of
hypoventilation and apnea. It extends the duration of safe a
Volume xx, . x : Month

pnea, defined as the time until a patient reaches a saturationevel of 88% to 90%, to allow for placement of a definitiveirway. When patients desaturate below this level, their status isn the steep portion of the oxyhemoglobin dissociation curvend can decrease to critical levels of oxygen saturation (�70%)ithin moments (Figure 1).3

The standard anesthesia induction of elective operativeatients is performed by administering a sedative, providinganual ventilations, administering a muscle relaxant, and then

ontinuing manual ventilations until placement of a definitiveirway. Preoxygenation is not mandatory in these patientsecause ventilation is continued throughout the inductioneriod and because they have normal physiology and lowetabolic needs.For operative patients with high aspiration risk caused by

owel pathology, body habitus, or critical illness,nesthesiologists developed rapid sequence induction. Asriginally conceived, this technique is the simultaneousdministration of the sedative and paralytic with no ventilationhile waiting for the paralytic to take effect, unless needed torevent hypoxemia. This induction method has been adapted tohe emergency department (ED), where all patients requiringirway management are assumed to be at risk for aspiration; ourefault technique is a rapid sequence tracheal intubation.

In a patient breathing room air before rapid sequenceracheal intubation (PaO2 �90 to 100 mm Hg), desaturationill occur in the 45 to 60 seconds between sedative/paralytic

dministration and airway placement. In the 1950s,nesthesiologists realized that the safest way to perform rapidequence tracheal intubation would be by filling the patient’s
lveoli with a high fraction of inspired oxygen (FiO2) before the
Annals of Emergency Medicine 1

g6rw

dlcvdesamvo

fls

FP

ullmpt

paTap

bipUb

te

db

CA

Preoxygenation and Prevention of Desaturation During Emergency Airway Management Weingart & Levitan

procedure.4 Studies by Heller and Watson5 and Heller et al6

show markedly increased time to desaturation if the patientsreceived preoxygenation with 100% oxygen rather than roomair before tracheal intubation.5,6

For preoxygenation in the ED, we have 3 goals: (1) to bringthe patient’s saturation as close to 100% as possible; (2) todenitrogenate the residual capacity of the lungs (maximizingoxygen storage in the lungs); and (3) to denitrogenate andmaximally oxygenate the bloodstream.7 The first 2 goals areimperative; denitrogenating and oxygenating the blood addslittle to the duration of safe apnea8 because oxygen is poorlysoluble in blood, and the bloodstream is a comparatively smalloxygen reservoir compared with the lungs (5% versus 95%).

Recommendation: Preoxygenation extends the duration ofsafe apnea and is recommended for every ED trachealintubation.

WHAT IS THE BEST SOURCE OF HIGH FIO2 FORPREOXYGENATION?

The duration of safe apnea times in most of thepreoxygenation literature is predicated on anesthesia circuitsthat are capable of delivering 90% to 100% FiO2 when usedwith a well-fitting mask. However, the usual source of oxygenduring ED preoxygenation is a facemask with an oxygenreservoir. This device is erroneously referred to as thenonrebreather mask despite an absence of 1-way valves coveringall of its ports. True nonrebreather masks set at 15 L/minute forpatients with normal ventilatory patterns are capable ofdelivering near 90% FiO2,9 but these devices are rarely availablein EDs. Standardly available nonrebreather masks at flow ratesof 15 L/minute deliver only 60% to 70% FiO2, do not providecomplete denitrogenation, and accordingly do not maximize the

Figure 1. Oxyhemoglobin dissociation curve demonstratesthe SpO2 from various levels of PaO2. Risk categories areoverlaid on the curve. Patients near an SpO2 of 90% are atrisk for precipitous desaturation, as demonstrated by theshape of the curve.

duration of safe apnea.9 p

2 Annals of Emergency Medicine

Standardly available nonrebreather masks can deliver FiO2

reater than or equal to 90% by increasing the flow rate to 30 to0 L/minute.10 Such flow rates may be achievable on most flowegulators in EDs by continuing to open the valve, though thereill be no calibrated markings beyond 15 L/minute.

Some ED providers use the self-inflating bag-valve-maskevice to provide preoxygenation. Bag-valve-mask devices

acking 1-way inhalation and exhalation ports will deliver onlylose to room air FiO2 when not actively assistingentilations.11,12 Even with ideal 1-way valves, the devices willeliver oxygen only in 2 circumstances: the patient generatesnough inspiratory force to open the valve or the practitionerqueezes the bag. In both circumstances, to obtain any FiO2

bove that of room air, a tight seal must be achieved with theask, which usually requires a 2-handed technique.13 A bag-

alve-mask device hovering above the patient’s face providesnly ambient FiO2.

Recommendation: Standard reservoir facemasks with theow rate of oxygen set as high as possible are the recommendedource of high FiO2 for preoxygenation in the ED.

OR WHAT PERIOD OF TIME SHOULD THEATIENT RECEIVE PREOXYGENATION?

Ideally, patients should continue to receive preoxygenationntil they denitrogenate the functional residual capacity of their

ungs sufficiently to achieve greater than 90% end-tidal oxygenevel.14 Although the mass spectrometers in many EDs allow the

easurement of end-tidal oxygen levels, in practice this is rarelyerformed. Instead, expediency often demands an empiriciming of preoxygenation.

Three minutes’ worth of tidal-volume breathing (theatient’s normal respiratory pattern) with a high FiO2 source isn acceptable duration of preoxygenation for most patients.15,16

his tidal-volume breathing approach can be augmented bysking the patient to exhale fully before the 3-minuteeriod.17,18

Cooperative patients can be asked to take 8 vital-capacityreaths (maximal exhalation followed by maximalnhalation).16,19,20 This method generally can reduce thereoxygenation time to approximately 60 seconds.16

nfortunately, many ill ED patients cannot take vital-capacityreaths.

The above times are predicated on a source of FiO2 greaterhan or equal to 90% and a tightly fitting mask that preventsntrainment of room air.21

Recommendation: Patients with an adequate respiratoryrive should receive preoxygenation for 3 minutes or take 8reaths, with maximal inhalation and exhalation.

AN INCREASING MEAN AIRWAY PRESSUREUGMENT PREOXYGENATION?

Mean airway pressure may be increased during
reoxygenation through the use of techniques such as

phtnmnwFispas

dplr

Weingart & Levitan Preoxygenation and Prevention of Desaturation During Emergency Airway Management

noninvasive positive-pressure ventilation. If patients have notachieved a saturation greater than 93% to 95% before trachealintubation, they have a higher likelihood of desaturation duringtheir apneic and tracheal intubation periods.2,16,18,22,23 Ifpatients do not achieve this saturation level after 3 minutes oftidal-volume breathing with a high FiO2 source, it is likely thatthey are exhibiting shunt physiology; any further augmentationof FiO2 will be unhelpful.24 Shunt physiology refers to alveolithat are perfused but not ventilated because of conditions suchas pulmonary edema or pneumonia, in which the alveoli arefilled with fluid or collapsed. The net effect is a physiologicright-to-left shunt; blood coming from the pulmonary arteries isreturned to the pulmonary veins without oxygenation. In theshort term, shunt physiology can be partially overcome byaugmenting mean airway pressure, thereby improving theeffectiveness of preoxygenation and extending the safe apneatime.

Evidence for the use of increased mean airway pressure as a

Table 1. Evidence for increased mean airway pressure as a pre

Study Patients Intervention

Delay et al25 RCT of 28 obese,operative patients

Noninvasive ventilation

Futier et al26 RCT of 66 obese,operative patients

Two treatment groups: nventilation or noninvasventilation with post–tintubation recruitment

Cressey et al27 RCT of 20 morbidlyobese womenundergoingbariatric surgery

CPAP preoxygenation

Gander et al28 RCT of 30 morbidlyobese operativepatients

CPAP preoxygenation

Herriger et al29 RCT of 40 ASA I–IIoperative patients

CPAP preoxygenation

Antonelli et al30 RCT of 26 hypoxemicICU patientsrequiringbronchoscopy

Noninvasive ventilation

RCT, Randomized controlled trial; NPPV, noninvasive positive-pressure ventilationcan Society of Anesthesiologists; TI, tracheal intubation.

preoxygenation technique can be found in Table 1. In a study H


articularly relevant to the ED, Baillard et al23 examinedypoxemic critically ill patients requiring tracheal intubation inhe ICU. At the end of the preoxygenation period, theoninvasive positive-pressure ventilation group had a 98%ean SpO2, whereas the standard group had one of 93%. In the

oninvasive positive-pressure ventilation group, 6 of 26 patientsere unable to improve their hypoxemic saturations with highiO2 until they received positive pressure. During the tracheal

ntubation procedure, the standard group’s levels decreased toaturations of 81% compared with 93% in the noninvasiveositive-pressure ventilation group. Twelve of the control groupnd 2 of the noninvasive positive-pressure ventilation group hadaturation levels below 80%.

No negative cardiovascular effects27,31 or appreciable gastricistention was observed in noninvasive positive pressurereoxygenation studies.25 The latter result was likely due to the

ow pressures used in these studies; gastric distention andesulting aspiration is unlikely at pressures below 25 cm

enation technique.

Comparator Outcome

Spontaneous ventilationat zero pressure

The patients in the noninvasivepositive-pressure ventilationgroup achieved faster andmore completedenitrogenation than thestandard group, asmeasured by an exhaledoxygen level �90%.

asive

aleuver


At the end of preoxygenation,PaO2 was higher in the NPPVand NPPV�RM groupscompared with the spontvent group and remainedhigher after TI and the onsetof mechanical ventilation


Showed a 40-s increase intime to desaturation throughthe use of noninvasivepositive pressure.Nonsignificant primaryoutcome.


The time until reaching asaturation of 90% afterapnea was extended by aminute in the CPAP group


Application of positive airwaypressure during induction ofanesthesia in adultsprolongs the nonhypoxicapnea duration by �2 min


The PaO2/FiO2 ratio improvedin the noninvasive positive-pressure ventilation groupand worsened in the high-FiO2-alone group

recruitment maneuver; CPAP, continuous positive airway pressure; ASA, Ameri-

oxyg

oninviveracheman

; RM,

2O.32-35 The data on the absence of any cardiovascular side


sta

IR

pttct

pvorfrgwd

ocpcrif1apfsip

hut

e

aip

HT

ib


effects may not be applicable to volume-depleted critically illpatients.36

The benefits of noninvasive positive-pressure ventilation forpreoxygenation in the ED should primarily be observed inpatients who cannot achieve acceptable saturations with highFiO2 alone.31 If tracheal intubation is attempted withsaturations below 90%, these patients can critically desaturate inseconds.37 Positive pressure may be applied with standalonedisposable continuous positive airway pressure (CPAP) masks38;with CPAP masks connected to noninvasive machines orstandard ventilators; or by using a positive end-expiratorypressure (PEEP) valve on a standard bag mask (Figure 2). Evenin departments without immediate CPAP systems, single-usePEEP valves are inexpensive and require minimal modificationof practice.

In critically ill patients with very high degrees of shunting,apneic oxygenation (discussed below) alone is unlikely to behelpful.39 If patients require CPAP during their preoxygenationperiod, it may benefit them to have the device left on until themoment of tracheal intubation. Whatever predisposed them toexperience shunting will recur during the apneic period if theyremain at zero airway pressure.40 PEEP also prevents absorptionatelectasis caused by breathing high FiO2 gas level, increasingthe efficacy of apneic oxygenation.41

Recommendation: CPAP masks, noninvasive positive-

Figure 2. A disposable PEEP valve. This inexpensive itemis a strain gauge capable of PEEP settings from 5 to 20cm H2O. When placed on the exhalation port of a bag-valve-mask device (inset), it allows the device to providePEEP/CPAP when the patient is spontaneously breathingand during assisted ventilations. If combined with a nasalcannula set to 15 L/minute, it will provide CPAP evenwithout ventilations. The generation of positive pressure ispredicated on a tight mask seal.

pressure ventilation, or PEEP valves on a bag-valve-mask device o


hould be considered for preoxygenation and ventilation duringhe onset phase of muscle relaxation in patients who cannotchieve saturations greater than 93% to 95% with high FiO2.

N WHAT POSITION SHOULD THE PATIENTECEIVE PREOXYGENATION?Supine positioning is not ideal to achieve optimal

reoxygenation. When one is placed flat, it is more difficult toake full breaths and more of the posterior lung becomes proneo atelectatic collapse,3 which reduces the reservoir of oxygenontained within the lungs and therefore reduces safe apneaime.

Lane et al42 performed a randomized controlled trial ofatients preoxygenated in a 20-degree head-up positionersus a control group that was left supine. After 3 minutesf preoxygenation, the patients received sedation and muscleelaxation and were then allowed to decrease their saturationrom 100% to 95%. The head-up group took 386 seconds toeach this saturation versus 283 seconds in the controlroup.42 Recently, Ramkumar et al43 confirmed these results,ith the 20-degree head-up group taking 452 seconds toesaturate versus 364 seconds for the supine group.

Altermatt et al44 examined specifically preoxygenation inbese patients (body mass index �35). This randomizedontrolled trial compared safe apnea times in intubatedatients who received preoxygenation in a sitting positionompared with those preoxygenated while lying flat. Afterapid sequence induction of anesthesia, the trachea wasntubated and the patient was left apneic and disconnectedrom the anesthesia circuit until SpO2 level decreased from00% to 90%. Using the time taken for desaturation to 90%s the outcome, the patients preoxygenated in a sittingosition took 214 seconds to desaturate versus 162 secondsor patients preoxygenated while lying flat.44 Dixon et al45

howed similar benefits in a third randomized controlled trialn patients with body mass index greater than 40 who werelaced in the 25-degree head-up position.

Reverse Trendelenburg position (head of stretcher 30 degreesigher than the foot) also improves preoxygenation and may beseful in patients who cannot bend at the waist or shoulders, ie,hose immobilized for possible spinal injury.46

An additional benefit of head elevation is better laryngealxposure during direct laryngoscopy.47

Recommendation: Patients should receive preoxygenation inhead-elevated position whenever possible. For patients

mmobilized for possible spinal injury, reverse Trendelenburgosition can be used.

OW LONG WILL IT TAKE FOR THE PATIENTO DESATURATE AFTER PREOXYGENATION?Although breathing at a high FiO2 level will slightly

ncrease the bloodstream stores of oxygen, the primaryenefit of preoxygenation is the creation of a reservoir of
xygen in the alveoli. When a patient is breathing room air,

stdpi

CD

dpfmaTtsosposcmta

dnrhsw

wwob

tipctdmcfLppeim


450 mL of oxygen is present in the lungs; this amountincreases to 3,000 mL when a patient breathes 100% oxygenfor a sufficient time to replace the alveolar nitrogen. Apatient breathing room air will have a total oxygen reservoirin the lungs and bloodstream of approximately 1.0 to 1.5 L,whereas an optimally preoxygenated patient will have 3.5 to4.0 L.3 Oxygen consumption during apnea is approximately250 mL/minute (3 mL/kg per minute); in healthy patients,the duration of safe apnea on room air is approximately 1minute compared with approximately 8 minutes whenbreathing at a high FiO2 level.3

Benumof et al48 used physiologic modeling to calculatethe time to desaturation less than 90% after theadministration of succinylcholine for various patient groupsafter apnea. The times were 8 minutes, 5 minutes, and 2.7minutes for healthy adults, moderately ill adults, and obeseadults, respectively.

The desaturation curves of Benumof et al48 have beenextensively reproduced in the emergency medicine literature,but the extended times in these models are predicated onfactors that are very different from those present in manyemergency tracheal intubations. The curves assume completedenitrogenation and alveolar concentrations of oxygen at80%. The model by Benumof et al48 assumes preoxygenationwith a device capable of generating approximately 90% FiO2

and optimal time for preoxygenation. It also ignores pulseoximeter lag time. In sick patients, especially those with poorcardiac output, the readings on a finger-probe pulse oximetermay lag behind the actual central arterial circulation by 30 to60 seconds.49 The times depicted by the desaturation curvesare not applicable to critically ill ED patients or those withpoor cardiac output.50-52

The effect of shunting, increased metabolic demand, anemia,volume depletion, and decreased cardiac output are synergisticin dramatically reducing oxygen storage in the lungs andshortening safe apnea in critically ill patients. As calculated byFarmery and Roe,51 desaturation to 85% may be as short as 23seconds in critically ill patients versus 502 seconds in a healthyadult.51

Mort52 studied ICU patients with blood gas measurementsbefore and after preoxygenation, using bag-valve-maskventilation. Average PaO2 was only 67 mm Hg at baseline andincreased to a mean of only 104 mm Hg after 4 minutes of bag-valve-mask ventilation. In less than 20% of patients didpreoxygenation increase the PaO2 by 50 mm Hg. The author’sconclusion was that preoxygenation is only marginally effectivein critically ill patients. It is important for clinicians toappreciate that PaO2 values in this range are on the steep sectionof the pulse oximetry curve (Figure 1).

Recommendation: Given the unique variables involved ineach ED tracheal intubation, it is impossible to predict theexact duration of safe apnea in a patient. Patients with highsaturation levels on room air or after oxygen administration
are at lower risk and may maintain adequate oxygen h

aturation as long as 8 minutes. Critically ill patients andhose with values just above the steep edge of theesaturation curve are at high risk of hypoxemia withrolonged tracheal intubation efforts and may desaturatemmediately.

AN APNEIC OXYGENATION EXTEND THEURATION OF SAFE APNEA?Alveoli will continue to take up oxygen even without

iaphragmatic movements or lung expansion. In an apneicatient, approximately 250 mL/minute of oxygen will moverom the alveoli into the bloodstream. Conversely, only 8 to 20L/minute of carbon dioxide moves into the alveoli during

pnea, with the remainder being buffered in the bloodstream.53

he difference in oxygen and carbon dioxide movement acrosshe alveolar membrane is due to the significant differences in gasolubility in the blood, as well as the affinity of hemoglobin forxygen. This causes the net pressure in the alveoli to becomelightly subatmospheric, generating a mass flow of gas fromharynx to alveoli. This phenomenon, called apneicxygenation, permits maintenance of oxygenation withoutpontaneous or administered ventilations. Under optimalircumstances, a PaO2 can be maintained at greater than 100m Hg for up to 100 minutes without a single breath, although

he lack of ventilation will eventually cause marked hypercapniand significant acidosis.54

Apneic oxygenation is not a new concept; it has beenescribed in the medical literature for more than a century, withames such as apneic diffusion oxygenation, diffusionespiration, and mass flow ventilation.55,56 A summary ofuman evidence for apneic oxygenation is available as aupplement to this article (Table E1, available online at http://ww.annemergmed.com).

Neurocritical care physicians and neurologists are familiarith the use of apneic oxygenation to prevent desaturationhile performing brain death examinations.63-65 Apneicxygenation has also been used to continue oxygenation duringronchoscopies and otolaryngeal procedures.66-68

Two studies merit specific mention because they extend theechnique to situations applicable to emergency trachealntubation. In a randomized controlled trial of anesthesiaatients, Taha et al69 demonstrated no desaturation during theourse of 6 minutes in patients receiving 5 L/minute of oxygenhrough a nasal catheter. Conversely, the control groupesaturated to the study cutoff of 95% in an average of 3.65inutes. Ramachandran et al70 performed a randomized

ontrolled trial of obese patients requiring tracheal intubationor elective surgery. The apneic oxygenation group received 5/minute of oxygen through nasal cannulas during their apneiceriod. The apneic oxygenation group had significantrolongation of the time spent with a SpO2 greater than orqual to 95% (5.29 versus 3.49 minutes), a significant increasen patients with SpO2 greater than or equal to 95% at the 6-

inute mark (8 patients versus 1 patient), and significantly
igher minimum SpO2 (94.3% versus 87.7%).

http://www.annemergmed.com

http://www.annemergmed.com

Lp

WMP

mtapos

aasppwabhii

peddtBHppepca

ma(acprse

chfr


Apneic oxygenation as described above will allow continuedoxygenation but will have no significant effect on carbondioxide levels. Although extracorporeal carbon dioxide removal,high oscillatory flow, or acid buffers can allow apneicventilation, as well as oxygenation, these therapies are outsidethe scope of current ED practice.

To provide apneic oxygenation during ED trachealintubations, the nasal cannula is the device of choice. Nasalcannulas provide limited FiO2 to a spontaneously breathingpatient,71 but the decreased oxygen demands of the apneic statewill allow this device to fill the pharynx with a high level ofFiO2 gas.70 By increasing the flow rate to 15 L/minute, near100% FiO2 can be obtained. Although providing high flowrates with a conventional, nonhumidified nasal cannula can beuncomfortable because of its desiccating effect on thenasopharynx, after the patient has been sedated it should causeno deleterious effects for the short interval of airwaymanagement. Tailor-made high-flow nasal cannulas are alsoavailable that will humidify the oxygen, allowing flow rates upto 40 L/minute.72

The patients’ mouths being open did not negatively affectthe FiO2 provided.73 If any potential obstruction caused byredundant nasal tissue is discovered, nasal trumpets will allow adirect conduit from the nasal cannula to the oropharynx.

Although facemasks and nonrebreather masks can providehigh FiO2 levels to spontaneously breathing patients (dependingon flow rates), they provide minimal oxygen to apneicpatients,74 likely because of the 2 exhalation valves venting thefresh gas flow. Bag-valve-mask devices provide no oxygen toapneic patients unless manual ventilations are delivered. Evenwith manual ventilations, a continuous flow of high-level FiO2

will not be available with this device.Conventional ventilators or noninvasive ventilation machines

do not supply a continuous flow of gas when placed onconventional or noninvasive settings. The minimal negativeinspiratory pressures generated during apneic oxygenation areinsufficient to trigger gas delivery with these machines.Although the high-flow CPAP setups found in many ICUs canprovide both positive pressure and high FiO2 levels for apneicoxygenation, they are not commonly available in EDs.

An additional benefit to the use of nasal cannula devices isthat they can be left on during the tracheal intubation attempts.This has been described with an acronym, NO DESAT (nasaloxygen during efforts securing a tube)75; it allows the continuedbenefits of apneic oxygenation while tracheal intubationtechniques are performed. The nasal cannula can be placedunder a facemask (or bag-valve-mask device) duringpreoxygenation, and then it remains on, administering oxygenthrough the nose throughout oral tracheal intubation withdirect or video laryngoscopy.

Recommendation: Apneic oxygenation can extend theduration of safe apnea when used after the administration of
sedatives and muscle relaxants. A nasal cannula set at 15 (

/minute is the most readily available and effective means ofroviding apneic oxygenation during ED tracheal intubations.

HEN AND HOW SHOULD WE PROVIDEANUAL VENTILATIONS DURING THE APNEIC

ERIOD?Practitioners should not initiate laryngoscopy before full

uscle relaxation to maximize laryngeal exposure and to avoidriggering the patient’s gag reflex and active vomiting just beforepnea. Ventilation provides 2 potential benefits during the onsethase of muscle relaxation: ventilation and increasedxygenation through alveolar distention and reduction inhunting.

The first benefit is minimal in most clinical scenarios. Onverage, PaCO2 increases 8 to 16 mm Hg in the first minute ofpnea and then approximately 3 mm Hg/minuteubsequently.53 It is rare that this degree of PaCO2 increase andH decrease will be clinically significant. An exception is arofound metabolic acidosis, such as severe salicylate toxicity, inhich patients compensate for the acidosis through hyperpnea

nd tachypnea. Aggressive ventilation is needed for such patientsecause cardiovascular collapse with cessation of self-ventilationas been reported.76 A second exception is in situations of

ncreased intracranial pressure, in which the carbon dioxidencrease can lead to cerebral vasodilation.

The second benefit, increased oxygenation, is crucial;atients starting with a pulse oximetry reading of less than orqual to 90% will not tolerate apnea for 60 seconds. Ventilationuring the onset phase of muscle relaxation can create alveolaristention and lengthen the duration of safe apnea duringracheal intubation efforts, assuming it is conducted carefully.ag-valve-mask device inspiratory pressures greater than 25 cm

2O can overwhelm the esophageal sphincter and put theatient at risk for regurgitation and aspiration.34,35 Whenroviders are inexperienced or under stress, this pressure is easilyxceeded.77 If ventilations during apnea are required, it may bereferable to use an automated device such as a handheld oronventional ventilator with built-in inspiratory pressure limitsnd PEEP.78,79

If a bag-valve-mask device is used during the onset ofuscular relaxation, a PEEP valve will provide sustained

lveolar distention. Ventilations should be delivered slowlyduring 1 to 2 seconds), involve a low volume (6 to 7 mL/kg),nd be administered at as low a rate as tolerable for the clinicalircumstances (6 to 8 breaths/min).80 Although not clinicallyroven, there may be a benefit to head elevation in reducing theisk of passive regurgitation in such patients, in addition to theignificant physiologic benefits of oxygenation in a head-levated position.

A significant risk of positive-pressure ventilation in theritically ill patient involves decreased venous return andypotension. This is especially significant in low flow statesrom any cause (hypotension), volume depletion, acuteespiratory distress syndrome, and obstructive airway disease
with attendant risks of intrinsic PEEP). Overventilation in such

vprme

mpmpkpea

DA

dppgssurs

smd

rs

R

ritTi

pi

bvtrr


patients may precipitate hemodynamic collapse, and cliniciansmust be mindful of rate, volume, and speed of ventilation inthese situations. Relative hypoventilation and resultantpermissive hypercapnia may be required to avoid hemodynamiccollapse.81

Recommendation: The risk/benefit of active ventilationduring the onset phase of muscle relaxants must be carefullyassessed in each patient. In patients at low risk for desaturation(�95% saturation), manual ventilation is not necessary. Inpatients at higher risk (91% to 95% saturation), a risk-benefitassessment should include an estimation of desaturation risk andthe presence of pulmonary pathology. In hypoxemic patients,low-pressure, low-volume, low-rate ventilations will be required.

WHAT POSITIONING AND MANEUVERSSHOULD THE PATIENT RECEIVE DURING THEAPNEIC PERIOD?

Apneic oxygenation requires a patent airway for oxygen toreach the hypopharynx and be entrained into the trachea; oncethe patient is sedated and paralyzed, it is imperative to keep theposterior pharyngeal structures and tongue from occluding thepassage of gas. Head elevation, chin lift, and jaw thrust willaccomplish this in most patients; a jaw thrust alone should beused if there is risk for cervical spine injury. In some patients, anasal trumpet or oral airway may also be required. Patients withsleep apnea or obesity often need a combination of jawdistraction, lifting of submandibular soft tissue, and nasal ororal airways.

Positioning the patient with their external auditory meatuson the same horizontal plane as their sternal notch maximizesupper airway dimensions and facilitates direct laryngoscopy.82,83

Head elevation relative to the thorax also permits optimal jawdistraction, and conversely atlanto-occipital extension pivots thebase of tongue and epiglottis against the posterior pharynx andpromotes obstruction. In all but the thinnest patients, a head-elevated position requires lifting of the head of the bedsomewhat, plus padding under the head and upper shoulders.The face plane of the patient should be parallel to the ceiling.For the superobese, this positioning requires a very large ramp.In cervical spine precautions, elevating the head relative to theneck is not possible, but as previously noted the foot of thestretcher should be tilted downward to improve pulmonaryfunction.

Cricoid pressure, considered an essential aspect of rapidsequence tracheal intubation when it was first conceived, hascome under increasing scrutiny within anesthesia andemergency medicine.84,85 Theoretically, the application of firmpressure to the cricoid cartilage compresses the esophagus whilekeeping the trachea patent, but in practice this is not always thecase.86 Computed tomography and magnetic resonance imagingscanning have shown that cricoid pressure causes lateraldisplacement of the esophagus in more than 90% of patientsand laryngeal/tracheal compression in 80%.87,88 Numerous
ventilation studies have found that cricoid pressure hinders bag- h

alve-mask device ventilation, increases peak inspiratoryressure, and reduces tidal volumes.34,84,89-94 For the sameeasons that the airway obstruction induced by cricoid pressureay preclude effective manual ventilation, it may limit the

ffectiveness of apneic oxygenation as well.

Recommendation: Patients should be positioned toaximize upper airway patency before and during the apneic

eriod, using ear-to–sternal notch positioning. Nasal airwaysay be needed to create a patent upper airway. Once the apneic

eriod begins, the posterior pharyngeal structures should beept from collapsing backwards by using a jaw thrust. Cricoidressure may negatively affect apneic oxygenation, but studiesxamining this question in the setting of modern emergencyirway management do not exist to our knowledge.

OES THE CHOICE OF PARALYTIC AGENTFFECT PREOXYGENATION?

The choice of paralytic agent may influence the time toesaturation during airway management. In a study of operativeatients, the time to desaturation to 95% was 242 seconds inatients receiving succinylcholine versus 378 seconds in a groupiven rocuronium.95 Similarly, in obese patients undergoingurgery, the succinylcholine group desaturated to 92% in 283econds versus 329 seconds in the rocuronium group.96 Whensed at a dose of greater than or equal to 1.2 mg/kg,ocuronium provides intubating conditions identical to those ofuccinylcholine.97

It is hypothesized that the fasciculations induced byuccinylcholine may cause increased oxygen use. Pretreatmentedications to prevent fasciculations minimize the difference in

esaturation times.95

Recommendation: In patients at high risk of desaturation,ocuronium may provide a longer duration of safe apnea thanuccinylcholine.

ISK STRATIFICATION AND CONCLUSIONSPatients requiring emergency airway management can be

isk stratified into 3 groups, according to pulse oximetry afternitial application of high-flow oxygen. The recommendedechniques to use for patients in each group are shown inable 2, and a logistic flow of preoxygenation steps is shown

n Figure 3.Head-elevated positioning is simple and easy to apply in all

atients; in the patient immobilized for cervical spine injury, its beneficial to tilt the foot of the bed downward.

Patients at lowest risk (saturations of 96% to 100%) shoulde properly positioned and receive preoxygenation; activeentilation is not needed. Passive apneic oxygenation duringracheal intubation efforts may not be necessary in these low-isk patients, but it will extend safe apnea in the event ofepeated tracheal intubation attempts.

Patients in the 91% to 95% saturation group after receiving
igh FiO2 levels are at high risk of critical desaturation during

rc

(


emergency tracheal intubation. Positioning, preoxygenation,and passive oxygenation should be used. For these patients,consideration should be given to using PEEP duringpreoxygenation and while awaiting muscle relaxation, but the

Table 2. Risk categorization of patients during preoxygenation.*

Risk Category, Basedon Pulse OximetryWhile Receiving High-Flow Oxygen

Preoxygenation Period(3 Minutes)

Low risk, SpO2

96%–100%Nonrebreather mask with

maximal oxygen flow rateNo

High risk, SpO2

91%–95%Nonrebreather mask or CPAP or

bag-valve-mask device withPEEP

No

Hypoxemic, SpO2

90% or lessCPAP or bag-valve-mask device

with PEEPCP

*Risk categories are based on patient’s initial response to high-flow oxygen thexhibit shunt physiology and are prone to rapid desaturation during the peri-inpice of the steep portion of the oxyhemoglobin dissociation curve and shouldare at low risk for peri-intubation desaturation. Patients in all risk categories sburg if there is a risk of spine injury).

Figure 3. Logistic flow of preoxygenatio


isks and benefits of these techniques must be assessed case byase.

For patients initially hypoxemic with high FiO2 levelssaturation of 90% or less), aggressive efforts must be made to

set of Muscle Relaxation(�60 Seconds)

Apneic Period During TrachealIntubation (VariableDuration, Depending onAirway Difficulty; Ideally<30 Seconds)

reather mask and nasaln at 15 L/min

Nasal oxygen at 15 L/min

reather mask, CPAP, or bag--mask device with PEEP andl oxygen at 15 L/min


r bag-valve-mask device withand nasal oxygen at 15 L/


a tightly fitting nonrebreather mask. Patients who are already hypoxemicon. Patients with saturations of 91% to 95% have values close to the preci-nsidered high risk. Patients with saturations greater than or equal to 96%receive preoxygenation in a head-elevated position (or reverse-Trendelen-

On

nreboxyge

nrebvalvenasa

AP oPEEPmin

roughtubatibe cohould

n and prevention of desaturation.


1

1

1

1

1

1

2

2

2

2

2

2

2

2

2

2

3

3

3

3


maximize saturation before tracheal intubation. These patientswill require PEEP during preoxygenation, ventilation during theonset of phase of muscle relaxants, and passive oxygenationduring tracheal intubation.

Videos of the techniques described in this article can befound at http://emcrit.org/preoxygenation.

Supervising editors: Gregory W. Hendey, MD; Donald M. Yealy,MD

Funding and support: By Annals policy, all authors are requiredto disclose any and all commercial, financial, and otherrelationships in any way related to the subject of this articleas per ICMJE conflict of interest guidelines (seewww.icmje.org). The authors have stated that no suchrelationships exist.

Publication dates: Received for publication June 25, 2011.Revisions received July 20, 2011; September 4, 2011; andSeptember 28, 2011. Accepted for publication October 4,2011.

Address for correspondence: Richard M. Levitan, MD, [email protected].

REFERENCES1. Mort TC. The incidence and risk factors for cardiac arrest during

emergency tracheal intubation: a justification for incorporating theASA guidelines in the remote location. J Clin Anesth. 2004;16:508-516.

2. Davis DP, Hwang JQ, Dunford JV. Rate of decline in oxygensaturation at various pulse oximetry values with prehospital rapidsequence intubation. Prehosp Emerg Care. 2008;12:46-51.

3. Lumb AB. Nunn’s Applied Respiratory Physiology. 7th ed. Oxford:Churchill Livingstone; 2010:568.

4. Morton HJ, Wylie WD. Anaesthetic deaths due to regurgitation orvomiting. Anaesthesia. 1951;6:190-201.

5. Heller ML, Watson TR Jr. Polarographic study of arterialoxygenation during apnea in man. N Engl J Med. 1961;264:326-330.

6. Heller ML, Watson TR Jr, Imredy DS. Apneic oxygenation in man:polarographic arterial oxygen tension study. Anesthesiology.1964;25:25-30.

7. Campbell IT, Beatty PC. Monitoring preoxygenation. Br J Anaesth.1994;72:3-4.

8. Baraka A, Ramez Salem M. Preoxygenation. In: Hagberg CA, ed.Benumof’s Airway Management: Principles and Practice. 2nd ed.Philadelphia, PA: Mosby; 2007:303-318.

9. Vender JS, Szokol JW. Oxygen delivery systems, inhalationtherapy, and respiratory therapy. In: Hagberg CA, ed. Benumof’sAirway Management: Principles and Practice. 2nd ed.Philadelphia, PA: Mosby; 2007:321-345.

10. Earl JW. Delivery of high FiO2. Available at: http://www.rcjournal.com/abstracts/2003/?id�OF-03-257. AccessedApril 11, 2011.

11. Nimmagadda U, Salem MR, Joseph NJ, et al. Efficacy ofpreoxygenation with tidal volume breathing. Comparison ofbreathing systems. Anesthesiology. 2000;93:693-698.

12. Mills PJ, Baptiste J, Preston J, et al. Manual resuscitators andspontaneous ventilation—an evaluation. Crit Care Med. 1991;19:1425-1431.

13. Joffe AM, Hetzel S, Liew EC. Anesthesiology. 2010;113:873-879.


4. Bhatia PK, Bhandari SC, Tulsiani KL, et al. End-tidal oxygraphyand safe duration of apnoea in young adults and elderly patients.Anaesthesia. 1997;52:175-178.

5. Hamilton WK, Eastwood DW. A study of denitrogenation withsome inhalation anesthetic systems. Anesthesiology. 1955;16:861-867.

6. Baraka AS, Taha SK, Aouad MT, et al. Preoxygenation:comparison of maximal breathing and tidal volume breathingtechniques. Anesthesiology. 1999;91:612-616.

7. Baraka AS, Taha SK, El-Khatib MF, et al. Oxygenation using tidalvolume breathing after maximal exhalation. Anesth Analg. 2003;97:1533-1535.

8. Baraka A, Haroun-Bizri S, Khoury S, et al. Single vital capacitybreath for preoxygenation. Can J Anaesth. 2000;47:1144-1146.

9. Pandit JJ, Duncan T, Robbins PA. Total oxygen uptake with twomaximal breathing techniques and the tidal volume breathingtechnique: a physiologic study of preoxygenation. Anesthesiology.2003;99:841-846.

0. Rapaport S, Joannes-Boyau O, Bazin R, et al. [Comparison ofeight deep breaths and tidal volume breathing preoxygenationtechniques in morbid obese patients]. Ann Fr Anesth Reanim.2004;23:1155-1159.

1. Benumof JL. Preoxygenation: best method for both efficacy andefficiency. Anesthesiology. 1999;91:603-605.

2. El-Khatib MF, Kanazi G, Baraka AS. Noninvasive bilevel positiveairway pressure for preoxygenation of the critically ill morbidlyobese patient. Can J Anaesth. 2007;54:744-747.

3. Baillard C, Fosse JP, Sebbane M, et al. Noninvasive ventilationimproves preoxygenation before intubation of hypoxic patients.Am J Respir Crit Care Med. 2006;174:171-177.

4. Nunn JF. Applied Respiratory Physiology. 4th ed. Oxford, England:Butterworth-Heinemann; 1995:156–197.

5. Delay JM, Sebbane M, Jung B, et al. The effectiveness ofnoninvasive positive pressure ventilation to enhancepreoxygenation in morbidly obese patients: a randomizedcontrolled study. Anesth Analg. 2008;107:1707-1713.

6. Futier E, Constantin JM, Pelosi P, et al. Noninvasive ventilationand alveolar recruitment maneuver improve respiratory functionduring and after intubation of morbidly obese patients: arandomized controlled study. Anesthesiology. 2011;114:1354-1363.

7. Cressey DM, Berthoud MC, Reilly CS. Effectiveness of continuouspositive airway pressure to enhance pre-oxygenation in morbidlyobese women. Anaesthesia. 2001;56:680-684.

8. Gander S, Frascarolo P, Suter M, et al. Positive end-expiratorypressure during induction of general anesthesia increasesduration of nonhypoxic apnea in morbidly obese patients. AnesthAnalg. 2005;100:580-584.

9. Herriger A, Frascarolo P, Spahn DR, et al. The effect of positiveairway pressure during pre-oxygenation and induction ofanaesthesia upon duration of non-hypoxic apnoea. Anaesthesia.2004;59:243-247.

0. Antonelli M, Conti G, Rocco M, et al. Noninvasive positive-pressure ventilation versus conventional oxygen supplementationin hypoxemic patients undergoing diagnostic bronchoscopy.Chest. 2002;121:1149-1154.

1. Jaber S, Jung B, Corne P, et al. An intervention to decreasecomplications related to endotracheal intubation in the intensivecare unit: a prospective, multiple-center study. Intensive CareMed. 2010;36:248-255.

2. Vyas H, Milner AD, Hopkin IE. Face mask resuscitation: does itlead to gastric distension? Arch Dis Child. 1983;58:373-375.

3. Ho-Tai LM, Devitt JH, Noel AG, et al. Gas leak and gastricinsufflation during controlled ventilation: face mask versus
laryngeal mask airway. Can J Anaesth. 1998;45:206-211.

http://emcrit.org/preoxygenation

http://www.icmje.org

mailto:[email protected]

http://www.rcjournal.com/abstracts/2003/?id=OF-03-257

http://www.rcjournal.com/abstracts/2003/?id=OF-03-257

5

5

5

5

5

6

6

6

6

6

6

6

6

6

6

7

7

7

7

7

7

7


34. Lawes EG, Campbell I, Mercer D. Inflation pressure, gastricinsufflation and rapid sequence induction. Br J Anaesth. 1987;59:315-318.

35. Ruben H, Knudsen EJ, Carugati G. Gastric inflation in relation toairway pressure. Acta Anaesthesiol Scand. 1961;5:107-114.

36. Jellinek H, Krafft P, Fitzgerald RD, et al. Right atrial pressurepredicts hemodynamic response to apneic positive airwaypressure. Crit Care Med. 2000;28:672-678.

37. Tanoubi I, Drolet P, Donati F. Optimizing preoxygenation in adults.Can J Anaesth. 2009;56:449-466.

38. Leman P, Greene S, Whelan K, et al. Simple lightweightdisposable continuous positive airways pressure mask toeffectively treat acute pulmonary oedema: randomized controlledtrial. Emerg Med Australas. 2005;17:224-230.

39. Engstrom J, Hedenstierna G, Larsson A. Pharyngeal oxygenadministration increases the time to serious desaturation atintubation in acute lung injury: an experimental study. Crit Care.2010;14:R93.

40. Neumann P, Berglund JE, Fernandez Mondejar E, et al. Dynamicsof lung collapse and recruitment during prolonged breathing inporcine lung injury. J Appl Physiol. 1998;85:1533-1543.

41. Rothen HU, Sporre B, Engberg G, et al. Prevention of atelectasisduring general anaesthesia. Lancet. 1995;345:1387-1391.

42. Lane S, Saunders D, Schofield A, et al. A prospective,randomised controlled trial comparing the efficacy of pre-oxygenation in the 20 degrees head-up vs supine position.Anaesthesia. 2005;60:1064-1067.

43. Ramkumar V, Umesh G, Philip FA. Preoxygenation with 20° head-up tilt provides longer duration of non-hypoxic apnea thanconventional preoxygenation in non-obese healthy adults. JAnesth. 2011;25:189-194.

44. Altermatt FR, Munoz HR, Delfino AE, et al. Pre-oxygenation in theobese patient: effects of position on tolerance to apnoea. Br JAnaesth. 2005;95:706-709.

45. Dixon BJ, Dixon JB, Carden JR, et al. Preoxygenation is moreeffective in the 25 degrees head-up position than in the supineposition in severely obese patients: a randomized controlledstudy. Anesthesiology. 2005;102:1110-1115; discussion 1115A.

46. Boyce JR, Ness T, Castroman P, et al. A preliminary study of theoptimal anesthesia positioning for the morbidly obese patient.Obes Surg. 2003;13:4-9.

47. Lee BJ, Kang JM, Kim DO. Laryngeal exposure duringlaryngoscopy is better in the 25 degrees back-up position than inthe supine position. Br J Anaesth. 2007;99:581-586.

48. Benumof JL, Dagg R, Benumof R. Critical hemoglobindesaturation will occur before return to an unparalyzed statefollowing 1 mg/kg intravenous succinylcholine. Anesthesiology.1997;87:979-982.

49. Ding ZN, Shibata K, Yamamoto K, et al. Decreased circulationtime in the upper limb reduces the lag time of the finger pulseoximeter response. Can J Anaesth. 1992;39:87-89.

50. Drummond GB, Park GR. Arterial oxygen saturation beforeintubation of the trachea. An assessment of oxygenationtechniques. Br J Anaesth. 1984;56:987-993.

51. Farmery AD, Roe PG. A model to describe the rate ofoxyhaemoglobin desaturation during apnoea. Br J Anaesth. 1996;76:284-291.

52. Mort TC. Preoxygenation in critically ill patients requiringemergency tracheal intubation. Crit Care Med. 2005;33:2672-2675.

53. Eger EI, Severinghaus JW. The rate of rise of PaCO2 in the apneicanesthetized patient. Anesthesiology. 1961;22:419-425.

54. Nielsen ND, Kjaergaard B, Koefoed-Nielsen J, et al. Apneic
oxygenation combined with extracorporeal arteriovenous carbon

dioxide removal provides sufficient gas exchange in experimentallung injury. ASAIO J. 2008;54:401-405.

5. Hirsch H. Uber kunstliche Atmung durch Ventilation der Trachea[dissertation]. Giessen; 1905.

6. Volhard F. Uber kunstliche Atmung durch Ventilation der Tracheaund eine einfache Vorrichtung zur hytmischen kunstlichenAtmung. Munch med NVochensch. 1908:209-211.

7. Comroe JH Jr, Dripps RD. Artificial respiration. JAMA. 1946;130:381-383.

8. Enghoff H, Holmdahl MH, Risholm L. Oxygen uptake in humanlungs without spontaneous or artificial pulmonary ventilation. ActaChir Scand. 1952;103:293-301.

9. Holmdahl MH. Pulmonary uptake of oxygen, acid-basemetabolism, and circulation during prolonged apnoea. Acta ChirScand Suppl. 1956;212:1-128.

0. Frumin MJ, Epstein RM, Cohen G. Apneic oxygenation in man.Anesthesiology. 1959;20:789-798.

1. Babinski MF, Sierra OG, Smith RB, et al. Clinical application ofcontinuous flow apneic ventilation. Acta Anaesthesiol Scand.1985;29:750-752.

2. Teller LE, Alexander CM, Frumin MJ, et al. Pharyngeal insufflationof oxygen prevents arterial desaturation during apnea.Anesthesiology. 1988;69:980-982.

3. al Jumah M, McLean DR, al Rajeh S, et al. Bulk diffusion apneatest in the diagnosis of brain death. Crit Care Med. 1992;20:1564-1567.

4. Marks SJ, Zisfein J. Apneic oxygenation in apnea tests for braindeath. A controlled trial. Arch Neurol. 1990;47:1066-1068.

5. Perel A, Berger M, Cotev S. The use of continuous flow of oxygenand PEEP during apnea in the diagnosis of brain death. IntensiveCare Med. 1983;9:25-27.

6. Barth L. [Therapeutic use of diffusion breathing in bronchoscopy].Anaesthesist. 1954;3:227-229.

7. Payne JP. Apnoeic oxygenation in anaesthetised man. ActaAnaesthesiol Scand. 1962;6:129-142.

8. Lee SC. Improvement of gas exchange by apneic oxygenation withnasal prong during fiberoptic intubation in fully relaxed patients. JKorean Med Sci. 1998;13:582-586.

9. Taha SK, Siddik-Sayyid SM, El-Khatib MF, et al. Nasopharyngealoxygen insufflation following pre-oxygenation using the four deepbreath technique. Anaesthesia. 2006;61:427-430.

0. Ramachandran SK, Cosnowski A, Shanks A, et al. Apneicoxygenation during prolonged laryngoscopy in obese patients: arandomized, controlled trial of nasal oxygen administration. J ClinAnesth. 2010;22:164-168.

1. Kory RC, Bergmann JC, Sweet RD, et al. Comparative evaluationof oxygen therapy techniques. JAMA. 1962;179:767-772.

2. Waugh JB, Granger WM. An evaluation of 2 new devices for nasalhigh-flow gas therapy. Respir Care. 2004;49:902-906.

3. Wettstein RB, Shelledy DC, Peters JI. Delivered oxygenconcentrations using low-flow and high-flow nasal cannulas.Respir Care. 2005;50:604-609.

4. Tiep B, Barnett M. High flow nasal vs high flow mask oxygendelivery: tracheal gas concentrations through a head extensionairway model. In: Respiratory Care 2002 Open Forum 2002;October 5-8, 2002; Tampa, FL.

5. Levitan RM. NO DESAT! Nasal oxygen during efforts securing atube. Emergency Physicians Monthly. December 9, 2010.Available at: http://www.epmonthly.com/features/current-features/no-desat-/. Accessed October 22, 2011.

6. Stolbach AI, Hoffman RS, Nelson LS. Mechanical ventilation wasassociated with acidemia in a case series of salicylate-poisoned
patients. Acad Emerg Med. 2008;15:866-869.

http://www.epmonthly.com/features/current-features/no-desat-/

http://www.epmonthly.com/features/current-features/no-desat-/

8

8

8

9

9

9

9

9

9

9

9


77. Aufderheide TP, Lurie KG. Death by hyperventilation: a commonand life-threatening problem during cardiopulmonary resuscitation.Crit Care Med. 2004;32:S345-351.

78. von Goedecke A, Voelckel WG, Wenzel V, et al. Mechanicalversus manual ventilation via a face mask during the induction ofanesthesia: a prospective, randomized, crossover study. AnesthAnalg. 2004;98:260-263.

79. von Goedecke A, Wenzel V, Hormann C, et al. Effects of facemask ventilation in apneic patients with a resuscitationventilator in comparison with a bag-valve-mask. J Emerg Med.2006;30:63-67.

80. von Goedecke A, Wagner-Berger HG, Stadlbauer KH, et al. Effectsof decreasing peak flow rate on stomach inflation during bag-valve-mask ventilation. Resuscitation. 2004;63:131-136.

81. Oddo M, Feihl F, Schaller MD, et al. Management of mechanicalventilation in acute severe asthma: practical aspects. IntensiveCare Med. 2006;32:501-510.

82. Collins JS, Lemmens HJ, Brodsky JB, et al. Laryngoscopy andmorbid obesity: a comparison of the “sniff” and “ramped”positions. Obes Surg. 2004;14:1171-1175.

83. Levitan RM, Mechem CC, Ochroch EA, et al. Head-elevatedlaryngoscopy position: improving laryngeal exposure duringlaryngoscopy by increasing head elevation. Ann Emerg Med.2003;41:322-330.

84. Ellis DY, Harris T, Zideman D. Cricoid pressure in emergencydepartment rapid sequence tracheal intubations: a risk-benefitanalysis. Ann Emerg Med. 2007;50:653-665.

85. Brimacombe JR, Berry AM. Cricoid pressure. Can J Anaesth.1997;44:414-425.

86. Petito SP, Russell WJ. The prevention of gastric inflation—aneglected benefit of cricoid pressure. Anaesth Intensive Care.
1988;16:139-143.

7. Smith KJ, Dobranowski J, Yip G, et al. Cricoid pressure displacesthe esophagus: an observational study using magnetic resonanceimaging. Anesthesiology. 2003;99:60-64.

8. Smith KJ, Ladak S, Choi PT, et al. The cricoid cartilage and theesophagus are not aligned in close to half of adult patients. CanJ Anaesth. 2002;49:503-507.

9. Allman KG. The effect of cricoid pressure application on airwaypatency. J Clin Anesth. 1995;7:197-199.

0. Hartsilver EL, Vanner RG. Airway obstruction with cricoidpressure. Anaesthesia. 2000;55:208-211.

1. Hocking G, Roberts FL, Thew ME. Airway obstruction with cricoidpressure and lateral tilt. Anaesthesia. 2001;56:825-828.

2. Saghaei M, Masoodifar M. The pressor response and airwayeffects of cricoid pressure during induction of general anesthesia.Anesth Analg. 2001;93:787-790.

3. Mac GPJH, Ball DR. The effect of cricoid pressure on the cricoidcartilage and vocal cords: an endoscopic study in anaesthetisedpatients. Anaesthesia. 2000;55:263-268.

4. Palmer JH, Yentis SM. Cricoid pressure application to awakevolunteers: discomfort cannot be used to indicate appropriateforce. Can J Anaesth. 2005;52:114-115.

5. Taha SK, El-Khatib MF, Baraka AS, et al. Effect ofsuxamethonium vs rocuronium on onset of oxygen desaturationduring apnoea following rapid sequence induction. Anaesthesia.2010;65:358-361.

6. Tang L, Li S, Huang S, et al. Desaturation following rapidsequence induction using succinylcholine versus rocuronium inoverweight patients. Acta Anaesthesiol Scand. 2011;55:203-208.

7. Perry JJ, Lee JS, Sillberg VA, et al. Rocuronium versussuccinylcholine for rapid sequence induction intubation. Cochrane
Database Syst Rev. 2008;(2):CD002788.


Table E1. Evidence for apneic oxygenation to extend the duratio

Study Patients Interventio

Comroe et al57 Obs trial of 2 patientswith neurologicinjuries

Endotracheal insufof 6–11 L/min ooxygen

Enghoff et al58 Obs study of 7operative patients

Tubing placed dowtube connectedFiO2

Holmdahl59 Documentation ofseparate Obsstudies

Endotracheal insufof 100% FiO2

Frumin et al60 Obs study of 8operative patients

Intubated, adminis100% FiO2 and lapneic

Babinski et al61 Obs study of 5operative patients

Two endobronchialcatheters placed

Teller et al62 RCT, blinded,crossover trial of 12pts

Nasopharyngeal caattached to 100at 3 L/min

Taha et al69 RCT of 30 pts Nasal catheters atto 5L/min of 10

Ramachandran et al70 RCT of 30 obese,operative patients

Nasal cannula atta5 L/min 100% F

Obs, Observational trial.

n of safe apnea.

n Comparator Outcome

flationf

None Observation of long duration tillSaO2 �90% in numerousseparate experiments

n ETto 100%

None No decrease in ABG PaO2 for 5–7min

flation None Extended time until desaturationin separate studies

teredeft

None No desaturation for between 18and 55 min. Patients hadmarked hypercapnia andcommensurate decreased pH.

None 30 min of apnea withoutsignificant desaturation

theters% FiO2

Nasopharyngeal cathetersattached to room air

Outcome was a sat of �92% or10 min. None of the patients inthe insufflation armdesaturated below 98% duringthe 10 min.

tached0% FiO2

Room air No desaturation during the courseof the 6-min predeterminedstopping point in patientsreceiving apneic oxygenation.The control group desaturatedto the study cutoff of 95% in anaverage of 3.65 min.

ched toiO2

Room air The apneic oxygenation group hadsignificant prolongation of SpO2

�95% time (5.29 versus 3.49min), a significant increase inpatients with SpO2 �95% atthe 6-min mark (8 patientsversus 1 patient), andsignificantly higher minimumSpO2 (94.3% versus 87.7%).

11.e1 Annals of Emergency Medicine Volume xx, . x : Month

preoxygenation and prevention of desaturation during ... · pdf fileairway/review article...

Documents