airway management of the critically ill patient: rapid ...airway management of the critically ill...
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DOI 10.1378/chest.127.4.1397 2005;127;1397-1412 Chest
Stuart F. Reynolds and John Heffner
Patient: Rapid-Sequence IntubationAirway Management of the Critically Ill
http://chestjournal.org/cgi/content/abstract/127/4/1397and services can be found online on the World Wide Web at: The online version of this article, along with updated information
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2007Physicians. It has been published monthly since 1935. Copyright CHEST is the official journal of the American College of Chest
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Airway Management of the Critically IllPatient*Rapid-Sequence Intubation
Stuart F. Reynolds, MD; and John Heffner, MD, FCCP
Advances in emergency airway management have allowed intensivists to use intubation tech-niques that were once the province of anesthesiology and were confined to the operating room.Appropriate rapid-sequence intubation (RSI) with the use of neuromuscular blocking agents,induction drugs, and adjunctive medications in a standardized approach improves clinicaloutcomes for select patients who require intubation. However, many physicians who work in theICU have insufficient experience with these techniques to adopt them for routine use. Thepurpose of this article is to review airway management in the critically ill adult with an emphasison airway assessment, algorithmic approaches, and RSI. (CHEST 2005; 127:1397–1412)
Key words: airway management; ICU; induction agents; intensivist; intubation; neuromuscular blocking agents;rapid-sequence intubation; respiratory failure
Abbreviations: NMBA � neuromuscular blocking agent; RSI � rapid-sequence intubation; V̇o2 � oxygen uptake
T he ability to place a secure airway in a variety ofpatients and clinical circumstances represents an
obligatory skill for critical care physicians. In theICU, these skills are regularly tested by the suscep-tibility of critically ill patients to hypoxic injury whenemergency intubation is required. These patientstypically have varying degrees of acute hypoxemia,acidosis, and hemodynamic instability when intuba-tion is required, and tolerate poorly any delays inestablishing an airway.1 Associated conditions, suchas intracranial hypertension, myocardial ischemia,upper airway bleeding, or emesis can be aggravatedby the intubation attempt itself. And many criticallyill patients, especially elderly patients, have a highfrequency of comorbid conditions and underlying
vascular disease that may further increase the risk formyocardial or cerebral ischemia when intubationattempts are prolonged.2
Unfortunately, multiple factors complicate rapidstabilization of the airway for critically ill patients inthe ICU. Patients who require emergency intubationfrequently become combative during intubation at-tempts. Conditions that complicate assisted ventila-tion and airway intubation, such as supraglotticedema, may go undetected before airway placementattempts. Also, critical care physicians cannot alwayscount on having the most highly skilled members ofthe nursing and respiratory therapy staff on duty toassist with difficult intubations.
All of these factors warrant the standardization ofthe approaches used for emergency intubation in theICU to ensure proper airway placement. Emergencymedicine physicians have adopted algorithmic ap-proaches for airway assessment and for rapid-sequence intubation (RSI) as the primary approachfor emergency airway management.3,4 RSI is thenearly simultaneous administration of a potent in-duction agent with a paralyzing dose of a neuromus-cular blocking agent (NMBA). When applied byskilled operators for appropriately selected patients,RSI increases the success rate of intubation to 98%
*From the Medical-Surgical Intensive Care Unit (Dr. Reynolds),University Health Network and Mount Sinai Hospital, Toronto,ON, Canada; and the Division of Pulmonary and Critical CareMedicine, Allergy, and Clinical Immunology (Dr. Heffner),Medical University of South Carolina, Charleston, SC.Manuscript received April 14, 2004; revision accepted August 31,2004.Reproduction of this article is prohibited without written permis-sion from the American College of Chest Physicians (e-mail:[email protected]).Correspondence to: John Heffner, MD, FCCP, Medical Univer-sity of South Carolina, 169 Ashley Ave, PO Box 250332, Charles-ton, SC 29425; e-mail: [email protected]
critical care review
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while reducing complications.4–15 Moreover, adjunc-tive medications incorporated into the RSI algorithmreduce the physiologic pressor response to endotra-cheal intubation, which can induce cardiovascularcomplications. The present review outlines thesestandardized approaches for airway assessment andRSI with the intent of widening the use of thesetechniques in the ICU setting.
Airway Assessment
The American Society of Anesthesiology defines adifficult airway by the existence of clinical factorsthat complicate either ventilation administered byface mask or intubation performed by experiencedand skilled clinicians. Difficult ventilation has beendefined as the inability of a trained anesthetist tomaintain the oxygen saturation � 90% using a facemask for ventilation and 100% inspired oxygen,provided that the preventilation oxygen saturationlevel was within the normal range.16 Difficult intu-bation has been defined by the need for more thanthree intubation attempts or attempts at intubationthat last � 10 min.16 This latter definition provides amargin of safety for preoxygenated patients who areundergoing elective intubation in the operatingroom. Such patients in stable circumstances canusually tolerate 10 min of attempted intubationwithout adverse sequelae. Critically ill patients withpreexisting hypoxia and poor cardiopulmonary re-serve, however, may experience adverse events aftershorter periods of lack of response to ventilation orintubation.1,2,17 Schwartz and coworkers1 reportedthat 3% of hospitalized critically ill patients die
within 30 min of emergency intubation, and as manyas 8% of intubation attempts result in an esophagealplacement. Li and coworkers7 have demonstratedthat complications occur in up to 78% of patientsrequiring emergency intubation. The incidence ofesophageal intubation and aspiration ranged from 8to 18%, and 4 to15%, respectively.1,7 Identificationof the difficult airway before initiating intubationattempts, therefore, has heightened importance inthe ICU.
Examination of the airway to predict difficultieswith face mask ventilation and intubation is anessential component of the preoperative assessmentof patients who are scheduled for elective surgery.Multiple approaches exist to identify patients with adifficult airway. Unfortunately, the utility of theseairway assessment methods has not been adequatelyevaluated in critically ill patients who undergo urgentintubation. Moreover, a recent retrospective analysisby Levitan and coworkers18 has indicated that per-forming a thorough airway assessment of a criticallyill patient in the emergency department is often notfeasible in 70% of patients. Nevertheless, intensivistswho are skilled in intubation should have an under-standing of these techniques to allow their applica-tion when it is practical to do so.
Assessment for Difficult Ventilation
Both anatomic and functional factors can interferewith the use of a face mask for ventilation. Anatomicfactors include abnormalities of the face, upperairway, lower airway, and thoracoabdominal compli-ance (Table 1). Obesity represents an important
Table 1—Anatomic Factors Associated With Difficult Ventilation*
Anatomic Location Airway Issue Intervention
Face Facial wasting; facial hair;edentulous snoring history
Patient positioning: sniffing position, and/or jaw thrust; ensure proper fitof mask to face; variety of different mask sizes; oropharyngeal andnasopharyngeal airways; team ventilation, with one person “bagging”while the other person ensures a proper seal; leave the dentures inwhile ventilating the patient
Upper airway Abscess; hematoma;neoplasm; epiglottitis
Assist ventilation and avoid neuromuscular paralysis; awake intubation,possible fiberoptic with double set up for cricothyrotomy; call for helpif an upper airway obstruction is suspected
Lower airway Reactive airways Preinduction administration of bronchodilators, nitrates, and diureticsAirspace disease
PneumoniaARDSPulmonary edemaHemo/pneumothorax
PEEP valve for oxygenation in pulmonary edema, ARDS, and pneumonia;decompress a pneumothorax if you are going to apply positive pressureventilation
Thorax-abdomen Ascites; obesity;hemoperitoneum;abdominal compartmentsyndrome
Use of a bag-valve-mask with a PEEP valve may help oxygenation andventilation
*PEEP � positive end-expiratory pressure.
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anatomic barrier to successful face-mask ventila-tion.19 Obese patients experience an increased risk ofarterial oxygen desaturation due to difficulties withface mask ventilation and intubation because ofredundant oral tissue, decreased respiratory systemcompliance due to chest and diaphragmatic restric-tion, and cephalomegaly, which interferes withproper face-mask placement.20
Altered mental status with loss of airway tone isthe most common functional hindrance to assistedventilation.21 Critical illness and medications com-monly used in the ICU, such as sedatives, NMBAs,and opioids, produce increased upper airway resis-tance by relaxing the muscles of the soft palate.22,23
Because the soft palate rather than the tongue is thesite of obstruction, ventilation is assisted by a jawthrust or head tilt, the placement of either a naso-pharyngeal or oropharyngeal airway, and the appli-cation of positive-pressure assisted ventilation. Con-versely, inadequate sedation, saliva levels, andoropharyngeal instrumentation can precipitate laryn-gospasm, which can result in an obstructed airway.This involuntary spasm of the laryngeal musculaturemay be ablated with positive-pressure ventilation,suctioning of secretions, cessation of airway manip-ulation, and jaw thrust. Severe instances may requireneuromuscular blockade.
Assessment for Difficult Intubation
Multiple methods exist to identify patients who areat risk for difficult intubations in the operating room.Unfortunately, no studies have assessed their utilityfor patients in the ICU.
The Mallampati classification system,24 as modi-fied by Samsoon and Young,25 is a widely utilizedapproach for evaluating patients in the preoperativesetting. This system predicts the degree of antici-pated difficulty with laryngoscopy on the basis of the
ability to visualize posterior pharyngeal structures(Fig 1). The Mallampati class is devised by havingpatients sit up, open their mouth, and pose in the“sniffing position” (ie, neck flexed with atlantoaxialextension) with the tongue voluntarily protrudedmaximally while the physician observes posteriorpharyngeal structures. A tongue blade is not used. AMallampati class of I or II predicts a relatively easylaryngoscopy. A Mallampati class � II indicates anincreased probability of a difficult intubation and theneed for specialized intubation techniques.
The Mallampati system has an application in theICU, however, for the evaluation of mentally alertpatients who require elective intubation for proce-dures. Critically ill patients with altered mentalstatus or acute respiratory failure are unlikely tocooperate with the procedure. In approaching suchpatients, the evaluation of the oropharyngeal cavitywith a tongue blade or laryngoscope allows theintensivist who is familiar with the Mallampati sys-tem to assess the patient to some degree for adifficult intubation and also provides an opportunityto detect any obvious signs of upper airway obstruc-tion.26
Other factors that predict a difficult intubationinclude a mouth opening � 3 cm (ie, two fingertips),a cervical range of motion of � 35° of atlantooccipi-tal extension, a thyromental distance of � 7 cm (ie,three finger breadths), large incisor length, a short,thick neck, poor mandibular translation, and a nar-row palate (ie, three finger breadths).27–31 Modelsdeveloped by multivariate analysis have incorporatedmultiple clinical factors to derive highly accuratepredictive models (sensitivity, 86.8%; specificity,96.0%) for identifying difficult intubations amongpatients who are undergoing elective intubations inthe operating room.32 Because the incidences ofboth difficult laryngoscopy (1.5 to 8.0%) and failedintubation (0.1 to 0.3%) are low in the operating
Figure 1. Mallampati classification for grading airways from the least difficult airway (I) to the mostdifficult airway (IV). Class I � visualization of the soft palate, fauces, uvula, and anterior and posteriorpillars; class II � visualization of the soft palate, fauces, and uvula; class III � visualization of the softpalate and the base of the uvula; and class IV � soft palate is not visible at all.
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room with expert anesthesiologists working withpatients from the healthy population, these modelshave a high negative predictive value (99.7%) but alow positive predictive value (30.7%).32–34 Theirroutine use in the operating room, therefore, hasquestionable cost-effectiveness. Although the inci-dence of difficult intubations is higher in the ICU,these multivariate predictive models have not beentested in that setting. In the emergency department,nearly 70% of patients undergoing RSI have eitheraltered mental status or cervical spine collars in placethat prevent the assessment of these predictivefactors.18 Consequently, no data support the value ofthese predictive models for routine use of RSI in theICU to identify patients who will experience adifficult or failed intubation.
Despite the absence of validation studies to dem-onstrate the utility of airway assessment techniquesto identify patients who will experience difficultintubations in the ICU, a quick examination of thepatient for functional and anatomic factors has beenshown to be predictive in the operating room settingand can assist preintubation planning.
Advanced Airway Pharmacology
Advanced airway management requires the selec-tion of appropriate drugs for a particular clinicalsituation. Proper drug selection facilitates laryngos-copy, improves the likelihood of successful intuba-tion, attenuates the physiologic response to intuba-tion, and reduces the risk of aspiration and othercomplications of intubation by a factor of 50 to70%.35–38 Depending on the clinical circumstances,the intensivist may utilize a combination of prein-duction agents, an induction agent, and a paralyticagent.
Preinduction Drugs
Stimulation of the airway with a laryngoscope andendotracheal tube presents an extremely noxiousstimulus,39 which is associated with an intense sym-pathetic discharge resulting in hypertension andtachycardia (called the pressor response). The phys-iologic consequences of this pressor response arewell-tolerated by healthy persons undergoing elec-tive intubation. A hypertensive response, however,may induce myocardial and cerebrovascular injury incritically ill patients with limited reserves for ade-quate tissue oxygenation.2 Moreover, critically illpatients who require emergent intubation experi-ence hypoxia, hypercarbia, and acidosis, which in-duce an extreme sympathetic outflow that is associ-ated with tachycardia, labile BP, and an increasedmyocardial contractility.40 Attenuation of these phys-
iologic stresses after the placement of an airway mayunmask relative hypovolemia and/or vasodilation,which result in postintubation hypotension.40 Endo-tracheal intubation also can provoke bronchospasmand coughing that may aggravate underlying condi-tions, such as asthma, intraocular hypertension, andintracranial hypertension. Patients who are at risk foradverse events from airway manipulation benefitfrom the use of preinduction drugs, which includeopioids, lidocaine, �-adrenergic antagonists, andnon-depolarizing neuromuscular blockers (Table 2).
Opioids have a long history of use in anesthesiabecause of their analgesic and sedative effects. Fen-tanyl is commonly used because of its rapid onset ofaction and short duration of action. Fentanyl bluntsthe hypertensive response to intubation (40% inci-dence of hypertensive response compared with 80%in control subjects),41 although it has only marginaleffects on attenuating tachycardia.41,42 Derivatives offentanyl, sufentanil and alfentanil, are more effectivethan fentanyl at blunting both the tachycardic andhypertensive responses to intubation.42–45 Fentanyland its derivatives can occasionally cause rigidity ofthe chest wall. This idiosyncratic reaction appears tooccur more commonly with higher doses and rapidinjections. Studies in rats46 and case reports inadults47,48 have suggested that opioid-induced chestwall rigidity may be reversed by treatment with IVnaloxone, although some patients in our experiencemay require neuromuscular blockade.
Caution is advised when using opioids in patientswho are in severe shock states. Opioids can block thesympathetic compensatory response to hypotension,resulting in cardiovascular collapse.
Lidocaine, a class 1B antiarrhythmic drug, hasbeen used to diminish the hypertensive response, toreduce airway reactivity, to prevent intracranial hy-pertension, and to decrease the incidence of dysr-rhythmias during intubation.49–51 Demonstrated ef-fectiveness for these end points, however, has variedamong reports,50,52,53 and no evidence has clearlyestablished that lidocaine improves outcomes interms of a lower incidence of myocardial infarctionor stroke. North American physicians use lidocainemore commonly as a preinduction agent for patientswho are at risk of elevated intracranial pressurecompared with physicians in Europe.52 To be mosteffective, lidocaine should be administered 3 minprior to intubation at a dose of 1.5 mg/kg.
Esmolol is a rapid-onset, short-acting, cardioselec-tive �-adrenergic receptor-site blocker that effec-tively mitigates the tachycardic response to intuba-tion with an inconsistent effect on the hypertensiveresponse.41,42,54–56 However, most studies,41,54,56 butnot all,53 have indicated that esmolol is more effec-tive than lidocaine or fentanyl in reducing the pres-
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sor response. The combined use of esmolol (2mg/kg) and fentanyl (2 �g/kg) has a synergistic effectfor reducing both the tachycardia and hypertensionassociated with tracheal intubation and laryngealmanipulation.35,41 Caution is needed with the use ofesmolol in trauma victims and other patients who areat risk for hypovolemia and may require a tachy-cardic response to maintain BP.
Some protocols for RSI recommend the use of asubparalytic preinduction dose of a non-depolarizingneuromuscular blocking drug for patients with sus-pected raised intracranial or intraocular pressure (eg,those with acute traumatic brain injury) who willreceive succinylcholine during induction for intuba-tion.42,57 Succinylcholine can cause fasciculationsthat may promote transient intracranial hyperten-sion, hyperkalemia, and postintubation myalgia. Alow “defasciculating dose” dose (ie, one tenth of theintubation dose) of a non-depolarizing NMBA, suchas rocuronium, has been recommended58–60 to pre-vent fasciculations and a succinylcholine-inducedrise in intracranial pressure. One systematic litera-ture review,57 however, found no evidence thatpretreatment with a defasciculating dose of compet-itive neuromuscular blockers in patients with acutebrain injury is beneficial. The available studies werelimited by weak designs and small sample sizes, so apositive effect has not yet been excluded. Level IIevidence exists that pretreatment before succinyl-choline administration lowers intracranial pressurein patients undergoing neurosurgery for brain tu-mors.57 It is not the practice of the authors, however,to use a subparalyzing dose of rocuronium or anyother non-depolarizing muscle relaxant as an adjunc-tive premedication because of the limited evidencefor efficacy.
Induction Agents
Induction agents are used to facilitate intubationby rapidly inducing unconsciousness. Familiaritywith a range of induction drugs is important becausethe specific clinical circumstance dictates the appro-priate induction method (Table 3). Agents that areindicated for patients with respiratory failure may becontraindicated in other clinical settings. Intensivistsshould, therefore, avoid using a single standardizedinduction approach.
Etomidate is a nonbarbiturate hypnotic agent thatis used for the rapid induction of anesthesia. Thisimidazole derivative has a rapid onset of action and ashort half-life. It predictably does not affect BP.Etomidate has cerebral-protective effects by reduc-ing cerebral blood flow and cerebral oxygen uptake
Tab
le2—
Pre
indu
ctio
nA
gent
sU
sed
for
RSI
Dru
gD
osag
eO
nset
Dur
atio
nIn
dica
tions
Cau
tions
Fen
tany
l2–
3�
g/kg
slow
IVpu
shov
er1–
2m
in
Alm
ost
imm
edia
te0.
5–1
hPr
imar
ypr
eind
uctio
nag
ent
that
prov
ides
seda
tion
and
anal
gesi
ain
hem
odyn
amic
ally
stab
lepa
tient
sw
ithth
efo
llow
ing:
coro
nary
arte
rydi
seas
e;hy
pert
ensi
veem
erge
ncie
s;ar
teri
alan
eury
sms
and
diss
ectio
ns;
cere
brov
ascu
lar
acci
dent
s;an
din
trac
rani
al/in
trao
cula
rhy
pert
ensi
on
Hyp
oten
sion
;mas
sete
ran
dch
est
wal
lrig
idity
ifbo
lus
inje
cted
;bra
dyca
rdia
with
larg
ebo
lus
dose
s
Lid
ocai
ne1.
5m
g/kg
IV2–
3m
inbe
fore
intu
batio
n
45–9
0s
10–2
0m
inA
sw
ithfe
ntan
yl;a
sthm
a;C
OPD
;oft
enus
edin
conj
unct
ion
with
fent
anyl
Hyp
oten
sion
Esm
olol
2m
g/kg
IV2–
10m
in10
–30
min
Syne
rgis
ticw
ithfe
ntan
yl;m
ost
com
mon
lyus
edfo
rne
uros
urgi
calp
atie
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with
rais
edin
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essu
res;
limite
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gex
peri
ence
inis
olat
edhe
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aum
ain
the
emer
genc
yde
part
men
t
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dyca
rdia
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oten
sion
;inc
reas
edai
rway
reac
tivity
Roc
uron
ium
ata
defa
scic
ulat
ing
dose
0.06
mg/
kg1–
2m
in�
5–10
min
Ele
vate
din
trac
rani
al/in
trao
cula
rpr
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re;p
reve
ntio
nof
succ
inyl
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ine-
indu
ced
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lgia
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iddo
ses
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beca
use
apa
raly
ticef
fect
may
occu
r.
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(V̇o2). It does not, however, attenuate the pressorresponse that is related to intubation or provideanalgesia.
Adverse effects of etomidate include nausea, vom-iting, myoclonic movements, lowering of the seizurethreshold in patients with known seizure disorders,and adrenal suppression.43,49,61–63 Etomidate, evenafter a single bolus dose, inhibits cortisol productionin the adrenal gland at various enzymatic levels andreduces adrenal responsiveness to exogenous adrenalcorticotrophin hormone for up to12 h.49,64 Deleteri-ous effects of etomidate-induced adrenal suppres-sion have not been established after a single induc-tion dose.
Because of its rapid onset, short half-life, and goodrisk-benefit profile, etomidate has become the pri-mary induction agent for emergency airway manage-ment. It is especially useful for patients with hypo-tension and multiple trauma because it does not altersystemic BP.
Propofol is a rapid-acting, lipid-soluble inductiondrug that induces hypnosis in a single arm-braincirculation time. The characteristics of propofol in-clude a short half-life and duration of activity, anti-convulsive properties, and antiemetic effects. Propo-fol reduces intracranial pressure by decreasingintracranial blood volume and decreasing cerebralmetabolism.65,66 These mechanisms may underliethe improved outcomes with the use of propofol thathave been demonstrated in patients with traumaticbrain injury who are at risk of raised intracranialpressure.42,63,67
At doses that induce deep sedation, propofolcauses apnea and produces profound relaxation oflaryngeal musculature. This profound muscular re-laxation effect allows propofol, when used in combi-nation with a non-depolarizing NMBA (rocuronium)or opioids (remifentanil or alfentanil) to produceintubation conditions that are similar to those ob-tained with succinylcholine.68–71 However, we con-tinue to favor its use with succinylcholine to ensureadequate intubating conditions. Propofol facilitatesRSI, to a greater degree than etomidate, because itprovides a deeper plane of anesthesia, thereby atten-uating any effects of incomplete muscle paralysis.38
The most important adverse effect of propofol isdrug-induced hypotension, which occurs by reducingsystemic vascular resistance and, possibly, by de-pressing inotropy.63 Hypotension usually responds toa rapid bolus of crystalloid fluids and can be pre-vented by expanding intravascular volume beforegiving propofol or by pretreating patients withephedrine.72 Some patients with allergies to soy oreggs may experience hypersensitivity reactions topropofol. Propofol has no analgesic properties.
For hemodynamically stable patients who have
Tab
le3—
Dru
gsU
sed
for
Indu
ctio
n*
Dru
gD
osag
eO
nset
Dur
atio
nIn
dica
tions
Cau
tions
Eto
mid
ate
Stab
le,0
.3m
g/kg
IVP,
unst
able
,0.1
5m
g/kg
IVP;
onse
t,30
s
30–6
0s
3–5
min
Mul
titra
uma;
exis
ting
hypo
tens
ion
Inhi
bits
cort
isol
synt
hesi
s;de
crea
ses
foca
lse
izur
eth
resh
old
Prop
ofol
Stab
le,2
mg/
kgIV
P;un
stab
le,0
.5m
g/kg
IVP;
onse
t,30
s
9–50
s3–
10m
inIs
olat
edhe
adin
jury
;sta
tus
epile
ptic
usH
ypot
ensi
on;l
ecith
inal
lerg
y
Thi
open
tal
Stab
le,3
mg/
kgIV
P;un
stab
le,1
.5m
g/kg
IVP;
onse
t,30
s
30–6
0s
5–30
min
Nor
mot
ensi
ve;n
orm
ovol
emic
befo
reba
rbitu
rate
ther
apy
for
stat
usep
ilept
icus
orco
ntro
lof
intr
acra
nial
hype
rten
sion
Bro
ncho
spas
m;h
ypot
ensi
on;p
oor
avai
labi
lity
beca
use
ofco
ntro
lled
drug
stat
us
Ket
amin
e2
mg/
kgIV
P1–
2m
in5–
15m
inA
sthm
a/C
OPD
Hea
din
jury
;isc
hem
iche
art
dise
ase;
hype
rten
sive
emer
genc
ies
Scop
olam
ine
0.2–
0.4
mg
IVP
10m
in2
hU
ncom
pens
ated
shoc
kT
achy
card
ia
*IV
P�
IVpu
sh.
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either a contraindication to succinylcholine or re-ceive non-depolarizing neuromuscular blockers forparalysis, propofol may be the induction agent ofchoice. Many clinicians use propofol as an inductiondrug for patients with isolated head injury or statusepilepticus.
Ketamine, a phencyclidine derivative, is a rapidlyacting dissociative anesthetic agent that has potentamnestic, analgesic, and sympathomimetic qualities.Ketamine acts by causing a functional disorganiza-tion of the neural pathways running between thecortex, thalamus, and limbic system.49 It does so byselectively inhibiting the cortex and thalamus whilestimulating the limbic system. Ketamine is also aunique induction agent because it does not abateairway-protective reflexes or spontaneous ventila-tion.49
The central sympathomimetic effects of ketaminecan produce cardiac ischemia by increasing cardiacoutput and BP, thereby increasing myocardial V̇o2.Patients can experience “emergence phenomena” asthey resurface from the dissociative state induced byketamine. This frightening event, characterized byhallucinations and extreme emotional distress, canbe attenuated or prevented with benzodiazepinedrugs. Because ketamine is a potent cerebral vaso-dilator, intracranial hypertension is a contraindica-tion for its use. Other side effects include salivationand bronchorrhea, both of which can be preventedwith the administration of an anticholinergic agentsuch as glycopyrrolate or scopolamine.
The bronchodilator properties of ketamine make itsuitable for patients with bronchospasm due to statusasthmaticus or COPD. No outcome studies exist,however, to demonstrate improved outcomes inthese clinical settings. The sympathomimetic effectsof ketamine warrant avoiding its use in patients withacute coronary syndromes, intracranial hypertension,or raised intraocular pressure.
Sodium thiopental is a thiobarbiturate with a rapid30-s onset of action and a short half-life. Its use forRSI is limited because it is a controlled substanceand propofol has similar characteristics. Barbituratesin general decrease cerebral V̇o2, cerebral bloodflow, and intracranial pressure. They are associated,however, with hypotension secondary to the inhibi-tion of CNS sympathetic outflow, which results indecreased myocardial contractility, systemic vascularresistance, and central venous return.63,73 Hypovole-mia accentuates barbituate-induced hypotension.Sodium thiopental, therefore, should not be used asan induction agent in patients who have hypovolemicor distributive shock. The central sympatholytic ef-fect induced by barbiturates has a positive effect inits blunting of the pressor response to intuba-tion.58,74,75
Barbituates cause allergic reactions in 2% of pa-tients, and also induce laryngospasm, hypersaliva-tion, and bronchospasm.63 Just as barbiturates aregenerally not used in the ICU for sedation purposes,they are not used to the same extent for emergencyairway management. Sodium thiopental is rarelyused in the ICU for emergency intubation, althoughit has applications for normotensive, normovolemicpatients who have status epilepticus or require intu-bation prior to entering barbiturate coma for thecontrol of intracranial hypertension.
Scopolamine is a muscarinic anticholinergic agentwith a short half-life that has sedative and amnesticeffects, but no analgesic properties. It can causetachycardia but otherwise produces no hemody-namic consequences.74 Scopolamine induces lesstachycardia, however, compared with other availablemuscarinic agents (eg, atropine and glycopyrro-late).49 This hemodynamic profile makes scopol-amine a preferred induction agent for patients withuncompensated shock when RSI is used. Adverseeffects include psychotic reactions in addition totachycardia and occur related to the dose adminis-tered.49 Scopolamine causes profound papillary dila-tion, complicating neurologic evaluations.
NMBAs
NMBAs are used to facilitate laryngoscopy andtracheal intubation by causing profound relaxation ofskeletal muscle. There are two classes of NMBAs,depolarizing and non-depolarizing (Table 4). Bothclasses act at the motor end plate. These drug classesdiffer in that depolarizing agents activate the acetyl-choline receptor, whereas non-depolarizing agentscompetitively inhibit the acetylcholine receptor.NMBAs have no direct effect on BP.
Depolarizing Agents: Succinylcholine
Succinylcholine, a depolarizing NMBA, is a dimerof acetylcholine molecules that causes muscular re-laxation via activity at the motor end plate.74 Succi-nylcholine acts at the acetylcholine receptor in abiphasic manner. It first opens sodium channels andcauses a brief depolarization of the cellular mem-brane, noted clinically as muscular fasciculations.49 Itthen prevents acetylcholine-medicated synaptictransmission by occupying the acetylcholine recep-tor. Succinylcholine is enzymatically degraded byplasma and hepatic pseudocholinesterases.76
Succinylcholine is the most commonly adminis-tered muscle relaxant for RSI, owing to its rapidity ofonset (30 to 60 s) and short duration (5 to 15 min).76
Effective ventilation may return after 9 to 10 min.The effects of succinylcholine on potassium balance
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and cardiac rhythm represent its major complica-tions. It can also induce malignant hyperthermia.77
Most reports76,78,79 of deaths, secondary to succi-nylcholine-induced hyperkalemia, involve childrenwith previously undiagnosed myopathies who under-went surgery. Although deaths related to succinyl-choline-induced hyperkalemia are rare, cardiac ar-rest has been reported.80–83 Three studies84–86 ofadult patients have reported that the mean values ofserum potassium levels for the study populationsbefore and after an intubating dose of succinylcho-line changed by as little as �0.04 mmol/L to as muchas 0.6 mmol/L.
The hyperkalemic effect may be exaggerated inpatients with subacute or chronic denervation con-ditions (eg, congenital or acquired myopathies, cere-brovascular accidents, prolonged pharmacologicneuromuscular blockade, wound botulism, criticalillness polyneuropathy, corticosteroid myopathies,and muscle disuse atrophy), burns, intraabdominalinfections, sepsis, and muscle crush injuries.81,83,87–91
The exaggerated hyperkalemic response is mediatedthrough the up-regulation of skeletal muscle nico-tinic acetylcholine receptors.88 Acute rhabdomyoly-sis can produce hyperkalemia, which is aggravated bythe effects of succinylcholine, through mechanismsof drug-induced increases in muscle cell membranepermeability.83,88,92
A personal or family history of malignant hyper-thermia represents an absolute contraindication tosuccinylcholine therapy, which may trigger a hyper-thermic response. Patients who experience masseterspasm on induction with either thiopental or fentanylare at an increased risk of developing malignanthyperthermia when treated with succinylcholine.93,94
Other contraindications that require special precau-tions include denervation of muscles due to under-lying neuromuscular diseases or injury to the CNS,
myopathies with elevated serum creatine kinase val-ues, sepsis after the seventh day, narrow-angle glau-coma, cutaneous burns, penetrating eye injuries,hyperkalemia, and disorders of plasma pseudocho-linesterase. Succinylcholine may be used safelywithin 24 h of experiencing acute burns,95–97 andwithin 3 days of experiencing acute denervationsyndromes and crush injuries.97–100 The drug shouldbe used with caution in patients with preexistingchronic renal insufficiency, although a literaturereview101 has indicated that succinylcholine may beused safely in this setting in the absence of other riskfactors for drug-induced hyperkalemia. Such pa-tients must be closely monitored for severe hyper-kalemia.
Succinylcholine-associated dysrrhythmias are me-diated by postganglionic muscarinic receptors andpreganglionic sympathetic receptors. Bradydysr-rhythmias are most commonly observed, with rarereports of asystole and ventricular tachyarrhythmias.Most instances occur in pediatric patients or inadults after the use of multiple doses of succinylcho-line.76,102,103 Dysrrhythmias may be prevented inadults by premedication with a vagolytic dose ofatropine (0.4 mg IV) prior to repeating a dose ofsuccinylcholine.75,76
Succinylcholine may cause an increase in intragas-tric pressure, presumably because of drug-inducedmuscular fasciculation. Aspiration usually does notoccur by way of this effect because of a coincidentincrease in tone of the esophageal sphincter.104,105
Succinylcholine increases both intraocular and intra-cranial pressure, but these effects are transient andclinically unimportant.106,107 Patients should receivesuccinylcholine only if adequate face-mask ventila-tion can be achieved if intubation fails.
Because of the extensive risks associated with theuse of succinylcholine in critically ill patients, some
Table 4—Neuromuscular Blocking Agents
Drug Dosage Onset, sDuration,
min Indications Cautions
Succinylcholine 1.5 mg/kg IV push 30–60 5–15 Use as default paralyticagent unless there iscontraindication
Contraindications: personal or familyhistory of malignant hyperthermia;likely difficult intubation or maskventilation; known uncontrollablehyperkalemia; myopathy; chronicneuropathy/stroke; denervationillness or injury after � 3 d; crushinjury after � 3 d; sepsis after � 7d; severe burns after � 24 h
Caution: chronic renal insufficiencyRocuronium High dose: 1 mg/kg IV push 45–60 45–70 When succinylcholine
is contraindicatedPredict difficult intubation and
ventilation; allergy to aminosteroidneuromuscular blocking agents
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intensivists have argued that its role in the ICU isobsolete.108 We believe that its superiority to otheravailable neuromuscular blocking drugs (infra vida)warrant its use in patients without risk factors foradverse events. Its use requires extensive educationof critical care physicians to ensure their understand-ing of the contraindications for use of the drug. Onesurvey study109 observed that there was a poorunderstanding among critical care physicians of therisks of succinylcholine for patients with criticalillness polyneuropathy.
Succinylcholine is given in a dose of 1.5 mg/kg forintubation because a lower dose may induce relax-ation of the central laryngeal muscles before periph-eral musculature. This circumstance may promoteaspiration and complicate intubation by relaxinglaryngeal muscles and promoting glottic incompe-tence, while leaving masseter muscle function in-tact.49 A recent study,110 however, suggests thatcomparable intubation conditions for surgical pa-tients undergoing elective intubation can beachieved after 0.3, 0.5, or 1.0 mg/kg succinylcholinewhen induced with propofol or fentanyl. These lowerdoses allow a more rapid return of spontaneousrespiration and airway reflexes.110 In the absence ofsuch data for critically ill patients who require urgentintubation, we continue to recommend the use ofsuccinylcholine, 1.5 mg/kg, for RSI.
Non-Depolarizing NMBAs
Non-depolarizing NMBAs provide an alternativeto succinylcholine for RSI. Rocuronium, an aminos-teroid drug, has a short onset of action (1 to 2 min)and an intermediate duration of action (45 to 70min).
A systematic review68 compared relative outcomeswith the use of succinylcholine for intubation tothose with the use of rocuronium. This study con-cluded that the use of succinylcholine producedsuperior intubation conditions compared to that ofrocuronium (0.6 mg/kg) when rigorous standardswere used to define the term excellent conditions(relative risk of poor conditions with rocuronium use,0.87; 95% confidence interval, 0.81 to 0.94;n � 1,606). The two agents had similar efficacy whenless rigorous definitions were used to define ade-quate intubation conditions. No differences werefound, however, if propofol was used for induction,or if the dose of rocuronium was 1.0 mg/kg. The useof this higher dose of rocuronium prolongs theduration of paralysis. The success rate of intubationwas similar for both rocuronium and succinylcholineunder all of the study conditions.68
The effects of non-depolarizing blocking drugs canbe reversed using acetylcholinesterase inhibitors,
such as neostigmine or edrophonium, and vagolyticdoses of glycopyrolate or atropine. The only absolutecontraindication to the use of rocuronium is allergyto aminosteroid neuromuscular drugs. Extreme cau-tion should be exercised in selecting appropriatepatients for its use. Patients for whom intubationappears likely to be difficult may experience hypoxiaif face mask ventilation is unsuccessful during theprolonged period of drug-induced paralysis (45 to 70min) before intubation can be achieved.
Airway Management in the ICU
In 199316 and again in 2003,111 the AmericanSociety of Anesthesiologists task force on difficultairways published guidelines for the management ofdifficult airways in the operating room. The applica-tion of these structured approaches to airway man-agement appears to have decreased closed claimscosts in anesthesia.112 The guidelines are widelyendorsed by anesthesiologists, with 86% stating thatthey use the algorithms in their clinical practice.113
These particular algorithms, however, have limitedapplicability to the ICU because they rely on preop-erative assessment and exercise the option of delay-ing surgery in the operating room if it appears thatintubation will be overly difficult.
Although not validated, algorithms reported byWalls and coworkers114 provide a standardized ap-proach to emergency airway management. Suchalgorithmic approaches for emergent intubation thatappropriately select patients for RSI have demon-strated improved outcomes in both emergency de-partment and field intubation settings.5–13,15 Emer-gency medicine practitioners who utilize airwaymanagement protocols that incorporate RSI experi-ence airway failures with a need to progress toemergency cricothyrotomy in only 0.5% of intuba-tions.5,6 The National Emergency Airway RegistryII,6 a data bank of 7,712 intubations, has demon-strated that RSI is the most common technique ofintubation with a success rate � 98.5%. These re-sults contrast with the 18% incidence of failedintubation in the absence of RSI reported by Li andcoworkers.7 This prospective study compared com-plications arising from intubation utilizing paralyticagents within an RSI protocol to intubations thosearising from intubations without the use of NMBAs.Esophageal intubations and airway trauma occurredwith greater frequency in the group that did notreceive RSI (18% vs 3%, respectively, and 28% vs0%, respectively).7
The intubation algorithms modified from Wallsand coworkers114 (Figs 2–5) classify intubation at-tempts into the following categories: (1) universal;
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(2) crash; (3) difficult; and (4) failed. The universalalgorithm (Fig 2) is the beginning point for intuba-tion for all patients. The initial assessment requiresthe intensivist to determine whether the patient isunresponsive or near death, or whether a difficultairway appears likely. The former requires activationof the crash airway algorithm (Fig 3), and the latteractivation of the difficult airway algorithm (Fig 4).The absence of any of these conditions allows thephysician to initiate RSI.
Failure to intubate a patient with three or moreattempts directs the intensivist to the failed airwayalgorithm (Fig 5). This algorithm calls for immediateassistance in preparation for emergency criciothy-roidotomy if measures to oxygenate or intubate thepatient have failed. Success with the use of thesealgorithms requires the presence of personnel whoare skilled in the specialized techniques needed tomanage a difficult airway and failed intubation.These algorithms can serve as a training curriculumfor preparing critical care physicians to manageairways in the ICU.
RSI
As described above, RSI is a critical element in theestablishment of a secure airway during emergency
intubation. First developed to facilitate intubation inthe operating room and to reduce the risks ofaspiration for patients with full stomachs, RSI hasbeen adopted by emergency physicians and is nowbeing used for intubating patients in the field.Studies4–15 have demonstrated increased intubationsuccess rates and decreased complications with air-way protocols that utilize RSI compared with thoseusing traditional intubation techniques.
Several factors underlie the improved outcomeswith RSI. Preoxygenation reduces the need forface-mask ventilation in preparation for intubation,and thereby decreases the risks for gastric insuffla-tion and the aspiration of stomach contents. The useof a potent induction agent with a neuromuscularblocking drug allows the airway to be rapidly con-trolled, further reducing the risk of aspiration. Theuse of adjunctive medications in appropriate clinicalsettings can reduce the pressor response and otherphysiologic consequences of laryngoscopy and tra-cheal intubation. Table 5 presents an example of theauthors’ typical RSI protocol.
Not all critically ill patients are candidates for RSI,however. The presence of severe acidosis, intravas-
Figure 3. Crash airway algorithm. See Fig 2 for abbreviationsnot used in text.
Figure 2. Universal airway algorithm. BNTI � blind nasotra-cheal intubation.
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cular volume depletion, cardiac decompensation,and severe lung injury may complicate the adminis-tration of preinduction and induction agents, whichmay result in vasodilation and hypotension. Acutelung injury may prevent an adequate response topreoxygenation efforts. Such patients require crashintubation and usually tolerate intubation attemptswithout extensive premedication because of thepresence of depressed consciousness.
The general sequence of RSI consists of the “sixP’s,” as follows: preparation, preoxygenation, pre-medication, paralysis, passage of the endotrachealtube, and postintubation care. Preparation beginswhen the clinician identifies the need for intubation.A period of 5 to 10 min before intubation allows forthe evaluation of the patient for signs of a difficultairway, as described above, and for the preparationof the equipment. Among the various mnemonicsthat are used to assist preparation, the phrase “YBAG PEOPLE?” (Table 6) allows physicians torecall the essential elements of the preparatory phaseand emphasizes the need to avoid positive-pressureface mask ventilation whenever possible.
Preoxygenation, also termed alveolar denitrogena-tion, is performed with the patient breathing 100%oxygen through a nonrebreather mask for 5 min.Mentally alert patients are asked to perform eightdeep breaths to total lung capacity. Alveolar denitro-genation creates a reservoir of oxygen in the lungthat limits arterial desaturation during subsequentintubation attempts. The use of positive-pressureventilation administered by face mask is reserved forpatients who cannot achieve adequate oxygenationwhile breathing 100% oxygen by nonrebreathermask.
Premedication entails the use of drugs to providesedation and analgesia, and to attenuate the physio-logic response to laryngoscopy and intubation. Twoto three minutes before the patients undergoes
Figure 5. Failed airway algorithm. See Fig 2 for abbreviationsnot used in text.
Figure 4. Difficult airway algorithm. BNTI � blind nasotra-cheal intubation.
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Tab
le5—
Sche
mat
ized
Exa
mpl
eof
anR
SI
Tim
e�
10m
in(P
repa
re)
Tim
e�
5m
in(P
reox
ygen
ate)
Tim
e�
2m
in(P
retr
eat)
Tim
e0
(Par
alys
is)
Tim
e�
30–4
5s
(Pas
sth
eT
ube)
Tim
e�
45s
(Pos
tintu
batio
nM
anag
emen
t)
Pred
ict
diff
icul
tin
tuba
tion:
stop
ifno
tR
SIca
ndid
ate
Hyp
oten
sive
patie
nt:
1.G
ood
vasc
ular
acce
ss2.
Vas
opre
ssor
sre
adily
avai
labl
eW
eus
eas
need
edPh
enyl
ephr
ine
10m
gin
100
mL
NS
(100
�g/
mL
)—an
dgi
ve1
mL
aliq
uots
prn
Or
Eph
edri
ne,5
–10
mg
bolu
ses
asne
eded
Prov
ide
100%
with
nonr
ebre
athe
rm
ask
orB
VM
Susp
ecte
din
trac
rani
alhy
pert
ensi
on,m
yoca
rdia
lis
chem
ia,o
rhy
pert
ensi
veem
erge
ncy.
Fen
tany
lwith
orw
ithou
tlid
ocai
ne(m
ore
com
mon
lyw
eus
efe
ntan
ylal
one)
Indu
ctio
n:1.
Eto
mid
ate
(def
ault
indu
ctio
nag
ent)
or2.
Prop
ofol
or3.
Ket
amin
eor
4.Sc
opal
amin
e
Intu
bate
Obs
erve
ET
Tpa
ssbe
twee
nvo
calc
ords
Ifpr
oble
ms
with
visu
aliz
atio
nre
mem
ber
to“B
UR
P”1.
Bac
kwar
ds2.
Upw
ard,
and
3.R
ight
war
d4.
Pres
sure
onth
eth
yroi
dca
rtila
ge
Con
firm
plac
emen
taf
ter
infla
tion
ofcu
ff:
1.A
uscu
ltate
abdo
men
,the
nhe
mith
orac
esfo
rai
ren
try
2.D
etec
tE
Tco
2
colo
rch
ange
orw
avef
orm
3.R
eass
ess
oxyg
enat
ion
stat
us4.
Onc
eE
TT
plac
emen
tco
nfir
med
,cea
seSe
llick
man
euve
r5.
Secu
retu
be
Mne
mon
ic“Y
BA
GPE
OPL
E”
No
PPV
unle
sspa
tient
’sSp
o2
�90
%If
PPV
requ
ired
,the
npr
ovid
ecr
icoi
dpr
essu
re(S
ellic
km
aneu
ver)
Ast
hma
lidoc
aine
Selli
ckm
aneu
ver
with
adm
inis
trat
ion
ofin
duct
ion
agen
t
Con
side
rpl
acem
ent
ofO
Gt
orN
GPo
stE
TI,
AB
Gan
alys
isan
dC
XR
Ifpa
tient
ishy
pote
nsiv
e,en
sure
good
vasc
ular
acce
ss,a
ndha
veav
aila
ble
drug
s
Itis
not
our
prac
tice
tous
ede
fasc
icul
atin
gdo
ses
ofro
curo
nium
orot
her
nond
epol
ariz
ing
NM
BA
s
Neu
rom
uscu
lar
bloc
kade
:1.
Succ
inyl
chol
ine
or2.
Roc
uron
ium
Ifpa
tient
Spo
2�
90%
duri
ngat
tem
pt,s
top
and
prov
ide
PPV
and
oxyg
enat
ion
until
Spo
2�
90%
As
man
yof
the
drug
sus
edin
RSI
have
shor
tha
lf-lif
eco
nsid
erco
ntin
ued
seda
tion
with
orw
ithou
tpa
raly
sis
*AB
G�
arte
rial
bloo
dga
s;SC
I�
spin
alco
rdin
jury
;B
VM
�ba
g-va
lve-
mas
kve
ntila
tion;
CX
R�
ches
tra
diog
raph
;E
Tco
2�
end-
tidal
CO
2;E
TI
�en
dotr
ache
alin
tuba
tion;
NG
�na
soga
stri
ctu
be;
OG
�or
ogas
tric
tube
;PPV
�po
sitiv
e-pr
essu
reve
ntila
tion;
SPo
2�
puls
eox
imet
ryox
ygen
satu
ratio
n;E
TT
�en
dotr
ache
altu
be.
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laryngoscopy, a combination of drugs individualizedto a patient’s needs and clinical circumstances isadministered (Table 2).
The induction and neuromuscular blocking drugsare administered immediately after the patientachieves adequate preoxygenation and receives thepreinduction medication. An assistant performs theSellick maneuver (ie, cricoid pressure) to preventpassive aspiration and reduce gastric insufflation ifthe patient is receiving positive-pressure ventilationby face mask. If the patient vomits, cricoid pressureshould be released and the patient should be log-rolled to allow dependent suctioning of the pharynx.
Although many emergency physicians use etomi-date as their primary induction drug, other drugshave specific advantages in certain clinical settings(Table 3). The selection of a neuromuscular blockingdrug also depends on clinical circumstances, aspreviously described. Succinylcholine provides safeand effective neuromuscular blockade for most pa-tients. Rocuronium may be a more appropriatechoice for patients if there are contraindications orconcerns about the use of succinylcholine.
Forty-five seconds to 1 min after induction andparalysis, the adequacy of paralysis is assessed bychecking mandibular mobility. Resistance to motionindicates incomplete paralysis, which requires thatthe patient start to receive oxygen again, with reas-sessment of relaxation taking place in 15 to 30 s.
Once the patient is relaxed, laryngoscopy is per-formed and the vocal cords visualized. Visualizationof the vocal cords and the glottic opening may beimproved by placing pressure on the thyroid carti-lage in a backward, upward, and rightward direction(the mnemonic “BURP” or backwards, upwards,right, and pressure).8 If laryngoscopy is not immedi-ately successful and the patient’s oxygen saturation
level falls to � 90%, assisted ventilation is initiatedwith a bag-valve-mask device and cricoid pressure tooxygenate and ventilate the patient before attempt-ing laryngoscopy again. After successful trachealintubation and cuff inflation, the confirmation ofintubation is required.
The goal in the immediate postintubation period isto confirm correct tracheal intubation, and the ade-quacy of oxygenation and ventilation. Epigastricauscultation followed by auscultation of bothhemithoraces in the axillas assists in assessing for anesophageal or mainstem intubation. The rise and fallof the chest and the maintenance or improvement ofoxygenation should be noted. The measurement ofend-tidal CO2 by either a colorimetric or waveformdevice has become a necessary step in confirmingtracheal intubation. Once satisfied that the endotra-cheal tube is in the trachea, cricoid pressure may bereleased. The cuff is then rechecked, and the endo-tracheal tube is secured to the patient. A postintu-bation chest radiograph and arterial blood gas assess-ment should be obtained. Many of the inductionagents and succinylcholine have a short duration ofaction. Thus, sedation should be considered at thispoint.
Conclusion
Advanced airway management is an obligatory skillfor critical care physicians to acquire. The adoptionof algorithmic approaches and RSI by anesthesiolo-gists and emergency medicine physicians has im-proved the success rates for the emergency intuba-tion of unstable patients and has decreased thenumber of complications related to airway control.3,4
Although limited outcomes data exist for the use ofthese techniques in the ICU, similarities of patientsand conditions with the emergency setting warrantthe adoption of algorithmic approaches and RSI asthe standard mode of intubation for critically illpatients. RSI requires a thorough understanding ofthe physiology of intubation, and of the various drugsused for induction and paralysis in addition to carefulpatient selection. The standardization of intubationefforts with well-conceived algorithms requires aregimented approach that is similar to that employedfor cardiopulmonary resuscitation. The training ofcritical care physicians requires greater attention toteaching these advanced airway management skills,more collaboration between anesthesiologists andcritical care physicians to promote these skills,4 andcareful monitoring for adverse events and outcomesto improve patient selection for the various intuba-tion approaches that are available.115
Table 6—Preparation for Intubation Mnemonic
Mnemonic Description
Y Yankauer suctionB Bag-valve-maskA Access veinG Get your team, get help if predict a difficult airwayP Position patient (sniffing position if no
contraindications) and place on monitorE Endotracheal tubes and check cuff with syringeO Oxygen, oropharyngeal airway availableP Pharmacy: draw up adjunctive medications,
induction agent, and neuromuscular blockerL Laryngoscope and blades: ensure a variety and that
they are workingE Evaluate for difficult airway: look for obstruction,
assess thyromental distance � 3 finger breadths,interincisor distance � 2 finger breadths, neckimmobilization
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DOI 10.1378/chest.127.4.1397 2005;127;1397-1412 Chest
Stuart F. Reynolds and John Heffner Intubation
Airway Management of the Critically Ill Patient: Rapid-Sequence
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