123 Posoperative Tracheal Extubacion[1]

8/11/2019 123 Posoperative Tracheal Extubacion[1]

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REVIEW ARTICLE

Postoperative Tracheal Extubation

Kirk A. Miller,

MD,

Christopher P. Harkin,

MD,

and Peter L. Bailey, MD

Department of Anesthesiology, Universi ty of Utah Medical Center, Salt Lake City, Utah

A

though tracheal intubation receives much at-

tention, especially with regard to management

of the difficult airway, tracheal extubation has

received relatively little emphasis. The scope and sig-

nificance of problems occurring after tracheal extuba-

tion are real. Adverse outcomes involving the respira-

tory system comprise the single largest class of injury

reported in the ASA Closed Claims Study (1). Obvious

adverse events related to tracheal extubation ac-

counted for 35 of the 522 or 7 of the respiratory-

related claims. Certainly additional morbidity related

to extubation could be accounted for in other catego-

ries of adverse respiratory events, such as inadequate

ventilation, airway obstruction, bronchospasm, and

aspiration. Others have documented a 4 -9 inci-

dence of serious adverse respiratory events in the

immediate postextubation period (2,3) and prevent-

able anesthesia-related etiologies were noted as im-

portant by Ruth et al. (2). Mathew et al. (4), in a

retrospective review of more than 13,000 anesthetics,

noted that emergency tracheal reintubations occurred

in only 0.19 of patients, and that the majority of

tracheal reintubations were due to preventable anes-

thesia-related factors. Perhaps a greater percentage of

patients experience postextubation difficulties but do

not require reintubation of the trachea. Reasons for

tracheal reintubation in the intensive care setting may

differ, but the reported incidence in that arena is sim-

ilarly 4 (5).

Anesthesiologists recognize the immediate postex-

tubation period as one where patients are particularly

vulnerable. Events such as laryngospasm, aspiration,

inadequate airway patency, or inadequate ventilatory

drive can occur and frequently result in hypoxemia.

Such hypoxemia is most often corrected within min-

utes. Less frequently, postextubation hypoxemia can

rapidly result in serious morbidity. In this report we

will review the known physiologic and pathophysio-

logic changes associated with anesthesia and surgery

that can influence respiratory function after tracheal

Accepted fo r publication August 10, 1994.

Address correspondence and reprint requests to Peter L. Bailey,

MD, Department of Anesthesiology, University of Utah Medical

Center, 50 North Medical Drive, Salt Lake Cit y, UT 84132.

01994 by the International Anesthesia Research Society

0003-2999/95/$5.00

extubation, the physiologic impact of extubation itself,

criteria used for predicting successful extubation, and

different techniques and interventions used for tra-

cheal extubation. It is not our intent to review the

complications of laryngoscopy and tracheal intuba-

tion. However, common complications of tracheal in-

tubation, with special emphasis on the airway, will be

discussed in detail as they frequently affect respira-

tory function after tracheal extubation. More uncom-

mon and miscellaneous complications, such as prob-

lems related to the endotracheal tube cuff, recently

have been reviewed (6).

Effects of Anesthesia and Surgery on

Respiratory Function After Extubation

After the ideal extubation, patients would exhibit

adequate ventilatory drive, a normal breathing pat-

tern, a patent airway with intact protective reflexes,

normal pulmonary function, and the absence of any

mechanical perturbations such as coughing. Unfortu-

nately, all of these conditions are rarely, if ever,

achieved in patients extubated after anesthesia. Un-

derstanding the potential interactions between anes-

thesia, surgery, and extubation on respiratory function

helps define many of the complications that occur at

this crucial juncture in anesthesia care. This section

will include a discussion of the effects of anesthesia

and surgery on the respiratory system which are com-

mon during extubation, with major emphasis on the

airway and lung.

Airway Changes

Any form of airway dysfunction, such as obstruction

after tracheal extubation, is an immediate threat to

patient safety. Significant airway compromise leads to

diminished minute ventilatory volumes and hypox-

emia ensues in a variable, but often rapid fashion. A

differential diagnosis of acute postoperative obstruc-

tion of the upper airway after extubation includes:

laryngospasm, relaxed airway muscles, soft tissue

edema, cervical hematoma, vocal-cord paralysis, and

vocal-cord dysfunction (Table 1). Airway obstruction

from foreign body aspiration (e.g., temperature probe

condoms) will not be reviewed but deserves mention.

Anesth Analg 1995;80:149-72

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POSTOP ERATIVE TRACHEAL EXTUBATION 1995:80:149-72

Table 1. Differential Diagnosisof Postoperative

Airway Obstruction

1. Laryngospasm

2. Airway muscle elaxation

a. Residual muscle elaxants

b. Residual anesthetics

3. Soft tissue edema (allergic reaction/mechanical

trauma)

a. Uvular

c. Paryngolaryngeal

4. Cervical hematoma

5. Vocal cord paralysis/dysfunction

6. Foreign body aspiration

Laryngospasm Laryngospasm, defined by Keating

(7) as a protective reflex, can be life-threatening when

it occurs after extubation. Historically, a patient in

Stage II anesthesia has been thought to be particularly

vulnerable to laryngospasm (8). Stimulation of a vari-

ety of sites from the nasal mucosa to the diaphragm

can evoke laryngospasm (9). Most commonly, laryn-

gospasm is a reaction to a foreign body or substance

near the glottis. Blood or saliva, even in small

amounts, can elicit laryngospasm. It has been sug-

gested that laryngospasm can be prevented by extu-

bating a patient under deep anesthesia, while the la-

ryngeal reflexes are depressed (8). However,

substantial proof of this tenet is lacking.

Suzuki and Sasaki (10) contend that laryngospasm

is solely attributable to prolonged adduction of the

vocal cords mediated via the superior laryngeal nerve

and cricothyroid muscle. Ikari and Sasaki (11) have

demonstrated that the firing threshold of the laryngeal

adductor neurons involved in laryngospasm varies in

a sinusoidal manner during spontaneous ventilation.

Interestingly, reflex laryngeal closure occurs more

readily during expiration than inspiration (Figure 1).

Others believe that laryngospasm also involves clo-

sure of the glottis in addition to adduction of the vocal

cords. Closure of the glottis results from contraction of

the lateral cricoarytenoid and thyroarytenoid muscles,

which are innervated by the recurrent laryngeal nerve

(9). Clinical recognition and treatment of laryngo-

spasm must be expedient (see below), if complications

such as hypoxemia or pulmonary edema are to be

avoided (12).

Airway Relaxation Airway obstruction related to

relaxation of airway soft tissue is frequently associated

with residual effects of anesthesia. Such obstruction is

purported to be most commonly due to relaxation of

the airway (pharyngolaryngeal) muscles. Physiologic

maintenance of upper airway patency occurs by a

complex mechanism that involves the muscles in-

serted into the hyoid bone and thyroid cartilage (13).

During normal inspiration, an increase in tonic activ-

ity of these strap muscles precedes contraction of the

diaphragm and prevents apposition of the tongue and

soft palate against the posterior pharyngeal wall (141.

Drummond (15), administered sodium thiopental to

14 patients which resulted in a decrease in electromyo-

graphic activity of the strap muscles that was associ-

ated with airway obstruction. Airway collapse has

been prevented by stimulation of the strap muscles in

rabbits (16). The mechanisms of airway obstruction in

sleep disorders also involves a decrease in the tonic

activity of these upper airway muscles.

The actual tissue producing obstruction is a point of

debate, but likely sites include the tongue, soft palate,

and/or epiglottis. Evidence implicating the tongue as

responsible for upper airway obstruction after extuba-

tion is derived from several sources including descrip-

tions of the mechanism of obstruction in unconscious

patients, other sleep apnea studies, and several anes-

thesia reports (17-21). Safar et al. (17), after evaluating

lateral radiographs in anesthetized patients concluded

that obstruction is secondary to posterior prolapse of

the tongue. Sleep apnea patients also experience ob-

struction from relaxation of the tongue secondary to

decreased airway muscle tone that occurs during

rapid eye movement sleep (18,191. Studies using elec-

tromyograms in obstructive sleep apnea patients have

recorded decreased activity of the genioglossus mus-

cle concurrent with airway obstruction (19). Nishino et

al. (20), reported decreases n hypoglossal nerve activ-

ity which correlated inversely with increasing halo-

thane concentrations in cats; however, there were no

observations concerning airway obstruction. In addi-

tion, reports of intraoperative airway obstruction dur-

ing bilateral carotid endarterectomy under cervical

plexus block suggest bilateral hypoglossal nerve dys-

function as a contributing factor (21).

Using fluoroscopy and lateral radiography, others

have demonstrated that obstruction occurs at the level

of the soft palate in sleep apnea patients (22). Nandi et

al. (23) demonstrated obstruction at the soft palate in

17 of 18 patients, the epiglottis in 4 of 18 patients, and

the tongue in 0 of 18 patients (Figures 2 and 3). Boiden

(24), using bronchoscopy, had similar findings, and

proposed that the relative position of the hyoid bone

to the thyroid cartilage determines the degree of air-

way patency (24). Thus, the head tilt and jaw thrust

recommended by Morikawa et al. (25) results in ven-

tral movement of the hyoid bone relative to the thy-

roid cartilage, and is effective in opening the airway.

The soft palate appears to be the most likely site of

airway obstruction. Nevertheless, prolapse of the

tongue, especially when it is large, can probably also

impair airway patency.

Pharyngolaryngeal Edema Uvular and/or soft pal-

ate edema is a potential cause of postextubation air-

way obstruction (26). The pathophysiology of uvular

edema is undetermined, but suggested possibilities

include mechanical trauma and/or impeded venous


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1995;80:149-72

REVIEW ARTICLE MILLER E T AL. 151

POSTO PERATIVE TRACHEAL EXTUBATION

Figure 1. Mean threshold in volts for reflex glottic

closure (laryngospasm) plotted with respect to respi-

ratory phase. Note the increased threshold during

inspiration. (Adapted with permission f rom: Ikari T,

Saski CT. Glottic closure reflex control mechanisms.

Ann oto1 1980;89:220-4.)

Figure2. Radiographic evidence before (le ft) and

after (right) induction of anesthesia, demonstrating

sof t palate obstruction of the airway during anesthe-

sia. Arrows indicate airway opening and narrowing.

(Adapted with permission from Nandi PR. Effect of

general anaesttiesia on the pharynx. Br J Anaesth

1991;66:157-62.)

I

I

I I I I I

early late early late early late early late early late early late

lNSPlRATlON EXPIRAT ION INSPIR ATION EXPIRATION lNSPlRATlONEXPlRATlON

drainage from airway devices including endotracheal

tubes (271, oral airways (281, nasal a irways (291, laryn-

geal mask airways (30), and vigorous suctioning of the

airway (31). Pregnant patients, and especially those

with toxemia, may experience significant uvular

and/or pharyngolaryngeal edema and related airway

obstruction (32).

Surgery involving the anterior neck, including dis-

sections or cervical spine operations, may also result

in pharyngolaryngeal edema and airway obstruction.

Avoiding bilateral neck dissections in an attempt to

prevent serious edema has been recommended (331,

but, significant edema and supraglottic obstruction

can occur even after delayed contralateral second

stage procedures (34). One proposed mechanism of

edema after neck surgery is the physical disruption of

lymphatic drainage. Emery et al. (35) presented a re-

view of seven cases of postoperative upper airway

obstruction after anterior cervical spine surgery. Five

of the seven patients had evidence of pharyngolaryn-

geal edema, while none of the seven cases had evi-

dence of cervical hematoma.

Cervical Hem&ma Cervical hematoma after ante-

rior neck surgery can also cause airway obstruction.

Such hematomas can develop postoperatively, and

cause delayed airway obstruction after extubation.

The purported mechanism of airway obstruction as-

sociated with cervical hematoma is the obstruction of

venous and lymphatic systems by the expanding

mass, resulting in pharyngolaryngeal edema (36).

Edematous mucosal folds can eventually obliterate the

glottis (36). Compression of adjacent airway struc-

tures, such as the trachea, by a hematoma is not com-

monly found (37).

OSullivan et al. (36), described the postoperative

course of six carotid endarterectomy patients who

formed cervical hematomas. Stridor and respiratory

compromise, which required immediate surgical in-

tervention, developed in four of six patients. After

induction of general anesthesia, three of these pa-

tients were impossible to manually ventilate and two

could not be intubated. The two patients without

evidence of stridor also returned to the operating

room. One of these two could not be manually ven-

tilated and both were difficult to intubate. Another

reported case of cervical hematoma involved a 57-

yr-old patient who developed airway obstruction 12


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POSTO PERATIVE TRACHEAL EXTUBATION 1995;80:149-72

- pre-induction

. apnoea

I I I

I I I I I

0 10 20 30 40 50 60 70

Distance (mm)

Figure 3. Diagramm atic representation of the pharyngeal outline

based on radiograph (Figure 2) measurem ents before (solid line)

and after (dotted line) induction of anesth esia. 1, soft palate; 2, base

of tongue; 3, hyoid bone; 4, epiglottis. (Adapted with permission

from Nunn JF. Effect of general anaes thesia on the pharynx. Br

J Anaesth 1991;66:157-62.)

h after thyroidectomy. A significant hematoma de-

veloped, but its evacuation did not relieve airway

obstruction. The persistent airway obstruction was

thought to be secondary to pharyngolaryngeal edema

(38).

The incidence of cervical wound hematoma after

carotid endarterectomy is cited as 1.9 , with an un-

known percentage of these patients developing air-

way obstruction (39). When these patients return to

the operating room for reexploration, the absence of

stridor or respiratory distress does not predict free-

dom from diff icult airway problems. Hematoma, as

well as pharyngolaryngeal edema, may render man-

ual ventilation by mask and/or visualization of the

vocal cords and tracheal intubation difficult or impos-

sible. In addition, evacuation of the hematoma may

not ameliorate existing airway compromise. Such

patients should be extubated cautiously and when

there is evidence that pharyngolaryngeal edema has

diminished.

Linglnal Edema Oral surgery can produce edema of

the tongue and compromise postoperative airway

function, especially after palatoplasty or pharyngeal

flap surgery (40). Prolonged placement of a mouth

gag, commonly used in cleft palate repair, can result in

lingual edema as described by Schettler (41). Periodic

relie f of pressure from mouth gag devices should help

reduce associated lingual edema (42). Head position

during neurosurgery has also been reported to con-

tribute to lingual edema. Patients undergoing a

craniotomy in the sitting position may have their head

in such extreme flexion that obstruction of venous

drainage of the tongue results in lingual edema, mac-

roglossia, and airway obstruction (43). During such

head flexion the presence of an oral airway may exac-

erbate compression of the tongue and further compro-

mise lingual circulation.

An allergic reaction to glutaraldehyde solution,

used to sterilize laryngoscope blades, is another

unique cause of lingual edema. Edema can be so se-

vere as to lead to reintubat ion during recovery (44).

Severe allergic reactions in general may involve part

or al l of several airway structures and can also result

in edema and airway compromise.

Vocal Cord Paralysis Unilateral vocal cord paraly-

sis may cause persistent hoarseness after extubation

(45). Bilateral vocal cord paralysis may produce upper

airway obstruction (46,47). Vocal cord paralysis is usu-

ally secondary to injury of the recurrent laryngeal

nerve resulting in unopposed superior laryngeal

nerve mediated adduction of the vocal cords. Such an

injury can occur with neck surgery (especially thyroid-

ectomy) (48), thoracic surgery (49,501, internal jugular

line placement (51), and endotracheal intubation (52-

55). Endotrachealtubes are frequently cited as a cause

of vocal cord paralysis, and suggested mechanisms

include endotracheal tube cuff compression of the re-

current laryngeal nerve against the lamina of the thy-

roid cartilage. Positioning of the endotracheal tube

cuff just below or adjacent to the vocal cords may

increase the incidence of this problem. Excessive cuff

inflation and/or high cuff pressures resulting from

diffusion of nitrous oxide can also contribute to vocal

cord damage, especially in cuffs that are positioned

just below the cords.

Vocal Cord Dysfunction Vocal cord dysfunction

(VCD) is an uncommon clin ical cause of airway ob-

struction. VCD was first described in 1902 by Osler

(56). It has since been described by various synonyms,

including paroxysmal vocal cord motion (57), facti-

tious asthma (58), emotional laryngeal wheezing (59),

and Munchausens stridor (60). Al l of the above enti-

ties are similar in their clinical presentation. The pa-

tient population, from the few reported cases (61,621,

appears to consist predominantly of young females

with a recent history of an upper respiratory tract

infection and emotional stress (59,61,63). VCD pre-

sents with laryngeal stridor or upper airway wheezing

similar to asthma (59,64), but the wheezing is unre-

sponsive to bronchodilator therapy (58,63,65). Patients

complain of inspiratory difficulties that result from


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1995;80:149-72 POSTO PERATIVE TRACHEAL EXTUBATION

paradoxical adduction of the vocal cords during inspi-

ration (59). Obstruction can be severe and require the

institution of an arti ficia l or surgical airway (61,66).

Flow volume loops will reveal variable extrathoracic

obstruction with a marked decrease in inspiratory

flow compared to expiratory flow (611, but visualiza-

tion of the vocal cords during a symptomatic episode

is necessary for a def initive diagnosis (67). Recommen-

dations for successful extubation of these patients in-

clude avoiding an awake extubation or, if possible,

providing adequate sedation at the time of extubation.

Sedation alleviates the dynamic inspiratory obstruc-

tion by reducing inspiratory effort and flow. Treat-

ment of a VCD episode includes verbal reassurance,

asking the patient to focus on the expiratory phase of

breathing (621, and sedation if the diagnosis of VCD as

the cause of respiratory distress is certain (58).

Laryngeal Incompetence Several investigations have

demonstrated that laryngeal incompetence occurs af-

ter extubation whether or not residual anesthetic ef-

fects are present. Tom lin et al. (68) evaluated 56 pa-

tients undergoing simple surface surgery under

light balanced anesthesia; 12 patients developed

postoperative atelectasis, 6 of whom aspirated when

asked to swallow 10 mL of contrast medium 2 or more

hours after surgery. The majority of these patients (4

of 6) demonstrating this finding had been intubated.

Gardner (69) demonstrated aspiration in 10 of 94 pa-

tients 2 to 4 days after extubation, and Siedlecki et al.

(70) found that 27 of responsive patients aspirated

radiopaque dye immediately after extubation. Cardiac

surgery patients also have a high risk (33 ) of aspira-

tion when extubated early (less than 8 h) after surgery,

even if awake. This risk sign ificantly decreases to 5

when extubation is performed later (71). Residual an-

esthetic effects may contribute to this high incidence of

aspiration in the early postoperative period. In sum-

mary, laryngeal incompetence is common and the risk

of aspiration after extubation is not elimina ted by the

presence of consciousness.

Swallowing Swallowing, another airway protec-

tion reflex, can also be impaired by a host of factors

after surgery and anesthesia. As recently reviewed

(72), topical anesthetics, tracheostomy, tracheal intu-

bation, neurologic or airway structure injury, con-

scious intravenous sedation, inhalat ion of 50 nitrous

oxide, and even sleep can depress swallowing and

permit pulmonary aspiration. Pavlin et al. (73) and

Isono et al. (74) have also demonstrated that partial

paralysis with neuromuscular blockers depresses

swallowing, too.

Control of Breathing

While it is not the purpose of this review to completely

describe the impact of anesthesia on the control of

breathing, it is necessary to highlight the major factors

affecting ventilatory drive during tracheal extubation.

Airway function is also linked to the central neural

control of breathing and, like spontaneous ventilation,

is depressed by anesthesia. Inhalation drugs, opioids,

sedative-hypnotics, and muscle relaxants are the com-

mon anesthetics that can depress the ventilatory re-

sponse to carbon dioxide and/or hypoxia. Significant

residual drug effects are often present at the time of

tracheal extubation.

Inhalation drugs alter the regulation of CO, partial

pressures, as evidenced by the correlation between

increasing alveolar concentrations of various potent

inhaled anesthetics, and increases in resting CO, ten-

sions and declines in ventilatory responses to CO2

(75-77). Low concentrations of the potent inhalation

drugs (less than 0.5 minimum alveolar anesthetic con-

centration (MAC)) should not, in and of themselves,

produce clin ically troublesome blunting of ventilatory

response to CO2 during extubation and recovery from

surgery (78). However, low concentrations of potent

inhalation drugs may blunt the hypoxic ventilatory

response and such an effect can pose a significant risk.

Halothane, enflurane, and isoflurane, at 1 MAC in

dogs, produce significant depression of hypoxic ven-

tilatory drive. Enflurane has been reported to be the

greatest depressant of hypoxic ventilatory drive and

isoflurane the least (79). Knil l et al. (78,80,81) per-

formed several investigations of hypoxic ventilatory

drives in humans and demonstrated that even low

concentrations (0.1 MAC) of halothane and enflurane

greatly decrease the ventilatory response to isocapnic

hypoxia. A more recent report suggests that hypoxic

ventilatory drive may not be depressed by low con-

centrations of isoflurane (82). Decreases in hypoxic,

but not hypercapnic, ventilatory drive occur with ni-

trous oxide as well (83).

All p receptor opioid agonists, including morphine,

fentanyl, sufentanil, and alfentanil, produce dose-de-

pendent depression of ventilation, primarily through

a direct action on the medullary respiratory center

(84). The responsiveness of the respiratory center to

CO, is significantly reduced by opioids. The slope of

the ventilatory response to CO, is decreased, and

minute vent ilatory responses to increases in Pace, are

shifted to the right. The apneic threshold and resting

arteria l Pco, are also increased by opioids. Thus, the

primary mechanism whereby the body regulates

minute ventilation and protects itself from significant

increases in COP and respiratory acidosis is signifi-

cantly impaired by opioids. Opioids also decrease hy-

poxic ventilatory drive (85,86), and blunt the increase

in respiratory drive normally associated with in-

creased loads, such as increased airway resistance

(85).


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154 REVIEW ARTICLE MILLER ET AL. ANESTH ANALG


Delayed or recurrent respiratory depression can oc-

cur in patients recovering from general anesthesia

who have received fentanyl (87), morphine (88), me-

peridine (89), alfentanil (90), and sufentanil (91). Ex-

planations for this phenomenon include a lack of stim-

ulation or pain, administration of supplemental

analgesics and other medications, renarcotization after

naloxone administration, motor activity causing re-

lease of opioids stored in skeletal muscle, hypother-

mia, hypovolemia, and hypotension. Investigators

have noted second peaks in plasma fentanyl levels

during the drugs elimination phase (92). Secondary

peaks in fentanyl plasma levels produce parallel de-

creases in CO, sensitivity and breathing (93).

Benzodiazepines have also been shown to decrease

the acute ventilatory response to hypercarbia and hy-

poxia (94). This action is not as profound as that

observed after opioid agonists. Antagonism of signif-

icant residual benzodiazepine effects with flumazenil

can be followed by resedation because of the shorter

duration of action of the latter drug. Vecuronium and

d-tubocurarine can also decrease hypoxic ventilatory

drive, supposedly by blocking nicotinic cholinergic

receptors in the carotid body (95,96). Acety lcholine is

one of the carotid body neurotransmitters involved in

facilitating hypoxic ventilatory drive (96).

Recurrence of troublesome ventilatory depression

can occur after extubation without obvious cause. Tra-

cheal extubation, patient transport, and init ial recov-

ery room nursing assessment can result in significant

patient stimulation. Once these events have passed,

overall stimulation can subside, and possibly result in

an apparent renarcotization with inadequate

and/or obstructed ventilation. Sleep, too, especially in

association with the actions of opioid analgesics, re-

sults in significant depression of ventilatory drive (97).

Pulmonary Function

The lung routinely undergoes significant physiologic

and, at times, pathophysiologic changes during gen-

eral anesthesia that can persist after tracheal extuba-

tion. These changes frequently include decreased lung

volumes, abnormalities in gas exchange, augmented

work of breathing, and depressed mucociliary func-

tion. These changes are rarely, if ever, of benefit. They

can be detrimental and, at times, may result in signif-

icant patient morbidity. Thus, the impact of anesthesia

and surgery on lung function can significantly influ-

ence results after tracheal extubation.

Lung Volumes The most apparent and easily ex-

plained lung volume change after extubation is an

increase in dead space, which occurs as a result of

substituting the endotracheal tube volume with the

upper airway volume. Significant changes in func-

tional residual capacity (ERC) also occur periopera-

tively. FRC usually decreases by approximately 18

of total lung capacity or approximately 500-1000 mL

with induction of general anesthesia (98,991. Postop-

erative decreases in FRC are associated with surgery

of the abdomen or thorax (100,101). It is unclear

whether FRC is decreased immediately after tracheal

extubation. Ali et al. (100) and Colgan and Whang

(101) demonstrated that, although FRC is not de-

creased immediately after extubation, it is decreased

several hours later. Strandberg et al. (102) demon-

strated a decrease in FRC in 90 of patients 1 h after

surgery.

The decrease in ERC seen after induction of anes-

thesia and after extubation may be caused by different

mechanisms (103). The decrease in FRC seen immedi-

ately after induction was well illustrated by Brismar et

al. (99). In that study computed tomography revealed

areas of compression atelectasis (Figure 4). The mech-

anism for this decrease in FRC after induction of an-

esthesia has been attributed to a cephalad shift of the

diaphragm (1041, rib cage instability (105,106), and

increased intrathoracic blood volume (105). Interest-

ingly, neuromuscular block (NMB) after induction of

general anesthesia does not result in a further decrease

in FRC (105). The mechanism underlying postopera-

tive decreases in FRC is usually related to diaphrag-

matic dysfunction (102,107,108). Simonneau et al. (107)

reported that diaphragmatic dysfunction after abdom-

ina l surgery could last up to 1 wk and resulted in a

greater reliance on rib cage movement for breathing.

Diaphragmatic dysfunction is though to be secondary

to surgical irritation, inadequate pain control, and/or

abdominal distention. In addition to diaphragmatic

dysfunction, another cause of postoperative decreases

in FRC is guarded breathing (splinting). Relief of pain

can part ially restore FRC (108) and vital capacity (109),

and improve oxygenation (110).

While the clin ical consequences of decreases in FRC

are often not problematic, decreases in FRC are often

large enough to cause atelectasis (Figure 4) and ven-

tilation-perfusion abnormalities that impair gas ex-

change and decrease oxygen stores. Such lung volume

changes, if present at the time of extubation, can com-

promise a patients abi lity to tolerate airway difficul-

ties by decreasing the time available for intervention

and prevention of hypoxemia.

Hypoxemiu The incidence of hypoxemia, most fre-

quently defined as an oxyhemoglobin saturation less

than 90 , after extubation and recovery from general

anesthesia is high. As many as 24 of children (111)

and 32 of adults after a general anesthetic will be

hypoxemic upon arrival at a postanesthesia care uni t if

no supplemental oxygen is provided during transport


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ANESTH ANALG REVIEW ARTICLE MILLER ET AL.

155


Figure 4. Transverse computed tomography scan s of the thorax

before (upper) and after (lower) induction of anesthe sia, demon-

strating areas of comp ression atelecta sis (arrows) in the dependent

regions of both lungs. (Adapted with permission from Brismar B, et

al. Pulmonary dens ities during ane sthesia w ith muscu lar relax-

ation-a proposal of atelectas is. Anesthes iology 1985;62:422-8.)

(112). Marshall and Wyche (1131, in a review of hy-

poxemia during and after anesthesia, categorized

postoperative hypoxia into early and late causes. Be-

sides inadequate minute ventilation or airway ob-

struction, other causes of early hypoxemia include

increased ventilation/perfusion mismatch (114), in-

creased alveolar-to-arterial gradient (115), diffusion

hypoxia (116), obligatory posthyperventilation hy-

poventilation (117,118), shivering (1191, inhibi tion of

hypoxic pulmonary vasoconstriction (120), and a de-

crease in cardiac output (121). Late causes include

increased ventilation/perfusion mismatch (122,123)

preexisting pulmonary disease (124), old age (124),

gender (with males experiencing hypoxemia more fre-

quently than females) (125), and obesity (126). Al-

though the intraoperative administration of opioids

occasionally has been reported to increase postopera-

tive hypoxemia (127), the vast majority of studies have

not demonstrated that the use of opioids in anesthesia

is associated with an increased incidence of postoper-

ative hypoxemia (128).

Diffusion hypoxia, another cause of hypoxemia in

patients emerging from anesthesia was first reported

by Fink (116), who thought the outward diffusion of

N,O could dilu te alveolar oxygen. With the continu-

ous application of supplemental oxygen during emer-

gence and recovery from anesthesia the incidence of

clinically significant diffusion hypoxia is rare but not

unheard of (129,130).

Mucociliary dysfunction associated with anesthesia

and surgery can also contribute to postoperative hy-

poxemia. Bronchial epithelial cell cilia normally clear

mucous from the respiratory tract (131). Patients with

atelectasis have been shown to have delayed mucocili-

ary clearance (132). Anesthesia, tracheal intubation

and surgery result in mucociliary dysfunction and

abnormal or retrograde mucous flow. Mucous pooling

in dependent areas can contribute to impaired gas

exchange.

Work of Breathing Tracheal extubation of a spon-

taneously breathing patient can decrease the work of

breathing (WOB) by decreasing airway resistance and

minute ventilation (133). The presence of an endotra-

cheal tube augments spontaneous ventilation increas-

ing respiratory rate and tidal volume (134). Some

studies demonstrate transient increases in minute ven-

tilation after extubation produced by increases in re-

spiratory rate, tidal volume, and inspiratory flow, all

of which return to preextubation values within 30 min

(135). Most often, if airway obstruction is minimal,

tracheal extubation results in a decrease in the WOB.

The impact of other artificial airways, such as an oral

airway, on the WOB is unknown. Although the de-

crease in WOB after extubation should be beneficial,

as noted above, the presence of an endotracheal tube

may stimulate breathing and counteract the respira-

tory depressant effects of anesthesia while simulta-

neously maintaining the airway. An apparently ade-

quate spontaneous minute ventilation prior to

extubation may not be sustained once the trachea is

extubated.

Coughing/Bucking

Coughing frequently occurs during tracheal extuba-

tion. Bucking is a more forceful and often protracted

cough that physiologically mimics a Valsalva maneu-

ver. Unlike a Valsalva maneuver, bucking occurs at

variable lung volumes, which are often less than vital

capacity. Coughing and bucking are not only estheti-

cally unpleasant, but can also be harmful. They can

cause abrupt increases in intracavitary pressures. For

example, patients with an open eye injury or increased

intracranial pressure, can be placed at risk. Increased

intraocular and intracranial pressures result from an


8/24



increase in intrathoracic pressure that decreases ve-

nous return to the right atrium (136). Abdominal

wound separation, although rarely associated with

emergence from anesthesia, is another potential com-

plication associated with an increase in intraabdomi-

nal pressure secondary to bucking.

Bucking also results in a decrease in FRC (137).

Bucking, especially in pediatric patients, can rapidly

cause hypoxemia, not only due to the decrease in

minute vent ilation but also subsequent to the associ-

ated loss in lung volume and resultant atelectasis. The

persistence of relative hypoxemia after bucking itself

resolves illustrates the greater time and difficulty

needed to reexpand the lung compared to the ease

with which it collapses. The avoidance of bucking

during the extubation of patients is an important clin-

ical skill and art, and is one of the clin ical hallmarks

of the smooth extubation.

Cardiovascular Effects of Extubation

Many investigators have documented that tracheal

extubation causes modest (10 30 ) and transient

increases in blood pressure and heart rate, lasting 5-15

min (138-143). Although such cardiovascular stimu-

lation is usually inconsequential, certain patients may

experience unfavorable or undesirable sequelae. For

example, Coriat et al. (144) demonstrated that patients

with coronary artery disease experience significant

decreases in ejection fractions (from 55 2 7 to

45 ? 7 ) after extubation. The changes in ejection

fraction occurred in the absence of electrocardio-

graphic signs of myocardial ischemia. Wellwood et al.

(145) reported that patients with a cardiac index of less

than 3.0 L * min- * m-*

did demonstrate an ischemic

response to the stress of postoperative tracheal extu-

bation after myocardial revascularization. These pa-

tients experienced decreases in myocardial lactate ex-

traction, left ventricular compliance, and cardiac

performance. Others, however, have failed to confirm

electrocardiographic or enzymatic evidence of myo-

cardial ischemia related to tracheal extubation in pa-

tients after coronary artery surgery (146,147). Tracheal

extubation after caesarean section in parturients with

gestational hypertension can cause significant in-

creases of 45 and 20 mm Hg in mean arterial and

pulmonary artery pressures, respectively. It was con-

cluded that tracheal extubation and related hemody-

namic changes increased the risk of cerebral hemor-

rhage and pulmonary edema in those parturients

(148).

Finally, as described above, coughing often occurs

during tracheal extubation. Coughing can lead to in-

creases in intrathoracic pressure which can interfere

with venous return to the heart. The effects of cough-

ing on heart rate, systolic, diastolic , and arteria l pulse

pressure, and coronary flow velocity have been eval-

uated by Kern et al. (149). Fourteen patients undergo-

ing routine diagnostic coronary arteriography were

evaluated. Coughing significantly increased systolic

pressure (from 137 -+ 25 to 176 -+ 30 mm Hg), diastolic

pressure (from 72 + 10 to 84 + 18 mm Hg), and

arteria l pulse pressure (from 65 -t 27 to 92 -+ 35 mm

Hg), without changing heart rate. Mean coronary flow

velocity decreased (from 17 + 10 to 14 2 12 cm/s> in

these patients.

In summary, significant hemodynamic stimulation,

to varying degrees, can be at least transiently pro-

duced by tracheal extubation. Although these changes

are usually inconsequential, patients at particular risk

may occasionally be adversely affected by tracheal

extubation. Thus, the potentia l for deleterious hemo-

dynamic events to follow extubation, while most often

rare, should not be ignored.

Neurologic Effects of Extubation

It is well established that laryngoscopy and intubation

increase intracranial pressure (ICI), the greatest in-

crease being elic ited in patients with decreased intra-

crania l compliance (150). However, the effects of tra-

cheal extubation on ICI have not been investigated.

Although it is likely that extubation causes at least

transient increases in ICI, the existence of such effects

must be extrapolated from other data.

Donegan and Bedford (151) reported that ICI in-

creased by 12 + 5 mm Hg in comatose patients whose

tracheas were suctioned. White et al. (152) also found

ICI? increased from 15 t 1 to 22 + 3 mm Hg after

endotracheal suctioning in fully resuscitated, coma-

tose intensive care unit (ICU) patients. The ICI in-

creases lasted for less than 3 min after suctioning. Both

authors hypothesized that coughing associated with

endotracheal suctioning causes ICI to increase by in-

creasing intrathoracic pressure, cerebral venous pres-

sure, and cerebral blood volume. Thus tracheal extu-

bation, especially when associated with suctioning

and/or coughing or bucking, is also likely to increase

ICP.

Increases in arterial blood pressure often result from

tracheal extubation as mentioned above, and arterial

hypertension can also lead to or be associated with

intracranial hemorrhage or increases in ICI (153). Pos-

sibly, associated hemodynamic changes, during and

after extubation, can also negatively impact patients

with intracranial pathology.

The problems and pitfalls of airway management in

patients with cervical spine injuries have been docu-

mented (154). Although not studied, the potential for

neurologic damage during the extubation of such pa-

tients after cervical spine stabil ization procedures

seems remote. However, the preoperative injury, as


9/24


157

1995;80:149-72 POSTO PERAT IVE TRACHEAL EXTUBATION

well as the cervical spine surgery, can result in signif-

icant postoperative edema formation and/or bleeding

and airway dysfunction. Cervical spine injury or

edema can also impair neural drive and phrenic nerve

and diaphragmatic function.

In summary, although the neurologic consequences

of tracheal extubation have not been evaluated, cough-

ing, bucking, and arterial hypertension during tra-

cheal extubation can all be detrimental, especially in

patients with existing intracranial pathology. The

maintenance of adequate ventilatory drive and airway

function after extubation is also likely to be more

difficult in patients undergoing intracranial or cervical

spine surgery.

Hormonal Effects of Extubation

Recognition that a significant and potentially deleteri-

ous stress response can result from the induction of

anesthesia, tracheal intubation, and surgery has led to

numerous documentations of this phenomenon. On

the other hand, the endocrine response to tracheal

extubation has received little attention. Lowrie et al.

(143) evaluated the impact of tracheal extubation on

changes in plasma concentrations of epinephrine and

norepinephrine in 12 patients undergoing major elec-

tive surgery. Epinephrine levels were significantly

increased from 0.9 to 1.4 pmol/mL only 5 min af-

ter extubation. Norepinephrine

levels remained

unchanged.

Adams et al. (155) performed an investigation in

which 40 patients, undergoing herniorraphy or chole-

cystectomy, were anesthetized with either isoflurane

or halothane and extubated at 0.5 MAC depth of an-

esthesia or awake. Significant but transient (lasting

minutes) increases in plasma epinephrine levels oc-

curred in all patients but to greater degrees in those

anesthetized with isoflurane versus halothane and in

those extubated prior to awakening. Norepinephrine

levels also increased in all patients except those extu-

bated awake after halothane anesthesia. Although an-

tidiuretic hormone levels increased in all patients after

extubation, neither adrenocorticotropic hormone nor

cortisol levels did.

These few investigations indicate that an endocrine

response to tracheal extubation can occur. This re-

sponse appears to be modest and transient in nature,

and unlikely to have a negative impact.

Extubation Criteria

The ability to predict adequate respiratory function

after extubation depends on many factors. In broad

terms, anesthesia and specific pharmacologic thera-

pies used to permit tracheal intubation and mechani-

cal ventilation must be sufficiently reversed. In addi-

tion, any underlying pathologic determinants of the

need for mechanical ventilation, whether they be med-

ical (e.g., pneumonia) or iatrogenic (e.g., thoracoto-

my), must be addressed, so that spontaneous ventila-

tion can sustain adequate cardiopulmonary function.

The operative setting often differs from the ICU in that

the factors leading to required mechanical ventilation

(anesthesia, surgical insult, residual anesthetics, neu-

romuscular blockers) are primarily iatrogenic. In ad-

dition, these factors are usually rapidly reversed. ICU

patients frequently require mechanical ventilation be-

cause of cardiopulmonary disease and pathologic pro-

cesses hat interfere with gas exchange. A discussion

of the process of weaning ICU patients from ventila-

tory support is not the objective of this paper; how-

ever, many of the criteria commonly used to predict

successful tracheal extubation are derived from the

study of such patients.

Predicting whether a patient will tolerate tracheal

extubation after general anesthesia requires knowl-

edge of the patients current cardiopulmonary status

as well as the presence and impact of residual anes-

thetics, including muscle relaxants. The cardiopulmo-

nary system is of particular concern, especially if or-

gan dysfunction and pathology might preclude

immediate postoperative extubation. Cardiopulmo-

nary function criteria focus primarily on ventilatory,

hemodynamic, neuromuscular, and hematologic con-

siderations. Specific respiratory concerns include

breathing pattern, ventilatory drive, airway function,

ventilatory muscle strength, and gas exchange. Car-

diovascular concerns include hemodynamic stability

in order to ensure adequate circulation and respira-

tory gas transport, both through the lungs and sys-

temically. The impact of residual NMB and determi-

nation of its adequate reversal is also key. Hemoglobin

levels sufficient for adequate oxygen transport and

hemostasis should be achieved (156). While the above

considerations are important and well known to clini-

cians, specific derived and objective criteria for pre-

dicting successful extubation are often lacking. For

instance, single independent factors, such as the he-

matocrit, cannot be considered in isolation but only as

part of larger formulas, organ system(s) function, and

the patient as a whole. Frequently used objective cri-

teria used to decide whether to extubate a patient will

be reviewed.

Breathing Patterns

Spontaneous breathing patterns provide information

about respiratory efficiency and the likelihood of suc-

cessful extubation. Two types of breathing patterns,

either a rapid shallow breathing pattern or a paradox-

ical breathing pattern (asynchronous motion of the rib

cage and abdomen) indicate an increased risk that

extubation will not be successful or that it is failing.


10/24

158

REVIEW ARTICLE MILLER E T AL.

POSTOPERATIVE TRACHEAL EXTUBATION

ANESTH ANALG

1995:80:149-72

Rapid shallow breathing is often secondary to me-

chanical dysfunction and causes inefficient gas ex-

change (157). Yang and Tobin (158) studied medical

ICU patients and found that the frequency of breaths

per minute divided by the tidal volume in liters (f/Vt>

is a reliable predictor of extubation success. Patients

with f/Vt values of less than 100 had successful tra-

cheal extubation. In that study, the f/Vt ratio proved

superior to minute ventilation, tidal volume, respira-

tory rate, maximal inspiratory pressure, and static or

dynamic compliance in predicting successful weaning

and extubation.

Paradoxical breathing, or asynchronous motion of

the rib cage and abdomen, can imply the onset of

respiratory failure, especially in cases of pulmonary

insufficiency (157). Respiratory muscle fatigue can un-

derlie this phenomenon and in an attempt to conserve

energy, the intercostal muscles and the diaphragm

contract alternately. Paradoxical or rocking boat

breathing patterns are also seen in patients with sig-

nificant residual NMB and/or airway obstruction.

Respiratory Muscle Strength

Neuromuscular Block Tracheal extubation after gen-

eral anesthesia is at times unsuccessful because resid-

ual muscle relaxation results in airway obstruction

and/or inadequate minute ventilation. The presence

of residual muscle relaxation is less likely to result in

inadequate minute ventilation than airway obstruc-

tion (73,159,160). Uncoordinated breathing, dyspnea,

and/or accompanying anxiety often further exacer-

bate conditions. Clinicians usually attempt to objec-

tively determine adequate neuromuscular function by

peripheral nerve stimulation, clinical strength tests,

and maximum inspiratory pressure (ME).

Ali et al. (161,162), using ulnar nerve evoked elec-

tromyograms, suggested that a train-of-four (TOF) ra-

tio of 0.6 to 0.7 correlated well with signs of adequate

clinical recovery and safe extubation. However, the

TOF ratio cannot always predict adequate ventilation

and airway muscle strength after tracheal extubation.

Possible explanations for this include the fact that

visual and/or tactile assessmentof the TOF ratio has

not been found to be clinically reliable (163,164). The

use of subjective rather than objective TOF ratio meas-

ures may explain the finding that up to 28 of recov-

ery room patients have a TOF ratio of less than 0.7

(165). Other factors, such as increases in Pace,, can

also impair the pharmacologic reversal of neuromus-

cular block.

The double-burst technique has been suggested to

improve the clinical accuracy of peripheral nerve stim-

ulation (166). Although visual observation of the dou-

ble-burst technique is 90 accurate at predicting a

TOF ratio less than 0.5, it is only 44 accurate in

-60

MIP

-40

(cmH20)

-30

J

Figure 5. Maximum inspiratory pressure (MB) below which the

indicated clinic al maneuvers could not be performed after incre-

mental neuromuscular block with curare in volunteers. Note that

the head lift is the most sen sitive clinic al indicator of residual

neuromuscu lar block with d-tubocurarine chloride. All asterisks

indicate different and statistically significan t P values for MIP indi-

cated by the bar graph versus a MIP of -25 cm H,O (dotted line).

(Adapted with permission from Pavlin EG, Holle RH, Schoen e RB.

Recovery of airway p rotection compared with ventilation in hu-

mans after paralysis curare. Anesthes iology 1989;70:381-5.

predicting a TOF ratio less han 0.7 (166). Thus, neither

the TOF ratio nor the double-burst technique, when

applied with a standard peripheral nerve stimulator,

permit great accuracy, and do not reliably permit the

diagnosis of significant residual NMB. The reliability

of a sustained tetanic response to peripheral nerve

stimulation as a predictor of successful tracheal extu-

bation has not been documented to our knowledge.

Clinical assessment of respiratory muscle strength

prior to extubation includes observation of head lift,

leg lift, hand grip strength and/or the MIP that can be

generated against an occluded airway. The head lift

was introduced by Varney et al. (167), who standard-

ized the assessmentof NMB by using the rabbit head

drop as an indication of muscle relaxation. The ability

to perform a 5-s head lift, perhaps the most reliable

test of adequate neuromuscular strength, correlates

with a TOF ratio of 0.7-0.8 (168). Dam and Guldmann

(169), and others (73,170,171), have advocated the use

of the head lift as a reliable test of adequate respiratory

muscle strength. Pavlin et al. (73) administered incre-

mental small doses of curare to awake volunteers,

decreasing MIP from -90 cm H,O to -20 cm H,O,

and studied the correlation between the progressive

muscle relaxation, airway obstruction, and clinical

tests including the 5-s head lift, leg lift, and grip

strength (Figure 5). The 5-s head lift was again found

to be the most reliable indicator of adequate airway

muscle strength and function. Interestingly, adequate

minute ventilation could be sustained when airway


11/24

ANESTH ANALG

1995;80:149-72

REVIEW ARTICLE MILLER ET AL. 159

POSTOFERATIVE TRACHEAL EXTUBATION

support was provided, despite the presence of signif-

icant paralysis.

The MIP is often quoted as a measure of adequate

respiratory muscle strength. Bendixen et al. (172) dem-

onstrated in a small series of patients that a MIP of

-20 to -25 cm H,O was necessary to maintain ade-

quate minute ventilation, and suggested that inspira-

tory force measurement could be a valid measure of

ventilatory capacity. Sahn and Lakshminarayan (173)

demonstrated that 100 of patients in the ICU with a

MIP of -30 cm H,O could be extubated successfully,

and others have agreed (174). Pavlin et al. (73) dem-

onstrated, however, that when volunteers were ad-

ministered incremental doses of curare in order to

decrease the mean MIP of -90 cm H,O to -20 cm

H,O, minute ventilation, but not airway function,

could be maintained (Figure 5). In fact, airway ob-

struction persisted unless a mean MIP of at least -40

cm H,O could be produced. A 5-s head lift could be

consistently reproduced only when patients demon-

strated a mean MIP of -53 cm H,O. A study that

tested both the MIP and the TOF ratio could not

demonstrate any correlation between the two tests

(168). The above studies are supported by the clin ical

observation that adequate minute ventilation prior to

extubation is at times not sustained once airway sup-

port (e.g., an endotracheal tube) is removed.

In conclusion, peripheral nerve stimulation is a

valuable tool for the intraoperative titration of muscle

relaxants and assessment of NMB (175); however, TOF

monitoring is fal lib le as a clin ical predictor of success-

ful extubation. Similarly, measurement of intraopera-

tive maximum inspiratory pressure to prove adequate

return of muscle function is variably predictive and

also used much less frequently. The abi lity of patients

to perform a 5-s head li ft is the simplest and most

reliable method to date to determine the return of

sufficient muscle strength after NMB and its reversal.

However, many anesthetized patients are extubated

prior to regaining responsiveness, an approach which

removes the abi lity of a patient to respond to a com-

mand requesting them to perform a head lift maneu-

ver. There is often little uncertainty concerning the

adequacy of neuromuscular and airway function, and

therefore little need to perform a head lift test. Nev-

ertheless, when there is concern for whether a patient

can maintain their airway and spontaneous venti-

lation, performance of a 5-s head lift prior to extuba-

tion is recommended as the best predictor of such

functions.

Extubation Techniques

The actual technique of tracheal extubation has re-

ceived remarkably lit tle scientific study. This fact is al l

the more curious in light of the attention and impor-

tance given to protecting the lungs from aspiration

during periods where airway function is compro-

mised. The lack of substantial information with regard

to the advantages or disadvantages of various tracheal

extubation techniques also stands in contradistinction

to the number and intensity of opinions on the matter.

Extubation and Trailing Suction Catheters

In 1972, Mehta (176) studied several endotracheal tube

(ETT) placement and extubation techniques and asso-

ciated pulmonary aspiration in 90 patients undergoing

different surgical procedures. After intubation, ETT

cuffs were inflated until an airtight seal was obtained.

Mehta evaluated the efficacy of six different extuba-

tion techniques in preventing aspiration of radio-

graphic dye placed on the back of the tongue. Only

two techniques resulted in no radiographic signs of

aspiration. One of these approaches involved placing

the ETT so that the proximal end of the cuff was just

beyond the true vocal cords. The second method in-

volved tilting the operating table 10 head down, suc-

tioning the pharynx, and then placing the suction

catheter through the ETT and removing both the ETT

and the trailing suction catheter while applying gentle

suction. In other patient groups, pharyngeal suction-

ing alone or trailing the suction catheter without some

head down positioning did not prevent radiographic

dye lung contamination. The authors concluded that

liquid matter (e.g., regurgitated gastric contents,

blood) can accumulate above the ETT cuff and be

aspirated. Others (177,178) have also demonstrated

that a column of fluid can accumulate around the ETT

above the cuff, and below the vocal cords. Recommen-

dations to minimize this phenomenon include using

the largest possible diameter ETT, use of gauze pads

in the hypopharynx, and use of the Trendelenburg

position (178).

Cheney (179), in a correspondence concerning

Mehtas report, agreed that ETT cuff placement just

below the true vocal cords and the head down posi-

tion prior to extubation was advantageous. However,

he argued against suctioning through the ETT at the

time of its withdrawal, fearing depletion of lung oxy-

gen stores as well as interruption of air and oxygen

flow into the lungs. Cheney suggested a method

where patients receive several positive pressure

breaths of 100 oxygen after endotracheal suctioning

and just prior to cuff deflation. Any accumulated en-

dotracheal contents above the cuff would then theo-

retically be expelled into the pharynx by the positive

pressure gradient established between the lungs and

the atmosphere after cuff def lation and tube with-

drawal. This technique would hypothetica lly leave the


12/24



1995:80:149-72

extubated patient with a clear airway and oxygen-

fil led lungs. In support of Cheneys assessment, both

Urban and Weitzner (180) and Jung and Newman

(181) have demonstrated that endotracheal suctioning

can lead to hypoxemia.

Positive-Pressure Breath and Extubation

The method of extubation that includes delivering a

large positive pressure breath immediately prior to

extubation has received support (182,183), and most

major anesthesiology textbooks describe tracheal ex-

tubation via this method. It is stated that the lungs

should receive a large sustained inflation (to near total

lung capacity), then the ETT cuff should be deflated

and the trachea extubated. This sequence often causes

the first postextubation respiratory event to be a cough

which, in theory, clears the airway and vocal cords of

secretions. Garla and Skaredoff (184) further recom-

mend that closure of anesthesia machines adjustment

pressure limiting valve can produce and sustain lung

inflation prior to deflating the cuff and extubation. It is

unknown to what extent, if any, material that has

accumulated in the trachea, above an endotracheal

tube cuff, is actually expelled by a positive pressure

breath prior to extubation. We could find no well

controlled clinical study or scientific evidence delin-

eating the merits or disadvantages of this extubation

maneuver or technique compared to others.

While the study by Mehta (176) represented a useful

beginning to research in this area, no further work has

since bui lt upon it . Thus, many questions remain un-

answered, especially since Mehtas work evaluated

radiographic evidence of aspiration as the only out-

come measure. Other concerns, not addressed by

Mehta but also of importance during and after tra-

cheal extubation, include the resultant degree of

breath holding or breathing pattern disturbance, air-

way patency or compromise, subsequent oxyhemo-

globin desaturation, and the number and type of in-

terventions necessary after each extubation method.

Deep Versus Awake Extubation

Historically, Guedel (185) was the first to describe the

clinical stages of ether anesthesia. During the second

stage, uninhib ited activity, unconsciousness, and ex-

citement are manifest. Clinically important reflex ac-

tivities (e.g., laryngospasm, vomiting) are readily elic-

ited during second stage by procedures such as

laryngoscopy and tracheal intubation or extubation.

Thus, the premise that tracheal extubat ion should oc-

cur when patients are either fully awake or at surgical

(deep) levels of anesthesia. The common use of bal-

anced anesthesia often obscures the clinical signs of

the second stage. It is also not clear to what extent a

second and excitatory stage even exists with balanced

or intravenous anesthetic techniques. Consequently,

proof of necessity for deep extubating conditions,

and what leve l of anesthesia is adequately deep, is

somewhat arbitrary and debatable.

Evaluation of tracheal extubation at deep or surgical

levels of general anesthesia versus during the awake

state has only been investigated in the pediatric pa-

tient population. Pate1 et al. (186) examined 70 healthy

children for differences in oxygen saturation and air-

way-related complications after awake or deep ex-

tubation. Patients were undergoing either elective

strabismus surgery or adenoidectomy and/or tonsil-

lectomy. Patients randomly assigned to be extubated

awake breathed 100 oxygen for at least 5 min and

had end-tidal halothane concentrations of less than

0.15 prior to extubation. Patients extubated at deep

levels of anesthesia had end-tidal halothane concen-

trations of greater than 0.8 at the time of extubation.

Both groups, breathed 100 oxygen for 5 min after

extubation. At 1, 2, 3, and 5 min after extubation,

patients extubated deep had significantly higher oxy-

hemoglobin saturations than patients extubated

awake (Spa, 97.6 + 3.7 to 99.8 + 0.5 vs

93.7 t 4.8 to 98.6 & 2.5 ). Oxygen saturation

values were similar thereafter. The incidence of post-

operative laryngospasm, excessive coughing, breath

hold ing, airway obstruction requir ing positive pres-

sure vent ilation after extubation, or arrhythmias was

not statistically different between patients extubated

awake or deep. These investigators concluded that for

healthy children undergoing elective surgery, clinical

conditions or the preference of the anesthesiologist

should dictate the choice of extubation technique.

A similar investigation was conducted by Pounder

et al. (187) comparing halothane and isoflurane with

respect to the incidence of complications after awake

and deep tracheal extubation. One hundred children

undergoing minor urologic surgery or abdominal her-

niotomy were studied. A comparison of patients who

underwent deep extubations with either inhalation

drug revealed no statistical differences in the inci-

dence of coughing, breath-holding, airway obstruc-

tion, laryngospasm, or the lowest oxyhemoglobin sat-

uration levels (halothane 97 -+ 1.9 and isoflurane

96.5 2 2.1 ). Patients extubated awake demon-

strated a higher incidence of coughing (18 vs 7), air-

way obstruction (9 vs 2), and total number of any

respiratory complications (20 vs 10) after isoflurane

versus halothane. There were no significant differ-

ences in the incidence of oxyhemoglobin desaturation

to less than 90 or lowest saturation recorded

(87.4 5 11.2 vs. 89.0 t 11.2 ) between isoflurane

and halothane anesthetized patients extubated awake.

Patients anesthetized with halothane experienced a

lower incidence of oxyhemoglobin desaturation to less

than 90 when extubated deep versus awake (0 vs 6).


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REVIEW ARTICLE MILLER ET AL.

161


Table 2. Number (and Percent) of Pediatric Patients Experiencing the Listed Complications After Halothane or Isoflurane

and Tracheally Extubated Awake or Deep

Complications Deep

Halothane Isoflurane

Awake

Deep Awake

Coughing

Breath-holding

Airway obstruction

Laryngospasm

Any complication

spo, < 90

Lowest saturation level

recorded (mean 2

SD)

3 (12) 7 (28) 1 (4) 18 (72)b,d

5 (20) 3 (12) 7 (28) 8 (32)

5 (20) 2 (8) 7 (28) 9 (36jb

0 1 (4) 1 (4) 3 (12)

10 (40) 10 (40) 12 (48) 20 (so)b,d

0 6 (24) 0 11 (44)d

97 t 1.9 89.0 +- Il.2 96.5 + 2.1 87.4 k 11.2

Adaoted from Pounder DR. Blackstock D. Steward DT . Tracheal e xtubation in children: halothane versus isoflurane. anesthetized versus awake. Anesthesi-

ology 1991; 74654-5, with permission.

a See text for details.

b Statistically different fro m awake/halothane group.

Statistically different fro m deep/halothane group.

d Statistically different fr om deep/isoflurane group.

Patients anesthetized with isoflurane and extubated

deep had significantly less coughing (1 vs 18) and a

lower incidence of at least one respiratory complica-

tion (12 vs 20) than those extubated awake. Awake

versus deep extubation after isoflurane anesthesia also

resulted in a higher incidence of oxyhemoglobin de-

saturations to less than 90 (11 vs 0). The authors

concluded that in children with normal airways,

awake extubations after either halothane or isoflurane

anesthesia results in more hypoxemia (Spa, < 90 )

than deep extubation. Anesthesia with isoflurane ver-

sus halothane also results in more coughing and air-

way obstruction after awake extubation (Table 2). The

authors also stated that, if it is desirable to extubate a

patient awake, the use of halothane, instead of isoflu-

rane, may improve emergence.

Many anesthesiologists believe, and it is widely

taught, that it is advantageous to extubate patients at

risk of developing bronchospasm at surgical levels of

anesthesia. Actual clinical investigations of this prin-

ciple could not be found. The basis for this approach

stems from multiple studies of the effects of general

anesthesia, and in particular the potent inhalation an-

esthetics, on bronchial smooth muscle and airway re-

activity. Shnider and Paper (188) concluded from a

retrospective study that during general anesthesia, pa-

tients who had their tracheas intubated experienced

significantly more wheezing than nonintubated pa-

tients. They also suggested that halothane was a valu-

able inhalation drug for anesthetizing patients with

reactive airway disease and for treating intraoperative

bronchospasm. Many investigators have evaluated the

effects of inhalational drugs on airway reflexes and

determined that ether (189), cyclopropane (190), enflu-

rane (20,191), and isoflurane (191) obtund or block

airway reflexes which could lead to bronchospasm by

directly relaxing smooth muscle or by inhibiting me-

diator release (192,193). Thus, there is significant evi-

dence to strongly suggest a role for the potent inhala-

tion drugs in relaxing bronchial smooth muscle tone

and controlling airway reflexes and reactivity. Al-

though deep extubation may represent a practice of

this principle and an effective technique for patients

with reactive airway disease, there is no adequate

clinical investigation substantiating any real benefit to

this approach.

Pharmacologic Interventions

Several pharmacologic approaches to attenuate the

physiologic changes associated with tracheal extuba-

tion have been evaluated. Local anesthetics, and in

particular lidocaine, have received the most attention.

Steinhaus and Howland (194) observed that patients

have a smoother anesthetic course when nitrous

oxide-thiobarbiturate anesthesia was combined with

lidocaine to suppress pharyngeal and laryngeal re-

flexes. Laryngospasm and coughing too was success-

fully treated with intravenous (IV) lidocaine. In a fol-

lowup study, Steinhaus and Gaskin (195) found IV

lidocaine (1.1 mg/kg) more effectively suppressed

coughing and resulted in no apnea compared to so-

dium thiopental(l.l mg/kg, IV) and meperidine (0.36

mg/kg, IV). Poulton and James (196) also found IV

lidocaine (1.5 mg/kg) compared to saline, produced

significant reductions in the number of cough re-

sponses (24 + 11 to 9 + 9) in subjects induced to cough

by the inhalation of nebulized aqueous citric acid.

In a study of 40 children undergoing elective ton-

sillectomy, Baraka (197) evaluated the effects of IV

lidocaine on preventing or controlling laryngospasm

associated with extubation. Anesthesia was induced

and maintained with halothane in oxygen and discon-

tinued 5 to 10 min prior to the end of surgery. None of


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1995;80:149 -72

the 20 patients receiving an IV bolus of 2 mg/kg of

lidocaine 1 min prior to extubation developed laryn-

gospasm after extubation; 4 of 20 patients in the con-

trol group had severe laryngospasm after extubation.

IV lidocaine, 2 mg/kg, rapidly controlled laryngo-

spasm in these children. The observations of Baraka

were not confirmed in a double-blind study by Leicht

et al. (1981, who evaluated the effect of prophylactic IV

lidocaine on laryngospasm after extubation in chil-

dren undergoing tonsillectomy. The incidence of la-

ryngospasm was the same between lidocaine and sa-

line groups. Leicht et al. (198) concluded that their

results differed from Barakas because of differences

in the time interval time (4.5 vs 0.5 to 1.5 min) between

lidocaine administration and extubation, and that the

central effect of lidocaine had already dissipated in the

children they evaluated. The duration of action of

lidocaine is such that it should be administered 60-90

s prior to tracheal stimulation or extubation. Although

a central mechanism of action of lidocaine is cited as

likely (198), peripheral airway suppressant effects (see

below) may also exist. Other IV drugs, including me-

peridine, doxapram, and diazepam, have occasionally

been reported to relieve laryngospasm (199,201).

The use of aerosolized loca l anesthetics to suppress

coughing has also been evaluated. For example, the

inhalat ion of nebulized 20 lidocaine or 5 bupiva-

Caine has been shown to abolish the cough reflex in

animals (202-204). Cross et al. (204) found that inha led

aerosolized bupivacaine significantly suppressed

coughing triggered by inhaled citric acid or tactile

stimulation of the trachea with a suction catheter via

tracheotomy stomas. However, the same effects were

not produced by IV bupivacaine. Thomson (205) as-

sessed the effects of nebulized 4 bupivacaine on

seven normal subjects and eight asthmatic patients. In

all cases, bupivacaine prevented coughing triggered

by inhaled aerosolized citric acid. Local anesthetics,

administered either systemically or as aerosols, can

also attenuate bronchospasm by directly relaxing air-

way smooth muscle, inh ibi ting mediator release,

and/or interrupting reflex arcs (206,207).

The effects of lidocaine on blood pressure and heart

rate responses to tracheal extubation were evaluated

by Bidwai et al. (138,139) and Wallin et al. (142). In

their first investigation, Bidwai et al. administered 1.5

mL of 4 lidocaine down the ETT 3 to 5 min prior to

extubation. While the tube was being slowly with-

drawn, they also sprayed a second dose of 1.0 mL of

4 lidocaine down the ETT. No statistically significant

increases of systolic and diastolic blood pressure or

heart rate occurred 1 or 5 min after extubation. In a

similar study, IV lidocaine (1 .O mg/ kg), administered

2 min prior to extubation, was also effective in block-

ing increases in blood pressure and heart rate 1 and 5

min after extubation (138). Wallin et al. (142) evalu-

ated the efficacy of a continuous IV lidocaine infusion

in attenuating the hemodynamic response periopera-

tively. Sign ificant blunting of increases in systolic

blood pressure (SBP) and heart rate were observed in

patients who received the lidocaine infusion 5 and 10

min after extubation.

IV lidocaine has also been used to treat increases in

ICI associated with endotracheal suctioning. Donegan

and Bedford (151) demonstrated that IV lidocaine (1.5

mg/kg) administered 2 min prior to endotracheal suc-

tion ing attenuated increases in ICI normally caused

by this procedure. However, White et al. (152) used

the same amount of IV lidocaine administered 2 to 3

min prior to endotracheal suctioning, and observed

significant increases in ICI (peak increase of 19 + 3

mm Hg from baseline). It is unclear why their results

differ from those of Donegan and Bedford (151). White

et al. (152) also evaluated IV fentanyl (1 pg/kg), thio-

pental (3 mg/kg), and intratracheal lidocaine (1.5

mg/kg), by the same protocol and observed similar

increases in ICI with endotracheal suctioning. Since

the test drugs in the amounts studied were unable to

suppress the cough reflex, they concluded that cough-

ing caused the ICI increases seen with endotracheal

suctioning. Thus, lidocaine may be an effective sup-

pressant of ICI increases during tracheal extubation if

coughing is eliminated.

In summary, the above results indicate that lido-

Caine is usually an effective therapeutic drug when

attempts to decrease or avoid several of the physio-

logic sequelae of tracheal extubation are merited. Al-

though some studies suggest that the mechanism of

loca l anesthetic action in cough suppression supports

their topical application (2021, the IV administration of

lidocaine, in an appropriate dose (l-2 mg/kg) and in

a timely fashion (l-2 min before extubation) will often

reduce the coughing or bucking as well as the cardio-

vascular responses to extubation. In addition, sponta-

neous vent ilation and respiratory pattern will usually

be preserved after an IV bolus of lidocaine.

Esmolol has also been used to attenuate hemody-

namic responses to tracheal extubation. Dyson et al.

(140) studied forty ASA grade I and II patients sched-

uled for elective surgery. Patients received either es-

molol(1.0 mg/kg, 1.5 mg/kg, or 2.0 mg/kg) or normal

saline IV in a randomized fashion 2 to 4 min prior to

extubation. While al l doses of esmolol controlled the

heart rate response to extubation, 1.0 mg/kg of esmo-

101 did not attenuate increases in SBP whereas 1.5

mg/kg and 2.0 mg/kg did. The largest dose of esmo-

101 esulted in significant hypotension and the authors

recommended 1.5 mg/kg of IV esmolol as the best

dose to control hemodynamic responses to tracheal

extubation. Muzzi et al. (208) also found IV esmolol

(500 pg/kg loading dose followed by a 50-300


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1995;80:149-72


pg * kg- * min- infusion) and labetolol (0.25 to 2.5

mg/kg) equally effective in treating increases in blood

pressure during emergence and recovery from anes-

thesia after intracranial surgery.

Fuhrman et al. (141) compared the effects of esmolol

and alfentanil on heart rate and SBP during emergence

and extubation in a randomized double-blind investi-

gation of 42 healthy patients having elective surgery.

Their patients received either a normal saline bolus

followed by a normal saline infusion, a 5 pg/kg alfen-

tanil bolus followed by normal saline infusion, or a

500 pg/kg esmolol bolus followed by a 300

pg. kg- * mini esmolol infusion when end-tidal

isoflurane levels were 0.25 or less. Only the bolus

dose with subsequent infusion of esmolol significantly

controlled the heart rate and SBP response to emer-

gence and extubation. Alfentanil controlled these he-

modynamic variables during emergence, but both

heart rate and SBP increased (from 81 to 108 bpm and

from 121 to 147 mm Hg, respectively) with extubation.

The time to extubation was also significantly pro-

longed with alfentanil (12.6 min), versus the esmolol

group (8.8 min) and the placebo group (8.1 min).

These studies demonstrate that esmolol can be used to

control the hemodynamic response to tracheal extuba-

tion. Significant hemodynamic responses to postoper-

ative tracheal extubation also occur less frequently in

patients taking P-adrenergic blockers prior to their

coronary artery surgery (209).

Finally, Coriat et al. (144) reported that a contin-

uous infusion of nitroglycerin (0.4 pg * kg- * min-1

significantly reversed or eliminated decreases in left

ventricular ejection fraction that occurred in patients

with mild angina 3 min after extubation. The nitro-

glycerin infusion was started prior to induction, con-

tinued throughout surgery, and terminated 4 h after

extubation. Nitroglycerin infusion did not, however,

prevent increases in heart rate (from 85 t 8 to 99 ?

7 bpm) and SBP (from 122 +- 9 to 140 + 8 mm Hg)

during extubation.

Routine Tracheal Extubation

It is clear that experience, clinical skill, and art form

the basis of techniques for routine postoperative tra-

cheal extubations. Our recommendations are based on

the literature reviewed herein, combined with our

own experience, as well as that of others. Prior to

extubation, patients should be free of processes

known to cause or exacerbate airway obstruction (Ta-

ble 1). The possibility of such a problem is likely to be

increased with surgery of the head and neck. Often a

quick, gentle look with a laryngoscope can detect po-

tential problems such as edema or persistent bleeding

in the airway. In addition to direct visualization, gen-

tle suctioning can also be diagnostic, as well as thera-

peutic, by removing substances such as blood. The

ease or difficulty with which patients were ventilated

by bag and mask and intubated during the induction

of anesthesia should also be considered. Obviously,

adequate spontaneous ventilation should be estab-

lished prior to tracheal extubation. As reviewed

above, this includes the return of adequate ventilatory

drive, tidal volumes, respiratory rate, breathing pat-

terns, and oxygenation. Pathology and/or surgery

that might preclude the maintenance of adequate

spontaneous ventilation after extubation should also

be considered. In certain circumstances, a conservative

approach to extubation may be preferable, especially

if baseline cardiovascular or respiratory function is

significantly impaired. NMB, if used, should be ade-

quately reversed. While the 5-s head lift test is fre-

quently not applied, it remains the most reliable test

when assurance of sufficient neuromuscular function

is required. Clinical experience, limiting the applica-

tion of muscle relaxants to appropriate surgical indi-

cations, and careful titration of muscle relaxants to

avoid overdose will help reduce complications associ-

ated with neuromuscular blockers.

Using appropriate but gentle pharyngolaryngeal

suctioning, administration of IV lidocaine in a timely

manner, and whether to provide a positive pressure

breath immediately prior to extubation have been dis-

cussed. Evidence, presented above (see Figure 11, hat

laryngeal adductor neuron firing is less active during

inspiration (11) actually implies that endotracheal

tube removal during this phase of the respiratory cy-

cle would produce less laryngospasm. Our own clin-

ical experience suggests that after IV lidocaine, 1.0-l .5

mg/kg, and gentle oropharyngeal suctioning, tracheal

extubation at the onset of an active inspiration without

any manual augmentation of the preceding tidal

breath results in less laryngospasm and minimal in-

terruption of the spontaneous ventilatory pattern. We

use this particular extubation technique with patients

who, as part of their anesthesia, have received anal-

gesic doses of an opioid and are breathing isoflurane,

usually 0.4 to 0.8 , with nitrous oxide in oxygen.

Nitrous oxide is discontinued when lidocaine is ad-

ministered permitting time for reoxygenation of the

lungs. Our intent is to provide the minimum level of

anesthesia necessary to prevent any response to ETT

cuff deflation and extubation. If swallowing, for ex-

ample, immediately precedes extubation, coughing

and/or bucking are likely to occur as the ETT is re-

moved. It is, however, only with time that each clini-

cian learns to include or omit the above-mentioned

and/or other maneuvers from their particular extuba-

tion technique. The concentrations of inhaled anes-

thetics, if any, that should be used at the time of


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extubation must also be tailored to each patients re-

quirements and conditions.

Immediately after routine tracheal extubation of the

spontaneously breathing patient, breathing pattern

and airway patency should be assessed.The applica-

tion of a gentle jaw thrust maneuver and neck exten-

sion, combined with 100 oxygen administered by

4-8 cm Hz0 of continuous positive airway pressure

(CPAP) via mask, optimizes diagnosis as well as ther-

apy. A hand on the rebreathing bag of a circle system

can assess he seal achieved by the face mask, quali-

tatively measure spontaneous respiratory functions,

and maintain CPAP which stents the airway open and

assists breathing. Excessive positive pressure can be

released easily by slightly lifting the mask or adjusting

the pressure limiting (pop-off) valve. With this sim-

ple approach, breathing pattern and airway function

can be assessed, and if necessary first interventions

(100 oxygen, administered via positive pressure)

made. In most experienced hands, breathing pattern

and tidal volume are adequate and further interven-

tion is unnecessary as patients emerge from general

anesthesia and tracheal extubation.

Prevention and Treatment of

Hypoxemia After Extubation

The incidence and risk of airway difficulties and hy-

poxemia after extubation can be diminished by several

measures taken prior to and during extubation. For

example, breathing 100 oxygen for 3 min and pro-

viding a large inspiration immediately prior to extu-

bation to decrease atelectasis has been recommended

(210,211). However, administration of a mixture of

oxygen and nitrogen versus 100 oxygen prior to

extubation may have theoretical advantages. Browne

et al. (212) observed that the incidence

123 Posoperative Tracheal Extubacion[1]

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