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Induction of general anesthesia: Overview


Authors: Adam King, MD, William Benedetto, MD, Alexandra Plichta, MD
Section Editor: Girish P Joshi, MB, BS, MD, FFARCSI
Deputy Editor: Nancy A Nussmeier, MD, FAHA

All topics are updated as new evidence becomes available and our peer review process is complete.

Literature review current through: Jul 2022. | This topic last updated: Aug 18, 2022.

INTRODUCTION

General anesthesia establishes a reversible state that includes:

● Hypnosis
● Amnesia
● Analgesia
● Akinesia
● Autonomic and sensory block

The goals for induction of general anesthesia are to rapidly, safely, and pleasantly produce
these conditions while maintaining adequate oxygenation, ventilation, and hemodynamic
stability. This topic provides an overview of preinduction preparations and selection of
anesthetic induction agents and techniques. Recommendations for specific types of
surgical procedures and for patients with specific comorbidities are discussed in individual
topics.

Specific intravenous (IV) and inhalation anesthetics and neuromuscular blocking agents
used during induction of general anesthesia are reviewed in separate topics:

● IV induction and adjuvant agents (see "General anesthesia: Intravenous induction


agents" and "Perioperative uses of intravenous opioids in adults: General
considerations", section on 'Induction')

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● Inhalation agents (see "Inhalation anesthetic agents: Clinical effects and uses",
section on 'Induction of general anesthesia' and "Inhalation anesthetic agents:
Properties and delivery")
● Neuromuscular blocking agents (see "Clinical use of neuromuscular blocking agents
in anesthesia")

Techniques used during induction of general anesthesia (eg, preoxygenation, airway


management) are also reviewed separately:

● (See "Preoxygenation and apneic oxygenation for airway management for


anesthesia".)
● (See "Airway management for induction of general anesthesia".)
● (See "Rapid sequence induction and intubation (RSII) for anesthesia".)
● (See "Management of the difficult airway for general anesthesia in adults".)

CONTINUUM OF SEDATION DURING ANESTHETIC INDUCTION

Anesthetic agents demonstrate a dose-response effect, with progressively higher doses


providing progressively deeper levels of sedation and anesthesia. During induction of
general anesthesia, sedation progresses as a continuum of effect rather than as a
consecutive series of distinct states with clear transitions ( table 1) [1].

Light/minimal sedation with anxiolysis and analgesia is a level in which responsiveness to


voice, airway patency, spontaneous ventilation, and cardiovascular function are preserved.
Moderate sedation, also termed conscious sedation, represents a deeper level of sedation
and analgesia, in which the patient remains responsive to voice, has intact airway patency
and spontaneous ventilation, but may have reduced blood pressure. Deep sedation is a
state in which the patient no longer responds to voice, and may have compromised airway
patency, ventilation, and cardiovascular function. However, movement in response to a
noxious surgical stimulus still occurs. General anesthesia is an anesthetic depth at which
the patient will not respond to voice or to noxious surgical stimuli.

As the patient progresses through deeper planes ("stages") of anesthesia, airway reflexes
and patency, spontaneous ventilation, cardiovascular function, and muscle tone become
increasingly depressed ( figure 1). Patients may rapidly transition from one stage of
anesthetic depth to the next. Thus, urgent interventions may become necessary to

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manage the airway or support respiratory and cardiovascular functions. For example,
during "Stage 2," of general anesthesia (ie, the "reactive stage"), the patient is prone to
laryngospasm requiring rapid intervention. During deeper states of general anesthesia,
over-dosing of sedative/hypnotics may cause hypotension and cardiovascular collapse.

Some degree of resistance to changes in consciousness typically occurs during induction


of general anesthesia such that a higher effect-site concentration of anesthetic agent may
be necessary to achieve loss of consciousness compared with the concentration noted
upon return of consciousness during emergence [2-4]. This phenomenon is termed
hysteresis or "neural inertia." (See "Emergence from general anesthesia".)

PREPARATION FOR ANESTHETIC INDUCTION

Before patient arrival — Before patient arrival in the operating room (OR) or


interventional suite, the following steps are necessary:

● Anesthesia machine checkout – The anesthesia machine checkout should be


performed prior to the patient's arrival in the operating room ( table 2) [5]. (See
"Anesthesia machines: Prevention, diagnosis, and management of malfunctions".)

● Airway equipment preparation – Since all anesthetic induction agents and


adjuvants may cause respiratory depression, preparations for advanced airway
management are necessary. (See "Airway management for induction of general
anesthesia", section on 'Preparation for induction of anesthesia'.)

● Drug preparation – Routinely administered anesthetic drugs should be prepared.


Drugs for treatment of common complications and emergencies should be
immediately available. These include but are not limited to:  

• A sedative/hypnotic, most commonly propofol; etomidate or ketamine can be


selected for hemodynamically unstable patients. (See "General anesthesia:
Intravenous induction agents".)

• A neuromuscular blocking agent (NMBA), either a nondepolarizing agent (eg,


rocuronium, vecuronium) or a depolarizing agent (succinylcholine). (See "Clinical
use of neuromuscular blocking agents in anesthesia".)

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• A vasopressor, most commonly phenylephrine. Alternatives include ephedrine or


dilute norepinephrine as appropriate ( table 3).

• An anticholinergic (atropine or glycopyrrolate).

After patient arrival — After patient arrival in the OR, the following steps are completed:

● Monitoring – In addition to continuous personal observation provided by the


anesthesia provider, the patient should be connected to standard American Society
of Anesthesiologists (ASA) monitors before induction of general anesthesia [6].
Standard monitors include but are not limited to: electrocardiogram (ECG), pulse
oximetry, blood pressure (BP), and temperature monitors, as well as an oxygen (O2)
analyzer and a continuous end-tidal carbon dioxide (ETCO2) analyzer (eg,
capnography, capnometry, or mass spectroscopy) in the patient breathing system
( table 4). Preinduction measurements are obtained to ensure proper functioning
of the monitors and to establish the patient's baseline values. (See "Basic patient
monitoring during anesthesia".)

● Intravenous access – Virtually all adult patients have at least one peripheral venous
or other vascular access catheter placed before induction. Catheters should be
checked to ensure that they are patent. Intravenous (IV) fluids and equipment to
obtain additional venous access should be immediately available. (See "Peripheral
venous access in adults".)

● Preprocedure checklist – An appropriate preprocedure checklist should be


completed; an example is provided in the table ( table 5). (See "Safety in the
operating room", section on 'Checklists'.)

Immediately before induction

● Positioning for induction – Before induction of anesthesia, the patient's head is


positioned in the sniffing position for optimal airway management (atlanto-occipital
extension with head elevation of 3 to 7 cm) [7], supported so that the neck is flexed
and the head extended (assuming an absence of cervical spine pathology). If not
contraindicated, the head of the bed is elevated 20 to 30 degrees. (See "Airway
management for induction of general anesthesia", section on 'Patient positioning'.)

● Preoxygenation (denitrogenation) – Before administration of any anesthetic

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induction or adjuvant agents, the patient is preoxygenated (denitrogenated) with


100 percent O2 to increase O2 reserve, thereby providing additional time to secure
the airway [8,9]. (See "Airway management for induction of general anesthesia",
section on 'Preoxygenation'.)

SELECTION OF INDUCTION TECHNIQUE

Induction of general anesthesia may be accomplished using primarily intravenous (IV) or


primarily inhalation anesthetic agents. Most adults prefer induction primarily with IV
agents. (See "General anesthesia: Intravenous induction agents" and "Inhalation
anesthetic agents: Clinical effects and uses", section on 'Induction of general anesthesia'.)

Notably, adults may be less satisfied with a primary inhalation induction technique
compared with IV induction due to the unpleasant odor of anesthetic gases [10], as well as
a higher incidence of postoperative nausea and vomiting compared with use of IV agents
such as propofol (see "Postoperative nausea and vomiting", section on 'Anesthetic factors')
[10-12]. Furthermore, inhalation induction time is longer compared with IV induction.
Several minutes of ventilation may be required. Thus, this technique is unsuitable for rapid
sequence induction and intubation (RSII). (See "Rapid sequence induction and intubation
(RSII) for anesthesia".)

The ideal induction agent has a rapid onset of action, minimal cardiopulmonary or other
side effects, and is cleared from the bloodstream quickly so that recovery is rapid.
However, none of the available induction agents is ideal for all patients, and all have side
effects. We typically administer combinations of agents from different pharmacologic
classes during induction and/or maintenance of general anesthesia. This strategy
minimizes the total dose of any one anesthetic agent, thereby reducing the incidence of
undesirable side effects. Age and coexisting diseases affect selection and dosing of
anesthetic induction and adjuvant agents. (See "General anesthesia: Intravenous
induction agents", section on 'Dosing considerations' and "Inhalation anesthetic agents:
Clinical effects and uses", section on 'Influence of patient-related factors'.)

INTRAVENOUS ANESTHETIC INDUCTION

Patient selection — Adult patients usually have intravenous (IV) access and typically

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prefer induction with IV agents.

Techniques and anesthetic agents

Induction with endotracheal intubation — Selection and dosing of sedative-hypnotic


and adjuvant agents are determined by patient-specific factors, including age and
comorbidities. (See "General anesthesia: Intravenous induction agents", section on
'Dosing considerations'.)

● Intravenous sedative-hypnotic agent – During IV induction with planned


endotracheal intubation, a primary IV sedative-hypnotic induction agent is typically
administered ( table 6). (See "General anesthesia: Intravenous induction agents".)

● Intravenous adjuvant agents – One or more adjuvant IV agents (eg, short-acting


opioid, lidocaine, midazolam ( table 7)) are also typically administered during
induction to blunt the sympathetic stress response and cough reflex during
laryngoscopy and intubation, minimize pain due to injection of the anesthetic
induction agents, and supplement effects of the primary sedative-hypnotic
anesthetic and reduce their dose. As an example, a reasonable combination of
adjuvant agents is fentanyl 25 to 100 mcg, followed by lidocaine 50 to 100 mg, with
both administered immediately prior to induction when either propofol or etomidate
is selected for the sedative-hypnotic induction agent. We start with the lower end of
these dose ranges in patients with conditions such as advanced age and/or frailty;
hemodynamic abnormalities caused by persistent bleeding or other factors resulting
in hypovolemia, vasodilation, or myocardial dysfunction; or impaired renal or hepatic
function. (See "General anesthesia: Intravenous induction agents", section on
'Adjuvant agents' and "General anesthesia: Intravenous induction agents", section on
'Dosing considerations'.)

However, scant evidence is available to support use of any particular combination of


agents. Notably, coadministration of agents acting on different receptor types may
produce synergistic anesthetic effects. Thus, avoiding use of multiple agents or
reducing doses may be prudent in older patients or those with significant
comorbidities, particularly impaired renal and/or hepatic function. Adjuvant agents
are typically avoided altogether in patients with actual or potential hemodynamic
instability.  

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● Neuromuscular blocking agent – A neuromuscular blocking agent (NMBA) is


usually administered before endotracheal intubation ( table 8). (See
'Neuromuscular blocking agents' below and "Clinical use of neuromuscular blocking
agents in anesthesia", section on 'Endotracheal intubation'.)

● Addition of an inhalation agent – Inhalation anesthetic agent(s) are often added


shortly after initial loss of consciousness is achieved using IV agents. Administration
of inhalation anesthetic(s) deepens anesthesia and blunts airway reflexes and
sympathetic stress responses during laryngoscopy. Potent volatile inhalation agents
also induce a dose-dependent decrease in skeletal muscle tone, which improves
conditions during insertion of either an endotracheal tube or supraglottic airway.
(See "Inhalation anesthetic agents: Clinical effects and uses", section on 'Use as a
supplement (all inhalation agents)'.)

Induction with supraglottic airway placement — During IV induction with planned


insertion of a supraglottic airway (SGA) such as a laryngeal mask airway (LMA), an
adequate depth is necessary to avoid coughing, gagging, breath-holding, laryngospasm,
or bronchospasm. (See "Supraglottic devices (including laryngeal mask airways) for airway
management for anesthesia in adults", section on 'Placement technique'.)

Similar to induction with planned endotracheal intubation (see 'Induction with


endotracheal intubation' above), lidocaine is typically administered before the selected
primary IV sedative-hypnotic induction agent [13]. (See "General anesthesia: Intravenous
induction agents".)

However, opioids may be avoided or minimized during the induction sequence if


spontaneous ventilation is planned after SGA insertion to avoid a period of apnea due to
opioid-induced respiratory depression. (See "Supraglottic devices (including laryngeal
mask airways) for airway management for anesthesia in adults", section on 'Choice of
mode of ventilation'.)

If difficulties are encountered with SGA placement or initial ventilation, additional doses of
the selected sedative-hypnotic agent can be administered. Alternatively, intubation with
an endotracheal tube can be performed. (See "Supraglottic devices (including laryngeal
mask airways) for airway management for anesthesia in adults", section on
'Troubleshooting'.)

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INHALATION ANESTHETIC INDUCTION

Properties, mechanisms of action, and delivery of inhalation agents are discussed


separately ( table 9). (See "Inhalation anesthetic agents: Properties and delivery".)

Patient selection — An inhalation induction technique is often selected for younger


pediatric patients or those with developmental delay to avoid fear of needles and
responses to the pain of a needle stick [14]. Inhalation induction may also be the
preferred method for adult patients when:

● Maintenance of spontaneous ventilation is desirable during induction. Examples


include patients with intraoral, pharyngeal, or mediastinal mass causing
compression of the airway if an awake intubation technique is not feasible.

● An in situ tracheostomy is present since unpleasant odor and irritation of the airway
are not problematic.

● Intravenous (IV) access is difficult to obtain. However, IV access should be


established immediately after induction so that common problems such as
hypotension during induction can be treated.

Techniques and specific inhalation agents — Inhalation induction of anesthesia


requires a high concentration of a volatile anesthetic agent, with or without nitrous oxide
(N2O). Development of non-pungent, nonirritant volatile anesthetics that have rapid onset
(eg, sevoflurane) has made inhalation induction of anesthesia via facemask less irritating
and viable option compared with induction using older inhalation agents [11].

Modified administration techniques can be used to facilitate the speed of anesthetic


induction. For example, the breathing circuit may be primed with a high sevoflurane
concentration (eg, 8 percent) plus N2O. Then the patient is instructed to take a vital
capacity breath (defined as a complete expiration followed by a complete inspiration),
followed by a period of apnea with inflated lungs (ie, "breath-holding") [15]. Typically this
single breath technique achieves the 2 percent alveolar sevoflurane concentration
required to tolerate painful interventions such as surgical incision [16]. (See "Inhalation
anesthetic agents: Properties and delivery", section on 'Technique-related
considerations'.)

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Potent volatile agents — Advantages shared by all potent volatile anesthetic agents


during induction of general anesthesia include excellent bronchodilation, dose-dependent
decrease in skeletal muscle tone, and decrease in cerebral metabolic rate of oxygen
consumption (CMRO2). Disadvantages of these agents include respiratory depression,
systemic vasodilation, and decreased blood pressure (BP), adverse effects which are dose-
dependent. In rare instances, all potent volatile agents can precipitate malignant
hyperthermia. (See "Inhalation anesthetic agents: Clinical effects and uses", section on
'Other clinical effects'.)

● Sevoflurane – Sevoflurane has many characteristics of the ideal induction agent, and
is the most commonly used potent volatile inhaled agent for this purpose. It has
minimal odor, lacks pungency, and has potent bronchodilating characteristics [10-
12,14,17-19]. Furthermore, sevoflurane has relatively rapid onset due to its low tissue
and blood solubilities, which also result in rapid clearance from the bloodstream and
rapid recovery. The time to loss of consciousness may be as little as 60 seconds if a
high concentration of sevoflurane (eg, 4 to 8 percent) is briefly delivered via a
facemask [14,15,20]. (See "Inhalation anesthetic agents: Clinical effects and uses",
section on 'Sevoflurane' and "Inhalation anesthetic agents: Clinical effects and uses",
section on 'Induction of general anesthesia'.)

● Isoflurane – Isoflurane is the most potent of the volatile anesthetics, but is not ideal
for use as the sole induction agent because of its relative pungency and slow onset
(and recovery) compared with sevoflurane. (See "Inhalation anesthetic agents:
Clinical effects and uses", section on 'Isoflurane'.)

● Halothane – Halothane is a sweet-smelling gas with only moderate pungency.


However, halothane is no longer commercially available in North America due to
adverse effects (particularly the possibility of halothane hepatitis). Also, halothane
has the slowest onset compared with all other potent inhalation agents during
induction of anesthesia because of its high tissue and blood solubility. Other
disadvantages include significant myocardial depression at higher doses and risk of
arrhythmias due to sensitization of the myocardium to catecholamines (either
endogenous or exogenously administered epinephrine or norepinephrine). For these
reasons, newer inhalation agents such as sevoflurane have been developed to
replace halothane. However, halothane is still used in many countries with limited
resources for both induction and maintenance of general anesthesia due to its low

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cost and wide availability. (See "Inhalation anesthetic agents: Clinical effects and
uses", section on 'Halothane'.)

● Desflurane – Desflurane is generally not used during induction of anesthesia via


facemask. It is the most pungent of the volatile anesthetics and has the highest
incidence of airway irritation (coughing, salivation, breath-holding, laryngospasm),
particularly at high concentrations [17,21]. Also, desflurane can cause sympathetic
stimulation, tachycardia, and hypertension when administered in high or abruptly
increased inspired concentrations. Since any inhalation agent must be rapidly
increased to produce a high concentration during induction of general anesthesia in
an awake patient, these properties limit use of desflurane during induction. (See
"Inhalation anesthetic agents: Clinical effects and uses", section on 'Desflurane'.)

Nitrous oxide gas — N2O is a sweet-smelling gas without pungency or potential for


airway irritation. N2O increases speed of anesthetic onset if coadministered with any
potent volatile inhalation agent, compared with administration of the potent agent alone,
due to a phenomenon termed the "second gas" effect. Thus, it is often used as an
adjuvant agent during inhalation induction of general anesthesia. (See "Inhalation
anesthetic agents: Properties and delivery", section on 'Second gas effect' and "Inhalation
anesthetic agents: Clinical effects and uses", section on 'Nitrous oxide'.)

Notably, N2O is avoided during induction in certain patients, including those with pre-
existing bowel distention, increased middle ear pressure, pneumothorax,
pneumoperitoneum, pneumocephalus, intraocular gas, or venous air embolism [22-24].
Further gaseous distension of such spaces during administration of N2O has potentially
significant adverse consequences (eg, nausea with emesis, tension pneumothorax,
increased intracranial pressure, vision loss, expansion of entrapped intravascular air).
Also, N2O is typically avoided during induction in patients with cardiomyopathy and/or
pulmonary hypertension because it causes mild myocardial depression and mild
sympathetic nervous system stimulation that may increase pulmonary vascular resistance.
(See "Inhalation anesthetic agents: Clinical effects and uses", section on 'Disadvantages
and adverse effects'.)

NEUROMUSCULAR BLOCKING AGENTS

● For endotracheal intubation – During induction of general anesthesia, a

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neuromuscular blocking agent (NMBA) is usually administered to facilitate


laryngoscopy and intubation if endotracheal intubation is planned ( table 8). (See
"Clinical use of neuromuscular blocking agents in anesthesia", section on
'Endotracheal intubation'.)

The choice of NMBA should be based on the desired speed of onset, reversibility,
patient comorbidities, and anticipated difficulty of airway intubation. If rapid
sequence intubation and induction is desired, either succinylcholine (SCh; 1 to 1.5
mg/kg) or rocuronium (1.2 mg/kg) is typically selected. If a relatively large dose of
rocuronium is used to achieve swift onset of optimal intubating conditions, the
neuromuscular blocking effect may be rapidly terminated by administering
sugammadex 16 mg/kg [25,26]. (See "Rapid sequence induction and intubation (RSII)
for anesthesia", section on 'Neuromuscular blocking agents (NMBAs)' and "Clinical
use of neuromuscular blocking agents in anesthesia", section on 'Sugammadex'.)

Nondepolarizing NMBAs administered in usual doses (eg, rocuronium 0.6 mg/kg,


vecuronium, cisatracurium, atracurium, and pancuronium) have a slower onset than
SCh but are often selected for elective intubation to avoid the side effects of SCh if
the patient does not need RSII and does not have a potentially difficult airway
( table 8).

● For supraglottic airway insertion – Occasionally, a small dose of an NMBA is


employed to facilitate supraglottic airway (SGA) placement by preventing coughing
and other airway responses. (See 'Induction with supraglottic airway placement'
above.)

VASOPRESSOR AGENTS

Vasopressor agents may be administered to treat hypotension during induction of general


anesthesia. Typical choices of agents are ( table 3) (see "Hemodynamic management
during anesthesia in adults", section on 'Vasopressor and positive inotropic agents'):

● Phenylephrine, a pure alpha1-adrenergic agonist that causes both arterial and


venous vasoconstriction. Administration of phenylephrine 40 to 100 mcg IV bolus
increases blood pressure (BP). Doses may be repeated if necessary.

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● Ephedrine, an alpha and beta receptor adrenergic agonist that causes release of
endogenous norepinephrine stores. Administration of ephedrine 5 to 10 mg IV bolus
increases both BP and heart rate (HR). Doses may be repeated if necessary.

Occasionally, continuous infusion of a phenylephrine or a more potent vasopressor (eg,


norepinephrine) may be necessary to maintain hemodynamic stability during and
immediately after induction of general anesthesia.

CLINICAL CASE EXAMPLES

Patient-specific or procedure-specific considerations may affect selection of anesthetic


induction techniques and agents. The following clinical examples are discussed in detail in
separate topics:

● Hemodynamically unstable patient – In a patient with actual or potential


hemodynamic instability (eg due to hypovolemia, vasodilation, or severe myocardial
dysfunction) (see "Intraoperative management of shock in adults"), we typically
select etomidate (0.2 to 0.4 mg/kg) or ketamine (0.5 to 2 mg/kg) to induce general
anesthesia [27].

● Need for rapid sequence induction and endotracheal intubation – In a patient


with high risk for pulmonary aspiration, rapid sequence induction and intubation
(RSII) is typically selected to minimize the time the patient is sedated with an
unprotected airway. A single rapid bolus of the sedative-hypnotic agent is
immediately followed by administration of the neuromuscular blocking agent
(NMBA). Underdosing either the sedative-hypnotic or the NMBA may result in
laryngospasm if intubation is not successful on first attempt or patient recall.
Notably additional adjuvant agents (eg, opioids, lidocaine, midazolam) are usually
minimized or avoided for a RSII technique. (See "Rapid sequence induction and
intubation (RSII) for anesthesia".)

In some patients with very high risk for aspiration, awake intubation is performed
rather than RSII, particularly if a potentially difficult airway is anticipated. (See
"Management of the difficult airway for general anesthesia in adults", section on
'Awake intubation'.)

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● Older patient – In general, doses of intravenous and inhalation induction agents


should be reduced in an older adult. (See "Anesthesia for the older adult", section on
'Selection and dosing of anesthetic agents'.)

● Patients with specific comorbidities:

• Heart disease – (See "Anesthesia for noncardiac surgery in patients with ischemic
heart disease", section on 'Induction' and "Intraoperative management for
noncardiac surgery in patients with heart failure", section on 'Induction'.)

• End stage renal disease – (See "Anesthesia for dialysis patients", section on
'Induction'.)

• Brain tumor or head injury – (See "Anesthesia for craniotomy", section on


'Induction of anesthesia' and "Anesthesia for patients with acute traumatic brain
injury", section on 'Choice of anesthetic agents'.)

• Eye injury – (See "Anesthesia for emergency eye surgery", section on 'Choice of
induction and adjuvant agents'.)

SUMMARY AND RECOMMENDATIONS

● Definition of general anesthesia – General anesthesia is a reversible state that


includes hypnosis, amnesia, analgesia, akinesia, and autonomic and sensory block
such that the patient will not respond to voice or to noxious surgical stimuli. During
induction of general anesthesia, sedation progresses as a continuum of effect rather
than as a consecutive series of distinct states with clear transitions ( table 1 and
figure 1). (See 'Continuum of sedation during anesthetic induction' above.)

● Preparations for induction

• Before patient arrival – Anesthesia machine checkout procedure ( table 2),


preparation for advanced airway management, and preparation of routinely
administered drugs. (See 'Before patient arrival' above.)

• After patient arrival – Connection of standard American Society of


Anesthesiologists (ASA) monitors, establishment of intravenous (IV) access,
completion of preprocedure checklist ( table 5). (See 'After patient arrival'

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above.)

• Immediately before induction – Head positioning in the sniffing position,


preoxygenation using 100 percent oxygen. (See 'Immediately before induction'
above.)

● Intravenous anesthetic induction – Most adults prefer induction with IV agents.


Combinations of agents from different pharmacologic classes are typically
administered to minimize dose of each anesthetic agent (see 'Intravenous anesthetic
induction' above):

• Sedative-hypnotic agent (eg, propofol, etomidate, ketamine) ( table 6)

• Adjuvant agent(s) (eg, short-acting opioid, lidocaine, midazolam) ( table 7)

• Neuromuscular blocking agent (NMBA) if endotracheal intubation is planned or to


facilitate supraglottic airway placement ( table 8) (see 'Neuromuscular blocking
agents' above)

• Inhalation anesthetic agent(s), often added shortly after achieving initial loss of
consciousness

● Inhalation anesthetic induction – Inhalation induction is often preferred by


children due to fear of needles, and may be selected for adults when spontaneous
breathing during induction is desirable. Agents include the potent volatile
anesthetics (eg, isoflurane, sevoflurane, desflurane) and the gas nitrous oxide
( table 9). (See 'Inhalation anesthetic induction' above.)

● Use of vasopressor agents – Phenylephrine or ephedrine may be administered if


necessary to treat hypotension. (See 'Vasopressor agents' above.)

● Patient-specific and procedure-specific considerations – (See 'Clinical case


examples' above.)

ACKNOWLEDGMENT

The UpToDate editorial staff acknowledges Liza M Weavind, MBBCh, FCCM, MMHC, who
contributed to an earlier version of this topic review.

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REFERENCES

1. ASA Continuum of Depth of Sedation: Definition of General Anesthesia and Levels of S


edation/Analgesia. Committee of Origin: Quality Management and Departmental Ad
ministration, 2009. https://www.asahq.org/standards-and-guidelines/continuum-of-d
epth-of-sedation-definition-of-general-anesthesia-and-levels-of-sedationanalgesia.
2. Sepúlveda PO, Tapia LF, Monsalves S. Neural inertia and differences between loss of
and recovery from consciousness during total intravenous anaesthesia: a narrative
review. Anaesthesia 2019; 74:801.
3. Friedman EB, Sun Y, Moore JT, et al. A conserved behavioral state barrier impedes
transitions between anesthetic-induced unconsciousness and wakefulness: evidence
for neural inertia. PLoS One 2010; 5:e11903.
4. Moppett IK, Shorrock ST. Working out wrong-side blocks. Anaesthesia 2018; 73:407.

5. https://www.asahq.org/For-Members/Clinical-Information/2008-ASA-Recommendatio
ns-for-PreAnesthesia-Checkout.aspx.

6. American Society of Anesthesiologists. Standards for Basic Anesthetic Monitoring. ww


w.asahq.org/Search.aspx?q=standards+basic+anesthetic+monitoring (Accessed on M
arch 29, 2016).

7. Kobayashi M, Ayuse T, Hoshino Y, et al. Effect of head elevation on passive upper


airway collapsibility in normal subjects during propofol anesthesia. Anesthesiology
2011; 115:273.
8. Tanoubi I, Drolet P, Donati F. Optimizing preoxygenation in adults. Can J Anaesth
2009; 56:449.
9. Nimmagadda U, Salem MR, Crystal GJ. Preoxygenation: Physiologic Basis, Benefits,
and Potential Risks. Anesth Analg 2017; 124:507.
10. Thwaites A, Edmends S, Smith I. Inhalation induction with sevoflurane: a double-blind
comparison with propofol. Br J Anaesth 1997; 78:356.
11. Joshi GP. Inhalational techniques in ambulatory anesthesia. Anesthesiol Clin North
America 2003; 21:263.
12. Suzuki KS, Oohata M, Mori N. Multiple-deep-breath inhalation induction with 5%
sevoflurane and 67% nitrous oxide: comparison with intravenous injection of

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propofol. J Anesth 2002; 16:97.


13. Xing J, Liang L, Zhou S, et al. Intravenous Lidocaine Alleviates the Pain of Propofol
Injection by Local Anesthetic and Central Analgesic Effects. Pain Med 2018; 19:598.
14. Sigston PE, Jenkins AM, Jackson EA, et al. Rapid inhalation induction in children: 8%
sevoflurane compared with 5% halothane. Br J Anaesth 1997; 78:362.
15. Lejus C, Bazin V, Fernandez M, et al. Inhalation induction using sevoflurane in
children: the single-breath vital capacity technique compared to the tidal volume
technique*. Anaesthesia 2006; 61:535.

16. Joo HS, Perks WJ. Sevoflurane versus propofol for anesthetic induction: a meta-
analysis. Anesth Analg 2000; 91:213.

17. White PF, Tang J, Wender RH, et al. Desflurane versus sevoflurane for maintenance of
outpatient anesthesia: the effect on early versus late recovery and perioperative
coughing. Anesth Analg 2009; 109:387.

18. Mostafa SM, Atherton AM. Sevoflurane for difficult tracheal intubation. Br J Anaesth
1997; 79:392.
19. Thomas Ebert and Larry Lindenbaum. Inhaled Anesthetics. In: Clinical Anesthesia, Sev
enth, Paul G. Barash (Ed), Lippincott Williams Wilkins, Philadelphia 2013. p.447-477.
20. Boonmak P, Boonmak S, Pattanittum P. High initial concentration versus low initial
concentration sevoflurane for inhalational induction of anaesthesia. Cochrane
Database Syst Rev 2016; :CD006837.
21. de Oliveira GS Jr, Girao W, Fitzgerald PC, McCarthy RJ. The effect of sevoflurane versus
desflurane on the incidence of upper respiratory morbidity in patients undergoing
general anesthesia with a Laryngeal Mask Airway: a meta-analysis of randomized
controlled trials. J Clin Anesth 2013; 25:452.
22. Torri G. Inhalation anesthetics: a review. Minerva Anestesiol 2010; 76:215.
23. Sun R, Jia WQ, Zhang P, et al. Nitrous oxide-based techniques versus nitrous oxide-
free techniques for general anaesthesia. Cochrane Database Syst Rev 2015;
:CD008984.
24. Myles PS, Chan MT, Kasza J, et al. Severe Nausea and Vomiting in the Evaluation of
Nitrous Oxide in the Gas Mixture for Anesthesia II Trial. Anesthesiology 2016;
124:1032.
25. de Boer HD, Driessen JJ, Marcus MA, et al. Reversal of rocuronium-induced (1.2

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mg/kg) profound neuromuscular block by sugammadex: a multicenter, dose-finding


and safety study. Anesthesiology 2007; 107:239.
26. Pühringer FK, Rex C, Sielenkämper AW, et al. Reversal of profound, high-dose
rocuronium-induced neuromuscular blockade by sugammadex at two different time
points: an international, multicenter, randomized, dose-finding, safety assessor-
blinded, phase II trial. Anesthesiology 2008; 109:188.
27. Jabre P, Combes X, Lapostolle F, et al. Etomidate versus ketamine for rapid sequence
intubation in acutely ill patients: a multicentre randomised controlled trial. Lancet
2009; 374:293.
Topic 94135 Version 45.0

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GRAPHICS

Continuum of sedation/analgesia/anesthesia

Moderate
Minimal
sedation/analgesia Deep General
  sedation
(conscious sedation/analgesia Δ anesthesia ◊
(anxiolysis)*
sedation) ¶

Responsiveness Normal Purposeful § Purposeful § Unarousable,


response to response to verbal response after even with
verbal or tactile repeated or painful painful
stimulation stimulation stimulation stimulus

Airway Unaffected No intervention Intervention may Intervention


required be required often required

Spontaneous Unaffected Adequate May be inadequate Frequently


ventilation inadequate

Cardiovascular Unaffected Usually Usually maintained May be


function maintained impaired

Because sedation is a continuum, it is not always possible to predict how an individual patient
will respond. Hence, practitioners intending to produce a given level of sedation should be
able to rescue patients whose level of sedation becomes deeper than initially intended.
Individuals administering moderate sedation/analgesia (conscious sedation) should be able to
rescue patients who enter a state of deep sedation/analgesia, while those administering deep
sedation/analgesia should be able to rescue patients who enter a state of general anesthesia.

* A drug-induced state during which patients respond normally to verbal commands.


Although cognitive function and coordination may be impaired, ventilatory and cardiovascular
functions are unaffected.
¶ A drug-induced depression of consciousness during which patients respond purposefully §
to verbal commands, either alone or accompanied by light tactile stimulation. No
interventions are required to maintain a patient airway, and spontaneous ventilation is
adequate. Cardiovascular function is usually maintained.
Δ A drug-induced depression of consciousness during which patients cannot be easily
aroused but respond purposefully § following repeated or painful stimulation. The ability to
independently maintain ventilatory function may be impaired. Patients may require assistance
in maintaining a patient airway, and spontaneous ventilation may be inadequate.
Cardiovascular function is usually maintained.
◊ A drug-induced loss of consciousness during which patients are not arousable, even by
painful stimulation. The ability to independently maintain ventilatory function is often

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impaired. Patients often require assistance in maintaining a patient airway, and positive
pressure ventilation may be required because of depressed spontaneous ventilation or drug-
induced depression of neuromuscular function. Cardiovascular function may be impaired.
§ Reflex withdrawal from a painful stimulus is not considered a purposeful response.

From: American Society of Anesthesiologists Task Force on Sedation and Analgesia by Non-Anesthesiologists. Practice
guidelines for sedation and analgesia by non-anesthesiologists. Anesthesiology 2002; 96:1004. Copyright © 2002
American Society of Anesthesiologists. Reproduced with permission from Wolters Kluwer Health. Unauthorized
reproduction of this material is prohibited.

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Signs indicating stages of anesthesia

Modified from: Gillespie NA. The signs of anesthesia. Anesth Analg 1943; 22:275. Copyright © 1943 International Anesthesia Researc
permission from Wolters Kluwer Health. Unauthorized reproduction of this material is prohibited.

Graphic 113985 Version 2.0

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American Society of Anesthesiologists Summary of Anesthesia Machine


Checkout Recommendations

Responsible
Item to be completed
party

To be completed daily

Item #1: Verify that auxiliary oxygen cylinder and self-inflating manual Provider and
ventilation device are available and functioning technician

Item #2: Verify that patient suction is adequate to clear the airway Provider and
technician

Item #3: Turn on anesthesia delivery system and confirm that AC power Provider or
is available technician

Item #4: Verify availability of required monitors, including alarms Provider or


technician

Item #5: Verify that pressure is adequate on the spare oxygen cylinder Provider and
mounted on the anesthesia machine technician

Item #6: Verify that the piped gas pressures are ≥50 psig Provider and
technician

Item #7: Verify that vaporizers are adequately filled and, if applicable, Provider or
that the filler ports are tightly closed technician

Item #8: Verify that there are no leaks in the gas supply lines between Provider or
the flowmeters and the common gas outlet technician

Item #9: Test scavenging system function Provider or


technician

Item #10: Calibrate, or verify calibration of, the oxygen monitor, and Provider or
check the low oxygen alarm technician

Item #11: Verify that carbon dioxide absorbent is not exhausted Provider or
technician

Item #12: Breathing system pressure and leak testing Provider and
technician

Item #13: Verify that gas flows properly through the breathing circuit Provider and
during both inspiration and exhalation technician

Item #14: Document completion of checkout procedures Provider and


technician

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Item #15: Confirm ventilator settings and evaluate readiness to deliver Provider
anesthesia care (anesthesia time out)

To be completed prior to each procedure

Item #2: Verify that patient suction is adequate to clear the airway Provider and
technician

Item #4: Verify availability of required monitors, including alarms Provider or


technician

Item #7: Verify that vaporizers are adequately filled and, if applicable, Provider
that the filler ports are tightly closed

Item #11: Verify that carbon dioxide absorbent is not exhausted Provider or
technician

Item #12: Breathing system pressure and leak testing Provider and
technician

Item #13: Verify that gas flows properly through the breathing circuit Provider and
during both inspiration and exhalation technician

Item #14: Document completion of checkout procedures Provider and


technician

Item #15: Confirm ventilator settings and evaluate readiness to deliver Provider
anesthesia care (anesthesia time out)

AC: alternating current; psig: pounds per square inch gauge.

Reproduced with permission from: Riutort KT, Eisenkraft JB. The Anesthesia Workstation and Delivery Systems for
Inhaled Anesthetics. In: Clinical Anesthesia, 7th ed, Barash PG, Cullen BF, Stoelting RK, et al. (Eds), Lippincott Williams
& Wilkins, Philadelphia 2013. Copyright © 2013 Lippincott Williams & Wilkins. www.lww.com.

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Vasopressors and inotropic agents used in the operating room: Adult


dosing* ¶

Functional class
Bolus
Drug (predominant receptor or Infusion dose
dose
mechanism of action)

Ephedrine Inotrope/chronotrope/vasopressor 5 to 10 mg N/A Tachyp


(alpha 1 -adrenergic receptor boluses occur w
agonist; beta 1 - and beta 2 - repeat
adrenergic receptor agonist) to indi
postsy
release
norepi
Cardio
effects
by dru
ephed
into ad
nerves
or thos
deplet
norepi
reserve
reserp
Admin
extrem
(eg, in
increm
of 2.5 m
patien
monoa
oxidas
inhibit
metha
since e
hypert
respon
threate
dysrhy
occur

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Phenylephrine Vasopressor (alpha 1 -adrenergic 50 to 100 10 to 100 Often s


receptor agonist) mcg mcg/minute treat h
boluses norma
or
(may begin HR is p
infusion if 0.1 to 1
Geneti
repeated mcg/kg/minute
polymo
bolus lead to
doses are individ
necessary) respon

Norepinephrine Inotrope/vasopressor (alpha 1 - and 4 to 8 mcg 1 to 20 mcg/minute Often s


beta 1 -adrenergic receptor (may begin first-lin
or
agonist) infusion if during
repeated 0.01 to 0.3 surger
bolus mcg/kg/minute for trea
doses are most t
necessary) Norepi
mcg is
approx
equiva
potenc
phenyl
mcg
Periph
extrava
high co
may ca
damag

Epinephrine Inotrope/chronotrope/vasopressor 4 to 10 1 to 100 mcg/minute First-lin


(alpha 1 -adrenergic receptor mcg for car
or
agonist; beta 1 - and beta 2 - initially; up and fo
adrenergic receptor agonist) to 100 mcg 0.01 to 1
May be
boluses mcg/kg/minute
admin
may be   or via a
used when endotr
Note changing
initial in eme
effects across dose
response is Low do
range:
inadequate bronch
Low doses
effects
have primarily
cause
beta 2 -
vasodi
adrenergic
decrea
effects at 1 to 2

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mcg/minute or Interm
0.01 to 0.02 cause
mcg/kg/minute HR and
Intermediate High d
doses have vasoco
primarily with po
beta 1 - and hypert
beta 2 - advers
adrenergic effects
effects at 2 to Individ
10 mcg/minute respon
or 0.02 to 0.1 related
mcg/kg/minute variabl
High doses
have primarily
alpha 1 -
adrenergic
effects at 10 to
100
mcg/minute or
0.1 to 1
mcg/kg/minute

Vasopressin Vasopressor (vasopressin 1 and 1 to 4 units 0.01 to 0.04 Effectiv


vasopressin 2 receptor agonist) units/minute treatm
hypote
 
refract
Doses >0.04 admin
units/minute up to catech
0.1 units/minute are sympa
reserved for salvage such a
therapy (ie, failure to phenyl
achieve adequate BP norepi
goals with other
No dire
vasopressor agents) ¶
HR
Little e
can ca
splanc
vasoco
Individ
respon
related
variabl

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Periph
extrava
cause

Dopamine Inotrope/vasopressor/dose- N/A 2 to 20 Low do


dependent chronotropy mcg/kg/minute exacer
(dopaminergic, beta 1 -, beta 2 -, and hypote
 
alpha 1 -adrenergic receptor beta
agonist) Note changing
High d
effects across dose
cause
range:
vasoco
Low doses advers
have primarily effects
dopaminergic arrhyth
effects at <3
mcg/kg/minute
Intermediate
doses have
primarily
beta 1 - and
beta 2 -
adrenergic
effects at 3 to
10
mcg/kg/minute
High doses
have primarily
alpha 1 -
adrenergic
effects >10
mcg/kg/minute

Dobutamine Inotrope/vasodilator/dose- N/A 1 to 20 Exacer


dependent chronotropy (beta 1 - mcg/kg/minute hypote
and beta 2 -adrenergic receptor possib
agonist) dose-d
vasodi
beta
concur
admin
potent
vasoco
such a
norepi

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vasopr
necess

Milrinone Inotrope/vasodilator N/A 0.375 to 0.75 Exacer


(phosphodiesterase inhibitor) mcg/kg/minute (a hypote
(decreases rate of cyclic adenosine loading dose of 50 due to
monophosphate [cAMP] mcg/kg over ≥10 (via
degradation) minutes may be phosph
administered, but inhibit
may be omitted to concur
avoid hypotension) admin
potent
vasoco
such a
norepi
vasopr
necess

Isoproterenol Inotrope/chronotrope/vasodilator N/A 5 to 20 mcg/minute Exacer


(beta 1 - and beta 2 -adrenergic hypote
or
receptor agonist) due to
0.05 to 0.2 depen
mcg/kg/minute vasodi
beta
May ca
arrhyth
Not av
most s

N/A: not applicable; HR: heart rate; IV: intravenous; IM: intramuscular; BP: blood pressure;
PVR: pulmonary vascular resistance.
* Dose ranges are based on adult patients of normal size.
¶ Refer to related UpToDate content on hemodynamic management during anesthesia and
surgery.

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Basic monitoring during anesthesia

Primary physiologic
Monitoring Derived Additio
process/parameter Principle
equipment information functi
targeted

Oxygenation Inspired gas O 2 analyzer Paramagnetic Inspired/expired A low-level a


O 2 content (with a low- sensor, fuel O 2 concentration automaticall
limit alarm in (galvanic) cell, when placed activated by
use) polarographic downstream from on the anest
(Clark) electrode, fresh flow control machine
mass valves
spectroscopy, or
Raman scattering

Blood Pulse The Beer-Lambert Hemoglobin Continuous


oxygenation oximeter law applied to saturation, pulse evaluation o
tissues and rate, relative pulse circulation, v
pulsatile blood amplitude pitch pulse t
flow. The relative displayed on and audible
absorbency at plethysmography threshold ala
wavelengths of waveform
660 and 940 nm is
used to estimate
saturation, which
is derived from
the ratio of
oxyhemoglobin to
the sum of
oxyhemoglobin
plus
deoxyhemoglobin.

Ventilation  Exhaled Capnograph CO 2 molecules ETCO 2 , inspired Instantaneo


CO 2 absorb infrared CO 2 , diagnostic information
radiation at 4.26 waveforms, Perfusion
micrometers, respiratory rate, effectivel
proportionate to apnea detection being
the CO 2 transport
concentration through t
present in the vascular
breath sample Metaboli
effectivel

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being pro
by cellula
metaboli
Confirma
tracheal t
placemen
intubatio

Integrity of Disconnection Detects the Alarms if a Alarms if hig


ventilation alarm cyclical changes in significant decrease pressures ar
system airway pressure in in rate or pressure sensed
during the normal range occurs
mechanical
ventilation

Pulmonary Pulmonary Volume of gas Inspired and Pressure vol


mechanics flow and proportional to a expired volume, and flow vol
(volume, pressure drum movement, flow, and airway loops
flow, sensors changes in pressure
pressure) differential
pressure (near the
Y-connector) or in
electrical
resistance (hot
wire housed in a
monitor or
ventilator)

Circulation Cardiac ECG The ECG monitor Heart rate and ST segment
activity detects, amplifies, rhythm depression/e
displays, and and trend ov
records the ECG with an audi
signal. alarm warni
significant
arrhythmias
asystole

Arterial BP Noninvasive Oscillometric Arterial BP Indicator of


BP monitor devices perfusion
automatically
inflate and deflate
the cuff, and have
electronic
pressure sensors
that record the

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pressure
oscillations of the
arteries. The
pressure at which
maximal
oscillations occur
as the cuff is
deflated
corresponds with
MAP. Proprietary
algorithms are
used to calculate
systolic and
diastolic BP.

Temperature   Temperature Devices with a Core or peripheral A greater th


monitor semiconductor, temperature core-to-perip
electrical temperature
resistance gradient is in
decreases as of low cardia
temperature output.
decreases

O 2 : oxygen; CO 2 : carbon dioxide; ETCO 2 : end-tidal carbon dioxide; ECG: electrocardiogram;


BP: blood pressure; MAP: mean arterial pressure.

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World Health Organization surgical safety checklist

Sign in Time out Sign out

Before induction of Before skin incision Before patient leaves


anesthesia operating room
__ Confirm all team members
__ Patient has have introduced Nurse verbally confirms
confirmed: themselves by name and with the team:
Identity role
__ The name of the
Site __ Surgeon, anesthesia procedure recorded
Procedure professional, and nurse
__ That instrument,
Consent verbally confirm
sponge, and needle
Patient
__ Site marked/not counts are correct (or
Site not applicable)
applicable
Procedure
__ Anesthesia safety __ How the specimen is
check completed Anticipated critical events labeled (including
patient name)
__ Pulse oximeter on __ Surgeon reviews: What are
patient and the critical or unexpected __ Whether there are any
functioning steps, operative duration, equipment problems to
anticipated blood loss? be addressed
Does patient have a:
__ Anesthesia team reviews: __ Surgeon, anesthesia
Known allergy? professional, and nurse
Are there any patient-
__ No specific concerns? review the key concerns
for recovery and
__ Yes __ Nursing team reviews: Has
management of this
sterility (including
Difficult airway/aspiration patient
indicator results) been
risk?
confirmed? Are there
__ No equipment issues or any
concerns?
__ Yes, and
equipment/assistance Has antibiotic prophylaxis been
available given within the last 60
minutes?
Risk of >500 mL blood loss
(7 mL/kg in children)? __ Yes

__ No __ Not applicable

__ Yes, and adequate Is essential imaging displayed?


intravenous access
__ Yes
and fluids planned

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__ Not applicable

This checklist is not intended to be comprehensive. Additions and modifications to fit local
practice are encouraged.

Reproduced with permission from: Weiser T, Haynes A, Dziekan G, et al. Effect of a 19-item surgical safety checklist
during urgent operations in a global patient population. Ann Surg 2010; 251:976. Copyright © 2010 Lippincott
Williams & Wilkins.

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Intravenous anesthetic induction agents

Suggested Potential adverse


Drug Uses Advantages
induction dose* effects

Propofol Induction agent 1 to 2.5 mg/kg Rapid onset Dose-dependent


of choice for Older age: 1 to and offset hypotension
most patients 1.5 mg/kg Antiemetic Dose-dependent
Hypovolemia or properties respiratory depressio
hemodynamic Antipruritic Pain during injection
compromise: ≤1 properties Microbial
mg/kg Bronchodilation contamination risk
Anticonvulsant Rare anaphylaxis in
properties patients with allergy t
Decreases its soybean oil emulsio
CMRO 2 , CBF, with egg phosphatide
and ICP

Etomidate May be selected 0.15 to 0.3 Rapid onset High incidence of PON
in patients with mg/kg and offset Pain during injection
hemodynamic Presence of Hemodynamic Involuntary myocloni
instability due to profound stability with no movements
any cause hypotension: 0.1 changes in BP, Absence of analgesic
to 0.15 mg/kg HR, or CO effects
Anticonvulsant Transient acute
properties adrenocortical
Decreases suppression
CMRO 2 , CBF,
and ICP

Ketamine May be selected 1 to 2 mg/kg Rapid onset Cardiovascular effects


in hypotensive Chronic use of Increases BP, Increases myocardial
patients or those tricyclic HR, and CO in oxygen demand due
likely to develop antidepressants: most patients increases in HR, BP, a
hypotension (eg, 1 mg/kg Profound CO
hypovolemia, Presence of analgesic Increases pulmonary
hemorrhage, profound properties arterial pressure (PAP
sepsis, severe hypotension: 0.5 Bronchodilation Potentiates
cardiovascular to 1 mg/kg Maintains cardiovascular toxicit
compromise)
Intramuscular airway reflexes of cocaine or tricyclic
dose: 4 to 6 and respiratory antidepressants

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mg/kg drive Exacerbates


Intramuscular hypertension,
route available tachycardia, and
if IV access lost arrhythmias in
pheochromocytoma
Direct mild myocardia
depressant effects
Neurologic effects

Psychotomimetic
effects (hallucinations
nightmares, vivid
dreams)
Increases CBF and ICP
may increase CMRO
Unique EEG effects m
result in
misinterpretation of B
and other processed
EEG values
Other effects 

Increases salivation

Methohexital Induction for 1.5 mg/kg Lowers seizure Limited availability


electroconvulsive threshold, Dose-
therapy (ECT) facilitating ECT dependent hypotensi
because it Decreases Dose-dependent
activates seizure CMRO 2 , CBF, respiratory depressio
foci and ICP Involuntary myocloni
movements
Pain during injection 
Contraindicated in
patients with porphyr

CMRO 2 : cerebral metabolic oxygen requirement; CBF: cerebral blood flow; ICP: intracranial
pressure; BP: blood pressure; HR: heart rate; CO: cardiac output; PONV: postoperative nausea
and vomiting; EEG:electroencephalographic; ECT: electroconvulsive therapy.
* Use adjusted body weight or estimated lean body weight for anesthetic drug dosing.

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Intravenous adjuvant agents used during induction of general


anesthesia

Potential adverse
Drug Suggested dose Advantages
effects

Opioids Fentanyl: 25 to 100 Suppresses airway Dose-dependent


mcg (or 0.5 to 1 reflexes to prevent respiratory
mcg/kg): may be coughing and/or depression; possible
administered in bronchospasm during apnea
divided doses laryngoscopy and Pruritus
Sufentanil: 0.05 to 0.1 intubation Postoperative nausea
mcg/kg: may be Attenuates stress and vomiting
administered in response to prevent
divided doses   tachycardia and
  hypertension during
laryngoscopy and
(Reduce dose in older
intubation
adults [≥70 years];
Minimizes pain
reduce or avoid dose in
caused by IV injection
patients with
of induction agent
hemodynamic
instability.) Supplements
sedation and reduces
dose requirement of
IV induction agent

Lidocaine 0.5 to 1.5 mg/kg for Suppresses airway Mild increases in


suppression of airway reflexes to prevent airway tone
reflexes (or 0.5 to 1 coughing during Increases ventricular
mg/kg in older adults laryngoscopy and rate in patients with
[≥70 years]) intubation atrial fibrillation (avoid
20 to 30 mg total is Reduces airway in patients with Wolff-
used to reduce pain responsiveness to Parkinson-White
on injection of other noxious stimuli; syndrome or high-
agents  reduces airway grade heart block)
  responsiveness to
drugs that cause
(Reduce or avoid dose in
bronchospasm
patients with
Minimizes pain
hemodynamic
caused by IV injection
instability.)
of induction agent

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Supplements
sedation and reduces
dose requirement of
IV induction agent

Midazolam 1 to 2 mg is typical, Reduces anxiety and Mild systemic


administered in 1-mg produces amnesia; vasodilation and
increments typically administered decreased cardiac
Older adults (≥70 in the immediate output; may cause
years): 0.5-mg preoperative period severe hypotension in
increments up to 2 Supplements hemodynamically
mg sedation and reduces unstable or
  dose requirement of hypovolemic patients
IV induction agent Dose-dependent
(Reduce or avoid dose in
Anticonvulsant respiratory
patients with
depression; possible
hemodynamic
apnea, particularly if
instability.)
coadministered with
an opioid

IV: intravenous.

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Properties of neuromuscular blocking agents

Agent* Vecuronium Rocuronium Pancuronium Mivacurium

Type (structure) Non- Non- Non- Non-depolarizing


depolarizing depolarizing depolarizing

Type (duration) Intermediate Intermediate Long Short

Potency - ED 95 0.04 0.30 0.07 0.08


(mg/kg)

Intubating dose 0.10 to 0.20 0.60 to 1.00 0.08 to 0.12 0.20


(mg/kg) (1.20 with RSII
dose)

Onset time (min) 3 to 4 1 to 2 2 to 3 3 to 4

Time to 25% 20 to 35 30 to 50 (60 to 60 to 120 15 to 20


recovery (min) 80 with RSII
dose)

Elimination half-life (min)

Normal organ 50 to 60 60 to 100 100 to 130 2 to 2.5


function

Renal Mild increase 100 to 300 Increased x2 3 to 4


impairment

Hepatic Significant 120 to 400 Increased x2 3 to 6


impairment increase

Maintenance 0.01 0.10 0.02 0.10


dose (mg/kg)

Infusion dose 1 to 2 5 to 12 Not 5 to 8


(mcg/kg/min) recommended

Elimination Renal 10 to Renal 30%; Renal 40 to 70%; Plasma


route/metabolism 50%; hepatic 70% hepatic 20% cholinesterase (70%
hepatic 30 to of succinylcholine
50% rate)

Active 3-desacetyl- 17-desacetyl- 3-OH- No active metabolites


metabolites vecuronium rocuronium pancuronium;
(minimal) 17-OH-
pancuronium

Side effects Vagal blockade Minimal Vagal block Histamine release

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with large (tachycardia),


doses catecholamine
release

Contraindications None None Short surgical Pseudocholinesterase


(other than procedures (<60 deficiency
specific allergy) min); not
recommended
for continuous
infusion

Comments Not for Pain on Significant Reversal by


prolonged ICU injection; accumulation, cholinesterase
administration easily prone to inhibitors; mixture of
(myopathy); reversible by residual block 3 isomers (cis-cis
reversible by sugammadex; (3-OH minimal);
sugammadex; elimination metabolite has edrophonium for
elimination half-life 50% activity of antagonism more
half-life halved prolonged in pancuronium) effective during deep
in late ICU patient; block
pregnancy; 3- 17-desacetyl
desacetyl metabolite has
metabolite has 20% activity
60% of the
parent
compound
potency

NA: data not available; ED 95 : effective dose to achieve 95% depression of baseline muscle
contraction; NMBA: neuromuscular blocking agents; RSII: rapid sequence induction and
intubation; K + : potassium; MH: malignant hyperthermia; ST: single twitch; ICU: intensive care
unit.
* The data are averages obtained from published literature and do not account for other
influences such as volatile anesthetics, muscle temperature, etc.

Adapted from: Brull SJ. Neuromuscular blocking agents. In: Clinical Anesthesia, 8th ed, Barash PG, Cullen BF,
Stoelting RK, et al (Eds), Wolters Kluwer, Philadelphia 2017.

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Inhalation anesthetic agents

Generic name Nitrous oxide Halothane Isoflurane Sevoflurane

Brand name N/A Fluothane Forane Ultane

Chemical formula N2O C 2 HBrClF 3 C 3 H 2 ClF 5 O C4H3F7

Odor Slightly sweet Sweet Sweet Sweet

Color Colorless Colorless Colorless Colorless

Pungency None Moderate High Low

Solubility:blood:gas Very low: 0.46 Very high: 2.40 Moderately Low: 0.65
partition coefficient high: 1.40

Redistribution:brain:blood 1.1 1.9 1.6 1.7


partition coefficient

Potency:oil:gas partition Very low: 1.4 Very high: 224.0 High: 97.0 Moderately
coefficient high: 42.0

Minimum alveolar 105.0% 0.8% 1.2% 2.0%


concentration
(MAC) = ED 50 for response
to surgery

MAC-awake/MAC-aware = 68.0% 0.4% 0.5% 0.6%


ED 50 for response to
voice/touch

Blood pressure effect Negligible Dose-dependent Dose- Dose-


hypotension dependent dependent
hypotension hypotension

Vascular effect Negligible Negligible Vasodilation Vasodilation

Inotropic effect Negligible Negative Slightly Slightly


negative negative

Chronotropic effect Negligible Bradycardia Tachycardia Tachycardia >


MAC

How supplied Pressurized Bottled liquid Bottled liquid Bottled liquid


bottled gas

How delivered Flowmeter Vaporizer Vaporizer Vaporizer

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Fire risk Supports Non-flammable Non-flammable Non-flammab


combustion

Notes Nausea/emesis Nausea/emesis; Nausea/emesis; Nausea/emes


bradycardia/asystole; potentially inhalational
inhalational significant induction
induction; no longer tachycardia
used in US

N/A: not applicable.

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Contributor Disclosures
Adam King, MD No relevant financial relationship(s) with ineligible companies to disclose. William
Benedetto, MD No relevant financial relationship(s) with ineligible companies to disclose. Alexandra
Plichta, MD No relevant financial relationship(s) with ineligible companies to disclose. Girish P Joshi,
MB, BS, MD, FFARCSI Consultant/Advisory Boards: Baxter [anesthesia]. All of the relevant financial
relationships listed have been mitigated. Nancy A Nussmeier, MD, FAHA No relevant financial
relationship(s) with ineligible companies to disclose.

Contributor disclosures are reviewed for conflicts of interest by the editorial group. When found, these
are addressed by vetting through a multi-level review process, and through requirements for
references to be provided to support the content. Appropriately referenced content is required of all
authors and must conform to UpToDate standards of evidence.

Conflict of interest policy

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