Induction of General Anesthesia - Overview

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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: Jan 2024.

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')
● Inhalation agents (see "Inhalation anesthetic agents: Clinical effects and uses", section
on 'Induction of general anesthesia' and "Inhalation anesthetic agents: Properties and
delivery")
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● 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 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".)
• 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 "Patient safety in the operating
room", section on 'Timeouts, briefing, and debriefing'.)
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

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 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.
● 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'.)
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'.)
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 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

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 "Intraoperative use of vasoactive
agents", 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.
● 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].
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● 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'.)
● 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 in adults", 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 anesthetic 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 ( figure 1 and
table 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' 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.
Use of UpToDate is subject to the Terms of Use.
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19. Thomas Ebert and Larry Lindenbaum. Inhaled Anesthetics. In: Clinical Anesthesia, Seven
th, 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 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 48.0
GRAPHICS
Continuum of depth of sedation: Definition of general anesthesia and levels

of sedation/analgesia*
Moderate
Minimal
sedation/analgesia Deep General
sedation
("conscious sedation/analgesia anesthesia
anxiolysis
sedation")
Responsiveness Normal Purposeful ¶ response Purposeful ¶ response Unarousable

response to to verbal or tactile following repeated or even with
verbal stimulation painful stimulation painful
stimulation stimulus
Airway Unaffected No intervention Intervention may be Intervention

required required often required
Spontaneous Unaffected Adequate May be inadequate Frequently

ventilation inadequate
Cardiovascular Unaffected Usually maintained Usually maintained May be

function impaired
Minimal sedation (anxiolysis) is a drug-induced state during which patients respond normally to
verbal commands. Although cognitive function and physical coordination may be impaired, airway
reflexes and ventilatory and cardiovascular functions are unaffected.
Moderate sedation/analgesia ("conscious sedation") is 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 patent
airway, and spontaneous ventilation is adequate. Cardiovascular function is usually maintained.
Deep sedation/analgesia is 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 patent airway, and spontaneous ventilation may be inadequate.
Cardiovascular function is usually maintained.
General anesthesia is 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 impaired. Patients often require assistance in maintaining a patent 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.
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 Δ patients whose level of sedation becomes deeper than initially intended. Individuals
administering moderate sedation/analgesia ("conscious sedation") should be able to rescue Δ
patients who enter a state of deep sedation/analgesia, while those administering deep
sedation/analgesia should be able to rescue Δ patients who enter a state of general anesthesia.
* Monitored anesthesia care (MAC) does not describe the continuum of depth of sedation; rather it
describes "a specific anesthesia service in which an anesthesiologist has been requested to participate
in the care of a patient undergoing a diagnostic or therapeutic procedure."
¶ Reflex withdrawal from a painful stimulus is not considered a purposeful response.
Δ Rescue of a patient from a deeper level of sedation than intended is an intervention by a

practitioner proficient in airway management and advanced life support. The qualified practitioner
corrects adverse physiologic consequences of the deeper-than-intended level of sedation (such as
hypoventilation, hypoxia, and hypotension) and returns the patient to the originally intended level of
sedation. It is not appropriate to continue the procedure at an unintended level of sedation.
Approved by the ASA House of Delegates on October 13, 1999, and last amended on October 15, 2014. Published in: 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 & 2014 American Society of
Anesthesiologists, Inc. Reproduced with permission from Lippincott Williams & Wilkins. Unauthorized reproduction of this
material is prohibited.
Graphic 109909 Version 4.0
Signs indicating stages of anesthesia
Modified from: Gillespie NA. The signs of anesthesia. Anesth Analg 1943; 22:275. Copyright © 1943 International Anesthesia
Research Society. Reproduced with permission from Wolters Kluwer Health. Unauthorized reproduction of this material is
prohibited.
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 is Provider or
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, that the Provider or
filler ports are tightly closed technician
Item #8: Verify that there are no leaks in the gas supply lines between the Provider or
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 check the Provider or
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 during Provider and
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)
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, that the Provider
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 during Provider and
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.
Vasopressors and inotropic agents used in the operating room: Adult

dosing* ¶
Functional class
Bolus
Drug (predominant receptor or Infusion dose Com
dose
mechanism of action)
Ephedrine Inotrope/chronotrope/vasopressor 5 to 10 mg N/A Tachy

(alpha1-adrenergic receptor boluses occur
agonist; beta1- and beta2- repea
adrenergic receptor agonist) to ind
postsy
releas
norep
Cardio
effect
by dru
ephed
into a
nerve
or tho
deple
norep
reserv
reserp
Admin
extrem
(eg, in
increm
of 2.5
patien
mono
oxida
inhibi
metha
since
hyper
respo
threat
dysrh
occur
Phenylephrine Vasopressor (alpha1-adrenergic 50 to 100 10 to 100 Often

receptor agonist) mcg mcg/minute treat
boluses norm
or
(may begin HR is
infusion if 0.1 to 1
Genet
repeated mcg/kg/minute
polym
bolus lead t
doses are indivi
necessary) respo
Norepinephrine Inotrope/vasopressor (alpha1- and 4 to 8 mcg 1 to 20 mcg/minute Often

beta1-adrenergic receptor agonist) (may begin first-li
or
infusion if durin
repeated 0.01 to 0.3
surge
bolus mcg/kg/minute
for tre
doses are most
necessary) Norep
mcg i
appro
equiv
poten
pheny
mcg
Periph
extrav
high c
may c
dama
Epinephrine Inotrope/chronotrope/vasopressor 4 to 10 1 to 100 First-l

(alpha1-adrenergic receptor mcg mcg/minute for ca
agonist; beta1- and beta2- initially; up and fo
or
adrenergic receptor agonist) to 100 mcg May b
boluses 0.01 to 1
admin
may be mcg/kg/minute
or via
used when endot
initial in em
Note changing
response is
effects across dose Low d
inadequate
range: bronc
Low doses effect
have primarily cause
beta2- vasod
adrenergic decre
effects at 1 to 2 Interm
mcg/minute or cause
0.01 to 0.02 HR an
mcg/kg/minute High d
Intermediate vasoc
doses have with p
primarily hyper
beta1- and adver
beta2- effect
adrenergic Indivi
effects at 2 to respo
10 mcg/minute
or 0.02 to 0.1 relate

mcg/kg/minute variab
High doses
have primarily
alpha1-
adrenergic
effects at 10 to
100
mcg/minute or
0.1 to 1
mcg/kg/minute
Vasopressin Vasopressor (vasopressin1 and 1 to 4 units 0.01 to 0.04 Effect

vasopressin2 receptor agonist) units/minute treatm
hypot
refrac
Doses >0.04
admin
units/minute up to
catech
0.1 units/minute are
symp
reserved for salvage
such a
therapy (ie, failure to
pheny
achieve adequate BP
norep
goals with other
No di
vasopressor
HR
agents) ¶
Little
can ca
splan
vasoc
Indivi
respo
relate
variab
Periph
extrav
cause
Dopamine Inotrope/vasopressor/dose- N/A 2 to 20 Low d

dependent chronotropy mcg/kg/minute exace
(dopaminergic, beta1-, beta2-, and hypot
alpha1-adrenergic receptor beta2
agonist) Note changing
High d
effects across dose
cause
range:
vasoc
Low doses
adver
have primarily
effect
dopaminergic
arrhyt
effects at <3
mcg/kg/minute
Intermediate
doses have
primarily
beta1- and
beta2-
adrenergic
effects at 3 to
10
mcg/kg/minute
High doses
have primarily
alpha1-
adrenergic
effects >10
mcg/kg/minute
Dobutamine Inotrope/vasodilator/dose- N/A 1 to 20 Exace

dependent chronotropy (beta1- mcg/kg/minute hypot
and beta2-adrenergic receptor possib
agonist) dose-
vasod
beta2
concu
admin
poten
vasoc
such a
norep
vasop
neces
Milrinone Inotrope/vasodilator N/A 0.375 to 0.75 Exace

(phosphodiesterase inhibitor) mcg/kg/minute (a hypot
(decreases rate of cyclic adenosine loading dose of 50 due to
monophosphate [cAMP] mcg/kg over ≥10 (via
degradation) minutes may be phosp
administered, but inhibi
may be omitted to concu
avoid hypotension) admin
poten
vasoc
such a
norep
vasop
neces
Isoproterenol Inotrope/chronotrope/vasodilator N/A 5 to 20 mcg/minute Exace

(beta1- and beta2-adrenergic hypot
or
receptor agonist) due to
0.05 to 0.2
depen
mcg/kg/minute
vasod
beta2
May c
arrhyt
Not av
most
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 average size.
¶ Refer to related UpToDate content on hemodynamic management during anesthesia and surgery.
Basic monitoring during anesthesia
Primary physiologic
Monitoring Derived Additio
process/parameter Principle
equipment information functi
targeted
Oxygenation Inspired gas O2 analyzer Paramagnetic Inspired/expired A low-level a

O2 content (with a low- sensor, fuel O2 concentration automaticall
limit alarm in (galvanic) cell, when placed activated by
use) polarographic downstream on the anest
(Clark) electrode, from fresh flow machine
mass control valves
spectroscopy, or
Raman scattering.
Blood Pulse The Beer-Lambert Hemoglobin Continuous

oxygenation oximeter law applied to saturation, pulse evaluation of
tissues and rate, relative circulation, v
pulsatile blood pulse 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 CO2 Capnograph CO2 molecules ETCO2, inspired Instantaneou

absorb infrared CO2, diagnostic information
radiation at 4.26 waveforms, Perfusi
micrometers, respiratory rate, effectiv
proportionate to apnea detection is being
the CO2 transpo
concentration throug
present in the vascula
breath sample. system
Metabo
(how ef
CO2 is b
produc
cellular
metabo
Confirm
of trach
tube
placem
after
intubat
Integrity of Disconnection Detects the Alarms if a Alarms if hig

ventilation alarm cyclical changes in significant pressures ar
system airway pressure in decrease in rate sensed
during the normal range. or pressure
mechanical occurs
ventilation
Pulmonary Pulmonary Volume of gas Inspired and Pressure vol

mechanics flow and proportional to a expired volume, and flow volu
(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 warnin
significant
arrhythmias
asystole
Arterial BP Noninvasive Oscillometric Arterial BP Indicator of o

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

monitor semiconductor, peripheral core-to-perip
electrical temperature temperature
resistance gradient is in
decreases as of low cardia
temperature output
decreases.
BP: blood pressure; CO2: carbon dioxide; ECG: electrocardiogram; ETCO2: end-tidal carbon dioxide;
MAP: mean arterial pressure; O2: oxygen.
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 confirmed: have introduced Nurse verbally confirms with
Identity themselves by name and the team:
Site role
__ The name of the
Procedure __ Surgeon, anesthesia procedure recorded
Consent professional, and nurse
__ That instrument, sponge,
verbally confirm
__ Site marked/not and needle counts are
Patient
applicable correct (or not applicable)
Site
__ Anesthesia safety check __ How the specimen is
Procedure
completed labeled (including patient
Anticipated critical events name)
__ Pulse oximeter on patient
and functioning __ Surgeon reviews: What are __ Whether there are any
the critical or unexpected equipment problems to
Does patient have a:
steps, operative duration, be addressed
Known allergy? anticipated blood loss?
__ Surgeon, anesthesia
__ No __ Anesthesia team reviews: professional, and nurse
Are there any patient- review the key concerns
__ Yes
specific concerns? for recovery and
Difficult airway/aspiration risk? management of this
__ Nursing team reviews: Has
patient
__ No sterility (including indicator
results) been confirmed?
__ Yes, and
Are there equipment issues
equipment/assistance
or any concerns?
available
Has antibiotic prophylaxis been
Risk of >500 mL blood loss (7
given within the last 60
mL/kg in children)?
minutes?
__ No
__ Yes
__ Yes, and adequate
__ Not applicable
intravenous access and
fluids planned Is essential imaging displayed?
__ Yes
__ 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.
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
hemodynamic Antipruritic depression
compromise: ≤1 properties Pain during injectio
mg/kg Bronchodilation Microbial
Anticonvulsant contamination risk
properties Rare anaphylaxis in
Decreases patients with allerg
CMRO2, CBF, to its soybean oil
and ICP emulsion with egg
phosphatide
Etomidate May be selected 0.15 to 0.3 Rapid onset High incidence of

in patients with mg/kg and offset PONV
hemodynamic Presence of Hemodynamic Pain during injectio
instability due to profound stability with no Involuntary myoclo
any cause hypotension: 0.1 changes in BP, movements
to 0.15 mg/kg HR, or CO Absence of analges
Anticonvulsant effects
properties Transient acute
Decreases adrenocortical
CMRO2, CBF, suppression
and ICP
Ketamine May be selected 1 to 2 mg/kg Rapid onset Cardiovascular effect

in hypotensive Chronic use of Increases BP, Increases
patients or those tricyclic HR, and CO in myocardial oxyge
likely to develop antidepressants: most patients demand due to
hypotension (eg, 1 mg/kg increases in HR, B
Profound
hypovolemia, and CO
Presence of analgesic
hemorrhage, Increases
profound properties
sepsis, severe pulmonary arteri
hypotension: 0.5 Bronchodilation
cardiovascular pressure (PAP)
to 1 mg/kg Maintains
compromise)
Intramuscular airway reflexes Potentiates
dose: 4 to 6 and respiratory cardiovascular
mg/kg drive toxicity of cocaine
or tricyclic
Intramuscular
antidepressants
route available
if IV access lost Exacerbates
hypertension,
tachycardia, and
arrhythmias in
pheochromocyto
Direct mild
myocardial
depressant effect
Neurologic effects
Psychotomimetic
effects
(hallucinations,
nightmares, vivid
dreams)
Increases CBF an
ICP; may increase
CMRO2
Unique EEG effec
may result in
misinterpretation
BIS and other
processed EEG
values
Other effects
Increases salivati
Methohexital Induction for 1.5 mg/kg Lowers seizure Limited availability

electroconvulsive threshold, Dose-dependent
therapy (ECT) facilitating ECT hypotension
because it Decreases Dose-dependent
activates seizure CMRO2, CBF, respiratory
foci and ICP depression
Involuntary myoclo
movements
Pain during injectio
Contraindicated in
patients with
porphyria
CMRO2: 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.
Intravenous adjuvant agents used during induction of general anesthesia
Potential adverse
Drug Suggested dose Advantages
effects
Opioids Fentanyl: 25 to 100 mcg Suppresses airway Dose-dependent

(or 0.5 to 1 mcg/kg): reflexes to prevent respiratory depression;
may be administered in coughing and/or possible apnea
divided doses bronchospasm during Pruritus
Sufentanil: 0.05 to 0.1 laryngoscopy and Postoperative nausea
mcg/kg: may be intubation and vomiting
administered in divided Attenuates stress
doses response to prevent
tachycardia and
hypertension during
(Reduce dose in older
laryngoscopy and
adults [≥70 years]; reduce
intubation
or avoid dose in patients
Minimizes pain caused
with hemodynamic
by IV injection of
instability.)
induction agent
Supplements sedation
and reduces dose
requirement of IV
induction agent
Lidocaine 0.5 to 1.5 mg/kg for Suppresses airway Mild increases in airway
suppression of airway reflexes to prevent 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 in
20 to 30 mg total is used Reduces airway patients with Wolff-
to reduce pain on responsiveness to Parkinson-White
injection of other noxious stimuli; reduces syndrome or high-grade
agents airway responsiveness heart block)
to drugs that cause
bronchospasm
(Reduce or avoid dose in
Minimizes pain caused
patients with hemodynamic
by IV injection of
instability.)
induction agent
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 in decreased cardiac
output; may cause
Older adults (≥70 the immediate severe hypotension in

years): 0.5-mg preoperative period hemodynamically
increments up to 2 mg Supplements sedation unstable or hypovolemic
and reduces dose patients
(Reduce or avoid dose in requirement of IV Dose-dependent

patients with hemodynamic induction agent respiratory depression;
instability.) Anticonvulsant possible apnea,
particularly if
coadministered with an
opioid
IV: intravenous.
Properties of neuromuscular blocking agents
Agent Vecuronium Rocuronium Pancuronium * Mivacurium ¶ A
Type (structure) Non- Non- Non-depolarizing Non-depolarizing N

depolarizing depolarizing
Type (duration) Intermediate Intermediate Long Short In
Potency – ED95 0.04 0.3 0.07 0.08 0

(mg/kg)
Intubating dose 0.1 to 0.2 Δ 0.6 to 1 (1.2 0.08 to 0.12 0.2 0

(mg/kg) with RSII
dose) ◊
Onset time (min) 3 to 4 1 to 2 2 to 3 3 to 4 3
Time to 25% 20 to 35 30 to 50 (60 to 60 to 120 15 to 20 20

recovery (min) 80 with RSII
dose)
Elimination half-life (min)
Normal 50 to 60 60 to 100 100 to 130 2 to 2.5 2

organ
function
Renal Mild increase 100 to 300 Increased ×2 3 to 4 2

impairment
Hepatic Significant 120 to 400 Increased ×2 3 to 6 2

impairment increase
Intermittent 0.01 0.1 0.02 0.1 0

maintenance
dose (mg/kg) ¥
Starting infusion 1 to 2 5 to 12 Not 5 to 8 4

dose recommended
(mcg/kg/min) ‡
Elimination Renal 10 to Renal 30%; Renal 40 to 70%; Plasma R

route/metabolism 50%; hepatic 70% hepatic 20% cholinesterase (70% H
hepatic 30 to of succinylcholine es
50% rate) 60
Active 3-desacetyl- 17-desacetyl- 3-OH- No active metabolites N

metabolites vecuronium rocuronium pancuronium; 17- m
(minimal) OH-pancuronium
Side effects Vagal Minimal Vagal block Histamine release H

blockade with (tachycardia), re
large doses catecholamine la
release ac
p
Contraindications None None Short surgical Pseudocholinesterase H

(other than procedures (<60 deficiency u
specific allergy) min); not d
recommended re
for continuous
infusion
Comments Not for Pain on Significant Reversal by O

prolonged ICU injection; accumulation, cholinesterase in
administration easily prone to residual inhibitors; mixture of e
(myopathy); reversible by block (3-OH 3 isomers (cis-cis
reversible by sugammadex; metabolite has minimal);
sugammadex; elimination 50% activity of edrophonium for
elimination half-life pancuronium) antagonism more
half-life halved prolonged in effective during deep
in late ICU patient; block
pregnancy; 3- 17-desacetyl
desacetyl metabolite has
metabolite 20% activity
has 60% of the
parent
compound
potency
The data in this table are averages obtained from published literature and do not account for other
influences such as the use of volatile anesthetics or muscle temperature. For further information refer
to UpToDate content on clinical use of neuromuscular blocking agents.
ED95: effective dose to achieve 95% depression of baseline muscle contraction; ICU: intensive care
unit; K + : potassium; MH: malignant hyperthermia; N/A: data not available; NMBA: neuromuscular
blocking agents; RSII: rapid sequence induction and intubation; ST: single twitch.
* Pancuronium is no longer available in the United States, Canada, or Europe. It is available in several
countries around the world.
¶ Mivacurium is no longer available in the United States or Canada. It is available in many other
countries.
Δ Vecuronium at a dose of 0.1 to 0.2 mg/kg may be used for RSII in patients for whom succinylcholine
is contraindicated and rocuronium is unavailable; onset of paralysis will be delayed compared with
those preferred agents.
◊ Some experts use a higher dose, 1.5 mg/kg IV, of rocuronium for rapid sequence induction in the
emergency department. Refer to UpToDate content on rapid sequence in duction for emergency
intubation.
§ Cisatracurium at a dose of 0.4 mg/kg may be used for RSII in patients for whom succinylcholine is
contraindicated and rocuronium is unavailable; onset of paralysis will be delayed compared with
those preferred agents.
¥ Intermittent dosing titrated to endpoints such as ventilator synchrony may be preferred to

continuous infusions in the ICU. Higher intermittent maintenance doses may be used in the ICU to
provide a longer duration of action and to avoid continuous infusion.
‡ The starting infusion dose presumes that an intubating dose or a similar loading dose has been
given prior to starting the infusion. The infusion dose should be adjusted thereafter based on
monitoring.
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.
Inhalation anesthetic agents
Generic name Nitrous oxide Halothane Isoflurane Sevoflurane
Brand name N/A Fluothane Forane Ultane
Chemical formula N2 O C2HBrClF3 C3H2ClF5O C 4 H3 F 7 O
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) = ED50 for response
to surgery
MAC-awake/MAC-aware = 68.0% 0.4% 0.5% 0.6%

ED50 for response to
voice/touch
Blood pressure effect Negligible Dose-dependent Dose- Dose-

hypotension dependent dependent
hypotension hypotensio
Vascular effect Negligible Negligible Vasodilation Vasodilatio
Inotropic effect Negligible Negative Slightly Slightly

negative negative
Chronotropic effect Negligible Bradycardia Tachycardia Tachycardia

MAC
How supplied Pressurized Bottled liquid Bottled liquid Bottled liqu

bottled gas
How delivered Flowmeter Vaporizer Vaporizer Vaporizer
Fire risk Supports Non-flammable Non-flammable Non-flamm

combustion
Notes Nausea/emesis Nausea/emesis; Nausea/emesis; Nausea/em

bradycardia/asystole; potentially inhalationa
inhalational induction
induction; no longer significant

used in US tachycardia
N/A: not applicable.

Induction of General Anesthesia - Overview

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23/2/24, 13:54 Induction of general anesthesia: Overview - UpToDate

Official reprint from UpToDate®

Induction of general anesthesia: Overview

Literature review current through: Jan 2024.

General anesthesia establishes a reversible state that includes:

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

● Neuromuscular blocking agents (see "Clinical use of neuromuscular blocking agents in

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

CONTINUUM OF SEDATION DURING ANESTHETIC INDUCTION

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

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

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

return of consciousness during emergence [2-4]. This phenomenon is termed hysteresis or

PREPARATION FOR ANESTHETIC INDUCTION

● Anesthesia machine checkout – The anesthesia machine checkout should be

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

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

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

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

• An anticholinergic (atropine or glycopyrrolate).

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

measurements are obtained to ensure proper functioning of the monitors and to

● Preprocedure checklist – An appropriate preprocedure checklist should be completed;

Immediately before induction

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

● Preoxygenation (denitrogenation) – Before administration of any anesthetic

SELECTION OF INDUCTION TECHNIQUE

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

INTRAVENOUS ANESTHETIC INDUCTION

Techniques and anesthetic agents

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

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

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

anesthesia: Intravenous induction agents", section on 'Adjuvant agents' and "General

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

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

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

Induction with supraglottic airway placement — During IV induction with planned

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

INHALATION ANESTHETIC INDUCTION

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

● Maintenance of spontaneous ventilation is desirable during induction. Examples

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

Techniques and specific inhalation agents — Inhalation induction of anesthesia requires a

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

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

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

particularly at high concentrations [17,21]. Also, desflurane can cause sympathetic

NEUROMUSCULAR BLOCKING AGENTS

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

'Neuromuscular blocking agents (NMBAs)' and "Clinical use of neuromuscular blocking

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

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

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

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

CLINICAL CASE EXAMPLES

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

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

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

● Patients with specific comorbidities:

SUMMARY AND RECOMMENDATIONS

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

● Preparations for induction