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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
● 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:
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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")
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.
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After patient arrival — After patient arrival in the OR, the following steps are completed:
● 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".)
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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'.)
Patient selection — Adult patients usually have intravenous (IV) access and typically
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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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● An in situ tracheostomy is present since unpleasant odor and irritation of the airway
are not problematic.
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● 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'.)
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cost and wide availability. (See "Inhalation anesthetic agents: Clinical effects and
uses", section on 'Halothane'.)
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'.)
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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'.)
VASOPRESSOR AGENTS
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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.
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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• 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'.)
• Eye injury – (See "Anesthesia for emergency eye surgery", section on 'Choice of
induction and adjuvant agents'.)
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above.)
• Inhalation anesthetic agent(s), often added shortly after achieving initial loss of
consciousness
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
5. https://www.asahq.org/For-Members/Clinical-Information/2008-ASA-Recommendatio
ns-for-PreAnesthesia-Checkout.aspx.
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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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GRAPHICS
Continuum of sedation/analgesia/anesthesia
Moderate
Minimal
sedation/analgesia Deep General
sedation
(conscious sedation/analgesia Δ anesthesia ◊
(anxiolysis)*
sedation) ¶
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.
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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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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.
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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 #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 #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
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Item #15: Confirm ventilator settings and evaluate readiness to deliver Provider
anesthesia care (anesthesia time out)
Item #2: Verify that patient suction is adequate to clear the airway Provider and
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 #15: Confirm ventilator settings and evaluate readiness to deliver Provider
anesthesia care (anesthesia time out)
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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Functional class
Bolus
Drug (predominant receptor or Infusion dose
dose
mechanism of action)
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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
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Periph
extrava
cause
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vasopr
necess
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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Primary physiologic
Monitoring Derived Additio
process/parameter Principle
equipment information functi
targeted
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being pro
by cellula
metaboli
Confirma
tracheal t
placemen
intubatio
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
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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.
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__ No __ Not applicable
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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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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
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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
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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Potential adverse
Drug Suggested dose Advantages
effects
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Supplements
sedation and reduces
dose requirement of
IV induction agent
IV: intravenous.
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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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Solubility:blood:gas Very low: 0.46 Very high: 2.40 Moderately Low: 0.65
partition coefficient high: 1.40
Potency:oil:gas partition Very low: 1.4 Very high: 224.0 High: 97.0 Moderately
coefficient high: 42.0
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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.
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