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Induction of general anesthesia: Overview

Author: Adam King, 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: Dec 2020. | This topic last updated: Oct 09, 2018.
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 hemodynamic stability and ventilation.
This topic will discuss preinduction preparations and selection of anesthetic induction techniques and agents. The
intravenous induction agents, supplemental adjuvant agents, inhalation anesthetic agents, and neuromuscular blocking
agents used to induce general anesthesia are reviewed in detail separately:
● (See "General anesthesia: Intravenous induction agents".)

● (See "Inhalation anesthetic agents: Properties and delivery".)
● (See "Clinical use of neuromuscular blocking agents in anesthesia".)
Considerations for preoperative evaluation and preparation of the patient are reviewed separately:
● (See "Preoperative fasting guidelines".)

● (See "Preoperative medical evaluation of the healthy adult patient".)
● (See "Perioperative medication management".)
● (See "Evaluation of cardiac risk prior to noncardiac surgery".)
● (See "Evaluation of preoperative pulmonary risk".)
● (See "Preanesthesia evaluation for noncardiac surgery".)
CONTINUUM OF SEDATION DURING ANESTHETIC INDUCTION
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Anesthetic agents demonstrate a dose-response effect, with progressively higher doses providing progressively deeper
levels of sedation and anesthesia ( table 1).
Notably, sedation progresses to general anesthesia as a continuum of effect rather than as a consecutive series of
distinct states with clear transitions ( table 2). Light/minimal sedation with anxiolysis and analgesia is the lightest
plane, 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 and has intact airway patency and spontaneous ventilation, although
blood pressure may be reduced. Deep sedation is a state in which the patient is no longer responsive to voice; airway
patency, spontaneous ventilation, and cardiovascular function may also be compromised. However, the patient still
moves in response to a noxious surgical stimulus.
General anesthesia represents an anesthetic depth at which the patient will not respond to voice or to noxious surgical
stimuli (stage III) ( table 1). As the patient progresses from Stage I to stage III surgical anesthesia, airway reflexes and
patency, spontaneous ventilation, cardiovascular function, and muscle tone become increasingly depressed ( figure 1
). Stage IV anesthetic depth is “too deep” with profound medullary depression that includes the cardiovascular and
respiratory centers and eventually leads to the need for cardiopulmonary resuscitation ( table 1). Notably, patients
may rapidly transition from one stage of anesthetic depth to the next, so that urgent interventions to support the airway
and respiratory and cardiovascular function may become necessary.
PREPARATION FOR ANESTHETIC INDUCTION
Preparation before patient arrival — The following steps are undertaken before the patient arrives:
● Anesthesia machine checkout – The anesthesia machine checkout should be performed prior to the patient's
arrival in the operating room ( table 3) [1]. (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. (See "Preanesthesia evaluation for noncardiac
surgery".)
Preparation after patient arrival — After patient arrival, the following should be completed:
● Monitoring – Prior to induction of general anesthesia, the patient should be connected to standard American
Society of Anesthesiologists (ASA) monitors [2]. Preinduction measurements are obtained to ensure proper
functioning of the monitors and to establish the patient's baseline values.
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). (See
"Monitoring during anesthesia".)
● Intravenous access – Virtually all adult patients have at least one peripheral venous or other vascular access
catheter placed prior to 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).
Preparation immediately before induction
● Positioning for induction – Before induction of anesthesia, the patient's head should be placed in the sniffing
position (atlanto-occipital extension with head elevation of 3 to 7 cm [3]), 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.
● Preoxygenation (denitrogenation) – Prior to administration of any anesthetic induction agents, the patient is
preoxygenated (denitrogenated) with 100 percent O2 to increase O2 reserve, thereby providing additional time to
secure the airway [4,5]. (See "Airway management for induction of general anesthesia", section on
'Preoxygenation'.)
SELECTION OF INDUCTION TECHNIQUE
Induction of general anesthesia may be accomplished by employing a technique with either primarily intravenous (IV) or
primarily inhalation agents.
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. None of the available induction agents is ideal for all patients,
and all have side effects. Age and coexisting diseases affect selection of anesthetic induction and adjuvant agents, as
well as estimation of safe and effective doses of each agent.
In order to minimize the total dose of any one anesthetic agent and thereby reduce the incidence of drug-related side
effects, we typically administer multiple agents to accomplish anesthetic induction, including one or more adjuvant
agents, and a neuromuscular blocking agent (NMBA) if endotracheal intubation is planned. Various combinations of
drugs are effective, and either IV or inhalation routes of administration, or both, may be employed.
Inhalation agents are also frequently employed as a component of anesthetic induction, after initial loss of
consciousness has been achieved with IV agents. All inhalation agents deepen anesthesia so that airway reflexes and
sympathetic stress responses are blunted during laryngoscopy. The potent volatile agents also induce a dose-
dependent decrease in skeletal muscle tone, which improves conditions for insertion of an endotracheal tube (ETT) or a
supraglottic airway (SGA). (See "Inhalation anesthetic agents: Clinical effects and uses", section on 'Use as a supplement
(all inhalation agents)'.)
INTRAVENOUS ANESTHETIC INDUCTION
Adult patients usually have intravenous (IV) access and prefer induction with IV agents. The commonly used IV sedative-
hypnotic induction agents and adjuvant IV agents (eg, an opioid and/or lidocaine) used to supplement anesthetic effects
of the sedative-hypnotic induction agents are reviewed in detail separately ( table 6 and table 7). (See "General
anesthesia: Intravenous induction agents".)
Induction with endotracheal intubation — During induction with planned laryngoscopy and endotracheal tube
insertion, one or more adjuvant IV agents are typically administered to supplement the anesthetic effects of the
selected sedative-hypnotic induction agent ( table 7).
● Typically, an opioid (eg, fentanyl 25 to 100 mcg [ie, 0.5 to 1 mcg/kg]) is administered three to five minutes before the
sedative-hypnotic agent (eg, propofol 1 to 2.5 mg/kg) to achieve an optimal synergistic effect [6]. For example,
fentanyl can reduce the induction dose requirement of propofol by 40 to 70 percent [6-10].
● In some cases, midazolam may be administered in the immediate preoperative period or several minutes before
the sedative-hypnotic agent for its amnestic and anxiolytic effects; midazolam also supplements sedation and
reduces dose requirement for the selected sedative-hypnotic induction agent [8]. However, routine use of pre-
induction midazolam should be avoided as the risks of administration outweigh the benefits [11].
● Lidocaine 0.5 to 1.5 mg/kg is often administered to blunt the airway responses to laryngoscopy and endotracheal
intubation and to supplement the anesthetic effects of the induction agent [12-25]. Due to its local anesthetic effect,
a lower dose of lidocaine (approximately 40 mg) reduces pain caused by IV injection of propofol if administered into
the same vein [26-32].
● A neuromuscular blocking agent (NMBA) may be administered to facilitate endotracheal intubation ( table 8). (See
'Neuromuscular blocking agents' below.)
Induction with supraglottic airway placement — During IV induction with planned insertion of a supraglottic airway
(SGA) such as a laryngeal mask airway (LMA), adequate depth of anesthesia must be achieved 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'.)
● Lidocaine is typically administered prior to the sedative hypnotic agent, similar to induction with planned
endotracheal intubation [32]. (See 'Induction with endotracheal intubation' above.)
● Opioid administration during the induction sequence may be minimized or avoided to allow spontaneous
ventilation immediately after induction and avoid a period of postinduction apnea. (See "Supraglottic devices
(including laryngeal mask airways) for airway management for anesthesia in adults", section on 'Choice of mode of
ventilation'.)
● If difficulty with SGA placement or initial ventilation is encountered, an additional sedative-hypnotic agent is
typically administered. (See "Supraglottic devices (including laryngeal mask airways) for airway management for
anesthesia in adults", section on 'Troubleshooting'.)
● Occasionally, a small dose of an NMBA is employed to facilitate SGA placement and prevent or treat airway
responses. (See "Supraglottic devices (including laryngeal mask airways) for airway management for anesthesia in
adults", section on 'Use of neuromuscular blocking agents'.)
INHALATION ANESTHETIC INDUCTION
An inhalation induction is often selected for the following types of patients:
● Pediatric patients – Primary induction with inhaled agents is usually preferred by pediatric patients because of
their fear of needles and response to the pain of a needle stick [33].
● Adult patients – Inhalation induction may be preferred if spontaneous breathing during induction is desired (eg,
tracheal stenosis or intraoral, pharyngeal, or mediastinal mass causing compression of the airway) or when IV
access cannot be obtained. Adult patient satisfaction may be lower with a primary inhalation induction compared
with IV induction due to the unpleasant odor of the gas [34] and a higher incidence of postoperative nausea and
vomiting (PONV) [34-36].
Compared with IV induction, inhalation induction time is longer, usually requiring several minutes of ventilation.
Therefore, this technique is not suitable for rapid sequence induction and intubation (RSII). (See "Rapid sequence
induction and intubation (RSII) for anesthesia".)
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, particularly
sevoflurane, has made inhalation induction of anesthesia via facemask a more pleasant and viable option compared
with older inhalation agents [35]. Properties, mechanisms of action, and delivery of inhalation agents are discussed
separately ( table 9). (See "Inhalation anesthetic agents: Properties and delivery", section on 'Factors affecting
inhalation anesthetic delivery'.)
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") [37]. Typically this single breath technique achieves the 2
percent alveolar sevoflurane concentration required to tolerate a painful intervention such as a surgical incision [38].
(See "Inhalation anesthetic agents: Properties and delivery", section on 'Technique-related considerations'.)
Volatile inhalation agents — Advantages for induction of general anesthesia that are shared by all potent volatile
anesthetic agents include excellent bronchodilation, dose-dependent decrease in skeletal muscle tone, and decrease in
cerebral metabolic rate of oxygen consumption (CMRO2). Disadvantages of all volatile agents include respiratory
depression, systemic vasodilation, and decreased blood pressure (BP); these are also dose-dependent. Also, all potent
volatile agents may precipitate malignant hyperthermia. (See "Inhalation anesthetic agents: Clinical effects and uses",
section on 'Other clinical effects'.)
● Sevoflurane – Sevoflurane is the most frequently used inhaled agent for induction of anesthesia. Sevoflurane has
many characteristics of the ideal induction agent, including relatively rapid onset due to its low tissue and blood
solubility, 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 [33,37,39]. It is the most commonly used potent volatile inhaled agent because of its
minimal odor, lack of pungency, and potent bronchodilating characteristics [33-36,40-42]. (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'.)
● Halothane – Halothane is a sweet-smelling gas with only moderate pungency. Halothane is no longer commercially
available in North America due to its adverse effects (particularly the possibility of halothane hepatitis), and the
development of newer inhalation agents that have replaced it, in particular sevoflurane. Also, halothane has the
slowest onset during induction of anesthesia compared with all other potent inhalation agents 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). However, halothane is still widely used for both induction and
maintenance of general anesthesia in many countries with limited resources due to its low cost and wide
availability. (See "Inhalation anesthetic agents: Clinical effects and uses", section on 'Halothane'.)
● Desflurane – Desflurane is not used for induction of anesthesia via facemask because it is the most pungent of the
volatile anesthetics and has the highest incidence of airway irritation (coughing, salivation, breath-holding,
laryngospasm) at high concentrations [40,43]. 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 of desflurane limit its use as an induction agent. (See "Inhalation anesthetic agents:
Clinical effects and uses", section on 'Desflurane'.)
● Isoflurane – Isoflurane, the most potent of the volatile anesthetics, is not ideal for use as the sole induction agent
because it is relatively pungent and has a slow onset (and recovery) compared with sevoflurane. (See "Inhalation
anesthetic agents: Clinical effects and uses", section on 'Isoflurane'.)
Nitrous oxide gas — N2O is a sweet-smelling gas without pungency or potential for airway irritation. It is often used as
an adjuvant agent during inhalation induction of general anesthesia. 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. (See "Inhalation anesthetic agents: Properties and delivery", section
on 'Second gas effect' and "Inhalation anesthetic agents: Clinical effects and uses", section on 'Nitrous oxide gas'.)
N2O is avoided during induction in patients with possible pre-existing bowel distention, increased middle ear pressure,
pneumothorax, pneumoperitoneum, pneumocephalus, intraocular gas, or venous air embolism [44-46]. Further
gaseous distension of such spaces 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 pulmonary hypertension because it causes mild
myocardial depression and sympathetic nervous system stimulation with increases in pulmonary vascular resistance.
(See "Inhalation anesthetic agents: Clinical effects and uses", section on 'Disadvantages and adverse effects'.)
NEUROMUSCULAR BLOCKING AGENTS
During induction of general anesthesia, a neuromuscular blocking agent (NMBA) is usually administered to facilitate
laryngoscopy if endotracheal intubation is planned, as discussed separately ( table 8). (See "Clinical use of
neuromuscular blocking agents in anesthesia", section on 'Endotracheal intubation'.)
Because of its rapid onset of action, we select SCh in patients requiring rapid sequence induction and intubation (RSII)
and in those with a potentially difficult airway (when the decision has been made to use an NMBA), unless SCh is
specifically contraindicated. (See "Clinical use of neuromuscular blocking agents in anesthesia", section on
'Succinylcholine'.)
Nondepolarizing NMBAs (eg, rocuronium, vecuronium, cisatracurium, atracurium, and pancuronium) have a slower
onset than SCh but are often selected for 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). If a relatively large dose of rocuronium is used to achieve
swift onset of excellent intubating conditions, the neuromuscular blocking effect may be terminated relatively rapidly by
administering sugammadex 16 mg/kg if necessary (eg, inability to intubate or ventilate) [47,48]. (See "Clinical use of
neuromuscular blocking agents in anesthesia", section on 'Nondepolarizing neuromuscular blocking agents'.)
Occasionally, a small dose of an NMBA is employed to facilitate supraglottic airway (SGA) placement and prevent
coughing and other airway responses. (See 'Induction with supraglottic airway placement' above.)
VASOPRESSOR AGENTS
Vasopressor agents are administered, if necessary, to treat hypotension during induction of general anesthesia.
● Phenylephrine – Phenylephrine is a pure alpha1-adrenergic agonist that causes both arterial and venous
vasoconstriction. Administration of phenylephrine 40 to 100 mcg increases blood pressure (BP); doses may be
repeated if necessary.
● Ephedrine – Ephedrine is an alpha and beta receptor adrenergic agonist that causes release of endogenous
norepinephrine stores. Administration of ephedrine 5 to 10 mg increases both BP and heart rate (HR); doses may be
repeated if necessary.
Occasionally an infusion of a vasopressor agent (eg, phenylephrine) is necessary during and immediately after
administration of induction agents ( table 10).
PATIENT-SPECIFIC AND PROCEDURE-SPECIFIC CONSIDERATIONS
Coexisting diseases, conditions, and the planned surgical procedure may affect selection of anesthetic techniques and
specific induction and adjuvant agents. These are discussed in separate topic reviews related to the condition and/or
surgical procedure. As examples:
● Hemodynamic instability – We typically select etomidate or ketamine to induce general anesthesia in patients with
actual or potential hemodynamic instability due to hypovolemia, vasodilation, or severe myocardial dysfunction.
(See "General anesthesia: Intravenous induction agents" and "Intraoperative management of shock in adults".)
Administration of a vasopressor (eg, phenylephrine and/or ephedrine) may be necessary to prevent or treat
hypotension. (See 'Vasopressor agents' above.)
Adjuvant agents (eg, opioids, lidocaine, midazolam) are usually eliminated, or at least reduced, in these patients.
(See "General anesthesia: Intravenous induction agents", section on 'Adjuvant agents'.)
● Older adults – The doses of intravenous and inhalation induction agents should be reduced in older patients. (See
"Anesthesia for the older adult", section on 'Sedative-hypnotics' and "Anesthesia for the older adult", section on
'Inhalation anesthetics'.)
● 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'.)
● Potentially difficult airway – (See "Management of the difficult airway for general anesthesia in adults", section on
'Induction of anesthesia'.)
● Aspiration risk – (See "Rapid sequence induction and intubation (RSII) for anesthesia", section on 'Induction
agents'.)
● Heart disease – (See "Anesthesia for noncardiac surgery in patients with ischemic heart disease", section on
'Induction' and "Anesthesia for noncardiac surgery in patients with heart failure", section on 'Induction'.)
● End stage renal disease – (See "Anesthesia for dialysis patients", section on 'Induction'.)
● Others – See other topic reviews for recommended modifications for the induction technique in specific conditions
and for specific procedures.
SUMMARY AND RECOMMENDATIONS
● The goals for induction of general anesthesia are to induce a state of amnesia, analgesia, akinesia, and autonomic
block while maintaining hemodynamic stability and ventilation. (See 'Introduction' above.)
● Anesthetic agents demonstrate a dose-response effect, with progressively higher doses providing progressively
deeper levels of sedation and anesthesia ( table 1). (See 'Continuum of sedation during anesthetic induction'
above.)
● Planning for induction includes the anesthesia machine checkout procedure, preparation for advanced airway
management, preparation of routinely administered drugs, and confirmation of availability of drugs for treatment
of common complications and emergencies. (See 'Preparation before patient arrival' above.)
● Prior to induction, the adult patient should be connected to the standard American Society of Anesthesiologists
(ASA) monitors and should have adequate intravenous (IV) access. An appropriate preprocedure checklist should be
completed. (See 'Preparation after patient arrival' above.)
● The patient is positioned for optimal airway management (eg, "sniffing" position), with the head up (ie, reverse
Trendelenburg or semi-sitting/"semi-Fowler" position). Preoxygenation is accomplished using 100 percent oxygen
(O2). (See 'Preparation immediately before induction' above.)
● Most adult patients prefer IV induction of anesthesia with a sedative-hypnotic agent (eg, propofol, etomidate,
ketamine) ( table 6) because they dislike the unpleasant odor of a volatile inhalation anesthetic agent. Also,
nausea and vomiting are less likely with some IV agents (eg, propofol). One or more adjuvant agents (eg, an opioid
and/or lidocaine) are typically administered during induction to minimize the pain of injection of the anesthetic
induction agent, blunt the reflex airway and sympathetic stress responses to laryngoscopy and endotracheal
intubation, and supplement the anesthetic effects of the induction agent ( table 7). (See 'Selection of induction
technique' above and 'Intravenous anesthetic induction' above.)
● Inhalation induction is often preferred by children because of their fear of needles. In adults, inhalation induction
may be preferred when spontaneous breathing is desirable during induction. 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, particularly sevoflurane, has made inhalation
induction of anesthesia via facemask a more pleasant and viable option compared with older inhalation agents (
table 9). (See 'Inhalation anesthetic induction' above.)
● A neuromuscular blocking agent (NMBA) is administered to facilitate laryngoscopy when endotracheal intubation is
planned ( table 8). Unless specifically contraindicated, succinylcholine (SCh) is selected for patients requiring rapid
sequence induction and intubation (RSII) and in those with a potentially difficult airway. For other patients, we
typically select a nondepolarizing NMBA (eg, rocuronium, vecuronium, cisatracurium) for intubation, particularly if
muscle relaxation is desired for longer than a few minutes. (See 'Neuromuscular blocking agents' above.)
● Vasopressor agents are administered, if necessary, to treat hypotension during induction of general anesthesia.
(See 'Vasopressor agents' above.)
● Patient-specific and procedure-specific considerations that affect induction technique and/or selection of agents
include hemodynamic instability, aspiration risk, potentially difficult airway, and specific disease states. (See
'Patient-specific and procedure-specific considerations' above.)
ACKNOWLEDGMENT
The editorial staff at UpToDate would like to acknowledge Liza M Weavind, MBBCh, FCCM, MMHC, who contributed to an
earlier version of this topic review.
Use of UpToDate is subject to the Subscription and License Agreement.
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rocuronium bromide induced pain on injection in children and adults. Cochrane Database Syst Rev 2016;
2:CD009346.
30. Aouad MT, Siddik-Sayyid SM, Al-Alami AA, Baraka AS. Multimodal analgesia to prevent propofol-induced pain:
pretreatment with remifentanil and lidocaine versus remifentanil or lidocaine alone. Anesth Analg 2007; 104:1540.
31. Rahman Al-Refai A, Al-Mujadi H, Petrova Ivanova M, et al. Prevention of pain on injection of propofol: a comparison
of remifentanil with alfentanil in children. Minerva Anestesiol 2007; 73:219.
32. 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.
33. 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.
34. Thwaites A, Edmends S, Smith I. Inhalation induction with sevoflurane: a double-blind comparison with propofol.
Br J Anaesth 1997; 78:356.
35. Joshi GP. Inhalational techniques in ambulatory anesthesia. Anesthesiol Clin North America 2003; 21:263.
36. Suzuki KS, Oohata M, Mori N. Multiple-deep-breath inhalation induction with 5% sevoflurane and 67% nitrous
oxide: comparison with intravenous injection of propofol. J Anesth 2002; 16:97.
37. 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.
38. Joo HS, Perks WJ. Sevoflurane versus propofol for anesthetic induction: a meta-analysis. Anesth Analg 2000; 91:213.
39. 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.
40. 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.
41. Mostafa SM, Atherton AM. Sevoflurane for difficult tracheal intubation. Br J Anaesth 1997; 79:392.
42. Thomas Ebert and Larry Lindenbaum. Inhaled Anesthetics. In: Clinical Anesthesia, Seventh, Paul G. Barash (Ed), Lip
pincott Williams Wilkins, Philadelphia 2013. p.447-477.
43. 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.
44. Torri G. Inhalation anesthetics: a review. Minerva Anestesiol 2010; 76:215.
45. 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.
46. 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.
47. 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.
48. 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.
Topic 94135 Version 36.0
GRAPHICS
Stages of anesthetic depth
Stage I Analgesia state: Patient is conscious and rational, with decreased perception of pain.
Stage II Delirium stage: Patient is unconscious; body responds reflexively; irregular breathing pattern with breathholding.
Stage III Surgical anesthesia: Increasing degrees of muscle relaxation; unable to protect airway.
Stage IV Medullary depression: There is depression of cardiovascular and respiratory centers.
Adapted from: Hewer CL. The stages and signs of general anesthesia. Br Med J 1937; 2:274.
Graphic 107796 Version 2.0
Continuum of sedation/analgesia/anesthesia
Moderate
Minimal sedation Deep
sedation/analgesia General anesthesia ◊
(anxiolysis)* sedation/analgesia Δ
(conscious sedation) ¶
Responsiveness Normal response to verbal Purposeful § response to Purposeful § response after Unarousable, even with
stimulation verbal or tactile stimulation repeated or painful painful stimulus
stimulation
Airway Unaffected No intervention required Intervention may be required Intervention often required
Spontaneous ventilation Unaffected Adequate May be inadequate Frequently inadequate
Cardiovascular function Unaffected Usually maintained Usually maintained 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 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 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.
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
Item to be completed Responsible party
To be completed daily
Item #1: Verify that auxiliary oxygen cylinder and self-inflating manual ventilation device are available and functioning Provider and 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 available Provider or 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 mounted on the anesthesia machine Provider and 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 filler ports are tightly closed Provider or technician
Item #8: Verify that there are no leaks in the gas supply lines between the flowmeters and the common gas outlet Provider or technician
Item #9: Test scavenging system function Provider or technician
Item #10: Calibrate, or verify calibration of, the oxygen monitor, and check the low oxygen alarm Provider or 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 both inspiration and exhalation Provider and technician
Item #14: Document completion of checkout procedures Provider and technician
Item #15: Confirm ventilator settings and evaluate readiness to deliver anesthesia care (anesthesia time out) Provider
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 filler ports are tightly closed Provider
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 both inspiration and exhalation Provider and technician
Item #14: Document completion of checkout procedures Provider and technician
Item #15: Confirm ventilator settings and evaluate readiness to deliver anesthesia care (anesthesia time out) Provider
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.
Basic monitoring during anesthesia
Primary physiologic
Monitoring
process/parameter Principle Derived information Additional function
equipment
targeted
Oxygenation Inspired gas O 2 analyzer Paramagnetic sensor, fuel (galvanic) cell, Inspired/expired O 2 A low-level alarm is
O 2 content (with a low- polarographic (Clark) electrode, mass concentration when placed automatically activated by
limit alarm in spectroscopy, or Raman scattering downstream from fresh flow turning on the anesthesia
use) control valves machine
Blood Pulse The Beer-Lambert law applied to tissues and Hemoglobin saturation, pulse Continuous evaluation of
oxygenation oximeter pulsatile blood flow. The relative absorbency rate, relative pulse amplitude circulation, variable pitch
at wavelengths of 660 and 940 nm is used to displayed on pulse tone, and audible low-
estimate saturation, which is derived from the plethysmography waveform threshold alarm
ratio of oxyhemoglobin to the sum of
oxyhemoglobin plus deoxyhemoglobin.
Ventilation Exhaled CO 2 Capnograph CO 2 molecules absorb infrared radiation at ETCO 2 , inspired CO 2 , Instantaneous information
4.26 micrometers, proportionate to the CO 2 diagnostic waveforms, about:
concentration present in the breath sample respiratory rate, apnea Perfusion (how effectively
detection CO 2 is being transported
through the vascular
system)
Metabolism (how
effectively CO 2 is being
produced by cellular
metabolism)
Confirmation of tracheal
tube placement after
intubation
Integrity of Disconnection Detects the cyclical changes in airway Alarms if a Alarms if high pressures are
ventilation alarm pressure in the normal range significant decrease in rate or sensed
system pressure occurs
during
mechanical
ventilation
Pulmonary Pulmonary Volume of gas proportional to a drum Inspired and expired volume, Pressure volume and flow
mechanics flow and movement, changes in differential pressure flow, and airway pressure volume loops
(volume, pressure (near the Y-connector) or in electrical
flow, sensors resistance (hot wire housed in a monitor or
pressure) ventilator)
Circulation Cardiac ECG The ECG monitor detects, amplifies, displays, Heart rate and rhythm ST segment
activity and records the ECG signal. depression/elevation and
trend over time, with an
audible alarm warning of
significant arrhythmias or
asystole
Arterial BP Noninvasive Oscillometric devices automatically inflate and Arterial BP Indicator of organ perfusion
BP monitor 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 semiconductor, electrical Core or peripheral A greater than 2°C core-to-
monitor resistance decreases as temperature temperature periphery temperature
decreases gradient is indicative of low
cardiac output.
O 2 : oxygen; CO 2 : carbon dioxide; ETCO 2 : end-tidal carbon dioxide; ECG: electrocardiogram; BP: blood pressure; MAP: mean arterial pressure.
World Health Organization surgical safety checklist
Sign in Time out Sign out
Before induction of Before skin incision Before patient leaves operating room
anesthesia
__ Confirm all team members have introduced themselves by Nurse verbally confirms with the team:
__ Patient has confirmed: name and role
__ The name of the procedure recorded
Identity
__ Surgeon, anesthesia professional, and nurse verbally
Site __ That instrument, sponge, and needle counts are
confirm
correct (or not applicable)
Procedure Patient
Consent __ How the specimen is labeled (including patient name)
Site
__ Site marked/not Procedure __ Whether there are any equipment problems to be

applicable addressed
Anticipated critical events
__ Surgeon, anesthesia professional, and nurse review
__ Anesthesia safety check __ Surgeon reviews: What are the critical or unexpected steps, the key concerns for recovery and management of this
completed operative duration, anticipated blood loss? patient
__ Pulse oximeter on __ Anesthesia team reviews: Are there any patient-specific
patient and functioning concerns?
Does patient have a: __ Nursing team reviews: Has sterility (including indicator
Known allergy? results) been confirmed? Are there equipment issues or any
concerns?
__ No
Has antibiotic prophylaxis been given within the last 60 minutes?
__ Yes
__ Yes
Difficult airway/aspiration
risk? __ Not applicable
__ No Is essential imaging displayed?
__ Yes, and __ Yes

equipment/assistance __ Not applicable
available
Risk of >500 mL blood loss (7

mL/kg in children)?
__ No
__ Yes, and adequate

intravenous access and
fluids planned
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
Drug Uses Suggested induction dose* Advantages Potential adverse effects
Propofol Induction agent of choice for 1 to 2.5 mg/kg Rapid onset and offset Dose-dependent hypotension
most patients Older age: 1 to 1.5 mg/kg Antiemetic properties Dose-dependent respiratory
Hypovolemia or hemodynamic Antipruritic properties depression
compromise: ≤1 mg/kg Bronchodilation Pain during injection
Anticonvulsant properties Microbial contamination risk
Decreases CMRO 2 , CBF, and Rare anaphylaxis in patients
ICP with allergy to its soybean
oil emulsion with egg
phosphatide
Etomidate May be selected in patients with 0.15 to 0.3 mg/kg Rapid onset and offset High incidence of PONV
hemodynamic instability due to Presence of profound Hemodynamic stability with no Pain during injection
any cause hypotension: 0.1 to 0.15 mg/kg changes in BP, HR, or CO Involuntary myoclonic
Anticonvulsant properties movements
Decreases CMRO 2 , CBF, and Absence of analgesic effects
ICP Transient acute adrenocortical
suppression
Ketamine May be selected in hypotensive 1 to 2 mg/kg Rapid onset Cardiovascular effects

patients or those likely to develop Chronic use of tricyclic Increases BP, HR, and CO in Increases myocardial oxygen
hypotension (eg, hypovolemia, antidepressants: 1 mg/kg most patients demand due to increases in
hemorrhage, sepsis, severe Presence of profound Profound analgesic properties HR, BP, and CO
cardiovascular compromise) hypotension: 0.5 to 1 mg/kg Bronchodilation Increases pulmonary arterial
Intramuscular dose: 4 to 6 Maintains airway reflexes and pressure (PAP)
mg/kg respiratory drive Potentiates cardiovascular
Intramuscular route available if toxicity of cocaine or tricyclic
IV access lost antidepressants
Exacerbates hypertension,
tachycardia, and
arrhythmias in
pheochromocytoma
Direct mild myocardial
depressant effects
Neurologic effects
Psychotomimetic effects
(hallucinations, nightmares,
vivid dreams)
Increases CBF and ICP;
may increase CMRO 2
Unique EEG effects may result
in misinterpretation of BIS and
other processed EEG values
Other effects
Increases salivation
Methohexital Induction for electroconvulsive 1.5 mg/kg Lowers seizure threshold, Limited availability
therapy (ECT) because it activates facilitating ECT Dose-dependent hypotension
seizure foci Decreases CMRO 2 , CBF, and Dose-dependent respiratory
ICP depression
Involuntary myoclonic
movements
Pain during injection
Contraindicated in patients
with porphyria
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.
Intravenous adjuvant agents used during induction of general anesthesia
Drug Suggested dose Advantages Potential adverse effects
Opioids Fentanyl: 25 to 100 mcg (or 0.5 to 1 Suppresses airway reflexes to prevent Dose-dependent respiratory depression;
mcg/kg): may be administered in divided coughing and/or bronchospasm during possible apnea
doses laryngoscopy and intubation Pruritus
Sufentanil: 0.05 to 0.1 mcg/kg: may be Attenuates stress response to prevent Postoperative nausea and vomiting
administered in divided doses tachycardia and hypertension during
laryngoscopy and intubation
(Reduce dose in older adults [≥70 years]; Minimizes pain caused by IV injection of
reduce or avoid dose in patients with induction agent
hemodynamic instability.) Supplements sedation and reduces dose
requirement of IV induction agent
Lidocaine 0.5 to 1.5 mg/kg for suppression of airway Suppresses airway reflexes to prevent Mild increases in airway tone
reflexes (or 0.5 to 1 mg/kg in older adults coughing during laryngoscopy and Increases ventricular rate in patients with
[≥70 years]) intubation atrial fibrillation (avoid in patients with
20 to 30 mg total is used to reduce pain on Reduces airway responsiveness to noxious Wolff-Parkinson-White syndrome or high-
injection of other agents stimuli; reduces airway responsiveness to grade heart block)
drugs that cause bronchospasm
(Reduce or avoid dose in patients with Minimizes pain caused by IV injection of

hemodynamic instability.) induction agent
Supplements sedation and reduces dose
requirement of IV induction agent
Midazolam 1 to 2 mg is typical, administered in 1-mg Reduces anxiety and produces amnesia; Mild systemic vasodilation and decreased
increments typically administered in the immediate cardiac output; may cause severe
Older adults (≥70 years): 0.5-mg increments preoperative period hypotension in hemodynamically unstable
up to 2 mg Supplements sedation and reduces dose or hypovolemic patients
requirement of IV induction agent Dose-dependent respiratory depression;
Anticonvulsant possible apnea, particularly if
(Reduce or avoid dose in patients with
coadministered with an opioid
hemodynamic instability.)
IV: intravenous.
Properties of neuromuscular blocking agents
Agent* Vecuronium Rocuronium Pancuronium Mivacurium Atracurium Cisatracurium Succinylcholine
Type (structure) Non- Non- Non-depolarizing Non-depolarizing Non- Non-depolarizing Depolarizing

depolarizing depolarizing depolarizing
Type (duration) Intermediate Intermediate Long Short Intermediate Intermediate Ultrashort
Potency - ED 95 0.04 0.30 0.07 0.08 0.21 0.04 to 0.05 0.25 to 0.30
(mg/kg)
Intubating dose 0.10 to 0.20 0.60 to 1.00 0.08 to 0.12 0.20 0.50 to 0.60 0.15 to 0.20 0.60 to 1.50
(mg/kg) (1.20 with RSII
dose)
Onset time (min) 3 to 4 1 to 2 2 to 3 3 to 4 3 to 5 4 to 6 1
Time to 25% 20 to 35 30 to 50 (60 to 60 to 120 15 to 20 20 to 35 30 to 60 5 to 10

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 21 23 to 30 <1

function
Renal Mild increase 100 to 300 Increased x2 3 to 4 21 Mild increase <1

impairment
Hepatic Significant 120 to 400 Increased x2 3 to 6 21 23 to 30 <1

impairment increase
Maintenance 0.01 0.10 0.02 0.10 0.10 0.01 N/A

dose (mg/kg)
Infusion dose 1 to 2 5 to 12 Not 5 to 8 10 to 20 1 to 3

(mcg/kg/min) recommended
Elimination Renal 10 to Renal 30%; Renal 40 to 70%; Plasma Renal 10%; Hoffman 30%; Butyrylcholinesterase
route/metabolism 50%; hepatic 70% hepatic 20% cholinesterase (70% Hoffman 30%; ester hydrolysis (plasma
hepatic 30 to of succinylcholine ester hydrolysis 60% cholinesterase,
50% rate) 60% pseudocholinesterase)
Active 3-desacetyl- 17-desacetyl- 3-OH- No active metabolites No active No active No active metabolites
metabolites vecuronium rocuronium pancuronium; metabolites metabolites
(minimal) 17-OH-
pancuronium
Side effects Vagal blockade Minimal Vagal block Histamine release Histamine None; histamine Myalgia; bradycardia/
with large (tachycardia), release; release at high asystole in children or
doses catecholamine laudanosine and doses with repeated dosing;
release acrylates dual (phase II,
production competitive) block;
anaphylaxis
Contraindications None None Short surgical Pseudocholinesterase Hemodynamically None High K +; MH;
(other than procedures (<60 deficiency unstable patients muscular dystrophy;
specific allergy) min); not due to histamine children; receptor up-
recommended release regulation settings;
for continuous pseudocholinesterase
infusion deficiency
Comments Not for Pain on Significant Reversal by Organ- Trivial histamine Fastest onset, most
prolonged ICU injection; easily accumulation, cholinesterase independent release; minimal reliable NMBA for
administration reversible by prone to residual inhibitors; mixture of elimination plasma rapid tracheal
(myopathy); sugammadex; block (3-OH 3 isomers (cis-cis laudanosine and intubation
reversible by elimination metabolite has minimal); acrylate levels
sugammadex; half-life 50% activity of edrophonium for
elimination prolonged in pancuronium) antagonism more
half-life halved ICU patient; 17- effective during deep
in late desacetyl block
pregnancy; 3- metabolite has
desacetyl 20% activity
metabolite has
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.
Inhalation anesthetic agents
Generic name Nitrous oxide Halothane Isoflurane Sevoflurane Desflurane
Brand name N/A Fluothane Forane Ultane Suprane
Chemical formula N2O C 2 HBrClF 3 C 3 H 2 ClF 5 O C4H3F7O C3H2F6O
Odor Slightly sweet Sweet Sweet Sweet Sweet
Color Colorless Colorless Colorless Colorless Colorless
Pungency None Moderate High Low Very high
Solubility:blood:gas Very low: 0.46 Very high: 2.40 Moderately high: 1.40 Low: 0.65 Very low: 0.45
partition coefficient
Redistribution:brain:blood 1.1 1.9 1.6 1.7 1.3

partition coefficient
Potency:oil:gas partition Very low: 1.4 Very high: 224.0 High: 97.0 Moderately high: 42.0 Low: 18.7
coefficient
Minimum alveolar 105.0% 0.8% 1.2% 2.0% 6.0%

concentration
(MAC) = ED 50 for response
to surgery
MAC-awake/MAC-aware = 68.0% 0.4% 0.5% 0.6% 2.5%

ED 50 for response to
voice/touch
Blood pressure effect Negligible Dose-dependent Dose-dependent Dose-dependent Dose-dependent

hypotension hypotension hypotension hypotension
Vascular effect Negligible Negligible Vasodilation Vasodilation Initial vasoconstriction,

later vasodilation
Inotropic effect Negligible Negative Slightly negative Slightly negative Initial positive, later
negative
Chronotropic effect Negligible Bradycardia Tachycardia Tachycardia >1 MAC Tachycardia
How supplied Pressurized bottled gas Bottled liquid Bottled liquid Bottled liquid Bottled liquid
How delivered Flowmeter Vaporizer Vaporizer Vaporizer Electric heated

vaporizer
Fire risk Supports combustion Non-flammable Non-flammable Non-flammable Non-flammable
Notes Nausea/emesis Nausea/emesis; Nausea/emesis; Nausea/emesis; Nausea/emesis; airway

bradycardia/asystole; potentially significant inhalational induction irritation; initial
inhalational induction; tachycardia sympathomimetic
no longer used in US
N/A: not applicable.
Vasopressors and inotropic agents used in the operating room: Adult dosing* ¶
Functional class
Drug (predominant receptor or Bolus dose Infusion dose Comments
mechanism of action)
Ephedrine Inotrope/chronotrope/vasopressor 5 to 10 mg boluses N/A Tachyphylaxis may occur with

(alpha 1 -adrenergic receptor multiple repeated doses due to
agonist; beta 1 - and beta 2 - indirect postsynaptic release of
adrenergic receptor agonist) norepinephrine
Cardiovascular effects attenuated by
drugs that block ephedrine uptake
into adrenergic nerves (eg, cocaine)
or those that deplete norepinephrine
reserves (eg, reserpine)
Administered with extreme caution
(eg, in small incremental doses of 2.5
mg) to patients using monoamine
oxidase (MAO) inhibitors or
methamphetamines since
exaggerated hypertensive responses
or life-threatening dysrhythmias may
occur
Phenylephrine Vasopressor (alpha 1 -adrenergic 50 to 100 mcg 10 to 100 mcg/minute Often selected to treat hypotension if
receptor agonist) boluses (may begin or normal or elevated HR is present
infusion if Genetic polymorphisms lead to
0.1 to 1 mcg/kg/minute
repeated bolus variable individual responses
doses are
necessary)
Norepinephrine Inotrope/vasopressor (alpha 1 - 4 to 8 mcg (may 1 to 20 mcg/minute Often selected as a first-line agent
and beta 1 -adrenergic receptor begin infusion if or during noncardiac surgery,
agonist) repeated bolus particularly for treatment of most
0.01 to 0.3 mcg/kg/minute
doses are types of shock
necessary) Norepinephrine 8 mcg is
approximately equivalent in potency
to phenylephrine 100 mcg
Peripheral extravasation of a high
concentration may cause tissue
damage
Epinephrine Inotrope/chronotrope/vasopressor 4 to 10 mcg 1 to 100 mcg/minute First-line treatment for cardiac arrest
(alpha 1 -adrenergic receptor initially; up to 100 or and for anaphylaxis
agonist; beta 1 - and beta 2 - mcg boluses may May be administered IV, IM, or via an
0.01 to 1 mcg/kg/minute
adrenergic receptor agonist) be used when endotracheal tube in emergencies
initial response is Low doses cause bronchodilatory
inadequate Note changing effects across dose effects and may cause arterial
range: vasodilation and decreased BP
Low doses have primarily beta 2 - Intermediate doses cause increases
adrenergic effects at 1 to 2 in HR and BP
mcg/minute or 0.01 to 0.02 High doses cause vasoconstriction,
mcg/kg/minute with possible severe hypertension
Intermediate doses have primarily and adverse metabolic effects
beta 1 - and beta 2 -adrenergic Individual responses to dose-related
effects at 2 to 10 mcg/minute or effect are variable
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 units/minute Effective for treatment of
vasopressin 2 receptor agonist) hypotension refractory to
administration of catecholamines or
Doses >0.04 units/minute up to 0.1
sympathomimetics such as
units/minute are reserved for salvage
therapy (ie, failure to achieve adequate ephedrine, phenylephrine, or

BP goals with other vasopressor norepinephrine
agents) ¶ No direct effect on HR
Little effect on PVR; can cause
splanchnic vasoconstriction
Individual responses to dose-related
effects are variable
Peripheral extravasation may cause
skin necrosis
Dopamine Inotrope/vasopressor/dose- N/A 2 to 20 mcg/kg/minute Low doses may exacerbate

dependent chronotropy hypotension via beta 2 stimulation
(dopaminergic, beta 1 -, beta 2 -, High doses may cause
Note changing effects across dose
and alpha 1 -adrenergic receptor vasoconstriction, adverse metabolic
range:
agonist) effects, and arrhythmias
Low doses have primarily
dopaminergic 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 mcg/kg/minute Exacerbation of hypotension is

dependent chronotropy (beta 1 - possible due to dose-dependent
and beta 2 -adrenergic receptor vasodilation (via beta 2 stimulation);
agonist) concurrent administration of a potent
vasoconstrictor such as
norepinephrine or vasopressin may
be necessary
Milrinone Inotrope/vasodilator N/A 0.375 to 0.75 mcg/kg/minute (a loading Exacerbation of hypotension is likely
(phosphodiesterase inhibitor) dose of 50 mcg/kg over ≥10 minutes due to vasodilation (via
(decreases rate of cyclic adenosine may be administered, but is often phosphodiesterase inhibition);
monophosphate [cAMP] omitted) concurrent administration of a potent
degradation) vasoconstrictor such as
norepinephrine or vasopressin may
be necessary
Isoproterenol Inotrope/chronotrope/vasodilator N/A 5 to 20 mcg/minute Exacerbation of hypotension is likely

(beta 1 - and beta 2 -adrenergic or due to dose-dependent vasodilation
receptor agonist) (via beta 2 stimulation)
May cause arrhythmias
Not available in most settings
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.
Contributor Disclosures
Adam King, MD Nothing to disclose Girish P Joshi, MB, BS, MD, FFARCSI Consultant/Advisory Boards: Pacira Pharmaceuticals [pain
management]. Speaker's Bureau: Baxter [anesthesia]. Nancy A Nussmeier, MD, FAHA Nothing 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

Induction of General Anesthesia Overview - UpToDate

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Induction of general anesthesia: Overview - UpToDate 17-01-21 13:19

Official reprint from UpToDate®

Induction of general anesthesia: Overview

General anesthesia establishes a reversible state that includes:

● (See "General anesthesia: Intravenous induction agents".)

● (See "Preoperative fasting guidelines".)

CONTINUUM OF SEDATION DURING ANESTHETIC INDUCTION

PREPARATION FOR ANESTHETIC INDUCTION

"Monitoring during anesthesia".)

● Preprocedure checklist – An appropriate preprocedure checklist should be completed; an example is provided in

Preparation immediately before induction

SELECTION OF INDUCTION TECHNIQUE

INTRAVENOUS ANESTHETIC INDUCTION

INHALATION ANESTHETIC INDUCTION

An inhalation induction is often selected for the following types of patients:

NEUROMUSCULAR BLOCKING AGENTS

PATIENT-SPECIFIC AND PROCEDURE-SPECIFIC CONSIDERATIONS

SUMMARY AND RECOMMENDATIONS

Use of UpToDate is subject to the Subscription and License Agreement.

2. American Society of Anesthesiologists. Standards for Basic Anesthetic Monitoring. www.asahq.org/Search.aspx?q=

44. Torri G. Inhalation anesthetics: a review. Minerva Anestesiol 2010; 76:215.

safety assessor-blinded, phase II trial. Anesthesiology 2008; 109:188.

Topic 94135 Version 36.0

Stages of anesthetic depth

Stage IV Medullary depression: There is depression of cardiovascular and respiratory centers.

Graphic 107796 Version 2.0

Spontaneous ventilation Unaffected Adequate May be inadequate Frequently inadequate

Cardiovascular function Unaffected Usually maintained Usually maintained May be impaired

Graphic 113984 Version 1.0

Signs indicating stages of anesthesia

Graphic 113985 Version 1.0

American Society of Anesthesiologists Summary of Anesthesia Machine Checkout Recommendations

Item to be completed Responsible party

Item #9: Test scavenging system function Provider or technician

Item #14: Document completion of checkout procedures Provider and technician

To be completed prior to each procedure

Item #14: Document completion of checkout procedures Provider and technician

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

Graphic 101563 Version 5.0

Basic monitoring during anesthesia

Graphic 110080 Version 3.0

World Health Organization surgical safety checklist

Sign in Time out Sign out

__ Site marked/not Procedure __ Whether there are any equipment problems to be

__ No Is essential imaging displayed?

__ Yes, and __ Yes

Risk of >500 mL blood loss (7

__ Yes, and adequate

Graphic 52392 Version 12.0

Intravenous anesthetic induction agents

Drug Uses Suggested induction dose* Advantages Potential adverse effects

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

Graphic 102350 Version 12.0

Intravenous adjuvant agents used during induction of general anesthesia

Drug Suggested dose Advantages Potential adverse effects

(Reduce or avoid dose in patients with Minimizes pain caused by IV injection of

Graphic 106541 Version 7.0

Properties of neuromuscular blocking agents

Site marked/not Procedure Whether there are any equipment problems to be

Yes, and Yes