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General anesthesia: Induction

Authors: Adam King, MD, Liza M Weavind, MBBCh, FCCM, MMHC

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: Sep 2017. | This topic last updated: Sep 07, 2017.

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 four 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 adult healthy 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 — 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. 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. 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 2) [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 3). (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 4).

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, lidocaine, and/or a benzodiazepine [usually
midazolam]) used to supplement anesthetic effects of the sedative-hypnotic induction agents are reviewed in detail separately (table 5 and table 6).
(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 6).

● 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 as part of the induction sequence 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 [11,12].

While fentanyl and midazolam should be administered a few minutes before induction, all other agents are typically administered in rapid
succession over a period of 60 to 120 seconds:
 ● Lidocaine 0.5 to 1.5 mg/kg may also be administered to blunt the airway responses to laryngoscopy and endotracheal intubation and
supplement the anesthetic effects of the induction agent [13-26]. A lower dose of lidocaine 20 to 30 mg is often administered prior to injection
of propofol and other induction agents to reduce pain caused by their injection [27-32].

● An NMBA may be administered to facilitate endotracheal intubation. Endotracheal intubation may be accomplished shortly after administration
of the NMBA (approximately 60 seconds after succinylcholine or 120 seconds after a nondepolarizing NMBA) (table 7). (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. (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. (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 rarely used to induce 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 7). (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 7). 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 8).

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 'Intravenous anesthetic induction agents' and "Anesthesia for the older adult", section on 'Inhalational anesthetic agents'.)

● 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 emergent eye surgery", section on 'Choice of induction and adjuvant agents'.)

● Potentially difficult airway – (See "Management of the difficult airway for general anesthesia", 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 the patient on dialysis", 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 5) 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 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 6). (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. (See 'Inhalation anesthetic induction' above.)

● A neuromuscular blocking agent (NMBA) is administered to facilitate laryngoscopy when endotracheal intubation is planned (table 7). 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.)

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Topic 94135 Version 28.0
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

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.

Graphic 101563 Version 4.0

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 oximeter The Beer-Lambert law applied to tissues and
oxygenation pulsatile blood flow. The relative absorbency
at wavelengths of 660 and 940 nm is used to
estimate saturation, which is derived from
the ratio of oxyhemoglobin to the sum of
oxyhemoglobin plus deoxyhemoglobin.
Hemoglobin saturation, pulse Continuous evaluation of
rate, relative pulse amplitude circulation, variable pitch
displayed on pulse tone, and audible low-
plethysmography waveform threshold alarm

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 Arterial BP Indicator of organ perfusion
BP monitor 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 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; ETT: endotracheal tube; ECG: electrocardiogram; BP: blood pressure; MAP: mean arterial
pressure

Graphic 110080 Version 2.0

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
__ That instrument, sponge, and needle counts are
Site confirm
correct (or not applicable)
Procedure Patient
Consent __ How the specimen is labeled (including patient name)
Site
Procedure __ Whether there are any equipment problems to be
__ Site marked/not
addressed
applicable Anticipated critical events
__ Surgeon, anesthesia professional, and nurse review
__ Anesthesia safety check __ Surgeon reviews: What are the critical or unexpected the key concerns for recovery and management of
completed steps, operative duration, anticipated blood loss? this 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
__ Yes
minutes?
Difficult airway/aspiration
__ Yes
risk?
__ Not applicable
__ No
Is essential imaging displayed?
__ Yes, and
equipment/assistance __ Yes
available __ Not applicable
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.

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Intravenous anesthetic induction agents
Drug Uses
Propofol Induction agent of choice for
most patients
Etomidate Often selected in patients with
hemodynamic instability due to
any cause
Ketamine Often selected in hypotensive
patients or those likely to develop
hypotension (eg, hypovolemia,
hemorrhage, sepsis, severe
cardiovascular compromise)
Methohexital Induction for electroconvulsive
therapy (ECT) because it
activates seizure foci
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.
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Suggested induction
dose
1 to 2.5 mg/kg
Older age: 1 to 1.5 mg/kg
Hypovolemia or hemodynamic
compromise: ≤1 mg/kg
0.15 to 0.3 mg/kg
Presence of profound
hypotension: 0.1 to 0.15
mg/kg
1 to 2 mg/kg
Chronic use of tricyclic
antidepressants: 1 mg/kg
Presence of profound
hypotension: 0.5 to 1 mg/kg
Intramuscular dose: 4 to 6
mg/kg
1.5 mg/kg
Advantages
Rapid onset and offset
Antiemetic properties
Antipruritic properties
Bronchodilation
Anticonvulsant properties
Decreases CMRO 2 , CBF, and
ICP
Rapid onset and offset
Hemodynamic stability with no
changes in BP, HR, or CO
Anticonvulsant properties
Decreases CMRO 2 , CBF, and
ICP
Rapid onset
Increases BP, HR, and CO in
most patients
Profound analgesic properties
Bronchodilation
Maintains airway reflexes and
respiratory drive
Intramuscular route available if
IV access lost
Lowers seizure threshold,
facilitating ECT
Decreases CMRO 2 , CBF, and
ICP
Potential adverse effects
Dose-dependent hypotension
Dose-dependent respiratory
depression
Pain during injection
Microbial contamination risk
Rare anaphylaxis in patients
with allergy to eggs and soy
products
High incidence of PONV
Pain during injection
Involuntary myoclonic
movements
Absence of analgesic effects
Transient acute adrenocortical
suppression
Cardiovascular effects
Increases myocardial oxygen
demand due to increases in
HR, BP, and CO
Increases pulmonary arterial
pressure (PAP)
Potentiates cardiovascular
toxicity of cocaine or tricyclic
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
Limited availability
Dose-dependent hypotension
Dose-dependent respiratory
depression
Involuntary myoclonic
movements
Pain during injection
Contraindicated in patients
with porphyria
Intravenous adjuvant agents used during induction of general anesthesia
Drug Suggested dose
Opioids Fentanyl: 25 to 100 mcg (or 0.5 to 1
mcg/kg): may be administered in divided
doses
Sufentanil: 0.05 to 0.1 mcg/kg: may be
administered in divided doses
(Reduce dose in older adults [≥70 years];
reduce or avoid dose in patients with
hemodynamic instability.)
Lidocaine 0.5 to 1.5 mg/kg for suppression of airway
reflexes (or 0.5 to 1 mg/kg in older adults
[≥70 years])
20 to 30 mg total is used to reduce pain on
injection of other agents
(Reduce or avoid dose in patients with
hemodynamic instability.)
Midazolam 1 to 4 mg, administered in 1-mg
increments
Older adults (≥70 years): 0.5-mg
increments up to 2 mg
(Reduce or avoid dose in patients with
hemodynamic instability.)
IV: intravenous.
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Advantages
Suppresses airway reflexes to prevent
coughing and/or bronchospasm during
laryngoscopy and intubation
Attenuates stress response to prevent
tachycardia and hypertension during
laryngoscopy and intubation
Minimizes pain caused by IV injection of
induction agent
Supplements sedation and reduces dose
requirement of IV induction agent
Suppresses airway reflexes to prevent
coughing during laryngoscopy and
intubation
Reduces airway responsiveness to noxious
stimuli; reduces airway responsiveness to
drugs that cause bronchospasm
Minimizes pain caused by IV injection of
induction agent
Supplements sedation and reduces dose
requirement of IV induction agent
Reduces anxiety and produces amnesia;
typically administered in the immediate
preoperative period
Supplements sedation and reduces dose
requirement of IV induction agent
Anticonvulsant
Potential adverse effects
Dose-dependent respiratory depression;
possible apnea
Pruritus
Postoperative nausea and vomiting
Mild increases in airway tone
Increases ventricular rate in patients with
atrial fibrillation (avoid in patients with
Wolff-Parkinson-White syndrome or high-
grade heart block)
Mild systemic vasodilation and decreased
cardiac output; may cause severe
hypotension in hemodynamically unstable
or hypovolemic patients
Dose-dependent respiratory depression;
possible apnea, particularly if
coadministered with an opioid
Properties of neuromuscular blocking agents

Agent* Vecuronium Rocuronium Pancuronium Mivacurium Atracurium Cisatracurium Succinylcholine

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

depolarizing depolarizing

Type (duration) Intermediate Intermediate Long Short Intermediate Intermediate

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 20 to 40 (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 No active No active No active metabolites

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

Side effects Vagal blockade Minimal Vagal block Histamine release Histamine None; histamine Myalgia; bradycardia/
with large doses (tachycardia), release; release at high asystole in children or
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 for release regulation settings;
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 half- metabolite has minimal); acrylate levels
sugammadex; life prolonged in 50% activity of edrophonium for
elimination half- ICU patient; 17- pancuronium) antagonism more
life halved in desacetyl effective during deep
late pregnancy; metabolite has block
3-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.

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Vasoactive infusions used in the operating room: Adult dosing*

Drug Class Predominant mechanism Infusion dose

Vasopressin Vasoconstrictor Vasopressin 1 and vasopressin 2 1 to 6 units/hour

receptors or
0.01 to 0.1 units/minute ¶

Phenylephrine Vasoconstrictor Alpha receptors 10 to 200 mcg/minute

or
0.1 to 2 mcg/kg/minute

Norepinephrine Inotrope/vasoconstrictor Alpha and beta 1 receptors 1 to 30 mcg/minute

or
0.01 to 0.3 mcg/kg/minute

Dopamine Inotrope/vasoconstrictor Dopaminergic receptors <3 mcg/kg/minute (D)

Beta 1 and beta 2 receptors 3 to 10 mcg/kg/minute (β1 and β2)

Alpha receptors >10 mcg/kg/minute (α)

Dobutamine Inotrope/vasodilator Beta 1 and beta 2 receptors 1 to 20 mcg/kg/minute

Epinephrine Inotrope/vasoconstrictor Alpha receptors 1 to 100 mcg/minute

Beta 1 and beta 2 receptors or
0.01 to 1 mcg/kg/minute
1 to 2 mcg/minute (β2) Δ
2 to 10 mcg/minute (β1, β2)
10 to 100 mcg/minute (α)

Milrinone Inotrope/vasodilator Phosphodiesterase inhibitor (decrease Loading dose 50 mcg/kg over ≥10
in rate of cyclic adenosine minutes (usually omitted), then 0.375
monophosphate [cAMP] degradation) to 0.75 mcg/kg/minute

Isoproterenol Inotrope/vasodilator Beta 1 and beta 2 receptors 5 to 20 mcg/minute

or
0.05 to 0.2 mcg/kg/minute

Clevidipine Vasodilator Inhibits calcium ion influx; selective 1 to 16 mg/hour

arteriolar smooth muscle relaxation or
0.02 to 0.27 mg/minute

Nicardipine Vasodilator Inhibits calcium ion influx; selective 5 to 15 mg/hour

arteriolar smooth muscle relaxation or
0.08 to 0.25 mg/minute

Nitroglycerin Vasodilator Increase in cyclic GMP (cGMP) 10 to 400 mcg/minute

or
0.1 to 4 mcg/kg/minute

Nitroprusside Vasodilator Smooth muscle relaxation 10 to 400 mcg/minute ◊

or
0.1 to 4 mcg/kg/minute

Esmolol Adrenergic antagonist and anti- Beta 1 receptors 10 to 50 mg boluses, then 25 to 300
arrhythmic mcg/kg/minute

Labetalol Adrenergic antagonist Beta 1 , beta 2 , and alpha 1 5 to 20 mg IV boluses, then 0.5 to 2
receptors mg/minute

V: vasopressin; D: dopaminergic; α: alpha adrenergic; β: beta adrenergic.

* Dose ranges are based on adult patients of normal size.
¶ Vasopressin doses >0.04 units/minute are reserved for salvage therapy (ie, failure to achieve adequate mean arterial pressure goal with other vasopressor agents).
Δ At low doses, epinephrine infusion has beneficial bronchodilatory effects and may cause arterial vasodilation and decreased blood pressure. Dose-related effect
ranges vary somewhat in clinical practice.
◊ Nitroprusside doses >400 mcg/minute are not recommended due to minimal added benefit and increased risk for thiocyanate or cyanide toxicity.

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