General anesthesia is a pharmacologically induced, reversible state characterized by unconsciousness, analgesia, amnesia, and skeletal muscle relaxation sufficient to permit surgical intervention. Unlike sedation or regional anesthesia, general anesthesia requires the suppression of protective airway reflexes and the complete abolition of conscious perception, and it is therefore associated with a correspondingly broader spectrum of physiological perturbation. Modern anesthetic practice achieves this state not through a single agent but through the deliberate combination of drugs that together address each of the four components: a strategy known as balanced anesthesia. Inhalational agents remain central to this framework, both for induction (in selected populations) and for maintenance of the anesthetic state, and an understanding of the pharmacokinetic principles governing their uptake and distribution is essential for rational clinical management.1 This module covers the fundamental principles that determine how quickly an inhalational anesthetic reaches effective brain concentrations, the concept of anesthetic potency, the pharmacological rationale for preanesthetic medications, and an overview of the role of intravenous agents in the balanced anesthesia construct.
The clinical speed of inhalational anesthetic induction is determined by how rapidly the partial pressure of the anesthetic in the brain equilibrates with the partial pressure being delivered to the alveoli. Because the brain and blood equilibrate rapidly (cerebral blood flow is high and the blood-brain barrier is readily traversed by lipid-soluble anesthetic vapors), the key determinant is how quickly alveolar partial pressure rises. Several interacting factors govern this process.12
Blood:Gas Partition Coefficient. The blood:gas partition coefficient (also called the Ostwald solubility coefficient) is the single most important pharmacokinetic property of an inhalational anesthetic. It describes the ratio of anesthetic concentration in blood to concentration in gas at equilibrium; in other words, how avidly the blood "absorbs" the drug from the alveolus at a given partial pressure. A high blood:gas partition coefficient means the drug is highly soluble in blood; blood acts as a large reservoir that must be progressively saturated before alveolar partial pressure can rise significantly, resulting in a slow induction. Conversely, an agent with a low blood:gas partition coefficient is poorly soluble in blood; alveolar partial pressure rises quickly, the brain equilibrates rapidly, and induction is fast.12 Nitrous oxide (blood:gas coefficient approximately 0.47) and desflurane (approximately 0.42) have low solubility and thus the fastest inductions among currently used agents. Halothane (approximately 2.4) and isoflurane (approximately 1.4) are more soluble and have correspondingly slower inductions. Sevoflurane (approximately 0.65) occupies an intermediate but clinically favorable position, accounting for its widespread use for inhalational induction, particularly in pediatric patients.3
Alveolar Ventilation. Increasing alveolar ventilation accelerates the rate at which fresh anesthetic-laden gas is delivered to the alveolus, thereby speeding the rise in alveolar partial pressure. This effect is most pronounced for highly soluble agents, because blood uptake constitutes a larger drain on alveolar concentration for those drugs. For poorly soluble agents such as desflurane or nitrous oxide, alveolar partial pressure rises quickly regardless, and the incremental benefit of increased ventilation is smaller. Clinically, hyperventilation (whether deliberate or as a result of surgical stimulation or metabolic acidosis) accelerates inhalational induction, while hypoventilation delays it. This principle has practical implications during induction in patients with obstructive lung disease or reduced respiratory reserve.12
Cardiac Output. Cardiac output influences the rate of anesthetic uptake from the alveolus into the pulmonary circulation. High cardiac output increases blood flow through the pulmonary capillaries, resulting in greater uptake of anesthetic from the alveolus per unit time and therefore a slower rise in alveolar partial pressure. Conversely, low cardiac output (as in shock or severe heart failure) reduces pulmonary blood flow, decreases the "sink" capacity of the circulation, and allows alveolar partial pressure to rise more rapidly, potentially leading to an unexpectedly rapid induction and cardiovascular depression in an already compromised patient. This physiological paradox (that the sickest patients may be most vulnerable to rapid anesthetic overdose during inhalational induction) is a clinically important consideration.1
Alveolar-to-Venous Partial Pressure Difference. As the tissues become progressively saturated with anesthetic, the partial pressure returning in venous blood increases, narrowing the alveolar-to-venous gradient and reducing net uptake. Early in an anesthetic, this gradient is large and uptake is rapid; as steady state is approached, uptake slows. Highly perfused tissues (brain, heart, liver, kidneys) equilibrate quickly, while skeletal muscle and fat, which have large capacities but lower blood flow, continue to act as a depot for hours. Obese patients may therefore show prolonged emergence when agents with significant lipid solubility are used for extended procedures, because adipose tissue has been progressively accumulating drug throughout the case.12
Concentration Effect. When a highly concentrated inspired mixture of an anesthetic is used, the rate of rise of alveolar partial pressure is disproportionately faster than would be predicted from simple diffusion kinetics. This phenomenon, the concentration effect, operates through two mechanisms. First, as the blood rapidly absorbs a highly soluble agent from the alveolus, the resulting decrease in alveolar volume is compensated by an inrush of additional gas from the conducting airways, which effectively concentrates the remaining anesthetic in the alveolus. Second, increased bulk flow of gas into the alveolus augments delivery. The concentration effect is most relevant to nitrous oxide, which is administered at concentrations of 50–70%, and to halothane, historically administered at higher concentrations during inhalational induction.13
Second Gas Effect The second gas effect is a direct extension of the concentration effect and occurs when nitrous oxide is administered simultaneously with a second volatile agent at lower concentration. The rapid absorption of the large volume of nitrous oxide augments both the alveolar concentration and the tidal volume delivery of the accompanying agent, accelerating its own rate of rise in alveolar partial pressure. The second gas effect is pharmacokinetically real and has been repeatedly demonstrated in human studies, although its clinical magnitude during routine practice is modest. It is most evident during the early minutes of a nitrous oxide-volatile agent induction.13
Minimum alveolar concentration (MAC) is the standard measure of inhalational anesthetic potency. It is defined as the alveolar concentration of an anesthetic (expressed as a percentage of one atmosphere) that prevents purposeful movement in response to a standard surgical skin incision in 50% of patients. MAC is therefore an ED50 for the anesthetic endpoint of immobility, and it allows potency comparisons across agents on a pharmacodynamically standardized basis.14 MAC values are additive: if 0.5 MAC of isoflurane is combined with 0.5 MAC of nitrous oxide, the combination produces an effect equivalent to 1.0 MAC of a single agent. This additivity is the pharmacological foundation of combined anesthetic techniques and explains why nitrous oxide, which has a MAC of 104% in pure form and therefore cannot produce surgical anesthesia alone at atmospheric pressure, can meaningfully reduce the required concentration of a volatile agent when used in combination.14
Several physiological and pharmacological factors shift MAC. MAC is decreased by advanced age, hypothermia, opioids, alpha-2 agonists (clonidine, dexmedetomidine), benzodiazepines, acute alcohol intoxication, and lithium. MAC is increased by chronic alcohol use, hyperthermia, hypernatremia, and monoamine oxidase inhibitor use. These modifiers have direct clinical relevance: elderly patients require substantially lower anesthetic concentrations to maintain the same depth of anesthesia, and failure to account for this predisposes to cardiovascular depression from relative overdose.1 The concept of MAC-awake (typically 0.3–0.4 MAC) is the concentration at which 50% of patients respond to verbal command and regain consciousness, a clinically useful threshold for managing emergence.
Diffusional hypoxia, also known as the Fink effect, occurs at the termination of nitrous oxide anesthesia. When nitrous oxide administration is discontinued, the large amount of dissolved nitrous oxide in blood and tissues rapidly diffuses into the alveoli, diluting alveolar oxygen and transiently reducing the partial pressure of oxygen in the alveolus, potentially to levels sufficient to cause hypoxemia. This effect is greatest in the first five to ten minutes following cessation of nitrous oxide and is readily prevented by administering 100% oxygen for several minutes at the end of the anesthetic. Failure to do so in a patient recovering from long nitrous oxide anesthesia can result in clinically significant oxygen desaturation, particularly in patients with reduced pulmonary reserve. The mechanism is the mirror image of the second gas effect: just as rapid nitrous oxide uptake concentrates co-administered gases early in anesthesia, rapid nitrous oxide efflux dilutes alveolar oxygen during emergence.13
Intravenous anesthetics serve three distinct roles in contemporary practice: induction of anesthesia, maintenance as part of total intravenous anesthesia (TIVA), and supplementation of inhalational techniques in a balanced anesthetic. Their pharmacokinetic behavior differs in a fundamental way from inhalational agents. Rather than being governed by alveolar partial pressures and partition coefficients, IV anesthetics follow multicompartmental distribution kinetics: rapid initial distribution to highly perfused tissues, including the brain, is followed by redistribution to muscle and eventually to fat, with hepatic metabolism as the predominant elimination pathway for most agents.1
Propofol (2,6-diisopropylphenol) is the most widely used IV induction and maintenance agent worldwide. Induction occurs within one arm-brain circulation time (approximately 30 seconds), and the clinical effect after a single bolus terminates within 5 to 10 minutes, primarily through redistribution rather than elimination. For TIVA maintenance, the pharmacokinetic behavior that matters most is the context-sensitive half-time: the time required for plasma concentration to fall by 50% after stopping a continuous infusion, which increases with infusion duration as peripheral compartments become progressively saturated.15 Propofol has a relatively favorable context-sensitive half-time compared to most IV agents, making prolonged TIVA infusions clinically manageable. Additional advantages include intrinsic antiemetic properties (through 5-HT3 receptor antagonism and central mechanisms), reduction of cerebral metabolic rate and cerebral blood flow, and smooth, rapid emergence.
Propofol is formulated in a lipid emulsion (10% soybean oil, 1.2% egg lecithin); pain on injection is common and can be reduced by prior lidocaine administration or use of a larger antecubital vein. A rare but life-threatening complication of prolonged high-dose propofol infusion is propofol infusion syndrome (PRIS), characterized by metabolic acidosis, rhabdomyolysis, cardiac arrhythmias, and renal failure. PRIS is most reported in severely ill patients receiving doses above 5 mg/kg/hr for more than 48 hours, and propofol should not be used for intensive care unit (ICU) sedation in pediatric patients for this reason.15
Etomidate is a carboxylated imidazole that produces anesthesia through gamma-aminobutyric acid type A (GABA-A) receptor potentiation. Its defining clinical advantage is hemodynamic stability: etomidate causes minimal reduction in cardiac output, heart rate, and systemic vascular resistance, making it the preferred induction agent in patients with severely compromised cardiovascular function, including cardiogenic shock, severe aortic stenosis, and tamponade. The induction dose is 0.3 mg/kg IV, with onset in approximately 30 seconds and duration of 5 to 15 minutes. The principal adverse effect limiting its use is adrenocortical suppression: a single induction dose inhibits 11-beta-hydroxylase, blocking cortisol synthesis for 6 to 24 hours in most patients.2 In patients with already-compromised adrenal reserve, this transient suppression may be clinically meaningful. Myoclonus on induction and a relatively high incidence of postoperative nausea are additional drawbacks. Etomidate is not used for TIVA maintenance because of the cumulative adrenal suppression that accompanies prolonged infusion.
Ketamine is a phencyclidine derivative that produces dissociative anesthesia through non-competitive antagonism of the N-methyl-D-aspartate (NMDA) receptor, blocking glutamate-mediated excitatory neurotransmission. At subanesthetic doses (0.1 to 0.5 mg/kg IV), ketamine provides potent analgesia without loss of consciousness. At induction doses (1 to 2 mg/kg IV or 4 to 6 mg/kg IM), it produces a characteristic dissociative state in which the patient appears conscious but is unresponsive to pain and unable to form memories. A critical practical feature is the preservation of pharyngeal and laryngeal protective reflexes, though this should not be interpreted as a guarantee of airway protection, and airway management equipment must always be available.16
Ketamine has sympathomimetic cardiovascular effects, increasing heart rate, blood pressure, and cardiac output through central stimulation of the sympathetic nervous system; this makes it useful for induction in hemodynamically unstable patients and for rapid sequence induction in shocked trauma patients where propofol would cause dangerous hypotension. It is a potent bronchodilator, an important advantage in patients with active bronchospasm or reactive airways disease. Ketamine increases cerebral blood flow and intracranial pressure, making it relatively contraindicated in patients with elevated intracranial pressure (ICP), though this contraindication has been partially revisited in patients who are already intubated and mechanically ventilated. Emergence phenomena, including vivid dreams, hallucinations, and dysphoria, occur in a proportion of patients (more in adults than children) and are reduced by concurrent benzodiazepine administration.
Dexmedetomidine is a highly selective alpha-2 adrenergic agonist with a selectivity ratio for alpha-2 over alpha-1 receptors of approximately 1,600:1, making it far more selective than clonidine. It produces sedation and anxiolysis through activation of alpha-2 receptors in the locus coeruleus, and analgesia through spinal and peripheral alpha-2 receptor agonism. Its most clinically distinctive feature is the production of a sedated state from which patients are readily arousable and cooperative, with minimal respiratory depression at standard doses. This profile makes dexmedetomidine particularly useful for procedural sedation, awake fiberoptic intubation, ICU sedation where daily awakening trials are planned, and as a premedication in patients in whom benzodiazepines are undesirable (obstructive sleep apnea, delirium-prone elderly patients).17 Dexmedetomidine also reduces anesthetic requirements, allowing reduction of volatile agent or propofol doses. Bradycardia and hypotension are the principal adverse effects, reflecting the alpha-2-mediated reduction in sympathetic outflow and norepinephrine release. A biphasic blood pressure response may be seen at higher loading doses, with transient hypertension from peripheral alpha-2B receptor stimulation followed by the more sustained central sympatholytic hypotension.
TIVA AS A TECHNIQUE Total intravenous anesthesia uses propofol as the primary hypnotic agent, typically combined with a short-acting opioid (most commonly remifentanil) for analgesia and anesthetic depth, and a nondepolarizing neuromuscular blocking agent for muscle relaxation where required. The pharmacokinetic rationale for remifentanil in TIVA is its ester hydrolysis by nonspecific plasma and tissue esterases, producing an ultra-short context-sensitive half-time of approximately 3 to 5 minutes regardless of infusion duration, enabling rapid titration of analgesia and very fast offset at emergence.2
TIVA is the preferred technique over volatile agents in several clinical settings: patients at very high risk for postoperative nausea and vomiting (PONV) (where propofol's antiemetic properties and the avoidance of volatile agents reduce PONV incidence substantially); patients known or suspected to be susceptible to malignant hyperthermia (where all volatile agents are contraindicated); cases requiring intraoperative neurophysiological monitoring of motor evoked potentials (where volatile agents suppress MEP amplitude in a dose-dependent fashion, while propofol-remifentanil TIVA allows reliable monitoring); and thoracic surgery cases requiring one-lung ventilation (where propofol does not inhibit hypoxic pulmonary vasoconstriction, preserving oxygenation during lung isolation). The principal challenge of TIVA is achieving reliable, consistent depth of anesthesia without the continuous readout provided by end-tidal gas analysis; processed electroencephalogram (EEG) monitoring (bispectral index, bispectral index (BIS), or similar indices) is increasingly used to guide propofol dosing and reduce the risk of awareness under anesthesia during TIVA.
Preanesthetic medication, defined as the pharmacological preparation of a patient prior to the induction of anesthesia, serves multiple simultaneous objectives: reduction of anxiety and facilitation of a smooth induction, provision of baseline analgesia, reduction of the incidence of postoperative nausea and vomiting (PONV), modification of autonomic reflexes, reduction of gastric volume and acidity, and (where relevant) amnesia for the perioperative period. No single agent accomplishes all of these goals, and contemporary premedication regimens are therefore multimodal, selecting agents that address the specific clinical needs of the individual patient.2
SEDATIVE-HYPNOTICS INCLUDING ANXIOLYTICS. Benzodiazepines are the most widely used sedative-hypnotics for premedication. Midazolam, by virtue of its rapid onset, short duration, and reliable amnestic properties, is the most commonly employed agent in this class perioperatively. Administered intravenously approximately 15 to 30 minutes before induction (typical adult dose 1 to 2 mg IV), midazolam produces anxiolysis, anterograde amnesia, and mild sedation without significant cardiovascular depression at standard doses. It also reduces the minimum alveolar concentration (MAC) of subsequently administered volatile agents, contributing to a smoother induction and lower anesthetic requirements for maintenance. Diazepam and lorazepam were used historically but have largely been displaced by midazolam in the perioperative setting because of their longer durations and less predictable onset when given orally.2 Dexmedetomidine provides anxiolysis and sedation via alpha-2 receptor agonism and is increasingly used as a premedication in patients in whom benzodiazepine use is undesirable, including those with obstructive sleep apnea or at elevated risk for postoperative delirium.
OPIOIDS. Opioids are incorporated into premedication regimens primarily for their analgesic and anesthetic-sparing properties. By providing baseline analgesia before the first surgical stimulus, they blunt the hemodynamic response to laryngoscopy and intubation, reduce intraoperative anesthetic requirements, and facilitate a more stable intraoperative course. Fentanyl, administered intravenously in the immediate pre-induction period (typical dose 1 to 2 mcg/kg), is the most commonly used opioid for this purpose owing to its rapid onset and short duration. The principal risks of opioid premedication include respiratory depression, nausea, and unpredictable pharmacokinetics with intramuscular dosing. In ambulatory surgical settings, opioid premedication must be balanced against the risk of increasing PONV and prolonging time to discharge.2
PONV RISK STRATIFICATION AND THE APFEL SCORE. Rational antiemetic premedication requires first establishing each patient's baseline PONV risk. The Apfel simplified risk score assigns one point each for: female sex, non-smoker status, history of PONV or motion sickness, and anticipated postoperative opioid use.5 Patients with 0, 1, 2, 3, or 4 risk factors have corresponding PONV incidences of approximately 10%, 20%, 40%, 60%, and 80%. A score of 3 or 4 defines a high-risk patient who warrants multimodal prophylaxis targeting at least two or three receptor systems simultaneously. The Apfel score guides not only antiemetic selection but also anesthetic technique: high-risk patients are reasonable candidates for total intravenous anesthesia (TIVA) with propofol rather than volatile agent maintenance, which by itself reduces PONV incidence by approximately 30% relative to inhalational techniques.10 Additional risk reduction comes from minimizing intraoperative and postoperative opioid use through multimodal analgesia, avoiding nitrous oxide (which independently increases PONV risk), and adequate intraoperative IV hydration.
ANTIEMETICS. Ondansetron and other 5-HT3 receptor antagonists are the most commonly administered antiemetics in the perioperative setting. They act by blocking serotonin signaling at vagal afferents in the gut and at the chemoreceptor trigger zone. The standard perioperative dose of ondansetron is 4 mg IV administered near the end of surgery, as its efficacy is greatest against PONV in the early postoperative period.10 Dexamethasone 4 to 8 mg IV at induction is a cost-effective PONV prophylactic with a mechanism that likely involves reduction of central serotonin release, anti-inflammatory effects on vagal afferents, and reduction of prostaglandin synthesis. Its onset of antiemetic effect is delayed (1 to 2 hours), which is why it is given at induction rather than at the end of surgery. Droperidol (0.625 to 1.25 mg IV) retains antiemetic efficacy through dopamine D2 blockade at the chemoreceptor trigger zone, but carries an FDA black box warning for QTc prolongation and risk of torsades de pointes, limiting its routine use. Scopolamine transdermal patch, applied the evening before surgery, provides sustained cholinergic blockade of the vomiting center and is particularly effective for PONV associated with opioid use and for motion-related nausea.
For patients with a score of 3 or 4, triple prophylaxis targeting three receptor systems (5-HT3, dopamine D2 or glucocorticoid, and cholinergic or neurokinin-1 (NK-1) pathways) is appropriate and supported by consensus guidelines.10
ANTIPSYCHOTICS. Butyrophenone antipsychotics, principally droperidol and haloperidol, have a well-established but now more circumscribed role in anesthetic premedication. Their dopamine D2 antagonism provides antiemetic, sedative, and anti-anxiety effects. Droperidol in low doses (0.625 to 1.25 mg IV) retains a role as a PONV prophylactic and was historically used in neuroleptanalgesia when combined with fentanyl, a technique now largely of historical interest. Haloperidol at low doses (0.5 to 1 mg IV) is used in some institutions as PONV prophylaxis and for management of emergence agitation, with a somewhat more favorable cardiovascular profile than droperidol at these doses.2
ANTIHISTAMINES. H1 antihistamines, particularly diphenhydramine and promethazine, were widely used as preanesthetic agents in earlier decades for their sedative, antiemetic, and anticholinergic properties. Their role has diminished with the availability of more targeted agents, but they retain a niche in patients with allergy history and in resource-limited settings. H2 blockers (famotidine; ranitidine was withdrawn from the US market in 2020 due to NDMA contamination) have a distinct role in aspiration prophylaxis through reduction of gastric acid production, unrelated to antiemetic activity.2
ANTICHOLINERGICS. Anticholinergic premedication with atropine, scopolamine, or glycopyrrolate was standard in the era of ether and cyclopropane anesthesia, when those agents caused copious airway secretions. Modern inhalational agents are far less secretagogue in effect, substantially reducing the routine need for antisialagogue premedication. Anticholinergics retain specific indications: glycopyrrolate when a dry surgical field is required (airway procedures, oral surgery), atropine to treat or prevent bradycardia including the bradycardia associated with succinylcholine in pediatric patients, and scopolamine transdermally for PONV prophylaxis. Glycopyrrolate is a quaternary ammonium compound that does not cross the blood-brain barrier, making it free of the central anticholinergic effects (sedation, confusion, delirium) that accompany atropine and scopolamine, both of which are tertiary amines with CNS penetration.2
ASPIRATION PROPHYLAXIS: PHARMACOLOGICAL RATIONALE. Pulmonary aspiration of gastric contents causes chemical pneumonitis (Mendelson syndrome) through the combined action of low-pH gastric fluid and particulate matter on bronchial mucosa and alveoli. The aspiration risk is determined by two independent factors: gastric volume and gastric pH. Reduction of gastric volume is the goal of preoperative fasting (ASA nil per os (nothing by mouth, NPO) guidelines: 2 hours for clear liquids, 6 hours for a light meal, 8 hours for a full meal), and pharmacological acceleration of gastric emptying in high-risk patients. Metoclopramide 10 mg IV given 30 to 60 minutes before induction acts through dopamine D2 and serotonin 5-HT4 receptor agonism in the gut to accelerate gastric emptying, increase lower esophageal sphincter tone, and augment peristalsis.2 It should not be used in patients with gastrointestinal obstruction, pheochromocytoma, or those on medications at risk for extrapyramidal interaction.
Elevation of gastric pH reduces the chemical burn potential of any aspirated material: gastric pH above 2.5 is associated with substantially reduced lung injury if aspiration occurs. Proton pump inhibitors (pantoprazole 40 mg IV or oral omeprazole the night before and morning of surgery) provide the most sustained elevation of gastric pH. H2 receptor antagonists (famotidine, ranitidine) act faster but have shorter duration. Sodium citrate 30 mL orally immediately before induction provides rapid neutralization of existing gastric acid through direct buffering; it is non-particulate and does not itself cause pulmonary injury if aspirated, unlike particulate antacids such as magnesium trisilicate.2 In high-risk patients (morbid obesity, diabetic gastroparesis, pregnancy, trauma, emergency surgery), a combination of these three approaches provides additive risk reduction across both gastric volume and gastric pH axes.
GASTROKINETIC DRUGS. Metoclopramide is the most commonly used gastrokinetic agent in the perioperative setting. Its mechanism combines dopamine D2 antagonism (centrally at the chemoreceptor trigger zone, providing antiemetic effect, and in the gut, accelerating motility) with 5-HT4 agonism (augmenting the prokinetic effect on gastric emptying and lower esophageal sphincter tone). The onset of gastrokinetic effect after IV administration is approximately 5 minutes, with a duration of 1 to 2 hours. Contraindications include mechanical bowel obstruction (where increased motility could worsen perforation risk), known or suspected pheochromocytoma (dopamine blockade may precipitate hypertensive crisis), and concurrent use of drugs with significant extrapyramidal liability. In patients for whom metoclopramide is not appropriate, domperidone (where available) is an alternative peripheral dopamine antagonist that does not cross the blood-brain barrier and therefore lacks the extrapyramidal and CNS adverse effects of metoclopramide, though it has limited parenteral availability in many countries.2
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Eger EI 2nd, Saidman LJ, Brandstater B. Minimum alveolar anesthetic concentration: a standard of anesthetic potency. Anesthesiology. 1965;26:756–763. [Seminal MAC paper.]
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Flood P, Rathmell JP, Shafer SL, eds. Stoelting's Pharmacology and Physiology in Anesthetic Practice. 5th ed. Philadelphia: Wolters Kluwer; 2015.
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Peyton PJ, Wu CY. Nitrous oxide-related postoperative nausea and vomiting depends on duration of exposure. Anesthesiology. 2014;120(5):1137–1145.
Franks NP. Molecular targets underlying general anaesthesia. Br J Pharmacol. 2006;147(Suppl 1):S72–S81.
Marik PE. Propofol: therapeutic indications and side-effects. Curr Pharm Des. 2004;10(29):3639–3649.
White PF, Ham J, Way WL, Trevor AJ. Pharmacology of ketamine isomers in surgical patients. Anesthesiology. 1980;52(3):231–239.
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