General anesthesia: high yield topics: 1

 General anesthesia discussion:

Q. What are the three major categories of anesthetic technique?

Anesthetic technique is often grouped into three major categories: general anesthesia, regional anesthesia, and monitored anesthesia care (MAC). 

Q. What four components are part of the clinically accepted definition of general anesthesia?

The four components of general anesthesia include immobility, amnesia, analgesia, and patient lack of harm. The concept of lack of harm was developed because of the potentially dangerous effects of general anesthetics, such as respiratory depression and hypotension. 

Q. What are the four levels on the continuum of sedation, as defined by the American Society of Anesthesiologists? Describe them in terms of patient responsiveness, ability to maintain a patent airway and spontaneous ventilation, and ability to maintain cardiovascular homeostasis.

The American Society of Anesthesiologists (ASA) defines the following four levels on the continuum of sedation:

  • Minimal sedation: A patient responds briskly to verbal stimulus, and airway and cardiovascular function are unaffected.
  • Moderate sedation: A patient responds purposefully to verbal or tactile stimuli, and airway and cardiovascular function are usually maintained.
  • Deep sedation: Repeated or painful stimulus is required for the patient to respond. Spontaneous ventilation may be inadequate, and airway intervention may be required. Cardiovascular function is usually maintained.
  • General anesthesia: The hallmark of general anesthesia is absence of patient responsiveness, even with a painful stimulus. Airway intervention is typically required, as spontaneous ventilation is usually inadequate. Cardiovascular homeostasis may be impaired by the medications required to induce general anesthesia. 

Q. Which of the four levels on the sedation continuum might an anesthesia provider encounter during monitored anesthesia care?

When caring for a patient receiving MAC, an anesthesia provider must be prepared for all degrees of sedation, from minimal sedation to an “unplanned” general anesthetic if the surgical procedure cannot be accomplished safely with sedation. The appropriate medications and airway equipment for general anesthesia should be available for a patient receiving MAC. 

Q. What major factors go into the choice of anesthetic technique?

The anesthesia provider must weigh several factors when deciding anesthetic technique, including 

  • The demands of the type of surgical procedure
  • The patient’s coexisting diseases
  • Patient preferences. 
Reconciling the requirements and risks inherent to the surgical procedure and pathology it is intended to treat (e.g., acute appendicitis, presenting for laparoscopic appendectomy) with the patient in whom the disease occurs (e.g., a 5-year-old with no current intravenous access) and designing a safe and effective anesthetic plan is one of the most important challenges for the anesthesia professional.

Q. What are some perioperative roles of peripheral nerve blockade and neuraxial anesthesia besides surgical analgesia? 

Peripheral nerve blockade or neuraxial anesthesia may be used in combination with general anesthesia to provide postoperative analgesia, reduce rates of postoperative chronic pain, and perhaps even reduce intraoperative blood loss.
For example, consider the development of “enhanced recovery after surgery” care pathways (e.g., for elective laparoscopic bowel resection), which emphasize the use of partial neuraxial analgesia via an epidural catheter both intraoperatively and postoperatively. In this situation an epidural catheter may be used despite the requirement for deep neuromuscular blockade and controlled ventilation to facilitate laparoscopic surgery, which necessitates general anesthesia during the surgical procedure itself.

Q. How is “preventive analgesia” defined?

Preventive analgesia is defined as analgesia lasting longer than 5.5 half-lives of an analgesic drug. 

Q. What is preoxygenation? Why is it performed prior to anesthesia induction?

Performed prior to induction of anesthesia for a general anesthetic, preoxygenation— also called denitrogenation—is the replacement of nitrogen in the patient’s functional residual capacity by the inhalation of 100% oxygen by face mask. 

Adequate preoxygenation can reduce or eliminate hypoxemia occurring between induction of anesthesia and institution of controlled ventilation. It does this by providing a reservoir of oxygen in the lungs, which is gradually absorbed even during periods of apnea. 

There are two regimens that typically achieve replacement of 80% of the functional residual capacity with oxygen:

• Allow the patient to take eight vital capacity breaths of 100% oxygen over 60 seconds.

• Allow normal tidal breathing of 100% oxygen for 3 minutes. 

Q. By what drug administration routes may induction of general anesthesia occur? 

Induction of anesthesia may be accomplished by an inhaled technique using volatile anesthetic gases or by an intravenous technique. In some cases, both techniques are used simultaneously. For example, a common method of inducing anesthesia in a pediatric patient is to perform an inhaled induction with the goal of immobility (deep sedation or general anesthesia) while an intravenous line is placed; then, to ensure adequate depth of anesthesia for intubation, an additional dose of intravenous hypnotic (e.g., propofol) is given prior to instrumenting the airway. 

Q. What is the most common high-potency volatile anesthetic gas used for inhaled induction of anesthesia, and why?

For inhaled anesthesia induction, sevoflurane is most commonly used because of its high potency, low pungency, and relatively low lipid solubility, resulting in desirable rapidity of onset. 

Desflurane is very pungent and causes airway irritability manifested as coughing, bronchospasm, or laryngospasm; it is poorly tolerated as an agent for inhaled induction. 

Isoflurane is less pungent than desflurane, but because of its high lipid solubility it cannot be used to induce general anesthesia rapidly as a sole agent. 

Q. When is a rapid sequence induction (RSI) technique used? What differentiates an RSI from a standard intravenous induction?

Rapid sequence induction (RSI) is used for patients at risk for aspiration of gastric contents. This group includes 

  • Patients with a known full stomach
  • An unknown fasting time
  • Clinically significant gastroesophageal reflux disease or delayed gastric emptying. 
The goal of RSI is to minimize the time between onset of unconsciousness and tracheal intubation. 

The hallmark of RSI is the administration of a rapid-onset neuromuscular blocking drug in “rapid sequence” with a hypnotic of choice. 

After preoxygenation, an intubating dose of a hypnotic is administered, followed immediately by an intubating dose of neuromuscular blocking drug. Tracheal intubation occurs as soon as intubating conditions are achieved, without the use of mask ventilation. If cricoid pressure is used, it is applied immediately upon loss of responsiveness and only released upon confirmation of correct endotracheal tube placement. 

Q. Why is mask ventilation not performed in a true RSI? What defines a modified RSI?

During RSI, mask ventilation is generally avoided because it can result in gastric insufflation, increasing the risk of aspiration of gastric contents. 

The RSI technique relies on rapid endotracheal intubation to avoid hypoxemia, which may progress to cardiac arrest if assisted ventilation cannot be provided. 

In a “modified” RSI, gentle positive-pressure ventilation using pressures less than 20 cm H2O may be judiciously attempted. Theoretically, low-pressure positive-pressure ventilation reduces the risk of gastric insufflation compared with standard mask ventilation and may be used to reduce the risk of hypoxemia prior to tracheal intubation. 

Q. How is cricoid pressure achieved? How efficacious is cricoid pressure?

Cricoid pressure is achieved by applying a force of 30 newtons (about 7 pounds) of pressure on the cricoid cartilage. This is thought to occlude the esophagus beneath and decrease the risk of the aspiration of gastric contents. 
Although the application of cricoid pressure for RSI has been the standard of care for decades, a recent meta-analysis did not demonstrate that its use has had a measurable impact on clinical outcomes during RSI. 

Q. What airway management technique is considered safest in a cooperative patient at high risk for difficult or impossible intubation?

Awake fiberoptic intubation is typically performed for patients at high risk of a “cannot intubate, cannot ventilate” situation. 

The hallmark of this technique is the maintenance of consciousness, and therefore a patent airway with adequate spontaneous ventilation, until endotracheal tube placement is confirmed. Induction hypnotics are administered until after endotracheal intubation. 

Q. What technique is used to achieve endotracheal intubation in a patient at risk for both aspiration of gastric contents and difficult or impossible intubation? 

Awake fiberoptic intubation may be selected for a patient at high risk for both aspiration and difficult or impossible intubation. 

Thus, an awake fiberoptic endotracheal intubation may be performed to 

  • maintain a patient’s conscious ability to clear regurgitated gastric contents away from the lungs 
  • maintain a patent airway and spontaneous ventilation until endotracheal tube placement is confirmed

Q. What are the complications of intubation?

  • During laryngoscopy and intubation 
    • Malpositioning

      • Esophageal intubation
      • Bronchial intubation 
      • Laryngeal cuff position
    • Airway trauma
      • Dental damage
      • Lip, tongue, or mucosal laceration Sore throat
      • Dislocated mandible 
      • Retropharyngeal dissection
    • Physiological reflexes 
      • Hypoxia, hypercarbia 
      • Hypertension, tachycardia 
      • Intracranial hypertension 
      • Intraocular hypertension 
      • Laryngospasm
    • Tube malfunction 
      • Cuff perforation

  • While the tube is in place 
    • Malpositioning
      • Unintentional extubation 
      • Bronchial intubation 
      • Laryngeal cuff position

    • Airway trauma
      • Mucosal inflammation and ulceration 
      • Excoriation of nose

    • Tube malfunction 
      • Fire/explosion 
      • Obstruction
  • Following extubation 
    • Airway trauma
      • Edema and stenosis (glottic, subglottic, or tracheal) 
      • Hoarseness (vocal cord granuloma or paralysis) 
      • Laryngeal malfunction and aspiration
    • Laryngospasm
    • Negative-pressure pulmonary edema

Q. What advantages do potent volatile anesthetics offer as a maintenance drug? 

Potent volatile anesthetics have several advantages for maintenance of anesthesia. They are:

  • Easy to titrate
  • Suppress the autonomic response to noxious stimulation
  • Provide a modest degree of muscle relaxation at clinically relevant doses, which can facilitate surgical exposure. 
  • Monitoring the end-tidal anesthetic gas concentration provides a surrogate measure for depth of hypnosis, which is as effective at preventing intraoperative awareness as purpose-built processed electroencephalogram monitors.

Q. What are the drawbacks of potent volatile anesthetics?

There are drawbacks to the potent volatile anesthetics for anesthesia maintenance. 

  • They increase the risk for nausea and vomiting. 
  • Emergence from anesthesia is associated with a paradoxical hyperreactivity state, which can clinically be manifested as airway hyperreactivity (bronchospasm, laryngospasm) and coughing. 
  • Volatile anesthetics also depress cardiac contractility and cause peripheral vasodilation, which may be manifested as clinically significant hypotension.

Q. What differentiates nitrous oxide from the potent volatile anesthetics?

There are key differences between nitrous oxide and the potent volatile anesthetics. 

  • Nitrous oxide provides relatively less vasodilation and cardiac depression than potent volatile anesthetics. 
  • It also has analgesic properties
  • Due to its low blood solubility also has rapid onset and offset.
  • The minimum alveolar concentration required to suppress movement to a painful stimulus is greater than can be delivered at atmospheric pressure, so it cannot be used as a sole agent to ensure hypnosis.

Q. What are the advantages and disadvantages of propofol as an anesthetic maintenance drug, compared with potent volatile anesthetics?

Propofol has distinct advantages and disadvantages compared to volatile anesthetics. 

  • Propofol reduces postoperative nausea and vomiting rates.
  • Emergence is associated with less coughing and laryngospasm risk. 
  • Delivery does not rely on controlled ventilation, so it may be more favorable for open- airway procedures (e.g., bronchoscopy, laryngeal surgery with intraoperative jet ventilation). 
  • Propofol does not suppress somatosensory and motor evoked potential signals as severely as volatile anesthetics and thus may facilitate intraoperative neurologic monitoring. 

  • However, propofol requires a reliable site of intravenous administration, there is no clinically available way to measure serum propofol concentrations, and the drug may be associated with higher rates of intraoperative awareness due to inadvertent interruption of intravenous administration. 
  • Depth of hypnosis monitoring using electroencephalography or auditory evoked potentials may protect against intraoperative awareness, particularly if neuromuscular blockade is concurrently used. 

Q. Name some procedural and patient requirements for successful regional anesthesia as the sole anesthetic technique.

In order to provide successful regional anesthesia, there are important procedural and patient requirements to consider, including the following:

Procedural: The location of the procedure must be amenable to regional anesthesia; for example, the distal extremities in the case of peripheral nerve block or the lower trunk and legs in the case of neuraxial anesthesia. Systemic neuromuscular blockade and controlled ventilation must not be required.

Patient: A cooperative patient who provides informed consent for any planned interventions is required for successful regional anesthesia.

Q. Why might regional or neuraxial anesthesia be particularly desirable for patients with severe systemic disease?

For a patient with severe systemic disease, there are unique aspects of regional anesthesia techniques that may be of benefit for the patient. 

Surgical anesthesia can theoretically be achieved without systemic sedation, assuming appropriate procedure selection. This avoids potential complications of deep sedation and general anesthesia including 

  • Cardiac depression in patients with marginal cardiac function
  • Difficult or impossible liberation from controlled ventilation in patients with severe underlying lung disease
  • Unpredictable or undesirable pharmacokinetic effects of organ failure (renal, hepatic) by systemic medications. 

Q. What are some options available to the anesthesiologist in the event that a peripheral nerve block is attempted but surgical anesthesia is not accomplished?

If surgical anesthesia is not achieved with a peripheral nerve block, either because it was difficult or the resultant block inadequate, several options are available to the anesthesiologist depending on the clinical situation. 

  • The block can be supplemented with local anesthetic infiltration, intravenous analgesics and/or sedatives can be administered
  • Surgery can be postponed and the block reattempted at a later time
  • General anesthesia can be administered. 

Q. List some pharmacologic and nonpharmacologic methods of providing sedation and anxiolysis during monitored anesthesia care (MAC).

Although many think first of medications as the means of providing sedation and anxiolysis during monitored anesthetic care, nonpharmacologic methods also have an important role in ensuring patient safety and comfort. 

Commonly used pharmacologic options include propofol, opioids, and hypnotic medications (most commonly benzodiazepines). 

Potential nonpharmacologic methods include video or audio distraction and verbal reassurance. Nonpharmacologic methods avoid undesirable side effects (e.g., respiratory depression, paradoxical agitation, or a duration of action longer than required for the procedure). These methods may provide sufficient comfort for well-selected patients who wish to avoid medications.

Q. What are common manifestations of respiratory depression from oversedation?

Respiratory depression is common with deep sedation. The respiratory effects of oversedation may be manifested as 
  • Upper airway obstruction (snoring, obstructive apnea)
  • Hypoventilation 
  • Hypoxemia. 
These risks require that the anesthesia provider be prepared to assist or take over ventilation as the clinical situation indicates. 
Sedatives that are less likely to cause hypoventilation include ketamine and dexmedetomidine, but these drugs have other side effects and may have synergistic sedative effects with other hypnotic medications. 

Q. What is the atmospheric impact of potent volatile anesthetics and nitrous oxide?

Waste anesthetic gases are typically scavenged by a suction mechanism from the operating room to limit occupational exposure for operating room personnel; however, scavenged gas is often vented outside the facility, into the environment. 

Potent volatile anesthetics and nitrous oxide are ozone-depleting greenhouse gases. Although the global warming potential by volume is greatest for desflurane, nitrous oxide is the most important inhaled anesthetic cause of atmospheric harm because it is used in relatively high concentrations (e.g., 50% to 70% by volume).

Q. What are techniques to minimise the environmental impact of inhaled anesthetics? 

Environmental impact is minimized by 

  • Using the lowest total amount of inhaled anesthetic, either by
    • Eliminating its use entirely (and providing anesthetic maintenance using total intravenous anesthesia) or
    • by reducing fresh gas flow in the context of low-flow or closed-circuit anesthesia. 
  • Choosing the lowest impact volatile anesthetic gas—sevoflurane or isoflurane, depending on acceptable fresh gas flow rates, and 
  • avoiding nitrous oxide—also minimizes impact. 
  • There exist collection systems for waste (scavenged) gases that are intended to capture anesthetic gases prior to atmospheric release and then potentially reprocess them for human reuse; however, none is yet widely used. 
As nitrous oxide (from all sources, including anesthetic) is likely to be the most significant ozone-depleting emission for the 21st century, the selection of an anesthetic regimen that takes environmental impact into account—while adding an extra layer of complexity to the choice of anesthetic technique—provides a sophisticated acknowledgment by the anesthesia provider that, as professionals, we have a duty not just to the patient before us but to future patients as well.

Q. What are the properties of an ideal anesthetic gas?

An ideal anesthetic gas would be 

  • Predictable in onset and emergence
  • Provide muscle relaxation
  • Cardiostability
  • Bronchodilation
  • Not trigger malignant hyperthermia or other significant side effects (such as nausea and vomiting)
  • Be inflammable
  • Undergo no transformation within the body
  • Allow easy estimation of concentration at the site of action

Q. What are the chemical structures of the more common anesthetic gases? Why do we no longer use the older ones?

Isoflurane, desflurane, and sevoflurane are the most commonly used volatile anesthetics. As the accompanying molecular structures demonstrate, they are substituted halogenated ethers, except halothane, a substituted halogenated alkane

Many older anesthetic agents had unfortunate properties and side effects such as 
  • Flammability (cyclopropane and fluroxene) 
  • Slow induction (methoxyflurane)
  • Hepatotoxicity (chloroform and fluroxene)
  • Nephrotoxicity (methoxyflurane)
  • Risk of seizures (enflurane)
Q. How are the potencies of anesthetic gases compared?

The potency of anesthetic gases is compared using minimal alveolar concentration (MAC).

One MAC is defined as ‘the minimum concentration (in volumes percent) of inhalational anaesthetic agent in the alveoli, at equilibrium, at one atmosphere pressure, in 100% oxygen, which produces immobility in 50% of unpremedicated adult subjects when exposed to a standard noxious stimulus.’

Of note, 1.3 MAC is required to abolish this response in 99% of patients. 

Other definitions of MAC include the 

MAC-BAR, which is the concentration required to block autonomic reflexes to nociceptive stimuli (1.7 to 2 MAC). 

MAC-awake, the concentration required to block appropriate voluntary reflexes and measure perceptive awareness (0.3 to 0.5 MAC). 

MAC appears to be consistent across species lines. The measurement of MAC assumes that alveolar concentration directly reflects the partial pressure of the anesthetic at its site of action and equilibration between the sites.

Q. What factors may influence MAC?

For every Celsius degree drop in body temperature, MAC decreases approximately 2% to 5%. 

Factors decrease MAC:

  • Increasing age and prematurity 
  • Pregnancy
  • Hyponatremia
  • Hypothermia 
  • Hypothyroidism 
  • Hypotension 
  • Opioids, barbiturates, benzodiazepines, calcium channel blockers
  • Acute alcohol intoxication
  • Drugs that reduce CNS catecholamine release (e.g. reserpine, methyl dopa, clonidine, dexmedetomidine, chronic amphetamine/cocaine use)

Factors increases MAC: 

  • Infants at 6 to 12 months of age
  • Hyperthermia
  • Hyperthyroidism
  • Hypernatremia 
  • Chronic alcoholism, opioid use 
  • Elevated CNS catecholamine release: anxiety states, drugs (e.g. ephedrine, acute amphetamine/cocaine use, MAOIs)

Factors that do not affect MAC include hypocarbia, hypercarbia, gender and hyperkalemia. 

MAC is additive. For example, nitrous oxide potentiates the effects of volatile anesthetics.

Q. Define partition coefficient. Which partition coefficients are important?

A partition coefficient describes the distribution of a given agent at equilibrium between two substances at the same temperature, pressure, and volume. 
Thus the blood-to-gas coefficient describes the distribution of anesthetic between blood and gas at the same partial pressure. 

A higher blood-to-gas coefficient correlates with a greater concentration of anesthetic in blood (i.e., a higher solubility). Therefore a greater amount of anesthetic is taken into the blood, which acts as a reservoir for the agent, reducing the alveolar concentration and thus slowing the rate of induction. 

Equilibration is relatively quick between alveolar and brain anesthetic partial pressure in insoluble volatile anesthetics. The alveolar concentration ultimately is the principal factor in determining onset of action.

Other important partition coefficients include brain to blood, fat to blood, liver to blood, and muscle to blood. Except for fat to blood, these coefficients are close to 1 (equally distributed). Fat has partition coefficients for different volatile agents of 30 to 60 (i.e., anesthetics continue to be taken into fat for quite some time after equilibration with other tissues).

Q. What factors influence speed of induction?

Factors that increase alveolar anesthetic concentration speed onset of volatile induction: 

  • Increasing the delivered concentrations of anesthetic
  • High flow within the breathing circuit
  • Increasing minute ventilation

Factors that decrease alveolar concentration slow onset of volatile induction: 

  • Increase in cardiac output
  • Decreased minute ventilation
  • High anesthetic lipid solubility
  • Low flow within the breathing circuit

Q. What is the second gas effect? Explain diffusion hypoxia.


Nitrous oxide is rapidly absorbed across the alveolar membrane into the pulmonary capillaries. Nitrous oxide is around 20 times more soluble in blood than oxygen or nitrogen. At high concentrations of nitrous oxide, a significantly greater volume of nitrous oxide is entering pulmonary blood than oxygen or nitrogen is entering the alveolus. This results in two phenomena, which together increase the speed of onset of anaesthesia:

• Concentration effect: As nitrous oxide is rapidly absorbed, the alveolar volume decreases, leading to a fractional concentration of the remaining gases in the alveolus. This results in an increased concentration gradient between the alveolus and pulmonary blood, favouring alveolus to blood transfer of anaesthetic agent. 

• Augmentation of alveolar ventilation. As nitrous oxide is rapidly absorbed, the volume and pressure in the alveolus falls, creating a pressure/volume gradient between the conducting airways and the alveolus. This augments alveolar ventilation by drawing more gas down its pressure gradient into the alveolus, thus increasing speed of onset of anaesthesia. 

Similarly, use of nitrous oxide will accelerate the offset of anaesthesia. During emergence from anaesthesia, nitrous oxide administration is ceased and an oxygen or oxygen/air mixture is delivered. Nitrous oxide rapidly diffuses from the bloodstream across the alveolar membrane into the alveolus. This dilutes the volatile agent in the alveolus (and therefore the partial pressure), resulting in a faster offset of anaesthesia. This also causes diffusion hypoxia.

However, even at high concentrations (70%) of nitrous oxide, this effect accounts for only a small increase in concentration of volatile anesthetic. 

Recent studies have yielded conflicting results as to whether this phenomenon is valid. 

When nitrous oxide is discontinued abruptly, its rapid diffusion from the blood to the alveolus decreases the oxygen tension in the lung, leading to a brief period of decreased oxygen concentration known as diffusion hypoxia. Administering 100% oxygen at the end of a case can mitigate this.

Q. Should nitrous oxide be administered to patients with pneumothorax? Are there other conditions in which nitrous oxide should be avoided?

Although nitrous oxide has a low blood-to-gas partition coefficient, it is 20 times more soluble than nitrogen (which comprises 79% of atmospheric gases). Thus nitrous oxide can diffuse 20 times faster into closed spaces than it can be removed, resulting in expansion of pneumothorax, bowel gas, or air embolism or in an increase in pressure within noncompliant cavities such as the cranium or middle ear.

Q. Which anesthetic agent is most associated with cardiac dysrhythmias?

Halothane has been shown to increase the sensitivity of the myocardium to epinephrine, resulting in premature ventricular contractions and tachydysrhythmias. 

The mechanism may be related to the 

  • Prolongation of conduction through the His-Purkinje system, which facilitates the reentrant phenomenon and β1-adrenergic receptor stimulation within the heart. 
  • Decrease automaticity of SA node, thereby favours the emergence of alternative pacemakers in atrium or the AV node.

Compared with adults, children undergoing halothane anesthesia appear to be relatively resistant to this sensitizing effect, although halothane has been shown to have a cholinergic, vagally induced bradycardic effect in children.

Q. What effects do volatile anesthetics have on hypoxic pulmonary vasoconstriction, airway caliber, mucociliary function, and intracranial pressure?

  • Hypoxic pulmonary vasoconstriction (HPV) is a locally mediated response of the pulmonary vasculature to decreased alveolar oxygen tension and serves to match ventilation to perfusion. Inhalational agents decrease this response.
  • All volatile anesthetics appear to decrease airway resistance by a direct relaxing effect on bronchial smooth muscle and by decreasing the bronchoconstricting effect of hypocapnia. The bronchoconstricting effects of histamine release also appear to be decreased when an inhalational anesthetic is administered.
  • Mucociliary clearance appears to be diminished by volatile anesthetics, principally through interference with ciliary beat frequency. The effects of dry inhaled gases, positive- pressure ventilation, and high inspired oxygen content also contribute to ciliary impairment.
  • Volatile anesthetics increase intracranial blood flow and may increase intracranial pressure (ICP). Use of an intravenous anesthetic may be preferred to volatile anesthetics when increasing ICP may impair effective intracranial blood flow.

Q. Discuss the biotransformation of volatile anesthetics and the toxicity of metabolic products.

For the most part, oxidative metabolism occurs within the liver via the cytochrome P-450 system and to a lesser extent within the kidneys, lungs, and gastrointestinal tract. 

Desflurane and isoflurane are metabolized less than 1%, whereas halothane is metabolized more than 20% by the liver. 

Under hypoxic conditions, halothane may undergo reductive metabolism, producing metabolites that may cause hepatic necrosis. Halothane hepatitis is secondary to an autoimmune hypersensitivity reaction.

Fluoride is another potentially toxic product of anesthetic metabolism. Fluoride- associated renal dysfunction has been linked to the use of methoxyflurane and greatly contributed to the withdrawal of methoxyflurane from the market. The fluoride produced by sevoflurane has not been implicated in renal dysfunction, perhaps because sevoflurane is not as lipid soluble as methoxyflurane and the time of exposure (fluoride burden) is much less.

Soda lime can also degrade sevoflurane. One of the metabolic by-products is a vinyl ether known as Compound A. Compound A has been shown to be nephrotoxic to rats, but no organ dysfunction in association with clinical use in humans has been noted. Compound A may accumulate during longer cases, low-flow anesthesia, and dry absorbent and with high sevoflurane concentrations. Anesthesia machines left on over the weekend with persistent gas flow desiccate the absorbent and make CO formation a possibility.

Q. Review the effects of COabsorbents on volatile anesthetic by-products.

Desflurane, much more than any other volatile anesthetic, has been associated with the production of carbon monoxide (CO). 

There are a number of key conditions. The volatile compound must contain a difluoromethoxy group (desflurane, enflurane, and isoflurane). This group interacts with the strongly alkaline and desiccated COabsorbent

A base-catalyzed proton abstraction forms a carbanion that can either be reprotonated by water to regenerate the original anesthetic or form CO when the absorbent is dry. Because of the greater opportunity to dry the absorbent out, the incidence of CO exposure is highest in the first case of the day, when machines have not been used for some time, or when fresh gas flow has been left on for a protracted period of time. The prior conditions are often found to be most significant on the first day of the week (e.g., mostly Mondays) if the machine has not been used during the weekend. Absorbents should be changed routinely despite lack of apparent color change, and moisture levels should be monitored.

Potassium hydroxide (KOH)–containing absorbents are the stronger alkalis and result in greater CO production. From greatest to least, KOH-containing absorbents are Baralyme (4.6%) > classic soda lime (2.6%) > new soda lime (0%) > calcium hydroxide lime (Amsorb) (0%). 

Choice of volatile anesthetic also determines the amount of CO produced, and at equiMAC concentrations desflurane > enflurane > isoflurane. Sevoflurane, once thought to be innocent, has recently been implicated as well when exposed to dry absorbent (especially KOH-containing). This leads to CO production and a rapid increase in absorbent temperature, generation of formic acid leading to severe airway irritation, and a lower effective circuit concentration of delivered sevoflurane compared with that of vaporizer dial concentration.

Q. Which anesthetic agent has been shown to be teratogenic in animals? Is nitrous oxide toxic to humans?

Nitrous oxide administered to pregnant rats in concentrations greater than 50% for over 24 hours has been shown to increase skeletal abnormalities. The mechanism is probably related to the inhibition of methionine synthetase; the mechanism may also be secondary to the physiologic effects of impaired uterine blood flow by nitrous oxide. Although, due to ethical reasons, this is not possible to study in humans, it may be prudent to limit the use of nitrous oxide in pregnant women.

Several surveys have attempted to quantify the relative risk of operating room personal exposure to nonscavenged anesthetic gases. Pregnant women were reported to have a 30% increased risk of spontaneous abortion and a 20% increased risk for congenital abnormalities. However, responder bias and failure to control for other exposure hazards may account for some of these findings.

Nitrous oxide can be toxic to humans because of its ability to prevent cobalamin (vitamin B12) to act as a coenzyme for methionine synthaseNitrous oxide interacts with vitamin B12 resulting in selective inhibition of methionine synthase, a key enzyme in methionine and folate metabolism. Thus, nitrous oxide may alter one-carbon and methyl-group transfer most important for DNA, purine and thymidylate synthesis. Long-term exposure to high concentrations of nitrous oxide may cause megaloblastic bone-marrow depression and neurological symptoms.

Toxic effects (e.g.,myelinopathies, spinal cord degeneration, altered mental status, paresthesias, ataxia, weakness, spasticity) generally are seen in persons abusing nitrous oxide for long periods of time. Other patients may be disposed to toxicity during routine nitrous-based anesthetics, including pernicious anemia and vitamin B12 deficiency. 

Patients having surgery where 70% nitrous oxide was used for over 2 hours have been shown to have more postoperative complications, including atelectasis, fever, pneumonia, and wound infections. It seems prudent then to limit the use of nitrous oxide in longer procedures.

Q. Factors to be considered before N2O use?

Patient factor:

  • Lung disease: Pneumothoraces, Bullous disease 
  • Increased intracranial pressure
  • Vit B12 deficiency 
  • Known history of nausea and vomiting
  • First trimester pregnancy
Surgical factors:

  • Middle ear surgery
  • Neurosurgery (risk of pneumocephalus, venous air embolism, increase in intracranial pressure)
  • Thoracic surgery 
  • Ophthalmic surgery 
  • Laparoscopic surgery 
  • Colorectal/bowel surgery 
  • Prolonged surgery (> 6 h)

Q. Describe the ventilatory effects of the volatile anesthetics.

Delivery of anesthetic gases results in dose-dependent depression of ventilation mediated directly through medullary centers and indirectly through effects on intercostal muscle function. 

Minute volume decreases secondary to reductions in tidal volume, although rate appears generally to increase in a dose-dependent fashion. 

Ventilatory drive in response to hypoxia can be easily abolished at 1 MAC and attenuated at lower concentrations. Increasing the delivered anesthetic concentration also attenuates the ventilatory response to hypercarbia.

Q. What are the different types of anesthesia breathing circuits?

Breathing circuits are usually classified as open, semiopen, semiclosed, or closed. They include various components configured to allow the patient to breathe (or be ventilated) with a gas mixture that differs from room air.

Q. Give an example of an open circuit.

An open circuit is the method by which the first true anesthetics were given 160 years ago. A bit of cloth saturated with ether or chloroform was held over the patient’s face. The patient breathed the vapors and became anesthetized. The depth of anesthesia was controlled by the amount of liquid anesthetic on the cloth; thus it took a great deal of trial and error to become good at the technique.

Q. Give an example of a semiopen circuit.

The various semiopen circuits were fully described by Mapleson and are commonly known as the Mapleson A, B, C, D, E, and F circuits. 

All have in common a source of fresh gas, corrugated tubing (more resistant to kinking), and a pop-off or adjustable pressure-limiting valve. Differences among the circuits include the locations of the pop-off valve, fresh gas input, and whether or not a gas reservoir bag is present. Advantages of the Mapleson series are simplicity of design, ability to change the depth of anesthesia rapidly, portability, and lack of rebreathing of exhaled gases (provided the fresh gas flow is adequate). Disadvantages include lack of conservation of heat and moisture, limited ability to scavenge waste gases, and high requirements for fresh gas flow. Semiopen circuits are rarely used today except for patient transport.

Q. Give an example of a semiclosed circuit.

The prototypical semiclosed circuit is the circle system. Every semiclosed system contains an inspiratory limb, expiratory limb, unidirectional valves, COabsorber, gas reservoir bag, and a pop-off valve on the expiratory limb. Advantages of a circle system include conservation of heat and moisture, the ability to use low flows of fresh gas (thereby conserving volatile anesthetic and the ozone layer), and the ability to scavenge waste gases. A disadvantage is its complex design; it has approximately 10 connections, each of which has the potential for disconnection.

Q. Give an example of a closed circuit.

Like the semiclosed circuit, the closed circuit is a circle system adjusted so the inflow of fresh gas just matches the patient’s Oconsumption and anesthetic agent uptake. The COis eliminated by the absorber.

Q. Rank the Mapleson circuits in order of efficiency for controlled and spontaneous ventilation.

  • Controlled: D > B > C > A (mnemonic: Dog Bites Can Ache) 
  • Spontaneous: A > D > C > B (mnemonic: All Dogs Can Bite)

Q. What circuit is most commonly used in anesthesia delivery systems today?

Almost every anesthesia manufacturer supplies a circle system with its equipment. When compared with other available circuits, the circle system provides the most advantages.

Q. How is a breathing circuit disconnection detected during delivery of an anesthetic?

Breath sounds are no longer detected with an esophageal or precordial stethoscope, and, if the parameters are properly set, the airway pressure monitor and tidal volume–minute volume monitor alarm will sound. The capnograph no longer detects CO2, and soon thereafter the Osaturation begins to decline. Exhaled COis probably the best monitor to detect disconnections; a decrease or absence of COis sensitive although not specific for disconnection.

Q. How is COeliminated from a circle system?

The exhaled gases pass through a canister containing a COabsorbent such as soda lime or Baralyme. Soda lime consists of calcium hydroxide (Ca[OH]2) with lesser quantities of sodium hydroxide (NaOH) and potassium hydroxide (KOH). Baralyme substitutes barium for calcium. Both soda lime and Baralyme react with COto form heat, water, and the corresponding carbonate. The soda lime reaction is as follows:

CO+ Ca(OH)= CaCO+ H2O + heat

Q. How much COcan the absorbent neutralize? What factors affect its efficiency?

Soda lime is the most common absorber and, at most, can absorb 23 L of COper 100 g of absorbent

However, the average absorber eliminates 10 to 15 L of COper 100 g absorbent in a single-chamber system and 18 to 20 L of COin a dual-chamber system. 

Factors affecting efficiency include 

  • the size of the absorber canister (the patient’s tidal volume should be accommodated entirely within the void space of the canister)
  • the size of the absorbent granule (optimal size is 2.5 mm or between 4 and 8 mesh)
  • the presence or absence of channeling (loose packing allowing exhaled gases to bypass absorber granules in the canister).

Q. How do you know when the absorbent has been exhausted? What adverse reactions can occur between volatile anesthetic and COabsorbents?

A pH-sensitive dye added to the granules changes color in the presence of carbonic acid, an intermediary in the COabsorption chemical reaction. The most common dye in the United States is ethyl violet, which is white when fresh and turns violet when the absorbent is exhausted

Q. How can you check the competency of a circle system?

You should close the pop-off valve, occlude the Y-piece, and press the Oflush valve until the pressure is 30 cm H2O. The pressure will not decline if there are no leaks. Then you should open the pop-off valve to ensure that it is in working order. In addition, you should check the function of the unidirectional valves by breathing down each limb individually, making sure that you cannot inhale from the expiratory limb or exhale down the inspiratory limb.

Q. For what reasons should general anaesthesia for elective cases be postponed?


  • Unstable coronary syndromes
    • Recent myocardial infarction 
    • Unstable or severe angina
  • Ischaemia heart disease causing crescendo or unstable angina pectoris
  • Decompensated heart failure - NYHA class IV or new onset 

  • Uncontrolled cardiac arrhythmia
    • Mobitz type II AV block
    • Third degree AV block
    • Symptomatic ventricular arrhythmia 
    • Symptomatic bradycardia 
  • Accelerated or stage III HTN, Hypertensive urgency, Hypertensive emergency 
  • Anaemia. Depends on level of anaemia and proposed surgery – but the ideal would be to restore haemoglobin to normal levels before proceeding.

  • Acute chest infection or upper respiratory tract infection. 
  • Some recommend deferring paediatric elective surgery for 4–6 weeks. Others believe this to be impractical.
  • Inadequately treated asthma or other chronic airways disease. 


  • Acute disorder not related to the surgery.

Systemic and metabolic

  • Acute or recent viraemia (risk of myocarditis).
  • Serious electrolyte abnormality, particularly hyper and hypokalaemia.

1. Miller's anesthesia review 
2. Secrets of anesthesia 
3. Short answer questions in anaesthesia 
4. Morgan and Mikhail's Clinical anaesthesiology
5. Smith and Aitkenhead's Text book of anaesthesia 


Popular posts from this blog

Blood Gas Partition Coefficient

Basic physiology of Neuromuscular junction