General Anesthesia Practice Questions

Q: Which of the following anesthetic agents have good analgesic property? a) Ketamine b) Nitrous oxide c) Thiopentone d) Propofol e) Midazolam

Ketamine and Nitrous oxide. ***Ketamine and Nitrous oxide*** - **Ketamine** is a dissociative anesthetic with potent **analgesic properties** secondary to its action as an **NMDA receptor antagonist**. - **Nitrous oxide** is an inhalational anesthetic known for its mild to moderate **analgesic effects**, making it useful for sedation and pain relief. *Ketamine only* - While **ketamine** has excellent analgesic properties, this option is incomplete as **nitrous oxide** also contributes significant analgesia among the choices. - Excluding other agents with analgesic properties makes this option less comprehensive than the correct answer. *Ketamine and Propofol* - **Ketamine** possesses strong analgesic effects, but **propofol** is a sedative-hypnotic agent with no significant intrinsic **analgesic properties**. - Propofol provides anesthesia and sedation but typically requires co-administration with opioids for pain control. *Nitrous oxide and Thiopentone* - **Nitrous oxide** provides analgesia, but **thiopentone** (a barbiturate) is primarily an anesthetic and sedative with **no significant analgesic properties**. - Thiopentone can induce unconsciousness rapidly but does not relieve pain. *Midazolam only* - **Midazolam** is a benzodiazepine primarily used for sedation, anxiolysis, and amnesia, with **no intrinsic analgesic properties**. - Its effects can reduce stress and perception of pain, but it does not directly act as an analgesic.

Q: A 70 kg young athlete was planned for surgery. During anesthesia, vecuronium was not available, so repeated doses of succinylcholine were given intermittently up to 640 mg. During recovery, the patient was not able to spontaneously respire and move limbs. What is the cause?

Phase II blockade. **Phase II blockade** - Prolonged administration of **succinylcholine** (> 30-60 minutes or high cumulative doses) can lead to a shift from Phase I to **Phase II block**. - In Phase II block, the neuromuscular junction exhibits characteristics similar to a **nondepolarizing block**, including fade on train-of-four stimulation and post-tetanic potentiation, leading to prolonged paralysis. *Muscle weakness due to repeated fasciculations* - While succinylcholine initially causes **fasciculations** due to depolarization, prolonged paralysis is not directly explained by muscle weakness from repeated fasciculations alone. - Fasciculations are a transient early effect and do not account for the sustained paralysis seen with high-dose, repeated administration. *Undiagnosed muscular dystrophy* - While certain **neuromuscular disorders** can alter response to muscle relaxants, there is no information in the scenario to suggest pre-existing muscular dystrophy. - Administering a large amount of succinylcholine accounts for the prolonged paralysis without needing to invoke an undiagnosed condition. *Pseudocholinesterase deficiency* - A deficiency in **pseudocholinesterase** would lead to a prolonged initial Phase I block with a typical dose of succinylcholine due to impaired metabolism. - However, the scenario describes **repeated doses** adding up to a very high cumulative amount (640 mg), pushing the patient into a Phase II block even if pseudocholinesterase levels were normal.

Q: With regard to ketamine, all of the following are true except:

Has no effect on intracranial pressure. ***Has no effect on intracranial pressure*** - Ketamine typically **increases intracranial pressure (ICP)** due to cerebral vasodilation, making it potentially problematic in patients with pre-existing elevated ICP. - Therefore, the statement that it has no effect on ICP is incorrect, and the question asks for the statement that is *not* true. *It may induce cardiac dysrhythmias in patients receiving tricyclic antidepressants* - Ketamine can increase **sympathetic nervous system activity** by activating the catecholamine system. - When combined with **tricyclic antidepressants (TCAs)**, which block norepinephrine reuptake, this can lead to an exaggerated cardiovascular response and **cardiac dysrhythmias**. *Emergence phenomena are more likely if anticholinergic premedication is used* - **Anticholinergic premedication** (e.g., scopolamine, atropine, glycopyrrolate) generally helps to reduce emergence phenomena by decreasing secretions and potentially mitigating vivid dreams or psychological reactions. - The statement suggests the opposite, which is incorrect; anticholinergic agents are often used precisely to *reduce* these effects. *It is a direct myocardial depressant* - Ketamine has an **intrinsic direct myocardial depressant effect** on isolated heart muscle preparations. - However, this direct effect is usually masked *in vivo* by its powerful **sympathomimetic effects**, which lead to an overall increase in heart rate, blood pressure, and cardiac output. *It has bronchodilator properties* - Ketamine is a **potent bronchodilator**, making it a useful anesthetic agent in patients with **asthma** or **bronchospasm**. - This effect is mediated partly through its sympathetic stimulating properties and direct relaxation of bronchial smooth muscle.

Q: Gas commonly used for rapid induction of anesthesia

Sevoflurane. ***Sevoflurane*** - Sevoflurane has a **low blood:gas partition coefficient**, leading to rapid equilibration between the lungs and blood, and thus rapid induction and emergence from anesthesia. - Its **non-pungent odor** and lack of airway irritation make it particularly suitable for children and adults requiring mask induction. *Nitrous oxide* - While it has a very low blood:gas partition coefficient, it is a **relatively weak anesthetic** and cannot achieve surgical depths of anesthesia on its own. - It is often used as an **adjunct** to other volatile anesthetics to reduce their required dose and speed up induction. *Isoflurane* - Isoflurane has a **higher blood:gas partition coefficient** compared to sevoflurane, resulting in a slower induction and emergence time. - Its **pungent odor** can cause coughing and airway irritation, making it less ideal for mask induction. *Desflurane* - Desflurane has the **lowest blood:gas partition coefficient** among the volatile anesthetics, leading to very rapid induction and emergence. - However, its **irritating effect on the airway** often causes coughing and laryngospasm, making it unsuitable for mask induction, especially in non-premedicated patients.

Q: An induction agent of choice for poor-risk patients with cardiorespiratory disease as well as in situations where preservation of a normal blood pressure is crucial:-

Etomidate. ***Etomidate*** - Etomidate is preferred in patients with **cardiac disease** or **hemodynamic instability** due to its minimal effects on cardiovascular function. - It maintains **cardiovascular stability**, including myocardial contractility and blood pressure, making it ideal for procedures where maintaining a normal blood pressure is crucial. *Ketamine* - Ketamine often causes a **sympathetic stimulating effect**, leading to increases in heart rate and blood pressure, which may be detrimental in such patients. - It is associated with **tachycardia** and **hypertension**, undesirable in a poor-risk patient with cardiorespiratory disease. *Propofol* - Propofol is a potent **vasodilator** and myocardial depressant, which can lead to significant **hypotension**, especially in volume-depleted or critically ill patients. - Its use can result in a dose-dependent decrease in **arterial blood pressure** and **cardiac output**. *Thiopentone* - Thiopentone can cause **myocardial depression** and significant **hypotension**, especially in patients with compromised cardiovascular function. - It leads to a notable decrease in **vascular tone** and venous return, thus lowering blood pressure.

Q: Succinylcholine when given for endotracheal intubation causes all of the following EXCEPT –

Hypokalemia in paraplegic patient. ***Hypokalemia in paraplegic patient*** - Succinylcholine is a **depolarizing neuromuscular blocker** that can cause a significant efflux of **potassium from cells**, leading to **transient hyperkalemia**, particularly in patients with muscle denervation (e.g., paraplegia, burns, crush injuries). - Therefore, it causes **hyperkalemia**, not hypokalemia, in predisposed patients. *Prolonged apnea* - **Prolonged apnea** can occur if a patient has atypical pseudocholinesterase, leading to a delayed metabolism of succinylcholine. - This enzyme deficiency causes **succinylcholine to remain active** for a longer duration, resulting in extended paralysis and respiratory depression. *Raised intraocular pressure* - Succinylcholine causes **contraction of extraocular muscles**, leading to an increase in **intraocular pressure**. - This effect is a concern in patients with **open globe injuries** or acute **narrow-angle glaucoma**. *Bradycardia* - Succinylcholine can stimulate **muscarinic receptors** at the sinoatrial node, leading to a **decrease in heart rate** (bradycardia). - This effect is more common with **repeated doses** or in **pediatric patients**.

Q: Why 100% oxygen has to be given to a patient after recovering from N2O anesthesia?

Diffusion hypoxia. ***Diffusion hypoxia*** - Upon discontinuation of N2O, its rapid diffusion out of the blood into the **alveoli** can dilute the partial pressures of **oxygen** and **carbon dioxide**, leading to hypoxemia and hypercapnia. - Administering 100% oxygen prevents this, ensuring adequate oxygenation while N2O is exhaled. *Second gas effect* - This phenomenon refers to the rapid uptake of a highly soluble anesthetic (like N2O) from the alveoli, which then concentrates the inspired partial pressure of a co-administered less soluble anesthetic, speeding its induction. - This effect is significant during the **induction phase** of anesthesia, not recovery. *Bronchoconstriction* - This is the narrowing of the airways, which can be caused by various factors like allergies, asthma, or irritants, but is not a direct consequence of recovering from N2O anesthesia or a reason for 100% oxygen administration. - While patients with **reactive airway disease** might experience bronchoconstriction under anesthesia, it is not specifically linked to N2O recovery for the general population. *Atelectasis* - This is the collapse of lung tissue, which can occur during or after surgery due to conditions like hypoventilation, airway obstruction, or pressure on the lungs. - Administering 100% oxygen is not used primarily to prevent atelectasis immediately after N2O cessation, although good ventilation and lung recruitment maneuvers are important in preventing it generally.

Q: Among the following anesthetic agents, portal vein flow is maximally reduced by:

Halothane. ***Halothane*** - **Halothane** causes the most significant reduction in **portal vein blood flow** due to its potent direct **myocardial depression** and systemic vasodilation, leading to a decrease in **hepatic perfusion pressure**. - Its effects can significantly compromise liver oxygen supply, particularly in patients with pre-existing hepatic dysfunction, making it less favorable for liver surgery compared to newer agents. *Isoflurane* - While **isoflurane** can reduce **portal vein flow**, it tends to maintain overall **hepatic oxygen delivery** better than halothane due to its favorable effect on the **hepatic arterial buffer response**. - It causes less profound **myocardial depression** and may maintain a more stable **hepatic blood flow** compared to halothane. *Ether* - **Ether** is an older anesthetic agent that is rarely used in modern practice due to its flammability and slower induction/recovery times. - Its effects on **portal vein flow** are less pronounced compared to halothane, and it generally maintains **hepatic blood flow** more effectively. *Enflurane* - **Enflurane** also causes **dose-dependent reductions** in **portal vein flow**, but generally less severely than halothane. - It can cause **renal toxicity** due to fluoride metabolites and is generally less favored than isoflurane or sevoflurane for maintaining optimal organ perfusion.

Q: Effect of Propofol on coagulation is?

No effect. ***No effect*** - Propofol is generally considered to have **no direct significant effect** on the coagulation cascade or platelet function in healthy individuals or during typical surgical procedures. - While some studies have explored potential minor antiplatelet effects in specific contexts or with very high doses, these are not clinically significant under normal usage and are not considered a primary action of the drug. *Inhibits platelet function* - While some in vitro studies have suggested a potential for propofol to **inhibit platelet aggregation**, these effects are not consistently observed in vivo at clinically relevant concentrations and are not considered a major pharmacological action. - Other medications, such as **aspirin** or **clopidogrel**, are specifically known for their antiplatelet effects, which are much more potent and clinically significant than any purported action of propofol. *Inhibits coagulation cascade* - Propofol does not directly interfere with the **coagulation cascade factors** (e.g., factors II, VII, IX, X) or their synthesis. - Drugs like **heparin** or **warfarin** are known inhibitors of the coagulation cascade, acting through different mechanisms. *Activates coagulation cascade* - There is no evidence to suggest that propofol causes the **activation of the coagulation cascade**. - In fact, conditions that would activate coagulation are usually independent of propofol administration, such as **trauma** or underlying **prothrombotic states**.

Q: All statements regarding ketamine are true except –

Raised ICT do not respond to CO2 level. ***Raised ICT do not respond to CO2 level*** - While ketamine generally **increases intracranial pressure (ICP)**, the statement that it *does not respond to CO2 levels* is incorrect. - Changes in arterial CO2 levels directly influence cerebral blood flow and, consequently, ICP, regardless of ketamine administration. Hyperventilation to lower PCO2 is still used to reduce ICP, even if ketamine is used. *Psychomimetic emergence* - **Psychomimetic emergence phenomena** (e.g., vivid dreams, hallucinations, delirium) are a well-known side effect of ketamine, particularly in adults. - This effect is due to ketamine's interaction with the **NMDA receptor** and other neurotransmitter systems. *May be arrhythmogenic* - Ketamine can cause **tachycardia** and **hypertension** due to sympathetic nervous system stimulation, which may lead to or exacerbate arrhythmias, especially in patients with pre-existing cardiac conditions. - Although it has a direct myocardial depressant effect *in vitro*, its *in vivo* effects are usually dominated by **sympathetic stimulation**, which can be arrhythmogenic. *Vasodilator and negative inotropic effect* - While ketamine has a direct **vasodilatory** and **negative inotropic effect** on cardiac muscle *in vitro* or in isolated heart preparations, these actions are typically overridden *in vivo* by its potent **sympathetic stimulating effects**. - *In vivo*, the net effect is usually **increased heart rate, blood pressure, and cardiac output**, due to catecholamine release and reuptake inhibition.

Question 1

Which of the following anesthetic agents have good analgesic property? a) Ketamine b) Nitrous oxide c) Thiopentone d) Propofol e) Midazolam

Accepted Answer

Ketamine and Nitrous oxide

Answer

Ketamine only

Answer

Nitrous oxide and Thiopentone

Answer

Ketamine and Propofol

Answer

Midazolam only

Question 2

A 70 kg young athlete was planned for surgery. During anesthesia, vecuronium was not available, so repeated doses of succinylcholine were given intermittently up to 640 mg. During recovery, the patient was not able to spontaneously respire and move limbs. What is the cause?

Accepted Answer

Phase II blockade

Answer

Muscle weakness due to repeated fasciculations

Answer

Undiagnosed muscular dystrophy

Answer

Pseudocholinesterase deficiency

Question 3

With regard to ketamine, all of the following are true except:

Accepted Answer

Has no effect on intracranial pressure

Answer

It may induce cardiac dysrhythmias in patients receiving tricyclic antidepressants

Answer

Emergence phenomena are more likely if anticholinergic premedication is used

Answer

It is a direct myocardial depressant

Answer

It has bronchodilator properties

Question 4

Gas commonly used for rapid induction of anesthesia

Accepted Answer

Sevoflurane

Answer

Nitrous oxide

Answer

Isoflurane

Answer

Desflurane

Question 5

An induction agent of choice for poor-risk patients with cardiorespiratory disease as well as in situations where preservation of a normal blood pressure is crucial:-

Accepted Answer

Etomidate

Answer

Ketamine

Answer

Propofol

Answer

Thiopentone

Question 6

Succinylcholine when given for endotracheal intubation causes all of the following EXCEPT –

Accepted Answer

Hypokalemia in paraplegic patient

Answer

Prolonged apnea

Answer

Raised intraocular pressure

Answer

Bradycardia

Question 7

Why 100% oxygen has to be given to a patient after recovering from N2O anesthesia?

Accepted Answer

Diffusion hypoxia

Answer

Second gas effect

Answer

Bronchoconstriction

Answer

Atelectasis

Question 8

Among the following anesthetic agents, portal vein flow is maximally reduced by:

Accepted Answer

Halothane

Answer

Isoflurane

Answer

Ether

Answer

Enflurane

Question 9

Effect of Propofol on coagulation is?

Accepted Answer

No effect

Answer

Inhibits platelet function

Answer

Inhibits coagulation cascade

Answer

Activates coagulation cascade

Question 10

All statements regarding ketamine are true except –

Accepted Answer

Raised ICT do not respond to CO2 level

Answer

Psychomimetic emergence

Answer

May be arrhythmogenic

Answer

Vasodilator and negative inotropic effect

General Anesthesia — MCQs

General Anesthesia — MCQs

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