General Anesthesia — MCQs

General Anesthesia Indian Medical PG Practice Questions and MCQs

Question 281: Hypotension is caused by all the following anesthetic agents except:

A. Halothane
B. Propofol
C. Ketamine (Correct Answer)
D. Thiopentone

Explanation: **Explanation:** The correct answer is **Ketamine**. This question tests the knowledge of the hemodynamic profiles of common anesthetic agents. **1. Why Ketamine is correct:** Ketamine is a unique "dissociative" anesthetic that acts as a **sympathomimetic**. It inhibits the neuronal reuptake of catecholamines (norepinephrine), leading to an increase in heart rate, cardiac output, and arterial blood pressure. This makes it the induction agent of choice for patients in **hypovolemic or septic shock**. *Note:* While Ketamine is a direct myocardial depressant, its indirect sympathetic stimulation usually overrides this effect in healthy individuals. **2. Why the other options are incorrect:** * **Propofol:** Known for causing the most significant drop in blood pressure among induction agents. it causes profound vasodilation (decreased systemic vascular resistance) and suppresses myocardial contractility. * **Thiopentone:** A barbiturate that causes hypotension primarily through peripheral venodilation (increasing venous capacitance) and a mild direct negative inotropic effect. * **Halothane:** A volatile anesthetic that causes a dose-dependent decrease in arterial pressure, primarily by **direct myocardial depression** and interference with calcium mobilization. **Clinical Pearls for NEET-PG:** * **Agent of choice in Shock:** Ketamine. * **Agent of choice in Day-care surgery:** Propofol (due to rapid recovery). * **Agent of choice in Head Injury:** Propofol or Thiopentone (they decrease ICP). **Avoid Ketamine** as it traditionally increases ICP (though this is currently debated). * **Halothane** sensitizes the myocardium to catecholamines, increasing the risk of arrhythmias.

Question 282: A 30-year-old man is scheduled for a laparoscopic cholecystectomy for biliary colic. He reports a family history of prolonged paralysis during general anesthesia. Which of the following medications should be avoided during his procedure?

A. Succinylcholine (Correct Answer)
B. Vecuronium
C. Pancuronium
D. Etomidate

Explanation: ### Explanation The correct answer is **Succinylcholine (Option A)**. **1. Why Succinylcholine is the Correct Answer:** The patient’s family history of "prolonged paralysis" strongly suggests **Pseudocholinesterase Deficiency** (also known as Butyrylcholinesterase deficiency). Succinylcholine is a depolarizing neuromuscular blocker that is normally rapidly hydrolyzed by the enzyme pseudocholinesterase, resulting in a short duration of action (5–10 minutes). In patients with a genetic deficiency or atypical form of this enzyme, succinylcholine cannot be metabolized efficiently, leading to prolonged neuromuscular blockade and respiratory paralysis lasting several hours. **2. Why the Other Options are Incorrect:** * **Vecuronium (B) and Pancuronium (C):** These are non-depolarizing neuromuscular blockers. While their action is reversed by Sugammadex or Neostigmine, they are primarily metabolized by the liver or excreted by the kidneys, not by pseudocholinesterase. They do not cause the specific "prolonged paralysis" associated with this genetic condition. * **Etomidate (D):** This is an intravenous induction agent. Its primary side effect is adrenal suppression (inhibition of 11-beta-hydroxylase); it has no effect on neuromuscular transmission or pseudocholinesterase levels. **3. NEET-PG High-Yield Pearls:** * **Inheritance:** Pseudocholinesterase deficiency is typically **Autosomal Recessive**. * **Diagnosis:** Confirmed by the **Dibucaine Number**. Dibucaine inhibits normal enzyme activity by 80%, but atypical enzyme by only 20%. A low Dibucaine number indicates the presence of atypical enzyme. * **Management:** If prolonged paralysis occurs, the patient must remain sedated and on **mechanical ventilation** until the block wears off spontaneously. Fresh Frozen Plasma (FFP) can theoretically provide the enzyme but is rarely used due to infection risks. * **Mnemonic:** Succinylcholine is the *only* muscle relaxant metabolized by pseudocholinesterase (along with the ester local anesthetic, Procaine).

Question 283: Which of the following anesthetic agents increases the requirement of curare?

A. Ketamine (Correct Answer)
B. Althesin
C. Nitrous oxide
D. Histotoxic hypoxia

Explanation: **Explanation:** The correct answer is **Ketamine**. **1. Why Ketamine is Correct:** Most general anesthetic agents (like volatile inhalational agents) **potentiate** the action of neuromuscular blocking agents (NMBAs) like curare (d-Tubocurarine). However, **Ketamine** is a notable exception. Ketamine increases the requirement of curare because it inhibits plasma cholinesterase and possesses sympathomimetic properties that can interfere with the neuromuscular blockade. Clinically, it has been observed that patients receiving ketamine may require higher doses of non-depolarizing muscle relaxants to achieve the same level of paralysis compared to other induction agents. **2. Why Other Options are Incorrect:** * **Althesin:** This was an intravenous anesthetic (a mixture of alphaxalone and alphadolone) that tended to **potentiate** the effects of non-depolarizing muscle relaxants, thereby decreasing the requirement. * **Nitrous Oxide (N₂O):** While N₂O has minimal effects on the neuromuscular junction compared to volatile agents (like Isoflurane), it does not increase the requirement for curare. * **Histotoxic Hypoxia:** This refers to the inability of cells to use oxygen (e.g., cyanide poisoning). It does not have a direct pharmacological interaction that increases the dose requirement of curare. **3. Clinical Pearls for NEET-PG:** * **Potentiators of NMBAs:** Volatile anesthetics (Desflurane > Sevoflurane > Isoflurane > Halothane), Aminoglycosides (e.g., Neomycin, Gentamicin), Magnesium, and Hypokalemia all **enhance** the block (decrease requirement). * **Ketamine Profile:** It is a "dissociative anesthetic" acting on NMDA receptors. It is the induction agent of choice for **hypovolemic shock** and **bronchial asthma** due to its sympathomimetic and bronchodilatory effects. * **Curare (d-Tubocurarine):** It is a prototype non-depolarizing NMBA known for causing significant **histamine release**, leading to hypotension and bronchospasm.

Question 284: If ketamine is the only agent used in reducing a dislocated shoulder, what are its actions?

A. Hypotension
B. Respiratory depression
C. Analgesia (Correct Answer)
D. Bradycardia

Explanation: **Explanation:** Ketamine is a unique anesthetic agent that produces **dissociative anesthesia**, characterized by a functional dissociation between the thalamocortical and limbic systems. **1. Why Analgesia is Correct:** Ketamine is a potent **NMDA receptor antagonist**. Even at sub-anesthetic doses, it provides profound **analgesia** (pain relief), making it an ideal choice for painful short procedures like reducing a dislocated shoulder. Unlike most other induction agents, it maintains protective airway reflexes and spontaneous respiration while eliminating pain. **2. Why Other Options are Incorrect:** * **Hypotension & Bradycardia (A & D):** Ketamine is a **sympathomimetic** agent. It inhibits the reuptake of catecholamines (norepinephrine), leading to an **increase** in heart rate (tachycardia) and blood pressure (hypertension). It is the induction agent of choice for patients in hemorrhagic or septic shock. * **Respiratory Depression (B):** One of ketamine’s primary advantages is that it causes **minimal respiratory depression**. It acts as a potent bronchodilator (useful in asthmatics) and generally preserves the patient's drive to breathe. **High-Yield Clinical Pearls for NEET-PG:** * **Emergence Delirium:** A common side effect characterized by hallucinations and vivid dreams; it can be prevented by co-administering **Benzodiazepines** (e.g., Midazolam). * **Secretions:** Ketamine increases salivation (sialagogue effect); **Atropine or Glycopyrrolate** is often given to counteract this. * **Contraindications:** Avoid in patients with raised Intracranial Pressure (ICP), Intraocular Pressure (IOP), or severe Ischemic Heart Disease. * **Status Asthmaticus:** Ketamine is the induction agent of choice due to its bronchodilatory properties.

Question 285: Which anesthetic agent is associated with "dissociative anesthesia"?

A. Propofol
B. Ketamine (Correct Answer)
C. Thiopental
D. Halothane

Explanation: **Explanation:** **Ketamine** is the classic agent associated with **dissociative anesthesia**. This unique state is characterized by a functional and electrophysiological dissociation between the thalamocortical and limbic systems. Clinically, the patient appears to be in a trance-like state—eyes may remain open with a slow nystagmic gaze, but they are unconscious and insensitive to pain (profound analgesia). This effect is primarily mediated by the non-competitive antagonism of **NMDA (N-methyl-D-aspartate) receptors**. **Analysis of Incorrect Options:** * **Propofol (A):** An intravenous sedative-hypnotic that acts via GABA-A receptors. It causes global CNS depression rather than dissociation and is known for rapid recovery and anti-emetic properties. * **Thiopental (C):** An ultra-short-acting barbiturate that also acts on GABA-A receptors. It provides hypnosis but lacks analgesic properties (it is actually considered "anti-analgesic"). * **Halothane (D):** A volatile inhalational anesthetic. While it produces unconsciousness, it does not produce the specific "disconnected" state characteristic of dissociation. **High-Yield Clinical Pearls for NEET-PG:** * **Sympathetic Stimulation:** Unlike most anesthetics, Ketamine increases HR, BP, and CO (useful in hypovolemic shock). * **Airway:** It preserves airway reflexes and causes bronchodilation (drug of choice for asthmatics). * **Side Effects:** Associated with **emergence delirium/hallucinations** (minimized by benzodiazepines) and increased intracranial/intraocular pressure. * **Analgesia:** It provides profound somatic analgesia but poor visceral analgesia.

Question 286: Which property is most important in determining the induction of a general anaesthetic agent?

A. Alveolar exchange
B. Pulmonary ventilation
C. Solubility of anaesthetic in blood (Correct Answer)
D. Solubility of anaesthetic in tissue

Explanation: ### Explanation The speed of induction of an inhalational anesthetic is primarily determined by the **Blood-Gas Partition Coefficient (Solubility)**. **1. Why Solubility in Blood is Correct:** For an anesthetic to reach the brain and exert its effect, it must first build up a partial pressure in the alveoli ($P_A$) and then in the arterial blood ($P_a$). * **Low Solubility (e.g., Desflurane, Nitrous Oxide):** The blood acts as a small reservoir. It saturates quickly, allowing the partial pressure to rise rapidly in the alveoli and brain, leading to **fast induction**. * **High Solubility (e.g., Halothane, Ether):** The blood acts as a large "sponge," soaking up the gas. This prevents the partial pressure from rising quickly, leading to **slow induction**. **2. Why Other Options are Incorrect:** * **Alveolar Exchange & Pulmonary Ventilation:** While an increase in ventilation can speed up induction (especially for soluble agents), they are physiological variables, not intrinsic properties of the anesthetic agent itself. * **Solubility in Tissue:** This primarily affects the **recovery (emergence)** phase rather than induction. High lipid solubility (Oil-Gas partition coefficient) determines the **potency** (MAC) of the drug, not the speed of onset. **3. High-Yield Clinical Pearls for NEET-PG:** * **Inverse Relationship:** Speed of induction is inversely proportional to blood solubility. * **Potency vs. Speed:** Potency is determined by the **Oil:Gas** coefficient (Meyer-Overton Hypothesis); Speed of induction is determined by the **Blood:Gas** coefficient. * **Second Gas Effect:** Nitrous oxide (low solubility, high concentration) can accelerate the uptake of a companion volatile anesthetic. * **Order of Solubility (Low to High):** Desflurane < Sevoflurane < Isoflurane < Halothane. (Desflurane is the fastest; Halothane is the slowest among these).

Question 287: Which of the following is a feature of depolarizing blockade?

A. Tetanic fade
B. Post-tetanic potentiation
C. Progression to dual blockade (Correct Answer)
D. Antagonism by anticholinesterases

Explanation: **Explanation:** Neuromuscular blockers are classified into **Depolarizing (Phase I)** and **Non-depolarizing (Phase II)** agents. Succinylcholine is the only clinically used depolarizing agent. **Why Option C is Correct:** A **Phase I (Depolarizing) block** occurs when succinylcholine mimics acetylcholine, causing persistent depolarization of the motor endplate. However, with prolonged exposure or high doses (typically >2-4 mg/kg), the block transitions into a **Phase II block (Dual Blockade)**. In this state, the membrane repolarizes but becomes desensitized to acetylcholine, clinically resembling a non-depolarizing block. **Why the other options are incorrect:** * **A & B (Tetanic fade and Post-tetanic potentiation):** These are classic features of **Non-depolarizing** blocks. In a pure Phase I depolarizing block, there is no fade; the muscle response is diminished but remains sustained (constant) during tetanic stimulation. * **D (Antagonism by anticholinesterases):** Anticholinesterases (like Neostigmine) increase acetylcholine levels. In a Phase I block, this actually **potentiates (worsens)** the blockade because it provides more substrate for depolarization. Neostigmine only antagonizes non-depolarizing blocks or a well-established Phase II block. **High-Yield NEET-PG Pearls:** * **Succinylcholine** is the drug of choice for Rapid Sequence Induction (RSI) due to its rapid onset and short duration. * **Fasciculations:** A hallmark of Phase I block, caused by the initial disorganized contraction of muscle units. * **Pseudocholinesterase:** The enzyme responsible for succinylcholine metabolism. Deficiency leads to prolonged apnea. * **Train-of-Four (TOF) Ratio:** In Phase I, the ratio is >0.7 (no fade); in Phase II/Non-depolarizing, the ratio is <0.7 (fade present).

Question 288: What is the recommended dose of Ketamine?

A. 0.5 mg/Kg IM
B. 2 mg/kg IV (Correct Answer)
C. 5 mg/kg IV
D. 10 mg/kg IM

Explanation: **Explanation:** Ketamine is a unique intravenous anesthetic agent that produces **dissociative anesthesia** by acting primarily as an antagonist at the **NMDA (N-methyl-D-aspartate) receptors**. **1. Why Option B is Correct:** The standard induction dose for Ketamine is **1–2 mg/kg IV**. At this dose, it produces rapid onset of anesthesia (within 30–60 seconds) and provides profound analgesia. It is the induction agent of choice in patients with hemodynamic instability or bronchial asthma due to its sympathomimetic and bronchodilatory properties. **2. Analysis of Incorrect Options:** * **Option A (0.5 mg/kg IM):** This dose is too low for induction via any route. Sub-anesthetic doses (0.1–0.5 mg/kg) are typically used for "pre-emptive analgesia" or chronic pain management. * **Option C (5 mg/kg IV):** This is an overdose for intravenous induction and may lead to prolonged recovery and increased risk of side effects. * **Option D (10 mg/kg IM):** While the IM induction dose of Ketamine is **4–10 mg/kg**, 10 mg/kg is the upper limit. In the context of NEET-PG, if both IV and IM doses are presented, the standard IV induction dose (2 mg/kg) is the more frequently tested and clinically standard benchmark. **High-Yield Clinical Pearls for NEET-PG:** * **Dissociative Anesthesia:** Characterized by a "trance-like" state where the eyes remain open with a slow nystagmic gaze. * **Hemodynamics:** Unlike other induction agents, Ketamine **increases** HR, BP, and CO (due to indirect sympathetic stimulation). * **Reflexes:** Pharyngeal and laryngeal reflexes are usually maintained. * **Contraindications:** Avoid in patients with raised Intracranial Pressure (ICP) or Intraocular Pressure (IOP), and in patients with Ischemic Heart Disease (due to increased myocardial oxygen demand). * **Emergence Delirium:** A common side effect (hallucinations/vivid dreams) which can be prevented by co-administering **Benzodiazepines** (e.g., Midazolam).

Question 289: The incidence of unpleasant dreams associated with emergence from ketamine anaesthesia can be reduced by the administration of what?

A. Atropine
B. Scopolamine
C. Physostigmine
D. Diazepam (Correct Answer)

Explanation: ### Explanation **Correct Answer: D. Diazepam** **Mechanism and Rationale:** Ketamine is a dissociative anesthetic that acts primarily as an NMDA receptor antagonist. A major side effect during the recovery phase is **Emergence Delirium**, characterized by vivid dreams, hallucinations, and psychomotor agitation. This occurs due to the depression of sensory association areas in the brain while the limbic system remains active. **Benzodiazepines**, specifically **Diazepam** or Midazolam, are the gold standard for preventing or mitigating these unpleasant dreams. They provide antegrade amnesia and exert a sedative effect on the limbic system, "smoothing out" the emergence profile. Administering a benzodiazepine toward the end of the procedure or as a premedication significantly reduces the incidence of these phenomena. **Analysis of Incorrect Options:** * **A. Atropine:** An anticholinergic used to reduce secretions (antisialagogue). However, it can cross the blood-brain barrier and potentially *worsen* postoperative delirium or "Central Anticholinergic Syndrome." * **B. Scopolamine:** Another anticholinergic that crosses the blood-brain barrier. It is known to cause significant sedation and amnesia but is more likely to *increase* the incidence of hallucinations and confusion in the elderly or when combined with ketamine. * **C. Physostigmine:** This is an acetylcholinesterase inhibitor that crosses the blood-brain barrier. It is used as an *antidote* to treat Central Anticholinergic Syndrome, not to prevent ketamine-induced dreams. **High-Yield Clinical Pearls for NEET-PG:** * **Ketamine "Stun" Dose:** Low-dose ketamine (0.1–0.5 mg/kg) provides excellent analgesia without significant respiratory depression. * **Contraindications:** Ketamine should be avoided in patients with **increased Intracranial Pressure (ICP)**, **increased Intraocular Pressure (IOP)**, and severe **Ischemic Heart Disease** (due to sympathetic stimulation). * **The "Dissociative" State:** Characterized by eyes remaining open with a slow nystagmic gaze (catalepsy). * **Drug of Choice:** Ketamine is the induction agent of choice for **hypovolemic shock** and **status asthmaticus**.

Question 290: Which of the following agents is known to cause pain on injection?

A. Ketamine
B. Methohexitone
C. Di-isopropyl Alcohol
D. Thiopentone (Correct Answer)

Explanation: **Explanation:** Pain on injection is a common side effect of several intravenous anesthetic agents, primarily due to the chemical nature of the drug or its solvent. **1. Why Thiopentone is the correct answer:** Thiopentone Sodium is a highly alkaline solution (pH 10.5). When injected into smaller veins, this high alkalinity causes significant chemical irritation to the vascular endothelium, resulting in **pain on injection**. If accidentally injected intra-arterially, it can lead to severe vasospasm and gangrene due to crystal formation. **2. Analysis of Incorrect Options:** * **Ketamine (A):** Ketamine is generally non-irritating to the veins and is not typically associated with pain on injection. It can be administered intravenously or intramuscularly. * **Methohexitone (B):** While Methohexitone is an oxybarbiturate, it is less commonly associated with significant injection pain compared to Thiopentone or Propofol. Its primary side effects are excitatory phenomena like hiccups and myoclonus. * **Di-isopropyl Alcohol (C):** This is a distractor. **Propofol** is chemically known as 2,6-diisopropylphenol. While Propofol is notorious for causing pain on injection (due to the activation of the kinin cascade), "Di-isopropyl Alcohol" is not the standard anesthetic agent used in clinical practice. **3. Clinical Pearls for NEET-PG:** * **Most common agents causing pain on injection:** Propofol (most common), Etomidate, Thiopentone, and Diazepam (due to propylene glycol solvent). * **Prevention:** Pain from Propofol/Thiopentone can be reduced by using larger veins (antecubital fossa) or pre-treatment with **Lidocaine**. * **Thiopentone Storage:** It is stored as a yellow powder under nitrogen to prevent reaction with atmospheric $CO_2$. * **Contraindication:** Thiopentone is strictly contraindicated in **Porphyria** (induces ALA synthetase).

Practice by Chapter

History of Anesthesia

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Preoperative Evaluation

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Pharmacology of Inhalational Anesthetics

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Pharmacology of Intravenous Anesthetics

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Neuromuscular Blocking Agents

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Airway Management

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Endotracheal Intubation

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Difficult Airway Algorithms

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Intraoperative Monitoring

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Depth of Anesthesia Monitoring

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Emergence from Anesthesia

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Postoperative Care

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