General Anesthesia — MCQs

General Anesthesia Indian Medical PG Practice Questions and MCQs

Question 431: A 60-year-old man undergoing an inguinal hernia repair is induced with propofol. Which of the following is most likely to be observed?

A. Hypertension
B. Apnea (Correct Answer)
C. Hyperthermia
D. Prolonged sedation

Explanation: **Explanation:** Propofol (2,6-diisopropylphenol) is the most commonly used intravenous induction agent. Its primary mechanism of action involves the enhancement of GABA-A receptors in the central nervous system. **Why Apnea is the Correct Answer:** Propofol is a potent respiratory depressant. Following an induction dose (1.5–2.5 mg/kg), it frequently causes **transient apnea** (lasting >30 seconds) by decreasing the sensitivity of the medullary respiratory center to carbon dioxide and reducing the tidal volume and respiratory rate. This effect is more pronounced than with other induction agents like thiopentone. **Analysis of Incorrect Options:** * **A. Hypertension:** Propofol typically causes **hypotension**, not hypertension. It reduces systemic vascular resistance (vasodilation) and myocardial contractility, making it the most hemodynamically unstable induction agent among common choices. * **C. Hyperthermia:** Propofol does not cause hyperthermia. In fact, it is the drug of choice for patients susceptible to **Malignant Hyperthermia**, as it is a non-triggering agent. * **D. Prolonged sedation:** Propofol is characterized by a **rapid recovery** profile. Due to its high lipid solubility and rapid redistribution from the brain to peripheral tissues, patients wake up quickly (usually within 5–10 minutes) with minimal "hangover" effect. **High-Yield Clinical Pearls for NEET-PG:** * **Drug of Choice:** For day-care (ambulatory) surgeries due to rapid recovery and anti-emetic properties. * **Pain on Injection:** A common side effect; minimized by using larger veins or pre-treatment with lidocaine. * **PRIS (Propofol Infusion Syndrome):** A rare, fatal complication of long-term high-dose infusion characterized by metabolic acidosis, rhabdomyolysis, and cardiac failure. * **Egg/Soy Allergy:** Use with caution as the emulsion contains egg lecithin and soybean oil.

Question 432: An anesthetic tension in the arterial blood is shown on the graph as a function of time after inhalation. A similar curve for nitrous oxide is also shown. Which of the following best describes the properties of the new anesthetic compared to nitrous oxide?

A. High blood:gas partition coefficient (Correct Answer)
B. Low solubility in the blood
C. Rapid onset of action
D. Low potency

Explanation: ***High blood:gas partition coefficient*** - The slower rise in **FA/FI ratio** (alveolar to inspired concentration) indicates the anesthetic has **high blood solubility**, meaning more drug dissolves in blood before reaching equilibrium. - A **high blood:gas partition coefficient** means the anesthetic is readily taken up by blood, delaying the rise in alveolar concentration compared to nitrous oxide. *Low solubility in the blood* - This would result in a **rapid rise** in FA/FI ratio, similar to or faster than nitrous oxide, which is not shown in the graph. - **Low blood solubility** means less drug dissolves in blood, allowing faster equilibration between alveolar and inspired concentrations. *Rapid onset of action* - The graph shows a **slower equilibration** compared to nitrous oxide, indicating **delayed onset** rather than rapid onset. - **Rapid onset** would be associated with a steep, quick rise in FA/FI ratio, which contradicts the shown curve. *Low potency* - **Potency** is determined by **MAC (Minimum Alveolar Concentration)**, not by the equilibration curve shown in the graph. - The blood:gas partition coefficient and equilibration speed are **independent of potency**, which relates to receptor binding affinity.

Question 433: Which of the following muscle relaxants is free of cardiovascular effects over the entire clinical dose range?

A. Pancuronium
B. Vecuronium (Correct Answer)
C. Atracurium
D. Pipecuronium

Explanation: **Explanation:** The cardiovascular stability of neuromuscular blocking agents (NMBAs) depends on their ability to trigger histamine release or interact with autonomic receptors (muscarinic or nicotinic). **Why Vecuronium is Correct:** Vecuronium is a monoquaternary aminosteroid NMBA known for its **cardiovascular stability**. It does not cause histamine release and has negligible effects on autonomic ganglia or muscarinic receptors. Consequently, it does not cause changes in heart rate or blood pressure, even at doses several times the $ED_{95}$, making it the drug of choice for patients where hemodynamic stability is critical. **Analysis of Incorrect Options:** * **Pancuronium:** This is a long-acting aminosteroid that causes **tachycardia** and hypertension. This is due to its vagolytic effect (blocking $M_2$ receptors in the heart) and its ability to stimulate norepinephrine release from sympathetic nerve endings. * **Atracurium:** This benzylisoquinolone is associated with **histamine release**, especially when administered rapidly or at high doses. This can lead to systemic vasodilation (hypotension) and reflex tachycardia. * **Pipecuronium:** While it is more stable than pancuronium, it can still exhibit mild cardiovascular effects at very high doses, though it is much closer to vecuronium in stability. However, vecuronium remains the classic textbook answer for "free of effects over the entire clinical range." **High-Yield NEET-PG Pearls:** * **Rocuronium:** Also cardiovascularly stable but may cause a slight increase in heart rate. * **Cisatracurium:** The most stable benzylisoquinolone (no histamine release), often used in renal/hepatic failure (Hofmann elimination). * **Mivacurium:** Shortest acting non-depolarizer; significant histamine release. * **Succinylcholine:** Can cause **bradycardia** (especially in children or on second dose) due to muscarinic stimulation.

Question 434: Which of the following statements about Halothane is FALSE?

A. Halothane is a good analgesic agent. (Correct Answer)
B. Halothane sensitizes the heart to catecholamines.
C. Halothane relaxes the bronchi.
D. Halothane causes hepatitis and liver cell necrosis.

Explanation: **Explanation:** Halothane is a potent inhalational anesthetic agent, but it is characterized by a significant clinical limitation: it is a **potent hypnotic but a poor analgesic**. In clinical practice, this means that while halothane can induce unconsciousness, it does not effectively block pain signals. Therefore, it must be supplemented with other analgesic agents (like opioids or nitrous oxide) to ensure a pain-free surgical state. **Analysis of Options:** * **Option A (Correct):** Halothane provides minimal analgesia. This makes the statement "Halothane is a good analgesic" false. * **Option B:** Halothane sensitizes the myocardium to the effects of circulating catecholamines (epinephrine/norepinephrine). This increases the risk of ventricular arrhythmias, especially if exogenous adrenaline is used during surgery. * **Option C:** Halothane is a potent bronchodilator. It is non-irritating to the airways and inhibits bronchial secretions, making it a historically preferred agent for patients with asthma or COPD. * **Option D:** "Halothane Hepatitis" is a well-known complication. It occurs due to the metabolism of halothane into trifluoroacetylated proteins, which can trigger an immune-mediated hepatotoxicity and centrilobular necrosis. **High-Yield Clinical Pearls for NEET-PG:** * **MAC of Halothane:** 0.75% (highly potent). * **Metabolism:** Approximately 20% is metabolized in the liver (highest among common inhalational agents). * **Uterine Effect:** It causes significant uterine relaxation, which can lead to postpartum hemorrhage (PPH) if used in obstetrics. * **Malignant Hyperthermia:** Like all volatile anesthetics, halothane is a known trigger.

Question 435: Which muscle relaxant can be used in a patient with high serum bilirubin of 6.0 mg/dL and serum creatinine of 4.5 mg/dL?

A. Atracurium (Correct Answer)
B. Vecuronium
C. Pancuronium
D. Mivacurium

Explanation: **Explanation:** The correct answer is **Atracurium**. The clinical scenario describes a patient with both hepatic impairment (Bilirubin 6.0 mg/dL) and renal failure (Creatinine 4.5 mg/dL). In such cases, the ideal muscle relaxant is one that does not rely on the liver or kidneys for metabolism or excretion. **Why Atracurium is correct:** Atracurium (and its isomer Cisatracurium) undergoes **Hofmann Elimination**—a unique organ-independent chemical degradation that occurs at physiological pH and temperature. It also undergoes ester hydrolysis by non-specific plasma esterases. Because it does not depend on hepatic or renal function, its duration of action remains predictable even in multi-organ failure. **Why other options are incorrect:** * **Vecuronium:** Primarily undergoes hepatic metabolism and biliary excretion (approx. 40-70%). Its duration is significantly prolonged in patients with liver disease. * **Pancuronium:** Primarily excreted by the kidneys (approx. 80%). It would lead to profound neuromuscular blockade and "recurarization" in a patient with a creatinine of 4.5 mg/dL. * **Mivacurium:** While metabolized by plasma cholinesterase, its clearance is significantly delayed in both liver and renal failure due to decreased enzyme production and altered distribution volumes. **NEET-PG High-Yield Pearls:** * **Hofmann Elimination:** Is a temperature and pH-dependent process. Acidosis and hypothermia *slow down* the elimination, prolonging the drug's effect. * **Laudanosine:** A major metabolite of atracurium. It is a CNS stimulant that can lower the seizure threshold (though rarely clinical at standard doses). * **Drug of Choice:** Cisatracurium is often preferred over Atracurium in clinical practice because it produces less histamine release and less laudanosine. * **Renal Failure:** Avoid Gallamine (100% renal excretion) and Pancuronium.

Question 436: Wooden chest rigidity is seen with which of the following agents?

A. Morphine
B. Fentanyl (Correct Answer)
C. Remifentanyl
D. Pentazocine

Explanation: **Explanation:** **Wooden Chest Syndrome** (also known as Opioid-Induced Muscle Rigidity) is a well-documented phenomenon characterized by intense, generalized muscle stiffness, particularly involving the thoracic and abdominal muscles. **Why Fentanyl is the correct answer:** While several potent opioids can cause this, **Fentanyl** is the most classic and frequently cited agent in medical examinations. The rigidity occurs due to the rapid intravenous administration of high-dose lipophilic opioids. It is mediated by the activation of **mu-opioid receptors** in the central nervous system (specifically the substantia nigra and striatum), which increases efferent motor nerve activity. This leads to decreased chest wall compliance, making manual ventilation extremely difficult or impossible. **Analysis of Incorrect Options:** * **Morphine:** Although a mu-agonist, it is less potent and slower-acting than fentanyl; it rarely causes significant chest wall rigidity compared to synthetic opioids. * **Remifentanil:** While Remifentanil *can* cause rigidity due to its high potency, Fentanyl remains the "textbook" answer for this specific clinical sign in the context of standard anesthesia induction. (Note: In some clinical scenarios, Remifentanil is a potent trigger, but Fentanyl is the primary association for NEET-PG). * **Pentazocine:** This is an opioid agonist-antagonist. It does not possess the potency or the specific mu-receptor profile required to induce wooden chest syndrome. **High-Yield Clinical Pearls for NEET-PG:** * **Management:** The definitive treatment is the administration of a **neuromuscular blocking agent** (e.g., Succinylcholine) to relax the muscles and allow ventilation. **Naloxone** can also reverse it but may also reverse analgesia. * **Prevention:** Administering opioids slowly and using pre-treatment with a small dose of non-depolarizing muscle relaxants can reduce the incidence. * **Associated Agents:** Other synthetic opioids like Sufentanil and Alfentanil are also high-risk triggers.

Question 437: During the second stage of general anesthesia, what is the typical state of the pupil?

A. Constricted
B. Partially dilated (Correct Answer)
C. Normal in size
D. Totally dilated

Explanation: **Explanation:** The stages of anesthesia are described by **Guedel’s Classification**, which tracks the progression of CNS depression. **Stage II (Stage of Delirium/Excitement)** is characterized by a loss of cortical inhibition, leading to a state of sympathetic overactivity. This surge in sympathetic discharge results in physiological responses such as tachycardia, hypertension, irregular breathing, and **pupillary dilation (mydriasis)**. The dilation is typically "partial" because the light reflex remains intact, unlike the paralytic dilation seen in deeper stages. **Analysis of Options:** * **A. Constricted:** This is characteristic of **Stage III, Plane 1** (Surgical Anesthesia). As the patient enters the surgical plane, the sympathetic surge of Stage II subsides, and the pupils become miotic (constricted). * **C. Normal in size:** This is seen in **Stage I** (Analgesia), where the patient is conscious and autonomic reflexes are not yet significantly altered. * **D. Totally dilated:** This occurs in **Stage IV** (Medullary Paralysis/Overdose). Here, the pupils are fixed and dilated due to complete paralysis of the pupillary constrictor muscles, signaling an anesthetic emergency. **NEET-PG High-Yield Pearls:** * **Stage II Danger:** This is the most unstable stage. Risk of laryngospasm, vomiting, and cardiac arrhythmias is highest here. Anesthesiologists aim to pass through this stage as quickly as possible (e.g., using rapid-acting IV agents like Propofol). * **Guedel’s Stages** were originally described using **Diethyl Ether**; they are less distinct with modern IV induction agents but remain a fundamental concept for exams. * **Stage III (Surgical Anesthesia)** is divided into 4 planes; **Plane 2** is generally considered the ideal depth for most surgeries.

Question 438: Which of the following intravenous anesthetic agents' pharmacokinetics does not change significantly with renal and hepatic dysfunction?

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

Explanation: **Explanation:** The correct answer is **Propofol**. This is due to its unique metabolic profile, specifically its **extrahepatic metabolism**. **1. Why Propofol is correct:** Propofol is primarily metabolized in the liver via conjugation to glucuronide and sulfate. However, its clearance rate exceeds hepatic blood flow, indicating significant **extrahepatic metabolism** (primarily in the **lungs** and to a lesser extent, the kidneys). Because of this high clearance rate and multiple metabolic pathways, its pharmacokinetics remain largely unaffected by moderate to severe renal or hepatic dysfunction. While metabolites are excreted by the kidneys, they are pharmacologically inactive. **2. Why the other options are incorrect:** * **Thiopentone:** It is almost entirely dependent on hepatic metabolism (oxidation). In hepatic dysfunction, its metabolism is slowed, leading to prolonged effects. In renal failure, increased free fractions (due to decreased protein binding) can lead to increased sensitivity. * **Etomidate:** It is metabolized by hepatic and plasma esterases. While it is relatively stable, its clearance can be significantly reduced in patients with cirrhosis, leading to a prolonged duration of action. * **Ketamine:** It undergoes extensive hepatic metabolism (N-demethylation) to form norketamine. Hepatic dysfunction significantly impairs its clearance, leading to prolonged sedation and emergence delirium. **3. High-Yield Clinical Pearls for NEET-PG:** * **Context-Sensitive Half-Time:** Propofol has a short context-sensitive half-time, making it the drug of choice for **TIVA (Total Intravenous Anesthesia)**. * **Antiemetic Property:** Propofol is the only induction agent with intrinsic antiemetic properties (at sub-hypnotic doses of 10–20 mg). * **Drug of Choice:** Propofol is preferred for day-care surgeries and neurosurgeries (as it reduces ICP and CMR02). * **Contraindication:** Avoid in patients with egg or soy allergy (due to the lipid emulsion vehicle).

Question 439: Which is the shortest acting muscle relaxant?

A. Pancuronium
B. Atracurium
C. Mivacurium (Correct Answer)
D. Vecuronium

Explanation: **Explanation:** The duration of action of neuromuscular blocking agents (NMBAs) is primarily determined by their metabolism and elimination pathways. **Mivacurium (Option C)** is the correct answer because it is a short-acting, non-depolarizing neuromuscular blocker with a duration of action of approximately **12–20 minutes**. Its short duration is due to its rapid metabolism by **plasma cholinesterase (pseudocholinesterase)**, the same enzyme that metabolizes succinylcholine. This makes it the shortest-acting non-depolarizing muscle relaxant available. **Analysis of Incorrect Options:** * **Pancuronium (Option A):** A long-acting steroid-based NMBA (duration >60 minutes). It is primarily excreted by the kidneys and is known for its vagolytic effect (tachycardia). * **Atracurium (Option B):** An intermediate-acting benzylisoquinolone (duration 30–45 minutes). It undergoes Hofmann elimination and ester hydrolysis, making it safe in renal or hepatic failure. * **Vecuronium (Option D):** An intermediate-acting steroid-based NMBA (duration 30–45 minutes). It is primarily metabolized by the liver and excreted in bile. **High-Yield Clinical Pearls for NEET-PG:** * **Shortest acting overall:** Succinylcholine (Depolarizing, ~5–10 mins). * **Shortest acting non-depolarizing:** Mivacurium. * **Metabolism:** Like succinylcholine, Mivacurium's action is prolonged in patients with **pseudocholinesterase deficiency**. * **Side Effect:** Mivacurium can cause significant **histamine release**, leading to hypotension and flushing if injected rapidly. * **Gantacurium:** A newer ultra-short-acting agent (investigational) that may be even shorter than Mivacurium.

Question 440: Ketamine is contraindicated in all except?

A. Congestive heart failure
B. Uncontrolled hypertension
C. Aortic aneurysm
D. Shock (Correct Answer)

Explanation: **Explanation:** **Ketamine** is a unique dissociative anesthetic agent known for its **sympathomimetic properties**. It acts by inhibiting the reuptake of catecholamines (norepinephrine), leading to an increase in heart rate, cardiac output, and blood pressure. **Why "Shock" is the correct answer:** In patients with **hypovolemic or septic shock**, Ketamine is often the induction agent of choice. Its ability to stimulate the sympathetic nervous system helps maintain hemodynamic stability by preventing the typical drop in blood pressure seen with other induction agents like propofol or thiopentone. (Note: In cases of extreme catecholamine depletion, it can occasionally act as a direct myocardial depressant). **Why the other options are contraindicated:** Because Ketamine increases myocardial oxygen demand and systemic vascular resistance, it is contraindicated in conditions where increased blood pressure or heart rate would be harmful: * **Uncontrolled Hypertension & Aortic Aneurysm:** The rise in blood pressure (pressor effect) can lead to hypertensive crisis or cause an aneurysm to rupture/dissect. * **Congestive Heart Failure (CHF):** The increase in afterload and heart rate can exacerbate heart failure and precipitate acute pulmonary edema. **High-Yield Clinical Pearls for NEET-PG:** * **Mechanism of Action:** Non-competitive antagonist at **NMDA receptors**. * **Airway:** It preserves airway reflexes and causes **bronchodilation** (drug of choice for status asthmaticus). * **Secretions:** It is a potent **sialagogue** (increases salivation); pretreatment with glycopyrrolate is often required. * **CNS:** It increases **Intracranial Pressure (ICP)** and **Intraocular Pressure (IOP)**, making it traditionally contraindicated in head injuries and glaucoma. * **Recovery:** Associated with **emergence delirium/hallucinations**, which can be mitigated by benzodiazepines.

Practice by Chapter

History of Anesthesia

Practice Questions

Preoperative Evaluation

Practice Questions

Pharmacology of Inhalational Anesthetics

Practice Questions

Pharmacology of Intravenous Anesthetics

Practice Questions

Neuromuscular Blocking Agents

Practice Questions

Airway Management

Practice Questions

Endotracheal Intubation

Practice Questions

Difficult Airway Algorithms

Practice Questions

Intraoperative Monitoring

Practice Questions

Depth of Anesthesia Monitoring

Practice Questions

Emergence from Anesthesia

Practice Questions

Postoperative Care

Practice Questions

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