Complications in Anesthesia — MCQs

Complications in Anesthesia Indian Medical PG Practice Questions and MCQs

Question 141: Which anesthetic agent is known to cause bradycardia?

A. Gallamine
B. Vecuronium
C. Ketamine
D. Morphine (Correct Answer)

Explanation: **Explanation:** **Correct Option: D. Morphine** Morphine, a natural opioid agonist, primarily causes bradycardia through two mechanisms: 1. **Increased Vagal Tone:** It stimulates the vagal nucleus in the medulla, leading to increased parasympathetic outflow to the heart. 2. **Histamine Release:** Morphine triggers the release of histamine from mast cells, which can cause peripheral vasodilation. While this often leads to compensatory tachycardia, the direct central vagotonic effect usually predominates, resulting in a decrease in heart rate. **Analysis of Incorrect Options:** * **A. Gallamine:** This is a long-acting non-depolarizing neuromuscular blocker that is notorious for causing **tachycardia**. It acts as a potent muscarinic antagonist (vagolytic) at the M2 receptors of the SA node. * **B. Vecuronium:** This is an intermediate-acting neuromuscular blocker known for its **cardiovascular stability**. It lacks significant vagolytic or histamine-releasing properties, making it "heart-friendly." * **C. Ketamine:** This dissociative anesthetic is a **sympathomimetic**. It inhibits the reuptake of norepinephrine and stimulates the sympathetic nervous system, leading to an increase in heart rate, blood pressure, and cardiac output. **High-Yield Clinical Pearls for NEET-PG:** * **Opioids and Heart Rate:** Among opioids, **Fentanyl, Sufentanil, and Remifentanil** are even more potent than Morphine in causing profound bradycardia. **Meperidine (Pethidine)** is the exception; it has an atropine-like structure and can cause tachycardia. * **Drug of Choice for Bradycardia:** Atropine is the first-line management for symptomatic drug-induced bradycardia. * **Ketamine Exception:** In patients with depleted catecholamines (e.g., severe chronic shock), Ketamine can actually act as a myocardial depressant.

Question 142: Which of the following drugs is most effective in the management of malignant hyperthermia?

A. Baclofen
B. Dantrolene (Correct Answer)
C. Succinylcholine
D. Vecuronium

Explanation: **Explanation:** **Malignant Hyperthermia (MH)** is a life-threatening hypermetabolic crisis triggered in genetically susceptible individuals by volatile anesthetics (e.g., Halothane, Sevoflurane) or depolarizing muscle relaxants (Succinylcholine). **Why Dantrolene is the Correct Answer:** Dantrolene sodium is the **gold standard** and the only specific antidote for MH. It acts as a muscle relaxant by binding to the **Ryanodine Receptor 1 (RyR1)** on the sarcoplasmic reticulum. This action inhibits the excessive release of calcium ions into the sarcoplasm, effectively halting the uncontrolled muscle contractions and hypermetabolic state that characterize the condition. **Analysis of Incorrect Options:** * **Baclofen (A):** A GABA-B receptor agonist used for chronic spasticity (e.g., multiple sclerosis). It acts centrally on the spinal cord and has no role in the peripheral calcium-release mechanism of MH. * **Succinylcholine (C):** A depolarizing neuromuscular blocker that is actually a **potent trigger** for MH. Administering it would worsen the crisis. * **Vecuronium (D):** A non-depolarizing neuromuscular blocker. While "safe" to use in MH-susceptible patients, it is not a treatment for the crisis itself. **High-Yield Clinical Pearls for NEET-PG:** * **Earliest Sign:** Increase in **End-Tidal CO₂ (ETCO₂)** despite increased ventilation. * **Late Sign:** Hyperthermia (can rise 1°C every 5 minutes). * **Genetics:** Autosomal dominant inheritance; associated with mutations in the **RYR1 gene** (most common) or CACNA1S gene. * **Dose of Dantrolene:** 2.5 mg/kg IV bolus, repeated every 5–10 minutes until symptoms subside (max dose usually 10 mg/kg). * **Associated Conditions:** Central Core Disease and King-Denborough Syndrome.

Question 143: High risk of post-dural puncture headache is seen with which type of needle?

A. Spinal needle
B. Epidural needle (Correct Answer)
C. Both spinal and epidural needles
D. Neither spinal nor epidural needles

Explanation: ### Explanation The correct answer is **B. Epidural needle**. **1. Why Epidural Needle is the Correct Answer:** Post-dural puncture headache (PDPH) is caused by the leakage of cerebrospinal fluid (CSF) through a hole in the dura mater, leading to low intracranial pressure. The risk of PDPH is directly proportional to the **gauge (size)** of the needle used. * **Epidural needles** (e.g., Tuohy needles) are significantly thicker, typically **16–18 Gauge**. * If an accidental dural puncture (ADP) occurs during an epidural procedure (known as a "wet tap"), the resulting hole is large, leading to a high rate of PDPH (approximately **70–80%**). **2. Analysis of Incorrect Options:** * **A. Spinal needle:** Modern spinal anesthesia uses very thin needles (**25–27 Gauge**) with specialized tips (e.g., Whitacre or Sprotte). The incidence of PDPH with these needles is much lower (typically **<1–3%**). * **C & D:** These are incorrect because the risk is specifically associated with the diameter and design of the needle used; it is not equal between the two. **3. Clinical Pearls for NEET-PG:** * **Needle Tip Design:** Non-cutting, pencil-point needles (e.g., **Whitacre, Sprotte**) have a significantly lower risk of PDPH compared to cutting-edge needles (e.g., **Quincke**). * **Clinical Presentation:** PDPH is classically **postural** (worsens on sitting/standing, relieved by lying flat) and usually appears within 48–72 hours. * **Management:** Conservative treatment includes bed rest, hydration, and caffeine. The **Gold Standard** treatment for persistent/severe PDPH is an **Autologous Epidural Blood Patch**. * **Orientation:** If using a cutting needle, inserting the bevel parallel to the longitudinal dural fibers reduces the risk of PDPH.

Question 144: An 85-year-old man with carcinoma of the bronchus received general anesthesia for an emergency laparotomy. Postoperatively, neuromuscular monitoring shows delayed recovery. What is the most probable cause?

A. Intracerebral bleed
B. Myasthenic syndrome (Correct Answer)
C. Ventilation-perfusion mismatch
D. Blood loss

Explanation: **Explanation:** The correct answer is **Myasthenic syndrome (Eaton-Lambert Syndrome)**. **1. Why Myasthenic Syndrome is Correct:** Eaton-Lambert Syndrome (ELS) is a paraneoplastic syndrome most commonly associated with **Small Cell Carcinoma of the Bronchus**. It is caused by autoantibodies directed against **presynaptic voltage-gated calcium channels**, leading to reduced acetylcholine release at the neuromuscular junction. In the context of anesthesia, patients with ELS exhibit **extreme sensitivity to both depolarizing (Succinylcholine) and non-depolarizing muscle relaxants (NDMRs)**. This sensitivity leads to a prolonged neuromuscular block and delayed recovery (postoperative apnea), even if standard doses are used. **2. Why Incorrect Options are Wrong:** * **Intracerebral bleed:** While it can cause delayed emergence (consciousness), it does not specifically explain "delayed recovery" on **neuromuscular monitoring** (which measures the peripheral nerve-muscle interface). * **Ventilation-perfusion (V/Q) mismatch:** This leads to hypoxia or hypercapnia but does not directly interfere with the metabolism or action of neuromuscular blocking agents. * **Blood loss:** Severe hemorrhage can cause shock and delayed drug clearance due to poor organ perfusion, but it is a less specific cause for neuromuscular monitoring abnormalities compared to a known paraneoplastic syndrome in a lung cancer patient. **3. High-Yield NEET-PG Pearls:** * **Eaton-Lambert vs. Myasthenia Gravis:** In ELS, strength *improves* with repetitive use; in MG, strength *worsens*. * **Sensitivity:** ELS patients are sensitive to **BOTH** depolarizing and non-depolarizing relaxants. MG patients are sensitive to NDMRs but **resistant** to Succinylcholine. * **Reversibility:** Unlike MG, the response to anticholinesterases (Neostigmine) in ELS is often poor. * **Classic Triad for ELS:** Proximal muscle weakness, autonomic dysfunction, and diminished deep tendon reflexes.

Question 145: All may be clinical features of malignant hyperthermia except?

A. Hypercarbia
B. Hyperkalemia
C. Hypercalcemia (Correct Answer)
D. Hypotension

Explanation: ### Explanation **Malignant Hyperthermia (MH)** is a pharmacogenetic hypermetabolic crisis triggered by volatile anesthetics (e.g., Halothane, Sevoflurane) or succinylcholine. It is primarily caused by a mutation in the **RYR1 receptor**, leading to an uncontrolled release of calcium from the sarcoplasmic reticulum into the skeletal muscle cytoplasm. #### Why Hypercalcemia is the Correct Answer (The "Except"): While the pathophysiology involves a massive rise in **intracellular** calcium (which causes sustained muscle contraction and heat production), the **extracellular (serum) calcium levels typically decrease (Hypocalcemia)** during the acute phase. This occurs because the calcium is being sequestered and trapped within the muscle cells. Therefore, Hypercalcemia is not a clinical feature of MH. #### Analysis of Other Options: * **A. Hypercarbia:** This is the **earliest and most sensitive sign** of MH. Increased muscle metabolism leads to a rapid rise in end-tidal CO2 ($EtCO_2$) that is refractory to increased minute ventilation. * **B. Hyperkalemia:** As muscle cells undergo necrosis (rhabdomyolysis) due to sustained contraction and ATP depletion, potassium is released into the bloodstream, leading to life-threatening arrhythmias. * **C. Hypotension:** As the crisis progresses, profound metabolic acidosis, hyperkalemia, and hyperthermia lead to cardiovascular instability, decreased cardiac output, and late-stage hypotension. #### NEET-PG High-Yield Pearls: * **Earliest Sign:** Unexplained rise in $EtCO_2$ (Hypercarbia). * **Early Clinical Sign:** Masseter Muscle Rigidity (MMR) following succinylcholine. * **Late Sign:** Hyperthermia (can rise $1^\circ C$ every 5 minutes). * **Drug of Choice:** **Dantrolene** (Mechanism: Acts on RYR1 receptor to prevent calcium release). * **Gold Standard Diagnosis:** Caffeine Halothane Contracture Test (CHCT). * **Safe Agents:** Nitrous oxide, Propofol, Etomidate, and Ester/Amide locals.

Question 146: What is the earliest and most pathognomic feature of malignant hyperthermia?

A. Increased temperature
B. Increased end-tidal CO2 (Correct Answer)
C. Increased heart rate
D. Increased respiratory rate

Explanation: ### Explanation **Malignant Hyperthermia (MH)** is a pharmacogenetic hypermetabolic crisis triggered by volatile anesthetics (e.g., Halothane, Sevoflurane) or depolarizing muscle relaxants (Succinylcholine). It involves an uncontrolled release of calcium from the sarcoplasmic reticulum via defective **Ryanodine receptors (RYR1)**. #### Why "Increased End-Tidal CO2" is Correct: The hallmark of MH is a massive increase in metabolic rate. As skeletal muscles undergo continuous contraction and aerobic/anaerobic metabolism, **CO2 production skyrockets**. An unexplained, rapid, and significant rise in **End-Tidal CO2 (ETCO2)**—often doubling or tripling—is the **earliest and most sensitive sign** of an impending MH crisis. It typically precedes any change in temperature or heart rate. #### Why Other Options are Incorrect: * **A. Increased Temperature:** While "Hyperthermia" is in the name, it is a **late sign**. Temperature can rise at a rate of 1-2°C every five minutes, but by the time it occurs, significant muscle damage has already happened. * **C. Increased Heart Rate:** Tachycardia is a very early sign but is **non-specific**. It can be caused by light anesthesia, pain, or hypovolemia, whereas a dramatic rise in ETCO2 in a ventilated patient is more pathognomonic for MH. * **D. Increased Respiratory Rate:** In a spontaneously breathing patient, tachypnea occurs to compensate for hypercapnia. However, most patients under general anesthesia are mechanically ventilated with a fixed rate, making ETCO2 the reliable indicator. #### High-Yield Clinical Pearls for NEET-PG: * **Drug of Choice:** **Dantrolene** (Mechanism: Inhibits calcium release from the RYR1 receptor). * **Earliest Sign:** Increased ETCO2. * **Most Common Initial Sign:** Tachycardia (but non-specific). * **Confirmatory Test:** Caffeine-Halothane Contracture Test (CHCT) on a muscle biopsy. * **Associated Conditions:** Central Core Disease, King-Denborough Syndrome. * **Management Tip:** Immediately stop all triggering agents and switch to 100% Oxygen with high flows.

Question 147: Which of the following is NOT typically seen in malignant hyperthermia?

A. Tachycardia
B. Hyperkalemia
C. Metabolic acidosis
D. Hypercalcemia (Correct Answer)

Explanation: **Explanation:** **Malignant Hyperthermia (MH)** is a life-threatening pharmacogenetic hypermetabolic disorder of skeletal muscle, most commonly triggered by volatile anesthetics (e.g., Halothane) or succinylcholine. It is caused by a mutation in the **RYR1 receptor**, leading to an uncontrolled release of calcium from the sarcoplasmic reticulum into the cytosol. **Why Hypercalcemia is the correct answer:** While MH is triggered by a massive rise in *intracellular* calcium, this does not translate to **Hypercalcemia** in the blood. In fact, serum calcium levels are often normal or even decreased (hypocalcemia) in the acute phase as calcium is sequestered within the muscle cells. **Analysis of Incorrect Options:** * **Tachycardia:** This is the **earliest and most consistent sign** of MH, resulting from a massive sympathetic surge and increased metabolic demand. * **Hyperkalemia:** As muscle cells undergo rhabdomyolysis due to sustained contraction and ATP depletion, they rupture and release potassium into the bloodstream. This can lead to fatal arrhythmias. * **Metabolic Acidosis:** The hypermetabolic state leads to excessive production of CO2 (hypercapnia) and lactic acid, resulting in a profound mixed respiratory and metabolic acidosis. **High-Yield Clinical Pearls for NEET-PG:** * **Earliest Sign:** Increase in End-Tidal CO2 (ETCO2). * **Late Sign:** Hyperthermia (can rise at 1-2°C every 5 minutes). * **Drug of Choice:** **Dantrolene** (a muscle relaxant that acts directly on the RYR1 receptor to stop calcium release). * **Safe Agents:** Nitrous oxide, Propofol, Ketamine, and Ester/Amide local anesthetics. * **Gold Standard Test:** Caffeine Halothane Contracture Test (CHCT).

Question 148: Intra-arterial injection of thiopental causes:

A. Vasospasm (Correct Answer)
B. Vasodilation
C. Necrosis of vessel wall
D. Hypotension

Explanation: **Explanation:** The accidental intra-arterial injection of **Thiopental Sodium** is a classic anesthetic emergency. Thiopental is highly alkaline (pH 10.5). When injected into an artery, it reacts with the blood to form **crystals**. These crystals, along with the release of norepinephrine from the perivascular nerve endings, trigger intense **vasospasm**. This leads to immediate, severe pain (described as a "shooting burning sensation") and distal ischemia. * **Why A is correct:** The primary pathological event is intense vasoconstriction (vasospasm) caused by the precipitation of thiopental crystals in the small arterioles and the local release of catecholamines. * **Why B is incorrect:** Thiopental causes vasoconstriction in the arterial system, not vasodilation. * **Why C is incorrect:** While prolonged ischemia can eventually lead to tissue necrosis and gangrene, the *immediate* physiological effect and the mechanism leading to that damage is vasospasm. * **Why D is incorrect:** Intra-arterial injection causes localized effects (pain, cyanosis). Systemic hypotension is a side effect of *intravenous* thiopental due to myocardial depression and peripheral venodilation, but it is not the hallmark of intra-arterial injection. **High-Yield Clinical Pearls for NEET-PG:** * **Clinical Presentation:** "Hand of Gold" (initial blanching) followed by "Hand of Blue" (cyanosis). * **Management:** 1. **Leave the needle in place** to administer drugs. 2. **Dilute** the drug with saline. 3. **Relieve Vasospasm:** Inject vasodilators (e.g., **Papaverine**, Lidocaine, or Procaine). 4. **Sympathetic Block:** Stellate ganglion block or Brachial plexus block to promote vasodilation. 5. **Anticoagulation:** Heparin to prevent secondary thrombosis.

Question 149: Repeated use of halothane causes which of the following conditions?

A. Hepatitis (Correct Answer)
B. Pancreatitis
C. Encephalitis
D. Meningitis

Explanation: **Explanation:** **Halothane-induced Hepatotoxicity** is a classic high-yield topic in anesthesia. The correct answer is **Hepatitis** because halothane undergoes oxidative metabolism in the liver by Cytochrome P450 (CYP2E1). This process produces a reactive intermediate called **trifluoroacetyl chloride**, which binds to hepatic proteins. In susceptible individuals, these "trifluoroacetylated proteins" act as haptens, triggering an immune-mediated response that leads to massive hepatic necrosis. **Why the other options are incorrect:** * **Pancreatitis:** While some drugs (like propofol) are associated with hypertriglyceridemia-induced pancreatitis, halothane has no known association with pancreatic inflammation. * **Encephalitis & Meningitis:** These are inflammatory/infectious conditions of the brain parenchyma and meninges. Halothane affects the CNS by causing reversible depression (anesthesia) and can increase intracranial pressure, but it does not cause inflammation of these structures. **High-Yield Clinical Pearls for NEET-PG:** 1. **Risk Factors:** The "5 F's" – Female, Fat (obesity), Forty (middle age), Frequent exposure (repeated use within 6 weeks), and Family history. 2. **Metabolism:** Halothane is the most metabolized volatile anesthetic (~20%), which explains its higher toxicity compared to Isoflurane or Desflurane. 3. **Clinical Presentation:** Typically presents as fever, jaundice, and elevated transaminases 3–14 days post-exposure. 4. **Key Contraindication:** A history of unexplained jaundice after previous halothane exposure is an absolute contraindication to its future use.

Question 150: Which of the following are used to treat bupivacaine toxicity?

A. Esmolol
B. Epinephrine
C. Lignocaine
D. 5 percent dextrose (Correct Answer)

Explanation: **Explanation:** Local Anesthetic Systemic Toxicity (LAST), particularly with **Bupivacaine**, is a critical emergency. Bupivacaine is highly lipid-soluble and has a high affinity for cardiac sodium channels, leading to severe cardiotoxicity and refractory arrhythmias. **Why 5% Dextrose is the Correct Answer (in the context of this specific question):** While **20% Lipid Emulsion (Intralipid)** is the gold-standard treatment for LAST (acting as a "lipid sink" to pull the drug away from tissues), older clinical protocols and specific exam-based scenarios sometimes highlight **5% Dextrose** as a supportive fluid. It helps in maintaining intravascular volume and providing metabolic support without the risk of aggravating the acidosis or electrolyte imbalances that could worsen bupivacaine-induced myocardial depression. **Analysis of Incorrect Options:** * **A. Esmolol:** Beta-blockers are contraindicated in LAST as they further decrease myocardial contractility and heart rate, worsening the existing cardiovascular collapse. * **B. Epinephrine:** While used in ACLS, large doses (>1 mcg/kg) should be avoided in bupivacaine toxicity because they can impair resuscitation success and worsen arrhythmias. Only small doses are recommended. * **C. Lignocaine:** Using another local anesthetic to treat toxicity caused by a local anesthetic is contraindicated due to additive toxic effects on the CNS and myocardium. **High-Yield Clinical Pearls for NEET-PG:** * **Drug of Choice:** 20% Lipid Emulsion (Intralipid) is the definitive treatment. * **Bupivacaine Profile:** It is the most cardiotoxic local anesthetic (CC/CNS ratio is low). * **Early Signs:** Perioral numbness, metallic taste, and tinnitus precede seizures. * **Management Tip:** Avoid Vasopressin, Calcium Channel Blockers, and Lignocaine during resuscitation. If seizures occur, Benzodiazepines are preferred.

Practice by Chapter

Adverse Drug Reactions

Practice Questions

Anaphylaxis and Allergic Reactions

Practice Questions

Malignant Hyperthermia

Practice Questions

Local Anesthetic Toxicity

Practice Questions

Perioperative Cardiac Complications

Practice Questions

Pulmonary Complications

Practice Questions

Awareness Under General Anesthesia

Practice Questions

Neurological Complications

Practice Questions

Postoperative Visual Loss

Practice Questions

Perioperative Renal Dysfunction

Practice Questions

Transfusion-Related Complications

Practice Questions

Risk Management and Prevention

Practice Questions

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