Apr 16, 2026

A 28-year-old male with ASA Grade I status is scheduled for emergency appendectomy. The patient develops severe jaw stiffness within 30 seconds after receiving succinylcholine. His body temperature increases to 40.2°C. End-tidal CO₂ shows an immediate and dramatic increase. The anaesthetist immediately reaches for a specific drug. What is it, and why? If you hesitated, Anaesthesia deserves more of your revision time, as it is one of the highest-scoring short subjects in recent NEET PG papers.
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The NEET PG Anaesthesia syllabus tests candidates on the stages of general anaesthesia, induction agents, inhalational agents, local anaesthetics, muscle relaxants, and regional techniques. The most commonly tested drug is succinylcholine (a depolarising muscle relaxant that causes fasciculations). Dantrolene (2.5 mg/kg IV) serves as the treatment for malignant hyperthermia. Propofol (2-2.5 mg/kg IV) acts as the most effective induction agent for brief medical procedures.

The sodium salt of dantrolene
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In the NEET PG exam, anaesthesia appears as a subject with a moderate-to-high frequency, accounting for 3-6 questions per exam. High-yield focus: stages of anaesthesia, MAC values of inhalational agents, spinal vs epidural differences, and malignant hyperthermia management. The recent examinations now require students to answer pharmacology-based questions that test their knowledge of drug mechanisms, adverse effects, and clinical applications.
In This Post:
General anaesthesia is the reversible state of unconsciousness, analgesia, amnesia, and muscle relaxation produced by a combination of intravenous and inhalational agents. Arthur Guedel described four stages using diethyl ether as the reference agent. While modern balanced anaesthesia bypasses most stages rapidly, examiners still love testing this classification.
On NEET PG, expect questions asking which stage is associated with laryngospasm (Stage II) or at which plane eyeball movements cease (Plane 3 of Stage III).
The most common cause of exam mistakes in this section is the confusion between induction and maintenance doses. I will explain which treatment agents are essential for this case.

A 20 ml ampoule of 1% propofol emulsion
Also Read : Important One Liners in Anesthesia
A classic NEET PG examination trap asks test-takers which induction method is safest for patients with hemodynamic instability. The answer is Ketamine for trauma/shock; Etomidate for cardiac patients with stable volume status.
Minimum Alveolar Concentration (MAC) is the concentration of an inhalational agent at 1 atmosphere that prevents movement in response to a surgical incision in 50% of patients. MAC is the single most important concept in inhalational anaesthesia for NEET PG.
Key MAC values you must memorise:
Here’s a mnemonic I teach my students: "No Dose Shall Impose Half Measures" (N₂O → Desflurane → Sevoflurane → Isoflurane → Halothane → Methoxyflurane) arranged from highest to lowest MAC, which is lowest to highest potency, since MAC is inversely proportional to potency.
Halothane makes the myocardium more sensitive to catecholamines, which leads to arrhythmias. The drug causes Halothane hepatitis through immune-mediated effects, which occur after repeated exposure to the substance.
Sevoflurane interacts with soda lime to create Compound A, which causes kidney damage in rats, although its actual impact on human health remains uncertain.
Methoxyflurane causes kidney damage through oxalic acid crystals, which depend on the amount of the drug administered.
N₂O causes diffusion hypoxia at the end of anaesthesia because it expands gas-filled cavities, which makes it dangerous to use in closed air spaces, such as in pneumothorax and middle ear surgery.
In NEET PG, questions often connect a specific agent with its particular toxic effects. You must learn these direct relationships in their entirety.

Local anaesthetics (LAs) work by blocking voltage-gated sodium channels that control nerve impulse transmission. The drug exists in an ionised state, which cannot pass through membranes, and in an uncharged state, it can. This concept drives the exam-favourite question: why do local anaesthetics fail in infected/acidic tissue? The answer - acidic pH shifts the equilibrium toward the ionised form, reducing membrane penetration. This process results in ion trapping.
LAs are divided into two groups based on their intermediate chain links:
Amides (Lidocaine, Bupivacaine, Ropivacaine) - contain "i" in the prefix before "-caine." The liver performs its metabolic breakdown. Esters (Procaine, Cocaine, Tetracaine) - their metabolites are processed by plasma cholinesterase (pseudocholinesterase). Esters are more likely to cause allergic reactions due to their metabolite, para-aminobenzoic acid (PABA).
Bupivacaine is considered the most dangerous local anaesthetic because it strongly binds to cardiac sodium channels, which function with fast-in slow-out kinetics. The medical procedure of 20% IV Intralipid emulsion (lipid rescue therapy) treats Bupivacaine cardiotoxicity. Ropivacaine serves as a safer alternative, which creates less danger to heart function and prevents muscle movement.
Lidocaine is known as the most versatile local anaesthetic because it is used for infiltration, nerve blocks, topical anaesthesia, epidural, spinal (5% hyperbaric), and IV antiarrhythmic (Class IB) use. The maximum safe dose of Lidocaine is 4.5 mg/kg without adrenaline and 7 mg/kg with adrenaline.
In clinical teaching, I educate students that doctors block nerves in the following sequence:
First, they block small unmyelinated C fibres (pain, temperature), and finally, they block large myelinated Aα fibres (motor).
The process of recovery happens in reverse order. The patient who receives spinal anaesthesia experiences pain relief before motor function loss, which occurs afterwards.
Succinylcholine (also known as suxamethonium) is the only depolarizing neuromuscular blocker in use. The drug binds to the nicotinic receptor as an acetylcholine mimic, which leads to initial muscle depolarization that manifests through visible muscle contractions before the drug establishes permanent muscle paralysis.
The drug reaches its full effects between 30 and 60 seconds, while its effects last for an ultra-short period which extends between 5 and 10 minutes because plasma cholinesterase enzymes, including pseudocholinesterase and butyrylcholinesterase, break down the substance.
Succinylcholine can cause hyperkalaemia (raises serum K⁺ by 0.5-1.0 mEq/L). The situation becomes life-threatening because burns, crush injuries, denervation injuries and upper motor neuron lesions cause receptor upregulation, which results in enormous potassium release.
The drug becomes forbidden for use in burn patients during the first 24 hours after their injury and in patients who have been diagnosed with pseudocholinesterase deficiency because this condition causes extended apnoea, which doctors identify through the Dibucaine number test that indicates normal results above 70.
Among non-depolarising agents, Atracurium, Vecuronium, Rocuronium and Pancuronium act as competitive blockers of the nicotinic receptor.
Atracurium undergoes Hofmann degradation (organ-independent elimination) - making it the agent of choice in hepatic and renal failure.
Rocuronium shows the quickest effect among non-depolarizing drugs, while Sugammadex functions as the exclusive method to reverse its effects through its selective relaxant binding capability; traditional methods require the combination of Neostigmine and Glycopyrrolate to achieve reversal.
Examiners often test this mechanism difference:
The Phase I depolarising block shows no fade on train-of-four testing and no post-tetanic facilitation.
The non-depolarising block displays fade patterns during train-of-four testing which leads to post-tetanic facilitation.
This is one of the most frequently tested comparisons in Anaesthesia for NEET PG. During ward postings, I always point out to students how the clinical differences follow directly from where the needle tip sits.
| Feature | Spinal Anaesthesia | Epidural Anaesthesia |
| Site of injection | Subarachnoid space | Epidural space |
| Needle used | 25G Quincke (cutting) or Whitacre (pencil-point) | 16-18G Tuohy needle |
| Level of insertion | Below L2 (usually L3-L4) | Any spinal level |
| Volume of drug | Small (2-4 mL) | Large (15-20 mL) |
| Onset | Rapid (2-5 minutes) | Slow (15-20 minutes) |
| Duration | Fixed (2-3 hours without catheter) | Continuous (via catheter) |
| Segmental blockade | Difficult to achieve | Easily achieved |
| Post-dural puncture headache | More common | Rare (unless accidental dural puncture) |
| Hypotension | Rapid, significant | Gradual, less severe |
| NEET PG pearl | Drug of choice: 0.5% Bupivacaine (heavy/hyperbaric) | Loss of resistance technique used to identify epidural space |
| Images |
The most common complication of spinal anaesthesia is hypotension (due to sympathetic blockade). Post-dural puncture headache (PDPH) is postural - worse on sitting up, relieved on lying down - and treated with an epidural blood patch if conservative measures fail.
For a deeper exploration of regional anaesthesia techniques, PrepLadder's video lectures provide clinical correlations and animated demonstrations.
Malignant hyperthermia (MH) is a life-threatening pharmacogenetic disorder triggered by volatile inhalational agents (Halothane, Sevoflurane, Isoflurane, Desflurane) and succinylcholine. It results from a mutation in the Ryanodine receptor (RYR1) gene on chromosome 19, leading to uncontrolled calcium release from the sarcoplasmic reticulum in skeletal muscle.
The result: sustained muscle contraction → massive hypermetabolism → hyperthermia, metabolic acidosis, hyperkalaemia, rhabdomyolysis, and eventually multi-organ failure if untreated.
The earliest sign is an unexplained rise in end-tidal CO₂ (ETCO₂). Masseter muscle rigidity after succinylcholine is a strong warning sign. The temperature may rise by 1-2°C every 5 minutes. Lab findings include respiratory and metabolic acidosis, elevated creatine kinase (CK), hyperkalaemia, and myoglobinuria.
The gold-standard diagnostic test is the Caffeine-Halothane Contracture Test (CHCT), performed on muscle biopsy in susceptible individuals.
TREATMENT ALGORITHM
Step 1: Stop all triggering agents immediately → switch to IV anaesthesia (Propofol/opioids) Step 2: Administer Dantrolene 2.5 mg/kg IV (repeat up to 10 mg/kg) - Dantrolene blocks RYR1 calcium release
Step 3: Active cooling (cold IV fluids, ice packs, gastric lavage) → correct hyperkalaemia (insulin + dextrose, calcium gluconate) → maintain urine output >2 mL/kg/hr (IV fluids + mannitol to prevent myoglobin-induced renal failure)
Step 4: Monitor in ICU for at least 24-48 hours - recrudescence occurs in ~25% of cases
On NEET PG, the single most tested fact: Dantrolene is the specific antidote for malignant hyperthermia. Do not confuse this with Dantrolene's other use as a skeletal muscle relaxant in spasticity.
The most dangerous stage of anesthesia occurs during Stage II, which scientists call Excitement or Delirium. The condition manifests through laryngospasm, breath-holding, vomiting and irregular breathing patterns. The modern IV induction agent Propofol allows rapid execution of this process, which leads to decreased anesthesia induction risks.
In patients with shock, Ketamine (1-2 mg/kg IV) becomes the preferred treatment for patients experiencing shock or hypovolemia because it stimulates their sympathetic nervous system, which leads to increased heart rate and blood pressure. Ketamine provides two benefits that Propofol and Thiopentone do not: it maintains cardiovascular stability while delivering pain relief.
The antidote for malignant hyperthermia is Dantrolene sodium (2.5 mg/kg IV, repeated up to 10 mg/kg). The drug operates by blocking Ryanodine receptors (RYR1) on the sarcoplasmic reticulum, thereby preventing uncontrolled calcium release from skeletal muscle.
Spinal anesthesia involves a drug injection method that targets the subarachnoid space located below L2 to create an immediate and complete blockage effect through a minimal drug volume requirement of 2-4 mL. Epidural anesthesia requires larger drug volumes, which range from 15-20 mL, to achieve effects that develop more slowly than spinal anesthesia while enabling continuous drug delivery through catheter-based systems.
Local anesthetics often fail in infected tissue because the tissue exhibits an acidic pH level which drops below 7.4. The unionized and ionized forms exist for local anesthetics. Acidic pH conditions create a situation where the charged ionized form becomes dominant because it cannot penetrate nerve membranes. The process known as ion trapping causes this effect, which makes anesthetics less effective.
NEET PG tests a candidate's knowledge of Anaesthesia through pharmacology-based MCQs, which include questions on drug mechanisms, dosage requirements, adverse effects and contraindications. The test includes questions that require people to compare two things which include spinal versus epidural and depolarizing versus non-depolarizing. The clinical scenario questions assess candidates' knowledge of how to manage malignant hyperthermia and select an appropriate induction agent.
"In anaesthesia, the drug you reach for in a crisis defines you more than the drug you chose for induction."
After 10 years of teaching, I can tell you that Anaesthesia questions in NEET PG reward those who know specific drugs, specific doses, and specific contraindications - not vague generalisations. Nail the tables, and you nail the marks.

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Propofol:
Thiopentone sodium:
Ketamine:
Etomidate:
Clinical Features & Diagnosis
Emergency Management
Q.1 What is the most dangerous stage of anaesthesia?
Q.2 Which induction agent is preferred in a patient with shock?
Q.3 What is the antidote for malignant hyperthermia?
Q.4 What is the difference between spinal and epidural anaesthesia?
Q.5 Why do local anaesthetics fail in infected tissue?
Q.6 How is Anaesthesia tested in NEET PG?
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