MBBS Anesthasia Syllabus

Why is epinephrine contraindicated in local anesthesia of end-arterial regions (fingers, toes, nose, penis, ears)?

Epinephrine causes vasoconstriction of end-arteries with no collateral supply, risking ischemia and tissue necrosis. The traditional teaching is to avoid epinephrine in "fingers, toes, nose, penis, and ears" (end-organs).

Compare depolarizing vs non-depolarizing neuromuscular blockers by mechanism and the prototype of each.

Depolarizing (prototype succinylcholine): an acetylcholine receptor AGONIST that causes persistent depolarization (initial fasciculations then flaccid paralysis); NOT reversed by neostigmine. Non-depolarizing (e.g., rocuronium, vecuronium, atracurium): competitive ACh receptor ANTAGONISTS, reversed by anticholinesterases or sugammadex.

What makes succinylcholine the fastest-onset, shortest-acting NMBA, and what enzyme terminates its action?

Succinylcholine has rapid onset ($30\text{--}60$ s) and short duration ($5\text{--}10$ min), ideal for rapid sequence intubation. It is metabolized by plasma pseudocholinesterase (butyrylcholinesterase); deficiency or atypical enzyme causes prolonged paralysis.

List the major adverse effects/contraindications of succinylcholine.

Succinylcholine can cause hyperkalemia (dangerous in burns, crush injury, denervation, prolonged immobility), malignant hyperthermia trigger, bradycardia (especially in children/repeat doses), increased intraocular/intracranial/intragastric pressure, myalgias, and prolonged apnea with pseudocholinesterase deficiency.

How does sugammadex reverse neuromuscular blockade, and which agents does it target?

Sugammadex is a modified $\gamma$-cyclodextrin that encapsulates (chelates) aminosteroid NMBAs in plasma, forming an inactive complex that is renally excreted. It rapidly reverses rocuronium and vecuronium (not benzylisoquinoliniums like atracurium).

By what unique organ-independent pathway is atracurium (and cisatracurium) eliminated, and why is this useful?

Atracurium/cisatracurium undergo Hofmann elimination (spontaneous, temperature- and pH-dependent non-enzymatic degradation) plus ester hydrolysis. This is independent of hepatic and renal function, making them ideal in liver or kidney failure.

What is the standard reversal regimen for non-depolarizing blockade using an anticholinesterase, and why is an antimuscarinic added?

Neostigmine (an acetylcholinesterase inhibitor) increases ACh at the junction to overcome the block. It is co-administered with an antimuscarinic (glycopyrrolate or atropine) to prevent muscarinic side effects such as bradycardia, salivation, and bronchospasm.

What does the Train-of-Four (TOF) ratio assess, and what TOF ratio indicates adequate recovery from neuromuscular blockade?

TOF delivers four supramaximal stimuli at 2 Hz; the TOF ratio is the amplitude of the 4th twitch divided by the 1st ($T4/T1$). A TOF ratio $\geq 0.9$ indicates adequate recovery and is the accepted threshold for safe extubation.

What is the Mallampati classification used for, and what do Classes I and IV indicate?

The Mallampati classification predicts difficulty of laryngoscopy/intubation based on visible oropharyngeal structures. Class I: soft palate, uvula, fauces, and pillars visible (easy). Class IV: only hard palate visible (predicts difficult intubation).

What is the mnemonic LEMON for difficult airway assessment?

LEMON: L = Look externally (facial trauma, beard, obesity), E = Evaluate the 3-3-2 rule, M = Mallampati score, O = Obstruction/Obesity, N = Neck mobility.

Explain the 3-3-2 rule for airway assessment.

The 3-3-2 rule predicts ease of laryngoscopy: 3 fingerbreadths mouth opening (inter-incisor distance), 3 fingerbreadths from chin (mentum) to hyoid bone, and 2 fingerbreadths from floor of mouth (hyoid) to thyroid notch. Failure to meet these suggests a difficult airway.

What is the most reliable confirmation of correct endotracheal tube placement?

Sustained waveform capnography (detection of exhaled $\ce{CO2}$ over $\geq 6$ breaths / continuous $\mathrm{ETCO_2}$) is the gold standard for confirming tracheal (not esophageal) placement, supplemented by bilateral chest auscultation, chest rise, and misting of the tube.

What are typical endotracheal tube internal diameter (ID) sizes for an average adult male and female?

Average adult male: ETT internal diameter $7.5\text{--}8.5\ \mathrm{mm}$; average adult female: $7.0\text{--}8.0\ \mathrm{mm}$. For children $>1$ year (uncuffed): $\text{ID} = \dfrac{\text{age}}{4} + 4\ \mathrm{mm}$.

What is the recommended endotracheal cuff pressure range, and why does it matter?

Cuff pressure should be kept at $20\text{--}30\ \mathrm{cmH_2O}$. Too high risks tracheal mucosal ischemia/necrosis and stenosis; too low allows aspiration and gas leak. Pressure should remain below tracheal capillary perfusion pressure ($\approx 25\text{--}35\ \mathrm{mmHg}$).

What is a supraglottic airway device (e.g., LMA), and where does it sit?

A supraglottic airway (e.g., laryngeal mask airway) is placed blindly in the hypopharynx with a cuff that seals around the laryngeal inlet (above the glottis), providing ventilation WITHOUT passing through the vocal cords. It is used for spontaneous or controlled ventilation in selected cases and as a difficult-airway rescue.

Name the main limitations/contraindications of a classic LMA compared with an endotracheal tube.

LMA does NOT provide a definitive sealed airway: it gives limited protection against aspiration, so it is relatively contraindicated in full stomach/high aspiration risk, morbid obesity, poor lung compliance, and surgery requiring high airway pressures or prone/lateral positioning.

According to difficult airway algorithms, what is the over-arching priority when intubation fails?

The priority is always oxygenation/ventilation, not intubation. The mantra is to avoid the "can't intubate, can't oxygenate" (CICO) catastrophe; if mask ventilation and supraglottic rescue fail, proceed to emergency front-of-neck access (cricothyroidotomy).

In a "can't intubate, can't oxygenate" (CICO) emergency, what is the definitive rescue procedure?

Emergency front-of-neck airway access, most commonly a cricothyroidotomy (surgical or needle/cannula with jet ventilation) through the cricothyroid membrane, to restore oxygenation when all other techniques have failed.

What is the difference between general anesthesia, regional anesthesia, and monitored anesthesia care (MAC)?

General anesthesia: drug-induced reversible loss of consciousness with no response even to painful stimuli, often with airway support. Regional anesthesia: LA blocks sensation to a body region (e.g., spinal, epidural, nerve block) while the patient may remain awake. MAC: titrated sedation/analgesia with monitoring, patient breathes spontaneously and can respond, used to supplement local anesthesia.

Contrast spinal (subarachnoid) and epidural anesthesia by site of injection and onset.

Spinal: LA injected into the CSF in the subarachnoid space (below L2 to avoid the cord); small volume, rapid dense block, fast onset. Epidural: LA injected into the epidural (potential) space; larger volume, slower onset, segmental block, and allows catheter for continuous infusion.

Why must a spinal anesthetic be performed below the L2 vertebral level in adults?

In adults the spinal cord (conus medullaris) typically terminates at L1-L2, so needle insertion at L3-L4 or L4-L5 (the line between iliac crests = Tuffier's line, $\approx$ L4) avoids cord injury while still reaching CSF of the cauda equina.

What is the classic complication of dural puncture, and how is a post-dural puncture headache (PDPH) characteristically described and treated?

PDPH results from CSF leak through the dural hole. It is a postural (positional) headache—worse upright, relieved when supine—often frontal/occipital. Treatment: bed rest, hydration, caffeine, analgesics; definitive treatment is an epidural blood patch.

What causes hypotension during spinal/epidural anesthesia and how is it managed?

Sympathetic blockade causes vasodilation (decreased SVR) and, with high blocks, bradycardia (block of cardiac accelerators $T1\text{--}T4$), reducing preload and cardiac output. Management: IV fluids, vasopressors (phenylephrine, ephedrine), leg elevation, and treating bradycardia with atropine.

Give the formula for mean arterial pressure (MAP) and the formula relating MAP to cardiac output and systemic vascular resistance.

$$\mathrm{MAP} = \mathrm{DBP} + \frac{1}{3}(\mathrm{SBP} - \mathrm{DBP})$$ and $$\mathrm{MAP} \approx \mathrm{CO} \times \mathrm{SVR}\ (+\ \mathrm{CVP}),\quad \mathrm{CO} = \mathrm{HR} \times \mathrm{SV}.$$

How is intraoperative hypotension commonly defined, and what is a structured framework for its causes?

Often defined as MAP $< 65\ \mathrm{mmHg}$ or a $>20\%$ drop from baseline. Causes follow the determinants of BP: decreased PRELOAD (hypovolemia, hemorrhage, caval compression), decreased CONTRACTILITY/RATE (anesthetic depression, arrhythmia, MI), and decreased AFTERLOAD/SVR (anaphylaxis, sepsis, sympathectomy, drugs).

Define hypoxemia, and give the alveolar gas equation for predicting alveolar oxygen tension.

Hypoxemia is low arterial oxygen, typically $\mathrm{PaO_2} < 60\ \mathrm{mmHg}$ or $\mathrm{SpO_2} < 90\%$. Alveolar gas equation: $$P_AO_2 = F_iO_2 (P_{atm} - P_{H_2O}) - \frac{P_aCO_2}{R}$$ where $R \approx 0.8$ and $P_{H_2O} = 47\ \mathrm{mmHg}$ at body temperature.

List the five physiologic mechanisms of hypoxemia.

(1) Ventilation/perfusion ($\dot V/\dot Q$) mismatch (most common), (2) right-to-left shunt (does not correct with 100% $\ce{O2}$), (3) hypoventilation (raised $\mathrm{PaCO_2}$, normal A-a gradient), (4) diffusion limitation, and (5) low inspired $\ce{O2}$ (high altitude). Calculate the A-a gradient to differentiate.

What is malignant hyperthermia, its triggers, and the underlying genetic defect?

MH is a life-threatening hypermetabolic crisis of skeletal muscle triggered by volatile anesthetics (halothane, sevoflurane, isoflurane, desflurane) and succinylcholine. It is an autosomal dominant disorder, most often a mutation in the ryanodine receptor ($RYR1$) causing uncontrolled $\mathrm{Ca^{2+}}$ release from the sarcoplasmic reticulum.

What are the early clinical signs of malignant hyperthermia and its specific drug treatment?

Earliest sign is a rapid rise in $\mathrm{ETCO_2}$ (hypercapnia) with tachycardia, masseter/generalized muscle rigidity, hyperthermia (late), and rhabdomyolysis/hyperkalemia. Treatment: stop triggers, hyperventilate with 100% $\ce{O2}$, and give dantrolene $2.5\ \mathrm{mg/kg}$ IV (repeat to max $10\ \mathrm{mg/kg}$), plus active cooling and correction of acidosis/hyperkalemia.

What are the Aldrete scoring criteria used to assess discharge readiness from the PACU?

The Aldrete score rates five parameters 0-2 each (max 10): Activity, Respiration, Circulation (BP), Consciousness, and $\ce{O2}$ Saturation (color in the original). A score $\geq 9$ generally indicates readiness for discharge from the post-anesthesia care unit.

What are the most common immediate postoperative complications managed in the PACU, including the major risk factors for PONV?

Common PACU issues: airway obstruction, hypoxemia, hypotension/hypertension, pain, hypothermia/shivering, emergence delirium, and postoperative nausea and vomiting (PONV). Apfel risk factors for PONV: female sex, non-smoker, history of PONV/motion sickness, and postoperative opioid use.