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Anaesthesia

 Isoflurane

  • Agent of choice in Cardiac patients.
  •  Vasodilation with least cardiovascular depression.
  •  Intracranial pressure (moderate increase).
  • Not ideal for asthmatics compared to Sevoflurane.

Desflurane

  •  Fastest induction & recovery.
  •  Minimally metabolized.
  • Preferred in shock & renal failure.

Sevoflurane

  •  Induction agent in children.
  • Maximum bronchodilation (non-asthmatics).
  • More cardiodepressant than Isoflurane.

Ether

  • Highly explosive  (not used today).
  • Classic: Complete anaesthetic agent.
  • Causes max emesis.
  • Basis of anaesthesia staging (Guedel’s classification).

Agent Key Features
Thiopentone Alkaline (pH 10.5), crosses placenta, no analgesia, safe in epilepsy
Short half-life due to redistribution
⛔ Intra-arterial injection → vasospasm
Propofol Pain on injection, use within 6 hrs, ideal for day care surgery
Etomidate Cardio-stable, safe in heart disease, 🚫 High nausea/vomiting
Ketamine High analgesia, ⬆️ ICP/Cerebral O₂, IM+IV routes, not ideal for head trauma
 Decreases hallucination: Midazolam

  • Benzodiazepines:
    • Produce anterograde amnesia
    • Act on α-subunit of GABA-A receptors
    • Muscle relaxation with Midazolam
    • Flumazenil: Specific antagonist
    • Lorazepam: Difficult reversal

1. Refractory periods: absolute (neuron cannot fire) and relative (can fire with greater than normal depolarization)

2. Specific receptor theory: local anesthetics bind inside Na channel, block entry of Na

3. Membrane expansion theory: anesthetics work by disrupting lipid bilayer around ion channel

4. Mechanism of action for local anesthetics: local must be in uncharged form to cross lipid bilayer of axon

a. Locals made as salts (usually mixed with HCl).  [Uncharged form] depends on pH of tissue, pKa of local-found by Henderson-Hasselbach equation- pH = pKa + log ( [RN] / [RNH+] )

b. Once inside axon, only charged form will bind to Na channel.

c. At physiologic pH, enough base exists outside nerve so anesthetic rapidly diffuses into axon.  Rate-limiting step is how much uncharged local is present outside neuron.

d. So, starts with 100 molecules of local, 25 of which are uncharged and 75 charged.  The 25 uncharged enter the neuron, leaving 0 on outside so the remaining 75 re-equilibrate to produce more uncharged which enters neuron .  Inside neuron the reverse happens as converted to ionic form then rapidly binds channel.

5. Inflammatory effects: ® an acidic environment, less of local can be converted to uncharged form (less enters).

6.  Pharmakokinetics: pool of local outside neuron depleted as local diffuses into adjacent muscles, tissues, enters blood vessels.  Since locals are water soluble, they go throughout body (even cross BBB and placenta)

7. Autonomic nervous system: sympathetic and parasympathetic divisions.  Both secrete pre-ganglionic acetylcholine.  Postganglionic NT is acetylcholine for parasympathetic, norepinephrine for sympathetic (also secrete E, dopamine, and seratonin, all are catecholamines).

a. Sympathetic catecholamines affect receptors (local anesthetics affect a1-mediated actions which cause vasoconstriction) ® fight or flight responses (pupil & bronchiole dilation, ­ HR, BP, blood glucose; ¯ GI)

b. Catecholamines inactivated by reuptake, diffusion, or metabolized by monoamine oxidase (MAO) and catechol-O-methyl transferase (COMT) then metabolites excreted in urine.

c.  When choosing sympathomimetic drug, consider receptor subtype in tissue and choose drug that affects it.

  • First Local Anaesthetic: Cocaine
  • First Muscle Relaxant: D-Tubocurarine (DTC)
  • Intubation Pioneer: Ivan Magill (Magill's forceps)

 Preoperative Considerations

  • Stop smoking ideally 8 weeks prior to surgery.
  • Urgent warfarin reversal: Fresh Frozen Plasma (FFP).
  • Atropine:
    • ↓ Salivation
    • Bronchodilation
    • Flushing in pediatric patients

  • Hypotension – Common post-op issue.
  •  Hypoxic hypoxia – MC intra-op type.
  •  Malignant hyperthermia – Not caused by Nitrous oxide.

Spinal Anesthesia

A. Anatomy

Spinal anesthesia targets the spinal cord, which arises from the foramen magnum and extends to the conus medullaris, typically ending around the third lumbar vertebrae (L3) in adults. The spinal column is protected by three layers: the dura mater, arachnoid mater, and pia mater. The subarachnoid space, where the spinal anesthetic is administered, contains cerebrospinal fluid (CSF), spinal nerves, and the arachnoid and pial vessels. The arachnoid membrane provides significant resistance to drug diffusion, accounting for approximately 90% of the barrier.

The epidural space lies outside the dura mater and is bounded by the ligamentum flavum, lamina, and spinous processes. It is important to distinguish between the epidural and subarachnoid spaces, as the needle placement determines the type of anesthesia administered.

Key anatomic landmarks for spinal anesthesia include the iliac crests, which can be used to approximate the L4-L5 interspace. The spinal needle is commonly inserted at the L3 or L4 level in adults to avoid the termination of the spinal cord.

B. Indications

1. Lower abdominal and pelvic surgeries: Spinal anesthesia is suitable for surgeries below the umbilicus, such as hernia repairs, gynecological and urological procedures.
2. Lower extremity surgeries: This includes orthopedic procedures and lower limb surgeries.
3. Cesarean sections: It provides adequate analgesia and muscle relaxation while allowing the mother to remain awake and participate in the birth.

C. Contraindications

Absolute contraindications:
1. Patient refusal or inability to cooperate and maintain a still position.
2. Coagulation disorders or use of anticoagulants, which increase the risk of spinal hematoma.
3. Local infection at the injection site.

Relative contraindications:
1. Sepsis: Due to the risk of spreading infection to the central nervous system.
2. Neurological conditions: Such as myelitis, which can be exacerbated by invasive procedures.
3. Intracranial hypertension: As spinal anesthesia can cause a sudden drop in systemic vascular resistance and increase intracranial pressure.
4. Severe spinal or spinal cord deformities: These may lead to complications in needle placement and drug distribution.
5. Cardiovascular conditions: Stenotic heart valve lesions and severe hypertrophic cardiomyopathy can be poorly tolerated due to the hemodynamic changes associated with spinal anesthesia.
6. Lack of anesthesiologist experience: This may increase the risk of complications.

D. Equipment

1. Patient monitors: ECG for heart rhythm monitoring, pulse oximeter for oxygen saturation, and a blood pressure cuff to assess circulation.
2. Resuscitation equipment: Oxygen supply, bag and mask for ventilation, and suction to clear the airway if needed.
3. Sterile environment: Sterile gloves, mask, gown (if required), and a clean field are essential to prevent infection.
4. Intravenous access: To administer fluids and medications during the procedure.
5. Sterile prep solution: Typically Betadine or a non-iodine alternative for skin preparation.
6. Spinal needle: Small gauge (24-26 gauge) for minimizing trauma.
7. Sterile drapes: To maintain the sterility of the area.
8. Local anesthetic: For skin infiltration to reduce pain during the spinal block.
9. Syringes: A small syringe for local anesthetic and a 3-5 mL syringe for the spinal anesthetic agent.
10. Anesthetic agent: Typically a local anesthetic with or without additives like epinephrine or opioids to prolong the block and enhance analgesia.
11. Bandage: For securing the needle site post-procedure

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