Description

SECTION 1 — CASE PRESENTATION AND CLINICAL CONTEXT

A 38-year-old healthy female (BMI 21) presented for a laparoscopic left donor nephrectomy. The anesthetic plan included multimodal general anesthesia with opioid-sparing strategy and regional blockade.

Anesthetic Regimen

• Premedication: Glycopyrrolate 0.2 mg

• Sedation: Midazolam 1 mg

• Analgesia: Fentanyl 200 µg

• Steroid: Dexamethasone 8 mg

• Induction: Propofol 100 mg

• Neuromuscular blockade: Atracurium 40 mg + infusion (30 mg/h)

• Adjuncts: Dexmedetomidine 30 µg, Magnesium sulfate 1 g, Paracetamol 1 g

• Maintenance gases: Oxygen, nitrous oxide, sevoflurane (MAC 0.8–1.4)

• Regional technique: Erector spinae plane (ESP) block after induction

• Pre-incision bolus: Propofol 40 mg for controlled hypotension

The case produced four distinct BIS and EEG physiological states, each driven by pharmacologic and surgical events:

1. BIS 36 — 10 minutes post-induction

2. BIS 15 — Following 40 mg propofol bolus

3. BIS 28 — Approximately 4 minutes after pneumoperitoneum

4. BIS 32 — At 45 minutes, during MAC ~1.4 volatile anesthesia

These phases reflect the evolutionary trajectory of cortical physiology under balanced anesthesia. The chapter uses these phases as an organizing framework to explore EEG neurobiology, pharmacology, anesthetic depth assessment, and clinical decision-making.

Why This Case is Ideal for Teaching BIS Interpretation

This case avoids many confounders (elderly age, hypothermia, shock, metabolic derangements) and includes:

• A young, healthy brain with intact thalamocortical connectivity

• Full neuromuscular blockade (eliminating EMG artifact)

• Highly standardized anesthetic regimen

• ESP block (stable analgesic background)

• Clear pharmacologic transitions

• Laparoscopy with predictable sympathetic surges

Thus, it provides a classic model to demonstrate how EEG and BIS evolve with:

• GABAergic sedation

• α2-adrenergic modulation

• Opioid-induced hyperpolarization

• NMDA inhibition

• Volatile anesthetic effects

• Sympathetic activation

• Propofol redistribution kinetics

This allows an unusually clean, high-fidelity demonstration of cortical electrophysiology under anesthesia.

References

1. Brown EN, Purdon PL. The Neuroscience of General Anesthesia. N Engl J Med. 2013;369:1015–1025.

2. Mashour GA, Hudetz AG. Neural Correlates of Unconsciousness in Anesthesia. Trends Neurosci. 2018;41:150–159.

3. Akeju O, Brown EN. Neural Oscillations Underlying General Anesthesia and Sleep. Curr Opin Anaesthesiol. 2017;30:441–451.

SECTION 2 — FOUNDATIONS OF EEG UNDER ANESTHESIA: MOLECULAR & CIRCUIT-LEVEL MECHANISMS

Understanding BIS requires understanding how anesthetics alter:

• Thalamocortical oscillators

• Inhibitory and excitatory synaptic currents

• Ion channel behavior

• Brainstem arousal systems

2.1 Thalamocortical Circuit Physiology

General anesthesia primarily acts on the thalamus, cerebral cortex, and brainstem arousal nuclei,...