Anesthesiology

01 Airway Anatomy & Physiology

Upper Airway Anatomy

The upper airway extends from the nares and oral cavity to the laryngeal inlet. The nasal cavity is lined with highly vascular mucosa (Kiesselbach plexus on the anterior septum is the most common site of epistaxis) and warms, humidifies, and filters inspired gas. Three turbinates (inferior, middle, superior) increase mucosal surface area. The oral cavity serves as the primary route for airway instrumentation; the tongue is the most common cause of upper airway obstruction in the unconscious patient because loss of genioglossus tone allows it to fall posteriorly against the soft palate and posterior pharyngeal wall. The pharynx is divided into the nasopharynx (posterior to nasal cavity, contains adenoids), oropharynx (posterior to oral cavity, from soft palate to epiglottis tip), and hypopharynx/laryngopharynx (epiglottis tip to cricoid cartilage, continuous with the esophageal inlet posteriorly).

Laryngeal Anatomy

The larynx extends from C3 to C6 and comprises a cartilaginous skeleton, intrinsic and extrinsic muscles, and mucosal lining. The epiglottis is a leaf-shaped elastic cartilage attached to the inner surface of the thyroid cartilage; during swallowing it folds posteriorly to cover the glottis, preventing aspiration. The thyroid cartilage (the largest, forming the laryngeal prominence or "Adam's apple") shields the vocal folds anteriorly. The cricoid cartilage is the only complete cartilaginous ring in the airway and defines the narrowest point of the adult airway at the subglottic level (in children <8 years, the cricoid ring — not the glottis — is the narrowest point). The cricothyroid membrane connects the thyroid and cricoid cartilages anteriorly and is the target for emergency surgical airway access (cricothyrotomy); it is approximately 9 mm high and 30 mm wide and lies 2–3 cm below the laryngeal prominence.

The vocal cords (true vocal folds) are paired mucosal folds stretched between the arytenoid cartilages posteriorly and the thyroid cartilage anteriorly. They are innervated by the recurrent laryngeal nerve (RLN) — a branch of the vagus — which controls all intrinsic laryngeal muscles except the cricothyroid (innervated by the external branch of the superior laryngeal nerve, which tenses the cords). Unilateral RLN injury causes ipsilateral vocal cord paralysis (cord fixed in paramedian position, hoarseness); bilateral RLN injury causes bilateral cord adduction and stridor — a potential airway emergency. The superior laryngeal nerve (SLN) has an internal branch providing sensation above the vocal cords and an external branch providing motor innervation to the cricothyroid muscle.

Trachea & Bronchial Anatomy

The trachea is approximately 10–12 cm long in adults, extending from the cricoid cartilage (C6) to the carina (T4–T5), supported by 16–20 C-shaped cartilaginous rings open posteriorly (the posterior membranous wall abuts the esophagus). The tracheal internal diameter averages 20 mm in men, 18 mm in women. At the carina, the trachea bifurcates into the right and left mainstem bronchi. The right mainstem bronchus is wider, shorter (~2.5 cm), and more vertically oriented (25° from midline) than the left (~5 cm, 45°) — this explains why aspiration, endobronchial intubation, and foreign body impaction occur preferentially on the right. The right upper lobe bronchus takeoff is only ~2.5 cm from the carina, which can be obstructed by an endobronchial tube or a deeply placed endotracheal tube.

Lung Volumes & Capacities

Understanding lung volumes is essential for ventilator management, preoxygenation efficacy, and predicting desaturation time during apnea.

Oxygen-Hemoglobin Dissociation Curve

The oxygen-hemoglobin dissociation curve plots hemoglobin saturation (SpO₂) against partial pressure of oxygen (PaO₂). Its sigmoid shape reflects cooperative binding: as each O₂ molecule binds, affinity for the next increases. At a PaO₂ of 60 mmHg, saturation is approximately 90% — below this, small decreases in PaO₂ produce precipitous desaturation. The P50 is the PaO₂ at which hemoglobin is 50% saturated; normal P50 is 26.7 mmHg.

Ventilation-Perfusion Matching & Shunt

Gas exchange efficiency depends on matching of ventilation (V) and perfusion (Q). The ideal V/Q ratio is 1.0. Shunt (V/Q = 0) occurs when blood passes through non-ventilated alveoli (atelectasis, pneumonia, pulmonary edema, endobronchial intubation) — cannot be corrected by increasing FiO₂ alone (the hallmark of true shunt). Dead space (V/Q = ∞) occurs when ventilated alveoli have no perfusion (PE, low CO states). Hypoxic pulmonary vasoconstriction (HPV) is a protective reflex that diverts blood away from poorly ventilated lung regions to better-ventilated areas, optimizing V/Q matching. All volatile anesthetics inhibit HPV in a dose-dependent manner (significant at >1 MAC), worsening V/Q mismatch and increasing shunt — this is one reason arterial oxygenation may be worse under general anesthesia. The lateral decubitus position creates V/Q mismatch because the dependent lung receives more perfusion (gravity) but less ventilation (compression); one-lung ventilation amplifies this significantly.

Dead Space

Anatomical dead space (~150 mL in adults, approximately 2 mL/kg) is the volume of the conducting airways (nose to terminal bronchioles) that does not participate in gas exchange. Physiological dead space = anatomical dead space + alveolar dead space (alveoli ventilated but not perfused). In healthy individuals, physiological ≈ anatomical dead space. Increased dead space (pulmonary embolism, hypovolemia, high PEEP, ARDS) widens the PaCO₂–ETCO₂ gradient and increases minute ventilation requirements. Dead space is quantified by the Bohr equation: V_D/V_T = (PaCO₂ − PECO₂) / PaCO₂; normal V_D/V_T ≈ 0.3.

02 Cardiovascular Physiology for Anesthesia

Frank-Starling Mechanism

The Frank-Starling law states that the force of ventricular contraction increases with increasing preload (end-diastolic volume) up to a physiologic limit, because stretching sarcomeres to optimal length improves actin-myosin overlap. On the Frank-Starling curve, the x-axis is preload (LVEDV or LVEDP) and the y-axis is stroke volume or cardiac output. On the ascending limb, volume administration increases output — the patient is "fluid responsive." On the flat portion, additional volume provides no hemodynamic benefit and risks pulmonary edema. Heart failure shifts the entire curve downward and rightward; inotropes shift it upward.

Cardiac Output & Its Determinants

Cardiac output (CO) = heart rate (HR) × stroke volume (SV). Normal resting CO is approximately 5 L/min. Stroke volume is determined by three factors: preload (ventricular end-diastolic volume, reflecting venous return), afterload (resistance the ventricle must overcome to eject — approximated by SVR for the LV), and contractility (intrinsic myocardial force independent of loading conditions). Cardiac index (CI) = CO / BSA; normal 2.5–4.0 L/min/m².

Mean Arterial Pressure

MAP = CO × SVR, or clinically estimated as (SBP + 2 × DBP) / 3. MAP must be maintained ≥65 mmHg to ensure adequate organ perfusion. Under anesthesia, MAP commonly falls due to decreased SVR (vasodilation from volatile agents and propofol), reduced CO (myocardial depression, decreased venous return), and loss of sympathetic tone. MAP <55 mmHg is associated with acute kidney injury and myocardial ischemia.

Myocardial Oxygen Supply & Demand

Myocardial oxygen supply depends on coronary blood flow and arterial oxygen content (CaO₂). The left ventricle is perfused primarily during diastole (unlike most organs, which are perfused during systole) because intramyocardial compressive forces during systole occlude subendocardial vessels. Coronary perfusion pressure (CPP) = aortic diastolic pressure (DBP) − left ventricular end-diastolic pressure (LVEDP). Tachycardia shortens diastole and reduces coronary perfusion time while simultaneously increasing demand. Myocardial oxygen demand is determined by: heart rate (single most important), wall tension (by Laplace: proportional to pressure × radius / wall thickness), and contractility. The anesthesiologist's goal in coronary patients is to maintain adequate CPP while minimizing demand: avoid tachycardia, maintain diastolic pressure, and prevent excessive increases in contractility or afterload.

Baroreceptor Reflex

The baroreceptors in the carotid sinus (glossopharyngeal nerve, CN IX) and aortic arch (vagus nerve, CN X) detect changes in arterial stretch. A drop in blood pressure decreases baroreceptor firing, which disinhibits the vasomotor center in the medulla, causing increased sympathetic outflow (tachycardia, vasoconstriction) and decreased parasympathetic tone. Volatile anesthetics, propofol, and neuraxial blockade blunt this reflex, contributing to hemodynamic instability. Chronic hypertension resets baroreceptors to a higher set point, making these patients more susceptible to hypotension under anesthesia.

Hemodynamic Profiles by Shock Type

Understanding hemodynamic profiles is essential for diagnosing and managing shock under anesthesia:

Autonomic Nervous System Effects on the Heart

03 Pharmacokinetics & Pharmacodynamics

Compartment Models

Anesthetic drug distribution is modeled using multi-compartment pharmacokinetics. In a one-compartment model, the drug distributes instantaneously throughout a single homogeneous volume; elimination follows first-order kinetics with a single half-life. Most IV anesthetics follow a two- or three-compartment model: the central compartment (plasma and highly perfused organs — brain, heart, kidneys), a rapidly equilibrating peripheral compartment (muscle, viscera), and a slowly equilibrating deep compartment (fat). After a bolus, plasma concentration falls in three phases: rapid distribution (α phase), slower redistribution (β phase), and terminal elimination (γ phase). For highly lipophilic drugs like propofol and thiopental, rapid redistribution from brain to muscle terminates clinical effect after a single bolus, even though elimination half-life is long.

Context-Sensitive Half-Time

The context-sensitive half-time (CSHT) is the time required for plasma concentration to fall by 50% after stopping a continuous infusion, where "context" refers to infusion duration. Unlike elimination half-life, CSHT accounts for tissue redistribution and is far more clinically relevant for predicting recovery. For remifentanil, CSHT remains constant (~3–4 minutes) regardless of infusion duration because of rapid ester hydrolysis — it is "context-insensitive." For fentanyl, CSHT increases dramatically with prolonged infusion (from ~20 min at 1 hour to >200 min at 6 hours) as peripheral compartments saturate. Propofol CSHT increases modestly (from ~10 min at 1 hour to ~40 min at 8 hours). This concept guides drug selection for cases of varying duration.

Minimum Alveolar Concentration (MAC)

MAC is the minimum alveolar concentration of an inhaled anesthetic at 1 atm that prevents purposeful movement in response to a standard surgical stimulus (skin incision) in 50% of patients. MAC is the ED50 for movement suppression and represents a single point on the dose-response curve. MAC values are additive: 0.5 MAC of sevoflurane + 0.5 MAC of nitrous oxide = 1.0 MAC total. Key MAC variants:

Cp50 & Pharmacodynamic Principles

For IV anesthetics, Cp50 is the plasma concentration producing a specified effect in 50% of patients (analogous to MAC for volatiles). Target-controlled infusion (TCI) pumps use pharmacokinetic models (e.g., Marsh or Schnider for propofol, Minto for remifentanil) to achieve a specified plasma or effect-site concentration. The effect-site equilibration constant (ke0) describes the rate of drug equilibration between plasma and the brain; a higher ke0 means faster onset. The biophase (effect-site compartment) cannot be measured directly but is modeled based on the time course of clinical effect.

04 Key Terminology & Abbreviations

05 ASA Physical Status Classification

The ASA Physical Status Classification System, developed by the American Society of Anesthesiologists, is a subjective assessment of a patient's overall health status before surgery. It is the single most widely used preoperative risk stratification tool and is documented for every anesthetic. It does not directly predict surgical risk but correlates with perioperative morbidity and mortality.

The ASA-E modifier is appended to any class (e.g., ASA IIIE) when the procedure is emergent. An emergent case is defined as one in which delay would lead to significant increase in the threat to life or body part. Emergency status independently increases perioperative risk.

06 Preoperative Assessment

Cardiovascular Risk Assessment — ACC/AHA Stepwise Approach

The 2014 ACC/AHA Guideline on Perioperative Cardiovascular Evaluation and Management provides a stepwise algorithm for non-cardiac surgery:

Revised Cardiac Risk Index (RCRI / Lee Index)

Each factor scores 1 point. Total score predicts major adverse cardiac events (MACE):

Functional Capacity — METs

Functional capacity is measured in metabolic equivalents (METs). 1 MET = resting oxygen consumption (~3.5 mL O₂/kg/min). Patients unable to achieve 4 METs of activity are at elevated perioperative cardiac risk.

Pulmonary Risk Assessment

The ARISCAT score (Assess Respiratory Risk in Surgical Patients in Catalonia) predicts postoperative pulmonary complications (PPCs). Seven independent risk factors are scored: age (≥51: 3 pts; ≥80: 16 pts), preoperative SpO₂ (91–95%: 8 pts; ≤90%: 24 pts), respiratory infection in past month (17 pts), preoperative anemia (Hb ≤10 g/dL: 11 pts), upper abdominal or intrathoracic incision (15 pts), surgery duration >2 hours (16 pts), emergency surgery (8 pts). Low risk: <26 pts (1.6%); intermediate: 26–44 pts (13.3%); high risk: ≥45 pts (42.1%).

Hepatic & Renal Considerations

MELD score (Model for End-Stage Liver Disease) = 3.78 × ln(bilirubin mg/dL) + 11.2 × ln(INR) + 9.57 × ln(creatinine mg/dL) + 6.43. MELD ≥15 carries significant perioperative mortality for non-hepatic surgery; MELD >20 is associated with >50% 90-day mortality. Active hepatitis and Child-Pugh class C cirrhosis are relative contraindications to elective surgery. For renal patients, assess dialysis schedule, potassium level, volume status, and acid-base balance preoperatively; schedule dialysis the day before surgery to optimize electrolytes while allowing post-dialysis volume reequilibration.

Preoperative Laboratory Testing

Routine preoperative laboratory testing in healthy patients undergoing low-risk surgery is no longer recommended (Choosing Wisely campaign). Testing should be guided by patient comorbidities and the planned procedure:

NPO Guidelines (ASA Fasting Recommendations)

07 Airway Assessment

Mallampati Classification

The modified Mallampati classification is assessed with the patient sitting upright, mouth open maximally, tongue protruded, without phonation. It predicts the relative size of the tongue to the pharynx and correlates with difficulty of laryngoscopy.

Additional Airway Assessment

Thyromental distance (TMD): measured from the thyroid notch to the mentum with the neck fully extended. Normal ≥6.5 cm (roughly three finger breadths). TMD <6 cm suggests anterior larynx and potential difficulty. Neck mobility: atlanto-occipital extension is essential for the "sniffing position." Decreased mobility (rheumatoid arthritis, ankylosing spondylitis, cervical spine fusion, morbid obesity) impairs alignment of oral, pharyngeal, and laryngeal axes. Inter-incisor distance: mouth opening <3 cm (two finger breadths) limits blade insertion. Upper lip bite test (ULBT): class I — lower incisors can bite above the vermilion of the upper lip (easy); class II — lower incisors can bite the upper lip below the vermilion (moderate); class III — lower incisors cannot bite the upper lip (difficult).

LEMON Mnemonic for Difficult Intubation

Predictors of Difficult Mask Ventilation — MOANS

Predictors of Difficult Intubation — HEAVEN

Cannot-Intubate-Cannot-Oxygenate (CICO) Preparation

Every anesthetic plan must include a CICO contingency. Before any induction: confirm availability of a surgical airway kit (scalpel-bougie-tube or commercial cricothyrotomy set), identify the cricothyroid membrane by palpation or ultrasound, and brief the team. In CICO: perform front-of-neck access (FONA) via cricothyrotomy — vertical skin incision, horizontal stab through cricothyroid membrane, insert bougie, railroad a cuffed 6.0 ETT or tracheostomy tube. Jet ventilation through a needle cricothyrotomy is a temporizing measure but carries risk of barotrauma and is not definitive.

08 Medication Management — Perioperative

Anticoagulants — Hold Times & Bridging

Antiplatelet Agents

Other Medications

09 Induction Agents

10 Volatile Anesthetics

Volatile (inhaled) anesthetics are halogenated ethers (except N₂O) that provide all components of general anesthesia: amnesia, unconsciousness, immobility, and some analgesia. They are administered via calibrated vaporizers (except desflurane, which requires a heated pressurized vaporizer due to its near-room-temperature boiling point of 22.8°C).

Nitrous Oxide — Special Concerns

N₂O is 34× more soluble in blood than nitrogen, so it diffuses into closed gas-filled spaces faster than nitrogen can diffuse out, causing expansion. Contraindicated in: pneumothorax, bowel obstruction, middle ear surgery, pneumocephalus, air embolism, recent intraocular gas injection (SF₂ bubble). Diffusion hypoxia: at emergence, rapid N₂O elimination from blood into alveoli dilutes alveolar O₂ — prevented by administering 100% O₂ for 5–10 minutes after discontinuing N₂O. N₂O irreversibly oxidizes the cobalt atom in vitamin B₂₁₂, inhibiting methionine synthase. Prolonged exposure (>6 hours) can cause megaloblastic anemia and subacute combined degeneration of the spinal cord (similar to B₂₁₂ deficiency). Avoid in B₂₁₂-deficient patients.

MAC Values Summary

Cardiovascular & Respiratory Effects (All Volatiles)

All volatile agents cause dose-dependent myocardial depression (decreased contractility and CO), systemic vasodilation (decreased SVR, decreased MAP), and respiratory depression (decreased tidal volume, increased respiratory rate, blunted ventilatory response to CO₂ and hypoxia). They increase cerebral blood flow (which can increase ICP — use cautiously in neurosurgery; sevoflurane has the least effect at <1 MAC). All volatiles are bronchodilators (useful in bronchospasm; sevoflurane preferred due to non-pungent nature). All trigger malignant hyperthermia in susceptible individuals. All potentiate non-depolarizing neuromuscular blockers in a dose-dependent manner.

11 Neuromuscular Blocking Agents

Depolarizing Agent — Succinylcholine

Succinylcholine (SCh) is the only depolarizing neuromuscular blocker in clinical use. It mimics acetylcholine at the nicotinic receptor, causing initial depolarization (fasciculations) followed by sustained depolarization and desensitization of the motor end plate, producing flaccid paralysis.

Other adverse effects: bradycardia (muscarinic stimulation — especially with repeat doses; pretreat children with atropine), increased IOP (transient, ~5–10 mmHg — relative concern in open globe injury, though evidence of actual extrusion is lacking), increased intragastric pressure (offset by increased lower esophageal sphincter tone), masseter muscle rigidity (may herald malignant hyperthermia), malignant hyperthermia trigger (the only NMBA that triggers MH), prolonged block with pseudocholinesterase deficiency (homozygous atypical: duration 4–8 hours; dibucaine number <30).

Non-Depolarizing Agents

Reversal of Neuromuscular Blockade

Neostigmine (0.03–0.07 mg/kg IV, max 5 mg): an acetylcholinesterase inhibitor that increases ACh at the neuromuscular junction, competing with residual non-depolarizing agent. Must be co-administered with an anticholinergic (glycopyrrolate 0.2 mg per 1 mg neostigmine, or atropine 0.4 mg per 1 mg neostigmine) to block muscarinic effects (bradycardia, salivation, bronchospasm). Neostigmine is ineffective at deep levels of block (requires at least 1–2 twitches on TOF).

Sugammadex is a modified γ-cyclodextrin that encapsulates rocuronium (and to a lesser extent vecuronium) in a 1:1 complex, rendering it inactive. It does not require anticholinergic co-administration and works at any depth of block:

TOF Monitoring

Train-of-four stimulation delivers four supramaximal stimuli at 2 Hz to a peripheral nerve (typically the ulnar nerve, measuring adductor pollicis response). The TOF ratio = T4/T1 amplitude. A TOF ratio ≥0.9 (by quantitative monitoring) is required before extubation to minimize residual neuromuscular blockade, which increases the risk of aspiration, hypoxia, and reintubation. Qualitative (subjective) assessment by tactile TOF is unreliable for detecting ratios between 0.4 and 0.9.

12 Opioids in Anesthesia

Opioids are the primary analgesic agents in anesthesia, acting at mu (μ), kappa (κ), and delta (δ) receptors in the CNS and periphery. Mu-receptor activation produces analgesia, euphoria, respiratory depression, miosis, decreased GI motility, and physical dependence.

Equianalgesic Dosing Table (Approximate)

13 Airway Management Techniques

Mask Ventilation

Bag-mask ventilation (BMV) is the foundational airway skill. The jaw thrust (bilateral mandibular angles lifted anteriorly) and chin lift displace the tongue from the posterior pharynx. Oral airways (Guedel) are sized from the corner of the mouth to the angle of the mandible and are contraindicated in conscious patients (provoke gag/laryngospasm). Nasal airways (nasopharyngeal trumpet) are better tolerated in semi-conscious patients; size = diameter of the patient's little finger; caution with coagulopathy and basilar skull fracture. The C-E technique: the thumb and index finger form a "C" over the mask; the remaining three fingers form an "E" on the mandible. Two-person technique improves seal in difficult cases.

Direct Laryngoscopy

Macintosh blade (curved): inserted into the vallecula between the base of tongue and epiglottis; pressure on the hyoepiglottic ligament indirectly lifts the epiglottis to expose the glottis. Available in sizes 1–4 (most adults: size 3 or 4). Miller blade (straight): tip placed posterior to the epiglottis, directly lifting it. Preferred in neonates and infants (floppy epiglottis), anterior airways, and situations where direct epiglottic lift is needed. Macintosh is generally preferred in adults because it provides more room for tube passage. View is graded by the Cormack-Lehane classification:

Video Laryngoscopy (VL)

Video laryngoscopes incorporate a camera near the blade tip, providing an indirect view of the glottis on a screen. They generally improve the Cormack-Lehane grade by 1–2 levels compared to DL. GlideScope: hyperangulated blade (60°), provides excellent view but requires a stylet with matching curvature for tube delivery. McGrath MAC: Macintosh-geometry disposable blade; can be used as standard DL or video-assisted. C-MAC (Storz): available in standard Macintosh and D-blade (hyperangulated) configurations. VL is recommended as the first-attempt strategy by many institutions, especially for anticipated difficult airways. Limitations: fogging, blood/secretions on camera, difficulty with tube delivery despite good view ("grade 1 view, grade 3 intubation").

Bougie (Tracheal Tube Introducer)

The bougie (gum elastic bougie, Eschmann introducer) is a critical rescue device for Cormack-Lehane grade IIb–III views. It is a 60–70 cm semi-rigid stylet with an angled (coupé) tip that is advanced blindly under the epiglottis toward the trachea during direct laryngoscopy. Confirmation of tracheal placement: (1) "clicks" felt as the tip slides over tracheal rings (positive in ~90%), and (2) "hold-up" at 30–40 cm as the tip reaches a distal bronchus (100% if present; in esophageal placement, the bougie slides freely without resistance). The ETT is then railroaded over the bougie into the trachea. Studies demonstrate that first-pass intubation success is significantly higher when the bougie is used routinely for DL compared to a standard stylet (BEAM trial). Many institutions now advocate routine bougie use for all DL intubations.

Supraglottic Airways (SGAs)

SGAs sit above the glottis and provide a hands-free airway without tracheal intubation. They are a key rescue device in the difficult airway algorithm. The laryngeal mask airway (LMA) is the prototypical SGA. Types include: LMA Classic (reusable, first-generation), LMA ProSeal (second-generation, with gastric drain tube and higher seal pressures up to 30 cmH₂O), LMA Supreme (disposable second-generation with gastric channel), i-gel (non-inflatable gel cuff, gastric channel), and LMA Fastrach/intubating LMA (designed for blind or fiberoptic-guided intubation through the SGA). Size selection: #3 for 30–50 kg, #4 for 50–70 kg, #5 for 70–100 kg.

Endotracheal Tube Selection & Positioning

Standard ETT sizing for adults: women 7.0–7.5 mm ID, men 7.5–8.0 mm ID. A smaller tube (6.0–6.5) should be selected for: anticipated difficult intubation (easier to pass), nasal intubation, subglottic stenosis, and pregnancy (airway edema). ETT depth at the lip: typically 21 cm for women, 23 cm for men (mnemonic: "21 for women, 23 for men"). Proper position places the tip 3–5 cm above the carina. Confirm placement by: (1) persistent ETCO₂ waveform (most reliable), (2) bilateral chest rise, (3) bilateral breath sounds, (4) absence of epigastric sounds, (5) chest X-ray (tip should project between T2 and T4). The cuff is inflated to achieve a seal at 20–30 cmH₂O (minimal leak technique) — pressures >30 cmH₂O risk tracheal mucosal ischemia and stenosis.

Fiberoptic Intubation

Awake fiberoptic intubation (AFOI) is the gold standard for anticipated difficult airway when mask ventilation is also expected to be difficult. The patient breathes spontaneously throughout. Preparation: antisialagogue (glycopyrrolate 0.2 mg IV), topicalization of the airway with lidocaine (nebulized 4%, oropharyngeal spray, transtracheal injection through cricothyroid membrane, or "spray-as-you-go" through the scope's working channel), and judicious sedation (dexmedetomidine or remifentanil infusion — maintain cooperation and airway reflexes). The flexible bronchoscope is advanced through the nose or mouth, the ETT is loaded on the scope, the scope is guided past the vocal cords, and the ETT is railroaded over the scope into the trachea. Confirm position by visualizing tracheal rings and carina through the scope.

Rapid Sequence Induction (RSI)

RSI is indicated when the patient is at risk for aspiration (full stomach, pregnancy, bowel obstruction, GERD, hiatal hernia, emergency surgery). Sequence: preoxygenation for 3–5 minutes (or 8 vital capacity breaths of 100% O₂), pre-treatment if indicated, induction agent + succinylcholine 1–1.5 mg/kg (or rocuronium 1.2 mg/kg) given simultaneously, cricoid pressure (Sellick maneuver — 30 N of posterior force on cricoid cartilage to occlude the esophagus; controversial, may impair laryngoscopic view), NO bag-mask ventilation between induction and intubation (to avoid gastric insufflation), and intubation within 60 seconds of apnea. Modified RSI: gentle bag-mask ventilation with low pressures (<20 cmH₂O) may be applied if desaturation occurs before intubation conditions are achieved.

ASA 2022 Difficult Airway Algorithm (Simplified)

14 Local Anesthetics

Mechanism of Action

Local anesthetics (LAs) reversibly block voltage-gated sodium channels from the intracellular side, preventing sodium influx, depolarization, and action potential propagation. They preferentially block small, myelinated (Aδ — pain, temperature) and unmyelinated (C — dull pain, postganglionic autonomic) fibers before large myelinated fibers (Aα — motor, proprioception). Clinical sequence of blockade: sympathetic → pain → temperature → touch → proprioception → motor.

Amides vs. Esters

Pharmacology of Key Agents

Local Anesthetic Systemic Toxicity (LAST)

LAST occurs from inadvertent intravascular injection or excessive absorption. Plasma levels rise and produce a biphasic toxicity pattern:

15 Neuraxial Anesthesia — Spinal & Epidural

Spinal Anesthesia

Spinal (subarachnoid) anesthesia involves a single injection of local anesthetic into the cerebrospinal fluid (CSF) in the lumbar subarachnoid space. The spinal cord terminates at L1–L2 in adults (the conus medullaris), so the needle is inserted at L3–L4 or L4–L5 interspace to avoid cord injury. The L4–L5 interspace is identified by a line connecting the iliac crests (Tuffier's line). Needle types include Quincke (cutting tip — higher PDPH risk) and Whitacre/Sprotte (pencil-point — lower PDPH risk, preferred). CSF confirmation (clear, free-flowing) confirms subarachnoid placement.

The most common agent is hyperbaric bupivacaine 0.75% (with 8.25% dextrose), which is denser than CSF and affected by gravity/patient position (baricity). Typical dose: 10–15 mg for lower abdominal/lower extremity surgery; 7.5–10 mg for C-section. Onset: 2–5 minutes. Duration: 90–150 minutes (depending on dose and adjuvants). Common adjuvants: fentanyl 10–25 mcg (faster onset, improved quality, minimal prolongation), morphine 0.1–0.2 mg (prolonged postoperative analgesia up to 24 hours but delayed respiratory depression risk up to 24 h).

Dermatome Levels by Procedure

Spinal Complications

Post-dural puncture headache (PDPH): incidence 1–3% with pencil-point needles, up to 30% with large-bore cutting needles. Frontal/occipital headache worsened by sitting/standing, relieved within 30 minutes of lying supine. Onset within 5 days of dural puncture. Mechanism: CSF leak through dural hole → decreased intracranial pressure → compensatory cerebral vasodilation and traction on meninges. Management: conservative (hydration, caffeine 300–500 mg PO/IV, analgesics) for 24–48 h; epidural blood patch (15–25 mL autologous blood injected into epidural space) for persistent symptoms — >90% effective. Hypotension: most common side effect of spinal anesthesia (sympathectomy → vasodilation + decreased venous return); treat with IV fluid, phenylephrine 50–100 mcg boluses (first-line), or ephedrine 5–10 mg (if bradycardia). High/total spinal: excessive cephalad spread → hypotension, bradycardia, respiratory insufficiency (diaphragmatic paralysis at C3–C5), loss of consciousness; treat with hemodynamic support, airway management, and intubation if needed. TNS (transient neurologic symptoms): pain/dysesthesia in buttocks/legs within 24 h, resolves in days; more common with lidocaine — a reason bupivacaine is preferred for spinals.

Epidural Anesthesia

The epidural space lies between the ligamentum flavum and the dura mater. Access is via the loss of resistance (LOR) technique: a syringe filled with saline (or air) is attached to the Tuohy needle; as the needle advances through the ligamentum flavum into the epidural space, resistance suddenly disappears. A catheter is then threaded 3–5 cm into the space for continuous infusion. Epidural anesthesia can be placed at any vertebral level (thoracic for chest/abdominal surgery, lumbar for lower extremity/obstetric).

Test dose: 3 mL of lidocaine 1.5% with 1:200,000 epinephrine (45 mg lidocaine + 15 mcg epinephrine). If intrathecal: rapid motor block within 3–5 minutes. If intravascular: heart rate increase ≥20 bpm within 60 seconds. Patient-controlled epidural analgesia (PCEA): typical regimen for labor — bupivacaine 0.0625–0.1% + fentanyl 2 mcg/mL; basal rate 6–10 mL/h, demand dose 5–8 mL, lockout 10–20 minutes.

Combined Spinal-Epidural (CSE)

The CSE technique provides the rapid onset and reliability of spinal anesthesia with the flexibility of an epidural catheter for prolonged procedures or postoperative analgesia. Needle-through-needle technique: the Tuohy needle is placed in the epidural space, a long spinal needle is advanced through it to puncture the dura, the intrathecal dose is injected, the spinal needle is withdrawn, and the epidural catheter is threaded. Commonly used for C-sections and labor analgesia.

16 Peripheral Nerve Blocks — Upper Extremity

Brachial Plexus Anatomy

The brachial plexus is formed by the ventral rami of C5–T1 and follows the mnemonic Robert Taylor Drinks Cold Beer — Roots, Trunks, Divisions, Cords, Branches:

Interscalene Block

The interscalene block targets the roots/trunks of the brachial plexus (C5–C7) in the interscalene groove between the anterior and middle scalene muscles at the level of the cricoid cartilage (C6). It provides excellent anesthesia for shoulder and proximal humerus surgery. The inferior trunk (C8–T1) is commonly spared, resulting in incomplete ulnar nerve blockade — not ideal for hand/forearm procedures. Key complications: phrenic nerve paralysis (virtually 100% ipsilateral hemidiaphragm paresis — avoid bilaterally and in patients with contralateral phrenic nerve dysfunction or significant pulmonary disease), Horner syndrome (miosis, ptosis, anhidrosis), recurrent laryngeal nerve block (hoarseness), vertebral artery injection, epidural/intrathecal spread.

Supraclavicular Block

The supraclavicular block targets the trunks/divisions at the level of the first rib, lateral to the subclavian artery, behind the clavicle. Often called the "spinal of the arm" because it provides rapid, dense blockade of the entire upper extremity below the shoulder. Excellent for elbow, forearm, wrist, and hand surgery. Under ultrasound guidance, the plexus appears as a "cluster of grapes" lateral and posterior to the subclavian artery, above the hyperechoic first rib. Risk: pneumothorax (historically ~1% with landmark technique, now <0.5% with ultrasound), phrenic nerve paresis (~50%).

Infraclavicular Block

The infraclavicular block targets the cords beneath the clavicle, around the axillary artery. The needle is inserted medial to the coracoid process, directed posteriorly. Advantages: catheter-friendly location (less prone to dislodgment), complete coverage below the mid-humerus including the musculocutaneous nerve (which may be missed with axillary block). Lower risk of pneumothorax and phrenic nerve paresis than supraclavicular approach.

Axillary Block

The axillary block targets the terminal branches (median, ulnar, radial) of the brachial plexus in the axilla around the axillary artery. Ideal for hand, wrist, and forearm surgery. Safest brachial plexus block (no pneumothorax, no phrenic nerve paresis). The musculocutaneous nerve leaves the brachial plexus sheath early and enters the coracobrachialis muscle — it must be blocked separately (injected within the coracobrachialis) for complete lateral forearm coverage. Under ultrasound, the nerves are identified relative to the axillary artery: median (superficial/lateral), ulnar (superficial/medial), radial (posterior/deep).

17 Peripheral Nerve Blocks — Lower Extremity & Truncal

Lower Extremity Blocks

Truncal & Fascial Plane Blocks

18 Standard ASA Monitors

The ASA Standards for Basic Anesthetic Monitoring (last affirmed 2020) mandate monitoring of oxygenation, ventilation, circulation, and temperature during all anesthetics. A qualified anesthesia provider must be continuously present.

Oxygenation

Pulse oximetry (SpO₂) is mandatory for every anesthetic. It measures the ratio of oxyhemoglobin to total hemoglobin using two wavelengths of light (660 nm red, 940 nm infrared) based on the Beer-Lambert law (light absorption is proportional to concentration of the absorbing substance and path length). Limitations: inaccurate with carboxyhemoglobin (CO-Hb reads falsely high ~100%), methemoglobinemia (SpO₂ trends toward 85% regardless of true saturation), severe peripheral vasoconstriction, nail polish (especially blue/green), motion artifact, and anemia (accurate until Hb <5 g/dL). An oxygen analyzer with a low-concentration alarm must be used in the breathing circuit to verify FiO₂.

Ventilation

Capnography (ETCO₂) is mandatory whenever an ETT or SGA is in use, and strongly encouraged during MAC/sedation. It is the most reliable method to confirm endotracheal tube placement (presence of CO₂ waveform) and is the earliest indicator of esophageal intubation (absent CO₂). Normal ETCO₂: 35–45 mmHg, typically 2–5 mmHg less than PaCO₂.

Circulation

ECG is continuously displayed. Standard 5-lead monitoring allows ST-segment analysis in leads II (inferior ischemia, P-wave analysis, arrhythmia detection) and V5 (anterior/lateral ischemia). Combined leads II + V5 detect ~95% of intraoperative ST changes. Non-invasive blood pressure (NIBP) is measured at intervals of ≤5 minutes. Cuff size matters: too small overestimates, too large underestimates (bladder width should be 40% of arm circumference).

Temperature

Monitoring is indicated whenever clinically significant changes in body temperature are anticipated. Sites (in order of accuracy for core temperature): pulmonary artery catheter (gold standard), distal esophageal, nasopharyngeal, tympanic membrane, bladder. Hypothermia (<36°C) is common under general anesthesia (impaired thermoregulation, cold OR environment, cold IV fluids, heat loss from surgical exposure) and increases bleeding (impaired coagulation), infection risk, and cardiac events. Active warming (forced-air warming blanket, fluid warmer) is standard of care.

Neuromuscular Monitoring Sites & Patterns

Beyond TOF, several other stimulation patterns are used: single twitch (1 Hz) — simple but insensitive (cannot detect residual block <75% receptor occupancy). Tetanic stimulation (50 Hz for 5 sec) — sustained stimulus; fade indicates non-depolarizing block. Post-tetanic count (PTC) — after tetanic stimulus, count the number of post-tetanic twitches; used to assess deep block when TOF = 0 (PTC 1–2 = deep; PTC ≥10 = approaching moderate block, TOF will reappear soon). Double burst stimulation (DBS) — two bursts of 3 stimuli at 50 Hz separated by 750 ms; easier to detect fade manually than TOF (clinician compares two discrete responses rather than four). Monitoring site: the adductor pollicis (ulnar nerve at the wrist) is the reference muscle for neuromuscular monitoring. The corrugator supercilii (facial nerve) has faster onset and recovery than the adductor pollicis — useful for predicting intubating conditions but overestimates recovery at the diaphragm and peripheral muscles.

Depth of Anesthesia — BIS Monitor

The bispectral index (BIS) is a processed EEG parameter scaled from 0 (isoelectric) to 100 (fully awake). Target range for general anesthesia: 40–60. BIS >60: increased risk of awareness; BIS <40: deeper than necessary, may increase postoperative delirium. Indications: TIVA (no end-tidal volatile to titrate), high-risk patients for awareness (cardiac surgery, C-section under GA, trauma, history of awareness), neuromuscular blockade (clinical signs of light anesthesia are masked).

19 Invasive Monitoring

Goal-Directed Fluid Therapy (GDFT)

Rather than relying on fixed formulas, goal-directed fluid therapy uses dynamic hemodynamic parameters to guide individual fluid administration. Static parameters (CVP, PCWP) are poor predictors of fluid responsiveness. Dynamic parameters include: pulse pressure variation (PPV) and stroke volume variation (SVV) — PPV >13% or SVV >12% during mechanical ventilation (in sinus rhythm, TV ≥8 mL/kg, closed chest) predicts fluid responsiveness with ~85% sensitivity and specificity. Passive leg raise (PLR) test: raising the legs to 45° from supine autotransfuses ~300 mL from the lower extremities; a ≥10% increase in CO within 1 minute predicts fluid responsiveness — this works even with spontaneous breathing, arrhythmias, and open chest (unlike PPV/SVV). Point-of-care cardiac output monitors (FloTrac/Vigileo, LiDCO, ClearSight) and transesophageal echocardiography enable real-time GDFT implementation.

Arterial Line

An arterial catheter provides continuous, beat-to-beat blood pressure measurement and facilitates repeated arterial blood gas sampling. Common sites: radial (most common — perform modified Allen test to confirm dual blood supply via ulnar artery before cannulation), femoral, brachial, dorsalis pedis. Indications: hemodynamic instability anticipated, vasoactive infusions, frequent ABGs, deliberate hypotension, morbid obesity (NIBP unreliable).

Arterial waveform analysis: the waveform shows a systolic upstroke, systolic peak, dicrotic notch (aortic valve closure), and diastolic runoff. Overdamping (air bubble, clot, kink, soft tubing): underestimates systolic and overestimates diastolic pressure, loss of dicrotic notch, slurred upstroke. Underdamping/resonance (long tubing, tachycardia): overestimates systolic and underestimates diastolic, ringing artifact. The fast-flush (square wave) test assesses system dynamics: 1–2 oscillations before settling = optimally damped; >2 oscillations = underdamped; no oscillation = overdamped. MAP is least affected by damping and is the most reliable value.

Central Venous Catheter (CVC)

A CVC is placed in a large central vein for venous access (vasoactive infusions, caustic drugs, TPN), hemodynamic monitoring (CVP), and rapid volume resuscitation (large-bore introducer sheath). Common sites: internal jugular vein (IJV) — preferred, ultrasound-guided, right side preferred (straight path to SVC); subclavian vein — lower infection rate but higher pneumothorax risk, not compressible if hemorrhage occurs; femoral vein — easiest landmark, no pneumothorax risk, but higher infection rate and DVT risk. Confirm tip position in the SVC-RA junction by chest X-ray.

CVP waveform has three positive waves and two descents: a wave (atrial contraction — absent in atrial fibrillation, giant "cannon" a waves in complete heart block or junctional rhythm when atrium contracts against a closed tricuspid valve), c wave (tricuspid valve bulging into atrium during isovolumetric contraction), v wave (passive atrial filling during ventricular systole, with tricuspid closed — giant v waves in tricuspid regurgitation), x descent (atrial relaxation), y descent (early ventricular filling after tricuspid opening). Normal CVP: 2–8 mmHg. CVP reflects right atrial pressure but is a poor predictor of fluid responsiveness.

Pulmonary Artery Catheter (PAC / Swan-Ganz)

The PAC is a flow-directed, balloon-tipped catheter inserted through a central vein introducer, advanced through the RA, RV, and PA, and "wedged" in a branch of the PA. It measures: RA pressure (CVP), RV pressure, PA pressure (systolic/diastolic/mean), pulmonary capillary wedge pressure (PCWP) (reflects LA pressure and LVEDP when mitral valve is normal; normal 6–12 mmHg), cardiac output (thermodilution), and mixed venous oxygen saturation (SvO₂; normal 65–75%, low = increased extraction from inadequate DO₂).

20 Fluid Management & Transfusion

Crystalloids vs. Colloids

Crystalloids are electrolyte solutions that distribute freely across the extracellular space. Approximately 25% of infused crystalloid remains intravascular after 30 minutes (the rest shifts to the interstitium). Balanced crystalloids — lactated Ringer's (LR: Na 130, K 4, Ca 3, Cl 109, lactate 28 mEq/L) and PlasmaLyte (Na 140, K 5, Mg 3, Cl 98, acetate 27, gluconate 23) — are preferred over normal saline (NS: Na 154, Cl 154) for large-volume resuscitation because NS causes hyperchloremic metabolic acidosis and may worsen AKI (SMART trial). Colloids (albumin 5%, hydroxyethyl starch) theoretically expand intravascular volume more efficiently (~75% remains intravascular), but HES increases renal injury and mortality in critically ill patients (6S and CHEST trials) and is no longer recommended in sepsis or ICU settings.

Maintenance Fluid Calculation — 4-2-1 Rule

Example: 70 kg adult = (4 × 10) + (2 × 10) + (1 × 50) = 110 mL/h. Intraoperative fluid management additionally accounts for: NPO deficit (hourly rate × hours fasted — replace 50% in first hour, 25% in second and third hours), ongoing losses (estimated blood loss, third-space losses — minimal for superficial surgery, 4–8 mL/kg/h for major abdominal), and urine output (target 0.5–1 mL/kg/h).

Transfusion

Massive transfusion protocol (MTP): activated for anticipated need of ≥10 units pRBCs in 24 hours (or ≥4 units in 1 hour). Goal-directed: transfuse pRBCs, FFP, and platelets in a 1:1:1 ratio (PROPPR trial). Adjuncts: tranexamic acid 1 g IV over 10 min then 1 g over 8 hours (CRASH-2 — give within 3 hours of injury), calcium replacement (citrate in blood products chelates calcium — monitor ionized calcium, give CaCl₂ 1 g per ~4 units), cryoprecipitate if fibrinogen <150 mg/dL.

Transfusion Reactions

TRALI (transfusion-related acute lung injury): non-cardiogenic pulmonary edema within 6 hours of transfusion, bilateral infiltrates, hypoxemia, no evidence of volume overload. Leading cause of transfusion-related death. Treatment: supportive (stop transfusion, oxygen, mechanical ventilation if needed). TACO (transfusion-associated circulatory overload): cardiogenic pulmonary edema from volume excess. Distinguishing feature: elevated BNP and JVP in TACO but not TRALI. Treatment: diuretics, slow transfusion rate.

Complications of Massive Transfusion

Beyond TRALI and TACO, massive transfusion carries several additional risks: hypothermia (stored blood is at 4°C — use fluid warmers for all rapid transfusions), hypocalcemia (citrate in blood products chelates ionized calcium — monitor iCa²+ and give CaCl₂ 1 g IV per approximately 4 units pRBCs; symptoms include hypotension, prolonged QT, and cardiac depression), hyperkalemia (potassium leaks from stored RBCs, especially older units — can reach 30–50 mEq/L in the supernatant of aged pRBCs; wash or use fresh units for neonates), dilutional coagulopathy (progressive depletion of factors and platelets with crystalloid and pRBC-only resuscitation — prevented by balanced ratio transfusion), metabolic alkalosis (citrate is metabolized to bicarbonate — late complication after massive transfusion), and 2,3-DPG depletion in stored blood (left-shifts the oxyhemoglobin curve, impairing O₂ release to tissues).

Viscoelastic Testing

TEG (thromboelastography) and ROTEM (rotational thromboelastometry) provide point-of-care assessment of the entire coagulation cascade from clot initiation through fibrinolysis. Key TEG parameters: R time (reaction time — time to initial clot formation; prolonged = factor deficiency → give FFP), K time (clot kinetics — time to reach 20 mm amplitude), α angle (rate of clot strengthening — low = fibrinogen deficiency → give cryoprecipitate), MA (maximum amplitude — reflects platelet function and fibrinogen; low = platelet deficiency/dysfunction → give platelets or DDAVP), LY30 (percent lysis at 30 minutes — >3% = fibrinolysis → give tranexamic acid).

21 Malignant Hyperthermia

Pathophysiology

Malignant hyperthermia (MH) is a pharmacogenetic syndrome triggered by exposure to volatile anesthetic agents (sevoflurane, desflurane, isoflurane, halothane) and/or succinylcholine in genetically susceptible individuals. The defect is most commonly an autosomal dominant mutation in the RYR1 gene (ryanodine receptor type 1 on skeletal muscle sarcoplasmic reticulum). Triggering agents cause uncontrolled release of calcium from the sarcoplasmic reticulum into the myoplasm, resulting in sustained muscle contraction, a hypermetabolic state (massively increased O₂ consumption and CO₂ production), heat generation, rhabdomyolysis, and ultimately cellular death if untreated. Mortality without treatment exceeds 70%; with early dantrolene, mortality is <5%.

Clinical Presentation

Treatment — Dantrolene Protocol

Safe Anesthesia for MH-Susceptible Patients

For patients with known or suspected MH susceptibility: avoid all triggering agents (volatile anesthetics and succinylcholine). Use TIVA (propofol + remifentanil or fentanyl), non-depolarizing NMBAs (rocuronium/cisatracurium), benzodiazepines, opioids, and regional/neuraxial anesthesia as appropriate. N₂O is safe (not a trigger). Prepare the anesthesia machine: flush with high-flow O₂ (≥10 L/min) for ≥20 minutes with fresh circuit and soda lime (or use a "clean" machine with activated charcoal filters), remove or disable vaporizers. Ensure dantrolene is immediately available (36 vials of standard dantrolene or 3 vials of Ryanodex). Monitor temperature and ETCO₂ continuously. Amide local anesthetics are safe (they do not trigger MH despite historical concern). Post-anesthesia: monitor in PACU for at least 1 hour; extended observation is not strictly required if the procedure was short and the patient is stable.

Diagnosis & Genetic Testing

The gold standard diagnostic test is the caffeine-halothane contracture test (CHCT), performed on a fresh muscle biopsy (vastus lateralis). Muscle strips are exposed to halothane and caffeine; MH-susceptible muscle demonstrates enhanced contracture. Sensitivity ~97%, specificity ~78%. Genetic testing for RYR1 and CACNA1S mutations is available but a negative genetic test does not exclude MH susceptibility (not all causative mutations are known). First-degree relatives of confirmed MH patients should be considered susceptible until tested.

22 Anaphylaxis in the OR

Common Triggers

Perioperative anaphylaxis occurs in approximately 1:10,000–1:20,000 anesthetics. The most common triggers are: neuromuscular blocking agents (~60% of cases — particularly rocuronium and succinylcholine, due to quaternary ammonium cross-reactivity), antibiotics (especially beta-lactams/cephalosporins given at induction), latex (declining with latex-free environments but still relevant), chlorhexidine (skin prep, CVC impregnation), colloids (gelatin, dextran), blood products, dyes (methylene blue, patent blue, isosulfan blue), and protamine.

Clinical Grading

Immediate Management

Differential Diagnosis of Intraoperative Anaphylaxis

Not all hemodynamic collapse during anesthesia is anaphylaxis. The differential includes: non-immune anaphylactoid reaction (direct mast cell degranulation without IgE — e.g., morphine, vancomycin "red man syndrome"), vasovagal response, high spinal, tension pneumothorax, air embolism, acute blood loss, cardiogenic shock, transfusion reaction, and propofol infusion-related hypotension. Bronchospasm without hypotension may represent reactive airway disease triggered by airway manipulation rather than anaphylaxis. The triad of hypotension + bronchospasm + cutaneous findings is most specific for anaphylaxis. In the anesthetized, draped patient, cutaneous signs (urticaria, flushing) may be hidden or absent, making tryptase levels essential for retrospective diagnosis.

Post-Event Workup

Draw serum tryptase levels at 3 time points: immediately when feasible, at 1–2 hours after symptom onset (peak), and at 24 hours (baseline). An elevated peak tryptase (>11.4 ng/mL or >2 + 1.2 × baseline) supports the diagnosis of mast cell degranulation. Refer the patient to an allergist for skin testing (intradermal testing with suspected agents, ideally at 4–6 weeks post-event) and specific IgE measurement. Results guide future anesthetic planning and drug avoidance.

23 Perioperative Cardiac Events

Intraoperative Myocardial Ischemia / Infarction

Intraoperative STEMI/NSTEMI may present as new ST elevation/depression ≥1 mm on ECG monitor, new regional wall motion abnormality on TEE, hemodynamic instability (hypotension, new arrhythmia), or elevated troponin postoperatively. Management: optimize hemodynamics (correct hypotension and tachycardia, maintain CPP), administer nitroglycerin for ischemia (avoid if hypotensive), heparin (if surgical bleeding is acceptable), consider emergent PCI if STEMI, and consult cardiology. Aspirin and dual antiplatelet therapy decisions are balanced against surgical bleeding risk.

Bradycardia

Intraoperative bradycardia (HR <50 bpm with hemodynamic compromise): common causes include high spinal/epidural, vagal stimulation (laryngoscopy, surgical manipulation of peritoneum/eye), opioids, beta-blockers, dexmedetomidine. Treatment ladder: atropine 0.5–1 mg IV (muscarinic antagonist — first-line), glycopyrrolate 0.2–0.4 mg IV (does not cross BBB), ephedrine 5–10 mg IV (indirect sympathomimetic, increases HR and BP), epinephrine 10–100 mcg IV for severe bradycardia, transcutaneous/transvenous pacing for refractory cases.

Intraoperative Hypertension

Intraoperative hypertension (SBP >20% above baseline) is common and has multiple causes: inadequate anesthesia depth (most common), pain/noxious stimulation, hypercarbia, hypoxemia, full bladder, medications (ketamine, vasopressors, ergot alkaloids), pheochromocytoma, aortic cross-clamping, malignant hyperthermia, and pre-existing essential hypertension. Management: first address the cause (deepen anesthesia, increase opioid, improve ventilation); pharmacologic options include increasing volatile agent concentration, labetalol 5–20 mg IV (combined alpha/beta blockade), esmolol 0.5–1 mg/kg bolus then 50–200 mcg/kg/min infusion (ultra-short-acting beta-1 selective), hydralazine 5–10 mg IV (direct vasodilator, slower onset 15 min), nicardipine infusion 2.5–15 mg/h (calcium channel blocker, smooth titratable vasodilation), or sodium nitroprusside 0.25–10 mcg/kg/min (potent, rapid, but risk of cyanide toxicity and rebound hypertension). Clevidipine (Cleviprex) is an ultra-short-acting IV calcium channel blocker with a 1-minute half-life, ideal for precise BP control.

Acute Pulmonary Embolism

Presents intraoperatively as sudden hemodynamic collapse (hypotension, tachycardia), acute right heart failure (elevated CVP, RV dilation on TEE), increased dead space (sudden drop in ETCO₂ with stable or increasing PaCO₂), and hypoxemia. Treatment: 100% FiO₂, volume resuscitation, vasopressors (norepinephrine, vasopressin), consider thrombolytics (alteplase 50–100 mg) if massive PE with hemodynamic collapse despite vasopressors (weigh against surgical bleeding), heparin bolus and infusion, inotropes (dobutamine/milrinone for RV failure), emergent surgical embolectomy or catheter-directed therapy in refractory cases.

Cardiac Arrest in the OR — ACLS Modifications

Tension Pneumothorax

Can occur from central line placement (especially subclavian), positive-pressure ventilation with barotrauma, or laparoscopic surgery. Signs: sudden hypotension, increased peak airway pressures, decreased breath sounds (unilateral), tracheal deviation (late). Treatment: immediate needle decompression (14G needle, 2nd intercostal space midclavicular line or 5th ICS anterior axillary line) followed by chest tube insertion.

Local Anesthetic Systemic Toxicity (LAST) in the OR

LAST can mimic other perioperative emergencies and must be in the differential for any seizure, arrhythmia, or cardiovascular collapse occurring within 60 minutes of local anesthetic administration (though delayed presentations up to 30 minutes after injection are well-documented). Under general anesthesia, the CNS prodromal symptoms (tinnitus, perioral numbness, metallic taste) are masked, and cardiac toxicity may be the first manifestation. Bupivacaine has the narrowest CC/CNS ratio (ratio of the dose causing cardiovascular collapse to the dose causing seizures) of any commonly used LA, meaning cardiac arrest may occur with little warning. Ropivacaine and levobupivacaine have wider safety margins. Always aspirate before injecting LA, use incremental dosing with epinephrine markers, observe for signs of intravascular injection (tachycardia with epinephrine-containing test dose), and keep intralipid 20% immediately available whenever performing regional anesthesia.

Venous Air Embolism

Risk during sitting craniotomy, posterior cervical spine surgery, central line placement/removal, laparoscopic surgery, and any procedure where the surgical site is above the heart (entrains air through open veins). The lethal volume in adults is approximately 3–5 mL/kg. Signs: sudden decrease in ETCO₂, hypotension, "mill wheel" murmur, desaturation. Treatment: flood surgical field with saline, lower the surgical site below the heart, aspirate air through CVC (if tip is at SVC-RA junction), Durant maneuver (left lateral decubitus and Trendelenburg position to trap air in the RA apex away from the RV outflow tract), hemodynamic support, consider hyperbaric oxygen for massive embolism.

24 Acute Postoperative Pain

Multimodal Analgesia

Modern postoperative pain management uses a multimodal approach — combining agents with different mechanisms to optimize analgesia while minimizing opioid consumption and side effects. This is a core principle of Enhanced Recovery After Surgery (ERAS) protocols.

IV Patient-Controlled Analgesia (PCA)

Opioid-Sparing Strategies

The opioid epidemic has driven a paradigm shift toward minimizing perioperative opioid use. Key strategies include: preemptive analgesia (administering analgesics before surgical stimulus to prevent central sensitization), regional anesthesia (peripheral nerve blocks and neuraxial techniques as primary analgesic modality), scheduled non-opioid analgesics (acetaminophen + NSAID scheduled around the clock, not PRN), IV lidocaine infusion (particularly effective for abdominal surgery), dexmedetomidine (alpha-2 agonist with analgesic, sedative, and opioid-sparing properties without respiratory depression), magnesium sulfate (NMDA antagonist, 30–50 mg/kg loading dose followed by 8–15 mg/kg/h infusion — reduces postoperative opioid consumption by 25%), and ketamine low-dose infusion (0.1–0.3 mg/kg/h intraoperatively, continued 24–48 h postoperatively in opioid-tolerant patients). These strategies collectively can reduce opioid consumption by 40–60% and shorten recovery time.

ERAS (Enhanced Recovery After Surgery) Pain Principles

ERAS protocols emphasize: preoperative education, preoperative multimodal analgesia (acetaminophen + gabapentinoid + celecoxib), regional anesthesia whenever possible, minimize intraoperative opioids (use short-acting agents like remifentanil), scheduled postoperative non-opioid analgesics, early mobilization, and early enteral nutrition. ERAS programs have been shown to reduce opioid consumption by 30–50%, shorten hospital length of stay, reduce complications, and improve patient satisfaction.

25 Chronic Pain Fundamentals

Pain Classification

Nociceptive pain results from activation of peripheral nociceptors by tissue damage (somatic = well-localized, sharp/aching from skin, muscle, bone; visceral = diffuse, cramping from internal organs). Neuropathic pain arises from damage or dysfunction of the nervous system itself (peripheral neuropathy, post-herpetic neuralgia, phantom limb, CRPS). Characterized by burning, shooting, electric-shock quality, allodynia (pain from normally non-painful stimulus), and hyperalgesia (exaggerated pain response). Nociplastic pain (IASP 2017) arises from altered nociception without clear evidence of tissue or nerve damage (fibromyalgia, irritable bowel syndrome, chronic widespread pain, tension-type headache). Driven by central sensitization and altered descending modulation.

Complex Regional Pain Syndrome (CRPS)

CRPS is a chronic pain condition characterized by pain disproportionate to the inciting event, accompanied by sensory, motor, sudomotor, vasomotor, and trophic changes. Type I (formerly reflex sympathetic dystrophy): no identifiable nerve injury; typically follows trauma, fracture, or surgery. Type II (formerly causalgia): identifiable peripheral nerve injury. Diagnosis requires the Budapest criteria: (1) continuing pain disproportionate to inciting event, (2) at least one sign in 2+ categories AND one symptom in 3+ categories (sensory: hyperesthesia/allodynia; vasomotor: temperature/color asymmetry; sudomotor/edema: asymmetric sweating/edema; motor/trophic: decreased ROM, weakness, dystonia, skin/nail/hair changes), (3) no other diagnosis better explains findings. Treatment: physical therapy (cornerstone), pharmacotherapy (gabapentinoids, duloxetine, corticosteroids in acute phase), sympathetic nerve blocks (stellate ganglion for upper extremity, lumbar sympathetic for lower extremity), spinal cord stimulation, and psychological support.

Central Sensitization & Gate Control Theory

Central sensitization is increased excitability of central neurons in the dorsal horn and brain, leading to amplified pain signals (hyperalgesia, allodynia, expanded receptive fields). Mediated by NMDA receptor activation, wind-up phenomenon, and glial cell activation. Gate control theory (Melzack & Wall, 1965): pain perception is modulated by a "gate" in the dorsal horn of the spinal cord. Large-diameter Aβ fibers (touch, vibration) activate inhibitory interneurons that "close the gate," reducing pain transmission by small C and Aδ fibers. This is the theoretical basis for TENS units, spinal cord stimulators, and rubbing a painful area.

Pain Assessment Tools

WHO Cancer Pain Ladder (3-Step)

Step 1 (mild pain): non-opioid analgesics (acetaminophen, NSAIDs) ± adjuvants. Step 2 (moderate pain): weak opioid (codeine, tramadol) + non-opioid ± adjuvants. Step 3 (severe pain): strong opioid (morphine, oxycodone, fentanyl, hydromorphone, methadone) + non-opioid ± adjuvants. Adjuvants at any step: antidepressants (duloxetine, amitriptyline for neuropathic pain), anticonvulsants (gabapentin, pregabalin), corticosteroids (bone metastases, neural compression), bisphosphonates, ketamine.

Neuropathic Pain Pharmacotherapy

First-line agents for neuropathic pain include: gabapentin (start 300 mg QHS, titrate to 300–1200 mg TID; NNT ~6 for 50% pain relief), pregabalin (start 75 mg BID, titrate to 150–300 mg BID; NNT ~4; faster onset than gabapentin, linear pharmacokinetics), duloxetine (30–60 mg daily; SNRI, effective for diabetic neuropathy, fibromyalgia, musculoskeletal pain; NNT ~6), tricyclic antidepressants (amitriptyline/nortriptyline 10–25 mg QHS, titrate to 75–150 mg; NNT ~4 — most effective but limited by anticholinergic side effects, sedation, cardiac conduction risk). Second-line: topical lidocaine 5% patch (for localized neuropathic pain, minimal systemic absorption), capsaicin 8% patch (applied in clinic for 30–60 minutes, depletes substance P; effective for post-herpetic neuralgia; reapply every 3 months), tramadol, and opioids (reserved for refractory cases due to risks of tolerance, dependence, and hyperalgesia).

Opioid Conversion & Rotation

When switching between opioids (rotation), calculate the total 24-hour morphine equivalent dose, convert to the new agent using equianalgesic tables, then reduce the calculated dose by 25–50% to account for incomplete cross-tolerance. Methadone has unique pharmacology: dual mechanism (mu-agonist + NMDA antagonist), extremely variable and long half-life (8–59 hours, mean 22 h), high oral bioavailability (~80%), QTc prolongation risk, and unpredictable conversion ratios (the higher the morphine equivalent dose, the more potent methadone is relatively — for morphine >500 mg/day, the ratio may be 12:1 or higher). Methadone conversions should only be performed by experienced clinicians.

26 Interventional Pain Procedures

Anticoagulation & Neuraxial/Regional Anesthesia Timing

The ASRA (American Society of Regional Anesthesia and Pain Medicine) guidelines provide evidence-based timing recommendations for neuraxial and deep peripheral blocks relative to anticoagulant administration:

Epidural Steroid Injection (ESI)

Used for radicular pain from disc herniation, spinal stenosis, or degenerative disease. Interlaminar ESI: needle enters the epidural space between laminae using loss of resistance — deposits medication in the posterior epidural space. Transforaminal ESI: fluoroscopy-guided needle enters the neural foramen, depositing medication in the anterior epidural space adjacent to the nerve root — more targeted, higher efficacy for unilateral radiculopathy, but carries risk of particulate steroid injection into the radicular artery (use dexamethasone, a non-particulate steroid, for cervical and some lumbar transforaminal injections to minimize stroke/paralysis risk). Typical agents: dexamethasone 8–10 mg or methylprednisolone 40–80 mg + preservative-free lidocaine or bupivacaine.

Facet Joint Procedures

Medial branch blocks (MBB): diagnostic blocks of the medial branches of the dorsal rami that innervate the facet (zygapophyseal) joints. Two concordant positive blocks (≥80% pain relief) confirm the facet joint as the pain generator. Each facet is innervated by the medial branch at that level and the level above (e.g., L4-5 facet is innervated by L3 and L4 medial branches). Radiofrequency ablation (RFA): thermal lesioning of the medial branch nerve using a radiofrequency probe heated to 80°C for 60–90 seconds. Provides 6–12 months of relief (nerve regenerates). Performed after two positive diagnostic MBBs.

Sacroiliac (SI) Joint Injection

Fluoroscopy- or ultrasound-guided injection of local anesthetic and corticosteroid into the SI joint for sacroiliac joint dysfunction (confirmed by provocation tests: FABER/Patrick, distraction, compression, thigh thrust, Gaenslen). If positive diagnostic block, options include intra-articular steroid, lateral branch RFA, or SI joint fusion for refractory cases.

Regenerative & Emerging Therapies

Platelet-rich plasma (PRP) injections concentrate autologous growth factors (PDGF, TGF-β, VEGF) for injection into tendons, ligaments, and joints. Evidence is strongest for lateral epicondylitis and knee osteoarthritis; evidence for spine pain is limited. Prolotherapy involves injection of dextrose (hyperosmolar solution) to provoke a localized inflammatory response and stimulate tissue repair at ligament/tendon insertions. Peripheral nerve stimulation (PNS) is gaining traction as an alternative to SCS for focal pain conditions (e.g., occipital neuralgia with occipital nerve stimulation, knee pain with genicular nerve stimulation). Advantages include less invasive implant and lower complication rates than SCS.

Spinal Cord Stimulation (SCS)

Spinal cord stimulation involves implanting epidural electrodes connected to a pulse generator that delivers electrical impulses to the dorsal columns. Mechanism: gate control theory — stimulation of large Aβ fibers in the dorsal columns inhibits pain transmission. Also modulates descending inhibitory pathways and neurochemical mediators. Indications: failed back surgery syndrome (most common), CRPS types I and II, peripheral neuropathy, refractory angina, peripheral vascular disease pain. Trial period (5–7 days with temporary percutaneous leads) required before permanent implant; success = ≥50% pain reduction. Modern waveforms: traditional tonic, burst, high-frequency (10 kHz — paresthesia-free), and closed-loop systems.

Intrathecal Drug Delivery Systems (IDDS)

Implanted pump delivers medication (morphine, ziconotide, bupivacaine, baclofen) directly into the intrathecal space. Provides potent analgesia at 1/300th of the systemic dose (intrathecal-to-oral morphine ratio is approximately 1:300). Indications: cancer pain refractory to systemic opioids, severe spasticity (baclofen), and selected non-cancer chronic pain. Requires MRI-compatible pump, regular refills (every 1–6 months), and monitoring for catheter-related complications (granuloma, migration, fracture).

Joint Injections & Viscosupplementation

Intra-articular corticosteroid injections are commonly performed for osteoarthritis and inflammatory arthritis. Typical agents: triamcinolone acetonide 40–80 mg (knee) or methylprednisolone 40–80 mg, mixed with 2–5 mL of 1% lidocaine. Fluoroscopy or ultrasound guidance improves accuracy, particularly for hip and shoulder injections. Limit frequency to 3–4 injections per joint per year (concern for accelerated cartilage degeneration with repeated injections). Patients scheduled for total joint arthroplasty should avoid corticosteroid injection within 3 months of surgery due to increased infection risk. Viscosupplementation (hyaluronic acid injections) provides lubrication and may offer 3–6 months of relief in knee OA. Evidence is mixed, with most guidelines providing a conditional recommendation.

Other Interventional Procedures

Trigger point injections (TPI): injection of local anesthetic (with or without corticosteroid) or dry needling into myofascial trigger points (taut bands of skeletal muscle). Stellate ganglion block: injection of local anesthetic at C6–C7 targeting the cervicothoracic sympathetic ganglion. Indications: CRPS type I of the upper extremity, phantom limb pain, vascular insufficiency of the upper extremity. Confirm by development of ipsilateral Horner syndrome. Complications: recurrent laryngeal nerve block, vertebral artery injection, pneumothorax, esophageal puncture. Celiac plexus block/neurolysis: injection of local anesthetic (block) or alcohol/phenol (neurolysis) at the celiac plexus (T12–L1, anterior to the aorta). Primary indication: upper abdominal cancer pain (pancreatic cancer). Neurolysis provides pain relief in 70–90% of pancreatic cancer patients. Side effects: orthostatic hypotension, diarrhea (sympatholysis).

27 Obstetric Anesthesia

Physiologic Changes of Pregnancy

Pregnancy produces profound physiologic changes relevant to anesthesia:

Labor Epidural Analgesia

Initiation: typically at patient request when active labor is established. Lumbar epidural catheter at L2–L3 or L3–L4. Test dose to exclude intrathecal or intravascular placement. Loading dose: bupivacaine 0.0625–0.125% + fentanyl 50–100 mcg in 10–15 mL. PCEA maintenance: bupivacaine 0.0625–0.1% + fentanyl 2 mcg/mL; basal rate 6–10 mL/h, demand 5–8 mL, lockout 10–20 min. Target: T10–L1 for labor pain (uterine contractions); extend to S2–S4 for second stage (perineal pain). Monitor for hypotension (treat with phenylephrine or ephedrine + fluid), fetal heart rate changes, pruritis (fentanyl-related, treat with nalbuphine 2.5–5 mg), and motor block (reduce concentration if excessive).

Spinal Anesthesia for Cesarean Section

Standard regimen: hyperbaric bupivacaine 0.75% (10–12 mg) + fentanyl 10–25 mcg + preservative-free morphine 0.1–0.2 mg (for postoperative analgesia up to 24 hours). Target dermatome level: T4. Hypotension is the most common complication (up to 80% without prophylaxis); prevention: left uterine displacement, crystalloid/colloid co-loading, prophylactic phenylephrine infusion (0.25–0.5 mcg/kg/min, titrated to maintain BP within 20% of baseline).

General Anesthesia for Emergent C-Section

Indicated when neuraxial anesthesia is contraindicated or insufficient and delivery is urgent. RSI technique with preoxygenation, cricoid pressure, propofol 2–2.5 mg/kg + succinylcholine 1–1.5 mg/kg (or rocuronium 1.2 mg/kg with sugammadex available). Maintain with sevoflurane or desflurane 1.0–1.5 MAC + N₂O/O₂ (50:50) or 100% O₂. After delivery: deepen anesthesia, add opioid, reduce volatile to 0.5–0.7 MAC, administer oxytocin. Keep induction-to-delivery time <8 minutes to minimize fetal drug exposure.

Postpartum Hemorrhage & Anesthetic Considerations

PPH is the leading cause of maternal mortality worldwide. Defined as blood loss ≥1000 mL with signs/symptoms of hypovolemia. The anesthesiologist's role includes: ensuring large-bore IV access (14–16G × 2), type and screen (or crossmatch), activating MTP early, maintaining hemodynamic stability with vasopressors and blood products, converting from neuraxial to general anesthesia if surgical intervention is needed (hemorrhage worsening under epidural anesthesia), and monitoring for coagulopathy (TEG/ROTEM-guided transfusion if available). Tranexamic acid 1 g IV within 3 hours of delivery reduces death from bleeding (WOMAN trial). The RCOG guideline recommends a stepwise approach to uterotonic therapy:

Uterotonic Medications

28 Pediatric Anesthesia

Weight-Based Dosing & Equipment Sizing

Pediatric drug dosing is universally weight-based (mg/kg or mcg/kg). ETT sizing: cuffed ETT (now preferred even in young children): internal diameter (mm) = (age in years / 4) + 3.5 for cuffed tubes. For uncuffed ETT (historically used in children <8 years): (age / 4) + 4. ETT depth at the lip (cm): ETT ID × 3 (e.g., 4.0 tube inserted to 12 cm). Cuffed ETTs are now standard even in neonates because they reduce gas leak, improve ventilation, decrease reintubation rates, and reduce waste gas pollution; cuff pressure must be monitored (<20–25 cmH₂O).

IV Access Challenges in Pediatrics

Peripheral IV access is the most common technical challenge in pediatric anesthesia. For patients without IV access, inhalation induction with sevoflurane is the standard approach. Once unconscious, IV access is obtained. If peripheral IV is impossible: options include intraosseous (IO) access (proximal tibia, distal femur, or distal tibia — 10–15 mL flush to clear marrow), external jugular vein cannulation, or central venous access (femoral preferred in emergencies). Ultrasound guidance significantly improves first-attempt success rates for peripheral and central access in children. Topical anesthetic cream (EMLA or LMX 4%) applied 30–60 minutes before reduces pain of IV insertion in awake children and should be offered whenever time permits.

Inhalation Induction

Inhalation induction with sevoflurane (up to 8% in 70% N₂O/30% O₂ or 100% O₂) is the standard technique for children without IV access. Sevoflurane's low blood-gas partition coefficient (0.65) allows rapid induction (loss of consciousness in 1–2 minutes). Incremental technique (starting at 2% and increasing by 1% every few breaths) or single-breath technique (vital capacity breath of 8%) can be used. Once unconscious, establish IV access and proceed with intubation or SGA placement.

Laryngospasm

Laryngospasm is involuntary sustained closure of the vocal cords, causing complete airway obstruction. Most common in children (especially ages 1–5), particularly during light anesthesia, airway manipulation, secretions, blood, or irritation. Incidence: 1–3% in children. Management: immediate CPAP with 100% O₂ and jaw thrust (gentle positive pressure may open the cords), deepen anesthesia with propofol 0.5–1 mg/kg if IV available, and if refractory: succinylcholine 0.5–1 mg/kg IV (or 4 mg/kg IM if no IV access) to break the spasm. Larson's maneuver: firm bilateral digital pressure in the "laryngospasm notch" (behind the lobule of the ear, between the ascending ramus of the mandible and the mastoid process) — causes a pain-mediated jaw thrust that may relieve spasm.

Temperature Regulation

Infants and neonates are extremely vulnerable to hypothermia due to large body surface area-to-weight ratio, thin skin, minimal subcutaneous fat, and immature thermoregulatory mechanisms. Hypothermia causes increased oxygen consumption, metabolic acidosis, delayed drug metabolism, and coagulopathy. Prevention: warm OR (26°C for neonates), forced-air warming blanket, heated humidified circuit gases, fluid warmer, minimal skin exposure.

Emergence Delirium

Emergence delirium (ED) is a dissociated state of consciousness with inconsolable crying, thrashing, and disorientation during emergence from general anesthesia. Incidence: 10–50% in preschool-age children (peak age 2–5 years). Risk factors: sevoflurane or desflurane anesthesia, young age, preoperative anxiety, ENT/ophthalmologic procedures. Prevention: midazolam premedication, IV propofol at emergence (1 mg/kg), fentanyl 1–2 mcg/kg, dexmedetomidine 0.3–0.5 mcg/kg, or TIVA. Treatment: ensure pain is adequately treated (pain and ED are easily confused), low-dose propofol, parental presence, calm environment.

Common Pediatric Anesthetic Drug Doses

Neonatal Considerations

Neonates have transitional circulation (patent foramen ovale, ductus arteriosus may remain open, especially in premature infants) which can cause right-to-left shunting with hypoxia, hypercarbia, or acidosis — maintaining normal pH, temperature, and oxygenation is critical to prevent persistent pulmonary hypertension of the newborn (PPHN). Premature infants are at risk for post-anesthetic apnea (apnea/bradycardia for up to 24 hours after general anesthesia in infants <60 weeks post-conceptual age — must monitor postoperatively). Regional anesthesia (spinal, caudal) is preferred when feasible to avoid GA-related apnea.

29 Geriatric & High-Risk Patients

Pharmacokinetic Changes with Aging

The elderly demonstrate decreased hepatic blood flow (by ~40%) and reduced Phase I metabolism (CYP450), leading to prolonged elimination of midazolam, fentanyl, and propofol. Decreased renal function (GFR declines ~1 mL/min/year after age 40) prolongs the effect of renally cleared drugs (morphine M6G metabolite, vecuronium metabolites, gabapentin). Decreased lean body mass and increased body fat alter the volume of distribution: lipophilic drugs (benzodiazepines, fentanyl) have larger Vd and prolonged effect; hydrophilic drugs (NMBAs) have smaller Vd and relatively higher initial plasma concentrations. Decreased plasma albumin increases the free (active) fraction of highly protein-bound drugs. Decreased total body water concentrates water-soluble drugs. The net result: the elderly are more sensitive to virtually all anesthetic agents, and doses must be reduced.

Dose Reduction Recommendations

Regional Anesthesia Preference in the Elderly

Regional anesthesia offers several theoretical advantages in geriatric patients: avoidance of airway manipulation and mechanical ventilation, reduced exposure to sedatives and volatile agents (which may contribute to delirium/POCD), better preservation of pulmonary function (especially thoracic epidural), superior postoperative analgesia with reduced opioid consumption, potential reduction in thromboembolic events (neuraxial sympathectomy improves blood flow), and earlier return of cognitive function. However, large randomized trials (RAGA trial for hip fracture) have not consistently shown mortality benefit of regional vs. general anesthesia. The decision should be individualized based on patient factors (anticoagulation status, spinal anatomy, patient preference) and surgical requirements. Peripheral nerve blocks (e.g., fascia iliaca block for hip fracture) provide excellent preoperative analgesia and reduce opioid requirements in the emergency department and perioperatively.

Frailty Assessment

Frailty is a clinical syndrome of decreased physiologic reserve. The Clinical Frailty Scale (CFS) ranges from 1 (very fit) to 9 (terminally ill). Frail patients (CFS ≥5) have 2–5× higher risk of postoperative complications, ICU admission, longer hospital stay, and 30-day mortality. Preoperative frailty screening should guide shared decision-making, choice of anesthetic technique (regional preferred), and postoperative disposition planning.

Postoperative Delirium & POCD

Postoperative delirium is an acute, fluctuating disturbance in attention and cognition. Incidence: 10–50% after major surgery in elderly patients. Risk factors: age >65, pre-existing cognitive impairment/dementia, sensory impairment (hearing/vision), major surgery, prolonged OR time, benzodiazepine use, opioid use, sleep deprivation, infection, electrolyte imbalance, urinary retention, pain, ICU admission. Prevention — the HELP protocol (Hospital Elder Life Program): orientation (reorientation boards, clock), early mobilization, sleep hygiene (minimize nighttime disruptions), hydration and nutrition, vision and hearing aids at bedside, avoid delirium-inducing medications (benzodiazepines, anticholinergics, meperidine). No pharmacologic agent reliably prevents delirium. Treatment: identify and correct underlying cause, non-pharmacologic interventions first; antipsychotics (haloperidol 0.5–1 mg) only for severe agitation with safety risk; avoid benzodiazepines (worsen delirium except for alcohol/benzodiazepine withdrawal).

Postoperative cognitive dysfunction (POCD) is a measurable decline in cognitive function (memory, attention, executive function) lasting weeks to months after surgery. More common after cardiac surgery and in the elderly. Risk factors overlap with delirium risk factors. No proven prevention or treatment; regional anesthesia may reduce POCD risk compared to general anesthesia (data conflicting). Distinguished from delirium by chronicity (weeks to months) and absence of fluctuating attention.

30 Drug Dosing Master Table

Induction Agents

Neuromuscular Blocking Agents

Opioids

Local Anesthetics — Maximum Doses

Vasopressors & Emergency Drugs

31 Classification Systems

ASA Physical Status Classification

Mallampati Classification

Cormack-Lehane Laryngoscopic View

Revised Cardiac Risk Index (RCRI)

Risk of MACE: 0 points = 3.9%, 1 = 6.0%, 2 = 10.1%, ≥3 = 15%.

Ramsay Sedation Scale

Aldrete Post-Anesthesia Recovery Score

Discharge from PACU requires score ≥9 out of 10.

Wilson Risk Sum Score for Difficult Intubation

Score ≥2: ~75% sensitivity for difficult intubation. SLux = subluxation of the mandible (lower incisors anterior to upper incisors).

32 Abbreviations Master List