Monitored Anaesthesia Care (MAC)

Definition and Terminology

• MAC - provided by a qualified anesthesiologist; may span the full spectrum from light anxiolysis to general anaesthesia
• Moderate sedation/analgesia ("conscious sedation") - may be provided by non-anesthesiologist providers and should NOT intend to attain a level where the patient is unresponsive

Key principle: If the patient loses consciousness and the ability to respond purposefully, the anaesthesia care is a general anaesthetic, irrespective of whether airway instrumentation is required.

Indications

1. The nature of the procedure warrants it (e.g., cataract surgery, colonoscopy, bronchoscopy, cardiac catheterization, minor dermatologic procedures)
2. The patient's clinical condition necessitates an anesthesiologist (e.g., extremes of age, hemodynamic instability, psychiatric disorders, morbid obesity)
3. A deeper level of analgesia/sedation is required than non-anesthesiologist providers can safely offer
4. The patient requests or requires supplementation to local/regional anaesthesia

Preoperative Assessment

• Medical status: Full history, physical, comorbidities (airway, cardiovascular, respiratory)
• Airway evaluation: The Mallampati score, mouth opening, neck mobility - because MAC can convert to general anaesthesia at any moment, a difficult airway plan is mandatory
• MAC candidacy: Patient ability to remain cooperative; psychological factors (claustrophobia, severe anxiety, dementia may make MAC impractical)
• Patient expectations: Must be counselled that awareness is possible and intentional during MAC

ASA Continuum of Sedation Depth

Monitoring Standards during MAC

1. Pulse oximetry - continuous; gives early warning of respiratory depression
2. Capnography (ETCO2) - increasingly recognized as the most sensitive and earliest indicator of respiratory depression; recommended alongside supplemental oxygen via modified face masks that allow CO2 sampling
3. ECG - continuously displayed
4. Non-invasive blood pressure - recorded at minimum every 5 minutes
5. Temperature - when clinically significant changes are anticipated; MAC is associated with inadvertent hypothermia especially at extremes of age and with neuraxial techniques
6. Depth of sedation monitoring:
   • Clinical: Ramsay Sedation Scale, Richmond Agitation-Sedation Scale (RASS), Observers' Assessment of Alertness/Sedation (OAA/S) scale
   • Electronic: Bispectral Index (BIS) or patient state index (PSI) using processed EEG; useful adjuncts but not substitutes for clinical assessment
7. Communication and observation - the anesthesiologist's continuous presence and attention remain the most important monitoring tool

Supplemental Oxygen and Fire Risk

• The combination of electrocautery + supplemental O2 + alcohol prep + flammable drapes is particularly dangerous
• Burns around the head and neck are an important cause of morbidity during MAC
• Risk mitigation: use lowest possible FiO2, allow 1 minute drying of alcohol preps, tent drapes to prevent O2 pooling

Pharmacology of MAC

Propofol

• Most commonly used drug for MAC
• Advantages: rapid onset, short context-sensitive half-time, antiemetic properties, smooth sedation
• Infusion rates: 25-75 mcg/kg/min for sedation
• Disadvantages: pain on injection, respiratory depression (apnoea with boluses), no analgesic properties, hypotension

Benzodiazepines

• Midazolam most commonly used: 0.5-2 mg IV titrated
• Provides anxiolysis, amnesia; does NOT provide analgesia
• Synergistic with opioids and propofol (significant respiratory depression risk)
• Long context-sensitive half-time makes recovery slower than propofol

Opioids

• Fentanyl, remifentanil, and alfentanil used
• Provide analgesia and sedation; potentiate other agents
• Remifentanil: ultra-short context-sensitive half-time; ideal for brief painful stimuli; risk of rapid tolerance
• Context-sensitive half-time concept: for infusions >8 hours, sufentanil's context-sensitive half-time is less than alfentanil's despite alfentanil's shorter elimination half-life

Ketamine

• Dissociative anaesthetic with analgesic, sedative, and amnestic properties
• Preserves airway reflexes and spontaneous ventilation
• Maintains or increases hemodynamic parameters
• Side effects: emergence reactions, increased secretions, nausea
• Combined with a benzodiazepine or low-dose propofol to reduce dysphoria

"Ketofol" (Ketamine + Propofol combination)

• The analgesic effect of ketamine reduces propofol requirements
• Advantages: hemodynamic stability, decreased PONV, improved procedural conditions, decreased airway complications
• Ratios range from 1:1 to 1:10 (ketamine:propofol)
• Dosing follows propofol: 0.25 mg/kg bolus, then infusion at 25-50 mcg/kg/min or incremental boluses of 0.25-0.5 mg/kg every 3-5 minutes

Dexmedetomidine

• Selective α2-agonist: sedation, analgesia, anxiolysis with minimal respiratory depression
• Produces a "cooperative sedation" - patients are calm but arousable
• Potentiates opioid analgesia and benzodiazepine hypnosis
• Loading dose: 1 mcg/kg over 10 minutes; maintenance: 0.2-0.7 mcg/kg/hour
• Side effects: bradycardia, hypotension

Complications

1. Respiratory Depression

• The leading cause of death and serious CNS injury during MAC is hypoxia from suppression of spontaneous respiration by sedative-hypnotic drugs
• Risk factors: elderly, obese, OSA, opioid-sedative combinations
• Management: reduce/stop infusions, jaw thrust, supplemental O2, airway adjuncts, bag-mask ventilation, naloxone/flumazenil if needed

2. Aspiration

• Risk increased with sedation as laryngeal reflexes may be blunted
• Pre-procedure fasting (NPO) guidelines apply equally to MAC patients

3. Laryngospasm

• Can occur if protective airway reflexes are stimulated during deep sedation
• Management: continuous positive airway pressure, deepen anaesthesia, succinylcholine if severe

4. Cardiovascular Complications

• Hemodynamic instability from vasodilation (propofol), vagal stimulation, or patient's underlying disease

5. Local Anaesthetic Systemic Toxicity (LAST)

• Must be prepared to recognize and treat LAST when MAC is provided alongside local/regional techniques
• Treatment: stop injection, 20% lipid emulsion, airway management, benzodiazepines for seizures

6. Fire/Burns

• As above; vigilance required with O2 and electrocautery in head/neck region

Conversion to General Anaesthesia

• Patient movement during a critical step
• Patient uncooperativeness
• Excessive sedation requiring airway instrumentation
• Surgical complications requiring deeper anaesthesia
• Hemodynamic deterioration

Medicolegal and Closed Claims Considerations

• MAC closed claims are associated with death and severe brain damage
• Most adverse outcomes involved respiratory depression from oversedation
• Documentation of appropriate pre-procedural assessment, intra-procedural monitoring, and post-procedure care is legally important
• MAC providers are held to the same standard of care as general anaesthesia

Future Directions

• Patient-controlled sedation/analgesia (PCS): Patient self-titrates sedation (e.g., propofol via lockout device)
• Target-controlled infusions (TCI): Pharmacokinetic models (Marsh, Schnider) drive pumps to achieve desired plasma or effect-site concentrations
• Closed-loop anaesthesia delivery systems: BIS or other EEG biomarkers used as real-time feedback to automate sedation delivery

Summary Points for Exam

1. MAC = anesthesiologist-provided service; spans full sedation spectrum including potential conversion to GA
2. Standards of preoperative evaluation and monitoring = identical to GA
3. No single drug is ideal; multimodal titrated approach preferred
4. Leading cause of serious injury = respiratory depression/hypoxia
5. Supplemental O2 + electrocautery = fire risk (especially head/neck)
6. Convert to GA promptly if patient loses purposeful responsiveness
7. Capnography is the most sensitive early monitor for respiratory depression
8. Dexmedetomidine = least respiratory depression; "cooperative sedation"
9. Remifentanil = ultrashort context-sensitive half-time; ideal for brief stimuli
10. MAC closed claims: mostly respiratory, mostly preventable

Local Anesthetic Systemic Toxicity (LAST)

Definition

Incidence and Epidemiology

• Overall incidence: 0.004% to 0.18% depending on study methodology and regional technique used
• Majority of cases (>75%) occur within 5 minutes of injection; rare cases present hours later with continuous infusion catheters
• A gradual decline in yearly incidence has been observed, likely reflecting improved awareness, ultrasound guidance, and incremental dosing practice
• Upper extremity blocks carry greater odds of LAST than lower extremity blocks
• Populations at highest risk: extremes of age (elderly, neonates), patients with pre-existing cardiac disease

Risk Factors

Pathophysiology and Mechanisms

General Mechanism

Factors that increase LAST risk:

• Acidosis and hypercapnia (reduce protein binding, increase ionized free fraction)
• Hyponatraemia
• Reduced cardiac output (decreases clearance, increases peak plasma concentration)
• Pharmacogenomic variation in metabolism (especially for ester-linked agents)

CNS Toxicity Mechanism

1. Excitatory phase - due to preferential blockade of inhibitory interneurons first
2. Inhibitory/depressive phase - global CNS suppression at higher concentrations

Cardiovascular Toxicity Mechanism

• Dose-dependent Na⁺ channel blockade → slowed cardiac conduction (PR prolongation, QRS widening)
• Bupivacaine has uniquely prolonged Na⁺ channel binding ("fast in, slow out") - responsible for refractory ventricular dysrhythmias
• Impairs CNS regulation of the baroreflex (brainstem level)
• At high concentrations: peripheral vasodilatation + pulmonary artery hypertension (the latter precedes fall in cardiac output)
• Ropivacaine and levobupivacaine are 30-40% less cardiotoxic than bupivacaine milligram-for-milligram due to their S(-) stereoisomer configuration and smaller alkyl side chain

Dose-Dependent CNS Effects (Lidocaine as Prototype)

Clinical Presentation

CNS Signs (occur at lower plasma concentrations than CV signs - the "CNS first, CV second" rule)

• Perioral/tongue numbness or tingling
• Metallic taste
• Tinnitus, visual disturbances, dizziness
• Restlessness, agitation
• Slurred speech, confusion

• Seizures (tonic-clonic)
• Loss of consciousness
• Respiratory arrest, coma

Cardiovascular Signs

• Hypertension and tachycardia initially
• Bradycardia, hypotension
• PR prolongation, QRS widening on ECG
• Ventricular tachycardia / ventricular fibrillation
• Asystole
• Complete cardiovascular collapse

Comparative Cardiotoxicity of Local Anaesthetics

Prevention

1. Aspiration before injection - mandatory, even though a negative aspiration does NOT guarantee extravascular placement
2. Incremental injection technique - 3-5 mL aliquots with pauses for observation
3. Epinephrine test dose - 1.5 mcg/kg (in adults: 15 mcg = 3 mL of 1:200,000); tachycardia (>20% HR increase), hypertension, or new T-wave changes suggest intravascular placement
4. Ultrasound guidance - real-time visualization of needle tip and local anesthetic spread; most effective prevention strategy
5. Adherence to maximum safe doses:
   • Lidocaine: 4-5 mg/kg (7 mg/kg with epinephrine)
   • Bupivacaine: 2-3 mg/kg
   • Ropivacaine: 3 mg/kg
6. Continuous monitoring (ECG, SpO2, BP) throughout block performance
7. Avoid high-vascularity sites for large-volume injections when possible
8. Avoid 0.75% bupivacaine for epidural use (associated with cardiac arrest on intravascular injection)

Treatment - ASRA Practice Advisory (2017/2020)

Immediate Steps

• Stop local anesthetic injection immediately
• 100% oxygen via face mask; if unconscious - secure airway (intubate if needed)
• Avoid and correct: hypoxia, hypercapnia, acidosis (these potentiate cardiotoxicity)

• Benzodiazepines first-line: Midazolam 1-5 mg IV, or diazepam
• If benzodiazepines unavailable: propofol or thiopentone in small doses (caution - cardiovascular depression)
• If seizures persist: succinylcholine to prevent metabolic acidosis from prolonged muscular contractions (does NOT stop CNS electrical activity)

Administer at first sign of dysrhythmia in suspected LAST - do not delay

• "Lipid sink/shuttle" theory: lipid particles scavenge free local anesthetic from tissue, redistributing it away from electrically sensitive organs
• Direct cardiotonic effect: restores vascular tone, improves cardiac contractility
• Acts as alternative mitochondrial energy substrate

• Epinephrine: use small doses - <1 mcg/kg bolus (large doses of epinephrine can trigger ventricular fibrillation in the setting of bupivacaine cardiotoxicity; animal data shows worse outcomes with standard ACLS doses of 1 mg)
• AVOID:
  • Vasopressin
  • Calcium channel blockers
  • Beta-blockers
  • Lidocaine as antiarrhythmic (obvious reason)
• Amiodarone may be used for ventricular dysrhythmias (particularly bupivacaine-induced)
• Defibrillation for VF as per standard ACLS

• If lipid emulsion and vasopressors fail - cardiopulmonary bypass (ECMO) should be considered; it is the ultimate rescue
• Contact perfusion team/ECMO team early if collapse is refractory

• Monitor for at least 2-6 hours after resolution of symptoms
• Patients with significant cardiovascular morbidities warrant longer observation
• Lipid infusion may cause propofol infusion syndrome-like lipemia if used at excessive doses

Summary of LAST Treatment Protocol (Cognitive Aid)

STOP injection → Call for HELP
↓
100% O₂ → Secure airway
↓
Benzodiazepine → Treat seizures
↓
20% Intralipid 1.5 mL/kg bolus → 0.25 mL/kg/min infusion
↓
ACLS (epinephrine <1 mcg/kg, NO vasopressin/Ca-blockers/β-blockers)
↓
Amiodarone for VF/VT
↓
Refractory? → Cardiopulmonary Bypass / ECMO
↓
Monitor ≥2-6 hours post-event

Key Exam Points

1. Bupivacaine is the most cardiotoxic local anesthetic; 0.75% bupivacaine is contraindicated for epidural use
2. Ropivacaine and levobupivacaine are 30-40% less cardiotoxic than bupivacaine
3. Classic presentation: CNS excitation → CNS depression → cardiovascular collapse (but with bupivacaine, CVS collapse may occur without CNS warning)
4. 20% Intralipid is the cornerstone of LAST treatment; start at first sign of dysrhythmia
5. Lipid emulsion: bolus 1.5 mL/kg, then 0.25 mL/kg/min; max 12 mL/kg
6. Epinephrine dose in LAST is reduced (<1 mcg/kg); standard ACLS doses worsen outcome
7. Vasopressin, Ca-channel blockers, beta-blockers are contraindicated in LAST
8. Negative aspiration does NOT exclude intravascular placement
9. Ultrasound guidance + incremental injection = best prevention strategy
10. Monitor for 2-6 hours post-event even after apparent recovery