Anesthesia is the pharmacologically induced, reversible state of controlled unconsciousness, amnesia, analgesia, and muscle relaxation that enables surgical and diagnostic procedures. Post anesthesia nurses must understand anesthetic agents, techniques, and their physiological effects to anticipate patient needs during emergence and recovery.
The four components of anesthesia are hypnosis (unconsciousness), amnesia (lack of memory formation), analgesia (pain control), and akinesia (immobility/muscle relaxation). Modern anesthesia balances these components using multiple drug classes rather than relying on high doses of single agents.
General Anesthesia
General anesthesia produces complete unconsciousness with loss of protective reflexes. It is indicated for major surgical procedures, patients unable to cooperate, procedures requiring complete immobility, and cases where regional techniques are contraindicated.
Stages of general anesthesia (Guedel's classification):
Stage I (Analgesia)
From induction to loss of consciousness; patient may be drowsy but responsive
Stage II (Excitement/Delirium)
From loss of consciousness to onset of regular breathing; characterized by irregular breathing, breath-holding, laryngospasm, and hyperreactivity; modern rapid-acting agents minimize time in this dangerous stage
Stage III (Surgical Anesthesia)
Regular breathing, progressive muscle relaxation, loss of reflexes; divided into four planes of increasing depth
Stage IV (Medullary Depression)
Respiratory and cardiovascular collapse; anesthetic overdose; requires immediate intervention
Regional Anesthesia
Regional anesthesia blocks nerve conduction to a specific body area while maintaining consciousness. Types include:
Neuraxial anesthesia:
Spinal (subarachnoid block)
Local anesthetic injected into cerebrospinal fluid at L2–L4 level; rapid onset; profound motor and sensory block; used for lower abdominal, pelvic, and lower extremity surgery
Epidural
Local anesthetic injected into epidural space; slower onset; can place catheter for continuous infusion; segmental block; used for labor analgesia, thoracic, abdominal, and lower extremity procedures
Combined spinal-epidural (CSE)
Combines rapid spinal onset with epidural catheter for extended analgesia
Peripheral nerve blocks:
Single-injection or continuous catheter techniques
Upper extremity
interscalene, supraclavicular, infraclavicular, axillary blocks
Lower extremity
femoral, sciatic, popliteal, adductor canal blocks
Truncal blocks
transversus abdominis plane (TAP), rectus sheath, paravertebral, erector spinae plane blocks
Monitored Anesthesia Care (MAC)
MAC involves anesthesia provider monitoring with sedation ranging from minimal to deep. The patient maintains protective reflexes and spontaneous ventilation. It is used for procedures requiring patient cooperation, minor surgeries, and diagnostic procedures. MAC can convert to general anesthesia if needed.
Local Anesthesia
Local anesthesia involves direct infiltration of anesthetic into surgical site without anesthesia provider involvement. The surgeon administers the agent. It is appropriate for minor procedures and superficial surgeries.
Intravenous Induction Agents
Propofol:
Mechanism
GABA-A receptor agonist; enhances inhibitory neurotransmission
Onset
30–45 seconds; duration 5–10 minutes
Effects
Rapid, smooth induction; antiemetic properties; decreases cerebral metabolic rate and intracranial pressure; causes dose-dependent respiratory depression and hypotension due to vasodilation and myocardial depression
PACU considerations
Rapid emergence; patients typically wake clear-headed; watch for hypotension especially in hypovolemic patients; pain on injection common
Etomidate:
Mechanism
GABA-A receptor agonist
Onset
30–60 seconds; duration 3–5 minutes
Effects
Hemodynamically stable; minimal cardiovascular depression; maintains cerebral perfusion pressure; causes adrenocortical suppression (avoid repeated doses or infusions)
PACU considerations
Myoclonus during induction; higher incidence of postoperative nausea and vomiting (PONV); used for hemodynamically unstable patients
Ketamine:
Mechanism
NMDA receptor antagonist; also affects opioid, monoamine, and muscarinic receptors
Onset
30–60 seconds IV; 3–4 minutes IM; duration 10–20 minutes
Effects
Dissociative anesthesia; profound analgesia; bronchodilation; increases heart rate, blood pressure, and cardiac output via sympathetic stimulation; maintains respiratory drive and airway reflexes (relative); increases cerebral blood flow and intracranial pressure
PACU considerations
Emergence delirium and hallucinations (reduced with benzodiazepine pretreatment); increased salivation; nystagmus; may cause purposeless movements; maintain quiet, calm environment
Barbiturates (Thiopental, Methohexital):
Mechanism
GABA-A receptor agonist
Effects
Rapid induction; decreases cerebral metabolic rate and intracranial pressure; causes significant cardiovascular and respiratory depression; no analgesic properties; contraindicated in porphyria
PACU considerations
Prolonged sedation with repeated doses; may cause laryngospasm; extravasation causes tissue necrosis
Inhalational Anesthetics
Volatile agents (Sevoflurane, Desflurane, Isoflurane):
Mechanism
Exact mechanism unclear; affects multiple ion channels including GABA-A receptors
Minimum alveolar concentration (MAC)
The concentration at which 50% of patients will not move in response to surgical incision; lower MAC indicates higher potency
Sevoflurane
MAC 2.0%; non-pungent; preferred for mask induction; minimal airway irritation; may cause emergence agitation in children; produces Compound A with CO2 absorbents
Desflurane
MAC 6.0%; most rapid emergence; pungent (causes coughing/laryngospasm if used for induction); sympathetic stimulation with rapid increases in concentration
Isoflurane
MAC 1.15%; pungent; cerebral vasodilation; rarely used for induction
Common effects
Dose-dependent cardiovascular depression, respiratory depression, bronchodilation, decreased systemic vascular resistance, muscle relaxation, decreased cerebral metabolic rate
PACU considerations for volatile agents:
Residual effects depend on duration of exposure and agent solubility
Desflurane and sevoflurane allow most rapid emergence
Watch for shivering (increases oxygen consumption)
Diffusion hypoxia: When nitrous oxide rapidly exits blood into alveoli, it dilutes alveolar oxygen; administer supplemental oxygen during early emergence
Malignant hyperthermia trigger: All volatile agents can trigger MH in susceptible patients
Nitrous Oxide:
Mechanism
NMDA receptor antagonist; also affects opioid receptors
MAC
105% (cannot produce surgical anesthesia alone at atmospheric pressure)
Effects
Anxiolysis; analgesia; minimal cardiovascular depression; rapid onset and offset due to low blood-gas solubility
Concerns
Diffusion into closed air spaces (avoid in pneumothorax, bowel obstruction, middle ear surgery); diffusion hypoxia on discontinuation; inactivates vitamin B12 with prolonged use; weak trigger for PONV
Opioids
Commonly used: Fentanyl, morphine, hydromorphone, remifentanil, sufentanil
Mechanism: Mu-opioid receptor agonists producing analgesia, sedation, and euphoria
Effects:
Analgesia without amnesia
Dose-dependent respiratory depression (decreased respiratory rate, tidal volume, and response to CO2)
Bradycardia via vagal stimulation
Minimal direct myocardial depression
Decreased gastrointestinal motility; increased biliary pressure
Nausea and vomiting via chemoreceptor trigger zone stimulation
Pruritis (especially with neuraxial administration)
Muscle rigidity (especially chest wall) with rapid high-dose administration
Miosis
PACU considerations:
Monitor respiratory rate and depth closely
Naloxone (0.04–0.4 mg IV) reverses respiratory depression but also analgesia
Titrate naloxone to respiratory rate, not consciousness
Duration varies: morphine 3–4 hours; fentanyl 30–60 minutes; remifentanil minutes
Delayed respiratory depression possible with morphine due to active metabolite (morphine-6-glucuronide) especially in renal impairment
Benzodiazepines
Commonly used
Midazolam, diazepam, lorazepam
Mechanism
GABA-A receptor agonist; enhances inhibitory neurotransmission
Effects
Anxiolysis, amnesia, sedation, anticonvulsant activity, muscle relaxation; minimal respiratory depression alone but synergistic with opioids; minimal cardiovascular effects
PACU considerations:
Prolonged sedation possible especially in elderly and hepatically impaired patients
Flumazenil (0.2 mg IV, repeat to 1 mg) reverses effects but may precipitate seizures in benzodiazepine-dependent patients or unmask seizure activity controlled by benzodiazepines
Watch for resedation as flumazenil duration (45–90 minutes) shorter than most benzodiazepines
Neuromuscular Blocking Agents (NMBAs)
Depolarizing agents (Succinylcholine):
Mechanism
Depolarizes motor end plate; initial fasciculations followed by flaccid paralysis
Onset
30–60 seconds; duration 5–10 minutes
Indications
Rapid sequence intubation; short procedures
Side effects
Hyperkalemia (especially in burns, crush injuries, denervation, immobility); malignant hyperthermia trigger; increased intragastric, intraocular, and intracranial pressure; bradycardia (especially with repeat doses); masseter muscle rigidity; prolonged block with pseudocholinesterase deficiency
Non-depolarizing agents (Rocuronium, Vecuronium, Cisatracurium, Pancuronium):
Mechanism
Competitive antagonism at nicotinic acetylcholine receptors
Duration varies
Rocuronium 30–60 minutes; vecuronium 30–40 minutes; cisatracurium 40–60 minutes; pancuronium 60–90 minutes
Effects
No fasciculations; no hyperkalemia; some agents cause histamine release (hypotension, bronchospasm)
Reversal
Neostigmine (with glycopyrrolate or atropine to prevent bradycardia) or sugammadex (specifically binds rocuronium and vecuronium)
PACU considerations for NMBAs:
Residual neuromuscular blockade is common and dangerous
Signs of residual blockade: Weak grip, inability to sustain head lift for 5 seconds, diplopia, difficulty swallowing, shallow breathing
Train-of-four (TOF) ratio greater than 0.9 indicates adequate recovery
Risk factors for residual blockade: Hypothermia, acidosis, hypokalemia, hypermagnesemia, aminoglycoside antibiotics, advanced age, renal/hepatic impairment
Sugammadex provides complete reversal of rocuronium/vecuronium without muscarinic side effects
Local Anesthetics
Mechanism: Block sodium channels, preventing nerve depolarization and impulse conduction
Classification:
Esters (chloroprocaine, procaine, tetracaine)
Metabolized by plasma pseudocholinesterase; higher allergic potential due to PABA metabolite
Amides (lidocaine, bupivacaine, ropivacaine, mepivacaine)
Metabolized by liver; rare true allergy
Factors affecting block:
pKa
Determines onset (lower pKa equals faster onset)
Lipid solubility
Determines potency
Protein binding
Determines duration
Vasoconstrictors (epinephrine)
Prolong duration by decreasing systemic absorption
Local anesthetic systemic toxicity (LAST):
Occurs from inadvertent intravascular injection or excessive absorption
CNS symptoms first: Circumoral numbness, metallic taste, tinnitus, visual disturbances, dizziness, confusion, seizures
Cardiovascular symptoms: Hypotension, bradycardia, arrhythmias, cardiovascular collapse
Bupivacaine most cardiotoxic
Treatment: Stop injection; call for help; manage airway; benzodiazepines for seizures; ACLS for cardiac arrest; intralipid 20% bolus (1.5 mL/kg) followed by infusion (0.25 mL/kg/min)
