Pain, Analgesia and Anesthesia

Pain

• protective signal indicates tissue injury or threat

• nociceptors is perception of pain

• influenced by: biological, psychological, social factors

• nociception does not equal pain

• patient’s perception of pain is key

Pain Pathway

• Transduction

  • tissue injury sends inflammatory mediators > nociceptor activation

• Transmission

  • signal travels to peripheral nerve > spinal cord > brain

• Perception

  • brain interprets signal > “pain experience”

• Modulation

  • CNS increase or decrease pain signal (endorphins, descending pathways)

drugs act at different steps of pathway

Transduction

• activates pain

• Mechanical (pressure, injury), Thermal (extreme heat/cold), Chemical (inflammation by prostaglandins, bradykinins, ATP)

• stimulus opens ion channels > sends action potential > signal to CNS

• inflammation = lowers pain threshold

Pain Facilitators

increase pain

• prostaglandins - sensitive nociceptors

• bradykinin - direct nociceptor activation

• substance P - amplifies signal in spinal cord

• histamine - inflammation & swelling

Pain Inhibitors

decrease pain

• endorphins - natural opioids, mood booster

• endocannabinoids - modulate pain, balance

Acute Pain

• protective - signals injury

• sympathetic activation - increased HR, BP, RR, and sweating (diaphoresis)

• resolves with healing

Chronic Pain

• no longer protective

• CNS remodeling + persistent signaling

• minimal physiologic response

• psychological + functional impact

• = disease, not just a symptom

Types of Acute Pain

• nociceptive (tissue injury)

  • somatic - sharp, localized

  • visceral (organ) - deep, diffuse

• neuropathic (nerve damage)

  • burning, tingling, electric

• inflammatory

  • swelling, aching, throbbing

• central (processing disorder)

  • no clear injury (fibromyalgia)

*identify pain type > guides drug choice

Where Pain Drugs Work

• transduction - NSAIDs, corticosteroids

• transmission - local anesthetics

• perception - opioids

• modulation - antidepressants, anticonvulsants

NSAIDs

• MOA: inhibit COX > decrease prostaglandins

• Effects: decreased pain, inflammation, fever

• prostaglandins = key pain sensitizers

• ADR:

  • GI bleeding > lowers protective PGs

  • renal injury > lowers renal perfusion *hypovolemia or older adults

  • increased BP

• Nursing:

  • monitor GI, renal function, dosing limits

Acetaminophen

not an NSAID

• MOA: acts in CNS > lowers prostaglandins (minimal peripheral effect)

• effects: lowers pain, fever / no anti-inflammatory effect

• Major ADR: hepatotoxicity - dose dependent

• Max Dose:

  • 4g/day in healthy ppl

  • 3g/day or less in high risk

Opioid Agonists

central pain modulation

• MOA: bind mu receptors > reduced pain, perception, emotional response

• Effects: analgesia, sedation, euphoria (taken when non-pain)

• Major ADR: respiratory depression (HIGH risk), constipation, dependence

• antidote: naloxene - reverses opioid effects

Opioid Receptors

• mu - analgesia, respiratory depression, euphoria

• kappa - spinal analgesia, sedation

• delta - minor role

Combination Opioids

Opioid + non-opioid (ex: acetaminophen (APAP))

• benefit: better pain control

• risk: dose ceiling - toxicity from non-opioid

Ex:

• APAP with hydrocodone, oxycodone, or codeine

Safety Check:

• taking multiple APAP products?

• total daily dose ~ 3-4g/day

• liver disease, alcohol use, malnutrition?

acetaminophen OD → liver failure

Pain Assessment

• onset

• location

• quality

• intensity - 0 to 10 scale

• aggravating/relieving factors

• effect on function (ADLs, mobility)

• influencing factors: biological, psychological, social

Effects of Ineffective Pain Management

• cardiovascular - increased HR, BP, cardiac workload

• pulmonary - hypoventilation, atelectasis, infection

• GI - post-op ileus, constipation, urinary retention

• muscular - weakness, fatigue

• psychological - anxiety, fear, frustration

long term - chronic stress

Pain Management Principles

• Goal: decrease pain → improved function

• Multimodal: non-pharm + pharmacologic

• Non-pharm:

  • physical (heat/ice, PT, TENS)

  • cognitive (distraction, biofeedback)

  • mind-body (acupuncture, meditation)

• Adjuvant meds (not primary analgesics):

  • antidepressants - neuropathic pain

  • anticonvulsants - neuropathic pain

  • corticosteroids - inflammatory pain

• individualize dosing, manage ADRs, reassess pain + function

Drug: Morphine

• MOA: bind to opioid receptors (mu/kappa) in CNS → alter pain perception

• For severe acute pain, chronic pain, preanesthetic sedation

• ADR: respiratory depression, sedation, N/V, constipation, urinary retention

• Nursing:

  • monitor for resp depression, bowel function

  • use naloxone (Narcan) for OD

  • oral, IV, subcutaneous

  • BBX warning - schedule II

  • release slowly for opioid tolerant

Drug: Fentanyl

• MOA: binds to opioid receptors (mu/kappa) for potent, rapid analgesia

• For short duration, chronic pain, surgery

• ADR: respiratory depression, bradycardia, hypotension, muscle rigidity

• Nursing:

  • BBX - schedule II

  • ensure airway support

  • monitor resp. depression + CNS depressant interaction

  • titrate carefully

Drug: Tramadol

• MOA: binds to opioid receptor (mu), weak, inhibits pain transmission impulse

• For moderate pain, neuropathic pain, restless leg syndrome

• ADR: dizziness, N/V, lethargy, CNS stimulation, seizures

• X: history of seizures, combination with SSRIs/MAOIs, sudden death with ethanol

• Nursing:

  • monitor for seizures

  • avoid alcohol/CNA depressants

  • risk of serotonin syndrome

  • schedule IV

Anesthesia

• reversible state of loss of sensation

• with or without loss of consciousness

• prevent pain during procedures

• levels:

  • sedation - calm, awake

  • moderate sedation - drowsy, arousable

  • deep sedation - difficult to arouse

  • general anesthesia - unconscious

Types of Anesthesia

• General

  • loss of sensation + loss of consciousness

  • major surgery

• Regional

  • loss of sensation in a body region + conscious

  • for lower body procedures

• Local

  • loss of sensation in small area + conscious

  • for minor procedures

• Sedation

  • reduced awareness, drowsiness

  • for procedures for relaxation / reduce anxiety

General Anesthesia

• MOA: increase GABA (inhibitory) & lower NMDA (excitatory)

• Result: global CNS depression - unconscious

• Risks: resp depression, hypotension

Drug: Isoflurane

• Class: general anesthetic

• MOA: increase GABA (inhibitory) & lower NMDA (excitatory)

• For induction (inhaled) + maintenance

• ADR: hypotension, resp depression, N/V

  • serious: malignant hypothermia, arrhythmias, hepatotoxicity

• X: MH, hepatic disease

• Nursing:

  • Pre-op: assess risk (MH, liver)

  • monitor BP, ECG, resp status

  • Post-op: resp depression, hypotension, delirium

Drug: Nitrous Oxide

• Class: CNS depressant

• MOA: NMDA receptor antagonist → blocks excitatory → mild anesthesia + analgesia

• For dental procedures, labor analgesia, adjunct to general anesthesia

• rapid onset + rapid recovery; weak anesthetic, use with other agents

• ADR: nausea, dizziness, sedation

  • serious: diffusion hypoxia (when w/o O₂)

• X: air-filled space conditions

• Nursing:

  • MUST administer with oxygen

  • monitor O2 sat, resp status

Drug: Propofol

• MOA: GABA agonist → increase inhibitory signal → rapid CNS depression → sedation/anesthesia

• rapid onset + short duration, no analgesic effect

• For induction + maintenance of anesthesia, ventilated patients ICU

• ADR: resp depression, hypotension, bradycardia

  • serious: propofol infusion syndrome (PRIS)

• X: egg/soy allergy

• Nursing:

  • often combined with analgesics

  • ensure airway + ventilation support

  • monitor BP, ECG, resp status

  • watch for PRIS

Sedatives for Anesthesia

• MOA: CNS depressants that induce relaxation and amnesia

• Ex: Midazolam, Diazepam (Valium)

• For conscious sedation during minor procedures

• ADR: resp depression, hypotension, dizziness

• Nursing: monitor resp rate + BP, ensure safe recovery

Drug: Midazolam

• MOA: enhances GABA → increase inhibitory → sedation, anxiolysis, amnesia

• rapid onset, causes anterograde amnesia, no analgesic effect

• ADR: resp depression, hypotension, dizziness

  • serious: resp arrest

• X: severe resp despression, concurrent CNS depressants

• Reversible agent: Flumazenil

• Nursing:

  • ensure airway support, monitory resp status, BP, sedation level

  • combine with analgesics if needed

Neuromuscular Blockers

• causes paralysis

• Ex: succinylcholine, rocuronium

• For intubation, surgical/mechanical ventilation

• ADR: resp paralysis, MH, bradycardia, hypotension

• Nursing:

  • sedate FIRST, analgesia SECOND, then NM blocker

  • have airway + reversal agents ready

  • monitor for MH

Drug: Succinylcholine

• MOA: persistent activation of nicotinic receptors → sustained depolarization → paralysis

• initial may fasciculations (twitching) or flaccid paralysis (floppy, no reflexes)

• For rapid sequence intubation, short procedures

• ADR: Hyperkalemia, bradycardia, MH, resp arrest

• X: high potassium, history of MH

• Nursing:

  • must be given with sedation

  • ensure airway + ventilation support

  • monitor K+, ECG, resp status, MH

Drug: Rocuronium

• MOA: blocks acetylcholine at nicotinic receptors → prevents depolarization → skeletal muscle paralysis

• no depolarization, no fasciculations / flaccid paralysis

• For RSI, surgical muscle relaxation, mechanical ventilation support

• ADR: resp paralysis, hypotension, prolonged paralysis

• Reversal Agent: sugammadex, neostigmine

• Nursing:

  • ensure support

  • continuous monitoring O2 sat, resp status

  • assess neuromuscular function (train-of-four) for response

Malignant Hyperthermia (MH)

Genetic → get family history before anesthesia

• Triggers: Volatile (inhaled) anesthetics + succinylcholine

• MOA: increased Ca²⁺ → sustained muscle contraction → hypermetabolism

• Effects: hyperthermia, acidosis, hyperkalemia, rhabdomylosis

• Treatment:

  • strop trigger

  • dantrolene

  • supportive care

Drug: Dantrolene

• MOA: blocks Ca²⁺ release → decrease muscle contraction & hypermetabolism

• For MH, neuroleptic malignant syndrome, severe muscle spasticity

• ADR: muscle weakness, drowsiness

  • serious: hepatotoxicity

• X: severe liver disease

• Nursing:

  • early administration life saving

  • monitor LFTs

  • assess muscle strenght, resp status

  • supportive care (IV fluids, electrolytes)

Local Anesthetics

• MOA: block sodium channels → prevent depolarization, stop action potentials → stop transmission (pain signal never reaches CNS)

• Ex: lidocaine, bupivacaine

• Toxicity:

  • CNS → siezures

  • cardiac → arrhythmias

Drug: Lidocaine

• MOA: blocks voltage-gated sodium channels → prevents depolarization → stops nerve conduction

• pain signal never reaches CNS

• For local / regional anesthesia (inject/topical), ventricular arrhythmias (IV use)

• ADR:

  • CNS: dizziness, confusion, siezures

  • cardiac: arrhythmias, hypotension

• X: severe heart block

• Nursing:

  • monitor ECG, BP, neurologic status

  • watch for early toxicity (tinnitus, metallic taste, confusion)

  • ensure safe dosing