Pain is whatever the patient says it is — the 5th vital sign, and the single most reported symptom in healthcare. Assess it, believe it, and treat it with the smallest effective combination of pharmacologic and nonpharmacologic tools.
🎯 Pain = subjectiveBelieve the patient's number, not your own guess.
🪜 WHO ladderNon-opioid → weak opioid → strong opioid, adding not replacing.
🔤 PQRST / OLDCARTStructured pain history — don't skip the assessment for the med.
🚨 Respiratory depression#1 opioid safety priority — assess RR before & after every dose.
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PATHOPHYSIOLOGY
STEP 1 · HOW PAIN WORKS
Nociception is the whole pathway from tissue injury to the brain's perception of pain.
⚡ Nociception — the 4-step pain pathway
Nociceptors are pain receptors on nerve endings that respond selectively to painful stimuli. Nociception is the transmission of that pain signal. Chemical substances at the injury site (prostaglandins, bradykinin, substance P) increase pain sensitivity; others (endorphins, enkephalins) decrease it.
🧠 "TTPM" — Transduction, Transmission, Perception, Modulation. Pain isn't a single event, it's a relay race.
⭐ COX-1 vs. COX-2 — why it matters for NSAIDs
COX-1
COX-2
"Housekeeping" enzyme — protects gut lining, supports platelet function
Induced by inflammation — drives pain, fever, swelling
Blocking it → GI ulcers/bleeding risk
Blocking it → reduces pain/fever/inflammation
🧠 COX-1 protects, COX-2 provokes. Non-selective NSAIDs block both — that's why they can cause GI upset while also relieving pain. See NG-256 NSAIDs for drug-level detail.
⚠️ Endogenous pain relief
Endorphins and enkephalins are the body's own opioids — they inhibit substance P (a neurotransmitter that amplifies pain signals), naturally decreasing pain sensation.
🧠 "Endorphins are the body's built-in morphine." Exercise, laughter, and touch can boost this system — part of why nonpharmacologic care genuinely reduces pain, not just distracts from it.
📈 Acute vs. chronic pain — different bodies, different exam answers
Acute pain
Chronic pain
Sudden onset, specific to an injury; lasts seconds up to 6 months
Persistent, often malignant or non-malignant, lasts longer than 6 months
Often NO visible signs — normal vitals do not rule out chronic pain
🧠 NCLEX trap: A calm patient with normal vitals reporting 8/10 chronic pain is not lying — chronic pain rarely shows the classic acute stress-response vitals. Believe the number.
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ASSESSMENT
STEP 2 · ASK BEFORE YOU TREAT
A structured history plus the right scale for the right patient — assessment always comes before the medication.
🔤 Focused pain history — PQRST
Letter
What it means
P
Provocation/Palliation — aggravating & alleviating factors: what makes it worse? What makes it better?
Q
Quality — dull, sharp, stabbing, burning?
R
Region/Radiation — where is the pain? Does it radiate?
S
Severity — rate on a 0–10 scale
T
Timing — when did it start? What was happening at onset? Duration?
🧠 "Please Quit Radiating, Send Timely help." Many programs also teach OLDCART (Onset, Location, Duration, Characteristics, Aggravating/Alleviating, Radiation, Treatment) — same core questions, different order. Use whichever your program tests.
🎚️ Numeric rating scale — self-report, ages ~9+
0 None
1-3 Mild
4-6 Mod
7-9 Severe
10 Worst
Gold standard when the patient can self-report — always use the patient's own number over a nurse's visual guess.
🧠 Pain is whatever the patient says it is, at the intensity they say it is.
🧒 Scales for special populations
Wong-Baker FACES scale — young children or anyone who can't use numbers; picks a face from smiling to crying.
FLACC scale — infants, nonverbal, or cognitively impaired patients. Scores Face, Legs, Activity, Cry, Consolability, 0–2 each (0–10 total).
CPOT / behavioral pain scales — sedated or intubated ICU patients; observe facial expression, body movement, muscle tension, ventilator compliance.
🧠 "Can't talk? Watch, don't guess." Nonverbal patients still feel pain — behavior is the vital sign when words aren't available.
⭐ Factors that influence how pain is expressed
Past experience with pain shapes current perception and coping.
Anxiety and depression both decrease the pain threshold — psych distress makes pain feel worse.
Age and gender influence reporting and treatment bias.
Culture — different cultures teach different "appropriate" pain responses; stoicism does not mean absence of pain.
🧠 Never assume — ask. A stoic patient from a culture that discourages outward pain expression can still be in severe pain; the number they give you is still the truth.
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TREATMENT
STEP 3 · MULTIMODAL & STEPPED
The WHO pain ladder steps therapy up with severity — and nonpharmacologic care belongs at every step, not just the mild ones.
🪜 WHO analgesic ladder — match the drug class to the severity
Multimodal analgesia = combining drug classes with different mechanisms (e.g., an NSAID + an opioid + a nonpharmacologic measure) to get better relief at lower opioid doses — fewer side effects, less respiratory depression risk.
🧠 The ladder adds, it doesn't just replace. Non-opioids often continue alongside opioids at every rung unless contraindicated — that's the whole point of multimodal care.
💊 Pharmacologic categories — see the dedicated pages for drug detail
Non-opioids: NSAIDs (ketorolac, ibuprofen) for mild pain; acetaminophen can be given with NSAIDs and carries a hepatotoxicity risk at high/chronic doses.
Adjuvants/routes: topical agents, local anesthesia, intraspinal (epidural/intrathecal) analgesia.
Delivery methods: routine around-the-clock dosing for constant pain; PRN for breakthrough pain; PCA (patient-controlled analgesia) pump for self-titrated IV opioid dosing.
➡️ Drug mechanisms, doses, and side effects are covered in full on NG-257 Opioids, NG-256 NSAIDs, and NG-232 Acetaminophen (Tylenol) — this page focuses on the assessment and care-planning process, not re-explaining each drug.
✅ Nonpharmacologic interventions — real tools, not "just distraction"
🧠 Nonpharm ≠ optional extra. These work through real physiologic pathways (e.g., gate-control theory, endorphin release) and should be layered in at every rung of the ladder, not reserved for "mild" pain only.
🚨 Opioid safety priorities — assess before AND after every dose
Priority
Why
Respiratory rate
Hold and notify provider if RR < 12/min — respiratory depression is the #1 life-threatening opioid adverse effect.
Sedation level
Increasing sedation precedes respiratory depression — a rising sedation score is an earlier warning sign than the RR itself.
Bowel function
Opioid-induced constipation is nearly universal — prophylactic bowel regimen, not PRN.
Naloxone
Opioid antagonist reversal agent — know where it is and keep it available for any patient on IV/high-dose opioids.
🧠 "Sedation before suffocation." A patient gets drowsy before their breathing drops — rising sedation is your earliest cue to hold the next dose.
⚡
QUICK RECALL
SAY IT OUT LOUD
🎯 Pain = subjectiveTrust the patient's number over your own guess
Q2: A calm patient with normal vital signs rates their chronic pain 8/10 — what should the nurse do?
Believe the reported number and treat accordingly — chronic pain often shows no visible physiologic signs, unlike acute pain.
Q3: Which scale is used for a nonverbal, cognitively impaired patient?
The FLACC scale (Face, Legs, Activity, Cry, Consolability) or another validated behavioral pain scale — not the numeric rating scale.
Q4: A patient on a morphine PCA becomes increasingly drowsy but is still arousable and RR is 14. What's the priority nursing action?
Treat rising sedation as an early warning sign of respiratory depression — increase monitoring frequency, reassess RR and sedation closely, and be ready to hold the next dose and notify the provider before RR drops further.