Narcotics or Narcotic drugs (also known as "opioids") are drugs that react with different types of opioid receptors—receptor sites that respond to naturally occurring peptides, enkephalins, and endorphins. The term "narcotic" comes from the Greek word "to be numb" (narcosis), and originally referred to a variety of substances that dulled the senses and relieved pain.

• The term "narcotic" was coined by the Greek physician Galen, who referred to agents that numb or deaden, causing loss of feeling or paralysis.
• It is based on the Greek word narcosis, a term originally used by Hippocrates for the process of numbing or the numbed state.
• Galen listed seeds of poppy juice (opium) as the chief examples.
• Narcotics in the form of opium were first abused by China.
• The leaf of the poppy was chewed beginning in the 1700s for relaxation.
• Beginning in 1806, morphine began to be extracted from the poppy flower.

• Opium is the dried latex obtained from the opium poppy plant.
• Scientific name: Papaver somniferum.
• Approximately 12 percent of the opium latex is made up of the analgesic alkaloid morphine.
• The latex is processed chemically to produce heroin and other synthetic opioids for medicinal use and for the illegal drug trade.
• The latex also contains closely related opiates like codeine and thebaine, as well as non-analgesic alkaloids such as papaverine and noscapine.

• Morphine
• Heroin (illicit drug)
• Codeine
• Thebaine
• Oxycodone
• Methadone
• Hydrocodone
• Hydromorphone

• The Single Convention on Narcotic Drugs of 1961 is an international treaty.
• It prohibits the production and supply of specific (nominally narcotic) drugs except under license for specific purposes, such as medical treatment and research.
• The principal objectives of the Convention are to limit the possession, use, trade, distribution, import, export, manufacture, and production of drugs exclusively to medical and scientific purposes, and to address drug trafficking through international cooperation to deter and discourage drug traffickers.
• The adoption of this Convention is regarded as a milestone in the history of international drug law.
• The 1961 Convention seeks to control more than 116 drugs that it classifies as narcotic. These include:
  • Plant-based products such as opium and its derivatives morphine, codeine, and heroin (the primary category of drugs listed).
  • Synthetic narcotics such as methadone and pethidine.
  • Cannabis, coca, and cocaine.

Drugs and substances are classified depending upon the drug's acceptable medical use and the drug's abuse or dependency potential.

• Schedule I: Drugs, substances, or chemicals defined as drugs with no currently accepted medical use and a high potential for abuse. Example: Heroin.
• Schedule II: Drugs, substances, or chemicals defined as drugs with a high potential for abuse, with use potentially leading to severe psychological or physical dependence. These drugs are considered dangerous. Examples: Combination products with less than 15 milligrams of hydrocodone per dosage unit (Vicodin), cocaine, methadone, hydromorphone (Dilaudid), meperidine (Demerol), oxycodone (OxyContin), fentanyl.
• Schedule III: Drugs with a moderate to low potential for physical and psychological dependence. Examples: Products containing less than 90 milligrams of codeine per dosage unit (Tylenol with codeine).
• Schedule IV: Drugs with a low potential for abuse and low risk of dependence.
• Schedule V: Drugs, substances, or chemicals defined as drugs with lower potential for abuse. Generally used for antidiarrheal, antitussive, and analgesic purposes. Examples: Cough preparations with less than 200 milligrams of codeine or per 100 milliliters.

Pain is mostly a subjective experience of unpleasant sensation and emotional experience. People respond to pain differently because of cultural differences, learned experiences, and environmental stimuli.

A-delta and C-fibers are two sensory nerves that respond to stimulation by generating nerve impulses that produce pain sensations.

Narcotic drugs work as central nervous system (CNS) depressants by slowing down neural activity in both the brain and the body. Since narcotics effects specifically target the CNS, once drugs enter the brain, their effects can spread quickly throughout the body and slow down overall communications between the brain and the body. These receptors are found in the CNS, peripheral nerves, and GI tract cells. In the spinal cord, they integrate and relate pain information. Pain relief and side effects depend on the type of receptor site.

1. Mu-receptors: Primarily pain-blocking receptors; also account for respiratory depression, euphoria, and development of physical dependence.
2. Beta-receptors: Modulate pain transmission by reacting with enkephalins in the periphery.
3. Kappa-receptors: Associated with some analgesia, pupillary constriction, sedation, and dysphoria.
4. Sigma-receptors: Associated with pupillary dilation, hallucinations, and psychoses with narcotic use.

Narcotics are divided into 3 major classes based on their interaction with opioid receptors:

• Narcotic Agonists: React with opioid receptors in the CNS to cause analgesia, sedation, or euphoria. They are classified as controlled substances because they have a high potential for physical dependence.
• Narcotic Agonists-Antagonists: Stimulate certain opioid receptors but block others. They exert a similar analgesic effect to that of morphine but have less potential for abuse. However, they are associated with more psychotic-like reactions.
• Narcotic Antagonists: Bind strongly to opioid receptors without causing receptor activation. They block opioid receptor effects as well as reverse the effects of too many opioids in the system.

These drugs react with specific opioid receptors in the CNS to cause analgesia, sedation, or euphoria. They are primarily derived from the opium poppy or synthesized as chemicals with similar properties to natural opiates.

• Therapeutic Action:
  • Narcotic agonists act as agonists to specific opioid receptors (primarily Mu, Kappa, and Delta) in the CNS to produce analgesia, euphoria, and sedation.
  • Mu-receptors: Primarily responsible for pain relief, respiratory depression, euphoria, and physical dependence.
  • Kappa-receptors: Associated with spinal analgesia, sedation, and miosis (pupil constriction).
  • Delta-receptors: Play a role in modulating emotional response and potentially cardiovascular function.
• Indications:
  • Relief of moderate to severe acute pain or chronic pain. While historically overprescribed, modern clinical guidelines emphasize their role for short-term, intense pain, such as post-operative recovery or acute trauma.
  • Preoperative medication to induce sedation, provide preemptive analgesia, and reduce the dose of anesthetic required.
  • Component of combination therapy for severe chronic pain, particularly in palliative care, oncology, or end-of-life care, where the focus shifts from long-term dependency concerns to quality of life and comfort.
  • Intra-spinal (epidural or intrathecal) administration to manage intractable pain while minimizing systemic side effects.
  • Treatment of severe cough (antitussives like codeine) and severe diarrhea (antidiarrheals like loperamide).

• Children:
  • Safety and effectiveness have not been universally established for all agents.
  • Narcotic agonists with established pediatric dosage guidelines include codeine, fentanyl (injection), hydrocodone, meperidine, and morphine.
  • Naloxone is the essential antidote for pediatric narcotic overdose or the reversal of accidental ingestion.
  • Strict monitoring for respiratory depression is vital, as children may be more sensitive to the ventilatory effects of opioids.
• Adults:
  • Education is key; patients should be reassured that the risk of addiction is minimal when narcotics are used for short-term, acute pain in a hospital setting.
  • Proactive pain management: Patients should be taught to request medication when pain begins rather than waiting for it to become unbearable (the "pain ladder" approach).
  • Pregnancy/Lactation: Caution is advised due to the risk of Neonatal Opioid Withdrawal Syndrome (NOWS), characterized by irritability, high-pitched crying, and poor feeding.
  • Most narcotic agonists are pregnancy category B except oxycodone (category C). In labor, morphine, meperidine, and oxymorphone are commonly used, though they can cause respiratory depression in the neonate.
• Older adults:
  • Susceptibility: Increased risk for toxic effects due to decreased hepatic metabolism and renal clearance.
  • Safety Protocol: Use "start low, go slow" dosing. Establish fall precautions, including side rails, call lights within reach, and mandatory assistance for ambulation to prevent hip fractures or head injuries.
  • Cognitive Risk: Higher incidence of "sundowning" or delirium when treated with narcotics.

• Allergy to narcotic agonists: Prevent hypersensitivity reaction.
• Diarrhea caused by toxic poisons: Drug depresses GI activity and this could lead to increased absorption of the toxin and severe toxicity.
• Respiratory dysfunction: Exacerbated by respiratory depression caused by drugs.
• Recent GI/GU surgery, acute abdomen, ulcerative colitis: Can be worsened by the GI depressive effects of the narcotics.
• Head injuries, alcoholism, delirium tremens, cerebral vascular disease: Can be exacerbated by the CNS effects of the drug.
• Liver, renal dysfunction: Can interfere with the metabolism and excretion of the drug.
• Pregnancy, lactation: Potential adverse effects to the fetus and the baby, including respiratory depression and withdrawal.

• CNS: Light-headedness, dizziness, psychoses, anxiety, fear, hallucinations, pupil constriction (miosis), impaired mental processes, extreme drowsiness, feeling like you might pass out. Low cortisol levels can cause nausea, vomiting, loss of appetite, dizziness, worsening tiredness, or weakness.
• Respiratory: Narcotic-induced respiratory center depression resulting in labored breathing, decreased respiratory effort, apnea, cardiac arrest, and shock. Narcotics overdose can lead to complications including coma, brain damage, and death.
• GI: Nausea, vomiting, constipation, biliary spasm.
• GU: Ureteral spasm, urinary retention, hesitancy, loss of libido.
• Others: Sweating, reduced heart rate, physical and psychological dependence, withdrawal upon abrupt dose reduction after long-term use.

• Barbiturates, phenothiazines, MAOIs, Benzodiazepines: Increased likelihood of profound sedation, respiratory depression, hypotension, coma, and death. The FDA warns that concomitant prescribing should be reserved for patients for whom alternative treatment options are inadequate.
• SSRI, MAOI, TCA, St. John's Wort: Increased risk of potentially life-threatening serotonin syndrome, especially if taken with tapentadol (a newer narcotic agonist that also blocks norepinephrine reuptake in the CNS).
• Note: Methylnaltrexone bromide (Relistor) is an essential adjunct used as a treatment for opioid-induced constipation in palliative care patients who are no longer responding to traditional laxatives.

Morphine is a natural phenanthrene alkaloid present in opium (about 10% of the poppy capsule Papaver somniferum). It acts directly on the CNS to decrease the feeling of pain. Morphine is the ‘gold standard’ against which other opioid analgesics are measured.

• Trade Names: Astramorph PF, Roxanol, Roxanol-T, Infumorph, MorphaBond ER, MS Contin, Kadian.
• Key Features:
  • When used correctly for acute/severe pain, patients don’t become dependent, tolerance is uncommon, and respiratory depression doesn’t usually occur because the pain stimulus acts as a physiological antagonist to respiratory depression.
  • Morphine has no ceiling effect to the analgesia: Unlike NSAIDs, increasing the dose will continue to increase pain relief until limited by side effects.
  • The correct dose is the one that gives pain relief without intolerable side effects; it must be individually titrated due to significant inter-individual variation in metabolism.
  • It causes peripheral vasodilation, which can result in orthostatic hypotension.
• Indications:
  • Post-operative pain and trauma management.
  • Myocardial infarction: Reduces pain, anxiety, and cardiac preload/afterload, thereby decreasing myocardial oxygen demand.
  • Premedication before surgery to provide sedation and analgesia.
  • Severe pain associated with malignancy or end-of-life care.
  • Sickle cell crisis and vaso-occlusive episodes.
  • Acute pulmonary oedema: Helps by redistributing blood volume through venodilation and reducing patient anxiety/air hunger.
  • Chronic pain (cancer) where non-opioids have failed.
• Contraindications:
  • Renal impairment: Morphine-6-glucuronide (active metabolite) accumulates, increasing toxicity risks.
  • Severe hepatic dysfunction and biliary tract surgery (may cause spasm of the Sphincter of Oddi).
  • Significant pulmonary disease: Severe bronchial asthma or COPD where respiratory drive is already compromised.
  • CNS depression, head injuries, or increased intracranial pressure (CO2 retention from respiratory depression further increases ICP).
  • Paralytic ileus or acute abdomen conditions.
• Side Effects:
  • Constipation: Occurs in nearly all patients; tolerance to this effect does not develop. (Always give a laxative alongside, e.g., Bisacodyl 5mg at night or stimulant/softener combinations).
  • Nausea/vomiting: Stimulates the chemoreceptor trigger zone (CTZ). (Give anti-emetics e.g., Plasil 10mg 8 hourly).
  • Drowsiness and sedation: Usually improves after 3-5 days as tolerance develops.
  • Itching (pruritus): Caused by non-immunological histamine release, not necessarily a true allergy.
  • Urinary retention: Increases tone of the bladder sphincter, especially in elderly males.
  • Miosis (pinpoint pupils): A classic sign of opioid effect and overdose.
• Dosage Ranges:
  • Acute/Post-op Pain: Oral 5-20mg every 4 hours. Adult SC/IM 10mg every 4 hours. Neonate 150mcg/kg every 6 hours. 6-12 yrs 5-10mg every 4 hours.
  • Chronic Pain: Adult Oral/SC/IM 10-15mg every 4 hours; for long-term use, converted to sustained-release formulations every 12 or 24 hours.
  • Myocardial Infarction: Slow IV injection (2mg/min), 10mg initial dose, followed by 5-10mg if necessary.
  • Acute Pulmonary Oedema: Slow IV injection (2mg/min) 5-10mg to relieve dyspnea.
• Useful Tips for Morphine Administration:
  • Titration & Dosage Adjustment: Titrate the regular dose over several days until the patient is pain-free. To calculate a new dose, either add the total daily dose and the total breakthrough dose given in 24 hours and divide by six to get the new 4-hourly dose, OR give 30-50% increments (e.g., 5mg—10mg—15mg given as 4-hourly doses). Increments of less than 30% are ineffective.
  • Alternative Routes: If the patient cannot swallow, use other routes such as subcutaneous (SC), intravenous (IV), or an alternative enteral route (e.g., gastrostomy tube). Oral morphine can also be absorbed through the mucosa of the buccal cavity (mouth) or rectum, allowing administration in unconscious patients or those with severe dysphagia.
  • Conversion Ratios: The ratio of PO to SC is 2:1 (e.g., 10mg oral = 5mg SC). The ratio of PO to IV is 2-3:1 (e.g., 30mg oral = 10mg IV).
  • Immediate vs. Slow-Release: Morphine is available in immediate and slow-release oral forms. Use slow-release morphine once the pain is controlled by dividing the total 24-hour dose in half to get the twice-daily dosage.
  • Breakthrough Pain: Always allow additional doses (usually 1/6th of the total daily dose) for breakthrough pain. While this may be a one-off incidence, if frequent breakthrough doses are required, it means the regular 4-hourly dose needs increasing.
  • Addressing "Total Pain": Pain must be controlled before other problems can be addressed—it is impossible to have meaningful discussions about psychosocial concerns if a patient has uncontrolled pain. Conversely, psychosocial or spiritual problems can cause or aggravate pain; no amount of well-prescribed analgesia will relieve this pain until the responsible issues are identified and addressed.
  • Chronic vs. Short-Term Use: Oral morphine is effective for chronic severe pain and can be given for many years safely, with doses occasionally reaching several hundred mgs 4-hourly. Opiates can also be used as short-term analgesia for painful conditions like AIDS opportunistic infections (e.g., cryptococcal meningitis), sickle cell crisis, or burns, and does not cause addiction.
  • Tapering Doses: If the pain stimulus is removed (e.g., via a nerve block or healing), the dose of morphine should be decreased gradually (tapered) to minimize the effects of physical dependence withdrawal.

• Pharmacology:
  • Heroin is the diacetylated derivative of morphine, making it more lipid-soluble.
  • Because of its lipophilicity, it crosses the blood-brain barrier much faster than morphine, resulting in a rapid "rush."
  • Once in the brain, it is rapidly metabolized back into 6-monoacetylmorphine and then morphine.
• Effects:
  • Onset of effects is usually rapid (seconds via IV, minutes via smoking) and lasts for 3-5 hours.
  • When given by injection into a vein, heroin has two to three times the analgesic potency as a similar dose of morphine.
  • Causes intense CNS depression and profound miosis.
• Clinical Status:
  • It is a Schedule I illicit drug in the US with no accepted medical use.
  • In the UK and other nations, it is used medically (Diamorphine) for severe pain, MI, and acute pulmonary edema because its high solubility allows for smaller injection volumes.
  • Used in supervised injectable opioid treatment (SIOT) for refractory addiction.
• Adverse Effects:
  • Extreme respiratory depression, which is the primary cause of death in overdose.
  • Intense physical and psychological addiction (dependence).
  • Infected heart valves (endocarditis), skin abscesses, and blood-borne infections (HIV, Hepatitis B/C) due to IV drug abuse practices.
  • Risk of "Cotton Fever" and talc granulomas from impurities in street-grade heroin.

• Pharmacology:
  • A natural phenanthrene alkaloid present in opium (about 0.2%). It is a prodrug with low affinity for opioid receptors itself.
  • Codeine works by being converted by the liver into morphine via the CYP2D6 enzyme.
  • Genetics play a massive role: "Ultra-rapid metabolizers" can face toxicity from normal doses, while "Poor metabolizers" get no pain relief.
• Indications:
  • Mild to moderate pain relief (Step 2 of the WHO Pain Ladder).
  • Antitussive (cough suppressant) for dry, non-productive coughs.
  • Symptomatic treatment of acute diarrhea.
  • Greater benefit occurs when combined with paracetamol (Co-codamol) or NSAIDs due to synergistic effects.
• Dosage Ranges:
  • Relief of pain (Adult): 30-60mg PO every 4-6 hours PRN; max dose 240mg daily.
  • Children (1-12 yrs): 0.5-1 mg/kg every 4-6 hours. Note: Use is strictly discouraged in children post-surgery (tonsillectomy) due to fatal cases in ultra-rapid metabolizers.
  • Diarrhea (Adult): 30mg up to 4 times daily.
• Key Issues to Note:
  • Has a "ceiling effect" for analgesia; doses above 60mg often increase side effects without increasing pain relief significantly.
  • Significant risk of constipation; increase fluids and fiber intake.
  • Avoid alcohol during therapy as it potentiates CNS depression.
  • Codeine is not recommended for treatment of productive cough because suppressing the cough reflex prevents the clearance of secretions.

• Indications:
  • Short-term management of acute analgesia, post-operative pain, and moderate to severe acute pain.
  • Obstetric analgesia (traditionally favored as it was thought to cause less respiratory depression in the neonate, though this is debated).
  • Treatment of post-operative shivering (rigors).
• Dosage Ranges:
  • Acute pain (Adult): 50-150mg SC/IM repeated after 4 hours.
  • Obstetric analgesia: 50-100mg repeated 1-3 hours later if necessary (max 400mg/24h).
  • Post-operative pain: 25-100mg repeated every 2-3 hours if necessary.
• Key Issues:
  • Metabolizes into normeperidine, a CNS stimulant with a long half-life (15-20 hours).
  • Normeperidine accumulation causes neurotoxicity: tremors, muscle twitches, hyperreflexia, and grand mal seizures.
  • Avoid in patients with renal failure (high risk of normeperidine accumulation).
  • Strictly contraindicated with MAOIs (risk of serotonin syndrome and hyperpyrexic crisis).
  • Not recommended for chronic pain due to toxicity and short duration of action (2-3 hours).

• Trade Names: OxyContin (Extended Release), Roxicodone (Immediate Release), Percocet (with Acetaminophen).
• Indications:
  • Relief of moderate to severe acute or chronic pain.
  • Often used as a second-line opioid if morphine is not tolerated (e.g., due to hallucinations or severe itching).
• Dosage:
  • Immediate release: 5-15mg every 4-6 hours.
  • Extended-release: 10–20 mg PO q12h (never crush or chew ER tablets).
  • Approximately 1.5 to 2 times as potent as oral morphine.
• Caution:
  • Extremely high potential for abuse and diverted use.
  • Metabolized by CYP3A4 and CYP2D6; watch for interactions with grapefruit juice or macrolide antibiotics.
  • Pregnancy Category C; sometimes preferred if opioids are mandatory as it has a slightly different safety profile than morphine.

• Pharmacology:
  • A synthetic mu-opioid agonist and NMDA receptor antagonist.
  • The NMDA antagonism may help in treating neuropathic pain and preventing opioid tolerance.
  • Has a very long and unpredictable half-life (8 to 59 hours), leading to high risk of accumulation and overdose during the first week of treatment.
• Indications:
  • Maintenance therapy for opioid-use disorder to prevent withdrawal and reduce "drug-seeking" behavior.
  • Chronic, severe pain management, especially neuropathic pain or cancer pain.
  • Detoxification protocols.
• Adverse Effects & Risks:
  • QT Prolongation: Can lead to Torsades de Pointes; baseline and follow-up ECGs are recommended.
  • Severe respiratory depression that lasts longer than the analgesic effect.
  • Sweating (diaphoresis) is more common with methadone than other opioids.
  • Fatal overdoses frequently involve concomitant use of benzodiazepines or other CNS depressants.

• Pharmacology: A synthetic phenylpiperidine opioid that is 50-100 times more potent than morphine. Highly lipophilic with a rapid onset and short duration of action when given IV.
• Indications:
  • Induction and maintenance of general anesthesia.
  • Transdermal patches (Duragesic) for stable, chronic pain in opioid-tolerant patients.
  • Actiq (lozenge) or Fentora (buccal) for breakthrough cancer pain.
• Warning: The patch is not for acute pain or opioid-naive patients; heat (fever, heating pads) can dangerously increase the rate of absorption from the patch.

• Pharmacology: A semi-synthetic opioid derived from codeine or thebaine. It is roughly equal in potency to oral morphine.
• Formulations: Most commonly found combined with acetaminophen (e.g., Vicodin, Norco) or ibuprofen. Pure hydrocodone ER (Zohydro) exists for severe chronic pain.
• Key Note: It is a Schedule II drug. Often used as an antitussive in syrup form (Tussionex). High risk of liver toxicity if taken in excess due to the acetaminophen component.

• Hydromorphone (Dilaudid):
  • 5-7 times more potent than morphine.
  • Highly soluble, allowing for low-volume injections; useful for cachectic patients.
  • Has fewer active metabolites than morphine, making it potentially safer in renal failure.
• Oxymorphone (Opana):
  • Potent mu-agonist; should be taken on an empty stomach (food significantly increases absorption, increasing overdose risk).
• Propoxyphene (Darvon):
  • Relatively weak analgesia (similar to aspirin).
  • Withdrawn in many markets (including US/UK) because of cardiotoxicity and narrow therapeutic index.

These drugs stimulate certain opioid receptors (like kappa) but block or partially block others (like mu). They have less potential for abuse compared to pure narcotic agonists but are able to exert a similar analgesic effect as morphine.

• Therapeutic Action: Produce analgesia, sedation, and sometimes euphoria or hallucinations. They have a "ceiling effect" for respiratory depression.
• Indications: Relief of moderate to severe pain; pre-anesthetic medication and a supplement to surgical anesthesia. Desirable for relieving chronic pain in patients who are susceptible to narcotic dependence. Often used for pain relief during labor and delivery.
• Contraindications and Cautions:
  • Physical dependence on pure narcotics: Can precipitate a severe withdrawal symptom in opioid-dependent patients
  • COPD, other respiratory dysfunction.
  • MI, CAD, hypertension (can be exacerbated by cardiac stimulatory effects).
  • Renal, hepatic dysfunction.
  • Pregnancy, lactation.
  • Nalbuphine is specifically contraindicated in patients who are allergic to sulfites to prevent cross-hypersensitivity reactions.
• Interactions: Barbiturates, phenothiazines, MAOIs increase the likelihood of respiratory depression and coma. Interaction with Tripelennamine causes increased hallucinogenic and euphoric effects (notably with Pentazocine, known as “Ts and Blues” on the street).

Narcotic antagonists bind strongly to opioid receptors without causing receptor activation. They block opioid receptor effects as well as reverse the effects of too many opioids in the system.

• Indications: Complete or partial reversal of narcotic depression (respiratory depression, sedation); diagnosis of suspected opioid overdose.
• Contraindications and Cautions: Allergy, pregnancy/lactation, CV disease (exacerbated by rapid reversal of depressive effects). Narcotic addiction: Precipitation of violent withdrawal symptoms.
• Adverse Effects:
  • CNS: excitement, immediate reversal of analgesia.
  • CV: tachycardia, blood pressure changes, dysrhythmias, pulmonary edema.
  • Acute narcotic abstinence syndrome: nausea, vomiting, sweating, tachycardia, hypertension, tremulousness, feelings of anxiety. A naloxone challenge should be administered before giving long-acting naltrexone to avoid acute reactions.

• Assess for mentioned cautions and contraindications (e.g. drug allergy, respiratory dysfunction, myocardial infarction, CAD, hepatorenal dysfunction, history of narcotic addiction) to prevent untoward complications.
• Conduct pain assessment with the patient to establish a baseline and evaluate the effectiveness of drug therapy.
• Perform thorough physical (CNS, vital signs, bowel sounds, urine output, neurological status, respiratory rate and rhythm) to establish baseline status before beginning therapy, determine drug effectiveness, and evaluate for any potential adverse effects.
• Obtain an electrocardiogram as appropriate to evaluate for cardiac effects (especially with Methadone).
• Monitor laboratory results (liver function, kidney function) to determine the need for possible dose adjustment and identify toxic drug effects.

• Impaired Gas Exchange related to respiratory depression.
• Disturbed Sensory Perception related to CNS effects.
• Constipation related to GI effects.
• Risk for Injury related to CNS effects (dizziness, sedation).
• Decreased Cardiac Output related to CV effects (with antagonists).
• Acute Pain related to withdrawal and CV effects.

• Unless the patient has received a recent dose of opioid, a loading dose should be administered (according to the prescription) at the commencement of the infusion to ensure therapeutic plasma levels are quickly reached.
• For rapid relief of pain (or anticipated pain), the prescribed bolus dose should be reached.
• The infusion rate may be adjusted by the nurse within the dose range specified, according to the patient’s level of pain.
• It takes approximately four half-lives (8 hrs for morphine/hydromorphone, ~1.5 hrs for fentanyl) to reach steady state plasma concentration if given as an infusion. Therefore, if the rate is to be increased, a bolus should be given as well.
• Ideally, the infusion rate should not be increased unless 3 boluses are required in a 1 hour period.
• The volume infused should be checked every hour and the rate verified on the fluid balance flow chart.

• Monitor patient response to therapy (relief of pain, appropriate sedation vs. over-sedation).
• Monitor for adverse effects (e.g., GI depression, respiratory depression, arrhythmias, hypertension during reversal).
• Evaluate patient understanding of drug therapy by asking the patient to name the drug, its indication, and adverse effects to watch for.
• Monitor patient compliance to drug therapy.

• Food and Drug Administration (FDA) Post-Market Drug Safety Information (Guidelines on Opioid Analgesic REMS, Neonatal Opioid Withdrawal Syndrome, and CNS Depressant Interactions).
• Single Convention on Narcotic Drugs, 1961 (United Nations Treaty Series).
• Standard Pharmacological Guidelines for Opioid Agonists, Partial Agonists, and Antagonists.
• Clinical Management of Acute and Chronic Pain (Textbook Reference Material provided via user documentation).