Learn — CNS, psychiatric & pain drugs

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Fentanyl

Fentanyl is a synthetic, highly lipid-soluble pure mu-opioid agonist roughly 100 times more potent than morphine, used for induction and maintenance of anaesthesia, for procedural and severe acute pain, in patient-controlled analgesia, and as a transdermal patch for stable chronic cancer pain. It matters at the bedside because its dose is measured in micrograms rather than milligrams, so a decimal error is a fatal error, and because it depresses breathing before it depresses consciousness enough to look alarming.

Mechanism: fentanyl binds mu-opioid receptors in the brainstem, the dorsal horn of the spinal cord and the periphery, blunting both the perception of pain and the medullary response to a rising carbon dioxide — that second effect is exactly what produces respiratory depression.
Dose and route: the usual adult analgesic dose is 25 to 100 micrograms (about 1 to 2 micrograms/kg) by slow intravenous injection titrated to effect; the transdermal patch is only for opioid-tolerant chronic pain and is changed every 72 hours, never used for acute or breakthrough pain.
Onset and duration: intravenous fentanyl acts in 1 to 2 minutes, peaks at about 5 minutes and a single dose wears off in 30 to 60 minutes by redistribution rather than elimination; the patch takes 12 to 24 hours to reach effect and the skin depot keeps releasing drug for about 24 hours after it is removed.
Repeated boluses or an infusion saturate fat and muscle so the context-sensitive half-time lengthens, and the patient can stop breathing hours after the last dose — the reason a post-anaesthetic patient needs continuous monitoring and not a single check.
The adverse effect that decides nursing action is respiratory depression heralded by increasing sedation and a falling respiratory rate; fentanyl also causes chest-wall and glottic rigidity when a large dose is pushed rapidly, which makes bag-mask ventilation impossible and needs anaesthetic help and a muscle relaxant.
The reversal agent is naloxone, titrated in small intravenous increments to restore adequate breathing rather than full wakefulness; because naloxone lasts only 30 to 90 minutes and fentanyl outlasts it, the patient stays monitored and may need repeat doses or an infusion.
Monitoring: record the respiratory rate and a sedation score at least as often as the pain score, keep the respiratory rate above 8 to 10 per minute with the patient rousable, and use continuous pulse oximetry — with capnography where it is available — for any infusion or patient-controlled pump.
Cautions and contraindications: the patch is contraindicated in the opioid-naive patient and in acute pain; heat over the patch from fever, a heating pad or a hot bath accelerates absorption and can cause overdose, and the dose must be reduced when benzodiazepines or other central depressants are running.

Gaseous anaesthetics

Inhalational anaesthetics are the gases and volatile liquids delivered through a vaporiser and the lungs to produce and maintain unconsciousness, and their potency is expressed as MAC — the minimum alveolar concentration that abolishes movement to a skin incision in half of patients. They matter at the bedside because their speed depends on blood solubility rather than on dose, because they are the agents that trigger malignant hyperthermia, and because nitrous oxide expands every closed air space it reaches.

MAC measures potency and a low MAC means a potent agent: halothane about 0.75%, isoflurane about 1.2%, sevoflurane about 2%, desflurane about 6% and nitrous oxide over 100%, which is why nitrous oxide can never anaesthetise alone. MAC falls with age, hypothermia, pregnancy and concurrent opioids or sedatives, and rises in infants and in chronic alcohol use.
Speed of induction and recovery is set by the blood-gas partition coefficient — the less soluble the agent, the faster the alveolar concentration rises and the faster the patient wakes; desflurane and nitrous oxide are the quickest and halothane the slowest.
Nitrous oxide gives good analgesia and amnesia but no muscle relaxation, so it is used as a carrier with a volatile agent; it enters closed gas spaces far faster than nitrogen leaves them, so it is contraindicated in pneumothorax, bowel obstruction, air embolism, middle-ear surgery and after an intraocular gas injection.
Sevoflurane is sweet-smelling and non-pungent with low blood solubility, which makes it the agent of choice for inhalational induction in children and in the difficult airway; isoflurane is cheap and stable for maintenance; desflurane has the fastest offset but is pungent and irritates the airway, so it is not used to induce.
Halothane still appears in Indian practice and in examinations: it sensitises the myocardium to catecholamines and provokes arrhythmias, depresses the myocardium in a dose-dependent way, and can cause halothane hepatitis, so it is avoided within about 3 months of a previous halothane anaesthetic.
The adverse effect that decides nursing action is malignant hyperthermia — a rising end-tidal carbon dioxide, masseter and generalised rigidity, tachycardia, a climbing temperature and dark urine — triggered by any volatile agent or by suxamethonium; nitrous oxide is the one inhalational agent that does not trigger it.
The reversal agent for malignant hyperthermia is dantrolene 2.5 mg/kg intravenously, repeated until the signs settle, alongside removing the trigger, ventilating with 100% oxygen at high flow, active cooling and treatment of the hyperkalaemia and acidosis.
Monitoring: end-tidal carbon dioxide, oxygen saturation, temperature, heart rate and blood pressure run continuously, and an unexplained rise in end-tidal carbon dioxide that does not settle with increased ventilation is the earliest and most sensitive sign of malignant hyperthermia.
In recovery every volatile agent causes nausea, vomiting and shivering, so the patient is nursed on the side with suction to hand, and supplemental oxygen is continued after nitrous oxide is stopped because diffusion hypoxia can follow its sudden withdrawal.

General anaesthesia — stages

Guedel's stages describe the orderly depression of the nervous system as an anaesthetic is taken up, read at the bedside from respiration, the pupils, the eye reflexes and muscle tone. They matter because stage II is the dangerous one in which laryngospasm, vomiting and arrhythmia occur, stage III is the target for surgery, and stage IV is an overdose that must be recognised and reversed at once.

Stage I, analgesia, runs from the start of induction to loss of consciousness: the patient is drowsy but rousable, still talks, breathes regularly and keeps every reflex, and analgesia is already present, which is why this plane alone is used for short procedures such as dressings with nitrous oxide.
Stage II, excitement or delirium, runs from loss of consciousness to the return of regular automatic breathing: the pupils dilate with a divergent gaze, breathing is irregular with breath-holding, muscle tone rises and reflexes are exaggerated, so laryngospasm, vomiting, aspiration and arrhythmia peak here and the theatre must be silent and free of stimulation until it is passed.
Stage III, surgical anaesthesia, is the target: automatic regular breathing, loss of the eyelash and then the eyelid reflex, pupils that centre and then fix, and stepwise loss of muscle tone through planes 1 to 4, with intercostal paralysis and diaphragmatic breathing marking the deepest plane.
Stage IV, medullary paralysis, is an overdose: apnoea, widely dilated non-reacting pupils, an imperceptible pulse and collapsing blood pressure — the agent is turned off, 100% oxygen and ventilation are begun and circulatory support started immediately.
Guedel described these stages for slow ether induction in an unpremedicated patient, so modern intravenous induction with propofol or thiopental carries the patient through stages I and II in seconds; the stages are now seen clearly only in slow inhalational induction and, running backwards, during emergence.
Emergence retraces the stages in reverse, so every waking patient passes through stage II again — which is why extubation is performed either deep or fully awake and never in stage II, and why the recovery nurse keeps suction, oxygen and an airway immediately to hand.
Depth today is judged by the clinical signs together with end-tidal agent concentration, haemodynamic response and, where available, a processed EEG depth-of-anaesthesia monitor, kept in the recommended range because an inadequate depth during paralysis causes awareness.
The nurse's job at induction is to have working suction, an oxygen source with a self-inflating bag, a checked laryngoscope and correctly sized tubes ready before the drug is drawn up, and to apply cricoid pressure on request during a rapid-sequence induction of a patient with a full stomach.

Spinal anaesthesia position and complications

Spinal or subarachnoid anaesthesia is the injection of a small dose of local anaesthetic into the cerebrospinal fluid below the end of the spinal cord, producing a dense sensory, motor and sympathetic block of the lower body while the patient keeps their own airway. It matters at the bedside because the sympathetic block is immediate and predictable — hypotension and bradycardia in the first twenty minutes — and because a block that climbs too high paralyses the intercostal muscles and then the diaphragm.

The puncture is made at the L3-L4 or L4-L5 interspace, safely below the conus medullaris which ends at about L1 in the adult and L3 in the newborn; Tuffier's line, joining the highest points of the iliac crests, crosses the body of L4 and is the surface landmark used.
The needle passes skin, subcutaneous tissue, supraspinous ligament, interspinous ligament, ligamentum flavum, the epidural space and finally the dura and arachnoid, and free flow of clear cerebrospinal fluid is the only proof of correct placement.
Position is sitting with the back arched, chin on chest, arms crossed and feet supported, or lateral with the knees drawn up to the abdomen and the back at the edge of the table; in both the aim is maximum flexion to open the interspinous spaces, and the nurse's task is to hold the patient still, support them so they cannot fall, and keep them from moving when the needle goes in.
The usual drug is hyperbaric bupivacaine 0.5% in dextrose, about 2 to 3 mL, often with a small dose of an opioid; because it is heavier than cerebrospinal fluid, the patient's position after injection is what determines the height the block reaches.
Onset of sensory block is 2 to 5 minutes and the level is fixed by about 15 to 20 minutes; a bupivacaine spinal gives roughly 90 to 150 minutes of surgical anaesthesia, after which sensation returns before motor power and the patient must not walk until the block has fully worn off.
The adverse effect that decides nursing action is hypotension from sympathetic blockade, with bradycardia when the block reaches the cardio-accelerator fibres at T1 to T4; the other complications are post-dural-puncture headache, urinary retention, total spinal, transient neurological symptoms, backache and, rarely, epidural haematoma or abscess.
There is no antidote — hypotension is treated by head-down tilt (left uterine displacement in the pregnant woman), a rapid crystalloid bolus, oxygen and a vasopressor such as phenylephrine or ephedrine when the pulse is slow, and bradycardia with atropine; a total spinal needs intubation, ventilation and full circulatory support.
Monitoring: check blood pressure every 2 to 3 minutes for the first 15 to 20 minutes and then every 5 minutes, keeping the systolic pressure within about 20% of baseline, test the sensory level with cold or pinprick, and watch the patient's ability to speak a full sentence and to grip, because hand tingling and a weak voice mean the block is climbing.
Post-dural-puncture headache is a postural frontal or occipital headache appearing 24 to 48 hours later, worse on sitting or standing and relieved by lying flat; it is commoner with a large cutting needle and in young women, and is managed with bed rest, hydration, caffeine and simple analgesia, with an epidural blood patch if it persists.
Absolute contraindications are patient refusal, raised intracranial pressure, infection at the puncture site, uncorrected hypovolaemia or shock, coagulopathy or therapeutic anticoagulation, and severe fixed cardiac output lesions such as tight aortic stenosis; the bladder is watched afterwards because urinary retention is common until the block resolves.

Regional anaesthesia

Regional anaesthesia is the deliberate interruption of nerve conduction to a defined part of the body with a local anaesthetic, either neuraxially as a spinal, epidural or caudal block, or by blocking a named peripheral nerve or plexus, so that surgery is done while the patient keeps their own airway. It matters at the bedside because the whole dose is deposited beside a nerve and a vessel, so an accidental intravascular injection or a simple overdose produces local anaesthetic systemic toxicity — an emergency the nurse must recognise from the patient's first words and treat with lipid emulsion.

Mechanism: local anaesthetics are weak bases that cross the nerve membrane unionised and then block the sodium channel from the inside, so conduction fails; small unmyelinated fibres go first, which is why sympathetic block precedes loss of pain and temperature, then touch and pressure, then motor power, and why recovery runs in the opposite order.
Epidural anaesthesia places a catheter in the epidural space without puncturing the dura, needs a large volume of 10 to 20 mL, takes 15 to 30 minutes to work, is segmental and can be topped up for hours or days for labour and postoperative analgesia; a spinal uses 2 to 3 mL into the cerebrospinal fluid and gives a dense block in minutes.
The named blocks that appear in examinations are interscalene for shoulder surgery, supraclavicular and infraclavicular for arm and forearm, and axillary for forearm and hand; femoral, sciatic, popliteal and adductor canal blocks for the lower limb; and transversus abdominis plane blocks for abdominal wall analgesia.
Maximum safe doses are what keep the patient alive: roughly 3 mg/kg for plain lignocaine and 7 mg/kg with adrenaline, and about 2 mg/kg for bupivacaine; adrenaline 1 in 200000 is added to slow absorption, prolong the block and act as an intravascular marker, and traditional teaching still avoids adrenaline-containing solutions in end-arterial fields such as digits.
Onset and duration: lignocaine acts in 3 to 5 minutes and lasts 1 to 2 hours (longer with adrenaline), while bupivacaine takes 10 to 20 minutes and lasts 3 to 8 hours, so bupivacaine is chosen when postoperative analgesia is the goal and lignocaine when speed is.
The adverse event that decides nursing action is local anaesthetic systemic toxicity, which begins with circumoral tingling, a metallic taste, tinnitus, slurred speech, dizziness and agitation, then convulsions, and finally a cardiac phase of arrhythmia and arrest; bupivacaine is the agent most likely to reach the cardiac phase with little warning.
The antidote is 20% lipid emulsion given as an intravenous bolus of about 1.5 mL/kg followed by an infusion while standard resuscitation continues; the seizure is controlled with a benzodiazepine, adrenaline is used in reduced doses in this arrest, and no local anaesthetic antiarrhythmic such as lignocaine is given.
Monitoring: every block needs intravenous access, full monitoring and resuscitation drugs including lipid emulsion in the room before the needle is inserted; aspirate before each 5 mL increment, inject slowly and keep talking to the patient, because the first sign of toxicity is something the patient tells you rather than something the monitor shows.
Contraindications are patient refusal, infection at the injection site, allergy to the agent, and coagulopathy or therapeutic anticoagulation for any neuraxial or deep block, for which the ASRA time intervals for stopping and restarting anticoagulants must be followed.

Alcohol withdrawal symptoms — CIWA-Ar

The Clinical Institute Withdrawal Assessment for Alcohol, revised (CIWA-Ar), is a ten-item bedside scale that turns the severity of alcohol withdrawal into a number so that benzodiazepine can be given when the patient actually needs it rather than by a fixed clock. It matters at the bedside because withdrawal follows a predictable timeline that ends in delirium tremens, a condition with real mortality, and because the nurse who scores the patient is the person who decides when the next dose is given.

CIWA-Ar scores ten items — nausea and vomiting, tremor, paroxysmal sweats, anxiety, agitation, tactile disturbance, auditory disturbance, visual disturbance, headache, and orientation or clouding of sensorium — each from 0 to 7 except orientation which is 0 to 4, giving a maximum of 67.
Interpretation: under about 8 to 10 is minimal withdrawal needing no drug, 8 to 15 is mild, 16 to 20 is moderate and above 20 is severe with a high risk of progressing to delirium tremens.
Symptom-triggered therapy gives a benzodiazepine dose whenever the score reaches the threshold and rescores the patient hourly; compared with fixed-schedule dosing it uses less drug and shortens treatment, but it depends entirely on a nurse who can score reliably and who documents each score.
The timeline is examinable and clinically useful: tremor, anxiety, sweating and tachycardia at 6 to 12 hours after the last drink; alcoholic hallucinosis with a clear sensorium at 12 to 24 hours; generalised tonic-clonic withdrawal seizures at 12 to 48 hours; and delirium tremens with clouded sensorium, disorientation, visual hallucinations, fever and marked autonomic overactivity at 48 to 96 hours.
Delirium tremens is the emergency of the list and is separated from hallucinosis by the confusion; untreated it carries a substantial mortality from arrhythmia, hyperthermia, aspiration and cardiovascular collapse, so it is nursed in a high-dependency setting.
Treatment is a benzodiazepine: a long-acting agent such as chlordiazepoxide or diazepam gives a self-tapering course, while lorazepam is chosen in liver disease, in the elderly and in delirium because it has no active metabolites; antipsychotics are only an adjunct because they lower the seizure threshold and do not treat the withdrawal itself.
Thiamine goes in before glucose: give parenteral thiamine (commonly 100 mg intramuscularly or intravenously as prophylaxis, and higher parenteral doses when Wernicke encephalopathy is suspected) before any dextrose-containing fluid, because a glucose load into a thiamine-depleted brain precipitates Wernicke encephalopathy.
Flumazenil, the benzodiazepine antidote, is deliberately not used here because it precipitates seizures in an alcohol-withdrawing patient; oversedation is managed instead by withholding the next dose, supporting the airway and continuing to monitor.
Monitoring: rescore CIWA-Ar hourly while it is at or above the threshold, record pulse, blood pressure and temperature, and check magnesium, potassium, sodium and glucose with liver function, keeping the glucose above 70 mg/dL and correcting magnesium and potassium; nurse the patient in a quiet, well-lit room with repeated reorientation and constant observation.

Lithium — therapeutic range

Lithium is a monovalent cation used as a mood stabiliser in bipolar disorder, damping intracellular second-messenger signalling through inhibition of inositol monophosphatase and glycogen synthase kinase 3; it is the agent with the best evidence for preventing both mania and depression and for reducing suicide. It matters at the bedside because the therapeutic and toxic ranges almost touch, and because the level is set less by the prescribed dose than by the patient's sodium and water balance.

Dose and route: the usual adult dose is 600 to 1200 mg a day orally in divided doses, or as a single night-time dose of a sustained-release preparation, but the dose figure means little on its own because the drug is titrated entirely to the serum level.
The therapeutic range is 0.6 to 1.2 mEq/L, aiming at 0.8 to 1.2 in acute mania and 0.6 to 1.0 for maintenance and in the elderly; the blood sample is taken 12 hours after the last dose, and a sample drawn too soon reads falsely high and leads to a wrong dose reduction.
Onset: lithium reaches steady state in about 5 to 7 days and takes one to two weeks to show an antimanic effect, so an antipsychotic or benzodiazepine covers the acute agitation meanwhile; levels are checked 5 to 7 days after starting and after every dose change.
Toxicity climbs a recognisable ladder: above 1.5 mEq/L brings coarse tremor, nausea, vomiting, diarrhoea, drowsiness and ataxia; above 2.0 brings confusion, myoclonus, hyperreflexia and slurred speech; and above 2.5 brings seizures, arrhythmia, renal failure, coma and death — and an elderly or dehydrated patient can show all of it at a lower level.
Lithium is handled by the kidney like sodium, so anything that depletes sodium or reduces renal perfusion raises the level: dehydration, vomiting and diarrhoea, a low-salt diet, fever with heavy sweating, thiazide diuretics, NSAIDs, ACE inhibitors and angiotensin receptor blockers, and metronidazole.
There is no antidote and lithium is not protein-bound, so toxicity is treated by stopping the drug, restoring volume and sodium with intravenous normal saline, and haemodialysis when the level is very high or there is neurological impairment or renal failure; activated charcoal does not bind lithium.
Long-term adverse effects are a fine tremor, polyuria and polydipsia from nephrogenic diabetes insipidus, hypothyroidism with goitre, weight gain, acne and flares of psoriasis, benign leucocytosis, and rarely hyperparathyroidism with hypercalcaemia; the ECG may show benign T-wave flattening.
Monitoring once stable is the level every 3 to 6 months with thyroid function, calcium, urea and creatinine every 6 to 12 months, all against baseline tests taken before starting; the patient is taught to keep salt and fluid intake steady, to withhold the drug and telephone if vomiting or diarrhoea starts, and to avoid over-the-counter NSAIDs.
Lithium in the first trimester is associated with Ebstein anomaly of the tricuspid valve and levels swing rapidly around delivery, so it is continued in pregnancy only after specialist counselling and with frequent monitoring.

Phenytoin — side effects

Phenytoin blocks voltage-gated sodium channels in their inactivated state and prolongs their recovery, so it stops the high-frequency repetitive firing of a seizure focus without depressing normal neuronal traffic; it is used for focal and generalised tonic-clonic seizures and in status epilepticus, and it does not work in absence seizures. It matters at the bedside because its saturation kinetics turn a small dose increase into a large rise in level, and because giving it intravenously too fast causes hypotension and asystole.

Dose and route: adult maintenance is about 300 to 400 mg a day (roughly 4 to 6 mg/kg) orally in divided doses or as one dose of the extended-release capsule, and the loading dose in status epilepticus is 15 to 20 mg/kg intravenously.
The intravenous rate is a nursing safety rule in its own right: never faster than 50 mg per minute in an adult and no more than 25 mg per minute in the elderly or in cardiac disease, because the propylene glycol diluent causes hypotension, bradycardia and asystole; fosphenytoin may be given faster and is prescribed in phenytoin-equivalent units.
Phenytoin precipitates in dextrose, so it is diluted only in normal saline, given through an in-line filter into a large vein with a saline flush before and after, and never mixed with another drug in the same line; extravasation causes purple glove syndrome with severe local injury.
Phenytoin follows zero-order or saturation kinetics within the therapeutic range, so once the metabolising enzymes are saturated a small increase in dose produces a disproportionate rise in level — this is why a modest increment can tip a stable patient into toxicity and why no dose is changed without a level.
The therapeutic total level is 10 to 20 micrograms/mL, and toxicity climbs a predictable ladder: nystagmus from about 20, ataxia and slurred speech from about 30, and lethargy progressing to coma above about 40; a free level is used in hypoalbuminaemia and renal failure because the drug is highly protein-bound.
The chronic effects that decide adherence and nursing care are gingival hyperplasia, hirsutism and coarsening of the facial features, megaloblastic anaemia from folate interference, osteomalacia and vitamin D deficiency from enzyme induction, peripheral neuropathy, and fetal hydantoin syndrome in pregnancy.
The dangerous idiosyncratic reactions are Stevens-Johnson syndrome and toxic epidermal necrolysis — strongly associated with the HLA-B*1502 allele in patients of Asian ancestry — and DRESS, the drug reaction with eosinophilia and systemic symptoms; both require the drug to be stopped and never restarted.
Phenytoin is a potent hepatic enzyme inducer, so it reduces the effect of oral contraceptives, warfarin, corticosteroids and many antiretrovirals — a woman on phenytoin needs contraceptive counselling — while isoniazid, fluconazole and cimetidine raise the phenytoin level.
There is no antidote: toxicity is managed by withholding the drug with supportive care, activated charcoal after a recent large ingestion and continuous cardiac monitoring after rapid intravenous administration, and the level falls slowly because of the saturation kinetics.
Monitoring and teaching: check the trough level, full blood count and liver function, run continuous ECG and blood pressure during and after an intravenous load, teach brushing, flossing and six-monthly dental review to limit gum overgrowth, and never stop the drug abruptly because withdrawal precipitates status epilepticus.

Morphine — respiratory depression

Morphine is the reference pure mu-opioid agonist: it closes presynaptic calcium channels and opens postsynaptic potassium channels, damping transmission in the dorsal horn and the brainstem, and it also blunts the medullary chemoreceptor response to carbon dioxide. That last action is the mechanism of respiratory depression, which is why the respiratory rate and the sedation score — not the pain score — decide whether the next dose is given.

Dose and route: for severe acute pain the adult dose is about 0.1 mg/kg intramuscularly, or 2 to 4 mg intravenously titrated in small increments every few minutes to effect; it is never given as a single large intravenous push, and doses are reduced and spaced in the elderly, the frail and in renal or hepatic impairment.
Onset and duration: intravenous morphine begins within about 5 minutes and peaks at 15 to 20 minutes, intramuscular begins in 15 to 30 minutes and peaks at about an hour, and the analgesic effect lasts 3 to 4 hours — so the observations after a dose must cover the peak, because that is when respiration is most depressed.
The adverse effects that decide nursing action are respiratory depression preceded by sedation, hypotension from histamine release and venodilatation, pinpoint pupils, constipation to which tolerance never develops and which needs a laxative prescribed from day one, nausea and vomiting, pruritus, urinary retention and biliary colic from spasm of the sphincter of Oddi.
The classic triad of opioid overdose is a depressed conscious level, pinpoint pupils and a respiratory rate below 8 to 12 per minute; the rate and the rousability, not the saturation, are the early measures, because in a patient on supplemental oxygen desaturation appears late.
The reversal agent is naloxone in small titrated intravenous increments to restore adequate ventilation rather than full wakefulness, repeated as needed and sometimes given as an infusion, because naloxone lasts only 30 to 90 minutes while morphine lasts longer.
Monitoring: record respiratory rate, sedation score and pain score together at every observation with continuous pulse oximetry after intravenous doses and during patient-controlled analgesia, and hold the dose and reassess if the respiratory rate falls below about 8 to 10 per minute or the patient cannot be roused.
Morphine is metabolised to morphine-6-glucuronide, which is itself active and cleared by the kidney, so in renal impairment it accumulates and produces delayed, prolonged respiratory depression and myoclonus — another opioid such as fentanyl is preferred in that setting.
Contraindications and cautions: acute severe asthma and existing respiratory depression, raised intracranial pressure and head injury where it obscures the pupils and conscious level while raising carbon dioxide, paralytic ileus, and a monoamine oxidase inhibitor taken within the previous two weeks; the dose is cut when a benzodiazepine or another central depressant is running.
In cancer pain morphine is given by the clock rather than as required, with breakthrough doses of about one sixth of the total daily dose, and tolerance to respiratory depression develops alongside tolerance to analgesia; in India it is a narcotic drug requiring a statutory register, double-locked storage and a count check at every shift change.

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