In: Management of anxiety disorders, acute alcohol withdrawal, muscle relaxation, treatment of tetanus,

antiepileptic adjunct in status epilepticus, preoperative relief of anxiety and tension.

Ac: Acts in the limbic system and reticular formation to potentiate the effects of GABA, an inhibitory
neurotransmitter; may act in spinal cord and supraspinal sites to produce muscle relaxation.
Pharmacokinetics:
Rout
e Onset Peak Duration
Oral 30–60 min 1–2 h 3h
IM 15–30 min 30–45 min 3 h
IV 1–5 min 30 min 15–60 min
Recta Rapid 1.5 h 3h
l
T1/2: 20 to 80 hours, metabolized in the liver, excreted in urine.
Ae: Mild drowsiness, depression, lethargy, apathy, fatigue, restlessness, bradycardia, tachycardia,
constipation, diarrhea, incontinence, urinary retention, changes in libido, drug dependence with withdrawal
syndrome.
Adult: 2–10 mg PO b.i.d. to q.i.d.; or 0.2 mg/kg PR; or 2–30 mg IM b.i.d. or IV; 2–2.5
mg PO b.i.d. for elderly patients
Pediatric: 1–2.5 mg PO t.i.d. to q.i.d.; 0.3–0.5 mg/kg PR; or 1–3 mg IM or IV

Special considerations: Monitor injection sites; drug of choice if route change is

anticipated; taper after long-term therapy
In: Sedation, short-term treatment of insomnia, long-term treatment of tonic–clonic seizures and cortical
focal seizures, emergency control of certain acute convulsive episodes, preanesthetic.
Ac: Inhibits conduction in the ascending RAS; depresses the cerebral cortex; alters cerebellar function;
depresses motor output; can produce excitation, sedation, hypnosis, anesthesia, and deep coma; and has
anticonvulsant activity.
Pharmacokinetics:
Route Peak Onset Duration
Oral 15 min 30–60 min10–16 h
IM,   10–30 min4–6 h
SQ
IV up to 15 min5 min 4–6 h
T1/2: 79 hours; metabolized in the liver, excreted in urine.
Ae: Somnolence, agitation, confusion, hyperkinesias, ataxia, vertigo, CNS depression, hallucinations,
bradycardia, hypotension, syncope, nausea, vomiting, constipation, diarrhea, hypoventilation, apnea,
withdrawal syndrome, rash, Stevens–Johnson syndrome.
Adult: 30–120 mg/day PO, IM, or IV; reduce dosage in elderly patients Pediatric: 1–3
mg/kg IV or IM

Special considerations: Taper gradually after long-term use; give IV slowly; monitor
injection sites
In: Relief of symptoms of depression; enuresis in children older than 6 years;
off-label consideration— control of chronic pain.
Ac: Inhibits presynaptic reuptake of norepinephrine and serotonin;
anticholinergic at CNS and peripheral receptors; sedating.
Pharmacokinetics:
Rout
e Onset Peak
Oral Varies2–4 h
T1/2: 8 to 16 hours, metabolized in the liver, excretion in the urine.
Ae: sedation, anticholinergic effects, confusion, anxiety, orthostatic
hypotension, dry mouth, constipation, urinary retention, rash, bone marrow
depression.
Adult: 50–200 mg/d PO
Pediatric: 30–40 mg/d PO
In: Treatment of patients with depression who are unresponsive to other
antidepressive therapy or in whom other antidepressive therapy is
contraindicated.
Ac: Irreversibly inhibits MAO, allowing norepinephrine, serotonin, and
dopamine to accumulate in the synaptic cleft; this accumulation is thought to be
responsible for the clinical effects.
Pharmacokinetics:
RouteOnsetDuration
Oral Slow 48–96 h
T1/2: Unknown; metabolized in the liver, excreted in urine.
Ae: Dizziness, vertigo, headache, overactivity, hyperreflexia, tremors, mania,
weakness, drowsiness, fatigue, sweating, orthostatic hypotension, constipation,
diarrhea, dry mouth, edema, anorexia, potential for hypertensive crisis.
15 mg PO t.i.d.; maintenance 15 mg/day PO
In: Treatment of depression, OCDs, bulimia, PMDD, panic disorders; off-label
uses include chronic pain, alcoholism, neuropathies, obesity.
Ac: Inhibits CNS neuronal reuptake of serotonin, with little effect on
norepinephrine and little affinity for cholinergic, histaminic, or alpha-adrenergic
sites.
Pharmacokinetics:
Rout
e OnsetPeak
Oral Slow 6–8 h
T1/2: 2 to 4 weeks; metabolized in the liver, excreted in urine and feces.
Ae: Headache, nervousness, insomnia, drowsiness, anxiety, tremor, dizziness,
sweating, rash, nausea, vomiting, diarrhea, dry mouth, anorexia, sexual
dysfunction, upper respiratory infections, weight loss, fever.
20 mg/d PO in the AM; do not exceed 60 mg/d; reduce dose with hepatic impairment;
also available in a 90-mg, once-a-week formulation
In: Management of manifestations of psychotic disorders; relief of preoperative
restlessness; adjunctive treatment of tetanus; acute intermittent porphyria; severe
behavioral problems in children; control of hiccups, nausea, and vomiting.
Ac: Blocks postsynaptic dopamine receptors in the brain; depresses those parts
of the brain involved in wakefulness and emesis; anticholinergic; antihistaminic;
alpha-adrenergic blocking.
Pharmacokinetics:
Route Onset Peak Duration
Oral 30–60 min2–4 h 4–6 h
Intramuscula 10–15 min15–20 min4–6 h
r
T1/2: 2 hours, then 30 hours; metabolized in the liver, excreted in the urine.
Ae: Drowsiness, insomnia, vertigo, extrapyramidal symptoms, orthostatic
hypotension, photophobia, blurred vision, dry mouth, nausea, vomiting,
anorexia, urinary retention, photosensitivity.
Adult: 25 mg IM for acute episode, may be repeated; switch to 25–50 mg PO t.i.d.
Pediatric: 0.5–1 mg/kg q4–8h PO, IM, or PR

In: Management of severely ill patients with schizophrenia who are

unresponsive to standard drugs; reduction of risk of recurrent suicidal behavior
in patients with schizophrenia or schizoaffective disorder.
Ac: Blocks dopamine and serotonin receptors; depresses the RAS;
anticholinergic; antihistaminic; alpha-adrenergic blocking.
Pharmacokinetics:
Rout
e Onset Peak Duration
Oral Varies1–6 hWeeks
T1/2: 4–12 hours; metabolized in the liver, excreted in the urine and feces.
Ae: Drowsiness, sedation, seizures, dizziness, syncope, headache, tachycardia,
nausea, vomiting, fever, neuroleptic malignant syndrome.
Adult: initially 25 mg PO b.i.d. to t.i.d.; up to 500 mg/d; available only through the
Clozaril Patient Management System, which monitors white blood cell count and
compliance issues, only 1-wk supply given at a time

In: Treatment of manic episodes of bipolar, manic-depressive illness.

Ac: Alters sodium transport in nerve and muscle cells; inhibits the release of
norepinephrine and dopamine, but not serotonin, from stimulated neurons;
increases the intraneuronal stores of norepinephrine and dopamine slightly; and
decreases the intraneuronal content of second messengers.
Pharmacokinetics:
Route Onset Peak Duration
Oral Unknow 0.5–3 h8–12 h
n
Oral, extended releaseUnknow 4–12 h 12–18 h
 n
T1/2: 24 hours; excreted in the urine.
Ae: CNS problems, including lethargy, slurred speech, muscle weakness, and
fine tremor; polyuria, gastric toxicity, with nausea, vomiting, and diarrhea
progressing; CV collapse, coma; adverse effects are related to serum drug levels.
600 mg PO t.i.d. for acute episodes; 300 mg PO t.i.d. to q.i.d. for maintenance; reduce
dose with elderly patients

In: Narcolepsy and attention-deficit disorder.

Ac: Mild cortical stimulant with CNS actions similar to those of amphetamines.
Pharmacokinetics:
Rout
e Onset Peak Duration
Oral Varies1–3 h4–6 h
T1/2: 1–3 hours; metabolized in the liver; excreted in the urine.
Ae: Nervousness, insomnia, increased or decreased pulse rate and blood
pressure, tachycardia, loss of appetite, nausea, abdominal pain.
Adult: 10–60 mg/day PO in divided doses, depending on preparation
Pediatric: 5 mg PO b.i.d.; increase gradually, do not exceed 60 mg/d

In: Control of tonic–clonic and psychomotor seizures; prevention of seizures

during neurosurgery; control of status epilepticus.
Ac: Stabilizes neuronal membranes and prevents hyperexcitability caused by
excessive stimulation; limits the spread of seizure activity from an active focus;
has cardiac antiarrhythmic effects similar to those of lidocaine.
Pharmacokinetics:
Rout
e OnsetPeak Duration
Oral Slow 2–12 6–12 h
h
IV 1–2 h Rapid 12–24 h
T1/2: 6 to 24 hours; metabolized in the liver, excreted in the urine.
Ae: Nystagmus, ataxia, dysarthria, slurred speech, mental confusion, dizziness,
fatigue, tremor, headache, dermatitis, Stevens–Johnson syndrome, nausea,
gingival hyperplasia, liver damage, hematopoietic complications, sometimes
fatal.
Adult: 100 mg PO t.i.d., up to 300–400 mg/d; 10–15 mg/kg IV
Pediatric: 5–8 mg/kg per day PO; 5–10 mg/kg IV in divided dose

In: Long-term treatment of generalized tonic–clonic and cortical focal seizures; emergency
control of certain acute convulsive episodes (status epilepticus, tetanus, eclampsia, meningitis);
anticonvulsant treatment of generalized tonic– clonic seizures and focal seizures (parenteral).
Ac: General CNS depressant; inhibits impulse conduction in the ascending RAS; depresses the
cerebral cortex; alters cerebellar function; depresses motor output; and can produce excitation,
sedation, hypnosis, anesthesia, and deep coma.
Pharmacokinetics:
Route Onset Duration
Oral 30–60 min10–16 h
IM, SC10–30 min4–6 h
IV 5 min 4–6 h
T1/2: 79 hours; metabolized in the liver, excreted in the urine.
Ae: Somnolence, insomnia, vertigo, nightmares, lethargy, nervousness, hallucinations, insomnia,
anxiety, dizziness, bradycardia, hypotension, syncope, nausea, vomiting, constipation, diarrhea,
hypoventilation, respiratory depression, tissue necrosis at injection site, withdrawal syndrome.
Adult: 60–100 mg/d PO; 200–320 mg IM or IV for acute episodes, may be repeated in
6 h; reduce dose with elderly and with renal or hepatic impairment
Pediatric: 3–6 mg/kg per day PO; 4–6 mg/kg per day IM or IV; 15–20 mg/kg IV over
10–15 min for status epilepticus

In: Management of anxiety disorders; acute alcohol withdrawal; muscle relaxant; treatment of tetanus;
adjunct in status epilepticus and severe recurrent convulsive seizures; preoperative relief of anxiety and
tension; management of epilepsy in patients who require intermittent use to control bouts of increased
seizure activity.
Ac: Acts in the limbic system and reticular formation; potentiates the effects of GABA; has little effect on
cortical function.
Pharmacokinetics:
Rout
e Onset Peak Duration
Oral 30–60 min1–2 h 3h
IM 15–30 min30–45 min3 h
IV 1–5 min 30 min 15–60 min
Recta Rapid 1.5 h 3h
l
T1/2: 20 to 80 hours; metabolized in the liver, excreted in the urine.
Ae: Drowsiness, sedation, depression, lethargy, apathy, fatigue, disorientation, bradycardia, tachycardia,
paradoxical excitatory reactions, constipation, diarrhea, incontinence, urinary retention, drug dependence
with withdrawal syndrome.
Adult: 2–10 mg PO b.i.d. to q.i.d.; or 0.2 mg/kg PR, may repeat in 4–12 h; 2–20 mg IM
or IV
Geriatric or debilitated patients: 2–2.5 mg PO daily to b.i.d.; or 2–5 mg IM or IV
Pediatric: 1–2.5 mg PO t.i.d. to q.i.d.; or 0.3–0.5 mg/kg PR with a repeat in 4–12 h if
needed; 0.25 mg/kg IV over 3 min, may repeat in 15–30 min for up to three doses

In: Control of absence seizures.

Ac: May act in inhibitory neuronal systems; suppresses the
electroencephalographic pattern associated with absence seizures; reduces
frequency of attacks.
Pharmacokinetics:
Rout
e Peak
Oral 3–7 h
T1/2: 30 hours (children), 60 hours (adults); metabolized in the liver, excreted in
the urine and bile.
Ae: Drowsiness, ataxia, dizziness, irritability, nervousness, headache, blurred
vision, pruritus, Stevens– Johnson syndrome, nausea, vomiting, epigastric pain,
anorexia, diarrhea, and pancytopenia.
Adult and pediatric >6 yr: 500 mg/d PO
Pediatric (3–6 yr): 250 mg/d PO, increase cautiously as needed
In: Treatment of seizure disorders, including partial seizures with complex
patterns; tonic–clonic seizures; mixed seizures; trigeminal neuralgia.
Ac: Inhibits polysynaptic responses and blocks posttetanic potentiations;
mechanism of action is not understood; related to the tricyclic antidepressants.
Pharmacokinetics:
Onse
Route t Peak
Oral Slow 4–5 h
Extended release oralSlow 3–12 h
T1/2: 25 to 65 hours, then 12 to17 hours; metabolized in the liver, excreted in the
urine and feces.
Ae: Drowsiness, ataxia, dizziness, nausea, vomiting, CV complications,
hepatitis, hematological disorders, Stevens–Johnson syndrome.
Adult: 800–1200 mg/d PO in divided doses q6–8h
Pediatric (>12 yr): adult doses, do not exceed 1000 mg/d
Pediatric (6–12 yr): 20–30 mg/kg per day PO in divided doses t.i.d. to q.i.d.
Pediatric (<6 yr): 35 mg/kg per day PO

In: Treatment of parkinsonism and Parkinson disease.

Ac: Precursor of dopamine, which is deficient in parkinsonism; crosses the
blood–brain barrier, where it is converted to dopamine and acts as a replacement
neurotransmitter; effective for 2 to 5 years in relieving the symptoms of
Parkinson disease.
Pharmacokinetics:
RouteOnset Peak Duration
Oral Varies0.5–2 h5 h
T1/2: 1 to 3 hours; metabolized in the liver, excreted in the urine.
Ae: Adventitious movements, ataxia, increased hand tremor, dizziness,
numbness, weakness, agitation, anxiety, anorexia, nausea, dry mouth, dysphagia,
urinary retention, flushing, cardiac irregularities.
0.5–1 g/d PO in two divided doses; titrate up to 8 g/d; most often given in combination
with carbidopa as Sinemet: 25 mg carbidopa/100 mg levodopa PO t.i.d.
In: Adjunctive therapy for Parkinson disease; relief of symptoms of
extrapyramidal disorders (parkinsonism) that accompany phenothiazine therapy.
Ac: Acts as an anticholinergic, principally in the CNS, returning balance to the
basal ganglia and reducing the severity of rigidity, akinesia, and tremors;
peripheral anticholinergic effects help to reduce drooling and other secondary
effects of parkinsonism.
Pharmacokinetics:
Rout
e Onset Peak Duration
Oral 1 h 1–1.5 h 6–12 h
IM 15 minUnknownUnknown
T1/2: 18.4 to 24.3 hours; metabolized in the liver.
Ae: Disorientation, confusion, memory loss, nervousness, light-headedness,
dizziness, depression, blurred vision, mydriasis, dry mouth, constipation, urinary
retention, urinary hesitation, flushing, decreased sweating.
2 mg PO t.i.d. to q.i.d. to a maximum of 16 mg/d; 2 mg IM or IV, repeated in 12 h as
needed; do not give more than four doses per day
In: Alleviation of signs and symptoms of spasticity; may be of use in spinal cord
injuries or spinal cord diseases.
Ac: Gamma-aminobutyric acid (GABA) analogue; exact mechanism of action is
not understood; inhibits monosynaptic and polysynaptic spinal reflexes; CNS
depressant.
Pharmacokinetics:
Route Onset PeakDuration
Oral 1h 2 h 4–8 h
Intrathecal30–60 4 h 4–8 h
min
T1/2: 3 to 4 hours; not metabolized; excreted in the urine.
Ae: Transient drowsiness, dizziness, weakness, fatigue, constipation, headache,
insomnia, hypotension, nausea, urinary frequency.
Adult: 40–80 mg PO daily, 12–1500 mcg/d per intrathecal infusion pump
Pediatric: intrathecal infusion pump, 24–1199 mcg/day—base dose on patient response
In: Control of clinical spasticity resulting from upper motor neuron disorders; preoperatively to
prevent or attenuate the development of malignant hyperthermia in susceptible patients; IV for
management of fulminant malignant hyperthermia.
Ac: Interferes with the release of calcium from the sarcoplasmic reticulum within skeletal
muscles, preventing muscle contraction; does not interfere with neuromuscular transmission.
Pharmacokinetics:
Rout
e OnsetPeak Duration
Oral Slow 4–6 h8–10 h
IV Rapid 5 h 6–8 h
T1/2: 9 hours (oral), 4 to 8 hours (IV); excreted in the urine.
Ae: Drowsiness, dizziness, weakness, fatigue, diarrhea, hepatitis, myalgia, tachycardia, transient
blood pressure changes, rash, urinary frequency.
Adult: initially 25 mg PO; increase based on spinal cord injuries; prevention and
management of response to a maximum 400 mg/d for spasticity
Prevention of malignant hyperthermia: 4–8 mg/kg per day PO for 1–2 d before surgery,
or 2.5 mg/kg IV over 1 h, given 1 h before surgery; postcrisis, 4–8 mg/kg per day PO
for 1–3 d
Pediatric: initially 0.5 mg/kg per day PO b.i.d., titrate to a maximum 100 mg PO q.i.d.
for spasticity; for malignant hyperthermia, follow adult dose

In: Relief of moderate to severe acute or chronic pain; preoperative medication; component of
combination therapy for severe chronic pain; intraspinal to reduce intractable pain.
Ac: Acts as an agonist at specific opioid receptors in the CNS to produce analgesia, euphoria,
and sedation.
Pharmacokinetics:
Rout
e Onset Peak Duration
Oral Varies 60 min 5–7 h
PR Rapid 20–60 min5–7 h
SQ Rapid 50–90 min5–7 h
IM Rapid 30–60 min5–6 h
IV Immediate20 min 5–6 h
T1/2: 1.5 to 2 hours; metabolized in the liver, excreted in the urine and bile.
Ae: Light-headedness, dizziness, sedation, nausea, vomiting, dry mouth, constipation, ureteral
spasm, respiratory depression, apnea, circulatory depression, respiratory arrest, shock, cardiac
arrest.
Adult: 10 to 20-mg solution PO or 15- to 30-mg tablets PO q4h, or 10 mg SQ or IM
q4h, or 2–10 mg/70 kg IV over 4–5 min, or 10–20 mg PR q4h
Pediatric: 0.1–0.2 mg/kg IM or SQ q4h

In: Relief of moderate to severe pain; preanesthetic medication and a

supplement to surgical anesthesia.
Ac: An agonist at specific opioid receptors in the CNS, producing analgesia and
sedation; an agonist at sigma opioid receptors, causing dysphoria and
hallucinations; acts at mu-receptors to antagonize the analgesia and euphoria.
Pharmacokinetics:
Route Onset Peak Duration
PO, IM, 15–30 min1–3 h 3 h
SC
IV 2–3 min 15 min3 h
T1/2: 2 to 3 hours; metabolized in the liver, excreted in the urine and bile.
Ae: Light-headedness, dizziness, sedation, euphoria, nausea, vomiting,
constipation, tachycardia, palpitations, sweating, ureteral spasm, physical
dependence.
Adults and children >12 yr: 30 mg IM, SQ, or IV q3–4h as needed or 50 mg PO q3–4h
as needed; do not exceed 360 mg/d; 30 mg IM most common for labor

In: Complete or partial reversal of narcotic depression; diagnosis of suspected

opioid overdose.
Ac: Pure narcotic antagonist; reverses the effects of the opioids, including
respiratory depression, sedation, and hypotension.
Pharmacokinetics:
Route Peak Onset Duration
IV Unknown2 min 4–6 h
IM, Unknown3–5 min4–6 h
SQ
T1/2: 30 to 81 minutes; metabolized in the liver, excreted in the urine.
Ae: Acute narcotic abstinence syndrome (nausea, vomiting, sweating,
tachycardia, fall in blood pressure), hypotension, hypertension, pulmonary
edema.
Adult: for overdose, 0.4–2 mg IV, may repeat at 2- to 3-min intervals; for reversal of
opioid effects, 0.1–0.2 mg IV, may repeat at 2- to 3-min intervals
Pediatric: for overdose, 0.01 mg/kg IV, repeat as needed; for reversal of opioid effects,
0.005–0.01 mg IV at 2- to 3-min intervals

In: Prevention or abortion of vascular headaches.

Ac: Constricts cranial blood vessels, decreases pulsation of cranial arteries, and
decreases hyperperfusion of the basilar artery vascular bed; mechanism of action
is not understood.
Pharmacokinetics:
Route OnsetPeak
SublingualRapid 0.5–3 h
T1/2: 2.7 hours, then 21 hours; metabolized in the liver, excreted in the feces.
Ae: Numbness, tingling in the fingers and toes, muscle pain in the extremities,
pulselessness or weakness in the legs, precordial distress, tachycardia,
bradycardia, ergotism (nausea, vomiting, diarrhea, severe thirst, hypoperfusion,
chest pain, confusion).
One tablet sublingually at the first sign of headache, repeat at 30-min intervals for a
total of three tablets, or one inhalation at first sign of headache, repeat in 5 min to a
total of six inhalations per day

In: Treatment of acute migraine; treatment of cluster headaches (SC route).

Ac: Binds to serotonin receptors to cause vasoconstrictive effects on cranial
blood vessels.
Pharmacokinetics:
Route Onset Peak Duration
Nasal sprayVaries 5–20 minUnknown
Oral 1–1.5 2–4 h Up to 24 h
hr
SQ Rapid 1–5 h Up to 24 h
T1/2: 115 minutes; metabolized in the liver, excreted in the urine.
Ae: Dizziness, vertigo, weakness, myalgia, blood pressure alterations, tightness
or pressure in the chest, injection-site discomfort, tingling, burning sensations,
numbness.
50–100 mg PO at first sign of headache, may repeat in 2 h; by nasal spray in one nostril,
may repeat in 2 h; do not exceed 40 mg/d

In: Induction of anesthesia, maintenance of anesthesia; induction of a hypnotic

state.
Ac: Depresses the CNS to produce hypnosis and anesthesia without analgesia.
Pharmacokinetics:
Rout
e OnsetDuration
IV 1 min 20–30 min
T1/2: 3 to 8 hours; metabolized in the liver, excreted in the urine.
Ae: Emergence delirium, headache, restlessness, anxiety, cardiovascular
depression, respiratory depression, apnea, salivation, hiccups, skin rashes.

In: Sedation, anxiolysis, and amnesia before diagnostic, therapeutic, or

endoscopic procedures; induction of anesthesia; continuous sedation of
intubated patients.
Ac: Acts mainly at the limbic system and RAS; potentiates the effects of
GABA; has little effect on cortical function; exact mechanism of action is not
understood.
Pharmacokinetics:
Rout
e Onset Peak Duration
Oral 30–60 min12 h 2–6 h
IM 15 min 30 min 2–6 h
IV 3–5 min <30 min2–6 h
T1/2: 1.8 to 6.8 hours; metabolized in the liver, excreted in the urine.
Ae: Transient drowsiness, sedation, drowsiness, lethargy, apathy, fatigue,
disorientation, restlessness, constipation, diarrhea, incontinence, urinary
retention, bradycardia, tachycardia, phlebitis at IV injection site.

In: Induction and maintenance of anesthesia.

Ac: Depresses the CNS to produce anesthesia and analgesia.
Pharmacokinetics:
Rout
e Onset Duration
IV 1–2 min20 min
T1/2: minutes; not metabolized, excreted in the lungs.
Ae: Cardiovascular depression, respiratory depression, apnea, earache, sinus
pain, vomiting, malignant hyperthermia.

In: Induction and maintenance of general anesthesia.

Ac: Depresses the CNS, causing anesthesia; relaxes muscles; sensitizes the
myocardium to the effects of norepinephrine and epinephrine.
Pharmacokinetics:
Route OnsetPeak Duration
Inhale Rapid Rapi End of inhalation
d d
T1/2: Unknown; metabolized in the liver, excreted in the urine.
Ae: Transient drowsiness, sedation, lethargy, apathy, fatigue, disorientation,
restlessness, constipation, diarrhea, incontinence, urinary retention, bradycardia,
tachycardia, hypoxia, acidosis, apnea, arrhythmias, hepatic injury.

In: Infiltration anesthesia, peripheral and sympathetic nerve blocks, central

nerve blocks, spinal and caudal anesthesia, topical anesthetic for skin or mucous
membrane disorders.
Ac: Blocks the generation and conduction of action potentials in sensory nerves
by reducing sodium permeability, reducing the height and rate of rise of the
action potential, increasing the excitation threshold, and slowing the conduction
velocity.
Pharmacokinetics:
Route Onset Peak Duration
IM 5–10 min 5–15 min2 h
TopicalNot generally absorbed systemically   
T1/2: 10 minutes, then 1.5 to 3 hours; metabolized in the liver, excreted in the
urine.
Ae: Headache, backache, hypotension, urinary retention, urinary incontinence,
pruritus, seizures; when locally applied: burning, stinging, swelling, tenderness.

In: As an adjunct to general anesthesia; to induce skeletal muscle relaxation; to

reduce the intensity of muscle contractions in electroconvulsive therapy; to
facilitate the care of patients undergoing mechanical ventilation.
Ac: Occupies the muscular cholinergic receptor site, preventing ACh from
reacting with the receptor; does not cause activation of muscle cells; causes a
flaccid paralysis.
Pharmacokinetics:
Rout
e Onset Duration
IV 4–6 min120–180 min
T1/2: 89 to 161 minutes; metabolized in the tissues, excreted unchanged in the
urine.
Ae: Respiratory depression, apnea, bronchospasm, cardiac arrhythmias

In: As an adjunct to general anesthesia; to facilitate endotracheal intubation; to

induce skeletal muscle relaxation during surgery or mechanical ventilation.
Ac: Combines with ACh receptors at the motor endplate to produce
depolarization; this inhibits neuromuscular transmission, causing a flaccid
paralysis.
Pharmacokinetics:
Rout
e Onset Duration
IV 30–60 sec4–6 min
T1/2: 2 to 3 minutes; metabolized in the tissues, excreted unchanged in the urine.
Ae: Muscle pain, related to the contraction of the muscles as a first reaction;
respiratory depression, apnea.