KNOWLEDGE ENHANCEMENT PRIGRAM (KEP)

PHARMACOLOGY

DRUGS ACTING
ON THE
CENTRAL AND PERIPHERAL NERVOUS SYSTEM

ANTISEIZURE MEDICATIONS

Introduction:

Epilepsy the most prevalent of the neurological disorders is not a single disease
but a collection of different syndromes characterized by the same feature:
sudden discharge of excessive electrical energy from nerve cells located within
the brain, which leads to a seizure. The treatment of epilepsy varies widely,
depending on the exact problem and its manifestations. The drugs that are
used to manage epilepsy are called antiepileptics, or antiseizure agents, and
are sometimes referred to as anticonvulsants; however, because not all types
of epilepsy involve convulsions, this term is not generally applicable.

The drug of choice for any given situation depends on the type of epilepsy,
patient age, specific patient characteristics such as cultural variations, and
patient tolerance for associated adverse effects. Drugs can be used to treat
more than one type of seizure.

Mechanism of Action:
Anti-seizure drugs act by
• Blocking the Na+ channel
• Blocking the Ca++ channel
• Blocking the excitatory neurotransmitters and ↑ the activity of
inhibitory neurotransmitter (GABA)

Classification of anti-seizure drugs

A. Barbiturates
 Phenobarbital – all forms of epilepsy, status epilepticus, severe
recurrent seizures
B. Benzodiazepines
 clonazepam – petit mal
 lorazepate – focal seizures
 diazepam – all forms of epilepsy, status epilepticus, recurrent
seizures, tetanus
 C. Hydantoins
 phenytoin – grand mal and psychomotor seizures
D. Succinimides
 ethosuximide – petit mal seizures
E. Other Drugs
 valproic acid – petit mal seizures in adults and children
 carbamazepine – grand mal, mixed, psychomotor seizures
 topiramate – adjunctive therapy for partial-onset seizures in adults
and children
The main drugs in current use are:
Primary:
• phenytoin, carbamazepine, valproate and ethosuximide
Secondary:
• phenobarbitone: highly sedative
• clonazepam
• diazepam used in treating status epilepticus

Hydantoins
• Treatment of grand mal epilepsy and tonic-clonic seizure disorders, but
not in absence seizures
• Treatment on peripheral neuralgia - an abnormal condition characterized
by severe stabbing pain
• Antiarrhythmias
• Less sedating
• May cause gingival hyperplasia
• Enhances the rate of estrogen metabolism, which can decrease the
effectiveness of some birth control pills.
• Includes: Phenytoin (Dilantin)
• Therapeutic serum levels range from 10 to 20 mcg/ml
• Other Adverse Effects
 Ataxia
 Diplopia
 Blood dyscrasias
 Hirsutism
 Increased collagen proliferation
 Fetal malformations: fetal hydantion syndrome

Carbamazepine
• Derivative of tricyclic antidepressants
• Similar profile to that of phenytoin, but with fewer unwanted effects
• Effective in most forms of epilepsy (except absence seizures);
particularly effective in psychomotor epilepsy; also useful in trigeminal
neuralgia and mania.
Valproate
• Very effective against absence seizure
• Unwanted effects: anorexia, nausea, teratogenicity, liver damage (rare but
serious)

Ethusuximide
• The main drug used to treat absence seizures, may exacerbate other
forms
• Relatively few unwanted effects, mainly nausea and anorexia sometimes
mental disturbances

Benzodiazepines
• Diazepam: preferred drugs for status epilepticus
• Nitrazepam: petit mal, especially myoclonic seizures and infantile spasms
• Clonazepam: one of the most effective in some cases of myoclonic
seizures. Used in petit mal and status epilepticus
• Adverse effects: drowsiness, sedation, depression, disorientation, and
drug dependence
• Incoordination and drowsiness are common side effects of diazepam

Barbiturates
• phenobarbital (Luminal)
• Can produce sedation, hypnosis, anesthesia, and deep coma
• Long-term treatment of generalized tonic clonic seizures; status
epilepticus
• Adverse effects: somnolence, insomnia, vertigo, nightmares, lethargy,
nervousness, hallucinations, anxiety, and respiratory depression

Clinical Uses of Antiseizure Drugs

 Tonic-clonic (grand mal) seizures:

 carbamazepine is preferred because of low incidence of side-
effects
 phenytoin and valproate may be prescribed
 Use of single drug is preferred when possible, because of risk of
pharmacokinetic interactions
 Partial (focal) seizures: carbamazepine, valproate; clonazepam or
phenytoin are alternatives.
 Absence seizures (petit mal): ethosuximide or valproate
 Valproate is used when absence seizures coexist with tonic-clonic
seizures, since most drugs used for tonic-clonic seizures may
worsen absence seizures
 Myoclonic seizures: valproate or clonazepam
 Status epilepticus: must be treated as an emergency, with diazepam
intravenously
 ANTIPARKINSONIAN DRUGS

Parkinson’s disease may develop in people of any age, but it usually affects
those who are past middle age and entering their 60s or even later years. The
cause of the condition is not known. At this time, there is no cure for Parkinson’s
disease. Therapy is aimed at management of signs and symptoms to provide
optimal functioning for as long as possible.
Parkinson’s Disease:
• Disease of the basal ganglia & related neuronal groups +
neurotransmitter deficiencies
• “shaking palsy”
 Bradykinesia – slowing down in the initiation & execution of
movement
 Rigidity – increased muscle tone
 Tremor at rest
 Impaired postural reflexes

Drug Therapy
• Therapy is aimed at restoring the balance between the declining levels of
dopamine, which has an inhibitory effect on the neurons in the basal
ganglia, and the now-dominant cholinergic neurons, which are excitatory.
This may help to reduce the signs and symptoms of parkinsonism and
restore normal function for a time. The goal of pharmacotherapy for
Parkinson’s disease is to increase the ability of the client to perform
normal daily activities of living such as eating, walking, dressing, and
bathing.
• Correcting the imbalance of neurotransmitters within the CNS
 Dopaminergic – enhance release or supply of dopamine (DA)
 Anticholinergic – antagonize or block the effects of overactive
cholinergic neurons in the striatum
• Dopamine does not cross the blood–brain barrier. Therefore, other drugs
that act like dopamine or increase dopamine concentrations indirectly
must be used to increase dopamine levels in the substantia nigra or to
directly stimulate the dopamine receptors in that area. This action helps to
restore the balance between the inhibitory and stimulating neurons.
• Treating Parkinsonism with Dopaminergic Drugs:
 Increases dopamine levels in the corpus striatum of the brain
 Drug of choice is Levodopa, which is a precursor of dopamine
synthesis
 Levodopa is the mainstay of treatment for Parkinson’s disease. This
precursor of dopamine crosses the blood–brain barrier and is
converted into dopamine. In this way, it acts like a replacement
therapy.
  Although levodopa is almost always given in combination form with
carbidopa as a fixed-combination drug (Sinemet), other drugs
besides carbidopa may be used.
 When used with carbidopa, the enzyme dopa decarboxylase is
inhibited in the periphery, diminishing the metabolism of levodopa in
the gastrointestinal (GI) tract and in peripheral tissues, thereby
leading to higher levels crossing the blood–brain barrier. Because
the carbidopa decreases the amount of levodopa needed to reach a
therapeutic level in the brain, the dose of levodopa can be
decreased, which reduces the incidence of adverse side effects.
 Dopaminergic Drugs
1. carbidopa-levodopa (Sinemet) – mainstay in the treatment of
PD
2. amantadine (Symmetrel)
3. apomorphine (Apokyn)
4. bromocriptine (Parlodel)
5. pramipexole (Mirapex)
6. ropinirole (Requip

 Drug-Drug Interaction
 If dopaminergics are combined with monoamine oxidase inhibitors
(MAOIs), therapeutic effects increase and a risk of hypertensive
crisis exists. The MAOI should be stopped 14 days before
beginning therapy with a dopaminergic.
 Combination of levodopa with vitamin B6 or with phenytoin may
lead to decreased efficacy of the levodopa

 Client Teaching
1. Increase fiber and fluid intake to prevent constipation.
2. Avoid foods high in pyridoxine (vitamin B6) such as beef, liver, ham,
pork, egg yolks, sweet potatoes, and oatmeal because they will
decrease the effects of the medications.
3. Avoid all OTC drugs and fortified cereals because of
4. Immediately report muscle spasm, spasmodic winking, and an
increase in bradykinesia.
5. It may be several months before the full therapeutic effects is
achieved
 A second approach to changing the balance of between dopamine and
acetylcholine in the brain is to give cholinergic blockers or anticholinergics.
• Anticholinergic Drugs: decreases the activity of acetylcholine
 benztropine mesylate (Cogentin)
 trihexylhenidyl HCl (Artane)
 Other drugs to manage PD:
 Antihistamine – decreases rigidity; example: Benadryl
 Betablockers – decreases rigidity; example: Inderal
 ANESTHETIC DRUGS

Introduction:
 Anesthetics are drugs that are used to cause complete or partial loss of
sensation.
 The anesthetics can be subdivided into general and local anesthetics,
depending on their site of action.
 General anesthetics are central nervous system (CNS) depressants used
to produce loss of pain sensation and consciousness.
 Local anesthetics are drugs used to cause loss of pain sensation and
feeling in a designated area of the body without the systemic effects
associated with severe CNS depression.
 In addition, general anesthesia also blocks the body reflexes. Blockage of
autonomic reflexes prevents involuntary reflex response to body injury that
might compromise a patient’s cardiac, respiratory, gastrointestinal (GI),
and immune status. Blockage of muscle reflexes prevents jerking
movements that might interfere with the success of the surgical procedure.
 Anesthesia: the state of depressed CNS activity
 Two types:
 General anesthesia involves the administration of a combination of
several different general anesthetic agents to achieve the following
goals: analgesia, or loss of pain, perception; unconsciousness, or
loss of awareness of one’s surroundings; and amnesia, or inability
to recall what took place.
 Local anesthesia

GENERAL ANESTHESIA

Widespread CNS depression, which is not without risks, occurs with general
anesthesia. In addition, all other body systems are affected. Because of the wide
systemic effects, patients must be evaluated for factors that may increase their
risk. These factors include the CNS, cardiovascular, respiratory factors , and
renal and hepatic functions.
1. CNS - Underlying neurological disease (e.g., epilepsy, stroke, myasthenia
gravis) that presents a risk for abnormal reaction to the CNS-depressing
and muscle-relaxing effects of these drugs.
 2. Cardiovascular - Underlying vascular disease, coronary artery disease, or
hypotension, which put patients at risk for severe reactions to anesthesia,
such as hypotension and shock, dysrhythmias, and ischemia.
3. Respiratory - Obstructive pulmonary disease (e.g., asthma, chronic
obstructive pulmonary disease, bronchitis), which can complicate the
delivery of gas anesthetics, as well as the intubation and mechanical
ventilation that must be used in most cases of general anesthesia.
4. Renal and hepatic - Conditions that interfere with the metabolism and
excretion of anesthetics (e.g., acute renal failure, hepatitis) and could
result in prolonged anesthesia and the need for continued support during
recovery. Toxic reactions to the accumulation of abnormally high levels of
anesthetic agents may even occur.
 With the wide variety of drugs available, the therapeutic effects required need
to be balanced with the potential for adverse effects. This is accomplished by
balanced anesthesia—the combining of several drugs, each with a specific
effect, to achieve analgesia, muscle relaxation, unconsciousness, and
amnesia rather than using one drug.
 The practice of using smaller doses of many different kinds of medication
rather than higher doses of fewer medicines.
 Many of these drugs are given before the general anesthetic is administered to
facilitate the process.

 Balanced anesthesia involves the following agents:

 Preoperative medications, which may include the use of anticholinergics
that decrease secretions to facilitate intubation and prevent bradycardia
associated with neural depression.
 Sedative–hypnotics to relax the patient, facilitate amnesia, and decrease
sympathetic stimulation
 Antiemetics to decrease the nausea and vomiting associated with the
slowing of GI activity.
 Antihistamines to decrease the chance of allergic reaction and help to dry
up secretions.
 Narcotics to aid analgesia and sedation

 Stages of General Anesthesia

 Stage 1, the analgesia stage, refers to the loss of pain sensation, with the
patient still conscious and able to communicate.
 Stage 2, the excitement stage, is a period of excitement and often
combative behavior, with many signs of sympathetic stimulation (e.g.,
tachycardia, increased respirations, blood pressure changes).
  Stage 3, surgical anesthesia, involves relaxation of skeletal muscles,
return of regular respirations, and progressive loss of eye reflexes and
pupil dilation. Surgery can be safely performed in stage 3.
 Stage 4, medullary paralysis, is very deep CNS depression with loss of
respiratory and vasomotor center stimuli, in which death can occur rapidly.
If a patient reaches this level, the anesthesia has become too intense and
the situation is critical.

 The three phases in general anesthesias are the following:

1. Induction is the period from the beginning of anesthesia until stage 3, or
surgical anesthesia, is reached. The danger period for many patients
during induction is stage 2 because of the systemic stimulation that
occurs. Often a rapid-acting anesthetic is used to move quickly through
this phase and into stage 3. NMJ blockers may be used during induction
to facilitate intubation, which is necessary to support the patient with
mechanical ventilation during anesthesia
2. Maintenance is the period from stage 3 until the surgical procedure is
complete. A slower, more predictable anesthetic, such as a gas
anesthetic, may be used to maintain the anesthesia once the patient is in
stage 3.
3. Recovery is the period from discontinuation of the anesthetic until the
patient has regained consciousness, movement, and the ability to
communicate. During recovery, the patient requires continuous monitoring
for any adverse effects of the drugs used, and ensure support of the
patient’s vital functions as necessary.

General Anesthetic Agents

Agents that depress the central nervous system (CNS) by
 Depression of consciousness
 Loss of responsiveness to sensory stimulation (including pain)
 Muscle relaxation
 Signs of GA: total analgesia, loss of consciousness, memory, and body
movement, which is similar to sleep but are not exactly the same
 Goals of General Anesthesia
1. Analgesia or loss of pain perception
2. Unconsciousness, or loss of awareness of one’s surroundings
3. Amnesia or inability to recall what took place

Pre-anesthetic Medications
1. Benzodiazepines to relieve anxiety
 2. Barbiturates for sedation
3. Antihistamines to prevent allergic reactions
4. Antiemetics to prevent aspiration of stomach contents and postsurgical
nausea and vomiting
5. Opioids to provide analgesia
6. Anticholinergic to prevent bradycardia and secretion of fluids into the
respiratory tract
7. Muscle relaxants for facilitation of intubation and relaxation

Classification of General Anesthetic Drugs

Barbiturate Anesthetics
• Intravenous drugs used to induce rapid anesthesia, which is then
maintained with an inhaled drug
• Include:
 methohexital(Brevital)
 thiopental (Pentothal)
 Thiopental is probably the most widely used of the intravenous
anesthetics. Because it has no analgesic properties, the patient may need
additional analgesics after surgery.
 • Thiopental has a very rapid onset of action, usually within 10 to 30
seconds, and an ultrashort recovery period of 5 to 8 minutes.
• Methohexital has a rapid onset of action and a recovery period that is
usually 3 to 4 minutes.
• Adverse effects: related to the suppression of the CNS with decreased
pulse, hypotension, suppressed respirations, and decreased GI activity.
Nausea and vomiting after recovery are common.

Non-Barbiturate Anesthetics
Other parenteral drugs used for intravenous administration in anesthesia:
• droperidol (Inapsine)
• etomidate (Amidate)
• fospropofol (Lusedra)
• ketamine (Ketalar)
• midazolam (Generic Brand)
• propofol (Diprivan)

Adverse Effects
• midazolam should be monitored for respiratory depression and CNS
suppression
• droperidol during recovery period may cause hypotension, chills,
hallucinations, and drowsiness. It may also cause QT prolongation, which
puts the patient at risk for serious cardiac arrhythmias.
• etomidate many patients during the recovery, experience myoclonic and
tonic movements, as well as nausea and vomiting.
• ketamine crosses the blood–brain barrier and can cause hallucinations,
dreams, and psychotic episodes
• propofol often causes local burning on injection. It can cause bradycardia,
hypotension, and, in extreme cases, pulmonary edema
• fospropofol is associated with a sensation of perianal burning, stinging,
tingling, and rash.

There are two primary methods in inducing general anesthesia:

1. IV agents are usually administered first because they act within a few
seconds.
• After the client loses consciousness, inhaled agents are used to
maintain the anesthesia.
2. Inhaled gas

Anesthetic Gases
A. Nitrous oxide (blue cylinder)
• Very potent analgesic
• Depresses the CNS to produce anesthesia and analgesia
• Does not cause muscle relaxation
 • Rapid onset of action within 1-2 minutes and rapid recovery usually
within 20 minutes
• Nitrous oxide is usually combined with other agents for anesthetic use.
• Adverse effects: cardiovascular and respiratory depression, apnea,
earache, sinus pain, vomiting, and malignant hyperthermia
 Malignant hyperthermia
 Occurs during or after general anesthesia
 Sudden elevation in body temperature (>104° F)
 Life-threatening emergency

• Standard Names and Identifying Container Colors for Medical Gases

(taken from the Federal Food & Cosmetic Act Section 21b dated April 10,
2006)

Different types of medical gas used in the hospital aside from nitrous oxide:
 Oxygen - a medical gas required in every healthcare setting, and is used
for resuscitation and inhalation therapy.
 Medical Air- used during anesthesia as a substitute for nitrous oxide to
reduce the high concentration of oxygen exposure. It is also used in ICU
and NICU areas.
 Medical CO2 – used as an insufflation gas for minimal invasive surgery
(laparoscopy, endoscopy, and arthroscopy) to enlarge and stabilize body
cavities to provide better visibility of the surgical area.
 Medical Helium – as an adjunct therapy in a number of respiratory
ailments such as asthma, COPD
 Nitrogen (Medical Liquid Nitrogen) - a medical gas used for
cryosurgery removal of some cancers and skin lesions
 B. Volatile Liquids
 Inhaled anesthetics also can be volatile liquids
 Volatile anesthetics are liquid at room temperature but are converted
into a vapor and inhaled to produce their anesthetic effects.
 Inhaled volatile liquids:
 halothane (Fluothane)
 Desflurane (Suprane)
 enflurane (Ethrane)
 isoflurane (Forane)
 sevoflurane (Sevorane)
 methoxyflurane (Penthrane)

• Halothane is the prototype of the volatile liquids. It is usually used

for maintenance of anesthesia and can be effective as an induction
agent. Desflurane is widely used in outpatient surgery because of
its rapid onset and quick recovery time. Isoflurane is widely used to
maintain anesthesia after inductions. It can cause muscle
relaxation. Sevoflurane is used in outpatient surgery as an
induction agent and is rapidly cleared for quick

Intravenous Anesthetics
Uses:
1. To induce or maintain general anesthesia
2. To induce amnesia
3. As an adjunct to inhalation-type anesthetics
• When IV anesthetics are administered alone, they are generally reserved for
medical procedures that take less than 15 minutes.
• Intravenous Anesthetic Drugs:
 Barbiturates
 Benzodiazepines
 Etomidate
 Ketamine
 Opiods
 Propofol

• Concurrent administration of intravenous and inhaled anesthetics allows the

dose of the inhaled agent to be reduced, thus lowering the potential for serious
side effects. Furthermore, when intravenous and inhaled anesthetics are
combined, they provide greater analgesia and muscle relaxation than could be
provided by the inhaled anesthetic alone.
Adjunctive Agents
1. Sedative-hypnotics
• Barbiturates (secobarbital, thiopental)
• Benzodiazepines (diazepam, midazolam)
2. Opioids (narcotics)
• morphine, fentanyl, sufentanil
3. Neuromuscular blocking agents (NMBAs)
• Depolarizing agents (succinylcholine)
• Nondepolarizing agents (pancuronium, d-Tubocurarine,
vecuronium)
4. Anticholinergics
• atropine, glycopyrrolate, scopolamine

Nursing Implementation
1. Keep in mind that the drug must be administered by trained personnel
(usually an anesthesiologist) because of the potential risks associated with
its use.
2. Have emergency equipment to maintain airway and provide mechanical
ventilation readily available when patient is not able to maintain respiration
because of CNS depression.
3. Monitor temperature for prompt detection and treatment of malignant
hyperthermia. Maintain dantrolene on standby.
4. Monitor PR, RR, BP, ECG, and cardiac output continually during
administration to assess systemic response to CNS depression and
provide appropriate support as needed.
5. Monitor temperature and reflexes
6. Institute safety precautions, such as side rails
7. Provide comfort measures to help the patient tolerate drug effects.
8. Provide preoperative patient teaching, that most patients who receive the
drug will be unconscious or will be receiving teaching about a particular
procedure.

LOCAL ANESTHETIC DRUGS

Local anesthesia refers to a loss of sensation in limited areas of the body. Local
anesthesia can be achieved by several different methods: topical administration,
infiltration, field block, nerve block, and intravenous regional anesthesia.
 Local anesthetic agents are used primarily to prevent the patient from
feeling pain for varying periods of time after the agents have been
administered in the peripheral nervous system.
  The local anesthetics are very powerful nerve blockers, and it is very
important that their effects be limited to a particular area of the body. They
should not be absorbed systemically. Systemic absorption could produce
toxic effects on the nervous system and the heart like severe CNS
depression and cardiac arrhythmias.
 In increasing concentrations, local anesthetics can also cause loss of the
following:
 sensations (in this sequence): temperature, touch, proprioception
(position sense), and skeletal muscle tone
 If these other aspects of nerve function are progressively lost,
recovery occurs in the reverse order of the loss

Types of Local Anesthetics

A. Infiltration – involves injecting the anesthetic directly into the tissues to be
treated (e.g., sutured, drilled, cut).
 Brings the anesthetic into contact with the nerve endings in the area
and prevents them from transmitting nerve impulses to the brain
 May be given intradermally, subcutaneously, or submucosally
across the path of nerves supplying the target area
 For minor surgical and dental procedures
 May be given in a circular pattern around the operative area
B. Field block – involves injecting the anesthetic all around the area that will
be affected by the procedure or surgery. This is more intense than
infiltration anesthesia because the anesthetic agent comes in contact with
all of the nerve endings surrounding the area. This type of block is often
used for tooth extractions.
C. Nerve block – involves injecting the anesthetic at some point along the
nerve or nerves that run to and from the region in which the loss of pain
sensation or muscle paralysis is desired.
 Used for surgical, dental, and diagnostic procedures
 Also used for therapeutic management of pain
 Types of Nerve Block
1. Peripheral nerve block:
 Blockage of the sensory and motor aspects of a
particular nerve for relief of pain or for diagnostic
purposes.
 Include sciatic nerve blocks, femoral nerve blocks,
paravertabral blocks, and brachial plexus blocks
2. Central nerve block: injection of anesthetic into the roots of
the nerves in the spinal cord.
 3. Epidural anesthesia: injection of the drug into the epidural
space where the nerves emerge from the spinal cord.
a. Most commonly used in obstetrics during labor and
delivery
4. Caudal block: injection of anesthetic into the sacral canal,
below the epidural area
5. Spinal anesthesia: injection of anesthetic into the spinal
subarachnoid space or cerebral spinal fluid. Drug affects
large, regional area such as lower abdomen and legs

 Local Anesthetics are classified as esters or amides:

1. Esters:
 procaine (Novocain)
 benzocaine (Dermoplast)
 tetracaine ( Pontocaine)
2. Amides
 bupivacaine (Marcaine)
 lidocaine (Xylocaine)
 mepivacaine (Carbocaine)
 ropivacaine (Naropin)

Drug Effects
• First, autonomic activity is lost
• Then pain and other sensory functions are lost
• Motor activity is the last to be lost
• As local agents wear off, they do so in reverse order (motor, sensory, then
autonomic activity are restored)

Side/Adverse Effects
• Usually limited
• Adverse effects result if:
 Inadvertent intravascular injection occurs
 Excessive dose or rate of injection is given
 Slow metabolic breakdown
 Injection into a highly vascular tissue

Nursing Implementation
1. Have emergency equipment readily available to maintain airway and
provide mechanical ventilation if needed.
2. Ensure that drugs for managing hypotension, cardiac arrest, and central
nervous system (CNS) alterations are readily available in case of severe
reaction and toxicity.
3. Ensure that patients receiving spinal anesthesia or epidural anesthesia
are well hydrated and remain lying down for up to 12 hours after the
anesthesia to minimize headache
4. Establish safety precautions to prevent injury during the time that the
patient has a loss of sensation and/or mobility
5. Provide meticulous skin care to the site of administration to reduce the risk
of breakdown.

NON-ANESTHETIC DRUGS AS ADJUNCTS TO SURGERY

NEUROMUSCULAR BLOCKING AGENTS

Neuromuscular Blocking Agents

• Primary adjuncts during surgery so the surgical procedure can be carried
out safely
• Necessary to administer drugs that cause skeletal muscles to totally relax
• Prevent nerve transmission in certain muscles, resulting in paralysis of the
muscle
• Used with anesthetics during surgery
• When used during surgery, artificial mechanical ventilation is required
• Paralyze respiratory and skeletal muscles so patient cannot breathe on
their own
• Do not cause sedation or relief of pain
• Patient may be paralyzed yet conscious

• Classification:
1. Depolarizing:
 Short acting: Succinlycholine
2. Nondepolorizing:
 Short Acting: Gantacurium, Mivacurium
 Intemediate acting: Atracurium, Cisatracurium,
Vecoronium, Rocuronium
 Long acting: Pancuronium, Pipecuronium, Doxacurium

 Sequence of Paralysis

Fingers, orbits (small muscles) Limbs Trunk Neck

in Diaphragm

Recovery in reverse
A. Depolarizing Agent: Succinylcholine
• Due to the depolarization, causes stimulation of the muscle and
muscle contraction (seen as twitching) and then flaccid paralysis.
• Both effects cause muscles to stop responding to stimuli, and
paralysis occurs
• Serious Side Effects
1. Abnormal or irregular heartbeat (cardiac arrhythmias)
2. Breakdown of muscle tissues (rhabdomyolysis)
3. Cardiac arrest
4. Excessive salivation
5. Fast or slow heart rate
6. Increase potassium
7. High blood pressure
8. Life threatening increase in temperature (malignant
hyperthermia)
9. Muscle twitching
10. Post operative pain
11. Prolonged slow breathing

Nondepolarizing Agents
• First sensation felt is weakness
• Followed by total flaccid paralysis
• Small, rapidly moving muscles are affected first (fingers, eyes), then limbs,
neck, trunk
• Finally, intercostal muscles and the diaphragm are affected, resulting in
cessation of respirations
• Recovery of muscles usually occurs in reverse order
• Therapeutic Action and Indications:
1. Serve as an adjunct to general anesthetics during surgery when
reflex muscle movement could interfere with the surgical procedure
or the delivery of gas anesthesia.
2. Facilitate mechanical intubation by preventing resistance to passing
of the endotracheal tube and in situations in which patients “fight” or
resist the respirator.
3. Facilitate various endoscopic diagnostic procedures when reflex
muscle reaction could interfere with the procedure.
4. Facilitate electroconvulsive therapy when intense skeletal muscle
contractions as a result of electric shock could cause the patient
broken bones or other injury.

• Adverse Effects
 Prolonged and profound paralysis
 Depressed respiration, bronchospasm, and apnea
  Hypotension and cardiac arrhythmias
 Constipation, vomiting, and regurgitation
 Hyperkalemia

• Nursing Implementation
1. Always assess past history of surgeries and response to anesthesia
as well as allergies and use of other medications
2. Assess use of alcohol, illicit drugs, opioids
3. Assessment is vital during pre-, intra-, and postoperative phases
 Vital signs, baseline laboratory tests, ECG, pulse oximeter
(PO2), ABCs (airway, breathing, circulation)
 Monitor all body systems
4. Close and frequent observation of the patient and all body systems
5. During a procedure, monitor vital signs, ABCs
6. Watch for sudden elevations in body temperature, which may
indicate malignant hyperthermia; have the drug dantrolene readily
available for treatment of malignant hyperthermia if it should occur.
7. During recovery, monitor for cardiovascular and respiratory
depression, which are complications of anesthesia
8. Implement safety measures during recovery, especially if
motor/sensory loss occurs due to local anesthesia
9. Reorient patient to surroundings
10. Provide preoperative teaching about the surgical procedure and
anesthesia
11. Teach the patient about postoperative turning, coughing, deep
breathing
12. If an NMBA is to be used for a procedure when the patient is to be
awake, teach the patient that he/she may be paralyzed but still able
to hear and feel
13. Arrange for a small dose of a nondepolarizing neuromuscular
junction (NMJ) blocker before the use of succinylcholine to reduce
the adverse effects associated with muscle contraction.
14. Ensure that a cholinesterase inhibitor is readily available to
overcome excessive neuromuscular blockade caused by
nondepolarizing NMJ blockers.
15. Have a peripheral nerve stimulator on standby to assess the degree
of neuromuscular blockade, if appropriate.
16. Test patient response and recovery periodically if the drug is being
given over a long period to maintain mechanical ventilation.
Discontinue the drug if response does not occur or is greatly
delayed.
 DRUGS FOR CONTROL OF PAIN

Pain
• Pain, by definition, is a sensory and emotional experience associated with
actual or potential tissue damage. The perception of pain is part of the
clinical presentation in many disorders and is one of the hardest
sensations for patients to cope with during the course of a disease or
dysfunction.
• Universal, complex, subjective experience
• Generally is related to some type of tissue damage and serves as a
warning signal
• A psychological and emotional experience characterized by unpleasant
feelings associated with trauma or disease
• Number one reason people take medication

• Two Types of Pain

1. Acute pain occurs in response to recent tissue damage or injury
2. Chronic pain is constant or intermittent pain that keeps occurring
long past the time the injured area would be expected to heal

• Sources of Pain
1. Nociceptive—free nerve endings that receive painful stimuli.
Characterized by well localized, dull, aching, or throbbing. Example:
laceration, fracture, cellulitis, arthritis
Two kinds:
a. Visceral pain
b. Somatic pain
2. Neuropathic –are damaged nerves characterized by stabbing or
shooting pain superimposed over a background of aching and
burning.
Example: poststroke pain, trigeminal neuralgia

The three main principles of the WHO analgesic ladder are: “By the clock,
by the mouth, by the ladder”.

By the clock:
To maintain freedom from pain, drugs should be given “by the clock” or “around
the clock” rather than only “on demand” (i.e. PRN). This means they are given on
a regularly scheduled basis. The frequency will depend on whether it is a
long- or short-acting preparation.
By the mouth:
The oral route is usually the preferred route for ease of use in a variety of care
settings. However, it may not be possible for all patients (e.g. end-of-life,
unconscious, swallowing issues). When the oral route is not feasible, the least
invasive route should be considered (e.g. sublingual or subcutaneous before
intravenous.). The intramuscular route should never be used.

By the ladder (refer to picture on the next page)

If pain occurs there should be prompt administration of drugs in the following
order:
• non-opiods (e. g. acetaminophen)
• as necessary, mild opioids (e. g. codeine)
• then strong opiods (e. g. morphine or hydromorphone) until the patient is free of
pain.
 • Narcotic is a general term used to describe morphine like drugs that
produce analgesia and CNS depression
• Opioids exert their action with at least four types of receptors: mu (μ),
kappa (κ), sigma (σ), and beta (β)
• From the perspective of pain management, the mu and kappa receptors
are the most important
• Opioids are classified as
1. agonist,
2. partial agonist
3. agonist-antagonist
• Agonist means “to do”
• Antagonist means “to block”

A. Narcotic Analgesic
• Relieves moderate to severe pain by inhibiting the release of
Substance P in central and peripheral nerves
• Reduces the perception of pain, sensation in brain, thereby producing
sedation and decreasing emotional upsets associated with pain
• Can be given orally, IM, subcutaneous, IV or even transdermally
• Bind to opioid receptors in brain and spinal cord and even in periphery
• Orally are metabolized by liver, excreted by kidney
• morphine and meperidine produce metabolites
• Widespread effects: CNS, Respiratory, and GI
• Indications for Use:
1. Before and during surgery
2. Before and during invasive diagnostic procedures
3. During labor and delivery
4. Treatment of acute pulmonary edema
5. Treating severe, nonproductive cough
6. Relief of acute and chronic pain

• Effects of Narcotic Analgesics

1. Euphoria
2. Nausea and vomiting
3. Respiratory depression
 4. Urinary retention
5. Diaphoresis and flushing
6. Pupil constriction (miosis)
7. Constipation

• Contraindications and Cautions

1. Respiratory depression
2. Chronic lung disease
3. Chronic liver or kidney disease
4. Benign Prostatic Hyperplasia ( BPH)
5. Increased intracranial pressure
6. Hypersensitivity reactions

• Management Considerations
1. Age-specific considerations
 Elderly patients are more susceptible to the CNS and
constipation side effects of opioids
2. Morphine is often the drug of choice
3. Other non-ceiling drugs include hydromorphone, levorphanol
and methadone
4. Use non-narcotic when able
5. Combinations may work by different mechanisms thus greater
efficacy (e.g. Tylenol w/codeine)

• Route Selections
1. Oral is preferred
2. IV most rapid = patient controlled analgesia (PCA) allows self
administration. More effective, requires less dosing
3. Epidural
4. Intrathecal - administration for drugs via an injection into the
spinal canal
5. Local injection
6. Can use rectal suppositories or transdermal routes

• Dosages of narcotic analgesics should be reduced for clients receiving

other CNS depressants such as other sedative-type drugs,
antihistamines or sedating antianxiety medications
• Narcotics are given before turning, coughing and deep breathing in
post-surgical patients
• Stop administering after 72h
• In acute pain, narcotic analgesics are most effective when given
parenterally and at start of pain
• Classifications of Narcotic Analgesics
1. Strong Agonists
2. Moderate Agonists
3. Agonist/Antagonists
 4. Antagonists

A. Strong Agonists
1. alfentanil (Alfenta) —short duration
2. fentanyl (Sublimaze or Duragesic) —short duration
3. hydromorphone (Dilaudid )
4. meperidine (Demerol) —preferred in urinary and biliary colic, less
respiratory depression in newborns
5. morphine
6. heroin
7. oxycontin
8. tramadol
9. methadone
Dependence is most likely to occur when high doses are taken for
extended period of time.

 Indications:
1. Antitussives
2. Adjuncts to general anesthesia to produce rapid analgesia, sedation,
and respiratory depression
3. Relief of acute and chronic pain,
4. Preoperative medication

B. Moderate Agonists
1. Codeine
 Much less potent analgesic than morphine but has a higher oral
effectiveness
 Good antitussive activity that do not cause analgesia
2. Propoxyphene
 Weaker analgesic than codeine

Nursing Interventions
1. Opioids may be administered PO, SC, IM, IV
2. Monitor liver function tests since opioids are metabolized in the liver
3. Monitor vital signs especially depth and rate of respirations
4. Withhold the drug if the client’s respiratory rate is below 10
5. Monitor neurological status
6. If ordered PRN, administer on client request or when nursing
observations indicate client expressions of pain
7. Monitor renal status and urine output
8. Monitor for side effects such as restlessness, dizziness, anxiety,
depressions, hallucinations, nausea and vomiting
9. Monitor for constipation
 10. Ensure client safety

C. Agonists/Antagonists
• Drugs that stimulate one receptor but block another
• Lower abuse potential than pure agonists
 buprenorphine (Buprenex)
 nalbuphine (Nubain)
 pentazocine (Talwin)
 butorphanol (Stadol)

D. Antagonists
• Bind to opiate receptors and prevent a response
• Used for reversal of opioid-induced respiratory depression
 naloxone (Narcan)
 nalmefene (Revex) —longer duration of action than Narcan
 naltrexone (ReVia)

 Nursing Considerations
1. Assess the client’s respiratory status and administer the opioid
antagonist if respirations are below 10 breaths/minute
2. Resuscitating equipment should be readily available
3. Assess for the presence or history of cardiovascular disease
4. After administration of opioid antagonists, check vital signs every 3
to 5 minutes
5. Check for withdrawal symptoms like increased thirst, chills, fever,
joint/muscle pain, CNS stimulation, drowsiness, dizziness,
confusion, seizures, headache, nausea, vomiting, diarrhea, rash,
rapid pulse and respirations.

Opiates Withdrawal Symptoms:

A. Stage 1: up to 8 Hours
 Anxiety
 Drug craving

B. Stage 2: 8 – 24 hours
 Anxiety
 Insomnia
 GI disturbance
 Rhinorrhea
 Mydriasis
 Diaphoresis
C. Stage 3: up to 3 days
 Tachycardia
 Nausea
 Vomiting
  Hypertension
 Diarrhea
 Chills
 Fever
 Tremors
 Seizure
 Muscle spasm

Management of Withdrawal Symptoms

• Methadone
• Clonidine (norepinephrine)
• Gradually decrease dosing so not to cause withdrawal of the signs and
symptoms

NON-NARCOTIC ANALGESICS
Analgesic, Antipyretic and
Anti-inflammatory Drugs

The inflammatory response is designed to protect the body from injury and
pathogens. It employs a variety of potent chemical mediators to produce the
reaction that helps to destroy pathogens and promote healing. As the body
reacts to these chemicals, it produces signs and symptoms of disease, such as
swelling, fever, ache, and pains. Occasionally, the inflammatory response
becomes a chronic condition and can result in damage to the body, leading to
increased inflammatory reactions. Anti-inflammatory agents generally block or
alter the chemical reactions associated with the inflammatory response to stop
one or more of the signs and symptoms of inflammation.

A. Non-Steroidal Anti-inflammatory Drugs

(NSAIDs)
Mechanism of action: Inactivate cyclooxygenase, the enzyme required for the
production of prostaglandins.
Prostaglandins are important in:
1. protection of kidneys and stomach
2. regulate vascular tone and platelets in CV system

Cyclooxygenase 1 and 2
• COX 1 is present in all tissues especially GI, kidneys, endothelial cells and
in platelets
• COX 2 are found in brain, bone, kidneys, GI tract, and the female
reproductive system
• Overall, prostaglandins produced by COX 2 are associated with pain and
inflammation
• Action of the COX’s
 Act on hypothalamus to decrease response to pyrogens and reset
the thermostat
 Prevent prostaglandins from increasing the pain and edema
produced by other substances released by damaged cells
 COX 1 has an antiplatelet activity for 7-10 days plus interfere with
blood coagulation and increase risk for bleeding
• Indications for Use
 Treat mild to moderate pain or inflammation
 Musculoskeletal disorders; dysmenorrhea, minor trauma and
surgery
 Celebrex is indicated for familial polyposis

Types of Non-steroidal Anti-inflammatory Drugs (NSAIDs)

1. Propionic acid derivatives such as ibuprofen, ketoprofen, naproxen and
fenoprofen
2. Acetic acid derivatives include indomethacin (Indocin), sulindac (Clinoril)
and tolmetin (Tolectin)
 Acetic acid derivatives have more severe adverse reactions than
the propionic acid derivatives
 ketorolac (Toradol) is used only for pain
 The only NSAID that can be given by injection
 Use is limited to 5 days since it can cause bleeding
 Not used in labor and delivery or during any major surgery

3. Oxicam Derivative
 include meloxicam (Mobic) and piroxicam (Feldene)
4. Cyclooxygenase-2 Inhibitor
 celecoxib (Celebrex)
5. Fenamates Derivative
 mefenamic acid (Ponstan, Dolfenal)

Contraindications
• OTC preparations contraindicated in alcoholics due to possible liver
damage
• Peptic ulcer disease
• GI or bleeding disorders
 • Hypersensitivity reactions
• Impaired renal function
• Celebrex if allergic to sulfonamides

Effects of NSAIDs on Other Drugs

• Decrease effects of ACE inhibitor, beta blockers and diuretics
• Affect sodium and water retention
• Inhibit renal prostaglandin synthesis

B. Salicylates
• Anti-inflammatory agents that has the ability to block the inflammatory
response, but also antipyretic (fever-blocking) and analgesic (pain-
blocking) properties.
• Inhibit the synthesis of prostaglandin, an important mediator of the
inflammatory reaction
• At low levels, affects platelet aggregation by inhibiting the synthesis of
thromboxane A2, a potent vasoconstrictor that normally increases platelet
aggregation and blood clot formation.
• At higher levels, aspirin inhibits the synthesis of prostacyclin, a vasodilator
that inhibits platelet aggregation

acetylsalicylci Acid (Aspirin)

• Home remedy for headaches, colds, influenza and other respiratory
infections
• For fever
• For inflammation
• Can combine ASA and COX 2 since COX 2 have little effect on
platelet function
• Poisoning can occur with large doses
• Measure serum levels if an overdose occurs
• S/s of poisoning: nausea, vomiting, fever, fluid and electrolyte
deficiencies, tinnitus, decreased hearing, hyperventilation,
confusion, visual changes, delirium, stupor and coma.
• Contraindications
 Allergies to acetylsalicylic acid (ASA)
 ASA contraindicated in children with acute active viral infection
since it can cause Reye’s syndrome
 Seen in children under 15 years old
 Results in encephalopathy, fatty infiltration of the liver,
pancreas, kidneys, spleen, and lymph nodes
 Cause is unknown
Salicylism or Salicylate Toxicity
 Acute overdose:
 Early symptoms include nausea, vomiting, tinnitus, difficulty in
hearing, hyperventilation
 Late symptoms include hyperactivity, fever, confusion, seizures
hyperpnea, tachypnea, hemorrhage, excitement, confusion,
pulmonary edema, convulsions, tetany, metabolic acidosis, coma,
and cardiovascular (CV), renal, and respiratory
 Emergency Procedures:
• Gastric lavage
• Activated charcoal
• IV bicarbonate for more rapid excretion
• hemodialysis
Nursing Considerations
1. Monitor temperature to evaluate the drug’s effectiveness in lowering
temperature.
2. Evaluate central nervous system (CNS) status like orientation,
reflexes, eighth cranial nerve function, and affect to assess CNS
effects of the drug.
3. Monitor pulse, blood pressure, and perfusion to assess for bleeding
effects or cardiovascular effects of the drug.
4. Evaluate respirations and adventitious sounds to detect
hypersensitivity reactions.
5. Perform a liver evaluation and monitor bowel sounds to detect
hypersensitivity reactions, bleeding, and gastrointestinal (GI) effects
of the drug.
6. Monitor laboratory tests such as CBC, liver and renal function tests,
urinalysis, stool guaiac, and clotting times to detect bleeding or
other adverse effects of the drug and changes in function that could
interfere with drug metabolism and excretion.

acetaminophen (Parcetamol)
• Equal in effectiveness to ASA in analgesic and antipyretic effects
• Lacks anti-inflammatory actions
• Ethanol induces drug-metabolizing enzymes in liver. Resulting rapid
metabolism of acetaminophen, which produces enough toxic
metabolite to exceed glutathione
• Glutathione is needed to inactivate toxic metabolites)
• Acetamenophen toxicity
 Occurs with 20g or more
 Creates toxic metabolite that is inactivated by glutathione
 Toxic metabolite damages liver cells
 Taking of acetaminophen should not exceed 4g/day
 Treatment of Acetaminophen Poisoning
1. gastric lavage
2. charcoal
3. antidote is acetylcysteine (Mucomyst)