This document provides information on opioid analgesics and their use for pain management. It discusses the differences between acute and chronic pain and lists various causes of pain. It then describes different mechanisms for controlling pain, including both non-opioid and opioid options. The rest of the document focuses on opioid analgesics, outlining specific opioid medications, how they work in the body, their indications, contraindications, adverse effects, and considerations for nursing care when administering opioids.

1. Drugs Affecting the
Nervous System

2. 2
REVIEW Let us test your recall. Try and answer the following.
__ __ __ __ __ __ = Basic building block of the nervous system.
__ __ __ __ __ __ __ __ __ = Thin, bushy-like structures that receive information from outside the
neuron.
__ __ __ __ = It transmits signal from the cell to a terminal.
__ __ __ __ __ __ __ = it is the space between neurons.
__ __ __ __ __ __ __ __ __ __ __ __ __ __ __ __ __ = It contributes to the regulation of attention,
arousal and memory.
How well did your brain retained the information you read in the
Bluebook? Were you able to guess the words being described by the
aforementioned statements?
NEURON
DENDRITES
NEUROTRANSMITTERS
SYNAPSE
AXON

3. Opioid Analgesics and
Pain Management

4. PAIN ACUTE vs CHRONIC PAIN
▫ Acute occurs quickly, is short in
duration, usually can be resolved
▫ Chronic longer lasting, usually at
least 3 months in duration,
possibly will not go away
▫ PAIN IS THE SIXTH (6th) VITAL
SIGN
.
4

5. CAUSES OF PAIN /
DISCOMFORT
▫ Trauma
▫ Tissue damage
▫ Pressure on tissue and nerves
▫ Inflammation of tissues and
nerves
5

6. 6
Pain Scale

7. MECHANISMS
TO CONTROL
PAIN
▫ Massage
▫ Position change
▫ Biofeedback
▫ Exercise
▫ Non-opoid analgesics
▫ Antidepressants
▫ Opioid analgesics
▫ Steroids
7

8. Opioid
Analgesics
▫ Pain relievers that contain opium,
derived from the opium poppy or
chemically related to opium
▫ Very strong pain relievers
▫ Very addicting
8

9. Opioid
Analgesics
(contd)
▫ codeine sulfate
▫ meperidine HCl (Demerol)
▫ methadone HCl (Dolophine)
▫ morphine sulfate
▫ propoxyphene HCl
▫ hydromorphone
▫ oxycodone
▫ fentanyl
▫ Many Others
9

10. Agonists ▫ Bind to an Opioid receptor in the
brain
▫ Cause an analgesic response
(reduction of pain sensation)
10

11. Opioid
Analgesics
Indications
▫ Main use to alleviate moderate to
severe pain
▫ Often given with adjuvant drugs to
assist primary drugs with pain
relief
▫ Muscle relaxant
▫ Sedative
▫ Alternate with non-narcotic
analgesic
11

12. Opioid
Analgesics
Indications
(contd)
Opioids are also used for:
▫ Cough center suppression
▫ Treatment of diarrhea
▫ Balanced anesthesia
12

13. Opioid
Analgesics
Contraindications
▫ Known drug allergy
▫ Severe asthma
▫ Use with extreme caution if
▫ Respiratory insufficiency
▫ Elevated intracranial pressure
▫ Morbid obesity
▫ Sleep apnea
▫ Paralytic ileus
13

14. Opioid
Analgesics
Adverse
Effects
▫ Euphoria
▫ CNS depression
▫ Leads to respiratory depression
▫ Most serious adverse effect
▫ Nausea and vomiting
▫ Urinary retention
▫ Diaphoresis and flushing
▫ Pupil constriction (miosis)
▫ Constipation
▫ Itching
14

15. Opioids
Opioid
Tolerance
▫ A common physiologic result of
chronic Opioid treatment
▫ Result larger dose is required to
maintain the same level of
analgesia
15

16. Opioids
Physical
Dependence
▫ Physiologic adaptation of the body
to the presence of an Opioid
▫ Opioid tolerance and physical
dependence are expected with
long-term Opioid treatment and
should not be confused with
psychologic dependence
(addiction)
16

17. Opioids
Psychological
Dependence
▫ A pattern of compulsive drug use
characterized by a continued
craving for an Opioid and the
need to use the Opioid for effects
other than pain relief
17

18. Opioids ▫ Misunderstanding of these terms
leads to ineffective pain
management and contributes to
the problem of under treatment
▫ Physical dependence is seen
when the Opioid is abruptly
discontinued or when an Opioid
antagonist is administered
▫ Opioid withdrawal/Opioid
abstinence syndrome
18

19. Antagonists ▫ Reverse the effects of these drugs
on pain receptors
▫ Bind to a pain receptor and exert
no response
▫ Also known as competitive
antagonists
19

20. Toxicity and
Management
of Overdose
ANALEPTICS
▫ naloxone (Narcan)
▫ naltrexone (Revia)
▫ These drugs bind to opiate receptors and
prevent a response
▫ Used for complete or partial reversal of
Opioid-induced respiratory depression
▫ Regardless of withdrawal symptoms, when a
patient experiences severe respiratory
depression, an Opioid antagonist should be
given.
20

21. 21
NURSING CONSIDERATIONS WHEN GIVING
NALOXONE
 Administer medication very slowly
 Anticipate patient response to treatment
 Monitor patient very closely
 Vital signs, respiratory rate, pulse ox
 Continue to monitor closely
 ½ Life of narcan 60- 90 minutes
 ½ Life of morphine 2 - 4 hours

22. 22
Toxicity and Management of Overdose
 Symptoms of Abstinence Syndrome
 Pulmonary edema
 Withdrawal symptoms
 Nausea
 Vomiting
 Agitation
 Anxiety
 Confusion
 Pain

23. 23
Opioid Analgesics
Nursing Implications
 Oral forms should be taken with food to minimize
gastric upset
 Ensure safety measures, such as keeping side rails
up, to prevent injury
 Withhold dose and contact physician if there is a
decline in the patients condition or if vital signs are
abnormal, especially if respiratory rate is less than
10 to 12 breaths/min

24. 24
Opioid Analgesics Nursing Implications (contd)
o Check dosages carefully
o Follow proper administration guidelines for
IM
injections, including site rotation
o Follow proper guidelines for IV
administration,
including dilution and rate of administration

25. 25
Opioid Analgesics Nursing Implications (contd)
 Constipation is a common adverse effect and may
be prevented with adequate fluid and fiber intake
 Instruct patients to follow directions for
administration carefully and to keep a record of
their pain experience and response to treatments
 Patients should be instructed to change positions
slowly to prevent possible orthostatic hypotension

26. 26
Monitor for Therapeutic Effects
 Decreased complaints of pain
 Decreased severity of pain
 Increased periods of comfort
 Improved activities of daily living, appetite, and sense of
well-being
 Decreased fever (acetaminophen)

27. 27
Monitor for Adverse Effects
 Contact physician immediately if vital signs change,
patients condition declines, or pain continues
 Respiratory depression may be manifested by
respiratory rate of less than 10 breaths/min,
dyspnea, diminished breath sounds, or shallow
breathing

28. 28
Prototype Morphine
 Opioid agonist
 Schedule II narcotic
 Pregnancy Category C
 Given orally or parenterally
 Half life 2 4 hours
 Used for severe pain (chronic or acute)

29. Morphine
▫ Indications
Relief of severe/acute/chronic
pain, analgesia during labor.
▫ Morphine is the drug of choice for
pain due to Myocardial Infarction,
dyspnea from pulmonary edema
not resulting from chemical
respiratory irritant.
29

30. Morphine ▫ Contraindications
▫ Severe respiratory depression,
acute/severe asthma, severe
hepatic/renal impairment. Used
with extreme caution in COPD,
hypoxia, head injury, increased
intracranial pressure
▫
30

31. Morphine Drug-Drug Interactions
▫ Use with EXTREME CAUTION in
patients taking MAOIs
▫ Increased CNS depression and
hypotension with alcohol, sedatives,
hypnotics, barbiturates, tricyclic
antidepressants, antihistamines
▫ May INCREASE the anticoagulant
effect of Warfarin (Coumadin)
31

32. ADVERSE REACTIONS TO NARCOTIC PAIN
MEDICATION
▫ CNS
▫ Impaired judgment
▫ Drowsiness (decrease in LOC)
▫ Decrease in respiratory effort
32

33. ADVERSE REACTIONS TO NARCOTIC PAIN
MEDICATION
▫ Gastrointestinal
▫ Dry mouth
▫ Nausea, vomiting
▫ Decreased intestinal peristalsis
33

34. ADVERSE REACTIONS TO
NARCOTIC PAIN MEDICATION
CARDIOVASCULAR (CV)
▫ Bradycardia
▫ Vasodilation
▫ Tachycardia
▫ Flushing
34

35. ADVERSE REACTIONS TO NARCOTIC PAIN
MEDICATION
▫ GENITOURINARY
▫ URINARY RETENTION
▫ ALLERGIC
▫ RASH
▫ ITCHING
▫ RESPIRATORY
▫ RESPIRATORY DEPRESSION
35

36. Opioid
HERBAL
INTERACTIONS
Concurrent use of
▫ Kava kave
▫ Valerian root
▫ Camomile
▫ Can result in increased CNS
depression
36

37. ROUTES OF ADMINISTRATION FOR
NARCOTIC ANALGESIA
▫ IV
▫ PO
▫ IM
▫ IN (intra-nasal)
▫ SC (SQ)
▫ TRANSDERMAL
▫ EPIDURAL
▫ RECTAL 37

38. ROUTES OF ADMINISTRATION FOR
NARCOTIC ANALGESIA
▫ INTRAVENOUS
▫ Effective within 5 10 min. Of
administration
▫ Most common route (in hospitalized
patients)
▫ Frequently administered as patient
controlled analgesia (PCA)
38

39. 39
PCA PATIENT CONTROLLED ANALGESIA
▫ DOUBLE LOCK SYSTEM
▫ TIME
▫ AMOUNT
▫ NURSE MUST DOCUMENT
▫ AMOUNT USED
▫ EFFECTIVENESS
▫ VITAL SIGNS INCLUDING RESPIRATIONS
▫ ANY UNTOWARD EFFECTS
▫ TEACH FAMILY ABOUT USE AND ABUSE

40. 40
EPIDURAL PAIN MANAGEMENT
• Catheter is placed into the epidural space to
inject a narcotic or anesthetic drug
• Obstetrics
• Surgical procedures
• Pain management
• Catheter may be left in for follow up
injections by physician or patient controlled
analgesia

41. 41
TRANSDERMAL PATCH
 SEVERE PAIN CHRONIC PAIN
 FENTANYL PATCH (DURAGESIC) MOST COMMON
 Slower onset but more consistent pain relief
 Patch usually changed every 72h
 Treated just as any other narcotic must account
for every patch
 Patch must be dated, timed and signed when
placed
 Old patch must be removed when the new one is
placed

42. 42
Nursing Considerations when giving Opioid
Analgesic medication
▫ Assess effectiveness of medication
▫ Use the 0 10 scale to measure intensity of pain
▫ Assess for adverse effects
▫ Assess rate, depth, and rhythm of RESPIRATIONS
▫ Provide for patient safety

43. Analgesic-Antipyretic-
Anti-Inflammatory and
Related Drugs

44. Overview
▫ This kind of drug is a group of chemically dissimilar
agents that have antipyretic, analgesic and anti-
inflammatory effects.
▫ The structure of this kind of drug differs from that of
steroidal anti-inflammatory drugs.
▫ Nonsteroidal anti-inflammatory drugs NSAIDs

45. History
▫ In ancient Egypt & Greece, dried leaves of myrtle, the bark of
willow & poplar tree
▫ In England, active component from willow bark was identified
as salicin, which is metabolized to salicylate in 1763.
▫ In Germany, salicylic acid was synthesized in 1860.
▫ In 1875, acetylsalicylic acid was synthesized.

46. Common pharmacological effects
These drugs show the same pharmacological effects
▫ -- antipyretic effect
▫ -- analgesic effect
▫ -- anti-inflammatory effect

47. Antipyretic
Effects
▫ "normal" temperature: slightly
affected
▫ "elevated" temperature: reduced
▫ The higher temperature, the more
potent
▫ Mechanisms of Antipyretic Action
Blocks pyrogen-induced
prostaglandin production in
thermoregulatory center (CNS)

48. NSAIDs
Pyrogen
Prostaglandins
pGE2
thermoregulatory
center
heat production ↑
Heat dissipation ↓
set point ↑
Fever
• Antipyretic
Mechanism
Block prostaglandins
production
• Sites of action:
Central Nervous
System

49. Analgesic
Effects
Effective to mild to moderate pain
0.5g of aspirin is a weak or mild analgesic
that is effective in short, intermittent types
of pain as encountered in neuralgia, myalgia,
toothache.

50. Analgesic Effects
▫ Pain may arise from:
Musculature, dental work , vascular , postpartum
conditions, arthritis , bursitis
▫ Sites of action:
peripherally -- sites of inflammation
subcortical sites

51. NSAIDs
Prostaglandins
pGE2 pGF2
Nerve ending of
pain
Pain
Bradykinin
histamine
factors
+
• block prostaglandins
production
• Sites of action:
peripheral tissue

52. Anti-inflammatory Effects
▫ NSAIDs only inhibit the symptoms of
inflammation
▫ But they neither arrest the progress of
the disease nor do they induce
remission

53. Anti-inflammatory Effects
▫ Reduced synthesis:
--eicosanoid mediators
▫ Interference:
--kallikrein system mediators
--inhibits granulocyte adherence
--stabilizes lysosomes
--inhibits leukocyte migration

54. Mechanism of action
The principal pharmacological effect of NSAIDs is due
to their ability to inhibit prostaglandin synthesis by
blocking the cyclooxygenase （COX） activity of
both COX-1 and COX-2.
NSAIDs----- acetylation of COX
(reversible or irreversible)

55. NSAIDs
Prostaglandins
pGE2 pGF2
Symptoms of
inflammation
Red, swelling,
Heating, Pain
Bradrkinin
Histamine
5-HT
Inflammatory
factors
+
• block prostaglandins
production
• Sites of action:
peripheral tissue

56. ▫ vasodilatation, pain sensitization, gastric
cytoprotection [mucous/HCO3 secretion], fever
▫ bronchoconstriction, uterine contraction
▫ inhibition of platelet aggregation, gastric
cytoprotection
▫ platelet aggregation

57. Salicylates
▫ Acetylsalicyclic acid
▫ Aspirin
▫ Sadium Salicylate

58. Pharmacokinetics
▫ Rapidly absorbed: stomach and upper small
intestine
▫ Distribution：through the body
rapidly hydrolyzed --------- acetic acid +
salicylate, catalyzed by tissue/blood
esterases

59. Elimination-----Pharmacokinetics
▫ metabolite in liver
dose ＜1g/day：one-order elimination T1/2: 3--5 hrs
dose ＞1g/day：zero-order elimination
＞4g/day T1/2:
▫ Excretion: kidney, influenced by pH of urine

60. Pharmacodynamics
1. Analgesic Effects (300-600mg)
2. Antipyretic Effects (300-600mg)
3. Anti-inflammatory Effects (3-6g)
do not influence the progress of disease
4. Effects on Platelets (40-100mg)
Reduced platelet aggregation
reduces thromboxane A2 (TXA2) formation

61. Low doses 40-100mg/day
▫ Platelets
▫ No nuclei
▫ No new COX1
produce
▫ TXA2 production ↓
▫ Lifetime:
8-11 days
▫ Endothelial cell
▫ Has nuclei
▫ New COX1 produce

62. Pharmacodynamics
5. Other effects
▫ Immune inhibition
▫ Effect on metabolism of
connective tissue
▫ Effects on metabolism of
glucose, fat, protein ----
catabolism ↑
▫ ACTH release ↑

63. Clinical Uses
1. Commonly used for management of mild to moderate pain
(300-600mg)
2. Combination agents (cold)
3. Used for reducing fever (300-600mg)
4. Useful in treatment of:
(high doses 3-6g) T1/2 > 12 hours
0 rheumatic fever
0 rheumatoid arthritis
0 other inflammatory joint diseases

64. Clinical Uses
5. Antiplatelet: (low doses) 40-100mg
 reduce incidence of transient ischemic
attacks (prophylaxis)
 reduce incidence of unstable angina
(prophylaxis)
 may reduce incidents of coronary artery
thrombosis

65. Clinical
Uses
6. Hypertension in pregnancy :
(low doses) 60-100mg
TXA2↓
7. Local indication
GI inflammation : 5-amido-
salicylic acid

66. SIDE
EFFECTS
1. CNS: excitation----inhibition
salicylic acid reaction:
Headaches; confusion;
hallucinations; tremors; vertigo;
behavior disturbance
2. GI effects: direct stimulation
PGE2 & PGI2 ↓
Esophagitis; gastric
ulcerations; GI hemorrhage

67. SIDE
EFFECTS
3. Liver & renal toxicity
 Dose dependence toxicity
 Reye's syndrome
a potentially fatal disease that
causes numerous detrimental
effects to many organs, especially
the brain and liver.
The disease causes hepatitis with
jaundice and encephalopathy

68. SIDE
EFFECTS
4. Other reaction
Hematologic: decreased platelet
aggregation; prolonged
bleeding time.
Exacerbations of asthma
Hypersensitivity: rashes
Acid-base Imbalance

69. Acetaminophen ▫ Rapidly absorbed from GI
▫ Phenacetin is largely converted to
Acetaminophen
▫ Similar antipyretic, analgesia to aspirin
▫ Weak anti-inflammatory properties
▫ used to reduce fever and pains (a major
ingredient in numerous cold and flu
medications) (choice for child)
▫ used appropriately, side effects are rare

70. Indomethacin
▫ More potent than aspirin
▫ As an anti-inflammatory
agent
▫ More adverse reaction
Ibuprofen
▫ Fewer adverse reaction
▫ Brufen；Benzeneacetic
acid； Fenbid； Emodin；
Motrin

71. Phenylbutazone ▫ Powerful anti-inflammatory effects
▫ Weak analgesic & antipyretic
activities
▫ Promote excretion of uric acid
▫ Used for acute gout, rheumatic &
rheumatoid arthritis
▫ More adverse reaction
▫ Can induce activities of drug
metabolize-E
▫ Can displace other drugs from
plasma proteins

72. Selective
COX-2
inhibitors
 Less adverse reactions
 Do not impact platelet
aggregation
▫ Meloxicam
▫ Celecoxib
▫ Nimesulide
▫ Rofecoxib
▫ Valdecoxib

73. Antipyretic analgesic Anti-
inflammatory
Side action
Acetaminophen ++ ++ +
Indomethacin ++++ ++++
sulindac ++++ ++
tolmetin + + ++ ++
diclofenac ++ ++ ++
Ibuprofen + +++ + +
meloxicam ---- cox2
Phenylbutazone +++ +++
ketorolac +++ i.m

74. Skeletal Muscle
Relaxant

75. Skeletal Muscle Relaxants (SMRs)
• Drugs that act peripherally at neuromuscular
junction/muscle fiber or centrally in the cerebrospinal axis
to reduce muscle tone or cause paralysis
• A muscle relaxants is a drug that affects skeletal muscle
function and decreases the muscle tone.

76. Common Symptoms/Conditions in which SMRs are used
• In conjunction with GA:
– Facilitate intubation of the trachea
– Facilitate mechanical ventilation
– Optimized surgical working conditions
• In Muscle spasm: a sudden involuntary contractionof one or more muscle
groups and is usually an acute condition associated with muscle strain
(partial tear of a muscle) or sprain
– Musculoskeletal Injury or Sports Injury
– Low Back pain or neck pain
– Fibromyalgia, tension headaches
• It may be used to improve symptoms such as muscle spasms, pain, and
hyperreflexia.

77. History:
From Fun
hunting in
Jungles to
Operation
theatre
 Curare: The arrow poison
 Source: Chondrodendrone tomentosum
andStrychnos toxifera
 Derived from: "ourare“ meaning arrow poison in
South American Indian
 Tubocurarine name: Because of packing in
“hollow bamboo tubes”

78. Neuromuscular Junction (NMJ)

79. Physiology of Skeletal Muscle Contraction

80. Classification of SMRs

81. Classification: Peripherally acting SMRs
1. Neuromuscular Junction (NMJ)Blockers :
A. Nondepolarizing (Competitive) blockers:
a. Long acting: d-Tubocurarine, Pancuronium, Doxacurium,
Pipecuronium, Gallamine and Metocurine
b. Intermediate acting: Vecuronium, Atracurium, Cisatracurium,
Rocuronium,
Rapacuronium
c. Short acting: Mivacurium
A. Depolarizing blockers: Succinylcholine (suxamethonium),
Decamethonium
B. Botulinum Toxin
1. Directly acting: Dantrolene

82. Nondepolarizing (Competitive) blockers
• Nondepolarizing (Competitive) Blockers having no intrinsic activity
(antagonist)
• These are of 3 types based on their activity:
a. Long acting: d-Tubocurarine, Pancuronium, Doxacurium,
Pipecuronium, Gallamine and Metocurine
b. Intermediate acting: Vecuronium, Atracurium,
Cisatracurium, Rocuronium, Rapacuronium
c. Short acting: Mivacurium

83. Nondepolarizing (Competitive) blockers
Pharmacological actions:
• Skeletal muscles: Intravenous injection of nondepolarizing
blockers rapidly produces muscle weakness followed by flaccid
paralysis.
• Autonomic ganglia: produce some degree of ganglionic blockade
• Histamine release: d-TC releases histamine from mast cells.
Histamine release contributes to the hypotension produced by d-
TC. Flushing, bronchospasm and increased respiratory secretions are
other effects.

84. Pharmacological actions (Cont.,)
• Cardiovascular system: d-Tubocurarine produces significant fall in
BP.This is due to
– Ganglionic blockade
– Histamine release and
– Reduced venous return
• Gastrointestinal tract: The ganglion blocking activity of
competitive blockers may enhance postoperative paralytic ileus after
abdominal operations.
• Central nervous system: All neuromuscular blockers are quaternary
compounds— do not cross blood-brain barrier.

85. Nondepolarizing blockers - Individual compounds
• d-Tubocurarine: 1st agent to undergo clinical investigation
– 1-2 hr. duration of action
– Histamine releaser (Bronchospasm, hypotension)
– Blocks autonomic ganglia (Hypotension)
• Clinical Use:
– Not clinical used do to its histaminic effects.
– Long duration of action(60 to 120 mins) and CVS effects restricted
its use

86. Nondepolarizing blockers - Individual compounds
• Pancuronium:
– It is a synthetic steroidal compound, ~5 times more potent
than d-TC. use is now restricted and longer acting
– Because of longer duration of action, needing reversal, its
to prolonged operations, especially neurosurgery.
▫
• Pipecuronium:
▫ – Muscle relaxant with a slow onset and long
duration of action; steroidal in nature;
recommended for prolonged surgeries.

87. Nondepolarizing blockers - Individual compounds
• Vecuronium:
– It is a most commonly used muscle relaxant for routine surgery and
in intensive care units..
• Atracurium:
– Four times less potent than pancuronium and shorter acting.
• Rocuronium:
– Muscle relaxant with a rapid onset and intermediate duration of
action which can be used as alternative to SCh for tracheal
intubation without the disadvantages of depolarizing block and
cardiovascular changes.

88. Depolarizing Blockers - Succinylcholine
• Succinylcholine have affinity and sub-maximalintrinsic activity at Nm
receptor.
• It acts on sodium channels, open them and causes initial twitching
and fasciculation.
• It does not dissociate rapidly from the receptors resulting in
prolonged depolarization and inactivation of Na+ channels.

89. Mechanism of Action: Succinylcholine

90. Advantages of Succinylcholine
• Most commonly used for Tracheal intubation
• Rapid onset (1-2 min)
• Good intubation conditions – relax jaw, separated vocal
chords with immobility, no diaphragmatic movements
• Short duration of action (5-10 minutes)
• Dose 1-1.5mg/kg
• Used as continuous infusion occasionally

91. Side effects of Succinylcholine
• Cardiovascular: unpredictable BP, heart rate and arrhythmias
• Fasciculation
• Muscle pain
• Increased intraocular pressure
• Increased intracranial pressure
• Hyperkalemia: k+ efflux from muscles, life threatening in Cardiac
Heart Failure, patient with diuretics etc.
• Malignant hyperthermia

92. What is Malignant hyperthermia
 Rare genetically determined reaction to susceptible persons having
abnormal RyR receptor Ca+ channel
 Caused by Halothane and manifests as high temperature due to
persistent muscle contraction
 Increased intracellular Ca+
 Succinylcholine accentuates this condition
 Treatment:
 Rapid external cooling – ice pack
 Bicarbonate infusion
 100% oxygen inhalation
 Injection of dantrolene: Direct acting muscle relaxant

93. Indication of Neuro Muscular Junction Blockers
• Adjuvant to General anesthesia
• Assisted ventilation
• Convulsion and trauma from
electroconvulsive therapy
• Status epilepticus
Vocal cord

94. Directly acting relaxants - Dantrolene
 Different from neuromuscular blockers, no action on
neuromuscular transmission
 Mechanism of Action: Ryanodine receptors (RyR) calcium
channels – prevents depolarization – no intracellular release
of Ca++
 Absorbed orally, penetrate brain and produces sedation,
metabolized in liver, excreted in kidney. T1/2 8-12 hrs
 Dose: 25-100mg - 4 times daily
 Uses: Upper Motor Neuron disorders – paraplegia, hemiplegia,
cerebral palsy and malignant hyperthermia (drug of choice 2.5-
4 mg/kg)
 Adverse effects – Sedation, malaise, light headedness,
muscular weakness, diarrhea and hepatotoxicity

95. Centrally acting Muscle relaxants
Classification:
1. Mephenesin congeners –Mephenesin, Carisoprodol,
Chlorzoxazone, Methocarbamol and Chlormezanone
2. Benzodiazepines – Diazepam, lorazepam, Clonazepam
and others
3. GABA derivative – Baclofen
4. Central α-2 agonist – Tizanidine, clonidine

96. MOA: Centrally acting Muscle relaxants
• Drugs that reduce skeletal muscle tone by selective
action on cerebrospinal axis
• Depress the spinal and supraspinal reflexes of muscle tone
• Also depresses polysynaptic reflexes of ascending reticular
formation – wakefulness disturbed (sedation)
• No effect on NM junction but reduce Upper Motor
Neuron spasticity and hyperreflexia

97. Mephenesin (Relaxyl/medicreme)
• Mephenesin (Relaxyl/medicreme)
–Modulation of reflexes in spinal internuncialneuron
–Cannot be used systemically
–Irritant rather than relaxant – topical preparations
• Carisoprodol, Chlorzoxazone (Mobizox), Methocarbamol
(Robinax/Robiflam) and Chlormezanone – similar but can
be used orally

98. Benzodiazepines as muscle relaxant
• Very potent centrally acting muscle relaxant – supraspinal
• Mechanism of action is via “GABAA receptor Cl- complex”
enhancement
• Inhibitory in nature
• Diazepam and Clonazepam are the most potent ones
• Diazepam is the prototype of BZDs

99. Baclofen- GABAB agonist
• Mechanism of action: GABA B agonist
– Hyperpolarization of neurons by increasing K+
conductance and alteration of Ca++ flux
– Does not affect to Cl- conductance
• Site of action: spinal chord – depresses polysynaptic and
monosynaptic reflexes
• Clinical effects: decreased hyperreflexia; reduced painful
spasms; reduced anxiety
• Dose: orally 5 mg three times daily, gradually increase to
20 mg four times daily or higher
• Intrathecally initially 50 mcg/day increase to 300-800 mcg/day

100. Tizanidine/ clonidine
• Mechanism of action: alpha-2 receptor agonist –
inhibits the release of excitatory amino acids in spinal
interneurons
• Clinical effects: reduced tone, spasm frequency, and
hyperreflexia
• Doses: tizanidine initial 4 mg three times daily
increase to 36 mg/day; clonidine initial 0.1 mg twice
daily increase to 2.4 mg/day

101. Uses of Centrally acting relaxants
• Acute muscle spasms
• Backache and neuralgias
• Anxiety and tension
• Spastic neurological disorders
• Tetanus
• Electroconvulsive therapy
• Orthopedic manipulations

102. Centrally acting Vs Peripherally acting
Centrally acting Peripherally acting
• Decrease muscle tone
but no reduction in
power
• Polysynaptic reflexes in
CNS
• CNS depression
• Orally and parenterally
• Spastic conditions, muscle
spasm
• Cause muscle paralysis
• Block NM transmission
• No CNS effect
• Given IV
• Short term surgical
procedures

103. Non-pharmacologic interventions to relieve muscle spasm
and spasticity
Non-pharmacologic interventions include:
• Physical interventions (stretching, passive movements)
• Transcutaneous electric nerve stimulation (TENS)
• Transcranial direct current stimulation (tDCS)
• Shock wave
• Vibratory stimulation (whole body vibration)
• Electromyography biofeedback
• Repetitive transcranial magnetic stimulation (TMS)
• Therapeutic ultrasound & Acupuncture
• Orthotics (splints, casts)
• Thermotherapy & Cryotherapy

104. Nursing Role
• Monitor patient response to therapy (improvement in muscle spasm
and relief of pain; improvement in muscle spasticity).
• Monitor for adverse effects (e.g.CNS changes, GI depression,
urinary urgency, etc).
• Discontinue drug at any sign of liver dysfunction to prevent adverse
effects.
• Monitor patient compliance to drug therapy.
• Provide safety measures (e.g. adequate lighting, raised side rails,
etc.) to prevent injuries.
• Educate client on drug therapy to promote understanding and
compliance.

105. Anti Anxiety and
Sedative-Hypnotic
Drugs

106. SEDATIVE AND HYPNOTIC DRUGS
Sedative effect
Given during waking hours
May cause drowsiness
Hypnotic effect
Given at bedtime with the purpose of inducing sleep
MAY BE THE SAME DRUG GIVEN AT DIFFERENT
DOSAGES

107. 111
Benzodiazepines
 Prototype
 Diazepam (Valium)
 Antianxiety, anticonvulsant, sedative/hypnotic, skeletal muscle
relaxant
 Schedule IV drugs Moderate potential for abuse
 Pregnancy category D
 Half-life 20-50 hours (metabolites also cause sedation up to 100
hours)
 Drug of choice to treat status epilepticus (sustained seizures)

108. 112
BENZODIAZEPINES
 alprazolam (Xanax)
 chlordiazepoxide (Librium)
 flurazepam (Dalmane)
 lorazepam (Ativan)
 midazolam (Versed)
 triazolam (Halcion)

109. 113
BENZODIAZEPINES
MECHANISM OF ACTION
 Binds with benzodiazepine receptors in nerve cells of the
brain these cells also have binding sites for GABA (gamma-
aminobutyric acid) which is an inhibitory neurotransmitter.
 Excitatory v. Inhibitory transmitters
 Excitatory Norepinephrine
 Inhibitory - GABA

110. 114
GABA
•Benzodiazapines and barbiturates work by increasing
the action of gaba in the brain
•Gaba is an amino acid that inhibits nerve transmissions
in the brain

111. 115
BENZODIAZEPINES
Indications
•Not all drugs are appropriate for all uses
•Antianxiety
•Hypnotic
•Anticonvulsant
•Preoperative sedation
•Prevent DTs in alcohol withdrawal

112. BENZODIAZEPINES
Contraindications
▫ Respiratory depression
▫ Liver disorder
▫ Kidney disorder
▫ History of alcohol or drug abuse
▫ Used cautiously with other CNS
depressants
116

113. 117
BENZODIAZEPINES
 Drug-Drug interactions
 Cimetidine, hormonal contraceptives, disulfiram, fluoxetine,
isoniazid, ketoconazole, metoprolol, propoxyohene,
propranolol, and valproic acid may enhance the effects of
sedatives by decreasing their metabolism.
 May decrease the efficacy of levodopa
 Rifampin, barbiturates may increase the metabolism of
benzodiazepines, decreasing their effectiveness.

114. 118
BENZODIAZEPINES
Herbal products to avoid when using benzodiazepines
 Kava kava
 Valerian root
 Camomile
CAN INCREASE SEDATION
THIS APPLIES TO ALL CNS DEPRESSANTS

115. 119
BENZODIAZEPINES
 Adverse Effects
 CNS depression drowsiness, lightheadedness
 Paradoxical effects insomnia, excitation
 Respiratory depression
 Hypotension
 Constipation/diarrhea
 Nausea, vomiting
 Rash

116. 120
BENZODIAZEPINES
 REVERSAL AGENT FOR OVERDOSE OF
BENZODIAZEPINES
 FLUMAZENIL
 INDICATED FOR THE REVERSAL OF MODERATE
SEDATION OR GENERAL ANESTHIA

117. 121
NURSING CONSIDERATIONS
 ASSESS PATIENT WITH FOCUS ON REASON FOR GIVING
 SEDATION
 ANXIETY
 NERVOUSNESS
 REASSESS PATIENT FOR RESPONSE TO DRUG
 SEDATIVE Q 4-6 H
 HYPNOTIC AT BEDTIME
 MONITOR VS AND POTENTIAL FOR DEPRESSION

118. 122
CONTRAINDICATIONS TO SEDATIVES
AND HYPNOTICS
 Patient with a history or current use of
recreational drugs or alcohol abuse
 Respiratory compromise
 Pregnancy or lactation

119. 123
NURSING IMPLICATIONS
 Administer accurately
 Teach patient about expected effects and
possible side effects
 Provide for patient safety
 Observe for therapeutic effects
 Decrease in anxiety
 Positive signs of sleep

120. 124
NURSING IMPLICATIONS
 Observe for adverse effects
 Excessive sedation
 Hypotension
 Observe for drug interactions
 Concurrent use of other CNS depressants

121. 125
Barbiturates Used as Anxiolytic-Hypnotics
These were once the sedative-hypnotic
drugs of choice but newer anxiolytics
have replaced them. Barbiturates have
high risk for addiction and dependency.

122. 12
Therapeutic Action
These are general CNS depressants that
inhibit neuronal impulse conduction in the
ascending RAS, depress the cerebral cortex,
alter cerebellar function, and depress motor
output. Therefore, they can cause sedation,
hypnosis, anesthesia, and even coma.

123. 127
Indications
•Generally indicated for anxiety, sedation,
insomnia, paresthesia, and seizures.
•Parenteral forms may be used for treatment
of acute manic reactions.

124. 128
Route Onset Peak Duration
Oral 15 min 30-60 min 10-16 h
IM, subcutaneous – 10-30 min 4-6 h
IV Up 10 15 min 5 min 4-6 h
Pharmacokinetics

125. Contraindications
and Cautions
▫ Allergy to barbiturates. Prevent severe
hypersensitivity reactions.
▫ History of addiction to sedative-hypnotic
drugs: barbiturates are more addicting than
most other anxiolytics
▫ Latent or manifest euphoria. May be
exacerbated by drug effects
▫ Marked hepatic impairment or
nephritis. May alter the metabolism and
excretion of drugs
▫ Respiratory distress and
dysfunction. Exacerbated by CNS
depression caused by drugs.
129

126. Contraindications
and Cautions
▫ Pregnancy. Associated with congenital
abnormalities
▫ Lactation. Has potential for adverse effects
on the infant.
▫ Acute or chronic pain. Can cause
paradoxical excitement which can mask
other symptoms
▫ Seizure disorder. Abrupt withdrawal of
barbiturates can precipitate status
epilepticus
▫ Chronic hepatic, cardiac, and respiratory
diseases. Can be exacerbated by the
depressive effects of these drugs.
130

127. Adverse
Effects
▫ CNS: drowsiness, somnolence, lethargy,
ataxia, vertigo, “hangover” feeling,
thinking abnormalities, paradoxical
excitement, anxiety, hallucinations
▫ CV: bradycardia, hypotension, syncope
▫ Respiratory: serious hypoventilation,
respiratory depression
▫ Hypersensitivity reactions: rash, serum
sickness, Steven-Johnson syndrome
▫ Development of physical tolerance and
psychological dependence
131

128. Nursing
Considerations
These are vital nursing interventions
done in patients who are taking
anxiolytic-hypnotics:
▫ Administer intravenous diuretics slowly
because rapid administration may cause
cardiac problems.
▫ Do not mix intravenous drugs in solution
with any other drugs to avoid potential
drug-drug interactions.
▫ Taper dose as ordered because abrupt
withdrawal can precipitate seizure attacks.
132

129. Nursing
Considerations
▫ Provide comfort measures (e.g.
small, frequent meals, access to
bathroom facilities, orientation, etc.)
to help patient tolerate drug effects
▫ Provide safety measures (e.g.
adequate lighting, raised side rails,
etc.) to prevent injuries.
▫ Educate client on drug therapy to
promote compliance.
133

130. Psychotherapeutic
Drugs

131. 135
Anxiety Disorders
A group of mental disorders characterized by a
vague uneasy feeling of discomfort or dread. The
symptoms of anxiety prevent the individual from
normal functioning . can be an exaggerated
response to an actual event or anxiety unrelated
to an identifiable event or condition.

132. 136
Anxiety disorders
 Panic disorder
 Generalized anxiety disorder
 Obsessive-compulsive disorder
 Post-traumatic stress disorder
 Simple phobia
 Social phobia

133. 137
Antianxiety Medications(Anxiolytics)
o Tricyclic antidepressants
o Benzodiazepines
o MAOIs
o Buspirone
o SSRIs

134. 138
BUSPIRONE (BuSpar)
 Mechanism of action unknown
 Interacts with serotonin and dopamine in
the brain
 No muscle relaxant effects
 No anticonvulsant effects
 Does not cause sedation

135. 139
BUSPIRONE (BuSpar)
Uses / indications
Short term management of anxiety
disorders
Not appropriate for immediate relief may
take
several weeks to see effects

136. 140
BUSPIRONE (BuSpar)
Side effects
 Dizziness, nausea, headache, anxiety, fatigue,
 Insomnia
Contraindications
 Renal/hepatic failure
 Use of MAOIs

137. 141
ANTIDEPRESSANTS AND MOOD
STABILIZERS DRUGS

138. 142
ETIOLOGY OF DEPRESSION
Monoamine neurotransmitter dysfunction
Deficiency of norepinephrine and/or
serotonin.
Balance, integration and interactions
among
norepinephrine, serotonin, and other
neurotransmission systems is an
important
etiological factors.

139. 143
ETIOLOGY OF DEPRESSION
 Neuroendocrine factors
 AN INCREASE IN CRF (corticotropin releasing
 factor/hormone) HAS BEEN NOTED IN
PATIENTS WITH DEPRESSION.

140. 144
CLASSIFICATIONS OF ANTIDEPRESSANT
MEDICATIONS
Tricyclic antidepressants
Monoamine oxidase inhibitors
Selective serotonin reuptake inhibitors
Unclassified drugs

141. 145
TRICYCLIC ANTIDEPRESSANTS
 imipramine (Tofranil) prototype
 nortriptyline (Pamelor)
 amitryptyline (Elavil)
 desipramine (Norpramin)

142. 146
TRICYCLIC ANTIDEPRESSANTS(TCAs)
 First generation of antidepressant therapy
 Mechanism of action
 Corrects the imbalance in the neurotransmitter
concentrations of serotonin and norepinephrine at
the nerve endings in the CNS. This is done by
blocking the reuptake of the neurotransmitters and
thus causing these neurotransmitters to accumulate
at the nerve endings.
 Also have nonselective receptor antagonism
causing many side effects.

143. 147
TRICYCLIC ANTIDEPRESSANTS
 Indications
 Depression
 Childhood enuresis(bed wetting)
 Imipramine
 Obsessive compulsive disorder
 Clomipramine
 Chronic pain syndromes
 Neuropathic pain (trigeminal neuralgia)

144. 148
TRICYCLIC ANTIDEPRESSANTS
Adverse effects
 Sedation
 Impotence
 Orthostatic hypotension
 Disturbs cardiac conduction
 Delayed micturation
 Edema
 Muscle tremors

145. 149
TRICYCLIC ANTIDEPRESSANTS
Interactions
 WHEN TAKEN WITH MAOIs MAY RESULT IN
INCREASED THERAPEUTIC LEADING TO
TOXIC EFFECTS (HYPERPYRETIC CRISIS)
 TCAs can inhibit the metabolism of
warfarin,resulting in an increase in
anticoagulation

146. 150
TRICYCLIC ANTIDEPRESSANTS
 Toxicity and management of overdose
 TCA overdoses are fatal 70 - 80 of the time
 Death usually results from seizures or
dysrhythmias
 THERE IS NO SPECIFIC ANTIDOTE FOR TCAs

147. 151
MONOAMINE OXIDASE INHIBITORS
(MAOIs)
 First generation of antidepressant drugs
 Highly effective
 Many side effects and drug/drug, drug/food
interactions
 Disadvantage potential to cause hypertensive crisis
when taken with tyramine

148. 152
MAOIs
 phenelzine (Nardil)
 tranylcypromine (Parnate)

149. 153
MAOIs Mechanism of Action
 Inhibit the MAO enzyme system in the CNS
 Amines (dopamine, serotonin, norepinephrine)
are not broken down, resulting in higher levels in
the brain
 Result alleviation of symptoms of depression

150. 154
MAOIs Indications
Depression, especially types characterized by
symptoms such as increased sleep and appetite
depression that does not respond to other drugs
such as tricyclics

151. 155
MAOIs Adverse Effects
 Tachycardia
 Dizziness
 Insomnia
 Anorexia
 Blurred vision
 Palpitations
 Drowsiness
 Headache
 Nausea
 Impotence

152. 156
MAOIs Overdose
 Symptoms appear 12 hours after
ingestion
 Tachycardia, circulatory collapse,
seizures, coma
 Treatment protect brain and heart,
eliminate toxin

153. 157
Hypertensive Crisis and Tyramine During
MAOI Therapy
Ingestion of foods and/or drinks with the
amino acid tyramine leads to hypertensive
crisis, which may lead to cerebral
hemorrhage, stroke, coma, or death

154. 158
Hypertensive Crisis and Tyramine (contd)
 Avoid foods that contain tyramine!
 Aged, mature cheeses (cheddar, blue, Swiss)
 Smoked/pickled or aged meats, fish, poultry
 (herring, sausage, corned beef, salami, pepperoni,
pâté)
 Yeast extracts
 Red wines (Chianti, burgundy, sherry, vermouth)
 Italian broad beans (fava beans)

155. 159
Antidepressants MAOIs
 Concurrent use of MAOIs and SSRIs may lead to
serotonin syndrome
 If the decision is made to switch to an SSRI, there
must be a 2- to 5-week wash-out period between
MAOI therapy and SSRI therapy

156. 160
Selective Serotonin Reuptake
Inhibitors(SSRIs)
 fluoxetine (Prozac)
 paroxetine (Paxil)
 sertraline (Zoloft)
 fluvoxamine (Luvox)
 citalopram (Celexa)
 escitalopram (Lexapro)

157. 161
SSRIs Newer-Generation
Antidepressants
 Fewer adverse effects than tricyclics and
MAOIs
 Very few drug-drug or drug-food
interactions
 Still takes about 4 to 6 weeks to reach
maximum clinical effectiveness

158. SSRIs
Mechanism of action
▫ Selectively inhibits serotonin reuptake
▫ Little or no effect on norepinephrine or
dopamine reuptake
▫ Result in increased serotonin
concentrations at nerve endings
▫ Advantage over tricyclics and MAOIs
little or no effect on cardiovascular
system
162

159. SSRIs INDICATIONS
▫ Depression
▫ Bipolar disorder
▫ Obesity
▫ Eating disorders
▫ Obsessive-compulsive disorder
163

160. SSRI
Antidepressants
Adverse Effects
▫ Body System Effects
▫ CNS Headache, dizziness,
tremor, nervousness,
insomnia, fatigue
▫ GI Nausea, diarrhea, constipation,
dry mouth
▫ Other Sexual dysfunction,
▫ weight gain, weight loss, sweating
▫ Most common and bothersome
164

161. 165
Serotonin-Norepinephrine Reuptake
Inhibitors
 Duloxetine (Cymbalta)
 Venlafaxine (Effexor)

162. 166
Serotonin-Norepinephrine Reuptake
Inhibitors
Indicated
For depression and general anxiety disorder
Also pain associated with diabetic peripheral
neuropathy
Contraindicated
CONCURRENT USE OF MAOIs
Angle closure glaucoma

163. SNRIs
Drug Interactions
 Highly bound to plasma proteins
 Compete with other protein-binding drugs, resulting in
more free, unbound drug to cause a more pronounced
drug effect
 Inhibition of cytochrome P-450 system

164. OTHER ANTIDEPRESSANTS NOT CLASSIFIED
 bupropion
 Wellbutrin, zyban
 Commonly prescribed for smoking cessation
 maprotiline
 Similar to TCAs
 Mirtazapine
 Remeron
 Often prescribed to enhance appetite

165. NURSING CONSIDERATIONS WHEN PATIENTS
ARE TAKING ANTIDEPRESSANTS
 Comprehensive patient history
 Complete medication history
 Monitor patient for therapeutic effects
 Monitor patients for adverse effects
 Education of patient on drug expectations and adverse
effects
 Educate patient regarding drug-drug, drug-food and drug-
herbal interactions

166. MOOD STABILIZING AGENTS
 lithium carbonate
 Eskalith, lithobid
 MOA not completely understood
 Managed using serum levels
 Indications : mania, bipolar disorder
Adverse effects
 vomiting, diarrhea, drowsiness, difficult
 coordination, hand tremors, muscle twitching,
 mental confusion

167. NURSING CONSIDERATIONS
 Monitor serum lithium levels
 Therapeutic levels are 1.0 1.5 meq/L
 Lithium is eliminated intact by the kidneys.
 Encourage fluids to completely eliminate the drug
 Monitor for therapeutic and adverse effects

168. PSYCHOSIS
 A severe mental disorder characterized by disordered
thought process and often bizarre thinking.
 Hypoactivity or hyperactivity
 Agitation
 Aggressiveness
 Hostility
 Social withdrawal

169. Antipsychotic Drugs
 Antipsychotic AKA Neuroleptic
 Any drug that modifies or treats psychotic
behaviors usually by blocking dopamine receptors
in the brain

170. Antipsychotic
Drugs
▫ Thioxanthenes
▫ thiothixene (Navane)
▫ Phenylbutylpiperidines
▫ haloperidol (Haldol)
▫ Dihydroindolones
▫ molindone (Moban)
▫ Dibenzodiazepines
▫ loxapine (Loxitane)
▫ Benisoxazoles
▫ Risperidone
▫ Quinolinine
▫ Aripiprazole (Abilify)
▫ Phenothiazines
▫ Chlorpromazine
(Thorazine)

171. HALDOL- FIRST GENERATION
ANTIPSYCHOTIC
 Schizophrenia
 Long half-life facilitates better
compliance by patients
 Long-term treatment of psychosis
 Can be given either IV or po

172. ADVERSE REACTIONS TO ANTIPSYCHOTIC
MEDICATION
▫ Seizures
▫ Extrapyramidal reactions
▫ Blurred vision, dry eyes
▫ Neuroleptic malignant syndrome
▫ Tartive dyskinesia

173. ATYPICAL ANTIPSYCHOTICS
NEWER-GENERATION ANTIPSYCHOTICS
▫ clozapine (Clozaril)
▫ risperidone (Risperdal)
▫ olanzapine (Zyprexa)
▫ quetiapine (Seroquel)
▫ ziprasidone (Geodon)
▫ aripiprazole (Abilify)

174. Mechanism of Action
▫ Block dopamine receptors in
the brain (limbic
system, basal ganglia)areas
associated with
emotion, cognitive function,
motor function
▫ Dopamine levels in the CNS
are decreased
▫ Result tranquilizing effect in
psychotic patients

175. ADVANTAGES OF NEWER GENERATION
ANTIPSYCHOTICS
 Reduced effect on Prolactin levels
 Stimulates mammary glands to produce milk
Lower risk of
o Neuroleptic malignant syndrome
o Extrapyramidal adverse effects
o Tartive dyskinesia

176. 180
Indications
 Treatment of serious mental illnesses
 Bipolar affective disorder
 Depressive and drug-induced psychoses
 Schizophrenia
 Autism
 Movement disorders (such as Tourettes
syndrome)
 Some medical conditions
 Nausea, intractable hiccups

177. 181
Adverse Effects
 Body System Adverse Effects
 CNS Sedation, delirium
 Cardiovascular Orthostatic hypotension,
syncope, dizziness, EKG changes
 Dermatologic Photosensitivity, skin rash,
 hyper-pigmentation, pruritus

178. 182
Adverse Effects (contd)
 Body System Adverse Effects
 GI Dry mouth, constipation
 GU Urinary hesitancy or retention,
impaired erection
 Hematologic Leukopenia and
agranulocytosis

179. 183
Adverse Effects (contd)
 Body System Adverse Effects
 Metabolic/endocrine Galactorrhea,
irregular menses, increased appetite,
polydipsia

180. 184
Nursing Implications
 Before beginning therapy, assess both
the physical and emotional status of
patients
 Obtain baseline vital signs, including
postural BP readings
 Obtain liver and renal function tests

181. 185
Nursing Implications (contd)
 Assess for possible contraindications to
therapy, cautious use, and potential drug
interactions
 Assess LOC, mental alertness, potential for
injury to self and others
 Check the patients mouth to make sure oral
doses are swallowed

182. 186
Nursing Implications (contd)
 Provide simple explanations about the
drug, its effects, and the length of time
before therapeutic effects can be
expected
 Abrupt withdrawal should be avoided
 Advise patients to change positions
slowly to avoid postural hypotension and
possible injury

183. 187
Nursing Implications (contd)
 The combination of drug therapy and psychotherapy
is emphasized because patients need to learn and
acquire more effective coping skills
 Only small amounts of medications should be
dispensed at a time to minimize the risk of suicide
attempts
 Simultaneous use of these drugs with alcohol or
other CNS depressants can be fatal

184. 188