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Central
Nervous
System
Agents
Ma. Tosca Cybil A. Torres, RN,
           MAN
CNS
Stimulants
CNS stimulants are drugs
  which increase the muscular
  (motor) and the mental
  (sensory) activities
 Their effects vary from the
  increase in the alertness and
  wakefulness (as with
  caffeine) TO the production
  of convulsion ( as with
  strychnine) or death due to
  over stimulation
Behavioral Manifestations of CNS
 Stimulation
• mild elevation in alertness, decrease in
  drowsiness and lessening of fatigue
  (Analeptic Effect)
• increased nervousness and anxiety -
  convulsions.
Molecular Basis of CNS
          Stimulation
Imbalance between inhibitory and excitatory
processes as in the brain. This
  hyperexcitability of neurons results from:
• potentiation or enhancement of excitatory
  neurotransmission(e.g. amphetamine)
• depression or antagonism of inhibitory
  transmission (e.g. Strychnine)
• presynaptic control of neurotransmitter
  release (e.g. picrotoxin)
Classification of CNS
     Stimulants
      • Analeptic Stimulants
        – Respiratory Stimulants
        – Convulsants
      • Psychomotor Stimulant
        – Sympathomimetics or
          Adrenergic CNS Stimulants
      • Methylxanthines
Analeptic Stimulants
• diverse chemical class of agents
• majority can be absorbed orally
• have a short duration of action -
  primary expression of
  pharmacological effect is
  convulsions (tonic-clonic)
  uncoordinated
• pharmacological effect is
  terminated through hepatic
  metabolism
• Possible Common Mechanism of
  Action -ability to alter movement of
  chloride ions across neuronal
  membranes
Respiratory CNS
                  Stimulants
• Doxapram - used to counteract postanesthetic
  respiratory depression and for acute
  hypercapnia in chronic pulmonary disease.
  –   Used with caution with neonatal apnea
  –   Administered IV
  –   Onset of action: within 20-40 secs
  –   SE: (overdose)
       •   Hypertension
       •   Tachycardia
       •   Trembling
       •   convulsions
Headaches: Migraine and
Cluster  Migraine headaches-
             characterized by a unilateral
             throbbing head
             pain, accompanied by N/V
             and photophobia
           Cluster headaches-
             characterized by severe
             unilateral nonthrobbing pain
             usually located around the
             eye. Usually not associated
             with N/V
Preventive Treatment for
 migraine

1. Beta adrenergic blockers
2. Anticonvulsants- Valproic
   acid (Depakote)
3. Tricyclic antidepressants-
   amitriptyline (Elavil)
Treatment or Cessation of
          Attacks

• Ergotamine tartrate
  – Nonspecific serotonin agonist and
    vasoconstrictor
  – Should be taken early during a
    migraine attack
  – May cause N and V
• Triptans
  – The most common recently developed group of
    drugs for tx of migraines and cluster headches
  – Prototype: sumatriptan(Imitrex)
     • Selective serotonin receptor agonist with a short
       duration of action
     • Considered more effective than ergotamine
     • MOA: causes vasoconstriction of cranial carotid
       arteries to relieve migraine attacks
     • SE: dizziness, fainting, tingling, numbness, warm
       sensation, drowsiness
     • AR: hypotension, heart block, angina, MI, cardiac
       arrest
• Amphetamines
 – Stimulates the release of
   norepinephrine and dopamine from the
   brain and SNS.
 – Can cause euphoria and alertness
CHARACTERISTICS


• all compounds are absorbed well orally
• large portion of untransformed amphetamine is
  excreted unchanged in the urine.
  Consequently, acidifying the urine with ammonium
  chloride hastens its clearance, and thus reduces
  its reabsorption in the renal tubules.
• Overdose: hyperreflexia, tremors, convulsions and
  irritability
• CV problems: increased heart rate, increased
  BP, palpitations and cardiac dysrythmias
• Therapeutic Uses:
  – Narcolepsy
    • Characterized by falling asleep during waking hours,
      such as driving a car or talking with someone. Sleep
      paralysis, a condition that is normal during sleep
      usually accompanies narcolepsy which affects the
      voluntary muscles making the person unable to move
      and collapse
• Therapeutic uses:
  – Attention Deficit/Hyperactivity Disorder
    • May be caused by disregulation of
      serotonin, norepinephrine, and dopamine.
    • Occurs primarily in children, usually before
      the age 7, but may continue through
      teenage years.
    • Characteristics involved include
      inattentiveness, poor coordination, inability
      to concentrate, restlessness, hyperactivity
      (excessive and purposeless activity),
      inability to complete tasks, and impulsivity.
Pharmacological Actions

• The primary effects of an oral dose are
  wakefulness, alertness, decrease fatigue; mood
  elevation, increased ability to concentrate; an
  increase in motor and speech activity.
  Amphetamines also diminish the awareness of
  fatigue; person may push exertion to the point of
  severe damage or even death.
• Stimulate the respiratory center,
  especially when respiration is
  depressed by centrally acting drugs,
  (barbiturates and alcohol).
• Amphetamine can reverse the marked
  sedation and behavioral retardation
  resulting from reserpine-like drug.
• Depresses appetite by their action on
  the lateral hypothalamus rather than
  an effect on metabolic rate.
Mechanisms of Action

• Releases monoamines at synapses
  in the brain and spinal cord.
• Inhibits neuronal uptake of
  monoamine
• Antagonist at certain
  adrenoreceptors
• May inhibit monoamine oxidase.
Adverse Effects
• CNS:
  Euphoria, dizziness, tremor, irritability
  , insomnia, Convulsion (at higher
  doses), hyperthermia and coma
• C.V. Cardiac stimulation leads to
  headache, palpitations, cardiac
  arrhythmias, anginal pain
• Other: Weight loss, Psychotic
  Reaction which are often
  misdiagnosed as schizophrenia.
• Addiction - including psychic
  dependence, tolerance and physical
  dependence.
• Drug Interactions:
  – Tricyclic antidepressant
  – Antihypertensive Agents
  – Foods high in tyramine content
• Amphetamine-like Drugs or ADHD and
  Narcolepsy
  – Given to increase a child’s attention span and
    cognitive performance and decrease
    impulsiveness, hyperactivity and restlessness
  Prototype:
  – Methylphenidate(Ritalin)
  – Dexmethypendate (Focalin)
  – Pemoline (Cylert)
  – Modafinil(Provigil)- drug for nacolepsy which
    increases the amount of time that clients feel
    awake
Side Effects:
  anorexia, vomiting,
  diarrhea, insomnia,
  dizziness, nervousness,
  restlessness, irritability
Adverse reaction:
  tachycardia, growth
  suppression,
  palpitations, transient
  loss of weight in
  children, and increased
  hyperactivity
Nursing
 considerations:
• Monitor V/S. report
  irregularities
• Record height, weight, and
  growth of children
• Observe for withdrawal
  symptoms (N and V,
  weakness, and headache)
• Monitor for side effects
Nursing considerations
• Instruct client to take drug with meals
• Avoid alcohol consumption
• Encourage use of sugarless gum to relieve
  dryness of mouth
• Monitor weight twice a week
• Advise not to drive and use hazardous
  equipments when experiencing palpitation,
  nervousness, tremors
Nursing
considerations
 • Instruct client not to discontinue the drug
   abruptly
 • Advise not to eat foods with caffeine
 • Instruct to eat nutritious food because
   drug may cause anorexic effect
 • Teach to report drug side effects such as
   tachycardia and palpitations
CNS
Depressa
nts
CNS Depressants: Classification
     They are classified
       according to their
       pharmacological action
       into:
     1- Sedative – hypnotics
     2- Anaesthetics
e
      -
Hypnoti
    cs
• Sedation
 –Mildest form of CNS depression
 –Diminishes physical and mental
  responses at lower dosages of
  certain CNS depressants but
  does not affect consciousness
ep
Definition:
Physiological depression of consciousness
Sleep cycle:
Starts with latency period → NREM → REM →
  cycles of NREM alternate with REM (about 4
  cycles)
 NREM                        REM
 - Non rapid eye movement - Rapid eye movement
 - Lasts for 90 min.      - Lasts for 20 min.
 - Thinking               - Dreaming
I- Sedative - Hypnotics
 Definitions

 Sedatives:
 Drugs which calm the patient & cause sedation and in large
   doses cause sleep


 Hypnotics:
 Drugs which induce sleep that resembles the natural sleep

 Ex. Barbiturates
Sedative Hypnotics
Mechanism of Action
• The GABA receptor is a pentameric structure that
  forms a Cl- channel.

• The receptor complex includes distinct binding
  sites for benzodiazepines, barbiturates and
  GABA-like substances.

• GABA transmission exerts an inhibitory effect on
  norepinephrine (NE), dopamine (DA), serotonin
  (5-HT), and acetylcholine (ACh) pathways.
Sedative – hypnotics:
         Classification
                                     Sedative-hypnotics


Barbiturates                                                                Non-barbiturates


          1-Long acting (12-24 hr)
          Ex. Phenobarbital
                                                          Benzodiazepines                 Non- benzodiazepine


          2-Intermediate acting (8-12hr)
          Ex. Amobarbital


          3-Short acting (4-8 hr)
          Ex. Pentobarbital


          4-Ultrashort acting (0.5-1hr)
          Ex. Thiopental
Barbiturates
MOA:
They have GABA like action → ↑ opening time
  of chloride channels → ↑conductance of
  chloride ions → hyperpolarization


Classification:
1-Long-acting
2-Intermediate-acting
3-Short acting
4-Ultrashort acting
• Barbiturates
  – Prototype:
     • Short acting: pentobarbital
       sodium(Nembutal sodium) – for
       sedation, sleep, or preanesthetic
     • Intermediate acting: amobarbital
       sodium(Amytal sodium)- sedative
       and short term hypnotic, to control
       acute convulsive episodes, and for
       insomia
     • Long acting: phenobarbital and
       mephobarbital-used to control
       seizures
     • Ultrashort-acting: thiopental
       sodium- used as a general
       anesthetic
Nursing Responsibilities:
• Recognize that continued use of
  barbiturate might result in drug abuse
• Monitor V/S, esp. RR and BP
• Raise side rails
• Check for rashes
• Administer phenobarbital IV at a rate of
  less than 50mg/min. do not mix with other
  medications. If to be given IM, use large
  muscle such as the gluteus max
Client teaching
  • Teach client the use on non pharmacological
    ways to induce sleep----enjoying a warm bath,
    listening to music, drinking warm fluids, and
    avoiding drinks with caffeine 6hrs before
    bedtime
  • Instruct to avoid alcohol and antidepressants,
    antipsychotics, and narcotic drugs----
    respiratory depression
  • Avoid taking herbs
  • Advise not to drive or operate a machinery
  • Instruct to take 30mins before bedtime
Benzodiazepines
• Can suppress stage 4 of NREM sleep, which may result
  in vivid dreams or nightmares and can delay REM sleep.
• Effective for sleep disorders for several weeks longer
  than other sedative-hypnotics but should not be longer
  than 3-4 weeks as a hypnotic to prevent REM rebound
Prototype:
Alprazolam(Xanax)- for alleviating anxiety that may cause
  sleeplessness
Estazolam(ProSom)- for treatment of insomia. Decreases
  the frequency of nocturnal wakefulness
Lorazepam(Ativan)-used as a pre operative sedative and
  to reduce anxiety
Nonbenzodiazepines
    used for short term treatment of insomia
    Well absorbed PO, onset 7-27 minutes
MOA: depression of the CNS, neurotransmitter
 inhibition

Prototype:
   zolpidem(Ambien)
S/E:
   drowsiness, lethargy, hangover, irritability, dizzine
   ss, anxiety
Adverse reactions:
tolerance, physiologic dependence
• Nursing responsibilities:
  – Monitor V/S. check for respiratory depression
  – Raise side rails
  – Observe for side effects (hangover, light-
    headedness, dizziness, or confusion)
  – Teach non pharmacological ways to induce
    sleep
  – Suggest to urinate before taking sedative
    hypnotics to prevent sleep disruption
  – Instruct to avoid alcohol and antidepressants,
    antipsychotics, and narcotic drugs----
    respiratory depression
Anaesthetics
Definition:
Drugs which cause unconsciousness &
  generalized loss of pain sensation, thus
  allow surgical procedures to be carried out
Classified as general and local
Ex. thiopental (IV) , halothane (inhalation)

MOA:
Interfering with propagation of nerve impulses
  by interfering with electrolytes movement
  through the cell membrane
General anesthesia
• Is a reversible loss of consciousness induced by
  inhibiting neuronal impulses in several areas of the
  central nervous system
• General anesthetics are agents that block the pain
  stimulus at the cortex

Produces a state of the ff:
 Analgesia
 Amnesia
 Unconsciousness characterized by loss of reflexes
  and muscle tone
Local anesthesia
•    Injection of a solution containing anesthetic
     into the tissues at the planned incision site.
•    Briefly disrupts sensory nerve impulse
     transmission form a specific body area or
     region.
Types of Local anesthesia
1.   Topical anesthesia – topical agents are
     applied directly to the area of skin or mucous
     membrane surfaced to be anesthetized

2.   Local infiltration – is the injection of an
     anesthetic agent directly into the tissue
     around an incision, wound, or lesion.
Purposes of Anesthesia

• To produce muscle relaxation
• To produce analgesia
• To produce artificial sleep or to cause loss
  of consciousness
• To block transmission of nerve impulses
• To suppress reflexes
• Nursing responsibilities:
  – Monitor client’s postoperative state of
    sensorium.
  – Check preoperative and postoperative urine
    output
  – Record V/S after induction of anesthesia----
    may result to hypotension and respiratory
    distress
  – Administer an analgesic or a narcotic-
    analgesic with caution until client fully
    recovers from the anesthetic

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Central Nervous System Agents

  • 3. CNS stimulants are drugs which increase the muscular (motor) and the mental (sensory) activities  Their effects vary from the increase in the alertness and wakefulness (as with caffeine) TO the production of convulsion ( as with strychnine) or death due to over stimulation
  • 4. Behavioral Manifestations of CNS Stimulation • mild elevation in alertness, decrease in drowsiness and lessening of fatigue (Analeptic Effect) • increased nervousness and anxiety - convulsions.
  • 5. Molecular Basis of CNS Stimulation Imbalance between inhibitory and excitatory processes as in the brain. This hyperexcitability of neurons results from: • potentiation or enhancement of excitatory neurotransmission(e.g. amphetamine) • depression or antagonism of inhibitory transmission (e.g. Strychnine) • presynaptic control of neurotransmitter release (e.g. picrotoxin)
  • 6. Classification of CNS Stimulants • Analeptic Stimulants – Respiratory Stimulants – Convulsants • Psychomotor Stimulant – Sympathomimetics or Adrenergic CNS Stimulants • Methylxanthines
  • 7. Analeptic Stimulants • diverse chemical class of agents • majority can be absorbed orally • have a short duration of action - primary expression of pharmacological effect is convulsions (tonic-clonic) uncoordinated • pharmacological effect is terminated through hepatic metabolism • Possible Common Mechanism of Action -ability to alter movement of chloride ions across neuronal membranes
  • 8. Respiratory CNS Stimulants • Doxapram - used to counteract postanesthetic respiratory depression and for acute hypercapnia in chronic pulmonary disease. – Used with caution with neonatal apnea – Administered IV – Onset of action: within 20-40 secs – SE: (overdose) • Hypertension • Tachycardia • Trembling • convulsions
  • 9. Headaches: Migraine and Cluster Migraine headaches- characterized by a unilateral throbbing head pain, accompanied by N/V and photophobia Cluster headaches- characterized by severe unilateral nonthrobbing pain usually located around the eye. Usually not associated with N/V
  • 10. Preventive Treatment for migraine 1. Beta adrenergic blockers 2. Anticonvulsants- Valproic acid (Depakote) 3. Tricyclic antidepressants- amitriptyline (Elavil)
  • 11. Treatment or Cessation of Attacks • Ergotamine tartrate – Nonspecific serotonin agonist and vasoconstrictor – Should be taken early during a migraine attack – May cause N and V
  • 12. • Triptans – The most common recently developed group of drugs for tx of migraines and cluster headches – Prototype: sumatriptan(Imitrex) • Selective serotonin receptor agonist with a short duration of action • Considered more effective than ergotamine • MOA: causes vasoconstriction of cranial carotid arteries to relieve migraine attacks • SE: dizziness, fainting, tingling, numbness, warm sensation, drowsiness • AR: hypotension, heart block, angina, MI, cardiac arrest
  • 13. • Amphetamines – Stimulates the release of norepinephrine and dopamine from the brain and SNS. – Can cause euphoria and alertness
  • 14. CHARACTERISTICS • all compounds are absorbed well orally • large portion of untransformed amphetamine is excreted unchanged in the urine. Consequently, acidifying the urine with ammonium chloride hastens its clearance, and thus reduces its reabsorption in the renal tubules. • Overdose: hyperreflexia, tremors, convulsions and irritability • CV problems: increased heart rate, increased BP, palpitations and cardiac dysrythmias
  • 15. • Therapeutic Uses: – Narcolepsy • Characterized by falling asleep during waking hours, such as driving a car or talking with someone. Sleep paralysis, a condition that is normal during sleep usually accompanies narcolepsy which affects the voluntary muscles making the person unable to move and collapse
  • 16. • Therapeutic uses: – Attention Deficit/Hyperactivity Disorder • May be caused by disregulation of serotonin, norepinephrine, and dopamine. • Occurs primarily in children, usually before the age 7, but may continue through teenage years. • Characteristics involved include inattentiveness, poor coordination, inability to concentrate, restlessness, hyperactivity (excessive and purposeless activity), inability to complete tasks, and impulsivity.
  • 17. Pharmacological Actions • The primary effects of an oral dose are wakefulness, alertness, decrease fatigue; mood elevation, increased ability to concentrate; an increase in motor and speech activity. Amphetamines also diminish the awareness of fatigue; person may push exertion to the point of severe damage or even death.
  • 18. • Stimulate the respiratory center, especially when respiration is depressed by centrally acting drugs, (barbiturates and alcohol). • Amphetamine can reverse the marked sedation and behavioral retardation resulting from reserpine-like drug. • Depresses appetite by their action on the lateral hypothalamus rather than an effect on metabolic rate.
  • 19. Mechanisms of Action • Releases monoamines at synapses in the brain and spinal cord. • Inhibits neuronal uptake of monoamine • Antagonist at certain adrenoreceptors • May inhibit monoamine oxidase.
  • 20. Adverse Effects • CNS: Euphoria, dizziness, tremor, irritability , insomnia, Convulsion (at higher doses), hyperthermia and coma • C.V. Cardiac stimulation leads to headache, palpitations, cardiac arrhythmias, anginal pain • Other: Weight loss, Psychotic Reaction which are often misdiagnosed as schizophrenia. • Addiction - including psychic dependence, tolerance and physical dependence.
  • 21. • Drug Interactions: – Tricyclic antidepressant – Antihypertensive Agents – Foods high in tyramine content
  • 22. • Amphetamine-like Drugs or ADHD and Narcolepsy – Given to increase a child’s attention span and cognitive performance and decrease impulsiveness, hyperactivity and restlessness Prototype: – Methylphenidate(Ritalin) – Dexmethypendate (Focalin) – Pemoline (Cylert) – Modafinil(Provigil)- drug for nacolepsy which increases the amount of time that clients feel awake
  • 23. Side Effects: anorexia, vomiting, diarrhea, insomnia, dizziness, nervousness, restlessness, irritability Adverse reaction: tachycardia, growth suppression, palpitations, transient loss of weight in children, and increased hyperactivity
  • 24. Nursing considerations: • Monitor V/S. report irregularities • Record height, weight, and growth of children • Observe for withdrawal symptoms (N and V, weakness, and headache) • Monitor for side effects
  • 25. Nursing considerations • Instruct client to take drug with meals • Avoid alcohol consumption • Encourage use of sugarless gum to relieve dryness of mouth • Monitor weight twice a week • Advise not to drive and use hazardous equipments when experiencing palpitation, nervousness, tremors
  • 26. Nursing considerations • Instruct client not to discontinue the drug abruptly • Advise not to eat foods with caffeine • Instruct to eat nutritious food because drug may cause anorexic effect • Teach to report drug side effects such as tachycardia and palpitations
  • 28. CNS Depressants: Classification They are classified according to their pharmacological action into: 1- Sedative – hypnotics 2- Anaesthetics
  • 29. e - Hypnoti cs
  • 30. • Sedation –Mildest form of CNS depression –Diminishes physical and mental responses at lower dosages of certain CNS depressants but does not affect consciousness
  • 31. ep Definition: Physiological depression of consciousness Sleep cycle: Starts with latency period → NREM → REM → cycles of NREM alternate with REM (about 4 cycles) NREM REM - Non rapid eye movement - Rapid eye movement - Lasts for 90 min. - Lasts for 20 min. - Thinking - Dreaming
  • 32. I- Sedative - Hypnotics Definitions Sedatives: Drugs which calm the patient & cause sedation and in large doses cause sleep Hypnotics: Drugs which induce sleep that resembles the natural sleep Ex. Barbiturates
  • 33. Sedative Hypnotics Mechanism of Action • The GABA receptor is a pentameric structure that forms a Cl- channel. • The receptor complex includes distinct binding sites for benzodiazepines, barbiturates and GABA-like substances. • GABA transmission exerts an inhibitory effect on norepinephrine (NE), dopamine (DA), serotonin (5-HT), and acetylcholine (ACh) pathways.
  • 34. Sedative – hypnotics: Classification Sedative-hypnotics Barbiturates Non-barbiturates 1-Long acting (12-24 hr) Ex. Phenobarbital Benzodiazepines Non- benzodiazepine 2-Intermediate acting (8-12hr) Ex. Amobarbital 3-Short acting (4-8 hr) Ex. Pentobarbital 4-Ultrashort acting (0.5-1hr) Ex. Thiopental
  • 35. Barbiturates MOA: They have GABA like action → ↑ opening time of chloride channels → ↑conductance of chloride ions → hyperpolarization Classification: 1-Long-acting 2-Intermediate-acting 3-Short acting 4-Ultrashort acting
  • 36. • Barbiturates – Prototype: • Short acting: pentobarbital sodium(Nembutal sodium) – for sedation, sleep, or preanesthetic • Intermediate acting: amobarbital sodium(Amytal sodium)- sedative and short term hypnotic, to control acute convulsive episodes, and for insomia • Long acting: phenobarbital and mephobarbital-used to control seizures • Ultrashort-acting: thiopental sodium- used as a general anesthetic
  • 37. Nursing Responsibilities: • Recognize that continued use of barbiturate might result in drug abuse • Monitor V/S, esp. RR and BP • Raise side rails • Check for rashes • Administer phenobarbital IV at a rate of less than 50mg/min. do not mix with other medications. If to be given IM, use large muscle such as the gluteus max
  • 38. Client teaching • Teach client the use on non pharmacological ways to induce sleep----enjoying a warm bath, listening to music, drinking warm fluids, and avoiding drinks with caffeine 6hrs before bedtime • Instruct to avoid alcohol and antidepressants, antipsychotics, and narcotic drugs---- respiratory depression • Avoid taking herbs • Advise not to drive or operate a machinery • Instruct to take 30mins before bedtime
  • 39. Benzodiazepines • Can suppress stage 4 of NREM sleep, which may result in vivid dreams or nightmares and can delay REM sleep. • Effective for sleep disorders for several weeks longer than other sedative-hypnotics but should not be longer than 3-4 weeks as a hypnotic to prevent REM rebound Prototype: Alprazolam(Xanax)- for alleviating anxiety that may cause sleeplessness Estazolam(ProSom)- for treatment of insomia. Decreases the frequency of nocturnal wakefulness Lorazepam(Ativan)-used as a pre operative sedative and to reduce anxiety
  • 40. Nonbenzodiazepines  used for short term treatment of insomia  Well absorbed PO, onset 7-27 minutes MOA: depression of the CNS, neurotransmitter inhibition Prototype: zolpidem(Ambien) S/E: drowsiness, lethargy, hangover, irritability, dizzine ss, anxiety Adverse reactions: tolerance, physiologic dependence
  • 41. • Nursing responsibilities: – Monitor V/S. check for respiratory depression – Raise side rails – Observe for side effects (hangover, light- headedness, dizziness, or confusion) – Teach non pharmacological ways to induce sleep – Suggest to urinate before taking sedative hypnotics to prevent sleep disruption – Instruct to avoid alcohol and antidepressants, antipsychotics, and narcotic drugs---- respiratory depression
  • 42. Anaesthetics Definition: Drugs which cause unconsciousness & generalized loss of pain sensation, thus allow surgical procedures to be carried out Classified as general and local Ex. thiopental (IV) , halothane (inhalation) MOA: Interfering with propagation of nerve impulses by interfering with electrolytes movement through the cell membrane
  • 43. General anesthesia • Is a reversible loss of consciousness induced by inhibiting neuronal impulses in several areas of the central nervous system • General anesthetics are agents that block the pain stimulus at the cortex Produces a state of the ff:  Analgesia  Amnesia  Unconsciousness characterized by loss of reflexes and muscle tone
  • 44. Local anesthesia • Injection of a solution containing anesthetic into the tissues at the planned incision site. • Briefly disrupts sensory nerve impulse transmission form a specific body area or region. Types of Local anesthesia 1. Topical anesthesia – topical agents are applied directly to the area of skin or mucous membrane surfaced to be anesthetized 2. Local infiltration – is the injection of an anesthetic agent directly into the tissue around an incision, wound, or lesion.
  • 45. Purposes of Anesthesia • To produce muscle relaxation • To produce analgesia • To produce artificial sleep or to cause loss of consciousness • To block transmission of nerve impulses • To suppress reflexes
  • 46. • Nursing responsibilities: – Monitor client’s postoperative state of sensorium. – Check preoperative and postoperative urine output – Record V/S after induction of anesthesia---- may result to hypotension and respiratory distress – Administer an analgesic or a narcotic- analgesic with caution until client fully recovers from the anesthetic