Central Nervous System AgentsMa. Tosca Cybil A. Torres,

RN, MAN

CNS Stimulant

s

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 excitatoryprocesses 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

• 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

Respiratory CNS Stimulants

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

• 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

Nursing considerations

CNS Depressants

CNS Depressants: Classification

They are classified according to their pharmacological action into:

1- Sedative – hypnotics2- Anaesthetics

Sedative

-Hypnot

ics

• Sedation–Mildest form of CNS depression

–Diminishes physical and mental responses at lower dosages of certain CNS depressants but does not affect consciousness

Sleep Definition: Physiological depression of consciousnessSleep cycle:Starts with latency period → NREM → REM →

cycles of NREM alternate with REM (about 4 cycles)

NREM REM- Non rapid eye movement- Lasts for 90 min.- Thinking

- Rapid eye movement- Lasts for 20 min.- Dreaming

I- Sedative - HypnoticsDefinitions

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 HypnoticsMechanism 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

BarbituratesMOA:They have GABA like action → ↑ opening time

of chloride channels → ↑conductance of chloride ions → hyperpolarization

Classification:1-Long-acting2-Intermediate-acting3-Short acting4-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

sleeplessnessEstazolam(ProSom)- for treatment of insomia. Decreases

the frequency of nocturnal wakefulnessLorazepam(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, dizziness, 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 anesthesia1. 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