Autonomic Nervous System Agents

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AUTONOMIC NERVOUS SYSTEM AGENTS

SYMPATHETIC NERVOUS SYSTEM

Aka. adrenergic system

Neurotransmitter: Norepinephrine

Adrenergic receptor organ cells alpha1,

alpha2, beta1 and beta2

Parasympathetic nervous system

Aka. cholinergic system

Neurotransmitter: acetyl choline

Cholinergic receptors organ cells Ni cotini c and

Muscarini c (stimulated by alkaloid nicotine and

muscarine)

Acetyl cholinester ase enzyme that

inactivates acetylcholine before reaching

receptor cell

Drugs that mimics SNS and PNS

Sympathetic Stimulants ParasympatheticStimulants

A. Sympathomimetics(adrenergic or adrenergicagonists)

A.P arasympathomimetics (cholinergic or cholinergicagonists)

1. Increase BP 1. Decrease BP

2. Increase PR 2. Decrease PR 3. Relax bronchioles 3. Constricts bronchioles 4. Dilate pupils 4. Constrict pupils

5. Relax uterine muscles

5. Increase urinarycontraction

6. Increase blood sugar 6. Increase peristalsis

SympatheticDepressants Parasympathetic

Depressants

B. Sympatholytics (adrenergic blockeror adrenergicantagonists)

B. P arasympatholytics(anticholinergics orcholinergicantagonists, orantispasmodics)

1. Decrease PR 1. Increase PR

2. Decrease BP 2. Decrease mucussecretions

3. Constrictbronchioles 3. Decrease GIT

motility 4. Increase urinaryretention 5. Dilates pupils

Adrenergics and adrenergic blockers

Adrenergics (sympathomimetics)

Adrenergic blockers (sympatholytics)

A. Adrenergics

Aka.

1. Adrenergi c agoni st s stimulates SNS

2. sympathomimeti cs mimics the SNS

neurotransmitters

Act on adrenergic receptor sites heart,

bronchiole walls, GIT, urinary bladder and ciliary

muscles of the eye

Adrenergic receptor sites alpha 1, alpha2,

bet a1 and bet a2

Effects of Adrenergics at Receptors

Alpha1 Increases force of heart contraction

Vasoconstriction (Increases blood pressure)

Decrease saliv ary gl and secretions

Increases urinary bl adder relaxation

Alpha2

Inhibits release of norepinephrine

Dilates blood vessels (hypotension)

Decreases GIT motility

Bet a1

Increases heart rate/force of contraction Increases renin secretion(increasing BP)

Bet a2

Dilates bronchioles

Gastrointestinal and uterine relaxation

Increase blood sugar (glycogenolysis)

Increase blood flow to the skeletal muscles

Inactivation of Neurotransmitters

Action of NT must be stopped to prevent

prolonging the effectInactiv ated through:

1. Reu pt ak e of the tr ansmitter back into the neuron

2. Enzymati c tr ans formation or degr ad ation

Monoamine oxidase (MAO) and catechol-O-

methyltransferase (COMT)

3. Diff usion away from the receptor

Classification of Sympathomimetics



A. Direct-acting sympathomimetics

Directly stimulate the adrenergic receptors

E.g. epinephrine or norepinephrine

B. Indirect-acting sympathomimetics

Stimulates the release of norepinephrine from

the terminal nerve endings

E.g. amphetamine

C. Mixed-acting sympathomimetics Stimulate the adrenergic receptor sites

stimulates the release of norepinephrine from

the terminal nerve endings

E.g. Ephedrine

Adrenergic drugs

1. Epinephrine (adrenalin)

Mode of action: acts on adrenergic sites(alpha 1, beta 1

& beta2), promotes CNS/cardiac stimulation and

bronchodilationPharmacok ineti cs

ROUTE: SQ, IV, topical, inhalation, intracardiac,

instillation

Not given orally (rapidly metabolized in the GI

tract/liver)

Metabolized in the liver and excreted in the

urine

Pharmacodynami cs

Frequently used in emergencies to treat

anaphylaxis

A potent inotropic drug (strengthen myocardial

contraction)

ACTION of Epinephrine:

1. Increases CO

2. Vasoconstriction

3. Elevates SBP

4. Increases HR

5. bronchodilation

High doses can result in cardi ac dy srhythmi as

(monitor ECG)

Onset/peak concentration times are rapid

Epinephrine with digoxin cardiac

dysrhythmias

Drugs that decreases the action of epinephrine:

1. beta-blockers

2. tricyclic antidepressants (TCA)

3. MAO inhibitors

T her a peuti c use/effect s

Treats

1. allergic reaction

2. anaphylaxis

3. bronchospasm

4. cardiac arrest

Side effect s

Anorexia, nausea, vomiting, nervousness,

tremors, agitation, headache, pallor, insomnia,

syncope, dizziness

Adver se reaction

Palpitations

Tachycardia

Dyspnea

Life-threatening Ventricular fibrillation,

pulmonary edema

C ontr aindi cation

Cardiac dysrhythmias

Pregnancy Cardiogenic shock

Hypertension

Hyperthyroidism

DM

2. ephedrine

Ephedrine HCL, ephedrine sulfate

T r ade names: Ephedsol, Ectasule

Acts on alpha1, beta1 and beta 2 receptors

Route: PO, SQ and IV T her a peuti c use

Treats hypotensive states

Bronchospasm

Orthostatic hypotension

Mild cases of asthma

3. Norepinephrine bitartrate

T r ade names: Levarterenol, Levophed

Acts on alpha1 and beta1

Given IV incorporated in D5W

Increases BP and CO

T her a peuti c use

Shock

Nur sing consider ation

BP monitoring every 2-5 min during infusion

4. Dopamine hcl

T r ade name: Intropin

Acts on alpha1 and beta1

Given PO and IV

T her a peuti c use

Correct hypotension

5. midodrine

T r ade name: ProAmatine

Given PO

Acts on alpha1

T her a peuti c use

Treat symptomatic orthostatic hypotension (BP

increases by 15-30 mm Hg in 1 hr)

5. Phenylephrine hcl

Trade name: Neo-Synephrine

Nasal decongestant

Given via nasal instillation

Acts on alpha receptors

T her a peuti c use

Nasal congestion



Common colds

Sinusitis and allergic rhinitis


Have the client blow the nose before

administration

6. Pseudoephedrine hcl

T r ade name: Sudafed, Actifed, Co-Tylenol,Pediacare

acts on alpha and beta2

Nasal decongestant

Given PO

T her a peuti c use

Nasal congestion


Avoid taking with hx of hypertension, cardiac

disease, DM

7. Phenylpropanolamine hcl

T r ade name: Dimetapp, Dristan, Triaminicol,

Triaminic

Given PO

Nasal decongestant

T her a peuti c use

Nasal congestion

8. Metaproterenol sulfate

Trade name: Alupent, Metaprel

Acts on beta1 (increased heart rate) and beta2

(bronchodilation)

Given PO

T her a peuti c use

Bronchospasm

Acute heart block

9. Dobutamine hcl

T r ade name: Dobutrex

Acts on beta1

Given IV

T her a peuti c use

Cardiac decompensation/Cardiogenic shock

(enhance cardiac contractility, SV & CO)

10. Isoetharine hcl

T r ade name: Bronko-sol

Acts on beta2

Given via inhalation

T her a peuti c use

Asthma and COPD (dilates bronchial tubes)

11. Terbutaline sulfate

T r ade name: Brethine, Brethaire, Bricanyl

Acts on beta2

Given PO and inhalation

T her a peuti c use

Bronchospasm (primary use)

Prevents premature birth during pregnancy

12. Ritodrine hcl

T r ade name: Yutopar

Acts on beta2 and beta1

Given PO and IV

T her a peuti c use

Decrease/stop uterine contraction

13. Albuterol

Beta2 adrenergic agonist

Mode of action: stimulates beta2 adrenergic

receptors in the lungs relaxation of bronchial

smooth muscles

T r ade name: Proventil, Salbutamol, Ventolin,

Novo-Salmol

Response bronchodilation

Given for asthmatic patient High doses may affect beta1 receptors

increase HR

Side effect s

tremors, restleness and nervousness

Adver se reactions

Palpitations, reflex tachycardia, hallucinations

Life-threatening: cardiac dysrhythmias

T her a peuti c Use

Treats bronchospasm, asthma, bronchitis and

other COPD

14. Clonidine & Methyldopa

Clonidine (Catapres)

Methyldopa (Aldomet)

Selective alpha2 adrenergic drugs used to treat

hypertension

Mode of action: inhibits the release of

norepinephrine and produces cardiovascular

depression decreasing BP

Nursing considerations (Adrenergics)

Record client VS

Report signs of increasing BP and HR

Monitor BP every 3-5 minutes when giving

alpha Adrenergics IV

Report side effects:

t achy cardi a, palpit ations, tremor s,

dizziness and increased blood pressure

Check urinary output and assess bladder

distension (urinary retention)

For cardiac resuscitation, epinephrine given

1mg/ml diluted in 10 ml of saline solution

Monitor IV site frequently when administering

norepinephrine bit artr ate (Levarterenol) or

dopamine (Intropin) because infiltration from

these cause ti ssue necrosi s



ANTIDOT E for norepinephrine (Levophed) and

dopamine is phentol amine mesyl ate (Regitine)

5-10mg, diluted in 10-15ml of saline

Offer food to avoid nausea and vomiting

Evaluate blood glucose levels

B. Adrenergic blockers (symphatholytics) Aka. Adrenergi c ant agoni st or sympatholyti cs

Blocks the effect of the adrenergic

neurotransmitters either by

1. directly occupying the alpha or beta

receptors or

2. inhibiting the release the release of

the neurotransmitters (norepinephrine and

epinephrine)

Effects of adrenergic blockers at receptors

Alpha 1 Vasodilation (decrease BP)

Miosis

Reflex tachycardia

Bet a 1

Decreases HR

Reduces force of contraction

Bet a 2

Constricts bronchioles

Contracts uterus

Decrease blood sugar (inhibits glycogenolysis)

Alpha adrenergic blockers

Block or inhibit a response at the alpha

adrenergic receptor sites

2 groups

a. Selective alpha block er s block alpha

1

b. Nonselective alpha block er s blocks

alpha 1 and alpha 2

EFFE CT S

1. Promotes vasodilation (decreasing

BP/ Orthostatic hypotension)

2. increase PR (compensatory

mechanism)

T her a peuti c use

a. used to treat peripheral vascular

disease e.g. Raynauds phenomenon, Buergers disease

E.g. tolazoline (Priscoline),

phentolamine mesylate (Regitine)

doxazoson mesylate (cardura)

prazoson HCL (Minipress)

terazosin HCL (Hytrin)

Beta adrenergic blockers

Aka. Bet a-block er s

Blocks beta adrenergic receptors sites

Decreases HR and BP

2 groups

a. Nonselective bet a block er s blocks

both beta 1 and beta 2 receptors

b. Selective beta blockers - blocks beta

1 receptors

Therapeutic use

1. cardiac dysrhythmias

2. mild hypertension

3. mild tachycardia4. angina pectoris

Side effects:

1. bradycardia

2. palpitations

3. hypotension

4. headache

5. dizziness

6. hyperglycemia

7. bronchospasm

Nonselective beta blockers

Prototype dr ugs: carvedilol (Coreg), labetalol

(Normodyne, Trandate), carteolol (Cartrol), penbutolol

(Levatol), propanolol HCL (Inderal), nadolol (Corgard),

pindolol (Visken), sotalol (Betapace), timolol maleate

(Blocadren)

Selective beta blockers

Prototype dr ugs: metoprolol (Lopressor), atenolol

(Tenormin), acebutol HCL (Secretal), Betaxolol

(Kerlone), bisoprolol fumarate (Zebeta), esmolol HCL

(Brevibloc)

C. Cholinergics (parasymphathomimetics)

Aka. Cholinergic stimulants, cholinergic agonists

Stimulate the parasympathetic nervous system

by mimicking the neurotransmitter

acetylcholine

Acetyl choline ( Ach) a neurotransmitter

located at the ganglions and the

parasympathetic terminal nerve endings

C holinergi c receptor s sites

1. Muscarinic receptors

Stimulate smooth muscle (GIT, GUT, glands,

heart) and slow heart rate

2. Nicotinic receptors (neuromuscular) which affect

skeletal muscles

2 types of Cholinergic drugs

1. Direct -acting cholinergi c dr ugs acts on receptors to

activate a tissue response

2. Indirect -acting cholinergi c dr ugs inhibit the action

of the enzyme cholinester ase

( C hE)/ acetyl cholinester ase( AC hE) to permit

acetylcholine to attach to the receptor sites



Effects of cholinergic drugs

C ardiov ascul ar : decrease HR, lower blood

pressure (vasodilation)

GIT : increase peristalsis

GUT : urinary bladder contraction

Ocul ar: pupil constriction (miosis)

Lung: bronchial constriction

Saliv ary gl and s: increase salivation muscle: maintains muscle strength (increase

neuromuscular transmission)

Direct acting cholinergics

Primarily selective to muscarinic receptors but

nonspecific (GIT, GUT, glands, heart)

Prototype dr ugs:

1. betanechol (Urecholine)- promotes urination

2. metoclopromide (Reglan) GERD, increases

gastric emptying time2. carbachol (Miostat), pilocarpine HCL (Pilocar)

reduce IOP, miosis

Side effect s: gastric pain/cramping, diarrhea,

increase salivary and bronchial secretions,

bradycardia, orthostatic hypotension

Indirect acting cholinergics

Aka. C holinester ase inhi bitor s,

acetyl cholinester ase inhi bitor s,

anti cholinester ase

Do not act on receptors

Binds with cholinesterase to allow acetylcholine

to activate muscarinic and nicotinic cholinergic

receptors

inhibit or inactivate enzyme cholinesterase,

permitting acetylcholine to accumulate at the

receptor sites

increases skeletal muscle contraction

T her a peuti c use:

1. Primarily used to treat my astheni a

gr avi s (neuromuscular disorder)

2. glaucoma

3. Alzheimers disease

Side effect s: increase GIT motility, bradycardia,

miosis, bronchial constriction and increase

urination

Prototype dr ugs:

demecarium bromide (Humorsol),

echothiophate iodide (Phospholine iodide),

isoflurophate (Floropryl) used to reduced IOP in

glaucoma

2 types of indirect acting:

1. Reversible Cholinesterase Inhibitors

Binds with enzyme cholinesterase for several

minutes to hours

Mode of action

1. Prod uce pu pill ary constri ction in the treatment of

gl aucoma

Prototype: phy sostigmine sali cyl ate ( E serine

Sali cyl ate)

2. Increase muscle strength in client w ith

my astheni a gr avi s

Prototype dr ugs:

Neostigmine (Prostigmin-short acting),pyridostigmin bromide (Mestinon-moderate acting),

ambenonium chloride (Mytelase- long acting),

edrophonium chloride (Tensilon-short acting for

diagnostic purposes)

2. Irreversible Cholinesterase Inhibitors

Bind with the enzyme permanently (long lasting

effect)

Used to produce pupillary constriction and to

manufacture organophosphate ANTIDOT E : pralidoxime (Protopam)

Nursing considerations

Monitor VS (HR/ BP)

Record fluid intake and output

Give cholinergics 1 hour before or 2 hours after

meals

Observe for side effects: cramping, diarrhea,

increase salivation and bronchial secretions,

bradycardia, orthostatic hypotension

Auscultate breath sounds for rales (crackling

sounds)

ANTIDOT E : atropine sulfate for cholinergic

overdose

Early signs of overdose: salivation, sweating,

abdominal cramps and flushing

For indirect acting drugs: monitor for

cholinergi c cri si s (overdose) muscular

weakness and increased salivation

D. Anticholinergics (Parasympatholytics)

Aka. Cholinergic blocking agents, cholinergic

antagonists, antispasmodics, muscarinic

antagonist

Inhibits the action of acetylcholine by occupying

the acetylcholine receptors - Blocking the PS

nerves producing SNS-like effects

Maj or res ponses to Anti cholinergi cs

1. decrease GIT motility

2. decrease salivation

3. mydriasis

4. increase pulse rate

5. decrease bladder contraction

6. decrease muscle rigidity and tremors

7. dilates bronchial airway

Antidote for Cholinesterase inhibitors

organophosphate ingestion

Prototype drugs:



- atropine sulf ate

- propantheline bromide (Pro-Banthine)

antispasmodic for peptic ulcer

- scopol amine hydrobromide

preanesthetic/motion sickness/IBS

- cy clopentol ate HC L (Cyclogyl) - mydriasis

Atropine sulfate Classic anticholinergic

Act on muscarinic receptor, but have little

effect on nicotinic receptor

Main use:

1. preoperative medication- decrease

saliv ary secretions

2. antispasmodic drug peptic ulcers,

relaxes smooth muscles of the GIT/decreasing

peri st al si s

3. increases heart r ate for bradycardicpatient

Pharmacok ineti cs

Well absorbed orally/parentally

Crosses BBB (CNS)

Has short half-life(little cumulative effect)

Mostly excreted in the kidneys

Pharmacodynami cs

Blocks acetylcholine by occupying muscarinic

receptor

Increases heart rate by blocking vagus

stimulation

Promotes pupil dilation by relaxing iris sphincter

Frequently used to decrease saliv ation and

res pir atory secretions preoper atively

Treat sinus bradycardia by increasing heart rate

Side effect s / Adver se reactions

Dry mouth

Decrease perspiration

Blurred vision

T achy cardi a

Constipation

Urinary retention

Nausea

Headache

Dry skin

Abdominal distention

Photophobia

coma

Neurologic and neuromuscular agents

Central nervous system stimulants

1. amphetamines

Stimulates release of the neurotransmitters

norepinephrine and dopamine from the brain

and the SNS.

Causes eu phori a and alertness; but causes

sleeplessness, restlessness, tremors and

irritability.

Continuous use may results to cardiovascular

problems - increased HR , palpit ations, cardi ac

dy srhythmi as, and increased BP

Acidic urine excretes amphetamines faster than

alkaline urine Given for nar colepsy , and in some cases for

ADHD( Attention defi cit hyper activity di sorder)

Side Effects & Adverse Reactions

Restlessness, insomnia, tachycardia, hypertension,

heart palpitations, dry mouth, anorexia, weight loss,

diarrhea, or constipation, and impotence

Amphetamine-likeDrugs for ADHD and Narcolepsy

Attention-deficit/hyperactivity

disorder (ADHD) caused by a dysregulation of the

neurotransmitters serotonin , norepinephrine ,

and dopamine

Occurs primarily in children usually before 7

years old

3-7 times more common in boys than girls

Characteristic behaviors include

1. Inattentiveness,

2. inability to concentr ate ,

3. restlessness,

4. hyper activity ,

5. inability to complete t asks, and

6. impul sive ,

7. poor coordination

N arcolepsy

Characterized by falling asleep during the

normal waking activities such as driving a car or

talking with someone

Sleep par aly si s - muscle paralysis that is normal

during sleep, usually accompanies narcolepsy

and affects the voluntary muscles

1. Methylphenidate (Ritalin) and demethylphenidate

(Focalin)

amphetamine-like drugs

Given to increase the childs attention-span and

cognitive performance (memory, reading) and

decrease impulsiveness, hyperactivity and

restleness

Methylphenid ate( Rit alin) most commonly

prescribed to treat ADHD and also used to treat

narcolepsy

Pharmacok ineti cs

well absorbed in the GI mucosa

Usually administered twice a day before

breakfast and lunch



given 30-45 minutes before meals for better

absorption

not be given within 6 hours before sleep

because it may cause insomni a

Side effect s

Insomnia, restlessness, nervousness, tremors,

irritability, tachycardia, elevated blood pressure

Pharmacodynami cs

Corrects ADHD by decreasing hyperactivity and

improving attention span

Amphetamines are generally avoided because

of higher potential for abuse, habituation, and

tolerance

sympathomimetics enhance the actions of

methylphenidate

Antihypertensives and barbiturates can

decrease the action of these drugs Foods that contain caffeine should be avoided

because they increase drug action

2. Modafinil (Provigil)

a new drug for narcolepsy

Increases the amount of time that clients with

narcolepsy feel awake

Does not disrupt night time sleep

Side effect s: headaches, nausea, diarrhea and

nervousness

Anorexiants

Appetite suppressants usually for obesity

Prototype dr ugs:

1. Amphet amines

Considered once as anorexiants for short-term

use (4-12 weeks)

Not recommended due tolerance, psychologic

dependence and abuse

2. Benzphet amine HC L (Didrex)

Similar to amphetamines

Potential for abuse

3. Dextroamphet amine (Dexedrine)

Treat obesity

Causes restlessness and insomnia

For short term use

4. Diethylpropion HC L (Dos pan , T enuate , T epanil)

For appetite suppression by stimulating the

appetite control in the hypothalamus

Take 1 hours before meals

For short term use

5. Mazindol (Mazanor , Sanorex)

Treat obesity

Give with meals to avoid GI discomfort

6.orli st at (X eni cal)

For long term weight loss and weight

maintenance by reducing fat absorption in the

GIT

Given tid during meals containing fat

Analeptics

CNS stimulants that mostly affect the brainstem

and spinal cord but also affect the cerebral

cortex

Primary use is to stimulate respiration

Xanthines ( methylx anthines )

1. C a ffeine

Stimulates CNS, large doses stimulate

respiration

Used for newborns with apnea to stimulate

respiration

Increases HR and BP

2. T heophylline

Given through NGT

Used mostly to relax bronchioles but also usedto increased respiration in newborns with

apnea

Side Effect s & Adver se Reactions

nervousness, restlessness, tremors, twitching,

palpitations, and insomnia

Other side effects include diuresis, GI irritation,

and rarely tinnitus (ringing in the ear)

High doses can cause psychologic dependence

Respiratory Central Nervous System Stimulant

1. Dox a pr am HC L (Dopr am)

CNS and respiratory stimulant

Used to treat respiratory depression caused by

drug overdose, pre- and post-anesthetic

respiratory depression, and COPD

Administered intravenously, and its onset of

action is within 20-40 seconds with a peak

action of 2 minutes

Overdose can cause hypertension, tachycardia,

trembling and convulsions

Headaches: Migr aine & C l uster

Migraine headaches

C har acterized by a unil ater al throbbing head

pain , accompanied by nausea, vomiting , and

photophobi a

Symptoms frequently per si st for 4 to 24 hour s

and for sever al d ay s in some cases

Pathophy siology

caused by infl ammation and dil ation of the

blood vessel s in the cr ani um

Etiology i s unk now n but some theories suggest

that an imbal ance in serotonin (causes

v asoconstri ction and su ppresses migr aine

head aches )

food s ri ch in thi s are cheese , chocol ate , and red

w ine



2 types

1. C l assi c migr aine associ ated w ith aur a that occur s

minutes to hour s before onset

2. C ommon migr aine not associ ated w ith aur a

C luster headaches

C har acterized by a severe unil ater al

nonthrobbing pain usually located around the eye/forehead

Occur s in a series of cl uster att acks one or

more att acks everyd ay for sever al w eeks

Not associ ated nausea and vomiting

T reatment for migr aine head aches

Preventive treatment incl udes

Bet a adrenergi c block er s li k e propanolol

( Inder al) , atenolol ( T enormin) , and metoprolol

( Lopressor) C al ci um channel block er s li k e ver a pamil ( C al an) ,

and nifedepine ( Procardi a )

T ri cy cli c antidepresant s li k e triptyline ( El avil)

and imipr amine ( T ofr anil)

T reatment depend s on the intensity of pain

mild migr aine att acks

1. Nonseroid al antiinfl ammatory dr ugs ( NS AIDs )

As pirin , acet aminophen , i bu profen , na proxen

( Aleve)

2. O pioid analgesi cs

Meperidine (Demerol) and butorphanol nasal

s pr ay ( St adol NS ) - occasional used

For moder ate to severe att acks

Ergot Al kaloid s

1. Ergot amine t artr ate

nons pecifi c serotonin agoni st and

v asoconstri ctor

Antimigr aine dr ug

t ak en early d uring an att ack

N&V may occur

Av ail able in SL and PO t ablet s

2. Dihydroergot amine mesyl ate

An ergot al kaloid

C an be admini stered SQ , IM, IV, or nasal s pr ay

Prevent or abort migr aine att acks

Selective serotonin receptor agoni st s ( tript ans )

1. sumatript an ( Imitrex)

5-HT 1 receptor agoni st

Latest dr ug developed

More effective than ergot amine in treating

migr aine att acks

T reat acute migr aine att acks and cl uster

head aches

Promotes v asoconstri ction

C entr al Nervous Sy stem Depressant s

Dr ugs that are C NS depressant s cause v arying

degrees of depression

T he broad cl assifi cation incl udes:

1. Sed ative-hypnoti cs

2. Gener al and local anestheti cs

3. Nar coti c and non-nar coti c analgesi cs4. Anti conv ul sant s

5. Antipsy choti cs

6. Antidepressant s

T ypes and St ages of Sleep

Normal sleep i s composed of t w o definite

phases:

1. Nonr a pid eye movement ( NRE M ) - st age I to

IV

2. Ra pid eye movement ( RE M ) sleep a per son

experience recall able dreams, diffi cult to arouse

Both these t w o occur cy cli cally d uring sleep at

about 90-minute interv al s

Dreams occur in the RE M st age

Individ ual s perform better d uring their wak ing

hour s if they experience all types and st ages of

sleep

Non- pharmacologi c Method s

Once the nur se di scover s that the client has

diffi culty f alling asleep , the follow ing method s

might be used fir st:

1. Ari se at a s pecifi c hour in the morning

2. T ak e few or no d aytime na ps

3. Avoid drinks that cont ain ca ffeine 6 hour s before

bedtime

4. Avoid heavy meal s or strenuous exer ci se before

bedtime

5. T ak e a warm bath , read , or li sten to musi c before

bedtime

6. Avoid drink ing copious amount s of fl uid before

bedtime

7. Decrease exposure to loud noi ses

8. Drink warm mil k before bedtime

Sedative-Hypnotics

1. Sed ation (sed atives )

mildest form of C NS depression char acterized by

dimini shed phy si cal and ment al res ponses at

low er dosages but does not a ffect consciousness

Used to red uce tension and anxiety

2. Hypnosi s ( hypnoti cs ) - a form of nat ur al sleep w hen

dr ug dose was Increased

Most frequently used for sleep di sorder s

Side-effect s / Adver se effect of Sed ative-Hypnoti cs

Hangover resid ual drowsiness resulting in impaired

reaction time



Dependence result s from chroni c hypnoti c use ,

char acterized by w ithdr awal symptoms from abr u pt

di scontinuation ( tremor s, dizziness, orthost ati c

hypotension , seizures, hall ucinations )

T oler ance result s w hen there i s a need to increase the

dosage over time to obt ain desired effect

Depression result s from long term use of hypnoti c

Res pir atory depression from high doses w hi ch su ppress the res pir atory center in the med ull a

Barbiturates

Used as a sed ative , treat s insomni a and

preoper ative medi cation

Mode of action: depression of the C NS , incl uding

the motor and sensory activities

3 C l assifi cations

1. Long-acting

used to control seizures or conv ul sive di sorder s,

anxiety

E .g. phenobar bit al and mephobar bit al

2. Intermedi ate-acting

usef ul as sleep sust ainer s for maint aining long

period s of sleep

Relieves anxiety , short term used for insomni a

E .g. but abar bit al ( Buti sol)

3. Short -acting

used to ind uce sleep for those

w ho have diffi culty f alling

asleep

may cause the per son to

awak en early in the morning

e.g. secobar bit al ( Seconal) and

pentobar bit al ( Nembut al)

4. Ultr a short -acting

used as a gener al anestheti c

E .g. thiopent al sodi um

( Penthot al)

Bar bit ur ates should be restri cted to short -term

use (2 w eeks or less ) because of their numerous

side effect s

Side effect s

Lethargy , drowsiness, hangover , dizziness

Adver se reactions

Dr ug dependence or toler ance

Life threatening: res pir atory di stress /depression

Pharmacok ineti cs

Pentobar bit al ( Nembut al) has been the hypnoti c

of choi ce until the introd uction of

benzodi azepines.

It has a slow absorption r ate and i s moder ately

protein-bound

It s long half -life i s mainly because of the

formation of active met abolites from liver

met aboli sm

Pharmacodynami cs

Pentobar bit al and secobar bit al are mainly used

for sleep ind uction and for sed ation need s.

has a r a pid onset w ith a short d ur ation of action.

T he onset of action i s slow er w hen admini stered

IM than w hen admini stered PO

Al cohol , nar coti cs and other sed ative-hypnoti cs

used in combination w ith bar bit ur ates may

f urther depress the C NS

Pentobar bit al increases hepati c enzyme action ,

causing increased met aboli sm and decreased

effect of dr ugs i .e. or al anti coagul ant s,

gl ucocorti coid s, TCA

Benzodiazepines

Anti -anxiety agent s used for allevi ating anxiety

thus, ind ucing sleep

Five benzodi azepines mar k eted as hypnoti cs are

1. fl ur azepam (Dalmane)

2. temazepam ( Restoril)

3. tri azol am (Hal cion)

4. est azol am ( ProSom)

5. aquazepam (Dor al)

As an anti anxiety

1. lor azepam ( Ativ an)

2. di azepam (Vali um)

Mode of action: increases the action of the

inhi bitory neurotr ansmitter , gamma

aminobutyri c acid ( G ABA )

su ppress st age 4 of NRE M sleep w hi ch may

result in vivid dreams and nightmares and del ay

RE M sleep

Fl umazenil - benzodi azepine ant agoni st , given

for benzodi azepine overdose

Pharmacok ineti cs

benzodi azepines are w ell absor bed through the

GI mucosa

Fl ur azepam i s r a pidly met abolized in the liver

It has a long half -life of 45 to 100 hour s.

Pharmacodynami cs

Benzodi azepines are used to treat insomni a by

ind ucing and sust aining sleep.

It has a r a pid onset of action and intermedi ate-

to long-acting effect s

Al cohol or nar coti cs t ak en w ith a

benzodi azepine may f urther depress C NS



Nonbenzodiazepines

Z olpidem ( Ambien) i s a non benzodi azepine that

differ s in it s str uct ure; how ever , it i s used for

short -term treatment (<10 d ay s ) of insomni a.

It s d ur ation of action i s 6-8 hour s w ith a short

half -life of 2-2.5 hour s.

Chloral Hydrate Other sed ative-hypnoti cs

It i s used to ind uce sleep and to decrease

noct urnal awak enings

T here i s less occurrence of hangover , res pir atory

depression , and toler ance.

Gastri c irrit ation i s a common compl aint , so the

dr ug should be t ak en w ith su ffi cient water/food

Nur sing res ponsi bilities (sed ative hypnoti cs )

1. Monitor V S es peci ally RR ( res pir atory depression and BP ( hypotension)

2. Assess patient for w ithdr awal symptoms w hen

t ak en for prolong period of time

3. Instr uct patient to avoid al cohol , antidepressant

and nar coti c dr ugs w hile t ak ing bar bit ur ate

because it can lead to res pir atory depression

4. Advi se client not to drive a motor vehi cle or

oper ate machinery

5. T ak e hypnoti cs 30 minutes before bedtime ,

short acting t ak e effect w ithin 15-30 minutes

Anesthetics

C l assified into:

Gener al

Local

Gener al anestheti cs depress the C NS , allevi ate

pain , and cause a loss of consciousness

Local anestheti cs eliminates sensation in a

s pecifi c area of the body

nitrous oxide ( l aughing gas) - fir st anestheti c

used was and still frequently used in dent al

surgery

Ether and chloroform w ere al so used in the past .

Ether i s highly fl ammable vol atile liquid , has a

pungent odor and can cause N&V a fter it has

been admini stered (seldom used)

C hloroform i s toxi c to liver cell s and i s no longer

used .

Balanced Anesthesia

It i s a combination of dr ugs used in gener al

anesthesi a w hi ch incl ude the follow ing:

1. A hypnoti c given the night before

2. Premedi cation such as a

benzodi azepine and an anti cholinergi c ( eg. atropine)

given 1 hour before surgery to decrease secretion

3. An ultr a short -acting bar bit ur ate

( thiopent al sodi um)

4. An inhaled gas such as nitrous oxide

& oxygen

5. muscle rel a x ant

T her a peuti c adv ant age:

1. Minimizes cardiov ascul ar problems2. Decreases amount of gener al anesthesi a needed

3. Red uces possi ble post anestheti c N/ V

4. Minimize di st ur bance of organ f unction

5. Decreases pain

St ages of Gener al anesthesi a

St age 1 Analgesi a( Ind uction st age)

Begins w ith consciousness and end s w ith loss of

consciousness

S peech i s diffi cult , lost pain and smell sensation

Auditory/vi sual hall ucination may occur

St age 2 Ex citement ( deliri um)

Prod uces loss of consciousness

C onf usion and ex citement occur s

St age 3 Surgi cal st age

Surgi cal proced ure i s performed d uring thi s

st age

St age 4 Med ull ary par aly si s

T oxi c st age of anesthesi a

Res pir ations are lost and cir cul atory coll a pse

occur s

Due to overdose of anesthesi a

I nhalation Anesthetics

C l assified into gas or vol atile liquid s

admini stered as gas and used to deliver gener al

anesthesi a

Usually absor bed qui ck ly , has r a pid action and

eliminated r a pidly

C y clopropane was a popul ar anestheti c from

1930-1960 but because of it s highly fl ammable

st ate , it i s no longer/ seldom used .

halothane was introd uced as a nonfl ammable

alternative in l ate 1950s

T ypi cally provides smooth ind uction and

recovery of consciousness usually occur s in

a pproximately 1 hour u pon di scontinuation

Usually combined w ith a bar bit ur ate

( thiopent al) , strong analgesi c ( morphine) and

muscle rel a x ant ( pancromi um) for surgi cal

proced ures

Adver se effect s:

1. res pir atory depression

2. hypotension

3. dy srhythmi as

4. hepati c dy s f unction



Ex ample of V ol atile liquid s inhal ation

anestheti cs

1. ether ( highly fl ammable)

2. halothane ( Fl uothane)

3. methoxyfl ur ane ( Penthr ane)

4. enfl ur ane ( Ethr ane)

5. i sofl ur ane ( For ane)

6. des fl ur ane ( Su pr ane) 7. sevofl ur ane (Ult ane)

Ex ample of Gas inhal ation anestheti cs

1. nitrous oxide ( l aughing gas )

2. cy clopropane

3. thiopent al sodi um ( Pentothal)

4. methohexit al sodi um ( Brevit al

sodi um)

5. thi amyl al sodi um ( Surit al)

I ntravenous Anesthetics Used for gener al anesthesi a or for the ind uction

st age of anesthesi a and for outpatient surgery

of short d ur ation

Have r a pid onset s and short d ur ations of actions

Adver se effect s from IV anestheti cs incl ude

res pir atory and cardiov ascul ar depression

Ex ample:

1. droperidol & fent anyl ( Innov ar)

2. etomid ate ( Amid ate)

3. propofol (Dipriv an)

4. k et amine hydrochloride (K et al ar)

T opical Anesthetics

Use of topi cal anestheti cs i s limited to mucous

membr anes, brok en or unbrok en sk in surf aces,

& burns

T hey come in different forms, such as sol ution ,

liquid s pr ay , ointment , cream , and gel .

decreases the sensitivity of the nerve endings of

the a ffected area.

Local Anesthetics

block pain at the site w here the dr ug i s

admini stered , allow ing consciousness to be

maint ained .

Uses:

1. Performing dent al proced ures

2. Sut uring sk in l acer ations

3. Performing short -term ( minor)

surgery at a localized area

4. Block ing nerve impul ses

5. Performing di agnosti c proced ures

such as l umbar punct ure and thor acentesi s

cl assifi cation

1. Short acting (1 / 2-1 hour)

Used for caud al , epid ur al anesthesi a and s pinal

anesthesi a

Ex ample:

C hloroprocaine ( Nesacaine)

Procaine HC L ( Novocain)

2. Moder ate acting (1-3 hour)

Used for infiltr ation , epid ur al and s pinal

anesthesi a

Ex ample:

Lidocaine (X ylocaine)

Mepiv acaine HC L ( C ar bocaine HC L / Isocaine/ Polocaine) Prilocaine HC L ( C it anest)

3. Long acting (3-10 hour)

Used for infiltr ation , caud al and epid ur al

anesthesi a

Ex ample

Bu piv acaine (Mar caine , Sensor caine)

Di bucaine HC L ( Nu per cainal) topi cal use

Etidocaine (Dur anest)

T etr acaine HC L ( Pontocaine) topi cal use i .e eye , nose

and throat for bronchoscopy

S pinal Anesthesia

Requires that a local anestheti c to be in j ected in

the subar achnoid s pace at the third or fourth

l umbar s pace

Head aches might result follow ing s pinal

anesthesi a, because of a decrease in C SF fl uid

pressure caused by a leak of fl uid at the needle

insertion point

encour aging the client to remain fl at on bed

/increasing fl uid s follow ing surgery decreases

the li k elihood s pinal head ache

Hypotension can al so result s from s pinal

anesthesi a

Various sites of the s pinal col umn used for a

nerve block w ith a local anestheti c:

1. S pinal block - i s the penetr ation of the

anestheti c into the subar achnoid membr ane (second

l ayer of the s pinal cord)

2. Epid ur al block - i s the pl acement of the local

anestheti c in the outer covering of the s pinal cord or the

d ur a mater



3. C aud al block - i s pl aced near the sacr um

4. Saddle block - i s given at the low er end of the

s pinal col umn to block the perineal area, used in l abor

d uring child birth

Monitor BP because hypotension i s the usual

side effect of anesthesi a

Anticonvulsants

Seizure disorder

Result s from overly active and hyper sensitive

neurons in the br ain that trigger ex cessive

electri cal di scharges, causing a seizure

C har acterized by loss of consciousness,

uncontrolled body movement s, changes in

behavior s and sensation

C hroni c and a lifelong di sorder

50% of case i s idiopathi c, other 50% considered

second ary to tr auma, br ain anoxi a, infection ,

C V A di sorder s

International C l assifi cation of Seizures

1. Gener alized seizures

a. T oni c-cloni c seizure

Aka. gr and mal seizure

toni c phase - sk elet al muscles contr act in a

s pasm l asting 3-5 second s

cloni c phase - there i s a dy srhythmi c muscul ar

contr action or j er k iness of the legs and arms

l asting 2-4 minutes.

b. T oni c seizures

c. C loni c seizures

d . Absence seizure( Petit mal)

Brief loss of consciousness l asting less than 10

second s

e. Myocloni c seizure

Isol ated cloni c contr action or j er ks

l asting 3-10 second s, may be limited to

one limb or involve the entire body

f . Atoni c seizure

Head drop , loss of post ure , sudden loss of

muscle tone

2. Parti al seizures

a. Simple seizure

i . Motor

y Formerly called

jacksoni an seizure.

y Involves s pont aneous

movement that s pread s

ii . Sensory

y V i sual , auditory , or

t aste hall ucination

i . Autonomi c res ponses

Paleness,

fl ushing ,

sw eating or vomiting

ii . Psy chologi c

Per sonality

changes

b. C omplex seizure

T here i s a loss of consciousness

C lient does not recall behavior

immedi ately before , d uring and

immedi ately a fter the seizure

i . Psy chomotor C omplex

symptoms ;

automati sms

( repetitive

behavior s such

as chew ing or

swallow ing

motions ) ,

behavior al

changes, and

motor seizures

ii . C ognitive

y C onf usion or memory

impairment

iii . A ffective

y Bizarre behavior

iv . C ompound

y May lead to gener alized

seizures such as toni c-

cloni c, toni c

Anticonvulsants

Aka. Antiepilepti c dr ugs ( AE Ds )

Dr ug used for epilepti c seizure

Mode of action: su ppress the abnormal electri c

impul ses from hyper active neurons focus to

corti cal areas, thus, preventing the seizure but

not eliminating the cause of the seizure

Anti conv ul sant s are al so cl assified as C NS

depressant s.

Anti conv ul sant s are usually t ak en throughout

the per sons lifetime.

Mode of Action

anti conv ul sant s w or k in 3 way s:

1. By su ppressing sodi um infl u x through

the dr ug binding to the sodi um channel w hen it i s



inactiv ated thus prolonging the channel inactiv ation and

thereby preventing neuron firing

e.g. Phenytoin , fos phenytoin ,

car bamazepine , ox car bazepine , v alproi c acid ,

topir amate , zoni samide , and l amotrigine

2. By su ppressing the cal ci um infl u x thus

preventing the electri c current gener ated by the cal ci um ions to the cal ci um channel

e.g. Valproi c acid and ethosu ximide

3. By increasing the action of G ABA ,

w hi ch inhi bit s neurotr ansmitter throughout the

br ain

e.g. Bar bit ur ates, benzodi azepines, and

ti agabine

Hydantoins

most commonly used dr ug for controlling

seizures ( gr and mal/ complex)

Ex ample:

phenytoin (Dil antin)

mephenytoin (Mesantoin)

Mode of action: inhi bit s sodi um infl u x , red uce

repetitive neuronal firing , thus limiting seizures

It has the least toxi c effect s, has a small effect

on gener al sed ation , and i s non-addi cting.

C ontr aindi cated to pregnancy because of it s

ter atogeni c effect s.

Side Effect s

gingiv al hyperpl asi a - overgrow th of the gum

ti ssues ( reddened gums that bleed easily)

neurologi c and psy chi atri c effect s such as

sl urred s peech , conf usion , depression and

thrombocytopeni a & leuk openi a

C lient s on hyd antoins for a long period may

have elev ated blood sugar w hi ch result s from

dr ug inhi biting the release of insulin

N/ V, constipation , drowsiness, alopeci a,

hir suti sm and ny st agmus

Barbiturates

Phenobar bit al - a long acting bar bit ur ate ,

prescri bed to treat gr and mal seizure and

epi sodes of st at us epilepti cus seizures ( r a pid

succession of epilepti c seizure)

Mode of action: red uce seizure by enhancing the

activity of G ABA , inhi bitory neurotr ansmitter

Succinimides

T hey are used to treat absence or petit mal

seizures, and it may be used in combination

w ith other anti conv ul sant s to treat such

seizures.

Ethosu xinimide ( Z arontin) i s the succinimide of

choi ce

Mode of action: decrease cal ci um infl u x through

the cal ci um channel s

Benzodiazepines

Aka. anxiolyti cs

3 benzodi azepines that have anti conv ul sant

effect s are:

C lonazepam C hlor azepate dipot assi um

Di azepam

C lonazepam - effective in controlling petit mal

seizures, how ever toler ance may occur 6

months a fter dr ug ther a py .

C lor azepate dipot assi um - frequently

admini stered in ad junctive ther a py for treating

parti al seizure

Di azepam(Vali um) - primarily prescri bed for

treating acute st at us epilepti cus and admini stered IV to achieve the desired res ponse ,

T he dr ug has a short term effect , thus, other

anti conv ul sant s are given a fter admini str ation

of di azepam

I minostilbenes

C ar bamazepine ( T egretol) i s effective in treating

refr actory seizure di sorder s that have not

res ponded top other anti conv ul sant ther a pies.

It i s used for gr and mal and parti al seizure

An inter action occur s w hen t ak en w ith

gr a pefr uit jui ce causing possi ble toxi city

V alproate

Valproi c acid (Depak ene) has been prescri bed

for petit mal , gr and mal , and mixed types of

seizures.

Hepatoxi city i s one of it s possi ble adver se

reactions

Nur sing res ponsi bilities (anti conv ul sant s )

1. Inform client not to combine al cohol and other

C NS depressant w hile t ak ing anti conv ul sant

because it f urther causes C NS depression

2. Patient should have a medi cal alert br ace let or

ID card w hi ch indi cates health problem and

dr ugs to be t ak en by client

3. Advi se patient not to abr u ptly stop t ak ing

anti conv ul sant but a gr ad ual w ithdr awal to

prevent seizure rebound and st at us epilepti cus

4. Monitor blood sugar level because phenytoin

(Dil antin) causes hypergly cemi a



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Autonomic Nervous System Agents