autonomic nervous system agents

Autonomic Nervous System AgentsMa. Tosca Cybil A. Torres, RN,

MAN

Central Nervous System(CNS)- the body’s primary nervous system which is composed of the brain and spinal cord.

Peripheral Nervous System(PNS)-located outside the brain and spinal cord. Two divisions:

Autonomic Somatic

† After the interpretation of the CNS, the PNS receives stimuli and initiates responses to those stimuli

Nervous system

Autonomic Nervous system (ANS)† also called the visceral system----

innervates (acts on) smooth muscles and glands† An involuntary nervous system † Functions: Control and regulation of the heart,

respiratory system, GIT, bladder, eyes, and glands

† Two sets of neurons: † Afferent (sensory) neurons- send impulses to the

CNS, where they are interpreted† Efferent (motor) neurons- receive the impulses from

the brain and transmit those impulse through the spinal cord to the effector organ cells

The efferent pathways in the ANS are divided into two branches:

1. Sympathetic nervous system→Also known as the adrenergic system→Smooth muscle innervated by the

neurotransmitter norepinephrine →Norepinephrine- released from the terminal nerve

ending and stimulates the cell receptors to produce a response

2. Parasympathetic nervous systemAlso called the cholinergic system Muscles innervated by the neurotransmitter

acetylcholine • Acetylcholine (ACh) is a neurotransmitter substance

that is found in both the CNS and in the PNS.• In the PNS, it is the NT released at synapses on skeletal

muscles and is also found in the cell bodies of the autonomic nervous system.

• In the brain, it appears to be involved in learning/memory, attention as well as sleeping and dreaming.

Body Tissue/Organ Sympathetic Response Parasympathetic Response

Eye Dilates pupils Constricts pupils

Lungs Dilates bronchioles Constricts bronchioles and increase secretions

Heart Increases heart rate Decreases heart rate

Blood vessels Constricts Dilates

GI Relaxes smooth muscles of GIT

Increases peristalsis

Bladder Relaxes bladder muscle Constricts bladder

Uterus Relaxes uterine muscles

Salivary gland Increases salivation

Autonomic Nervous System: Sympathetic and ParasympatheticSympathetic StimulantsSympathomimetics( adrenergics, adrenomimetics, or adrenergic agonists)

Parasympathetic StimulantsDirect-ActingParasympathomimetics (cholinergics or cholinergic agonists)

Action: Increase BPIncrease PRRelax bronchiolesDilates pupilsRelax uterine musclesIncrease blood sugar

Action: Decrease blood pressureDecrease pulse rateConstrict bronchiolesConstrict pupilsIncrease urinary contraction Increase peristalsisIndirect-ActingCholinesterase inhibitors (anticholinesterase) Action: Increase muscle tone

Sympathetic DepressantsSympatholytics(adrenergic blockers, adrenolytics, or adrenergic antagonists)

Parasympathetic DepressantsParasympatholytics (anticholinergics, cholinergics antagonists, or antispasmodics)

Action: Decrease PRDecrease BPConstrict Bronchioles

Action: Increase PRDecrease mucous secretions Decrease GI motilityIncrease urinary retentionDilate pupils

Cholinergic Agents

andCholinergic

Blocking Agents

Cholinergic

Agents

Cholinergic Agents

• Also called cholinomimetics, cholinergic stimulants, cholinergic agonists

• Drugs that stimulate theparasympathetic nervous system (PSNS)

• Mimic the effects of the PSNS neurotransmitter

• Acetylcholine (ACh)

Cholinergic Receptors

Two types, determined by:• Location• Action once stimulated

Nicotinic receptors and Muscarinic receptors

Nicotinic Receptors

• Located in the ganglia of both the PSNS and SNS

• Affects the skeletal muscle• Named “nicotinic” because can be

stimulated by the alkaloid nicotine

Nic

otin

ic

rece

ptor

si

tes

Mus

cle

cont

ract

ion

Muscarinic Receptors

• Located postsynaptically:– Smooth muscle– Cardiac muscle– Glands of parasympathetic fibers– Effector organs of cholinergic sympathetic fibers

• Named “muscarinic” because can be stimulated by the alkaloid muscarine

Cholinergic Agents: Mechanism of Action

• Direct-acting (agonist)– Bind to cholinergic receptors, causing

stimulation– Acts on the receptor sites to activate a tissue

response

Direct-Acting Cholinergic Drugs Ex:bethanechol chloride(Urecholine)- used to

increase urination metoclopramide HCL(Plasil)- usually used to

treat GERD---increases gastric emptying time

Cholinergic Agents: Mechanism of Action

• Indirect-acting– Inhibit the enzyme cholinesterase (chE)

(acetylcholinesterase)– Cholinesterase- destroys acetylcholine before it reaches

the receptor or after it has attached to the receptor site

– Result: more ACh is available at the receptors

Indirect Acting cholinergic drugs

Ex: demecarium bromide(Humorsol)-reduces IOP

in glaucoma, long acting mioticambenonium Cl (Mytelase)- to increase

muscle strength in MG, long acting edrophonium Cl(Tensilon)- to diagnose MG,

very short acting

Indirect-Acting Cholinergic Agents (Cholinesterase Inhibitors)

• Reversible– Bind to cholinesterase for a period of

minutes to hours• Irreversible

– Bind to cholinesterase and form a permanent covalent bond

– The body must make new cholinesterase

Drug Effects of Cholinergic Agents

• Effects seen when the PSNS is stimulated.• The PSNS is the “rest and digest” system.

Drug Effects of Cholinergic Agents

“SLUDGE”• Salivation

• Lacrimation

• Urinary incontinence

• Diarrhea

• Gastrointestinal cramps

• Emesis

Drug Effects of Cholinergic Agents

• Stimulate intestine and bladder– Increased gastric secretions– Increased gastrointestinal motility– Increased urinary frequency

• Stimulate pupil– Constriction (miosis)– Reduced intraocular pressure

• Increased salivation and sweating

Drug Effects of Cholinergic Agents

• Cardiovascular effects– Decreased heart rate– Vasodilation

• Respiratory effects– Bronchial constriction, narrowed airways

Drug Effects of Cholinergic Agents

• At recommended doses, the cholinergics primarily affect the MUSCARINIC receptors.

• At high doses, cholinergics stimulate the NICOTINIC receptors.

Cholinergic Agents: Therapeutic Uses

Direct-Acting Agents• Reduce intraocular pressure• Useful for glaucoma and intraocular surgery

Examples: acetylcholine, carbachol, pilocarpine

-Topical application due to poor oral absorption

Cholinergic Agents: Therapeutic Uses

Direct-Acting Agent—bethanechol• Increases tone and motility of bladder and GI tract• Relaxes sphincters in bladder and GI tract, allowing

them to empty• Helpful for postsurgical atony of the bladder

and GI tract

Cholinergic Agents: Therapeutic Uses

Indirect-Acting Agents• Cause skeletal muscle contractions• Used for diagnosis and treatment of

myasthenia gravis• Used to reverse neuromuscular blocking agents• Used to reverse anticholinergic poisoning (antidote)

Examples: physostigmine, pyridostigmine

Cholinergic Agents: Therapeutic Uses

Indirect-Acting Agent—donepezil (Aricept)• Used in the treatment of mild to moderate Alzheimer’s

disease.• Helps to increase or maintain memory and

learning capabilities.

Cholinergic Agents: Side EffectsSide effects are a result of overstimulation

of the PSNS.• Cardiovascular:

– Bradycardia, hypotension, conduction abnormalities (AV block and cardiac arrest)

• CNS:

– Headache, dizziness, convulsions• Gastrointestinal:

– Abdominal cramps, increased secretions, nausea, vomiting

Cholinergic Agents: Side Effects

• Respiratory:– Increased bronchial secretions,

bronchospasms• Other:

– Lacrimation, sweating, salivation, loss of binocular accommodation, miosis

Cholinergic Agents: Interactions

• Anticholinergics, antihistamines, sympathomimetics

• Antagonize cholinergic agents, resulting in decreased responses

Cholinergic Agents: Nursing Implications

• Keep in mind that these agents will stimulate the PSNS and mimic the action of ACh.

• Assess for allergies, presence of GI or GU obstructions, asthma, peptic ulcer disease, or coronary artery disease.

• Perform baseline assessment of VS and systems overview.

Cholinergic Agents: Nursing Implications

• Medications should be taken as ordered and not abruptly stopped.

• The doses should be spread evenly apart to optimize the effects of the medication.

• Overdosing can cause life-threatening problems. Patients should not adjust the dosages unless directed by the physician.

Cholinergic Agents: Nursing Implications

• Encourage patients with myasthenia gravis to take medication 30 minutes before eating to help improve chewing and swallowing.

• When donepezil is prescribed for Alzheimer’s disease, be honest with caregivers and patients that the drug is for management of symptoms, not for a cure.

• Therapeutic effects of donepezil may not occur for up to 6 weeks.

Cholinergic Agents: Nursing Implications

• Atropine is the antidote for cholinergics. It should be available in the patient’s room for immediate use if needed.

• Patients should notify their physician if they experience muscle weakness, abdominal cramps, diarrhea, or difficulty breathing.

Cholinergic Agents: Nursing Implications

Monitor for side effects, including:Increased respiratory Abdominal crampingsecretions

Bronchospasms Dysrhythmias

Difficulty breathing Hypotension

Nausea and vomiting Bradycardia

Diarrhea Increased sweating

Increase in frequency andurgency of voiding patterns

Cholinergic Agents: Nursing Implications

Monitor for therapeutic effects:• Alleviated signs and symptoms of myasthenia gravis

• In postoperative patients with decreased GI peristalsis, look for: – Increased bowel sounds– Passage of flatus– Occurrence of bowel movements

• In patients with urinary retention/hypotonic bladder, urination should occur within 60 minutes of bethanecol administration

Cholinerg

ic

Blocking

Agents

Cholinergic Blocking Agents

• Drugs that block or inhibit the actions of acetylcholine (ACh) in the parasympathetic nervous system (PSNS)

Cholinergic Blocking Agents: Mechanism of Action

• Competitive antagonists• Compete with ACh• Block ACh at the muscarinic receptors

in the PSNS– As a result, ACh is unable to bind to the

receptor site and cause a cholinergic effect.– Once these drugs bind to receptors, they inhibit

nerve transmission at these receptors.

Cholinergic Blocking Agents: Chemical Class

Natural Synthetic/Semisyntheticatropine anisotropine clidiniumbelladonna dicyclomine glycopyrrolatehyoscyamine hexocyclium homatropinescopolamine ipratropium isopropamide

oxybutynin propanthelinetolterodine tridihexethyl

Drug Effects of Cholinergic Blocking Agents

• Cardiovascular– Small doses: decrease heart rate – Large doses: increase heart rate

• CNS– Small doses: decrease muscle rigidity

and tremors– Large doses: drowsiness, disorientation,

hallucinations

Drug Effects of Cholinergic Blocking Agents

• Eye– Dilated pupils (mydriasis)– Decreased accommodation due to paralysis

of ciliary muscles (cycloplegia)• Gastrointestinal

– Relax smooth muscle tone of GI tract– Decrease intestinal and gastric secretions– Decrease motility and peristalsis

Drug Effects of Cholinergic Blocking Agents

• Genitourinary– Relaxed detrusor muscle– Increased constriction of internal sphincter– Result: urinary retention

• Glandular– Decreased bronchial secretions, salivation, sweating

• Respiratory– Decreased bronchial secretions– Dilated bronchial airways

Cholinergic Blocking Agents: Therapeutic Uses

CNS Decreased muscle rigidity and muscle

tremors• Parkinson’s disease• Drug-induced extrapyramidal reactions

Cholinergic Blocking Agents: Therapeutic Uses

CardiovascularAffect the heart’s conduction system• Low doses: slow the heart rate• High doses: block inhibitory vagal effects on

the SA and AV node pacemaker cells– Result: increased heart rate

Cholinergic Blocking Agents: Therapeutic Uses

Atropine Used primarily for cardiovascular

disorders• Sinus node dysfunction• Symptomatic second-degree heart block• Sinus bradycardia with hemodynamic compromise

(advanced life support)

Cholinergic Blocking Agents: Therapeutic Uses

RespiratoryBlocking the cholinergic stimulation of the PSNS

allows unopposed action of the SNS.• Results:

– Decreased secretions from nose, mouth, pharynx, bronchi

– Relaxed smooth muscles in bronchi and bronchioles

– Decreased airway resistance– Bronchodilation

Cholinergic Blocking Agents: Therapeutic Uses

Respiratory agents are used to treat:• Exercise-induced bronchospasms• Chronic bronchitis• Asthma• Chronic obstructive pulmonary disease

Cholinergic Blocking Agents: Therapeutic Uses

GastrointestinalPSNS controls gastric secretions and

smooth muscles that produce gastric motility.

• Blockade of PSNS results in:– Decreased secretions– Relaxation of smooth muscle– Decreased GI motility and peristalsis

Cholinergic Blocking Agents: Therapeutic Uses

Gastrointestinal agents are used to treat:• Peptic ulcer disease• Irritable bowel disease• GI hypersecretory states

Cholinergic Blocking Agents: Therapeutic Uses

Genitourinary• Relaxed detrusor muscles of the bladder• Increased constriction of the internal

sphincter• Reflex neurogenic bladder• Incontinence

Cholinergic Blocking Agents: Side Effects

Body System Side/Adverse Effects

Cardiovascular Increased heart rate, dysrhythmias

CNS CNS excitation, restlessness, irritability, disorientation, hallucinations, delirium

Cholinergic Blocking Agents: Side Effects

Body System Side/Adverse Effects

Eye Dilated pupils, decreased visual accommodation, increased intraocular pressure

Gastrointestinal Decreased salivation, decreased gastric secretions, decreased motility

Cholinergic Blocking Agents: Side Effects

Body System Side/Adverse Effects

Genitourinary Urinary retention

Glandular Decreased sweating

Respiratory Decreased bronchial secretions

Cholinergic Blocking Agents: Interactions

• Antihistamines, phenothiazines, tricyclic antidepressants, MAOIs

• When given with cholinergic blocking agents, cause ADDITIVE cholinergic effects, resulting in increased effects

Cholinergic Blocking Agents: Nursing Implications

• Keep in mind that these agents will blockthe action of ACh in the PSNS.

• Assess for allergies, presence of BPH, glaucoma, tachycardia, MI, CHF, hiatal hernia, and GI or GU obstruction.

• Perform baseline assessment of VS and systems overview.

Cholinergic Blocking Agents: Nursing Implications

• Medications should be taken exactly as prescribed to have the maximum therapeutic effect.

• Overdosing can cause life-threatening problems.

• Blurred vision may cause problems with driving or operating machinery.

• Patients may experience sensitivity to light and may want to wear dark glasses or sunglasses.

Cholinergic Blocking Agents: Nursing Implications

• When giving ophthalmic solutions, apply pressure to the inner canthus to prevent systemic absorption.

• Dry mouth may occur; can be handled by chewing gum, frequent mouth care, and hard candy.

• Check with physician before taking any other medication, including OTC medications.

• ANTIDOTE for atropine is physostigmine salicylate (Antilirium).

Cholinergic Blocking Agents: Nursing Implications

• Anticholinergics may lead to higher risk for heat stroke due to effects on heat-regulating mechanisms.

• Teach patients to limit physical exertion, and avoid high temperatures and strenuous exercise.

• Emphasize the importance of adequate fluid and salt intake.

Cholinergic Blocking Agents: Nursing Implications

• Patients should report the following to their physician: urinary hesitancy and/or retention, constipation, palpitations, tremors, confusion, sedation or amnesia, excessive dry mouth (especially if they have chronic lung infections or disease), or fever

Cholinergic Agents: Nursing Implications

• Monitor for therapeutic effects:• For patients with Parkinson’s disease:

fewer tremors and decreased salivation and drooling

• For patients with peptic ulcer disease: decreased abdominal pain

Cholinergic Blocking Agents: Nursing Implications

Monitor for side effects, including:Constipation TachycardiaTremors ConfusionHallucinations SedationUrinary retention Hot, dry skinFeverCNS depression (occurs with large doses of atropine)

&

Adrenerg

ics

• Adrenergics (adrenergic agonists, sympathomimetics, adrenomimetics)– Drugs that stimulate the sympathetic

nervous system– Mimics the sympathetic

neurotransmitters ( ie. epinephrine, norepinephrine)

– Act on one or more adrenergic receptor sites located on the smooth muscles

Effects of Adrenergics at ReceptorsReceptor Physiologic Responces

Alpha1 Increases force of heart contraction; vasoconstriction increases BP; mydriasis; salicary glands decrease secretions; bladder and prostate capsule increases contraction and ejaculation

Alpha2 Inhibits the release of norepinephrine; dilates blood vessels; produces hypotension; decreases GI motility and tone

Beta1 Increases heart rate and contraction; increases renin secretion----increase BP

Beta2 Dilates bronchioles; promotomes GI and uterine relaxation; promotes increase in blood sugar through glycogenolysis in the liver; increases blood flow in the skeletal muscles

Classification of Sympathomimetics/Adrenomimetics

1.Direct-Acting sympathomimetics directly stimulate the adrenergic receptor (e.g. epinephrine, norepinephrine)

2. Indirect-Acting sympathomimetics which stimulates the release of norepinephrine from the terminal nerve endings (e.g. amphetamine)

3.Mixed-Acting sympathomimetics (both direct and indirect acting)

Indications for use

• Emergency drugs in treatment of acute cardiovascular, respiratory and allergic disorders

• In children, epinephrine may be used to treat bronchospasm due to asthma or allergic reactions

• Phenylephrine may be used to treat sinus congestion

Indications of adrenergics cont.

• Stokes Adams• Shock• Inhibition of uterine contractions• For vasoconstrictive and hemostatic

purposes

Contraindications to use of adrenergics

• Cardiac dysrhythmias, angina pectoris• Hypertension• Hyperthyroidism• Cerebrovascular disease• Distal areas with a single blood supply such as

fingers, toes, nose and ears• Renal impairment use caution

Individual adrenergic drugs

• Epinephrine—prototype• Effects include: increased BP, increased

heart rate, relaxation of bronchial smooth muscle, vasoconstriction in peripheral blood vessels

epinephrine

• Increased glucose, lactate, and fatty acids in the blood due to metabolic effects

• Increased leukocyte and increased coagulation

• Inhibition of insulin secretion

epinephrine

• Affects both alpha and beta receptors• Usual doses, beta adenergic effects on

heart and vascular smooth muscle will predominate, high doses, alpha adrenergic effects will predominate

• Drug of choice for bronchospasm and laryngeal edema of anaphylaxis

epinephrine

• Excellent for cardiac stimulant and vasoconstrictive effects in cardiac arrest

• Added to local anesthetic• May be given IV, inhalation, topically• Not PO

epinephrine

• Physiologic antagonist to histamine• Those on beta blockers may need larger

doses• Drug of choice in PEA. Vasopressin has

now become drug of choice in ventricular tachycardia

• Single dose of Vasopressin, 40 units IV

Other adrenergics

• Ephedrine is a mixed acting adrenergic drug. Stimulates alpha and beta receptors. Longer lasting than epinephrine.

Pseudophed

• Used for bronchodilating and nasal decongestant effects

isuprel (Isoproterenol)

• Synthetic catecholamine that acts on beta 1 and 2 receptors

• Stimulates heart, dilates blood vessels in skeletal muscle and causes bronchodilation

• No alpha stimulation• Used in heart blocks (when pacemaker not

available) and as a bronchodilator

Neosynephrine (Phenylephrine)

• Pure alpha• Decreases CO and renal perfusion• No B1 or B2 effects• Longer lasting than epinephrine• Can cause a reflex bradycardia• Useful as a mydriatic

Toxicity of adrenergics in critically ill patients

• Affects renal perfusion• Can induce cardiac dysrhythmias• Increases myocardial oxygen consumption• May decrease perfusion of liver• Tissue necrosis with extravasation

Toxicity

• Do not give epinephrine and Isuprel at same time or within 4 hours of each other. Could result in serious dysrhythmias.

Nursing considerations• Monitor V/S. report signs of increasing BP and PR• Report side effects: tachycardia, tremors, dizziness,

increased BP• Check urine output and assess for bladder distension • Monitor IV site for IV forms----infiltration may cause

tissue necrosis• Give with food to avoid N/V• Evaluate blood glucose-----may elevate

Adrenergic

Blockers

Anti-adrenergics

• Sympatholytic• Block or decrease the effects of

sympathetic nerve stimulation, endogenous catecholamines and adrenergic drugs

Antiadrenergics—mechanisms of action and effects

• Can occur by blocking alpha 1 receptors postsynaptically

• Or by stimulation presynaptic alpha 2 receptors. Results in return of norepineprhine to presynaptic site. Activates alpha 2 resulting in negative feedback. Decreases release of additional norepinephrine.

Alpha-Adrenergic Agonists and blocking agents

• Alpha 2 agonists inhibit release of norepinephrine in brain; thus, decrease effects on entire body

• Results in decrease of BP• Also affects pancreatic islet cells, thus

some suppression of insulin secretion

Alpha 1 adrenergic blocking agents

• Act on skin, mucosa, intestines, lungs and kidneys to prevent vasoconstriction

• Effects: dilation of arterioles and veins, decreased blood pressure, pupillary constriction, and increased motility of GI tract

Alpha 1 adrenergic blocking agents

• May activate reflexes that oppose fall in BP such as fluid retention and increased heart rate

• Can prevent alpha medicated contraction of smooth muscle in nonvascular tissues

• Thus, useful in treating BPH as inhibit contraction of muscles in prostate and bladder

Alpha 1 antagonists

• Minipress (prazosin)—prototype.• Hytrin (terazosin) and Cardura (doxazosin)

—both are longer acting than Minipress.

Alpha 1 antagonists cont.

• Flomax (tamsulosin). Used in BPH. Produces smooth muscle relaxation of prostate gland and bladder neck. Minimal orthostatic hypotension.

• Priscoline (tolaxoline) used for vasospastic disorders. Pulmonary hypertension in newborns. Can be given sub Q, IM or IV.

Alpha 2 agonists

• Catapres (clonidine). PO or patch. • Tenex (guanfacine)• Aldomet (methyldopa). Can give IV.

Caution in renal and hepatic impairment.

Beta adrenergic blocking medications

• Prevent receptors from responding to sympathetic nerve impulses, catecholamines and beta adrenergic drugs.

Effects of beta blocking drugs

• Decreased heart rate• Decreased force of contraction• Decreased CO• Slow cardiac conduction• Decreased automaticity of ectopic

pacemakers

Effects of beta blocking drugs

• Decreased renin secretion from kidneys• Decreased BP• Bronchoconstriction• Less effective metabolism of glucose. May

result in more pronounced hypoglycemia and early s/s of hypoglycemia may be blocker (tachycardia)

Effects of beta blocking agents

• Decreased production of aqueous humor in eye

• May increase VLDL and decrease HDL• Diminished portal pressure in clients with

cirrhosis

Indications for use

• Alpha 1 blocking agents are used for tx of hypertension, BPH, in vasospastic disorders, and in persistent pulmonary hypertension in the newborn

• May be useful in treating pheochromocytoma• May be used in Raynaud’s or frostbite to

enhance blood flow

Regitine (phentolamine)

• Used for extravasation of potent vasoconstrictors (dopamine, norepinephrine) into subcutaneous tissues

Indications for use

• Alpha 2 agonists are used for hypertension—Catapres

• Epidural route for severe pain in cancer• Investigationally for anger management,

alcohol withdrawal, postmenopausal hot flashes, ADHD, in opioid withdrawal and as adjunct in anesthesia

Beta blocking medications

• Mainly for cardiovascular disorders (angina, dysrhythmias, hypertension, MI and glaucoma)

• In angina, beta blockers decrease myocardial oxygen consumption by decreasing rate, BP and contractility. Slow conduction both in SA node and AV node.

Beta blockers

• Possibly work by inhibition of renin, decreasing cardiac output and by decreasing sympathetic stimulation

• May worsen condition of heart failure as are negative inotropes

• May reduce risk of “sudden death”

Beta blockers

• Decrease remodeling seen in heart failure• In glaucoma, reduce intraocular pressur by

binding to beta-adrenergic receptors in ciliary body, thus decrease formation of aqueous humor

Beta blockers

• Inderal (propranolol) is prototype• Useful in treatment of hypertension,

dysrhythmias, angina pectoris, MI• Useful in pheochromocytoma in conjunction

with alpha blockers (counter catecholamine release)

• migraines

Beta Blockers

• In cirrhosis, Inderal may decrease the incidence of bleeding esophageal varices

• Used to be contraindicated in heart failure, now are standard

• Known to reduce sudden death• Often given with ACEIs• Indications include: htn, angina, prevention of MI

Receptor selectivity

• Acetutolol, atenolol, betaxolol, esmolol, and metoprolol are relatively cardioselective

• These agents lose cardioselection at higher doses as most organs have both beta 1 and beta 2 receptors

• Byetta is new agent that is cardioselective

Non-Receptor selectivity

• Carteolol, levobunolol, metipranolol, nadolol, propranolol, sotalol and timolol are all non-selective

• Can cause bronchoconstriction, peripheral vasoconstriction and interference with glycogenolysis

Combination selectivity

• Labetalol and carvedilol (Coreg) block alpha 1 receptors to cause vasodilation and beta 1 and beta 2 receptors which affect heart and lungs

• Both alpha and beta properties contribute to antihypertensive effects

• May cause less bradycardia but more postural hypotension

• Less reflex tachycardia

Intrinsic sympathomimetic activity

• Have chemical structure similar to that of catecholamines

• Block some beta receptors and stimulate others• Cause less bradycardia• Agents include: Sectral (acebutolol), Cartrol

(carteolol), Levatol (penbutolol) and Visken (pindolol)

Specific conditions-alpha agonists and antagonists

• In tx for BPH, patient should be evaluated for prostate cancer

• With alpha 2 agonists, sudden cessation can cause rebound BP elevation

• With alpha 1 blockers, first dose syncope may occurr from hypotension. Give low starting dose and at hs. May also cause reflex tachycardia and fluid retention.

Specific condtions-beta blockers

• With significant bradycardia, may need med with ISA such as pindolol and penbutolol

• Patient with asthma, cardioselectivity is preferred

• For MI, start as soon as patient is hemodynamically stable

Special conditions—beta blockers

• Should be discontinued gradually. Long term blockade results in increase receptor sensitivity to epinephrine and norepinephrine. Can result in severe hypertension. Taper 1-2 weeks.

Ethnic considerations

• Monotherapy in African Americans is less effective than in Caucasians.

• Trandate (labetalol) with both alpha and beta effects has been shown to be more effective in this population than Inderal, Toprol or timolol.

Nursing responsibilities• Monitor V/S. report marked changes in BP and PR• Note any complain of excessive dizziness and light

headedness• Report complaint of stuffy nose----nasal congestion may

occur• Determine if patient is diabetic------may cause

hypoglycemia. Teach to know early signs of hypoglycemia• Instruct client not to abruptly stop tx----may result to

rebound HTN,tachycardia, and angina