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Autonomic Nervous System Agents Ma. 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 system Also 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 Parasympathetic Sympathetic Stimulants Sympathomimetics (  adrenergics, adrenomimetics, or adrenergic agonists ) Parasympathetic Stimulants Direct-Acting Parasympathomimetics (cholinergics or cholinergic agonists) Action:  Increase BP Increase PR Relax bronchioles Dilates pupils Relax uterine muscles Increase blood sugar Action:  Decrease blood pressure Decrease pulse rate Constrict bronchioles Constrict pupils Increase urinary contraction  Increase peristalsis Indirect-Acting Cholinesterase inhibitors (anticholinesterase)  Action:  Increase muscle tone  Sympathetic Depressants Sympatholytics( adrenergic blockers, adrenolytics, or adrenergic antagonists ) Parasympathetic Depressants Parasympatholytics (anticholinergics, cholinergics antagonists, or antispasmodics) Action:  Decrease PR Decrease BP Constrict Bronchioles Action:  Increase PR Decrease mucous secretions  Decrease GI motility Increase urinary retention Dilate pupils
Cholinergic Agents  and Cholinergic Blocking Agents
Cholinergic Agents
Cholinergic Agents Also called cholinomimetics, cholinergic stimulants, cholinergic agonists Drugs that stimulate the parasympathetic 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
Nicotinic  receptor sites
Muscle contraction
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 miotic ambenonium 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” S alivation L acrimation U rinary incontinence D iarrhea G astrointestinal cramps E mesis
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 Effects Side 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 cramping secretions Bronchospasms Dysrhythmias Difficulty breathing Hypotension Nausea and vomiting Bradycardia Diarrhea Increased sweating Increase in frequency and urgency 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
Cholinergic 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/Semisynthetic atropine anisotropine clidinium belladonna dicyclomine glycopyrrolate hyoscyamine hexocyclium homatropine scopolamine ipratropium isopropamide oxybutynin propantheline tolterodine 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 Cardiovascular Affect 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  Respiratory Blocking 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  Gastrointestinal PSNS 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 block the 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 Tachycardia Tremors Confusion Hallucinations Sedation Urinary retention Hot, dry skin Fever CNS depression (occurs with large doses of atropine)
 &  
Adrenergics
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 Receptors Receptor Physiologic Responces Alpha 1 Increases force of heart contraction; vasoconstriction increases BP; mydriasis; salicary glands decrease secretions; bladder and prostate capsule increases contraction and ejaculation  Alpha 2 Inhibits the release of norepinephrine; dilates blood vessels; produces hypotension; decreases GI motility and tone  Beta 1 Increases heart rate and contraction; increases renin secretion----increase BP Beta 2 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 Direct-Acting sympathomimetics  directly stimulate the adrenergic receptor (e.g. epinephrine, norepinephrine) Indirect-Acting sympathomimetics  which stimulates the release of norepinephrine from the terminal nerve endings (e.g. amphetamine) 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

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Autonomic Nervous System Agents

  • 1. Autonomic Nervous System Agents Ma. Tosca Cybil A. Torres, RN, MAN
  • 2. 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
  • 4. 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
  • 5. 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
  • 6. 2. Parasympathetic nervous system Also 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.
  • 7. 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
  • 8. Autonomic Nervous System: Sympathetic and Parasympathetic Sympathetic Stimulants Sympathomimetics ( adrenergics, adrenomimetics, or adrenergic agonists ) Parasympathetic Stimulants Direct-Acting Parasympathomimetics (cholinergics or cholinergic agonists) Action: Increase BP Increase PR Relax bronchioles Dilates pupils Relax uterine muscles Increase blood sugar Action: Decrease blood pressure Decrease pulse rate Constrict bronchioles Constrict pupils Increase urinary contraction Increase peristalsis Indirect-Acting Cholinesterase inhibitors (anticholinesterase) Action: Increase muscle tone Sympathetic Depressants Sympatholytics( adrenergic blockers, adrenolytics, or adrenergic antagonists ) Parasympathetic Depressants Parasympatholytics (anticholinergics, cholinergics antagonists, or antispasmodics) Action: Decrease PR Decrease BP Constrict Bronchioles Action: Increase PR Decrease mucous secretions Decrease GI motility Increase urinary retention Dilate pupils
  • 9. Cholinergic Agents and Cholinergic Blocking Agents
  • 11. Cholinergic Agents Also called cholinomimetics, cholinergic stimulants, cholinergic agonists Drugs that stimulate the parasympathetic nervous system (PSNS) Mimic the effects of the PSNS neurotransmitter Acetylcholine (ACh)
  • 12. Cholinergic Receptors Two types, determined by: Location Action once stimulated Nicotinic receptors and Muscarinic receptors
  • 13. 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
  • 16. 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
  • 17. Cholinergic Agents: Mechanism of Action Direct-acting (agonist) Bind to cholinergic receptors, causing stimulation Acts on the receptor sites to activate a tissue response
  • 18. Direct-Acting Cholinergic Drugs Ex: bethanechol chloride(Urecholine)- used to increase urination metoclopramide HCL(Plasil)- usually used to treat GERD---increases gastric emptying time
  • 19. 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
  • 20. Indirect Acting cholinergic drugs Ex: demecarium bromide(Humorsol)-reduces IOP in glaucoma, long acting miotic ambenonium Cl (Mytelase)- to increase muscle strength in MG, long acting edrophonium Cl(Tensilon)- to diagnose MG, very short acting
  • 21. 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
  • 22. Drug Effects of Cholinergic Agents Effects seen when the PSNS is stimulated. The PSNS is the “rest and digest” system.
  • 23. Drug Effects of Cholinergic Agents “ SLUDGE” S alivation L acrimation U rinary incontinence D iarrhea G astrointestinal cramps E mesis
  • 24. 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
  • 25. Drug Effects of Cholinergic Agents Cardiovascular effects Decreased heart rate Vasodilation Respiratory effects Bronchial constriction, narrowed airways
  • 26. Drug Effects of Cholinergic Agents At recommended doses, the cholinergics primarily affect the MUSCARINIC receptors. At high doses, cholinergics stimulate the NICOTINIC receptors.
  • 27. 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
  • 28. 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
  • 29. 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
  • 30. 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.
  • 31. Cholinergic Agents: Side Effects Side 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
  • 32. Cholinergic Agents: Side Effects Respiratory: Increased bronchial secretions, bronchospasms Other: Lacrimation, sweating, salivation, loss of binocular accommodation, miosis
  • 33. Cholinergic Agents: Interactions Anticholinergics, antihistamines, sympathomimetics Antagonize cholinergic agents, resulting in decreased responses
  • 34. 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.
  • 35. 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.
  • 36. 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.
  • 37. 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.
  • 38. Cholinergic Agents: Nursing Implications Monitor for side effects, including: Increased respiratory Abdominal cramping secretions Bronchospasms Dysrhythmias Difficulty breathing Hypotension Nausea and vomiting Bradycardia Diarrhea Increased sweating Increase in frequency and urgency of voiding patterns
  • 39. 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
  • 41. Cholinergic Blocking Agents Drugs that block or inhibit the actions of acetylcholine (ACh) in the parasympathetic nervous system (PSNS)
  • 42. 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.
  • 43. Cholinergic Blocking Agents: Chemical Class Natural Synthetic/Semisynthetic atropine anisotropine clidinium belladonna dicyclomine glycopyrrolate hyoscyamine hexocyclium homatropine scopolamine ipratropium isopropamide oxybutynin propantheline tolterodine tridihexethyl
  • 44. 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
  • 45. 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
  • 46. 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
  • 47. Cholinergic Blocking Agents: Therapeutic Uses CNS Decreased muscle rigidity and muscle tremors Parkinson’s disease Drug-induced extrapyramidal reactions
  • 48. Cholinergic Blocking Agents: Therapeutic Uses Cardiovascular Affect 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
  • 49. 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)
  • 50. Cholinergic Blocking Agents: Therapeutic Uses Respiratory Blocking 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
  • 51. Cholinergic Blocking Agents: Therapeutic Uses Respiratory agents are used to treat: Exercise-induced bronchospasms Chronic bronchitis Asthma Chronic obstructive pulmonary disease
  • 52. Cholinergic Blocking Agents: Therapeutic Uses Gastrointestinal PSNS 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
  • 53. Cholinergic Blocking Agents: Therapeutic Uses Gastrointestinal agents are used to treat: Peptic ulcer disease Irritable bowel disease GI hypersecretory states
  • 54. Cholinergic Blocking Agents: Therapeutic Uses Genitourinary Relaxed detrusor muscles of the bladder Increased constriction of the internal sphincter Reflex neurogenic bladder Incontinence
  • 55. Cholinergic Blocking Agents: Side Effects Body System Side/Adverse Effects Cardiovascular Increased heart rate, dysrhythmias CNS CNS excitation, restlessness, irritability, disorientation, hallucinations, delirium
  • 56. 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
  • 57. Cholinergic Blocking Agents: Side Effects Body System Side/Adverse Effects Genitourinary Urinary retention Glandular Decreased sweating Respiratory Decreased bronchial secretions
  • 58. Cholinergic Blocking Agents: Interactions Antihistamines, phenothiazines, tricyclic antidepressants, MAOIs When given with cholinergic blocking agents, cause ADDITIVE cholinergic effects, resulting in increased effects
  • 59. Cholinergic Blocking Agents: Nursing Implications Keep in mind that these agents will block the 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.
  • 60. 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.
  • 61. 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).
  • 62. 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.
  • 63. 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
  • 64. 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
  • 65. Cholinergic Blocking Agents: Nursing Implications Monitor for side effects, including: Constipation Tachycardia Tremors Confusion Hallucinations Sedation Urinary retention Hot, dry skin Fever CNS depression (occurs with large doses of atropine)
  • 66.  &  
  • 68. 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
  • 69. Effects of Adrenergics at Receptors Receptor Physiologic Responces Alpha 1 Increases force of heart contraction; vasoconstriction increases BP; mydriasis; salicary glands decrease secretions; bladder and prostate capsule increases contraction and ejaculation Alpha 2 Inhibits the release of norepinephrine; dilates blood vessels; produces hypotension; decreases GI motility and tone Beta 1 Increases heart rate and contraction; increases renin secretion----increase BP Beta 2 Dilates bronchioles; promotomes GI and uterine relaxation; promotes increase in blood sugar through glycogenolysis in the liver; increases blood flow in the skeletal muscles
  • 70. Classification of Sympathomimetics/Adrenomimetics Direct-Acting sympathomimetics directly stimulate the adrenergic receptor (e.g. epinephrine, norepinephrine) Indirect-Acting sympathomimetics which stimulates the release of norepinephrine from the terminal nerve endings (e.g. amphetamine) Mixed-Acting sympathomimetics (both direct and indirect acting)
  • 71. 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
  • 72. Indications of adrenergics cont. Stokes Adams Shock Inhibition of uterine contractions For vasoconstrictive and hemostatic purposes
  • 73. 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
  • 74. Individual adrenergic drugs Epinephrine —prototype Effects include: increased BP, increased heart rate, relaxation of bronchial smooth muscle, vasoconstriction in peripheral blood vessels
  • 75. epinephrine Increased glucose, lactate, and fatty acids in the blood due to metabolic effects Increased leukocyte and increased coagulation Inhibition of insulin secretion
  • 76. 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
  • 77. epinephrine Excellent for cardiac stimulant and vasoconstrictive effects in cardiac arrest Added to local anesthetic May be given IV, inhalation, topically Not PO
  • 78. 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
  • 79. Other adrenergics Ephedrine is a mixed acting adrenergic drug. Stimulates alpha and beta receptors. Longer lasting than epinephrine.
  • 80. Pseudophed Used for bronchodilating and nasal decongestant effects
  • 81. 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
  • 82. 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
  • 83. 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
  • 84. Toxicity Do not give epinephrine and Isuprel at same time or within 4 hours of each other. Could result in serious dysrhythmias.
  • 85. 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
  • 87. Anti-adrenergics Sympatholytic Block or decrease the effects of sympathetic nerve stimulation, endogenous catecholamines and adrenergic drugs
  • 88. 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.
  • 89. 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
  • 90. 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
  • 91. 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
  • 92. Alpha 1 antagonists Minipress (prazosin)—prototype. Hytrin (terazosin) and Cardura (doxazosin)—both are longer acting than Minipress.
  • 93. 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.
  • 94. Alpha 2 agonists Catapres (clonidine). PO or patch. Tenex (guanfacine) Aldomet (methyldopa). Can give IV. Caution in renal and hepatic impairment.
  • 95. Beta adrenergic blocking medications Prevent receptors from responding to sympathetic nerve impulses, catecholamines and beta adrenergic drugs.
  • 96. Effects of beta blocking drugs Decreased heart rate Decreased force of contraction Decreased CO Slow cardiac conduction Decreased automaticity of ectopic pacemakers
  • 97. 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)
  • 98. 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
  • 99. 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
  • 100. Regitine (phentolamine) Used for extravasation of potent vasoconstrictors (dopamine, norepinephrine) into subcutaneous tissues
  • 101. 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
  • 102. 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.
  • 103. 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”
  • 104. 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
  • 105. 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
  • 106. 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
  • 107. 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
  • 108. Non-Receptor selectivity Carteolol, levobunolol, metipranolol, nadolol, propranolol, sotalol and timolol are all non-selective Can cause bronchoconstriction, peripheral vasoconstriction and interference with glycogenolysis
  • 109. 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
  • 110. 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)
  • 111. 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.
  • 112. 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
  • 113. 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.
  • 114. 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.
  • 115. 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