ANS Medications NUR 2303 Week 8 PDF

ANS Medications NUR 2303 – Week 8 Housekeeping Questions Kaplan reminder – practice tests, channel videos Glossary Chronotropic Sympatholytic Inotropic Sympathomimetic Dromotropic Parasympatholytic Adrenergic Parasympathomimetic Agonist Cholinergic Antagonist Anti-choli...

ANS Medications NUR 2303 – Week 8 Housekeeping Questions Kaplan reminder – practice tests, channel videos Glossary Chronotropic Sympatholytic Inotropic Sympathomimetic Dromotropic Parasympatholytic Adrenergic Parasympathomimetic Agonist Cholinergic Antagonist Anti-cholinergic ANS YouTube Review video Chapter 19 Adrenergic Drugs Automatic Nervous System Adrenergic Receptors Located throughout the body Are receptors for the sympathetic neurotransmitters α-Adrenergic receptors ß-Adrenergic receptors Dopaminergic receptors: respond only to dopamine Adrenergic drugs mimic the effects of Somatic Nervous System (SNS) neurotransmitters (catecholamines) norepinephrine epinephrine dopamine α-Adrenergic Receptors α1-Adrenergic receptors Located on postsynaptic effector cells (the cell, muscle, or organ the nerve stimulates) α2-Adrenergic receptors Located on presynaptic nerve terminals (the nerve that stimulates the effector cells) Control the release of neurotransmitters α2-Adrenergic agonists cause Vasoconstriction Central nervous system (CNS) stimulation ß-Adrenergic Receptors All are located on postsynaptic effector cells. ß1-Adrenergic receptors: located primarily in the heart ß2-Adrenergic receptors: located in smooth muscle of the bronchioles, arterioles, and visceral organs ß1-Adrenergic agonists cause Bronchial, gastrointestinal (GI), and uterine smooth muscle relaxation Glycogenolysis Cardiac stimulation Dopaminergic Receptors Additional adrenergic receptors Stimulated by dopamine Cause dilation of the following blood vessels, resulting in increased blood flow: Renal Mesenteric Coronary Cerebral Catecholamines Substances that can produce a sympathomimetic response Endogenous epinephrine, norepinephrine, dopamine Synthetic dobutamine, phenylephrine hydrochloride Physiological Response To Direct-acting Sympathomimetics Direct-acting sympathomimetic binds directly to the receptor and causes a physiological response Physiological Response To Indirect-acting Sympathomimetics Indirect-acting sympathomimetic causes release of catecholamine from storage sites (vesicles) in nerve endings. Catecholamine then binds to receptors and causes a physiological response. Physiological Response To Mixed-acting Sympathomimetics Mixed-acting sympathomimetic directly stimulates the receptor by binding to it. Indirectly stimulates the receptor by causing the release of stored neurotransmitters from vesicles in the nerve endings Stimulation of α-Adrenergic receptors Vasoconstriction of blood vessels Relaxation of GI smooth muscles (↓ motility) Constriction of bladder sphincter Contraction of uterus Male ejaculation Contraction of pupillary muscles of the eye (dilated pupils) Indications for α-Adrenergic agonists Reduction of intraocular pressure and dilation of pupils: treatment of open-angle glaucoma α-Adrenergic receptors Example: dipivefrin hydrochloride Stimulation of ß1-Adrenergic receptors On the myocardium, atrioventricular (AV) node, and sinoatrial node results in cardiac stimulation. Increased force of contraction (positive inotropic effect) Increased heart rate (positive chronotropic effect) Increased conduction through AV node (positive dromotropic effect) Dobutamine Hydrochloride Selective vasoactive ß1-adrenergic drug that is structurally like the naturally occurring catecholamine dopamine Stimulates ß1-receptors on heart muscle (myocardium); ↑ cardiac output by increasing contractility (positive inotropy), which ↑ stroke volume, especially in patients with heart failure. Intravenous drug; given by continuous infusion Stimulation of ß2-Adrenergic receptors On the airways results in bronchodilation (relaxation of the bronchi). Other effects of ß2-adrenergic stimulation: Uterine relaxation Glycogenolysis in the liver Increased renin secretion in the kidneys Relaxation of GI smooth muscles (decreased motility) Indications for ß2-Adrenergic Agonists Treatment of asthma and bronchitis Bronchodilators: drugs that stimulate ß2-adrenergic receptors of bronchial smooth muscles, causing relaxation Common bronchodilators that are classified as predominantly β2-selective adrenergic drugs formoterol fumurate dihydrate, salbutamol, salmeterol, xinafoate, and terbutaline sulphate. Vasoactive Sympathomimetics (AKA: Pressors, Inotropes) Also called cardioselective sympathomimetics Used to support the heart during cardiac failure or shock; various α- and ß-receptors affected Dopamine Hydrochloride Naturally occurring catecholamine neurotransmitter Potent dopaminergic as well as ß1- and α1-adrenergic receptor activity Low dosages: can dilate blood vessels in the brain, heart, kidneys, and mesentery, which increases blood flow to these areas (dopaminergic receptor activity) Higher infusion rates: improve cardiac contractility and output (ß1-adrenergic receptor activity) Highest doses: vasoconstriction (α1-adrenergic receptor activity) Epinephrine Hydrochloride (Adrenalin®) Endogenous vasoactive catecholamine Acts directly on both the α- and ß-adrenergic receptors of tissues innervated by the SNS Prototypical nonselective adrenergic agonist Administered in emergency situations One of the primary vasoactive drugs used in many advanced cardiac life support protocols Norepinephrine Betartrate (Levophed®) Stimulates α-adrenergic receptors Causes vasoconstriction Direct-stimulating ß-adrenergic effects on the heart (ß1- adrenergic receptors) No stimulation to ß2-adrenergic receptors of the lung Treatment of hypotension and shock Administered by continuous infusion Question A patient on a dobutamine drip reports that the intravenous line “hurts.” The nurse checks the insertion site and sees that the area is swollen and cool. What will the nurse do first? A. Slow the intravenous infusion. B. Stop the intravenous infusion. C. Inject the area with phentolamine. D. Notify the physician health care provider. α-Adrenergic Adverse Effects CNS Cardiovascular Other Headache, restlessness, Palpitations (dysrhythmias), Loss of appetite, dry mouth, excitement, insomnia, euphoria tachycardia, vasoconstriction, nausea, vomiting, taste changes hypertension (rare) ß-Adrenergic Adverse Effects Mild tremors, headache, nervousness, CNS dizziness, insomnia, euphoria Chest pain, increased heart rate, Cardiovascular palpitations (dysrhythmias), hypertension, vasoconstriction Sweating, nausea, vomiting, muscle Other cramps Interactions Anaesthetic drugs Digoxin Tricyclic antidepressants Monoamine oxidase inhibitors (MAOIs) Antihistamines Thyroid preparations Nursing Considerations Complete a comprehensive hx Assess for allergies and asthma Assess for hx of hypertension, dysrhythmias, and other CVD Assess renal, hepatic, and cardiac function before treatment. Baseline vs, peripheral pulses, skin colour, temperature, and cap refill Follow administration guidelines carefully. Monitor for therapeutic effects. Two adrenergic drugs may cause severe cardiovascular effects Question A patient on a dobutamine drip reports feeling a “tightness” in the chest that had not been felt before. What will the nurse do first? A. Check the infusion site for possible extravasation. B. Increase the infusion rate. C. Check the patient’s vital signs. D. Order an electrocardiogram. Question A 10-year-old child is brought to the emergency department while having an asthma attack. The child is given a nebulizer treatment with salbutamol. The nurse’s immediate assessment priority would be to: A. Determine the time of the child’s last meal. B. Monitor blood oxygen saturation (SpO2) with a pulse oximeter. C. Monitor the child’s temperature. D. Provide education on asthma management. Chapter 20 Adrenergic-Blocking Drugs Adrenergic Blockers Bind to adrenergic receptors block stimulation of the SNS Have the opposite effect of adrenergic drugs Inhibit (lyse) sympathetic stimulation Also known as: Adrenergic antagonists Sympatholytics α-blockers, β-blockers, and α-β–blockers Classified by the type of adrenergic receptor they block α1- and α2-receptors β1- and β2-receptors Alpha-blocker Mechanisms Drug Effects and Indications: α-Blockers Arterial and venous dilation, ↓ peripheral vascular resistance and BP ↓ resistance to urinary outflow, reduces urinary obstruction and relieves the effects of BPH Used to control and prevent hypertension in patients with pheochromocytoma Raynaud’s disease, acrocyanosis, and frostbite α-Blockers: Body System/Adverse Effects Cardiovascular: CNS: Dizziness, Palpitations, orthostatic headache, anxiety, hypotension, tachycardia, depression, weakness, edema, chest pain numbness, fatigue GI: Nausea, vomiting, Other: Incontinence, dry diarrhea, constipation, mouth, pharyngitis abdominal pain Question When the nurse is administering an α- blocker for the first time, which of the following is the most important development for the nurse to assess? A. Renal failure B. Hypotension C. Blood dyscrasia D. Dysrhythmias Common α-Blockers alfuzosin hydrochloride (Xatral®) phentolamine mesylate (Rogitine®) prazosin hydrochloride (Minipress®) terazosin hydrochloride (Hytrin®) tamsulosin (Flomax®) doxazosin mesylate (Cardura®) Phentolamine (Rogitine®) α-Blocker that reduces systemic vascular resistance and is sometimes used to treat hypertension Establish a diagnosis of pheochromocytoma Used to treat the extravasation of vasoconstricting drugs such as norepinephrine, epinephrine, and dopamine Contraindicated in known hypersensitivity, myocardial infarction (MI), and coronary artery disease Tamsulosin (Flomax®) α-Blocker used primarily to treat BPH; exclusively indicated for male patients Contraindications: known drug allergy and concurrent use of erectile dysfunction drugs such as sildenafil Adverse effects: headache, abnormal ejaculation, rhinitis, and others β-Blockers Block stimulation of β-receptors in the SNS Compete with norepinephrine and epinephrine Can be selective or nonselective Cardioselective β-blockers or β1-blocking drugs Nonselective β-blockers block both β1-receptors and β2-receptors. β2-Receptors are located primarily on the smooth muscles of the bronchioles and blood vessels. Cardioselective β-blockers (β1) ↓ SNS stimulation of the heart ↓ heart rate Prolong sinoatrial node recovery Slow conduction rate through the atrioventricular (AV) node ↓ myocardial contractility, thus reducing myocardial oxygen demand Nonselective β-blockers (β1 and β2) Cause same effects on heart as do cardioselective ß-blockers Constrict bronchioles, resulting in narrowing of airways and shortness of breath Produce vasoconstriction of blood vessels Other effects β-Receptors: Indications Angina, MI, hypertension Decrease demand for myocardial oxygen Cardioprotective Inhibit stimulation from circulating catecholamines Dysrhythmias Glaucoma (topical use) Migraine headache Lipophilicity allows entry into central nervous system. Question A 58-year-old patient is recovering in the Critical Care Unit after an MI. The nurse notes an order for the β- blocker metoprolol (Lopressor). The purpose of this drug is to A. Dilate the coronary arteries. B. Inhibit stimulation of the myocardium by circulating catecholamines. C. Provide a positive inotropic effect. D. Maintain the patient’s BP. β-Blockers: Adverse Effects Nonselective β-blockers may interfere with normal responses to hypoglycemia (tremor, tachycardia, nervousness). May mask signs and symptoms of hypoglycemia Use with caution in patients with diabetes mellitus. Atenolol (Tenormin®) Cardioselective β-blocker Commonly used to prevent future heart attacks in patients who have had one attack Hypertension and angina Management of thyrotoxicosis to help block the symptoms of excessive thyroid activity Available for oral use Esmolol (Brevibloc®) Very strong short-acting β1-blocker. Primary use: acute situations, to provide rapid temporary control of the ventricular rate in patients with supraventricular tachydysrhythmias Administered intravenously Question The adverse effects of a nonselective β-blocker are likely to be the most immediately life threatening in which of the following patients? A. Patient with type I diabetes B. Patient with asthma C. Patient with gastroesophageal reflux disease D. Patient with hypertension Nonselective β-Blockers carvedilol nadolol (Nadol®) labetalol (Trandate®) pindolol (Visken®) propranolol (Inderal®) sotalol (Rylosol®) timolol (Timoptic®) Cardioselective β-Blockers acebutolol (Sectral®) atenolol (Tenormin®) bisoprolol fumerate esmolol (Brevibloc®) nebivolol (Bystolic®) metoprolol (Lopressor®) Nursing Considerations Assess for allergies and perform a thorough cardiac assessment. Any pre-existing condition that might be exacerbated using these drugs α-blockers may cause hypotension. β-blockers may cause bradycardia, hypotension, heart block, heart failure, and bronchoconstriction. Encourage patients to take medications as prescribed. Instruct patients that these medications should never be stopped abruptly. Inform patients to report constipation or the development of urinary hesitancy or bladder distention. Nursing Considerations (cont.) Teach patients to change positions slowly to minimize postural hypotension. Instruct patients to avoid caffeine (causes excessive irritability). Instruct patients to initially avoid alcohol ingestion and hazardous activities Instruct patients to report palpitations, dyspnea, nausea, or vomiting occurs. Monitor for adverse effects. Monitor for therapeutic effects. Decreased chest pain in patients with angina Return to normal BP and heart rate Other specific effects, depending on the use Drug Interactions Avoid over-the-counter medications because of possible interactions. Possible drug interactions may occur with: Antacids (aluminum hydroxide type) Antimuscarinics or anticholinergics Diuretics and cardiovascular drugs Neuromuscular blocking drugs Oral hypoglycemic drugs Question A patient with type 2 diabetes is taking a β-blocker as part of treatment of hypertension. Which complication is most likely to develop? A. Hypertension B. Hyperkalemia C. Hypoglycemia D. Angina This Photo by Unknown Author is licensed under CC BY-SA Chapter 21 Cholinergic Drugs Cholinergic Drugs Drugs that stimulate the parasympathetic nervous system Also known as cholinergic agonists or parasympathomimetics Mimic effects of the parasympathetic nervous system neurotransmitter acetylcholine (ACh) Nicotinic receptors Muscarinic receptors Parasympathetic and Sympathetic Nervous Systems Cholinergic Drugs: Mechanism of Action Direct-acting cholinergic agonists Bind to cholinergic receptors, activating them Indirect-acting cholinergic agonists Also known as cholinesterase inhibitors Inhibit the enzyme acetylcholinesterase, which breaks down ACh Results in more ACh available at the receptors Indirect-Acting (Cholinesterase Inhibitors) Reversible Bind to cholinesterase for a short period of time Irreversible Bind to cholinesterase for a long period of time Bind to cholinesterase and form a permanent covalent bond The body must make new cholinesterase to break these bonds. Drug Effects Effects when parasympathetic system “rest and digest” is stimulated. Stimulate intestine and bladder ↑ gastric secretions ↑ gastrointestinal motility ↑ urinary frequency Stimulate pupils Constriction (miosis) ↓ intraocular pressure ↑ salivation and sweating Cholinergic Drug Effects Cardiovascular effects ↓ heart rate Vasodilation Respiratory effects Bronchial constriction, narrowed airways At recommended doses, cholinergics primarily affect muscarinic receptors. At high doses, cholinergics stimulate nicotinic receptors. Desired effects are from muscarinic receptor stimulation. Many undesirable effects are caused by stimulation of nicotinic receptors. Question The nurse is assessing a patient who has been taking a cholinergic drug for 3 days. The patient has flushed skin and orthostatic blood pressure changes and reports abdominal cramps and nausea. The nurse recognizes that the patient is most likely experiencing A. Early signs of a cholinergic crisis. B. Late signs of a cholinergic crisis. C. An allergic reaction to the drug. D. Expected adverse effects. Direct acting Cholinergic carbachol or pilocarpine Reduce intraocular pressure Useful for glaucoma and intraocular surgery Topical application because of poor oral absorption bethanechol Increases tone and motility of bladder and gastrointestinal (GI) tract Relaxes sphincters in bladder and GI tract, allowing them to empty Helpful for postsurgical atony of the bladder and GI tract Oral dose or subcutaneous injection succinylcholine Used as a neuromuscular blocker in general anaesthesia Intravenous Indirect-acting Cholinergic Increase ACh concentrations at the receptor sites, which leads to stimulation of the effector cells Cause skeletal muscle contractions Used for diagnosis and treatment of myasthenia gravis Used to reverse neuromuscular blocking drugs Used to reverse anticholinergic poisoning (antidote) Example: physostigmine Indirect-acting anticholinesterase drugs Used for treatment of mild to moderate Alzheimer’s disease donepezil (Aricept®) galantamine (Reminyl®) rivastigmine hydrogen tartrate (Exelon®) Contraindications Known drug allergy GI or genitourinary (GU) tract obstruction Bradycardia Defects in cardiac impulse conduction Hyperthyroidism Epilepsy Hypotension Chronic obstructive pulmonary disease Parkinson’s disease (exception rivastigmine) Adverse Effects Adverse effects are a result of overstimulation of the parasympathetic system. Bradycardia, hypotension, syncope, conduction abnormalities (atrioventricular block and cardiac arrest) Headache, dizziness, convulsions, ataxia Abdominal cramps, increased secretions, nausea, vomiting, diarrhea, weight loss Increased bronchial secretions, bronchospasms Other Lacrimation, sweating, salivation, miosis Cholinergic Crisis Circulatory collapse, hypotension, bloody diarrhea, shock, and cardiac arrest. SLUDGE (salivation, lacrimation, urinary incontinence, diarrhea, gastrointestinal cramps, and emesis) Early signs Abdominal cramps, salivation, flushing of the skin, nausea and vomiting, transient syncope, transient complete heart block, dyspnea, and orthostatic hypotension Treatment in early phase: atropine sulphate, a cholinergic antagonist Treatment of severe cardiovascular reactions or bronchoconstriction: epinephrine, an adrenergic agonist Interactions Anticholinergics, antihistamines, sympathomimetics Antagonize cholinergic drugs, resulting in decreased responses Other cholinergic drugs Additive effects Bethanechol (Duvoid®) Direct-acting cholinergic agonist Treatment of acute postoperative and postpartum nonobstructive urinary retention Management of urinary retention associated with neurogenic atony of the bladder Contraindications Known drug allergy, hyperthyroidism, peptic ulcer, active bronchial asthma, cardiac disease or coronary artery disease, epilepsy, and parkinsonism Donepezil (Aricept) Cholinesterase inhibitor that works centrally in the brain to increase levels of ACh by inhibiting acetylcholinesterase Used in the treatment of mild to moderate Alzheimer’s disease Similar cholinesterase inhibitors include galantamine and rivastigmine. Pyridostigmine (Mestinon®) Indirect-acting cholinergic drugs that work to increase ACh by inhibiting acetylcholinesterase Use: myasthenia gravis Edrophonium (Tensilon): indirect-acting cholinergic drug that is used to diagnose myasthenia gravis. It can also be used to differentiate between myasthenia gravis and cholinergic crisis. Question A patient with Alzheimer’s disease accidentally took 2 weeks’ worth of a cholinergic medication. Brought to the emergency department, the patient is going into shock and is experiencing severe hypotension and vomiting. The nurse will expect which initial treatment? A. Administration of physostigmine B. Administration of atropine C. Administration of epinephrine D. Cardiovascular support with dopamine This Photo by Unknown Author is licensed under CC BY-ND Nursing Considerations Note that these drugs will stimulate the parasympathetic nervous system and mimic the action of ACh. Assess for allergies, presence of GI or GU obstructions, asthma, peptic ulcer disease, and coronary artery disease. Perform baseline assessment of vital signs and systems overview. Medications should be taken as ordered and not abruptly stopped. Doses should be spread evenly apart to optimize the effects Overdosing can cause life-threatening problems. Patients should not adjust dosages unless directed by their health care provider. Nursing Considerations Atropine is the antidote for cholinergics, and it should be available in the patient’s room for immediate use if needed. Patients should notify their physicians if they experience muscle weakness, abdominal cramps, diarrhea, or difficulty breathing. Monitor for therapeutic effects Alleviated signs and symptoms of myasthenia gravis In postoperative patients with decreased GI peristalsis, monitor for: Increased bowel sounds Passage of flatus Occurrence of bowel movements Chapter 22 Cholinergic-Blocking Drugs Cholinergic-Blocking Drugs Drugs that block or inhibit the actions of acetylcholine (ACh) in the parasympathetic nervous system (PSNS) Also known as anticholinergics, parasympatholytics, and antimuscarinic drugs Compete with ACh for binding at muscarinic receptors ACh is unable to bind to the receptor site and cause a cholinergic effect. When these drugs bind to receptors, they inhibit nerve transmission at these receptors Site of Action of Cholinergic Blockers Cholinergic-Blocking Drugs: Examples Natural Plant Alkaloids atropine sulphate belladonna scopolamine hydrobromide Synthetic and semisynthetic dicyclomine (Bentylol®) glycopyrrolate oxybutynin (Ditropan®) tolterodine (Detrol®) Drug Effects Cardiovascular Small doses: decreased heart rate Large doses: increased heart rate Central nervous system (CNS) Small doses: decreased muscle rigidity and tremors Large dose: drowsiness, disorientation, hallucinations Drug Effects Eye Dilated pupils (mydriasis) Decreased accommodation caused by paralysis of ciliary muscles (cycloplegia) Gastrointestinal (GI) Relaxed smooth muscle tone of GI tract Decreased intestinal and gastric secretions Decreased motility and peristalsis Question Which finding would the nurse anticipate when assessing a patient with an atropine overdose? A. Moist skin B. Miosis C. Bradycardia D. Urinary retention This Photo by Unknown Author is licensed under CC BY-SA-NC Drug Effects Genitourinary (GU) Relaxed detrusor muscle Increased constriction of internal sphincter Result: urinary retention Glandular Decreased sweating Respiratory Decreased bronchial secretions Indications Atropine Used primarily for cardiovascular disorders Diagnosis of sinus node dysfunction Symptomatic second-degree heart block Severe sinus bradycardia with hemodynamic compromise (advanced life support) Indications: Respiratory Decreased secretions from the nose, mouth, pharynx, and bronchi Relaxed smooth muscles in the bronchi and bronchioles Decreased airway resistance Bronchodilation Cholinergic blockers are used to treat: Exercise-induced bronchospasms Asthma Chronic obstructive pulmonary disease Indications Decreasing muscle rigidity and muscle tremors Parkinson’s disease Drug-induced extrapyramidal reactions such as those associated with antipsychotic drugs Affects the heart’s conduction system Low doses: slow the heart rate High doses: block inhibitory vagal effects on sinoatrial and atrioventricular node pacemaker cells Results in increased heart rate Indications: Gastrointestinal The 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 GI drugs are used to treat: Irritable bowel disease GI hypersecretory states Indications: Genitourinary Reflex neurogenic bladder Incontinence Contraindications Known drug allergy Angle-closure glaucoma Acute asthma or other respiratory distress Myasthenia gravis (Immune Disorder) Acute cardiovascular instability GI or GU tract obstruction (e.g., BPH or illness) Body system/adverse effects Cardiovascular: Increased heart rate, dysrhythmias CNS: CNS excitation, restlessness, irritability, disorientation, hallucinations, delirium Eye: Dilated pupils (causing blurred vision), increased intraocular pressure GI: Decreased salivation, decreased gastric secretions, decreased motility (constipation) GU: Urinary retention Glandular: Decreased sweating Respiratory: Decreased bronchial secretions Interactions Amantadine, antihistamines, phenothiazines, digoxin When the above drugs are given with other cholinergic-blocking drugs, cause additive cholinergic effects, resulting in increased effects Toxicity and Overdose Symptomatic and supportive therapy Continuous electrocardiographic monitoring Activated charcoal Treatment of shock Physostigmine Atropine Naturally occurring antimuscarinic Uses: bradycardia, ventricular asystole, antidote for anticholinesterase inhibitor toxicity or poisoning, and preoperatively to reduce salivation and GI secretions Contraindications: angle-closure glaucoma, advanced hepatic and renal dysfunction, hiatal hernia associated with reflux esophagitis, intestinal atony, obstructive GI or GU conditions, and severe ulcerative colitis Glycopyrrolate Synthetic antimuscarinic drug Blocks receptor sites in the autonomic nervous system that control the production of secretions Use: preoperatively to reduce salivation and excessive secretions in the respiratory and GI tracts Contraindications: hypersensitivity, angle-closure glaucoma, myasthenia gravis, GI or GU tract obstruction, tachycardia, myocardial ischemia, hepatic disease, ulcerative colitis, and toxic megacolon Dicyclomine hydrochloride (Bentylol®) Synthetic antispasmodic cholinergic blocker Uses: functional disturbances of GI motility, such as irritable bowel syndrome Contraindications: known hypersensitivity to anticholinergics, angle-closure glaucoma, GI tract obstruction, myasthenia gravis, paralytic ileus, GI atony, and toxic megacolon Nursing Considerations Assess for allergies, presence of BPH, urinary retention, glaucoma, tachycardia, myocardial infarction, heart failure, hiatal hernia, and GI or GU obstruction. Perform baseline assessment of vital signs. Medications should be taken exactly as prescribed to have the maximum therapeutic effect. Overdosing can cause life-threatening problems. Blurred vision will cause problems with driving or operating machinery. Nursing Implications Patients may experience sensitivity to light and may want to wear dark glasses or sunglasses. 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. Patients should check with the physician before taking any other medication, including over-the-counter medications. Antidote for atropine overdose is physostigmine. Nursing Implications Anticholinergics taken by older adult patients may lead to higher risk for heatstroke because of the effects on heat-regulating mechanisms. Teach patients to limit physical exertion and to avoid high temperatures and strenuous exercise. Emphasize the importance of adequate fluid intake. Question Glycopyrrolate and an opioid are administered to a patient before surgery in the preoperative area. The anticholinergic is used to A. potentiate the action of the opioid. B. assist the patient in retaining urine during surgery. C. control secretions during surgery. D. prevent nausea. Wrap-up Questions? Next week: Renal Fluids and Electrolytes