NURS 3210 Active Learning Guide - Module 4 - CV Agents PDF

NURS 3210 Pharmacology and Nursing Active Learning Guide- Module 4- Medications Affecting and Protecting the CV System, Pa...

NURS 3210 Pharmacology and Nursing Active Learning Guide- Module 4- Medications Affecting and Protecting the CV System, Part 2 Purpose/Overview Active learning guides help students to focus their study time. They include knowledge level questions as well as those focusing on the application and analysis of information to provide greater context in relation to the course and career skills. Students should review the active learning guide before beginning to engage with the module content, then work to complete the guide during and after engaging with the content. An active learning guide is not the same as a study guide or a test blueprint. It serves as a guide to help the student navigate course or module content. Instructions Quickly review the active learning guide (ALG) before you begin reading and engaging with other content in the module. Looking at the questions beforehand will provide a preview of the information you should be alert to as your work through your reading or module resources. As you work through the module content, complete the active learning guide, topic-by-topic. You should use the resources provided and linked on the “Prepare” page in Canvas as the primary source for answering the questions in the active learning guide. Specific Agents for Module 4 1. Fill in the table with the drug’s classification/s. The drugs in the table are those you will be asked about on quizzes and exams. Keep in mind your assigned reading may include information about individual agents not listed here. You can check your work in the practice activity (flashcards) for each module. Common endings or other clues about the drug’s classification are italicized.  NURS 3210 Pharmacology and Nursing Coagulation Modifiers (Ch 26): Agent Name Classification Agent Name Classification Agent Name Classification Heparin Anticoagulant Warfarin Anticoagulan Vitamin K Fat soluable t Rivaroxaban Anticoagulant ASA Alteplase Thrombolytic Aminocaproic Antifibrinolytics Desmopressin Antihemophi Idarucizamab monoclonal Acid (DDAVP) lic antibodies Clopidogrel Antiplatelet Enoxaparin Anticoagulan Protamine t Sulfate Antianginals, Antidysrhythmics, and Antilipemics (Ch. 23, 27, 23): Agent Classification Agent Name Classification Agent Name Classification Name Niacin Adenosine antiarrhythm Nitroglyceri vasodilator ics n (NTG) Diltiazem Calcium Ezetimibe Anticholester Metoprolol beta-blockers channel ol agent blockers Atorvastatin Statin Procainamide antiarrhythm Amiodarone antiarrhythmics ics Isosorbide Antianginal Omega-3 Gemfibrozil antihyperlipidemic Lidocaine anesthetic Sotalol beta- Atenolol beta-blockers adrenergic blocking agents Flecainaide Antidysrhyth Magnesium sulfate anticonvulsa Verapamil calcium channel mics nt blockers Carvedilol non-selective Cholestyramine bile acid beta-blocker sequestrants Reading: Chapter 26 (Coagulation Modifiers) 1. Define thromboembolism and give three examples of thromboembolic events? Thromboembolism → The blocking of a blood vessel by a blood clot dislodged from its site of origin. Thromboembolic events → Events in which a blood vessel is blocked by an embolus carried in the bloodstream from the site of its formation. The tissue supplied by an obstructed artery may  NURS 3210 Pharmacology and Nursing tingle and become cold, numb, cyanotic, and eventually necrotic (dead). Once a clot forms on the wall of a blood vessel, it may dislodge and travel through the bloodstream. Such a clot is referred to as an embolus. If it lodges in a coronary artery, it can cause a myocardial infarction (MI); if it obstructs a brain vessel, it causes a stroke; if it goes to the lungs, it is a pulmonary embolism (PE); and if it goes to a vein in the leg, it is a deep vein thrombosis (DVT). 2. List 5 risk factors associated with thromboembolic events: Prolonged Immobility → Long flights or hospitalizations can lead to slow blood flow, exposing people to the possibility of forming blood clots. Age → Increasing in age puts an individual at significant risk. As we grow older our blood vessels can become narrower and less flexible. This can increase the chances of clot formation. Smoking → Smoking is a crucial risk factor for a thromboembolic event. Tobacco use damages the blood vessels, causes the blood pressure to increase and causes blood clots to form. Obesity → Obesity contributes to the creation of thromboembolic events due to excess weight putting additional stress on the cardiovascular system causing a cascade event to increase the opportunity to develop diabetes, increase blood pressure (hypertension) and blood clots. Family History → Inherited disorders in clotting can increase a family members chances having similar clotting disorders. 3. How does hemostasis occur? Write a 2-3 sentence summary of the process highlighting the major steps. Hemostasis is a general term for any process that stops bleeding. This can be accomplished by mechanical means (e.g., compression to the bleeding site) or surgical means (e.g., surgical clamping or cauterization of a blood vessel). When hemostasis occurs as a result of physiologic clotting of blood, it is called coagulation, which is the process of blood clot formation. The technical term for a blood clot is a thrombus. A thrombus that moves through blood vessels is  NURS 3210 Pharmacology and Nursing called an embolus. Normal hemostasis involves the complex interaction of substances that promote clot formation and other substances that either inhibit coagulation or dissolve the formed clot. Substances that promote coagulation include platelets, von Willebrand factor, activated clotting factors, and tissue thromboplastin. Substances that inhibit coagulation include prostacyclin, antithrombin III, and proteins C and S. In addition, tissue plasminogen activator is a natural substance that dissolves clots already formed. 4. Differentiate between Anticoagulants drugs → inhibit the action or formation of clotting factors and therefore prevent clots from forming. Antiplatelets drugs → prevent platelet plugs from forming by inhibiting platelet aggregation, which can be beneficial in preventing heart attacks and strokes. Thrombolytic drugs → lyse (break down) clots, or thrombi, that have already formed. This is a unique difference between thrombolytics and anticoagulants, which can only prevent the formation of a clot. 5. What is “bridge therapy” and explain its significance to prevention of thrombosis formation? The term bridge therapy refers to the fact that enoxaparin acts as a bridge to provide anticoagulation while the patient must be off of warfarin therapy. 6. A. What is the primary adverse event associated with anticoagulant or antiplatelet therapies? Anticoagulant Drug Subclass Heparins (unfractionated heparin, low–molecular-weight heparin) Adverse Effects Bleeding, hematoma, anemia, thrombocytopenia Drug Subclass  NURS 3210 Pharmacology and Nursing Direct thrombin inhibitors (lepirudin, argatroban, bivalirudin, dabigatran) Adverse Effects Bleeding, dizziness, shortness of breath, fever, urticaria Drug Subclass Selective factor Xa inhibitor (fondaparinux, rivaroxaban, apixaban, edoxaban, betrixaban) Adverse Effects Bleeding, hematoma, dizziness, rash, gastrointestinal distress, anemia Drug Subclass Warfarin (Coumadin) Adverse Effects Bleeding, lethargy, muscle pain, purple toes Antiplatelet Aspirin Central nervous → Drowsiness, dizziness, confusion, flushing Gastrointestinal → Nausea, vomiting, gastrointestinal bleeding Hematologic → Thrombocytopenia, agranulocytosis, leukopenia, neutropenia, hemolytic anemia, bleeding Clopidogrel Cardiovascular → Chest pain, edema Central nervous → Flulike symptoms, headache, dizziness, fatigue Gastrointestinal → Abdominal pain, diarrhea, nausea Miscellaneous → Epistaxis, rash, and pruritus (itching) Glycoprotein IIb/IIIa Inhibitors Cardiovascular → Bradycardia, hypotension, edema  NURS 3210 Pharmacology and Nursing Central nervous → Dizziness Hematologic → Bleeding, thrombocytopenia B. What would some more subtle signs of that adverse event look like in the patient? 7. Explain why a patient might prefer to take a medication like rivaroxaban might be preferred therapy compared to warfarin or enoxaparin (consider route and monitoring)? Rivaroxaban is a direct oral anticoagulant route administrated medication compared to Warfairin that requires the frequent monitoring of blood and dosage adjustment. Rivaroxaban does not require such monitoring. Enoxaparin is administered through injections. Patients may find this route of administration as painful and inconvienient. 8. Complete the Heparin Case Study, Questions #1, #2, and #3 found in Chapter 26, p. 423: 1. What nursing actions must be implemented to ensure the accuracy and safety of the continuous heparin infusion? Double Check Physician’s Order, Dosage, Rate of infusion, Bolus Dosage, Bolus Concentration. Infusion Smart Pump Properly configured and program correctly and the built in library used to prohibit dosing errors. aPTT levels need to be monitored and regularly checked to make sure the levels remain in the therapeutic range between 1.5 to 2.5 times the normal control value. The patient needs to be frequently assessed for bleeding, blood in urine/stool, petechiae, nosebleeds and increase bleeding from menstrual cycle. Patient education is needed to inform and update the patient about the reason for the Heparin therapy, the side effects, and the crucial need for reporting any signs of bleeding at once.  NURS 3210 Pharmacology and Nursing Nurse thorough documentation of the infusion rate, aPPT, signs of bleeding, patient response or toleration. Nurse will need to have emergency preparations ready of Protamine Sulfate for a possible overdose. 2. What patient findings would indicate a therapeutic response to the heparin therapy? aPPT Lecels are achieving and maintaining the needed aPTT range. The therapeutic benefit of no clots forming or new thromboembolic events like DVT or a Pulmonary Embolism forming. Benefits of a reduction of lower extremities swelling (Edema). Hematocrit and Hemoglobin levels remain stable and not dropping. Dropping would indicate significant bleeding. All vital signs will be stable. During Mr. L.’s hospital stay, the physician orders an extra bolus of 5000 units of heparin, IV push, because the results of Mr. L.’s laboratory tests indicate that his activated partial thromboplastin time (aPTT) is not at a therapeutic level. After giving the dose, the nurse notices that a dose of 20,000 units was given instead of 5000 units. What will the nurse do first, and what subsequent orders will the nurse prepare to carry out? HCP will be notified immediately to report the medication error and give details of administered dose. Stop the Heparin infusion to prevent an increases in anticoagulation. The patient will need to be monitored for signs of bleeding, and vital signs will need to be monitored. Assessment of stool for occult blood and skin assessment for bruising. The antidote of Protamine Sulfate will be prepared to neutralize the Heparin. The dosage of Protamine Sulfate will be calculated based on the amount of Heparin administered and the time elapsed during the overdose. The nurse will need to document the medication error,  NURS 3210 Pharmacology and Nursing patient assessment, intervention taken and the response of the patient. The hospital protocol for medication error will need to be followed. 9. Aspirin, which is both an anti-platelet drug and an anti-inflammatory drug. a. What are some indications for its use? Pain and Fever relief. Manage inflammation condition like rheumatoid arthritis. Reduce the risk for myocardial infarction, stroke and cardiovascular disease prevention. b. How does it affect platelets (what is it’s mechanism of action), and how long does this effect last? Irreversibly inhibiting the cyclooxygenase enzyme. The inhibition stops the formation of thrombozane A2. Aspiring will last for the platelet lifespan. This can be 7 to 10 days. The antiplatelet effect will stay until new platelets are produced. c. What are some common adverse effects associated with aspirin? Gastrointestinal Issues → Nausea, vomiting, heartburn, ulcers and gastrointestinal bleeding. Allergice reactions, hives, exacerbation of asthma and anaphylaxis in sensitive individuals. High risk of renal impairment during long term use. d. What are some signs and symptoms of salicylate toxicity, name three? Hyperventilation, CNS effects (Confusion, headache, dizziness, delirium and seizures). e. Say acetylsalicylic acid five times, fast.  10. Complete the Critical Thinking Question #1 from Chapter 44, p. 697 about aspirin therapy: 1. T., 68 years of age, is instructed to take aspirin, 81 mg, every morning with breakfast, as part of treatment after having a myocardial infarction. When discussing the aspirin therapy, he asks the nurse, “Will this also help my arthritis?” What is the nurse’s best answer? The nurse’s best answer would be to educate the patient on the main reasons why aspirin is administered for the antiplatet effect to combat blood clotting and to reduce the risk of  NURS 3210 Pharmacology and Nursing strokes and heart attacks. The nurse should also communicate the benefits of it antiinflammatory effects that can aid in relieving symptoms of arthritis. Reading: Chapter 23 (Antianginals) 1. In two to three sentences, distinguish between the pathophysiologic processes and effects that lead to angina/MI versus those that cause heart failure. The pathophysiologic process of anigin/MI usually involves atherosclerosis that leads to a reduced blood flow to the heart. This results in an ischemia that can lead to a potential myocardial infarction. Heart failure is manifested by the hearts inability to effectively pump. The cause can by hypertension, valve disorders, coronary artery disease progressing to symptoms like fluid retension, fatigue, and shortness of breath. The important distinction is in the underlying action that drives each separate condition and their clinical manifestations. 2. List five key lifestyle modifications to reduce risk for cardiovascular disease (hypertension, HF, MI). Smoking Cessation, Maintain a healthy diet, Regularly scheduled exercise, Weight Management, and Management/Coping mechanisms for stress and limit alcohol intake. 3. Describe the instructions you would provide to a patient prescribed sublingual NTG for recurrent angina about how to take the medication and what to do if symptoms are not relieved. Patient Instruction; How to take the Medication. Place one tablet under the tongue at onset of symptoms. Patient should be sitting or lying down when taking medication as an intervention for lightheadedness or dizziness. If symptoms not relieved, patient will need to wait 5 minutes, then take another dose. If symptoms persist after two doses, the patient should seek out emergency medical aid.  NURS 3210 Pharmacology and Nursing Patient will need to document angina episodes and medication use. Patient will also need to schedule follow up appointments to be assessed and evaluated for the effectiveness of the treatment plan. 4. Most antianginals have an effect on blood vessel diameter. a. What is this effect and why does it benefit a patient with angina? Antianginals dilate the blood vessels, particularly the coronary arteries. The dilation aids in increasing blood flow into the heart muscle. That increase in blood flow is crucial for patients that have been diagnosed with angina. Antianginals reverse the narrowed or blocked coronary arteries reducing chest pain and other clinical manifestations. b. What are the nursing implications that result from effect? It is critical for nurses to assess the vital signs of the patient that is receiving the antianginal therapy. Blood pressure and heart rate are impacted by hypotension and bradycardia as a side effect of the medication. Patient education should focus on medication adherence and lifestyle management and modification to manage angina. 5. Complete Critical Thinking Questions #1 and #2, found in Chapter 23, p. 368: 1. Mrs. A. has been shoveling snow all morning. As you work on the snow in your yard, you see her suddenly sit down in her driveway. When you go over to check on her, she says that she has nitroglycerin tablets in her jacket pocket but she forgot how to take them. What is your priority action at this time? Assess vital signs and distress level. If Mrs’ A, is experiencing shortness of breath, dizziness or chest pain, I would need to verify the dosage, route and assist with sublingual administration. And follow up with medical evaluation.  NURS 3210 Pharmacology and Nursing 2. Your patient has been switched from oral nitroglycerin capsules to a transdermal form. What are the priorities for patient teaching regarding transdermal nitroglycerin therapy? Patient education priority on how to apply the patch, possible side effects and patient ongoing assessment and monitoring. 6. Complete the NTG Case Study Questions #1, #3, & #4 found in Chapter 23, p. 365: 1. What type of angina is M.S. experiencing, and what are the therapeutic goals of the drug therapy he has received? M.S. is more than likely going through stable angina due to the signs and symptoms of chest pain during physical exertion that is relieved by nitroglycerin or rest. The therapeutic goals of the drug therapy are to resolve and relieve the clinical manifestations of angina symptoms, increase activity/exercise tolerance. Also, decrease the incidents and frequency/severity of angina attacks. NGT’s mechanism of action dialates blood vessels to decrease the workload on the heart by increasing the blood flow to the heart. 3. Two days after he begins the nitroglycerin, M.S. calls the office and says, “I’m having awful headaches. What is wrong?” What is the best explanation, and what can he do about the headaches? Headaches are the typical side effects of nitroglycerin because of the vasodilatory action of the medication. The result of the headache’s are due to the increased blood flow to the brain, is the best explanation to the patient. To manage the headaches, the patient can take acetaminophen/ibuprofen. If the symptoms do not resolve M.C. should contact an HCP to be assessed and evaluated for a possible dosage adjustment. 4. After 1 month, M.S. is switched from the extended-release capsules to a transdermal nitroglycerin patch. He says that he is glad he does not have to remember to “take those pills” three times a day. However, 3 months later, he calls and says, “I don’t think this patch is  NURS 3210 Pharmacology and Nursing working. I’m having more episodes of chest pain now when I jog.” What could be the explanation for this, and what can be done? Possible explanation is inefective symptom management that is leading to chest pain during exertion. Possible cause is the absorption rate of the transdermal patch (inadequate dosage). To resolve the patient can contact their HCP to be reevaluated and possibly get a new dosage. It is crucial to be properly reassessed and correct titration and monitoring to improve relief of clinical manifestations. Readings: Ch. 27 (Antilipemics) 1. In three to five sentences, explain the relationship between Hyperlipidemia, Angina, and Myocardial Infarction (MI)? Hyperlipidemia is the elevated levels of the lipids in the blood, cholesterol and triglycerides have the possibility to lead to atherosclerosis (build up of plaque in the arteries). The plaque has the potential to obstruct blood flow to the heart. This can lead to angina in the heart muscle. If after the plaque has built up and ruptures and then obstructs an artery to the heart, this has the potential to cause a heart attack or MI. due to the deprivation of oxygen enriched blood to the heart, leading to heart damage and or death of the heart muscle cells. 2. Where is cholesterol manufactured and what are the differences between “good” and “bad” cholesterol? Cholesterol is created in the liver and or supplied through diet. Low-density lipoprotein (LDL) cholesterol, or “bad” cholesterol, collects in the walls of the blood vessels, causing them to narrow. High-density lipoprotein (HDL), or “good” cholesterol, moves LDL cholesterol out of the bloodstream. 3. What common adverse effect is associated with most cholesterol-lowering medications, and why?  NURS 3210 Pharmacology and Nursing A clinically important adverse effect is myopathy (muscle pain), which may progress to a serious condition known as rhabdomyolysis. This is the breakdown of muscle protein accompanied by myoglobinuria, which is the urinary elimination of the muscle protein myoglobin. Rhabdomyolysis can lead to acute renal failure and even death. It appears to be dose- dependent and is more common in patients receiving a statin in combination with cyclosporine, gemfibrozil (a fibrate), or erythromycin. When recognized reasonably early, rhabdomyolysis is usually reversible with discontinuation of the statin drug. Risk factors for myopathy include age older than 65 years, hypothyroidism, renal insufficiency, and drug interactions. Instruct patients to immediately report any signs of toxicity, including muscle soreness or changes in urine color. 4. Which cholesterol-lowering medication can cause flushing as an adverse effect, and what antiplatelet/NSAID is effective in reducing this side effect? Niacin can cause flushing, pruritus, and gastrointestinal distress. Small doses of aspirin or a nonsteroidal antiinflammatory drug (NSAID) may be taken 30 minutes before the niacin dose to minimize cutaneous flushing. These undesirable effects also can be minimized by starting patients on a low initial dosage and increasing it gradually and by having patients take the drug with meals. 5. Complete the Antilipemic Case Study Questions #1 and #2 found in Chapter 27, p. 441: 1. S.P. says, “Isn’t there something else I can do instead of taking this medicine? I really don’t like taking pills.” What alternatives may be available to her? Alternatives are lifestyle modifications, change in diet, uptick in the amount of fiber added to diet. Regularly scheduled exercise, manage weight and learning stress coping. 2. After 4 months, S.P.’s lipid levels had not improved. The nurse practitioner discusses with S.P. the consequences of not improving her lipid levels. S.P. agrees to try the statin drug and schedules a follow-up appointment for 3 months. After 2 months, S.P. wakes up with some pain  NURS 3210 Pharmacology and Nursing in her legs and feels extremely tired. She thinks she is suffering the effects of a new workout program that she started the previous day. But when she goes to work, the pain gets worse, and she calls the office nurse to describe her symptoms. What could be happening? Myopathy, that has been caused by the statin prescribed. This adverse side effect will need to be recognized and resolve before it progresses to rhabdomyolysis. 6. Complete the Critical Thinking Question #1 found in Chapter 27, p. 443: 1. A patient has started taking niacin (nicotinic acid) as part of treatment for high cholesterol levels. After the first dose, he tells the nurse that he feels “hot” and that his face and neck are flushed. He says that he thinks he is having an allergic reaction. What is the nurse’s priority action at this time? The nurse’s priority action is to assess the patient to differentiate form an adverse side effect and a common side effect of niacin. Niacin’s mechanism of action is to cause vasodilation. This rush of blood can lead to a warm flushing of blood to the face and/or neck. The nurse will need to gain the time of onset, duration and level of discomfort and intensity of symptoms. Reading & Video: Chapter 25 (Antidysrhythmics) 7. From a physiologic perspective, what causes the heart muscle to contract in its usual pattern (atrial contraction, followed by ventricular contraction)? This contraction is due to a coordinated response of the cardiact conduction system. The Sinoatrial Node, in the right atrium is the natural pacemaker of the heart. This SA node generates electrical impulses that can trigger the atria to contract by pushing blood into the ventricles (atrial systole). Atrioventricular Node, receive the electrical signale/impulses from the SA Node located at the junction of the Atria and Ventricles. The AV node will delay the impluse, briefly, to allow the ventricles to fill with blood from the atria before the contraction.  NURS 3210 Pharmacology and Nursing After the impulse is delayed, at the AV Node, the impulse travels through the bundle of His along the right and left bundle branches and then finally through the Purkinje fibers. The Perkinje fibers then send the impulse throughout the ventricles. This causes the Ventricles to contract (systole), this contraction will pump the blood to the lungs and then on the to rest of the body. 8. What is the “normal” pathway for electrical signals in the heart: Where do they begin and where do they go? Starts at the SA Node → Atria → AV Node → Spreads Through Ventricles → Via Bundle of His and Purkinje Fibers → Results in effective pumping of blood throughout the body. 9. What is an action potential? Define it, and then draw or describe what is happening in each phase of the action potential. Action Potential → Electrical activity consisting of a series of polarizations and depolarizations that travel across the cell membrane of a nerve fiber during transmission of a nerve impulse and across the cell membranes of a muscle cell during contraction. Hypopolarization is the initial increase of the membrane potential to the value of the threshold potential. The threshold potential opens voltage-gated sodium channels and causes a large influx of sodium ions. This phase is called the depolarization. During depolarization, the inside of the cell becomes more and more electropositive, until the potential gets closer the electrochemical equilibrium for sodium of +61 mV. This phase of extreme positivity is the overshoot phase. After the overshoot, the sodium permeability suddenly decreases due to the closing of its channels. The overshoot value of the cell potential opens voltage-gated potassium channels, which causes a large potassium efflux, decreasing the cell’s electropositivity. This phase is the repolarization phase, whose purpose is to restore the resting membrane potential. Repolarization always leads first to hyperpolarization, a state in which the membrane potential is more negative than the default membrane potential. But soon after that, the membrane establishes again the values of membrane potential.  NURS 3210 Pharmacology and Nursing 10. An ECG or EKG is a picture of the electrical conduction of the heart. The usual pattern includes a p-wave, followed by a QRS complex, followed by a T-wave. a. What would the absence of a distinct, p-wave indicate? Dysfunction of electrical signal in Atria. Atria Fibrillation, Atrial Flutter, Atrioventricular nodal reentry tachycardia. b. What would the absence or a QRS-complex indicate? Dysfunction of electrical signal in Ventricul. Ventricular Fibrillation, bundle of branch blocks, other ventricular arrhythmias. 11. A. What are the absolute and relative refractory periods? B. When do they occur? The interval between phase 0 and phase 4 is called the action potential duration (Fig. 25.4). The period between phase 0 and midway through phase 3 is called the absolute or effective refractory period. During the effective refractory period, the cardiac cell cannot be restimulated to depolarize and generate another action potential. During the remainder of phase 3 and until the return to the RMP (phase 4), the cardiac cell can be depolarized again if it receives a powerful enough impulse (such as one induced by drug therapy or supplied by an electrical pacemaker). This period is referred to as the relative refractory period. Fig. 25.4 illustrates these various aspects of an action potential. Again, the actual shape of the action potential curve varies in different parts of the conduction system. C. How are they represented on the ECG?  NURS 3210 Pharmacology and Nursing  NURS 3210 Pharmacology and Nursing D. What do they mean for new electrical signals (generation of action potential)? (Some people relate this to flushing a toilet before it has finished filling!) Premature stimulation can interrupt the normal sequence of events that lead to action protential. When stimulus occurs (electrical signal) is transported and received by a neuron, it starts a cascade of events that lead to the opening of voltage-gated ion channels along with the influx of sodium ions. This results in the depoloarization and propagation of the action potential along the axon. If a new signal is sent before the neuron has completely repolarized and resets its potential it can be an obstacle to the process, causing a refractory period when another action potential cannot be created in a response to being stimulated. The refractory period is need so the action potentials do not overlap or are disrupted. 12. What are some risk factors that make dysrhythmias more likely to occur? Name at least five. Cardiac dysrhythmia, or an irregular heartbeat, can be caused by a number of factors, including underlying heart disease, lifestyle choices, and drugs. Some risk factors that may increase the likelihood of dysrhythmias include: Heart problems: Coronary artery disease, abnormal heart valves, cardiomyopathy, heart problems present at birth, and previous heart surgery Blood pressure: High blood pressure Electrolytes: Low levels of potassium, magnesium, or calcium, or electrolyte imbalance Medications: Some medicines and supplements, including those that make you more alert or increase your energy, cold medicines, or herbal supplements Alcohol: Heavy drinking (35 drinks in a week) or binge drinking (5 or more drinks in a row) Other factors: Thyroid disease, obstructive sleep apnea, viral illnesses, tobacco, changes in posture, exercise, and strong emotional stress  NURS 3210 Pharmacology and Nursing 13. Complete the table comparing the different classifications of antidysrhythmic drugs. Vaughn- If specified, Which phase of Does it affect Give an example Williams what receptor the action slow fibers of an arrhythmia Classification type or ion- potential is (nodal tissue) commonly channel is usually or fast fibers? treated with affected. affected? antidysrhythmics in this class. Class 1 Sodium Channel Phase 0 Fast Atrial fibrillation Blockers Class 2 beta-blocking Phase 4 Slow Both drugs supraventricular and ventricular dysrhythmias Class 3 ↑ action Fast Atrial fibrillation potential or flutter resistant duration to other drug therapy Class 4 calcium channel Blocks slow Slow Paroxysmal blockers calcium supraventricular channels tachycardia 14. Name two lethal arrhythmias and the pharmacologic therapies most commonly used to treat them. Ventricular Tachycardia (VT) → flecainide and propafenone. Ventricular Fibrillation (VF) → lidocaine and phenytoin 15. Amiodarone has an extremely long half-life. a. What are some common adverse effects of this medication? Pulmonary toxicity, thyroid disorders, bradycardia, hypotension, SA node dysfunction, AV block, ataxia, QT prolongation, torsades de pointes, vomiting, constipation, photosensitivity, abnormal liver function test results, jaundice, visual disturbances, hyperglycemia or hypoglycemia, dermatologic reactions including rash, toxic epidermal necrolysis, vasculitis, blue-gray coloring of the skin (face, arms, neck). b. How should the nurse assess for them or what testing is frequently done?  NURS 3210 Pharmacology and Nursing Nursing actions for the various antidysrhythmics include skillful nursing assessment and close monitoring of heart rate, blood pressure, heart rhythms, general well-being, skin color, temperature, and heart and breath sounds. c. Why does the half-life make a difference in the management of the adverse effects or toxicities? Amiodarone has an exceptionally long half-life, approaching many days. As a result, the therapeutic as well as any adverse effects of amiodarone may linger long after the drug has been discontinued. In fact, it may take as long as 2 to 3 months after the drug has been stopped for some adverse effects to subside. 16. Adenosine, which has an extremely short half-life, is used to treat only one type of dysrhythmia. a. What is it? Supreventricular Tachycardia b. What is unique about administration of Adenosine? Rapid onset and short duration. c. Why is it administered in this way? Allows for fast circulation to the cardiac tissue. The fast action of Adenosine is critical to the treatment of Supreventricular Tachycardia. 17. Complete Critical Thinking Questions #1 & #2 found in Chapter 25, p. 402: 1. A patient who was admitted to the hospital for treatment of atrial fibrillation is about to go home with a new prescription for diltiazem (Cardizem). As the nurse goes over the patient’s medication list, the patient complains, “I’m feeling very tired. And when I stand up, I can hardly walk because I’m so dizzy.” What is the nurse’s priority action at this time? Assess the patients vital signs. Blood pressure and heart rate specifically. Diltiazem is a calcium channel blocker that has the potential to cause hypotension and bradycardia. If found to be significantly low immediate intervention may be needed to stabilize the patient. 2. A patient has been admitted to the emergency department and is experiencing PSVT that has not responded to treatment with calcium channel blockers. Immediately after the patient  NURS 3210 Pharmacology and Nursing receives a dose of adenosine (Adenocard) by intravenous push, the monitor shows asystole. What is the nurse’s priority action in response to the asystole? CPR will need to be initiated to maintain the circulation of oxygenated blood throughout the body.