Week 11 Dysrythmia, Coags, Hyperlipidemia Class Slides PDF

Dysrhythmia, Coagulation Modifiers, Anti-lipemics NUR 2303 – Week 11 Housekeeping Questions Glossary Dysrhythmia Thrombus Heart failure Embolus Ejection fraction (65%) Triglycerides Hemostasis Cholesterol Lipoproteins C...

Dysrhythmia, Coagulation Modifiers, Anti-lipemics NUR 2303 – Week 11 Housekeeping Questions Glossary Dysrhythmia Thrombus Heart failure Embolus Ejection fraction (65%) Triglycerides Hemostasis Cholesterol Lipoproteins Chapter 26 Antidysrhythmic Drugs Cardiac Cell Inside the resting cardiac cell, there is a net negative charge relative to the outside of the cell. Difference in electronegative charge results from an uneven distribution of ions (sodium, potassium, calcium) across the cell membrane. A change in the distribution of ions causes cardiac cells to become excited. The movement of ions across the cardiac cell’s membrane results in an electrical impulse spreading across the cardiac cells. This electrical impulse leads to contraction of the myocardial muscle. Electrocardiography Electrocardiogram P wave PR interval QRS complex ST segment T wave Common Dysrhythmias Supraventricular dysrhythmias (‘above ventricle’ SA or AV node) A Fib (stroke risk) Ventricular dysrhythmias (below the AV node) Ectopic (outside the conduction system) Conduction blocks (disruption in impulse between atria and ventricle) Vaughan Williams Classification System commonly Based on the used to classify electrophysiological Class I Class II, III, IV antidysrhythmic effect of drugs on drugs the action potential Divided into Ia, Ib, Fast sodium and Ic drugs, channel blockers according to effects Class I Class Ia: procainamide Block sodium (fast) channels, delays repolarization Increase action potential duration (APD) Used for AF, PACs, PVCs, VTach, Wolff-Parkinson-White syndrome Class Ib: lidocaine (Xylocaine®) Block sodium channels, accelerates repolarization Increase or decrease APD Lidocaine is used for ventricular dysrhythmias only. Class Ic: flecainide Block sodium channels (more pronounced effect), little effect on APD or repolarization Used for severe ventricular dysrhythmias May be used in AF or flutter, WPW syndrome, SVT Class II Class II: ß-blockers Reduce or block SNS stimulation, thus reducing transmission of impulses in the heart’s conduction system Depress phase 4 depolarization General myocardial depressants for both supraventricular and ventricular dysrhythmias Class III amiodarone, dronedarone, sotalol, ibutilide Increase APD Prolong repolarization in phase 3 Used for dysrhythmias that are difficult to treat Life-threatening V Tach, tachycardia or fibrillation, AF or flutter that is resistant to other drugs Class IV Calcium channel blockers Inhibit slow channel (calcium-dependent) pathways Depress phase 4 depolarization Reduce atrioventricular node conduction Used for paroxysmal SVT (PSVT); rate control for AF and flutter Antidysrhythmics: Adverse Effects All antidysrhythmics can cause dysrhythmias! Hypersensitivity reactions Nausea, vomiting, and diarrhea Dizziness Headache, and blurred vision Prolongation of the QT interval  Antidysrhythmics: Toxicity & Interactions Toxicity Interactions Main effect involves the heart, Can result in dysrhythmias, circulation, and CNS hypotension or hypertension, Antidotes may not be available respiratory distress, or and requires maintenance of excessive therapeutic or toxic adequate circulation and drug effects respirations Most common is anticoagulant activity with Warfarin (Coumadin) Nursing Implications Monitor ECG for prolonged QT interval Administer IV infusions with an IV pump. Lidocaine that contains epinephrine can only be a local anaesthetic Teach patients how to take their own radial pulse for 1 full minute and to notify their physician before taking the next dose if the pulse is less than 60 beats/min. Careful with clients who are also on Coumadin Take with food to avoid GI upset Avoid grapefruit and caffeine Chapter 27 Coagulation Modifier Drugs Embolus If an embolus lodges in a coronary artery, it causes a myocardial infarction If it obstructs a brain vessel, it causes a stroke (a cerebrovascular accident). If it travels to the lungs, it is a pulmonary embolus. If it travels to a vein in the leg, it is a deep vein thrombosis (DVT). Collectively, these complications are called “thromboembolic events.” Fibrinolytic System Initiates the breakdown of clots and serves to balance the clotting process Fibrinolysis: opposite of clotting, mechanism by which formed thrombi are lysed to prevent excessive clot formation and blood vessel blockage Fibrin in the clot binds to a circulating protein known as plasminogen. This binding converts plasminogen to plasmin. Plasmin is the enzymatic protein that eventually breaks down the fibrin thrombus into fibrin degradation products. This keeps the thrombus localized to prevent it from becoming an embolus. Coagulation Modifier Drugs Inhibit the action or formation of clotting Anticoagulants factors or prevent clot formation Antiplatelet Inhibit platelet aggregation, prevent drugs platelet plugs Thrombolytic Lyse (break down) existing clots drugs Anticoagulants Also known as antithrombotic drugs Have no direct effect on a blood clot that is already formed Prevent intravascular thrombosis by decreasing blood coagulability Used prophylactically to prevent Clot formation (thrombus) An embolus (dislodged clot) MOA depends on which drug as they impact different areas along the clotting pathway Heparin Relatively large molecule that is derived from bovine or porcine intestine Inhibits circulating clotting factors (turning off factor II, X and IX) Weight-based protocol with lab confirmation of therapeutic level (aPTT) When heparin is given with a continuous IV infusion. Measurement of activated partial thromboplastin time (aPTT) is necessary Usually, every 6 hours until therapeutic effects are seen. DVT prophylaxis: 5 000 units subcutaneously two or three times a day. Does not need to be monitored when used for prophylaxis. Low Molecular Weight Heparin Synthetic smaller molecular structure Specifically binds to Factor X More predictable anticoagulant response Frequent laboratory monitoring of bleeding times not needed Bridge therapy Heparin is preferred in renal disease Warfarin (Coumadin) Inhibits vitamin K synthesis by bacteria in the gastrointestinal tract Action: inhibit vitamin K–dependent clotting factors II, VII, IX, and X Effect is the prevention of clot formation Careful monitoring of the PT/INR Normal INR (without warfarin) is 0.8 to 1.2 Therapeutic INR (with warfarin) ranges from 2 to 3.5, depending on the indication for use of the drug (e.g., atrial fibrillation, thrombo- prevention, prosthetic heart valve). Anticoagulants: Indications Used to prevent clot formation Myocardial infarction Unstable angina Atrial fibrillation Indwelling devices, such as mechanical heart valves Conditions in which blood flow may be slowed and blood may pool (e.g., major orthopedic surgery, prolonged periods of immobility) Anticoagulants: Contraindications and AEs Any acute bleeding process or high risk of such an occurrence Warfarin is contraindicated in pregnancy. LMWH in clients with an epidural - large risk of epidural hematoma. Bleeding Risk increases with increased dosages May be localized or systemic May also cause: Heparin-induced thrombocytopenia (HIT II can be fatal) Nausea, vomiting, abdominal cramps, thrombocytopenia, other effects Treatment for Toxic Effects: Heparin Aimed at reversing the underlying cause Symptoms: hematuria, melena (blood in the stool), petechiae, ecchymoses, and mucous membrane bleeding Stop drug immediately. Intravenous (IV) protamine sulphate: 1 mg of protamine can reverse the effects of 100 units of heparin (1 mg of protamine for each milligram of LMWH given). Heparin: Nursing Implications IV doses are double-checked with another nurse. Ensure that SC doses are given SC, not IM. Subcutaneous doses should be given in areas of deep subcutaneous fat, and sites should be rotated. Do not give SC doses within 5 cm of the umbilicus, abdominal incisions, open wounds, scars, drainage tubes, stomas, or areas of bruising or oozing. Do not aspirate subcutaneous injections or massage the injection site. Treatment for Toxic Effects: Warfarin Discontinue the warfarin. May take 36 to 42 hours before the liver can resynthesize enough clotting factors to reverse the warfarin effects Vitamin K1 can hasten the return to normal coagulation. Warfarin (Coumadin): Nursing Implications Many herbal products have potential Capsicum, garlic, ginger, ginkgo, St. John’s interactions; increased bleeding may wort, feverfew occur. Wearing a medical alert bracelet Education should include: Avoiding foods high in vitamin K (tomatoes, dark leafy green vegetables) Question A patient is receiving an IV infusion of heparin and was started on warfarin therapy the night before. Which statement is most correct? A. The patient is receiving a double dose of anticoagulants. B. The heparin therapy was ineffective, so the warfarin was started. C. The heparin provides anticoagulation until therapeutic levels of warfarin are reached. D. The heparin and warfarin work together synergistically to provide anticoagulation. Antiplatelet Drugs MOA: Prevent platelet aggregation at the site of the vessel injury Platelet stimulators (prostaglandin, thrombin, etc.) cause platelets to aggregate, then the platelets attract other platelets and cause vasoconstriction. Aspirin - inhibits regeneration of enzyme that leads to constriction and aggregation. Irreversible alteration to the platelet (7 days) clopidogrel (Plavix) –alters platelet membrane –no longer receives signals to aggregate Antithrombotic effects Adverse effects Pose a risk for inducing bleeding Vary according to drug Careful with other NSAIDs Thrombolytic Drugs Lyse preformed clots in the coronary arteries Older drugs streptokinase and urokinase Current drugs alteplase (Activase) tenecteplase (TNKase) MOA: Activates the fibrinolytic system to break down the clot in the blood vessel quickly. Activate plasminogen and convert it to plasmin, which lyses the thrombus. Thrombolytic Drugs: Indications and AEs Acute MI Bleeding Arterial thrombolysis Internal Intracranial DVT Superficial Occlusion of shunts or Other effects catheters Nausea, vomiting, hypotension, Pulmonary embolism hypersensitivity, anaphylactoid reactions Acute ischemic stroke Cardiac dysrhythmias Antifibrinolytic Drugs Prevent the lysis of fibrin Result in promoting clot formation Used for prevention and treatment of excessive bleeding resulting from hyperfibrinolysis or surgical complications Treatment of hemophilia A or type I von Willebrand’s disease with desmopressin Recombinant Factors: rVII, rVIII or rIX Question A 75-year-old man fell at home and hit his head against a table. His wife reports to their daughter that he does not have cuts or scratches, but there is a small lump on his upper scalp. She does not see any blood. He is taking warfarin and an antidysrhythmic as part of his treatment for chronic atrial fibrillation. What is the main concern at this time? A. Pressure should be applied to the lump for 3 to 5 minutes. B. He will need to take two doses of warfarin tonight to prevent blood clotting. C. He needs to be examined for possible internal bleeding from the fall. D. As long as there is no bleeding, there is no concern. Chapter 28 Antilipemic Drugs Lipid and Lipid Abnormalities Blood Lipids: Triglycerides & cholesterol Triglycerides: Energy source, stored in fat Cholesterol: Used in hormones, membranes, bile Lipoproteins: Transport triglycerides & cholesterol in blood Liver: Manages VLDL, HDL, regulates LDL Cholesterol Production: Liver uses acetyl CoA reductase Patient Education: Key for understanding lipid health Cholesterol Homeostasis Cholesterol Homeostasis: Managed mainly by the liver. Liver: Key organ for lipid metabolism. VLDL → IDL → LDL: Transports and processes cholesterol. LDL: Delivers cholesterol to tissues; excess returns to the liver. HDL: Recycles cholesterol, cardioprotective. Excess Cholesterol: Reduces liver LDL receptors, increases blood LDL. Atherosclerotic Plaque Formation Plaque Formation: Lipids and lipoproteins lead to atherosclerotic plaque, causing coronary artery disease (CAD). Foam Cells: High cholesterol leads monocytes to become fat- filled foam cells, forming fatty streaks in vessels. Restricted Blood Flow: Plaque reduces vessel size, limiting oxygen and nutrient supply to the heart. Cholesterol & Coronary Heart Disease Cholesterol & CAD: High cholesterol raises CAD-related death and disability. Treatment Goals: Primary Prevention: Prevent first cardiac events in high-risk individuals. Secondary Prevention: Prevent further events in those with past cardiac issues. Prevention Strategies: Early lifestyle changes in diet, weight, and activity can help prevent CAD. Therapy Benefits: Antilipemic drugs and omega-3s may reduce CAD and improve lipid levels. Dyslipidemias and Treatment Guidelines Primary prevention of CAD, secondary after event Canadian Cardiovascular Society Guidelines for the Diagnosis and Treatment of Dyslipidemia for the Prevention of CVD Framingham Risk Score All reasonable nondrug means of controlling blood cholesterol levels (e.g., diet, exercise, smoking cessation) Drug therapy based upon the specific lipid profile of the patient Four Classes: (1) hydroxymethylglutaryl–coenzyme A reductase inhibitors (statins), (2) bile acid sequestrants, (3) the B vitamin niacin (vitamin B3, nicotinic acid), and (4) the fibric acid derivatives (fibrates) Antilipemics Hydroxymethylglutaryl–coenzyme A (HMG–CoA) reductase inhibitors (statins) Bile acid sequestrants B vitamin niacin (vitamin B3, nicotinic acid) Fibric acid derivatives (fibrates) Cholesterol absorption inhibitor (Ezetrol®) Statins (Hydroxymethylglutaryl-Coenzyme A Reductase Inhibitors) First-line therapy for hypercholesterolemia Reduces plasma concentrations of LDL cholesterol by 30 to 40% Decrease in plasma triglycerides by 10 to 30% Increase in HDL cholesterol by 2 to 15% Dose dependent Potent LDL reducers pravastatin simvastatin (Zocor®) atorvastatin (Lipitor®) fluvastatin (Lescol®) rosuvastatin (Crestor®) lovastatin Statins: Mechanism of Action Inhibit HMG-CoA reductase, Lower the rate of cholesterol which is used by the liver to production produce cholesterol Lowers total and LDL cholesterol levels as well as Dosed once daily, usually with triglyceride levels and raises the evening meal or at bedtime “good” cholesterol, the HDL to correlate with diurnal rhythm component Statins: Adverse Effects Mild, transient gastrointestinal disturbances Rash Headache Myopathy (muscle pain), possibly leading to rhabdomyolysis, a serious condition Do not use for patients with elevated liver enzymes or liver disease Rhabdomyolysis Breakdown of muscle protein Myoglobinuria: urinary elimination of the muscle protein myoglobin Can lead to acute kidney injury and even death When recognized reasonably early, rhabdomyolysis is usually reversible with discontinuation of the statin drug. Instruct patients to immediately report any signs of toxicity, including muscle soreness or changes in urine colour (tea- coloured). Statins: Interactions Oral anticoagulants Drugs metabolized by CYP3A4 erythromycin azole antifungals quinidine sulphate verapamil hydrochloride diltiazem hydrochloride Human immunodeficiency virus (HIV) and hepatitis C protease inhibitors Grapefruit juice Question A patient with a new prescription for an HMG-CoA (statin) drug is instructed to take the medication with the evening meal or at bedtime. The patient asks why it must be taken at that time of day. The reason is that A. the medication is better absorbed at that time. B. that time frame correlates better with the natural diurnal rhythm of cholesterol production. C. there will be fewer adverse effects if the drug is taken at night instead of with the morning meal. D. this timing reduces the incidence of myopathy. Bile Acid Sequestrants: MOA and Indications cholestyramine resin (Olestyr®) Prevent resorption of bile acids from small intestine Bile acids are necessary for absorption of cholesterol. Relief of pruritus associated with partial biliary obstruction (cholestyramine) May be used along with statins Bile Acid Sequestrants: Adverse Effects Constipation Heartburn, nausea, belching, bloating These adverse effects tend to disappear over time. Increasing dietary fibre intake or taking a fibre supplement such as psyllium (Metamucil® and others), as well as increasing fluid intake, may relieve constipation and bloating. May also cause mild increases in triglyceride levels Bile Acid Sequestrants: Considerations Overdose can cause obstruction because the bile acid sequestrants are not absorbed. Treatment of overdose includes restoring gut motility. Drug interactions All drugs must be taken at least 1 hour before or 4 to 6 hours after the administration of bile acid sequestrants. High doses of a bile acid sequestrant decrease the absorption of fat- soluble vitamins (A, D, E, and K). Niacin (Niaspan®, nicotinic acid) Vitamin B3 Lipid-lowering properties require much higher doses than when used as a vitamin. Effective, inexpensive, often used in combination with other lipid-lowering drugs MOA: Thought to inhibit lipolysis in adipose tissue, decrease esterification of triglycerides in the liver, and increase the activity of lipoprotein lipase Reduces the metabolism or catabolism of cholesterol and triglycerides Niacin: Indications and Adverse Effects Effective in lowering triglyceride, total serum cholesterol, apolipoprotein B and LDL cholesterol levels Increases HDL levels Effective in the treatment of types IIa, IIb, III, IV, and V dyslipidemia Flushing (caused by histamine release) Pruritus Gastrointestinal distress Fibric Acid Derivatives: MOA Also known as fibrates (bezafibrate, gemfibrozil, fenofibrate) Believed to work by activating lipoprotein lipase, which breaks down cholesterol Also suppress the release of free fatty acid from adipose tissue, inhibit the synthesis of triglycerides in the liver, and increase the secretion of cholesterol in the bile Fibric Acid Derivatives: Contraindications Known drug allergy Severe liver or kidney disease Cirrhosis Gallbladder disease AE: Abdominal discomfort, diarrhea, nausea Blurred vision, headache Increased risk of gallstones Prolonged prothrombin time Fibric Acid Derivatives: Interactions Gemfibrozil enhances the action of oral anticoagulants. All are given with a statin, which increases risk of myositis, myalgia, and rhabdomyolysis. Laboratory test reactions: Decreased hemoglobin level, hematocrit value, and white blood cell count Increased aspartate aminotransferase, activated clotting time, lactate dehydrogenase level, and bilirubin level Cholesterol Absorption Inhibitor Ezetimibe (Ezetrol) Inhibits absorption of cholesterol and related sterols from the small intestine Results in reduced total cholesterol, LDL cholesterol, apolipoprotein B, and triglyceride levels Also increases HDL cholesterol levels Often combined with a statin drug Can be used as monotherapy Nursing Implications of Antilipemics Contraindications include biliary obstruction, liver dysfunction, and active liver dysfunction. Obtain results of baseline liver function studies. Patients on long-term therapy may need supplemental fat-soluble vitamins (A, D, K). Refer to guidelines regarding administration times and meals. Small doses of aspirin or NSAIDs may be taken 30 minutes before niacin to minimize cutaneous flushing. Case Study Jörg is a 70-year-old male patient with a history of atrial fibrillation that is controlled with medication. His medication regimen also includes warfarin (Coumadin). His daughter has taken him to the Coumadin Clinic today, and she has several questions for the nurse. a. Jörg’s daughter says, “I understand why my father takes a medication for his heart rhythm problems, but why does he need a blood thinner?” How will the nurse answer the daughter’s question? b. Jörg’s daughter also asks about her father’s clotting times. The nurse states that the prothrombin time (PT) is 19 seconds, and the international normalized ratio (INR) is 2.8. Are these values therapeutic? If the INR was 3.5 and Jörg showed signs of hemorrhage, what treatment would the nurse expect to be ordered? Take Home Reflection For next week: Be able to discuss the benefits of using an aerochamber (spacer) when giving teaching to a newly diagnosed asthmatic. Wrap-up Week 12: Respiratory