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1/16/24, 10:32 PM Realizeit for Student Introduction Primary medications used in the treatment of acute coronary syndrome include aspirin, nitroglycerin, morphine, beta-adrenergic blockers, angiotensin-converting enzyme (ACE) inhibitors, and thrombolytic (fibrinolytic) agents; and additional adjuv...

1/16/24, 10:32 PM Realizeit for Student Introduction Primary medications used in the treatment of acute coronary syndrome include aspirin, nitroglycerin, morphine, beta-adrenergic blockers, angiotensin-converting enzyme (ACE) inhibitors, and thrombolytic (fibrinolytic) agents; and additional adjuvant drugs based on the patient needs and scenario. These drugs relieve anginal pain by increasing blood supply to the myocardium as well as reducing the oxygen demand of the myocardium. This section includes a brief review of the current evidence related to the indications and effectiveness of the multiple drugs and nursing considerations related to their use in the management of acute coronary syndrome (ACS). Organic Nitrates The most widely used nitrate is the prototype nitroglycerin (Nitro-Bid, Nitro-Dur). Available in multiple forms, it is indicated for the management and prevention of acute chest pain caused by myocardial ischemia. Pharmacokinetics Nitroglycerin is 60% bound to protein, undergoes extensive first-pass metabolism in the liver, and has a half-life of 1 to 4 minutes. Excretion occurs in the urine. The onset of action, peak, and duration of action varies with the route of administration. Intravenous (IV) drip: onset, immediate; peak, immediate; duration of action, 3 to 5 minutes Sublingual (SL): onset, 1 to 3 minutes; peak, 4 to 8 minutes; duration of action, at least 25 minutes Translingual spray: onset, 1 to 3 minutes; peak, 4 to 10 minutes; duration of action, at least 25 minutes Oral (PO) tablets or capsules (sustained release): onset, about 60 minutes; peak, 2½ to 4 hours; duration of action, 4 to 8 hours Topical ointment: onset, 15 to 30 minutes; peak, 60 minutes; duration of action, 7 hours Topical transdermal disk: onset, about 30 minutes; peak, 120 minutes; duration of action, 10 to 12 hours Action Organic nitrates are converted to nitric oxide, a potent vasodilator, which relaxes smooth muscle in blood vessel walls. The drugs relieve anginal pain by several mechanisms: Venous dilation, which reduces venous pressure and decreases venous return to the heart. This decreases blood volume and pressure within the heart (preload), which in turn decreases cardiac workload and oxygen demand. This is the main mechanism by which nitroglycerin relieves angina. Coronary artery dilation at higher doses, which can increase blood flow to ischemic areas of the myocardium. Arteriole dilation, which lowers peripheral vascular resistance (afterload). This results in lower systolic blood pressure and, consequently, reduced cardiac workload and balancing supply and demand in the heart. Use For relief of sudden-onset angina, fast-acting preparations of nitroglycerin include SL and chewable tablets and transmucosal spray. Indications for these preparations include acute-onset chest pain and prophylaxis prior to activities known to provoke angina, such as walking, dancing, or mowing the lawn. For management of recurrent, chronic angina, long-acting preparations include PO sustained-release tablets and transdermal ointment. With these longer-acting forms, intolerance to their hemodynamic effects may develop, and therefore, the drugs do not relieve chest pain. In clinical practice, patients taking nitrates are usually nitrate free during the night, while sleeping, to prevent nitrate tolerance. The oral form of the drug undergoes rapid metabolism in the liver, and relatively small portions ultimately reach the systemic circulation. Thus, the PO form does not relieve acute chest pain but may be useful prophylactically in chronic chest pain. Nitroglycerin ointment is indicated for prevention of chronic angina. This route is convenient to use when the patient can have nothing by mouth (NPO) before surgery and cannot take the usually PO dose. Angina that is unresponsive to SL, PO, or transdermal preparations calls for IV nitroglycerin. Prescribers may typically order the IV form for management of pain associated with an MI. IV nitroglycerin is useful in the management of angina that is unresponsive to organic nitrates via other routes or to beta-adrenergic blockers. It also may be used to control blood pressure in perioperative or emergency situations and to reduce preload and afterload in severe heart failure. Use in Older Adults https://herzing.realizeithome.com/RealizeitApp/Student.aspx?Token=lqf9HhURQ5RqpgqAkzH2zbfuwFjUs0mdxkPeVey4KH2F7i%2fH0LC0NH7inQLoUzK%2f… 1/21 1/16/24, 10:32 PM Realizeit for Student Older adults may be more vulnerable to hypotension when taking nitroglycerin as a result of volume depletion, concurrent use of other medication, and loss of sympathetic tone. Use in Patients With Critical Illness IV nitroglycerin is commonly used in the critical care setting. Angina related to MI may be a patient's principal issue in the intensive care unit (ICU). However, he or she may also have heart failure, hypertension, renal failure, and/or anemia and therefore could be receiving multiple drugs such as heparin, epoetin alfa, and dobutamine. QSEN Alert: Safety The nurse must always check IV compatibility when administering drugs by that route. Close monitoring of vital signs, along with frequent titration of IV medications, is important in the critically ill. Adverse Effects The majority of adverse effects of nitroglycerin are related to the hemodynamic changes responsible for preload reduction and vasodilation. The most common adverse effect is a severe headache, which is typically treated with acetaminophen. Other common adverse effects include dizziness, bradycardia, syncope, hypotension, and orthostatic hypotension. Contraindications Contraindications to nitroglycerin include hypersensitivity reactions, severe anemia, hypotension, and hypovolemia. Caution is necessary in the following situations: In the presence of head injury or cerebral hemorrhage because it may increase intracranial pressure. With the use of other antihypertensive agents, such as beta-adrenergic blockers. It is essential to observe for extreme episodes of hypotension. With renal impairment. Nursing Implications Preventing Interactions Many drugs interact with nitroglycerin, increasing or decreasing its effects. Drug Interactions: Nitroglycerin Drugs That Increase the Effects of Nitroglycerin Adalat and other calcium channel blockers, alcohol, aripiprazole, benazepril and other angiotensin-converting enzyme inhibitors, codeine and oth Increase the risk of orthostatic hypotension Sildenafil, tadalafil, vardenafil Increase the risk of life-threatening hypotension Drugs That Decrease the Effects of Nitroglycerin Acetaminophen, chloral hydrate, dihydroergotamine, sulfonylureas, vasopressin Decrease vasodilating effects Administering the Medication It is important to take a patient’s vital signs prior to administration of any form of nitroglycerin. The nurse should withhold the medication with hypotension (systolic blood pressure less than 90 or 30 mm Hg below the patient’s normal blood pressure) as well as tachycardia with a heart rate greater than 100 beats/min. Administration of SL nitroglycerin or translingual spray is essential as soon as chest pain develops. If a patient is hospitalized, it is necessary to call the patient’s health care provider and obtain a 12-lead ECG at the onset of chest pain. The SL nitroglycerin container should stay in a dry, cool, dark environment, and replacement every 6 months is necessary. Exposure to light deactivates the nitroglycerin tablets. Once opened, the translingual spray has a shelf life of 2 to 3 years. https://herzing.realizeithome.com/RealizeitApp/Student.aspx?Token=lqf9HhURQ5RqpgqAkzH2zbfuwFjUs0mdxkPeVey4KH2F7i%2fH0LC0NH7inQLoUzK%2f… 2/21 1/16/24, 10:32 PM Realizeit for Student In acute coronary syndromes, after three SL doses, administered 5 minutes apart, patients outside of the hospital should seek medical attention. While hospitalized, IV dosing should be started and titrated to desired effect. Nitrate tolerance commonly develops within 24 hours in patients on a continuous infusion of nitroglycerin. Extended-release oral nitrate preparations are used post-MI if angina persists after revascularization. Application of nitroglycerin ointment requires using the dose-measuring application papers supplied with ointment. It is necessary to do the following: Squeeze the ointment onto a measuring scale printed on paper; typically, this is 1 or 1/2 inch, depending on the practitioner’s order. Use the paper to spread ointment onto a nonhairy area of skin (chest, abdomen, thighs; avoid distal extremities) in a thin, even layer, covering a 2- to 3-inch area. Do not allow the ointment to come in contact with the hand. Do not massage the ointment into the patient’s skin because absorption will be increased and interfere with the sustained action. People should take PO nitrates in the morning after a nitrate-free interval (typically during the night). They should take the tablets or capsules 1 to 2 hours before meals. It is important not to break, crush, or chew sustained-release preparations. IV nitroglycerin preparations come in glass bottles, polyvinyl chloride (PVC)-free partial-additive bags, and di(2-ethylhexyl) phthalate (DEHP)free, PVC-free plastic EXCEL containers. Nurses should use these only with special tubing provided by the manufacturer because PVC tubing absorbs up to 80% of the nitroglycerin. Inline IV filters that adsorb nitroglycerin should be avoided. In addition, nurses should ensure that IV nitroglycerin is administered via infusion pump and that patients are placed on cardiac monitors. Many hospitals require patients to be in ICUs or step-down units while the nitroglycerin drip is actively being titrated. As previously stated, it is essential to take vital signs frequently with IV administration and recheck them with each titration. Assessing for Therapeutic Effects Therapeutic effects of some forms of nitroglycerin may include the relief of acute chest pain as well as a modest decrease in blood pressure. With oral preparations, a decreased frequency of chronic chest pain should occur. Overall, patients should report that they feel better, have no symptoms of cardiac ischemia (i.e., chest pain), and have a higher activity tolerance. Medical Management The goals of medical management are to minimize myocardial damage, preserve myocardial function, and prevent complications. These goals are facilitated by the use of guidelines developed by the ACC and the AHA. https://herzing.realizeithome.com/RealizeitApp/Student.aspx?Token=lqf9HhURQ5RqpgqAkzH2zbfuwFjUs0mdxkPeVey4KH2F7i%2fH0LC0NH7inQLoUzK%2f… 3/21 1/16/24, 10:32 PM Realizeit for Student Beta-Adrenergic Blockers Beta-adrenergic blockers have become the cornerstone of drug therapy regimens people with angina, MI, hypertension, heart failure, and dysrhythmias. catecholamines epinephrine and norepinephrine by exerting effects on the three adrenergic receptors (betaforThey inhibit the chronotropic, inotropic, and vasoconstrictor responses to the1, beta2, and alpha). In the cardiac system, these drugs decrease cardiac workload by slowing heart rate, decreasing blood pressure, and reducing contractility. The drugs are as effective as the organic nitrates in reducing the frequency and severity of anginal symptoms during exercise. People taking the drugs do not develop tolerance during therapy as occurs with the organic nitrates. The 2013 ACCF/AHA Guidelines mized controlled trials demonstrating that when beta-adrenergic blockers are started early in patients without signs MI (primarily STEMI), MI reported evidence from randoAcute ofManagement thefor acute of heart failure with of death.the risk these drugs lower they reduce infarction size and early mortality. Also, with long-term use, these drugs lower the risk of death. The ability of a drug in this class to selectively block beta1 receptors, principally found in the myocardium, is known as cardioselectivity . Therefore, cardioselective beta-adrenergic blockers, such as atenolol, metoprolol, bisoprolol, and esmolol, offer the potential advantage of not interfering with bronchodilation or peripheral vasodilation. In addition to beta1-blockade, noncardioselective beta-adrenergic blockers block beta2 receptors found in smooth muscle in the lungs, blood vessels, and other organs. Examples of noncardioselective betaadrenergic blockers include propranolol, labetalol, nadolol, carvedilol, and timolol. Labetalol and carvedilol block both beta- and alphareceptors, thereby decreasing peripheral and coronary vascular resistance. During beta-adrenergic blocker therapy, the beta receptors undergo receptor up-regulation. This means that the number of receptors on the surface of target cells (the beta cells) becomes more sensitive to catecholamines. Pharmacokinetics With PO administration, atenolol undergoes limited first-pass metabolism in the liver. Absorption is rapid and consistent but incomplete. Approximately only 50% of an oral dose is absorbed from the gastrointestinal (GI) tract. The drug is modestly (6%–16%) bound to plasma, is distributed to the placenta, and is secreted in breast milk. It does not readily cross the blood–brain barrier. Peak blood levels occur https://herzing.realizeithome.com/RealizeitApp/Student.aspx?Token=lqf9HhURQ5RqpgqAkzH2zbfuwFjUs0mdxkPeVey4KH2F7i%2fH0LC0NH7inQLoUzK%2f… 4/21 1/16/24, 10:32 PM Realizeit for Student between 2 and 4 hours after ingestion. With IV atenolol, onset of action is immediate, duration of action is dose dependent (half-life 6–7 hours), and peak blood levels are reached in 5 minutes. The drug is not metabolized and is excreted in the urine and feces. Action Atenolol is a cardioselective beta-adrenergic blocker. The cardioselectivity is diminished at higher doses, where it inhibits beta2 receptors in the bronchial and vascular musculature. Use Atenolol is useful in the treatment of angina and hypertension as well as for the prophylaxis and treatment of MI. Health care providers use atenolol and other beta-adrenergic blockers in long-term management to decrease the frequency and severity of anginal attacks, decrease the need for sublingual nitroglycerin, and increase exercise tolerance. Evidence supports the use of a cardioselective beta-adrenergic blocker, such as atenolol, within the first 24 hours following an acute MI. QSEN Alert: Safety It is important to note that nonselective beta-adrenergic blockers should not be used in patients with variant angina because they are ineffective an coronary artery vasospasm. The U.S. Food and Drug Administration (FDA) has issued a BLACK BOX WARNING ♦ relating to the use of beta-adrenergic blockers in patients with CAD; abrupt withdrawal of oral forms may result in exacerbation of angina, increased incidence of ventricular dysrhythmias, MI, or death. Therefore, it is essential to slowly taper beta-adrenergic blockers before discontinuing them. Use in Older Adults The prevalence of CAD increases with age and is the major cause of disability, morbidity, and mortality in older adults. The elderly have a higher incidence of multivessel coronary disease, decreased left ventricular function, and comorbid conditions. For this reason, betaadrenergic blockers are one of the most frequently medications prescribed in older adults. Close monitoring of the patient’s heart rate is essential because the incidence of sick sinus syndrome and chronotropic intolerance increases with age and predisposes these patients to bradycardia, syncope, and falls. Use in Patients With Renal Impairment Atenolol is well tolerated in patients with renal impairment, but dosage reduction may be necessary. Study findings indicate beta-adrenergic blockers slow the deterioration of renal function in chronic kidney disease. Use in Patients With Critical Illness Administration of atenolol in the critical care setting may occur to reduce cardiovascular mortality in the management of hemodynamically stable patients with definite or suspected acute MI. IV administration should occur in a controlled setting equipped to monitor heart rate, blood pressure, and ECG. Hypotension may also occur with use, so the patient should be closely monitored for symptoms of hypotension. Unlike nitroglycerin, IV beta-adrenergic blockers are rarely used in the ICU for the control of angina. Adverse Effects The major cardiac adverse reactions related to beta-adrenergic blockers such as atenolol include heart failure and substantial negative chronotropy (causing slowing of the heart rate). A small number of people with chronic heart failure may have an exacerbation of heart failure when they begin taking atenolol or other beta-adrenergic blockers. In these people, sympathetic drive is maintaining cardiac output. The beta-adrenergic blockers decrease this sympathetic drive and therefore cause a low cardiac output state and heart failure. The majority of patients with heart failure do benefit from beta-blockade, and symptoms of heart failure abate. To manage the negative chronotropy, dosage adjustments may be necessary; the target heart rate should be 55 to 65 beats/min at rest. Use of beta-adrenergic blockers can lead to serious bradydysrhythmias and depression of the atrioventricular node. Noncardiac adverse effects include bronchospasm, especially in patients with chronic obstructive pulmonary disease (COPD) receiving high dosages because of beta2 receptor blockade. Note that many of the earlier signs of hypoglycemia are adrenergic warning symptoms (e.g., tremors, palpitation, tachycardia). Therefore, the use of beta-adrenergic blockers in patients with diabetes can mask the early warning symptoms of hypoglycemia. Contraindications https://herzing.realizeithome.com/RealizeitApp/Student.aspx?Token=lqf9HhURQ5RqpgqAkzH2zbfuwFjUs0mdxkPeVey4KH2F7i%2fH0LC0NH7inQLoUzK%2f… 5/21 1/16/24, 10:32 PM Realizeit for Student Contraindications to atenolol include known hypersensitivity to the drug, second- or third-degree heart block, and cardiogenic shock, as well as severe bradycardia, heart failure, or hypotension. Caution is warranted with milder bradycardia, heart failure, or hypotension, and asthma. Nursing Implications Preventing Interactions Many medications interact with atenolol, increasing or decreasing its effects. Drug Interactions: Atenolol Drugs That Increase the Effects of Atenolol Alcohol Increases the risk of hypotension Atazanavir, dolasetron, saquinavir Increase the risk of heart block Digoxin Increases the risk of bradycardia Diltiazem, verapamil Increase the risk of bradycardia, heart block, and increased left ventricular end-diastolic pressure Reserpine Increases the risk of hypotension and significant bradycardia Sildenafil, tadalafil, vardenafil Increase the risk of life-threatening hypotension Drugs That Decrease the Effects of Atenolol Adrenergic drugs (e.g., epinephrine, isoproterenol) Reverse bradycardia Anticholinergic drugs (e.g., diphenhydramine, ipratropium) Increase heart rate, offsetting slower heart rates of atenolol Indomethacin Decreases the hypotensive effects Administering the Medication Prior to giving atenolol, the nurse should check the patient’s vital signs. It is important to withhold atenolol and notify the prescriber for a resting heart rate of 60 beats/min and/or systolic blood pressure less than 90 mm Hg. The nurse gives IV beta-adrenergic blockers over 2.5 minutes. Continuous telemetry is necessary for patients receiving an IV bolus or a continuous drip. The effectiveness of beta-adrenergic blockers in relation to relieving angina is dose dependent. It is necessary to titrate the dose of the beta-adrenergic blocker for a target heart rate of 50 to 60 beats/min with normal blood pressure. The nurse monitors the blood pressure every 5 minutes, while the drip is being titrated, and assesses for signs of bronchoconstriction at higher drug dosages where cardioselectivity may be lost. Assessing for Therapeutic Effects The nurse evaluates for three main objectives in the patient with chronic angina. One, the patient's frequency and severity of angina is reduced. Two, the patient has improved exercise capacity. Three, there is a reduction or elimination in the use of sublingual nitroglycerin. Ideally, achievement of these goals results in fewer adverse effects. Assessing for Adverse Effects The nurse closely monitors the patient’s blood pressure and heart rate 2 to 4 hours after the first dose of atenolol. Signs of hypotension include dizziness and blurred vision; syncope is indicative of bradydysrhythmias. Increased shortness of breath and wheezing are adverse effects seen in patients with COPD who are taking noncardioselective beta-adrenergic blockers or high doses of cardioselective betaadrenergic blockers. In patients with diabetes prone to hypoglycemia, more frequent assessment of serum glucose levels may be necessary. Metroprolol (Lopressor, Toprol XL), is used alone or in combination with other medications to treat angina and hypertension. Like atenolol, metroprolol is cardioselective and improves survival after an MI. https://herzing.realizeithome.com/RealizeitApp/Student.aspx?Token=lqf9HhURQ5RqpgqAkzH2zbfuwFjUs0mdxkPeVey4KH2F7i%2fH0LC0NH7inQLoUzK%2f… 6/21 1/16/24, 10:32 PM Realizeit for Student Adjuvant Medications Angiotensin-Converting Enzyme Inhibitors Angiotensin-converting enzyme (ACE) inhibitors may be given to most patients routinely unless contraindicated, particularly in those with an anterior infarction, decreased left ventricular function, or heart failure. For those individuals who cannot tolerate an ACE inhibitor, an angiotensin receptor blocker can be given. Aspirin Aspirin produces an antiplatelet effect by irreversibly acetylating the active site of cyclooxygenase-1 (COX-1), which at lower doses effectively suppress platelet aggregation without affecting important endothelial cell functions. A growing body of evidence supports the use of aspirin in both primary and secondary prevention of cardiovascular events. However, in primary prevention, benefits may be outweighed by the risk of major bleeding. In secondary prevention, aspirin has been shown to substantially reduce mortality when administered during an evolving MI and should be given, unless contraindicated, as soon as possible after the onset of symptoms. The loading dose is 162 to 325 mg of uncoated aspirin; chewing or crushing the tablet establishes a high blood level quickly. Evidence suggests that long-term use of lower doses as opposed to higher dosages does not significantly affect cardiovascular outcomes and causes less risk of bleeding. With NSTEMI and STEMI, enteric-coated aspirin should be avoided initially because the enteric coating delays and reduces drug absorption. Adenosine Diphosphate Receptor Antagonists Clopidogrel and other adenosine diphosphate (ADP) receptor antagonists, prasugrel and ticagrelor, have antiplatelet effects similar to aspirin and inhibit the ADP (P2Y12) receptor on the surface of platelets. Clopidogrel has three shortcomings: delayed onset of action, irreversible inhibitory effects on platelets with no reversing agent or antidote, and significant individual variability in platelet response. Clopidogrel and ticagrelor are indicated for unstable angina and NSTEMI in patients who are to be treated medically or by planned primary PCI. Administering clopidogrel with aspirin (dual antiplatelet therapy) has been found superior to aspirin alone in decreasing the incidence of cardiovascular death and nonfatal MI—both acutely and for up to 9 to 11 months. Ticagrelor is used to reduce the rate of cardiovascular death, MI, and stroke in patients with a history of MI or acute coronary syndrome. The drug also decreases the rate of stent thrombosis in individuals requiring a stent for the treatment of acute coronary syndromes. Ticagrelor differs from clopidogrel and prasugrel in that receptor blockade is reversible. It is effective and relatively safe when compared to clopidogrel. The most recent data suggest that ticagrelor has broader applicability of use in individuals with acute coronary syndrome as compared to prasugrel. (However, prasugrel seems to be better tolerated.) In addition to aspirin, the ADP antagonists are usually continued for up to 12 months. Glycoprotein IIb/IIIa Receptor Antagonists The glycoprotein (GP) IIb/IIIa receptor antagonists eptifibatide and tirofiban inhibit platelet aggregation by preventing activation of GP IIb/IIIa receptors on the platelet surface and the subsequent binding of fibrinogen and von Willebrand factor to platelets. The drugs are used occasionally in combination with heparin or aspirin to prevent clotting before and during invasive heart procedures in patients with NSTEMI. Antiplatelet effects occur during intravenous drug infusion and diminish once the drug is stopped. Morphine Historically, morphine has been useful for relieving pain, reducing anxiety, and decreasing preload and remains a cornerstone in pain management in post-MI patients with unacceptable levels of pain. However, findings from the CRUSADE retrospective observational registry (57,039 patients with non–ST-elevation acute coronary syndrome) indicated that treating patients with morphine was associated with decreased survival. Although the exact cause of the negative outcome was not clear, recent studies ( Kubica et al., 2015 ; Parodi et al., 2014) have suggested that morphine acts by interfering with the antiplatelet effect of the P2Y12 receptor blockers commonly given to this group of patients. QSEN Alert: Evidence-Based Practice Interventions in acute MI are focused on the overall goal of prompt, complete, and sustained reperfusion of the myocardium. Interest in providing e management strategies that support that goal has given rise to concerns regarding morphine. One study found that the administration of morphine the risk of death. Another study of patients following a STEMI indicated that morphine may interfere with platelet inhibition by disrupting the absorp inhibitors) and other medications. By impeding normal gastric activity, morphine may delay absorption and decrease peak plasma levels of orally ad necessary to determine morphine’s ongoing role in pain management following acute MI. Thrombolytic Drugs The purpose of giving thrombolytic agents following a STEMI is to dissolve thrombi and reestablish blood flow as quickly as possible, prevent or limit tissue damage, and maximize functional improvement. These drugs stimulate conversion of plasminogen to plasmin, a https://herzing.realizeithome.com/RealizeitApp/Student.aspx?Token=lqf9HhURQ5RqpgqAkzH2zbfuwFjUs0mdxkPeVey4KH2F7i%2fH0LC0NH7inQLoUzK%2f… 7/21 1/16/24, 10:32 PM Realizeit for Student proteolytic enzyme that breaks down fibrin, the framework of a thrombus. In coronary circulation, restoration of blood flow reduces morbidity and mortality by limiting MI size. Maximal benefit is achieved when thrombolytic drugs are administered within the first 2 to 3 hours, especially within the first hour. In addition, anticoagulant drugs, such as heparin and warfarin, as well as antiplatelet agents are given following thrombolytic therapy to decrease reformation of a thrombus. Thrombolytic treatment is not recommended as treatment for a NSTEMI. Alternately, PCI (also called percutaneous transluminal coronary angioplasty) together with certain drugs may be used to reestablish blood flow with a STEMI. Adjunctive therapy with PCI includes antiplatelet and antithrombotic therapy to reduce thrombotic complications. Generally, aspirin, an ADP receptor antagonist, and a GP IIb/IIIa inhibitor are given. Intravenous fractionated heparin is also administered during the PCI to prevent acute coronary closure during the procedure. The goal in both approaches is to minimize total ischemic time and restore blood flow. Therapeutic effects include reversal of symptoms, stabilization of cardiac rhythm, decrease of the ST-segment elevation by 50%, and absence of bleeding complications. Heparins Heparin is a pharmaceutical preparation of the natural anticoagulant produced primarily by mast cells in pericapillary connective tissue, and it is the prototype anticoagulant. Endogenous heparin is found in various body tissues, most abundantly in the liver and lungs. Exogenous heparin is obtained from bovine lung or porcine intestinal mucosa and standardized in units of biologic activity. See later for a discussion of low-molecular-weight heparins (LMWHs). Pharmacokinetics It is necessary to give heparin intravenously or subcutaneously because the gastrointestinal (GI) tract does not absorb the drug. After IV injection, the drug acts immediately. After subcutaneous injection, heparin acts within 20 to 30 minutes. Metabolism takes place in the liver and the reticuloendothelial system. Excretion, primarily in the form of inactive metabolites, occurs in the urine. Hemodialysis does not remove it. Action Heparin combines with antithrombin III (a natural anticoagulant in the blood) to inactivate clotting factors IX, X, XI, and XII; inhibit the conversion of prothrombin to thrombin; and prevent thrombus formation. After thrombosis has developed, heparin can inhibit additional coagulation by inactivating thrombin, preventing the conversion of fibrinogen to fibrin, and inhibiting factor XIII (fibrin-stabilizing factor). Other effects include inhibition of factors V and VIII and platelet aggregation. Use Prophylactically, patients at risk for certain disorders take low doses of heparin prophylactically to prevent DVT and pulmonary embolism. These disorders include the following: Major illnesses (e.g., acute myocardial infarction, heart failure, serious pulmonary infections, stroke) QSEN Alert: Technology Several major adverse events have resulted from the use of heparin, and it is classified as a high-alert drug. Nurses demonstrate consistent practic heightened individual awareness of the risks and by advocating for systems to account for human error such as bar coding and “smart” pumps. Eff safety and quality include special safeguards to reduce the risk of errors that may harm the patient. Use in Older Adults Older adults often have atherosclerosis and thrombotic disorders, including myocardial infarction, thrombotic stroke, and peripheral arterial insufficiency, for which they receive an anticoagulant drug. They are more likely than younger adults to experience bleeding and other complications associated with this therapy. With standard heparin, general principles for safe and effective use apply. With LMWHs, elimination may be delayed in older adults with renal impairment, and the drugs should be used cautiously. Use in Patients With Renal Impairment https://herzing.realizeithome.com/RealizeitApp/Student.aspx?Token=lqf9HhURQ5RqpgqAkzH2zbfuwFjUs0mdxkPeVey4KH2F7i%2fH0LC0NH7inQLoUzK%2f… 8/21 1/16/24, 10:32 PM Realizeit for Student People with renal impairment may take heparin in usual dosages. However, the half-life of the drug may increase. Use in Patients With Hepatic Impairment Likewise, people with hepatic impairment may take heparin in usual dosages. However, the half-life of the drug may increase or decrease. Use in Patients With Critical Illness Heparin is often used in patients who are critically ill. However, the risk of bleeding is increased in the presence of other coexisting conditions. People who are critically ill have a high risk of DVT and pulmonary embolism, as well as a higher morbidity and mortality, including an increase in length of hospital stay, the need and duration of mechanical ventilation, and death. Effective prevention and treatment of thrombosis is necessary and typically includes LMWHs. In addition, it is essential to consider intermittent pneumatic compression devices and other measures to prevent DVT or pulmonary embolism. Use in Patients Receiving Home Care Patients may take standard heparin at home using the subcutaneous route, and use of LMWHs for home management of venous thrombosis has become standard practice. Daily visits by a home care nurse may be necessary if the patient or a family member is unable or unwilling to inject the medication. It is essential to take platelet counts before therapy begins and every 2 to 3 days during heparin therapy. If the platelet count falls below 100,000 platelets per microliter of blood or to less than half the baseline value, it is necessary to discontinue the heparin. Adverse Effects Hemorrhage is the major side effect of heparin therapy, hypersensitivity to the drug has occurred, and local irritation with subcutaneous injections of heparin can cause erythema and mild pain. Heparin-induced thrombocytopenia (HIT) (type II) is a potentially life-threatening complication of heparin administration, leading to a decrease in platelet count and detectable HIT antibodies. This condition occurs in 1% to 3% of people receiving heparin at therapeutic levels for 4 to 14 days, sometimes sooner in those who have previously received heparin. HIT is one of the most common immune-mediated adverse drug reactions. All patients exposed to any heparin at therapeutic or prophylactic doses or minute amounts in heparin flushes or on heparin-coated catheters, as well as those receiving LMWH, are at risk. If HIT occurs, it is necessary to discontinue all heparin and manage anticoagulation with a DTI such as argatroban. Contraindications Contraindications include GI ulcerations (e.g., peptic ulcer disease, ulcerative colitis), intracranial bleeding, dissecting aortic aneurysm, blood dyscrasias, severe kidney or liver disease, severe hypertension, polycythemia vera, and recent surgery of the eye, spinal cord, or brain. Caution is necessary in patients with hypertension, renal or hepatic disease, alcoholism, history of GI ulcerations, drainage tubes (e.g., nasogastric tubes, indwelling urinary catheters), threatened abortion, endocarditis, and any occupation with high risks of traumatic injury. Nursing Implications Preventing Interactions Many medications interact with heparin, increasing or decreasing its effect. Some herbs and foods increase the effects of the drug. No herbs or foods that decrease the effects of heparin have been identified. Drug Interactions: Heparin Drugs That Increase the Effects of Heparin Alteplase, direct thrombin inhibitors, platelet inhibitors Increase the risk of bleeding Antithrombin Increases pharmacologic effects Cephalosporins Lead to potential coagulopathies and risk of bleeding Penicillins (parenteral) Lead to altered platelet aggregation and increased risk of bleeding Warfarin May prolong and possibly invalidate the PT; if receiving both heparin and warfarin, draw blood for the PT at least 5 hours after the last IV heparin d Drugs That Decrease the Effects of Heparin Antihistamines, digoxin, nicotine, nitroglycerin (IV), tetracycline Decrease the anticoagulant effect https://herzing.realizeithome.com/RealizeitApp/Student.aspx?Token=lqf9HhURQ5RqpgqAkzH2zbfuwFjUs0mdxkPeVey4KH2F7i%2fH0LC0NH7inQLoUzK%2f… 9/21 1/16/24, 10:32 PM Realizeit for Student IV, intravenous; PT, prothrombin time. Herb and Dietary Interactions: Heparin Herbs and Foods That Increase the Effects of Heparin Chamomile, garlic, ginger, ginkgo, ginseng, high-dose vitamin E Administering the Medication Traditional anticoagulants have two major limitations: a narrow therapeutic window of adequate anticoagulation without bleeding and a highly variable individual dose–response that requires monitoring by laboratory testing. Prescribers use the activated partial thromboplastin time (aPTT), which is sensitive to changes in blood clotting factors, except factor VII, to regulate heparin dosage. Thus, normal or control values of aPTT indicate normal blood coagulation, and therapeutic values of adequate anticoagulation indicate low levels of clotting factors and delayed blood coagulation. During heparin therapy, the aPTT should be maintained at approximately 1.5 to 2.5 times the control or baseline value. The normal control value is 25 to 35 seconds; therefore, therapeutic values of adequate anticoagulation are approximately 45 to 70 seconds. With continuous IV infusion, blood for the aPTT may be drawn at any time; with intermittent administration, blood for the aPTT should be drawn approximately 1 hour before a dose of heparin is scheduled. It is not necessary to monitor aPTT with low-dose standard heparin given subcutaneously for prophylaxis of thromboembolism or with the LMWHs (e.g. enoxaparin). The nurse should be aware that heparin has disadvantages: parenteral injection is necessary, and the drug has a short duration of action, which means that there is a need for frequent administration. Assessing for Therapeutic Effects The nurse assesses for the absence or reduction of signs and symptoms of thrombotic disorders (e.g., less edema and pain with DVT, less chest pain and respiratory difficulty with pulmonary embolism, absence of uncontrolled bleeding). It is also necessary to ensure that aPTT values are within the therapeutic range. Assessing for Adverse Effects The nurse assesses the patient for signs of overt bleeding or HIT. Protamine sulfate, which is discussed in more detail later in the chapter, is an antidote for standard heparin and LMWHs. Protamine is typically given for bleeding that may not respond to merely withdrawing the heparin or when hemorrhaging is present. Patient Teaching Education related to bleeding risk is essential for patients receiving heparin. The nurse reinforces instructions for safe use of the drug and related anticoagulants, reminding patients to obtain laboratory tests and teaching how to observe for signs and symptoms of bleeding. Patient Teaching Guidelines for Anticoagulants General Considerations Anticoagulant drugs are given to people who have had, or who are at risk of having, a heart attack, stroke, or other problems from blood clots. Fo thrombosis, which usually occurs in the legs, you are likely to be given heparin injections for a few days, followed by warfarin for long-term thera blood clot from getting larger, traveling to your lungs, or recurring later. All anticoagulants can increase the risk of bleeding, so you need to take safety precautions to prevent injury. To help prevent blood clots from forming and decreasing blood flow through your arteries, you need to reduce risk factors that contribute to card low-fat, low-cholesterol diet (and medication if needed) to lower total cholesterol to below 200 mg/dL and low-density lipoprotein cholesterol to b overweight; control of blood pressure if hypertensive; avoidance of smoking; stress reduction techniques; and regular exercise. To help maintain a steady level of anticoagulation with warfarin, do not change your intake of foods that are high in vitamin K, which decreases th broccoli, brussels sprouts, cabbage, cauliflower, chives, collard greens, kale, lettuce, mustard greens, peppers, spinach, tomatoes, turnips, and w To help prevent blood clots from forming in your leg veins, avoid or minimize situations that slow blood circulation, such as wearing tight clothing prolonged sitting or standing, and bed rest. For example, on automobile trips, stop and walk around every 1 to 2 hours; on long plane trips, exerc walk around when you can. Following instructions regarding these medications is extremely important. Too little medication increases your risk of problems from blood clot f bleeding. While taking any of these medications, you need regular medical supervision and periodic blood tests. The blood tests can help your health care maintain your safety. https://herzing.realizeithome.com/RealizeitApp/Student.aspx?Token=lqf9HhURQ5RqpgqAkzH2zbfuwFjUs0mdxkPeVey4KH2F7i%2fH0LC0NH7inQLoUzK%2f… 10/21 1/16/24, 10:32 PM Realizeit for Student Notify your health care provider if you suddenly stop tobacco smoking, because this may result in a reduced clearance of warfarin. A dosage cha With enoxaparin, you need an injection, usually every 12 hours. You or someone close to you may be instructed in injecting the medication, or a v necessary. You need to take the drugs as directed. Avoid taking other drugs without the health care provider’s knowledge and consent, inform any health ca are taking an anticoagulant drug before any invasive diagnostic tests or treatments are begun, and keep all appointments for continuing care. With warfarin therapy, you need to avoid walking barefoot; avoid contact sports; use an electric razor; avoid injections when possible; and carry a bracelet (e.g., MedicAlert) stating the name of the drug and the health care provider’s name and telephone number. A routine blood test is necessary to ensure that your warfarin dose is appropriate. The results of this test determine your daily dose of warfarin. O blood tests are done less often (e.g., every 2 weeks). Report any sign of bleeding (e.g., excessive bruising of the skin, blood in urine or stool). If superficial bleeding occurs, apply direct pressure to th necessary. Self-Administration With enoxaparin, wash hands and cleanse the skin to prevent infection; inject deep under the skin, around the navel, upper thigh, or buttocks; an excessive bruising occurs at the injection site, rubbing an ice cube over an area before the injection may be helpful. With warfarin as with all medications, take as prescribed. Because the prescriber may set a dosing schedule that could vary from one day to the written record of the date and the amount of medication taken. Other Drugs in the Class LMWHs are synthetic heparins, have smaller molecular structures, and efficiently inactivate factor Xa via antithrombin. The drugs are as effective as IV heparin in treating thrombotic disorders and provide a more predictable anticoagulant response at recommended doses. The drugs do not cross the placenta. Indications for their use include prevention or management of thromboembolic complications associated with surgery or ischemic complications of unstable angina and myocardial infarction. The currently available LMWHs, dalteparin (Fragmin) and enoxaparin (Lovenox), differ from standard heparin and each other and are not interchangeable. LMWHs are typically given subcutaneously in fixed or weight-based dosing without monitoring of blood coagulation. These characteristics simplify outpatient anticoagulant therapy and safety. Enoxaparin may be administered intravenously in specific situations but should not be given intramuscularly. The drugs are also associated with less thrombocytopenia than is standard heparin. However, monitoring of platelet counts during therapy is necessary. With significant bleeding, protamine sulfate may be considered although it does not completely neutralize LMWHs; clinical bleeding may be reduced. The Institute for Safe Medication Practices (ISMP) classifies the LMWHs as high-alert drugs because there is a possible risk of significant harm when the drugs are used in error. Fondaparinux (Arixtra) indirectly and selectively inhibits factor Xa by mechanisms identical to LMWHs but without affecting thrombin activity. As a synthetic pentasaccharide, the drug binds to antithrombin and is administered for prophylaxis of DVT in people undergoing hip or knee surgery. It is administered subcutaneously and has a longer half-life than LMWHs, necessitating only a once-daily dose. The ISMP classifies fondaparinux as a high-alert drug because there is a possible risk of significant harm when the drug is used in error. Fondaparinux has no effect on prothrombin time, aPTT, platelet aggregation, or bleeding time, so it does not require routine coagulation monitoring. As with other anticoagulants, bleeding is a concern particularly in patients with renal dysfunction, because fondaparinux is primarily eliminated by the kidneys. Currently, no agent for reversal of fondaparinux is available. Direct Thrombin Inhibitors DTIs have benefits compared with agents such as heparin and warfarin, including the inhibition of both circulating and clot-bound thrombin. Other advantages of DTIs include a more predictable dose–response anticoagulant effect, inhibition of thrombin-induced platelet aggregation, and the lack of production of immune-mediated thrombocytopenia. Heparin and warfarin are indirect inhibitors of thrombin. The DTIs exert their effect by interacting directly with the thrombin molecule without the need of a cofactor, such as heparin cofactor II or antithrombin. As such, they inhibit thrombin’s ability to convert soluble fibrinogen to fibrin and to activate the fibrin-generating factors V, VIII, and IX. Because thrombin also stimulates platelets, DTIs also have antiplatelet activity. Both parenteral and oral DTIs are available. The original prototype of the bivalent type, hirudin, is not commercially available; however, its discovery led to the development through recombinant technology of parenteral derivatives, bivalirudin, desirudin, argatroban, and one oral DTI, dabigatran. Lepirudin, another derivative, was discontinued and is no longer on the market. In this discussion, the only oral DTI, dabigatran etexilate (Pradaxa), serves as the prototype. Pharmacokinetics https://herzing.realizeithome.com/RealizeitApp/Student.aspx?Token=lqf9HhURQ5RqpgqAkzH2zbfuwFjUs0mdxkPeVey4KH2F7i%2fH0LC0NH7inQLoUzK%2f… 11/21 1/16/24, 10:32 PM Realizeit for Student Dabigatran etexilate is an inactive prodrug that is rapidly and hydrolyzed to dabigatran, its active form, in the body by plasma and hepatic esterases. The drug is excreted in the urine, and the systemic elimination is proportional to the glomerular filtration rate. Typically, the elimination half-life is 12 to 17 hours, which can be extended in the elderly and those with renal failure. Action As an inactive prodrug, dabigatran etexilate lacks anticoagulant activity. With conversion to the active form in the body, dabigatran has been shown to specifically and reversibly inhibit both free and fibrin-bound thrombin, the key enzyme in the coagulation cascade, thereby inhibiting coagulation. DTIs have no known antagonists. Given orally, the drug peaks in 1 hour. Use Dabigatran etexilate is used to prevent strokes and systemic embolization in individuals with nonvalvular atrial fibrillation. In addition, it is given for the treatment and prevention of deep venous thrombosis and pulmonary embolism. Therapeutic drug monitoring is not necessary. Use in Older Adults Dabigatran etexilate is identified in the Beers Criteria as a potentially inappropriate medication; it should be used with caution in older adults who have a creatinine clearance less than 30 mL/min or those 75 years and older. However, no dosage adjustment of dabigatran etexilate is needed in elderly patients with normal renal function. Nevertheless, the risk of bleeding, a common side effect, increases with age. Use in Patients With Renal Impairment Because dabigatran etexilate is cleared by the kidneys, it accumulates in patients with renal insufficiency, and dosage adjustments may be required based on creatinine clearance calculations. The use of the drug is not recommended in patients receiving hemodialysis. Adverse Effects The most common adverse effects associated with the administration of dabigatran etexilate are bleeding, dyspepsia, abdominal pain, gastritis, and anemia. Contraindications Contraindications include a known hypersensitivity to any of the components of dabigatran etexilate and in patients with active pathologic bleeding or with a mechanical prosthetic heart valve. Use in pregnancy and lactation requires caution. Nursing Implications The ISMP classifies dabigatran etexilate as a high-alert drug because of the possible risk of significant harm that results when it is used in error. Preventing Interactions Many medications interact with dabigatran etexilate, altering its effect. No foods decrease the drug's bioavailability, although the drug's peak plasma concentration is delayed 2 hours if taken with food. Drug Interactions: Dabigatran Etexilate Drugs That Increase the Effects of Dabigatran Etexilate Anticoagulants, apixaban, aspirin, antiplatelet agents (especially clopidogrel), collagenase, dasatinib, defarasirox, deoxycholic acid, edoxaban, h inflammatory agents, pentosanpolysulfate sodium, prostacyclin analogues, salicylates, sugammadex, sulfinpyrazone, thrombolytics, tibolone, tic Increase the risk of bleeding Amiodarone, clarithromycin, dronedarone, ketoconazole P-glycoprotein/ABCB1 inhibitors, quinidine, verapamil May increase serum concentration Drugs That Decrease the Effects of Dabigatran Etexilate Antacids, atorvastatin, lumacaftor, P-glycoprotein/ABCB1 inducers, proton pump inhibitors May decrease serum concentration Estrogen derivatives, progestins May decrease the anticoagulant effects https://herzing.realizeithome.com/RealizeitApp/Student.aspx?Token=lqf9HhURQ5RqpgqAkzH2zbfuwFjUs0mdxkPeVey4KH2F7i%2fH0LC0NH7inQLoUzK%2f… 12/21 1/16/24, 10:32 PM Realizeit for Student Herb and Dietary Interactions: Dabigatran Etexilate Herbs and Foods That Increase the Effects of Dabigatran Etexilate Alfalfa, anise, bilberry, omega-3 fatty acids, vitamin E Administering the Medication The drug capsules should be administered intact with a full glass of water without regard to meals. If the capsules are open or chewed, absorption is increased, and the risk of adverse drug effects is enhanced. Assessing for Therapeutic Effects The nurse assesses for the absence of signs and symptoms of thrombotic disorders, including HIT, and for laboratory values within the normal range. A therapeutic range has not been established for tests of anticoagulant activity. Assessing for Adverse Effects The most common adverse effect associated with the administration of dabigatran etexilate is bleeding; therefore, assessing for signs of bleeding is a priority. Additionally, the nurse assesses for other adverse effects, including GI and hematologic effects. The anticoagulant effects of dabigatran can be reversed by idarucizumab (Praxbind). Patient Teaching Patients need to understand that stopping the drug without provider instruction could increase the risk of blood clots. Patients should notify other health care providers about taking dabigatran etexilate, particularly with spinal or epidural procedures that increase the risk of bleeding around the spine, because paralysis may occur. Other Drugs in the Class In comparison to heparin, which binds only circulating thrombin, DTIs such as bivalirudin and desirudin block circulating thrombin and clotbound thrombin. Bivalirudin is given intravenously as a specific and reversible DTI approved for the treatment of patients with unstable angina undergoing percutaneous transluminal coronary angioplasty (PTCA), as an anticoagulant in patients undergoing PTCA, and as an alternative to heparin in patients with or at risk of developing HIT. Desirudin has been shown to be more effective than enoxaparin in preventing DVT following total hip replacement. Desirudin is administered subcutaneously, and highly protein bound drugs do not modify its effects. Argatroban is indicated for HIT, is eliminated in the liver, and can be used in people with end-stage renal disease. Administered intravenously, argatroban is very short acting due to its reversible binding to thrombin. Direct Factor Xa Inhibitors Direct factor Xa inhibitors inactivate circulating and clot-bound factor Xa. Unlike fondaparinux, which acts indirectly, this class of drugs binds directly and, by doing so, inhibits the production of thrombin. These direct oral anticoagulants, along with dabigatran, are at least as effective as the vitamin K antagonists but are associated with less life-threatening bleeding. Currently, three orally acting direct factor Xa direct factor Xa inhibitors are available for intravenous infusion. are approved, rivaroxaban, apixaban, and edoxaban; no inhibitors Rivaroxaban serves as the prototype. Pharmacokinetics Rivaroxaban is rapidly absorbed and is highly bound to protein. The drug undergoes partial metabolism by CYP3A4 (an isozyme of the cytochrome P-450 system) and is excreted in the urine (36% as unchanged drug) and feces (7% as unchanged drug). Peak plasma levels are reached in 2 to 4 hours, and the half-life is 5 to 9 hours. Actions https://herzing.realizeithome.com/RealizeitApp/Student.aspx?Token=lqf9HhURQ5RqpgqAkzH2zbfuwFjUs0mdxkPeVey4KH2F7i%2fH0LC0NH7inQLoUzK%2f… 13/21 1/16/24, 10:32 PM Realizeit for Student Rivaroxaban inhibits platelet activation and formation of fibrin clotting by inhibition of factor Xa in both intrinsic and extrinsic coagulation pathways. Use Rivaroxaban is used in the treatment and secondary prevention of venous thromboembolism and in stroke prevention in patients with nonvalvular atrial fibrillation. Use in Children The safety of rivaroxaban in children has not been established. Use in Older Adults According to the Beers Criteria, dosage adjustment is indicated in older adults with creatinine clearance between 30 and 50 mL/min. Rivaroxaban is a potentially inappropriate medication in older adults with a creatinine clearance less than 30 mL/min because of increased risk of bleeding. Use in Patients With Renal Impairment Rivaroxaban is metabolized in the kidney and the liver. Therefore, the drug should not be used in individuals with a creatinine clearance of less than 15 mL/min; with delayed excretion of the drug, there may be increased risk of bleeding. Use in Patients With Hepatic Impairment Rivaroxaban should not be used in individuals with moderate to severe hepatic impairment. Use in Patients With Critical Illness Individuals who are critically ill may have complications that may necessitate the use of rivaroxaban, including treatment and secondary prevention of venous thromboembolism and for stroke prevention in patients with atrial fibrillation. The critically ill have a high risk of DVT and pulmonary embolism, as well as an increased risk of bleeding in the presence of other coexisting conditions, particularly those involving the kidneys or liver. Use in Patients Receiving Home Care Rivaroxaban for home use following knee or hip surgery for the prevention of venous thrombosis or management of nonvalvular atrial fibrillation has become common practice as the drug requires no INR monitoring. Additionally, rivaroxaban has fixed dosing schedule, a lower bleeding risk, and few drug interactions as compared to heparin. Regular home care by the nurse, particularly in the older adult, can enhance the safe use of the drug and recognition of signs and symptoms of bleeding before serious bleeding occurs. Adverse Effects Bleeding is the most common adverse effect of rivaroxaban, and this risk increases if the drug taken with other agents that alter hemostasis. Intracranial, gastric, and retinal bleeding has been reported. Additionally, the possibility of spinal or epidural hematoma exists in patients undergoing epidural anesthesia or spinal puncture with procedures or trauma that can lead to permanent paralysis. Dosage adjustment is recommended with anticipated procedures involving the spine. Contraindications Contraindications to rivaroxaban include a known hypersensitivity to the drug. The drug appears unsafe during pregnancy; it is associated with pregnancy-related hemorrhage and risk to the fetus. Benefits of therapy in pregnancy should outweigh risks. Nursing Implications Preventing Interactions Numerous drugs and some herbs are known to interact with rivaroxaban, increasing or decreasing its effect. Drug Interactions: Rivaroxaban Drugs That Increase the Effects of Rivaroxaban Anticoagulants, apixaban, aspirin, antiplatelet agents, collagenase, dasatinib, edoxaban, hemin, ibrutinib, limaprost, nonsteroidal anti-inflammato prostacyclin analogs, salicylates, sugammadex, thrombolytics, tibolone, tipranavir, vorapaxar, vitamin E Increase the risk of bleeding https://herzing.realizeithome.com/RealizeitApp/Student.aspx?Token=lqf9HhURQ5RqpgqAkzH2zbfuwFjUs0mdxkPeVey4KH2F7i%2fH0LC0NH7inQLoUzK%2f… 14/21 1/16/24, 10:32 PM Realizeit for Student Clarithromycin, osimertinib May increase serum concentration Drugs That Decrease the Effects of Rivaroxaban Bosentan, CYP3A4 inducers, deferasirox, estrogen derivatives, fusidic acid, nevirapine, progestins, siltuximab May decrease serum concentration Estrogen derivatives, progestins May decrease the anticoagulant effects Herb and Dietary Interactions: Rivaroxaban Herbs and Foods That Increase the Effects of Rivaroxaban Alfalfa, anise, bilberry, grapefruit juice Herbs and Foods That Decrease the Effects of Rivaroxaban St. John's wort Administering the Medication Rivaroxaban is generally given at a fixed dose. Although 10-mg tablets can be administered without regard to food, 15- and 20-mg tablets should be taken with food. The drug should be administered with the evening meal for nonvalvular atrial fibrillation. Assessing for Therapeutic Effects The nurse should assess for the absence of DVT or other unanticipated clotting. No routine monitoring of INR or other coagulation parameters is required. Assessing for Adverse Effects As with all anticoagulants, the nurse should observe for signs of bleeding, for any change in baseline renal or hepatic function that could enhance the risk of bleeding, and for concurrent administration of drugs known to interact with rivaroxaban. Patient Teaching Education related to bleeding risk is essential for patients receiving rivaroxaban. The nurse reinforces instructions for safe use of the drug and related anticoagulants and teaching how to observe for signs and symptoms of bleeding. Patients should notify other health care providers about taking rivaroxaban, particularly before spinal or epidural procedures that increase the risk of bleeding around the spine because paralysis may occur. Other Drugs in the Class Apixaban (Eliquis) and edoxaban (Savaysa) are additional oral direct factor Xa inhibitors. A major advantage of these drugs is fixed dosing, less variability in drug effect for a given dose, and the lack of required monitoring; although the overall risks of bleeding are similar to vitamin K antagonists, the risks for intracranial bleeding are less with the direct factor Xa inhibitors. These drugs carry the same risks in spinal or epidural procedures as rivaroxaban; the risk of paralysis may occur. As with rivaroxaban, and other anticoagulants, premature discontinuation of the direct factor Xa inhibitors without adequate alternative anticoagulation increases the risk of thrombosis. All drugs in the class pose a risk of hemorrhage and are classified as high-alert drugs by the ISMP because the drugs carry a heightened risk of causing significant patient harm when used in error. No drug that reverses the effects of the direct factor Xa inhibitors is currently available, and the drugs are not removed with dialysis. Should a patient experience hemorrhaging, oral activated charcoal may be given if the timing of administration would prove beneficial. Antiplatelet Drugs Antiplatelet drugs prevent one or more steps in the prothrombotic activity of platelets. As described previously, platelet activity is very important in both physiologic hemostasis and pathologic thrombosis. Arterial thrombi, which are composed primarily of platelets, may form https://herzing.realizeithome.com/RealizeitApp/Student.aspx?Token=lqf9HhURQ5RqpgqAkzH2zbfuwFjUs0mdxkPeVey4KH2F7i%2fH0LC0NH7inQLoUzK%2f… 15/21 1/16/24, 10:32 PM Realizeit for Student on top of atherosclerotic plaque and block blood flow in the artery. They may also form on heart walls and valves and embolize to other parts of the body. Drugs used clinically for antiplatelet effects act by a va

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