Cardiac Pharmacology Past Paper PDF 2025

Cardiac Pharmacotherapy PAT202 Winter 2025 Weeks 1 and 2 1  Weeks 1 & 2 Classification Pharmacotherapy Drug Opioids...

Cardiac Pharmacotherapy PAT202 Winter 2025 Weeks 1 and 2 1  Weeks 1 & 2 Classification Pharmacotherapy Drug Opioids -morphine (see PAT201 Pharmacology Key Concepts & Pain) Calcium channel blockers (selective for vessels) -diltiazem -amlodipine Vasodilators -nitroglycerin β1-Adrenergic receptor blockers -metoprolol (see PAT201 Hypertension) ACE inhibitors -enalapril (see PAT201 Hypertension) Neprilysin inhibitor/ARB -sacubitril & valsartan (combination drug) Cardiac glycosides -digoxin Antidysrhythmics (antiarrhythmics) -amiodarone Antiplatelets -clopidogrel (see PAT201 Atherosclerosis and Stroke) -ticagrelor Cyclooxygenase (COX) inhibitors -acetylsalicylic acid (see PAT201 Atherosclerosis and Stroke) Thrombolytics -tissue plasminogen activator (tPA): alteplase (see PAT201 Atherosclerosis and Stroke) Anticoagulants -heparin -warfarin Antidote for heparin therapy -protamine sulfate Antidote for warfarin therapy -vitamin K Low-molecular-weight heparins -enoxaparin Direct thrombin inhibitors -dabigatran Loop diuretics -furosemide (see PAT201 Hypertension) Thiazide diuretics -hydrochlorothiazide (see PAT201 Hypertension) Mineralocorticoid receptor antagonists -spironolactone 2  Factors Affecting Cardiac Treatments & management Performance strategies target decreasing cardiac workload & decreasing cardiac O2 demand 3 Figure 31.14 Rogers, 2023,  Overall Pharmacological Goals 1 2 3 4 5 Treating Decreasing Improving Improving Reducing symptoms heart oxygenation cardiac pain & workload & function anxiety oxygen demands 4  1. reduce frequency of angina episodes 2 main 2. terminate incidents of goals acute anginal pain once in progress Pharmacological Goals For Client With Angina 1. slow HR 2. dilate veins so heart receives less blood 4 different ↓ preload 3. cause heart to contract with less force mechanism ↓ contractility 4. dilate arterioles to lower BP s ↓ afterload gives heart less resistance when ejecting blood 5  Pharmacological Goals For Treatment of Acute MI 5 main goals 1. Restore perfusion to damaged myocardium as quickly as possible ⮚ through use of thrombolytics 2. Reduce myocardial oxygen demand ⮚ with nitrates and beta blockers to prevent further MIs 3. Control or prevent associated dysrhythmias ⮚ with beta blockers and antidysrhythmics 4. Reduce post-MI mortality ⮚ with acetylsalicylic acid and ACEIs 5. Control MI pain and associated anxiety ⮚ with narcotic analgesics 6  Pharmacological Goals For Treatment of HF 3 primary goals 1. Reduction of preload Both provide symptomatic relief but do not reverse HF progression 2. Reduction of SVR (↓ afterload) 3. Inhibition of both the RAAS and vasoconstrictor mechanisms of SNS results in significant reduction in morbidity & mortality from HF 7 Pharmacotherapy: Analgesics Classification Drug Opioids -morphine (see PAT201 Pharmacology Key Concepts & Pain) 8 Opioids 9  Indications acute MI pain, acute and chronic pain relieve SOB assoc. with HF and pulmonary edema Mechanisms of action binds with mu and kappa receptors in brain and dorsal horn of spinal cord Opioids: mimics endogenous opioids such as endorphins and enkephalins (also stimulate opioid receptors) Morphine ↓responsiveness of alpha-adrenergic receptors peripheral vasodilation (orthostatic hypotension and flushing of face and neck) Desired effects profound analgesia sedation, euphoria ↓ anxiety and fear But…how does morphine ↓ cardiac workload decrease preload and ↓ preload afterload? ↓ afterload Adverse effects CNS depression ⭢ respiratory depression, cardiac arrest dysphoria (restlessness, depression, and anxiety) hallucinations, dizziness, constipation, nausea itching sensation Urinary retention 10  Assessments: Respiratory assessment Pain assessment Vital signs Current medication usage, especially alcohol and other CNS depressants (alcohol, other opioids, general anesthetics, sedatives, and antidepressants such as monoamine oxidase (MAO) inhibitors and tricyclic antidepressants History of liver or renal disease Nursing Monitoring: Implicatio Agitation, slurred speech, euphoria, and constricted pupils orthostatic hypotension ns changes in level of consciousness increased intracranial pressure, seizures Changes in respiratory status and vital signs Contraindications: hypersensitivity and conditions such as acute asthma or upper airway obstruction Administration considerations: narcotic antagonists such as naloxone should be readily available if respirations fall below 10 breaths per minute. 11  When given to treat acute MI, morphine eliminates pain, reduces venous return to Morphine the heart, reduces vascular resistance, reduces cardiac workload, and reduces the oxygen demand of the heart. 12 Pharmacotherapy: Drugs Affecting The Cardiovascular System Classification Drug Calcium channel blockers -diltiazem (selective for vessels) -amlodipine Vasodilators -nitroglycerin β1-adrenergic receptor blockers -metoprolol (see PAT201 Hypertension) ACE inhibitors -enalapril (see PAT201 Hypertension) Neprilysin inhibitor/ARB -sacubitril & valsartan (combination drug) Cardiac glycosides -digoxin Antidysrhythmics (antiarrhythmics) -amiodarone 13  Calcium Channel Blockers (selective for vessels) 14  Calcium Channel Blockers (Selective for Vessels): Diltiazem Indications ▪ stable angina, atrial dysrhythmias, HTN Mechanisms of action inhibits transport of calcium into myocardial cells decreases HR and force of contraction, decreasing O2 demand of myocardium blocks calcium ions from entering cells so causes smooth muscle in arterioles to relax ↑ O2 supply in coronary arteries ↓ O2 demand by decreasing afterload (SVR) Desired effects relaxes both coronary and peripheral blood vessels Adverse effects 15  Assessment & Monitoring vital signs changes in level of consciousness dizziness postural hypotension Nursing signs of heart failure (CCBs can decrease myocardial contractility, increasing the risk for heart failure.) Implicatio fluid accumulation May need to measure intake and output and daily body weight. ns (Edema is a side effect of some CCBs.) Monitor liver and kidney function. Observe for constipation Safety: Monitor ambulation until response to drug is known 16 Calcium Channel Blockers (Selective for Vessels): Amlodipine Indications chronic stable angina, variant angina (Prinzmetal’s angina), HTN Mechanisms of action blocks calcium channels in myocardial and vascular smooth muscle, including the coronary arteries inhibits calcium ion influx across cell membranes Desired effects relaxes peripheral vascular smooth muscle ↓ BP dilates coronary vascular arteries ↑ myocardial oxygen delivery ↓ angina Adverse effects dizziness, flushing, hypotension, H/A, peripheral edema, dysrhythmias 17 Vasodilators 18  Vasodilators: Nitroglycerin (short- acting) Indications taken while acute anginal episode is in progress or just prior to physical activity (drug of choice for stable angina) – given SL Mechanisms of action precursor to nitric oxide (forms NO) NO relaxes vascular smooth muscle (both arterial, coronary, and venous) Desired effects produces vasodilation; venous greater than arterial ↓venous return ⭢↓preload thru venous dilation; or ↓SVR ⭢↓afterload thru arteriolar dilation; or both rapidly terminates angina pain by increasing O2 supply (good for variant angina) Adverse effects usually cardiovascular in nature and are rarely life-threatening Orthostatic hypotension H/A is common and may be severe reflex tachycardia 19  Monitoring: reflex tachycardia – problematic in a client with angina -often transient and asymptomatic Administration Considerations: Should be kept in a dark container Use gloves when applying nitroglycerin paste, patch or ointment to prevent self-administration – WHY? Nursing Blood pressure should be carefully monitored Implications nurse should hold nitrates and remove topical forms if serious hypotension is discovered – think of safety precautions Teaching: Clients should be instructed to use nitroglycerin at the first indication of chest pain or when anticipated stress or activity will occur. Clients should not wait until pain becomes severe. Should be taken in 5-minute intervals for up to three doses. If the pain does not subside after 2 doses, 911 should be called to obtain an ambulance to take the client to the emergency department. The client should not drive or not have a family member drive the client to the hospital Avoid taking sildenafil (Viagra), which has an expected outcome of an erection that can last up to 4 20 hours. Can result in an unsafe decrease in blood pressure β1-Adrenergic Receptor Blockers 21  Indications Desired effects used after MI to block ↓ HR → ↓ myocardial harmful effects of workload & O2 catecholamines demands target HR between 60 β 1- and 90 BPM also used for angina, Adverse effects bradycardia, Adrenergic HTN, MI hypotension bronchospasm is Receptor Mechanisms of Action negligible with cardio selectively blocks β1 Blockers receptors selective β1 blockers except in asthmatic (“olols”): Clients slows conduction clients care must be taken not velocity across should Metoprolol sudden stop th ly myocardium is as higher does may alsoattack. block β2 drug! Suddenly stopping can cause chest pain or heart Abrupt receptors! cessation of the drug may lead to a withdrawal syndrome that could cause angina or myocardial infarction. Tachycardia and hypertension are both common in the withdrawal syndrome. 22  Monitor for : BP, cardiac rhythm frequently assess 30 minutes before and 60 minutes after if taken orally paradoxal hypertension and tachycardia Nursing monitor for signs and symptoms of hypoglycemia– why? implicatio Safety: precautions when standing up ns Teach reduce salt intake Contraindications: first degree hard block, heart failure, bradycardia, shock 23  ACE Inhibitors These drugs block the renin-angiotensin-aldosterone system prevent the intense vasoconstriction caused by angiotensin II. These drugs also decrease blood volume, which enhances their antihypertensive effect. 24 RECALL: What Does the ACE Normally Do? So, what happens…if we inhibit it? Figure 51.6, Adams et al., 2025, p. 25 837  Prevents intense vasoconstriction caused by ACE angiotensin II → ↓SVR (↓afterload) Inhibitors Both decrease myocardial O2 Block the demand! ↓ blood volume by blocking RAAS aldosterone → ↓preload ACEI drugs (enalapril) stop ACE from breaking down bradykinin leading to ↑bradykinin levels causing ↑vasodilation which causes ↓BP BUT… ↑bradykinin causes an ↑in smooth muscle contraction leading to ↑contraction of bronchi causing a dry cough. Bradykinin - - inflammatory mediator that activates the kinin system 26 ACE Inhibitors (“prils”): Enalapril Cautio n with use of + Indications K sparin HTN, HF g diuret ics! Mechanisms of Action inhibits angiotensin-converting enzyme (ACE) angiotensin I cannot be converted to angiotensin II Desired effects promotes vasodilation → ↓ SVR (afterload) → ↓ work & O2 demands of heart ↓ blood volume & preload → ↓ work & O2 demands of heart and less cardiac remodeling Adverse effects hyperkalemia, orthostatic hypotension, headache, dizziness, persistent cough can cause life-threatening angioedema, neutropenia, agranulocytosis 27  Assess: The client’s current medications - avoid use with potassium supplements and potassium sparing diuretics – Nursing when initiating therapy watch for first dose effect (severe and profound hypotension in Implicatio angioedema) Monitor: ns dry nonproductive cough and dyspnea leukopenia, agranulocytosis cytosis &thrombocytopenia Serum potassium levels, liver enzymes, Bilirubin, BUN, Cr, Na and WBC 28  Neprilysin Inhibitor/AR B 29  Newer class (in 2015) called angiotensin receptor neprilysin inhibitors (ARNIs) Indications reduce mortality and hospitalizations in clients with HF Neprilysin Mechanisms of action inhibits neprilysin (enzyme normally in body that degrades Inhibitor /ARB: natriuretic peptides - NPs) via sacubitril & blocks Sacubitril/Valsar angiotensin II receptors via valsartan sacubitril: inhibits neprilysin →↑ cardioprotective (NPs) by tan ↓ their enzymatic breakdown valsartan: (ARB) blocks angiotensin II receptors → (combination vasodilation & ↓aldosterone release drug) Desired effects concentration of NPs increases → cardiac efficiency improves ↓ preload and afterload Is this a maintenance drug or used in Adverse effects crisis? What would you monitor here? hyperkalemia, hypotension, dizziness 30  Cardiac Glycosides 31  Indications primarily used for HF can stabilize some dysrhythmias Cardiac Mechanisms of action inhibits Na+/K+ ATPase causing Na+ to accumulate in Glycosid myocytes as Na+ accumulates, calcium ions released from es: storage areas in cell release of calcium ion produces more forceful Digoxin contraction of myocardial fibres suppresses sinoatrial (SA) node and slows electrical conduction through AV node Desired effects by ↑ myocardial contractility, digoxin directly ↑ CO, thus alleviating symptoms of HF and improving exercise tolerance improved CO results in ↑ urine production and a ↓ blood volume, relieving symptoms of pulmonary congestion and peripheral edema affects impulse conduction in heart Most dangerous adverse ↑ force of contraction (positive inotropic effect) effect of digoxin is its ability ↓ HR (negative chronotropic effect) to create dysrhythmias! Adverse effects Nausea/vomiting, anorexia, fatigue, H/A, dizziness 3 2  Assessments: apical pulse for 1 full minute before administering. If pulse is below 60 beats/minute, the drug is usually withheld and the health-care provider is notified Cardiac Recent serum digoxin level results before administering. If the level is higher than 1.8, withhold dose and notify the healthcare provider Glycosides: Monitor: Small increase in serum digoxin levels can produce serious Digoxin adverse effects, so the nurse must constantly be on the alert for drug-drug interactions and for changes in renal function that can affect blood levels. ⮚ Digoxin interacts with a several drugs: Antacids and Nursing cholesterol-lowering drugs can decrease absorption of digoxin. If calcium is administered IV together with Implication digoxin, it can increase the risk for dysrhythmias. When the client is also receiving quinidine, verapamil (Isoptin), or flecainide (Tambocor), digoxin levels will be s significantly increased. Doses may need to be changed. Teaching: Clients on cardiac glycosides should be strongly advised not to take any other prescription or OTC medication or herbal product without notifying the health-care provider. 3 3 Antidysrhythmics (Antiarrhythmics) 34  Antidysrhythmics (Antiarrhythmics): Amiodarone Indications resistant ventricular tachycardia that may prove life-threatening atrial dysrhythmias in clients with HF recurrent fibrillation (VF) Mechanisms of action blocks potassium and sodium ion channels Desired effects suppression of arrhythmias/dysrhythmias restores normal heart rhythm Prolongs repolarization and refractory period Adverse effects most serious adverse effect occurs in lung causes a pneumonia-like syndrome also causes blurred vision, rashes, photosensitivity, muscle weakness, N & V, anorexia, fatigue, dizziness, and hypotension, bradycardia, heart block 35  Antidysrhythmics (Antiarrhythmics): Amiodarone Amiodarone is 96% protein-bound, accumulates in body tissues, and is metabolized by the liver. Its onset of action may take several weeks when taken orally. It’s effects can last 4 to 8 weeks after the drug is discontinued, since it has a long half-life that may exceed 100 days. Amiodarone interacts with many other drugs and herbals. For example, it increases serum digoxin levels and enhances the actions of anticoagulants. Use with beta- blockers may potentiate sinus bradycardia, sinus arrest, or AV block. Amiodarone may increase phenytoin levels twofold to threefold. Use with echinacea may cause an increase in hepatotoxicity. Aloe may cause an increased effect of amiodarone. Grapefruit juice may decrease metabolism and worsen hypotension. 36  Monitor: BP Signs of pulmonary toxicity CNS changes Nursing Monitor client continually due to unusually long drug half life Implicatio ns Teaching: Recommend clients to avoid sunlight tanning beds and sun lamps Recommend baseline and regular ophthalmic examination Pharmacotherapy: Coagulation Modifiers Classification Drug Antiplatelets -clopidogrel (see PAT201 Atherosclerosis and Stroke) -ticagrelor Cyclooxygenase (COX) inhibitors -acetylsalicylic acid (see PAT201 Atherosclerosis and Stroke) Thrombolytics -tissue plasminogen activator (tPA): alteplase (see PAT201 Atherosclerosis and Stroke) Anticoagulants -heparin -warfarin Antidote for heparin therapy -protamine sulfate Antidote for warfarin therapy -vitamin K Low-molecular-weight heparins -enoxaparin Direct thrombin inhibitors -dabigatran 38  Mechanisms of Actions of Coagulation Modifiers Table 56.1 , Adams et al., 2025, p. 927 Figure 56.4, Adams et al., 2025, p. 928 39  Antiplatelet drugs cause an anticoagulant effect by interfering with various aspects of platelet function— primarily platelet aggregation. Unlike the anticoagulants, which are used primarily to prevent thrombosis in veins, antiplatelet agents are used to prevent Antiplatelets clot formation in arteries. Platelets play major role in thrombotic response to plaque rupture! So… inhibition of platelet aggregation is important aspect in treatment of ACS! 40 The Adenosine Diphosphate (ADP) Receptor Blockers Prevent and treat arterial thrombosis Once platelet adhesion occurs, stimulators like adenosine diphosphate (ADP) released from activated platelets causing platelets to aggregate -So…ADP promotes platelet aggregation by recruiting additional platelets to site of injury BUT…blocking ADP receptors inhibits aggregation -ADP receptor blockers alter platelet plasma membranes → unable to recognize chemical signals required to aggregate Drug examples: clopidogrel, ticagrelor 41  Indication - prophylaxis of arterial thromboembolism to reduce risk of stroke, MI, and death in clients with ACS - clients with ST-elevation MI → reduces risk of death, reinfarction, or stroke - prevent thrombi formation with coronary stents - prevent DVT Antiplatele Mechanisms of action ts: - blocks ADP receptors on platelets - inhibits platelet aggregation Clopidogre Desired effects l - Inhibits platelet function for life span of platelets (7-10 days) - platelet no longer receives signal to aggregate and form clot - extends clotting times When possible, clopidogrel should be - decreased possibility of stroke, MI discontinued at least 5 days prior to surgery to avoid excessive bleeding. Adverse effects - excessive bleeding, GI bleeds (less than Aspirin), flulike 42 syndrome, H/A, diarrhea, dizziness, bruising, upper  Indications reduces risk of thromboembolic events in ACS with PCI, reduces risk of stent thrombosis Mechanisms of action Antiplatelets blocks ADP receptors on platelets → prevents : Ticagrelor aggregation signal and platelet activation ⭢ ↓platelet Desired effects ↓ cardiovascular death, MI and stroke Adverse effects bleeding (can be serious/fatal) dyspnea 43  Monitor signs of bleeding (e.g., hematuria, tarry stools) Educate client that this drug is often Nursing used as adjunct therapy to anticoagulants implications Stop the drug at least seven days prior to planned surgery 44 Cyclooxygenase (COX) Inhibitors 45  Indications antiplatelet (unique to this NSAID) significant anticoagulant activity Cyclooxygenas secondary prevention of vascular events risk reduction of recurrent vascular events (thrombosis) in e (COX) those with hx of ACS, ischemic stroke, peripheral vascular Inhibitors: disease mild to moderate pain & inflammation, fever Acetylsalicylic Acid Mechanisms of Action inhibits cyclooxygenase (COX) enzyme pathway preventing production of prostaglandin & synthesis of thromboxane A 2 reco No lo n COX irreversibly inhibited for lifespan of platelet (7-10 mme ger nd days) prim ed for prev ar y h ar m e ntion s of as Desired effects could d ai l y inhibits platelet aggregation (effect on platelets almost outw use bene e igh immediate) fits. stron Still secondary prevention of thrombotic events gly for s indicate eco d Adverse effects prev ndary entio n gastric discomfort bleeding ↑ clotting time 46 salicylism (can occur with high dosing)  Monitor: GI upset, tinnitus, ototoxicity Platelet count ASA ASA is excreted in the urine and affects urine testing for glucose and other metabolites Nursing Safety: Platelet aggregation inhibition caused Implicatio by ASA is irreversible. ASA should be ns discontinued 1 week prior to elective surgery 47  Thrombolytics If given from 20 minutes to 12 hours after the onset of MI symptoms, thrombolytic agents can dissolve (breakdown) clots and restore perfusion to affected regions of the myocardium. If administered after 24 hours, the drugs are mostly ineffective. After the clot is successfully dissolved, anticoagulant therapy is initiated to prevent the formation of additional clots. 48  Re-establish blood flow! Main Goal is Early reperfusion can Reperfusio prevent necrosis and n! improve perfusion in infarct zone and salvage some cells that would have died BUT…reperfusion can cause further damage, inflammation, and increased phagocytosis of damaged but still viable myocytes 49 Thrombolytics Non-specific dissolve existing intravascular clots in clients with MI, CVA, PE, DVT etc. Narrow margin of safety Thrombolytics are Example: tPA - alteplase not the same as anticoagulants. Thrombolytics break down existing clots 50 Blockage & Reperfusion Following MI Figure 50.3, Adams et al., 2025, p. 51 813  Do NOT give if Thrombolytic Indications risk of bleeding is greater than s: Tissue the potential MI and CVA related to clots (thrombotic) benefit! Can you off-label use: restore IV catheter patency think of some Plasminogen examples when the risk may be Activator Mechanisms of action identical to human tPA enzyme greater than the benefit? mimics body’s process of clot destruction (tPA): converts plasminogen to plasmin (enzyme that breaks down Alteplase fibrin in clot) → dissolves thrombi Desired effects re-establishes bld flow to blood-starved tissues For maximum limits or prevents cell death effectiveness: causes clots to dissolve Must be given coronary artery opens allowing perfusion of myocardium within 6 hours of the onset of Adverse effects symptoms of MI severe risk of bleeding and within 3 spontaneous ecchymoses, hematomas, epistaxis, hours of intracranial bleeding thrombotic CVA 52 Nursing Implications: Monitoring: Closely monitor for signs of bleeding every 15 minutes for the first hour of therapy and then every 30 minutes thereafter. Signs of bleeding such as spontaneous ecchymoses, hematomas, or epistaxis should be reported to the healthcare provider immediately. Contraindications: clients with active bleeding or with a history of recent trauma (physical injury, surgery, biopsies, or childbirth (within the 10-day postpartum period). Any condition in which a favorable clot is in place that would be dissolved by thrombolytics condition where bleeding could be a significant hazard, such as severe renal or liver disease, coagulation disorders Safety: Use with caution with herbal supplements, such as ginkgo, which may cause an increased thrombolytic effect. What other safety considerations can you think of? Teaching: What would you need to educate the client about? 53 Anticoagulant s & Antidotes 54  Indications Anticoagulan acute thromboembolic disorders including DVT, PE, ts: Heparin UA, evolving MI prophylaxis for clotting Mechanisms of action binding of heparin to antithrombin III inactivates several clotting factors and inhibits thrombin activity Desired effects prevents the enlargement of existing clots prevents formation of new clots Natural substance found in liver and lining of Adverse effects blood vessels. Its normal function is to prolong abnormal bleeding coagulation time, preventing excessive heparin-induced thrombocytopenia(HITT) clotting within blood caused by abnormal antibodies that activate vessels. platelets, causing clots to form and depleting 55  Monitor: serum aPTT( activated partial thromboplastin time) normal value of aPTT is 25-40 seconds, therapeutic value while on medication is 1.5-2.0 times control serum platelet count due to risk of HITT Nursing signs of bleeding Implicatio Administration Considerations: Given sc or IV (intermittent or continuous) ns rotate sites if given subcutaneously do not massage the SC site do not pull back on the plunger once needle is in if given intravenously dedicated line must be used Should not be given with Aspirin and NSAIDs 56 Antidote For Heparin Therapy: REVERSES ANTICOAGULANT ACTIVITY OF Protamine HEPARIN Sulfate Indications Heparin overdose if serious hemorrhage occurs (also used in LWMH) onset of action → 5 minutes Mechanisms of action binds to heparin to form stable ion pair that does not have anticoagulant activity Desired effects neutralizes anticoagulant activity of heparin makes heparin ineffective Adverse effects severe respiratory distress, anaphylaxis, pulmonary edema, Hypotension, bradycardia, circulatory collapse 57  99% of the warfarin is bound to plasma proteins and is thus unavailable to produce its effect. Indications prophylaxis of thromboembolic events DVT, PE, AF prophylaxis of arterial thromboembolism Anticoagulan prevention of CVA/MI prevents clotting in long-term indwelling catheters ts: Warfarin can take several days to reach its maximum effect (overlapped with Heparin for a few days) Mechanisms of action inhibits action of vitamin K t i v i ty without adequate vitamin K, synthesis of a c a g u l a nt take clotting factors II, VII, IX, and X is diminished t i c o c a n An rf arin r ea c h ↓ production of clotting factors including of w a t o r a l days effect. thrombin seve ximum a ri n Desired effects m a h e p i ts why herapy s i s prevents intravascular clots/thrombosis Thi f ar i n t a r ed. Adverse effects and w overlapp a re abnormal bleeding 58  Educate avoid food high in potassium Consistent intake of leafy greens due to Vit K content Interactions: High risk for Food and Drug interactions can lead to Nursing ineffective therapy and toxicity Implicatio Monitor: ns serum PT/INR (prothrombin time – measure of extrinsic clotting response and international normalized ratio) – when on therapy PT levels are usually maintained at 1.5 to 2.5 times control value, INR 2.0-3.0 times higher) – report high or low values Serum platelet count signs of bleeding Administration Considerations: Only given early- in the day - requires close monitoring due to narrow therapeutic range 59  REVERSES ANTICOAGULANT ACTIVITY OF WARFARIN vitamin K is essential for synthesis of bld coagulation factors Indications Antidote for when PT/INR indicates blood taking too long to clot Warfarin Mechanisms of action Therapy: vitamin K overrides mechanism by which warfarin inhibits production of vitamin K-dependent clotting factors Vitamin K Desired effects effective blood clotting Adverse effects vitamin K is relatively nontoxic and thus causes minimal adverse effects may have hypersensitivity reactions 60  Foods high in vitamin K may decrease warfarin’s ability to prevent clots because…vitamin K is an antidote for warfarin! Warfarin: Warfarin maintenance dose can fluctuate Dietary significantly depending on amount of Requireme vitamin K in diet Clients do not need to avoid dietary nts vitamin K, but Vit K intake needs to be consistent once warfarin maintenance dose established leafy green veggies i.e. kale, Swiss chard, spinach, collard greens 61 Low-Molecular- Weight Heparins 62 Low-Molecular-Weight Heparin (LMWH): Enoxaparin Indications when anticoagulation required prevention of DVT, PE, UA, acute MI, coronary artery thrombosis prevention of DVT following surgery Mechanisms of action similar to heparin, except that inhibition is more specific to factor X Desired effects inhibits clotting factors lengthens clotting time and prevents thrombi from forming or growing larger Adverse effects hemorrhage, thrombocytopenia (less likely), pancytopenia, anaphylaxis, local site reactions 63  Low-Molecular-Weight Heparin (LMWH): Enoxaparin Nursing Considerations. The duration of action of LMWHs is two to four times longer, and they produce a more stable response than heparin. So, fewer follow-up laboratory tests are needed, and the client or family members can be trained to give the SC injections at home. 64 Direct Thrombin Inhibitors 65  Indication when anticoagulation is required stroke prophylaxis in clients with non-valvular AF treatment of DVT and pulmonary embolus in clients who have been treated with a parenteral anticoagulant for 5 to 10 days prophylaxis of DVT and PE in clients who have undergone hip Direct replacement surgery Thrombin Mechanisms of action directly inhibits action of thrombin and prevents Inhibitors: formation of fibrin Desired effects Dabigatra prevents clot formation and reduce risk of thrombotic n stroke & embolization prevents intravascular thrombosis by ↓ blood coagulation Extensively excreted by Adverse effects kidneys, so dose is serious internal hemorrhage, hypersensitivity dependent on reactions, dyspepsia, gastritis kidney function 66 Nursing Monitor for bleeding and allergic reaction Implicatio other considerations are similar to ns other anticoagulants 67  Pharmacotherapy: Diuretics Classification Drug Loop diuretics -furosemide (see PAT201 Hypertension) Thiazide diuretics -hydrochlorothiazide (see PAT201 Hypertension) Mineralocorticoid receptor -spironolactone antagonists Ensure you assess BP before giving these meds, WHY? 68 Loop Diuretics Thiazide Diuretics Potassium-Sparing Diuretics Figure 52-2, Adams et al., 2025, p. 69 854 Loop Diuretics 70 Loop Diuretics: Furosemide Indications - treatment of acute edema associated with liver cirrhosis, CKD, HF - HTN Mechanisms of action - blocks sodium/potassium/chloride symporter in ascending limb of loop of Henle - increased urinary excretion of sodium, chloride, potassium, hydrogen ions - region of nephron that normally filters bulk of sodium → causes +++ diuresis Desired effect - removes large amounts of fluid in a short time - ↓ preload, ↓ BP Adverse effects - hypovolemia (orthostatic hypotension, syncope) - electrolyte imbalances - tachycardia, dysrhythmias, nausea & vomiting - hypokalemia and metabolic alkalosis 71 Nursing Implications: Furosemide Monitor: Fluid and electrolyte imbalances Hypokalemia and dysrhythmias Blood pressure Safety: Ambulation and dizziness considerations Interactions: Furosemide may diminish the hypoglycemic effects of sulfonylureas and insulin. Concurrent use with NSAIDs can result in a diminished diuretic effect. Concurrent use with corticosteroids or other potassium-depleting drugs can result in hypokalemia. Additive hypotension will occur if furosemide is given at the same time as antihypertensives, including other diuretics. 72 Thiazide Diuretics 73 Thiazide Diuretics: Hydrochlorothiazide Normally, more than 99% of sodium entering the kidney is Indications Mechanisms of action reabsorbed by the reduces Na+ and Cl- body, and very little HF, HTN, edema leaves via urine. When reabsorption by inhibiting thiazides block this Na+/Cl- symporter, reducing reabsorption, more water reabsorption in nephron sodium is sent into the distal convoluted tubule urine. When sodium Desired effects moves across the tubule, water goes promotes diuresis→ ↓ with it; as a result, preload Adverse effects blood volume ↓ BP hypotension, orthostatic decreases and blood pressure falls. The hypotension (risk of falls), volume of urine dizziness, headache produced is directly electrolyte imbalances – proportional to the hypokalemia (dysrhythmias), amount of sodium reabsorption blocked hyponatremia, hypercalcemia by the diuretic 74  Monitor: Serum lab values: K+, Cl−, Na+, Ca+2, Mg+2, CBC, urea, creatinine Educate: potassium is lost along with the sodium Nursing clients must closely monitor their dietary potassium and are usually asked to increase their potassium Implicatio intake as a precaution. ns Interactions: Hydrochlorothiazide potentiates the action of other antihypertensives Thiazides may reduce the effectiveness of anticoagulants, sulfonylureas, antigout drugs, and antidiabetic drugs, including insulin. NSAIDs reduce the effectiveness of hydrochlorothiazide Use of calcium supplements may cause hypercalcemia Administration: given early in the day to prevent nocturia 75 Mineralocorticoid Receptor Antagonists 76  Indications severe stages of HF liver disease (aldosterone not metabolized) Mechanisms of action blocks aldosterone receptors (distal convoluted tubules & Mineralocortic collecting ducts); blocks sodium reabsorption oid Receptor Desired effects sodium and water excretion is increased Antagonists: ↓ cardiac preload ↓ morbidity and mortality rates in severe HF when added Spironolactone to standard therapy Activation of Adverse effects RAAS causes Na+ is lost, and hyperkalemia ↑ aldosterone K+ is retained muscle weakness, ventricular tachycardia, fibrillation → retention of K+ sparing Na+ and diuretic! water → edema that Potassium-sparing diuretics - should not be used in clients with can worsen renal insufficiency or hyperkalemia, since potassium levels may HF! rise to life-threatening levels 77  Assess and Monitor: Uric acid levels may increase, so clients with a history of gout or kidney stones may not tolerate Spironolactone Complete blood counts (CBCs), since agranulocytosis and other hematological disorders Nursing may occur Education: Implicatio Clients should avoid excess potassium in their diet ns and salts that contain potassium (e.g., KCl). Clients should report signs and symptoms of infection eg: fever, rash, and sore throat (since white blood cell levels may be too low to combat infections) 78