Pharmacology W1&2 Cardiac PDF

16 - Percutaneous coronary intervention (PCI) - Coronary artery bypass graft (CABG) - Minimally invasive direct coronary artery bypass (MIDCAB) - Gene & stem therapy for myocardial angiogenesis & spinal cord stimulation Coronary Artery Disease (CAD), Acute Coronary Syndrome (AC...

16 - Percutaneous coronary intervention (PCI) - Coronary artery bypass graft (CABG) - Minimally invasive direct coronary artery bypass (MIDCAB) - Gene & stem therapy for myocardial angiogenesis & spinal cord stimulation Coronary Artery Disease (CAD), Acute Coronary Syndrome (ACS) & Heart Failure (HF): How They Are All Related! WEEK 1: Cardiac Pharmacotherapy Classification Drug Opioids -morphine (see PAT201 Pharmacology Key Concepts & Pain) Calcium channel blockers (selective -diltiazem 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  17 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 Factors Affecting Cardiac Performance measurement of stretch - Don't need to know neural reflexes, atrial receptors, hormones  18 - Treatments & management strategies target decreasing cardiac workload & decreasing cardiac O2 demand Overall Pharmacological Goals - Treating symptoms - Decreasing heart workload & oxygen demands - Improving oxygenation - Improving cardiac function - Reducing pain & anxiety Pharmacological Goals For Client With Angina 2 main goals 1. reduce frequency of angina episodes 2. terminate incidents of acute anginal pain once in progress 4 different mechanisms 1. slow HR more allows expanding to hold a whichamon blood , ear t > - , 2. dilate veins so heart receives less blood ↓ preload 3. cause heart to contract with less force ↓ contractility 4. dilate arterioles to lower BP ↓ afterload gives heart less resistance when ejecting blood 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 Pharmacological Goals For Treatment of HF 3 primary goals 1. Reduction of preload 2. Reduction of SVR (↓ afterload) - Both provide symptomatic relief but do not reverse HF progression 3. Inhibition of both the RAAS and vasoconstrictor mechanisms of SNS - results in significant reduction in morbidity & mortality from HF Pharmacotherapy: Analgesics  19 Classification Drug Opioids -morphine (see PAT201 Pharmacology Key Concepts & Pain) Opioids: Morphine 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 - mimics endogenous opioids such as endorphins and enkephalins (also stimulate opioid receptors) - DECREASE responsiveness of alpha-adrenergic receptors - peripheral vasodilation (orthostatic hypotension and flushing of face and neck) Desired effects - profound analgesia(pain) - Sedation (resp drop) euphoria - DECREASE anxiety and fear - DECREASE cardiac workload - DECREASE preload - DECREASE afterload Adverse effects - CNS depression →respiratory depression, cardiac arrest - dysphoria (restlessness, depression, and anxiety) - hallucinations, dizziness, constipation, nausea - itching sensation - Urinary retention But…how does morphine decrease preload and afterload? Nursing Implications (things you need to assess for) 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 Monitoring: - Agitation, slurred speech, euphoria, and constricted pupils - orthostatic hypotension - changes in level of consciousness - increased intracranial pressure, seizures  20 - 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. Morphine - When given to treat acute MI, morphine eliminates pain, reduces venous return to the heart, reduces vascular resistance, reduces cardiac workload, and reduces the oxygen demand of the heart. 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 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 - related to vasodilation - H/A, dizziness, edema of ankles and feet Nursing Implications  21 Assessment & Monitoring - vital signs - changes in level of consciousness - dizziness - postural hypotension - signs of heart failure (CCBs can decrease myocardial contractility, increasing the risk for heart failure.) - fluid accumulation - May need to measure intake and output and daily body weight. (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 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 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  22 - usually cardiovascular in nature and are rarely life-threatening - Orthostatic hypotension - H/A is common and may be severe - reflex tachycardia Nursing Implications 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? - Blood pressure should be carefully monitored - 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: enhance blood flow to private area), which has an expected outcome of an erection that can last up to 4 hours. Can result in an unsafe decrease in blood pressure - Should NEVER be taken with alcohol as combined may cause severe hypotension and even cardiovascular collapse. β1-Adrenergic Receptor Blockers (“olols”): Metoprolol Indications - used after MI to block harmful effects of catecholamines - target HR between 60 and 90 BPM - also used for angina, HTN, MI Mechanisms of Action - selectively blocks β1 receptors - slows conduction velocity across myocardium Desired effects - ↓ HR → ↓ myocardial workload & O2 demands Adverse effects - bradycardia, hypotension - bronchospasm is negligible with cardio selective β1 blockers except in asthmatic clients - care must be taken as higher does may also block β2 receptors!  23 - Clients should not suddenly stop this drug! - Suddenly stopping can cause chest pain or heart attack. Abrupt 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. Nursing implications Monitor for : - BP, cardiac rhythm frequently - assess 30 minutes before and 60 minutes after if taken orally - paradoxal hypertension and tachycardia - monitor for signs and symptoms of hypoglycemia– why? Safety: - precautions when standing up Teach - reduce salt intake Contraindications: - first degree hard block, heart failure, bradycardia, shock 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. RECALL: What Does the ACE Normally Do? So, what happens…if we inhibit it? ACE Inhibitors Block the RAAS  24 - 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 ACE Inhibitors (“prils”): Enalapril Indications - HTN, HF 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 Caution with use of K+ sparing diuretics! Nursing Implications Assess: The client’s current medications - avoid use with potassium supplements and potassium sparing diuretics – - when initiating therapy watch for first dose effect (severe and profound hypotension in angioedema) Monitor: - dry nonproductive cough and dyspnea - leukopenia, agranulocytosis cytosis &thrombocytopenia - Serum potassium levels, liver enzymes, Bilirubin, BUN, Cr, Na and WBC Neprilysin Inhibitor /ARB: Sacubitril/Valsartan (combination drug) Newer class (in 2015) called angiotensin receptor neprilysin inhibitors (ARNIs) Indications - reduce mortality and hospitalizations in clients with HF  25 Mechanisms of action - inhibits neprilysin (enzyme normally in body that degrades natriuretic peptides - NPs) via sacubitril & blocks angiotensin II receptors via valsartan - sacubitril: inhibits neprilysin →↑ cardioprotective (NPs) by ↓ their enzymatic breakdown - valsartan: (ARB) blocks angiotensin II receptors → vasodilation & ↓aldosterone release Desired effects - concentration of NPs increases → cardiac efficiency improves - ↓ preload and afterload Adverse effects - hyperkalemia, hypotension, dizziness Is this a maintenance drug or used in crisis? What would you monitor here? Cardiac Glycosides: Digoxin Indications - primarily used for HF - can stabilize some dysrhythmias Mechanisms of action - inhibits Na+/K+ ATPase causing Na+ to accumulate in myocytes - as Na+ accumulates, calcium ions released from storage areas in cell - release of calcium ion produces more forceful 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 - ↑ force of contraction (positive inotropic effect) - ↓ HR (negative chronotropic effect) Adverse effects - Nausea/vomiting, anorexia, fatigue, H/A, dizziness - dysrhythmias - visual disturbances (halos, blurring, yellow and green tinge) - Most dangerous adverse effect of digoxin is its ability to create dysrhythmias! Nursing Implications 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  26 - Recent serum digoxin level results before administering. If the level is higher than 1.8, withhold dose and notify the healthcare provider Monitor: - Small increase in serum digoxin levels can produce serious 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 cholesterol-lowering drugs can decrease absorption of digoxin. If calcium is administered IV together with digoxin, it can increase the risk for dysrhythmias. When the client is also receiving quinidine, verapamil (Isoptin), or flecainide (Tambocor), digoxin levels will be 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. - Provide food high in K if pt is on K-wasting diuretics 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 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  27 increase in hepatotoxicity. Aloe may cause an increased effect of amiodarone. Grapefruit juice may decrease metabolism and worsen hypotension. Nursing Implications Monitor: - BP - Signs of pulmonary toxicity - CNS changes - Monitor client continually due to unusually long drug half life 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 Antidote for heparin therapy -warfarin Antidote for warfarin therapy -protamine sulfate -vitamin K Low-molecular-weight heparins -enoxaparin Direct thrombin inhibitors -dabigatran Mechanisms of Actions of Coagulation Modifiers  28 Antiplatelets - 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 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! 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 Antiplatelets: Clopidogrel 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 Mechanisms of action - blocks ADP receptors on platelets - inhibits platelet aggregation Desired effects - Inhibits platelet function for life span of platelets (7-10 days) - platelet no longer receives signal to aggregate and form clot - extends clotting times - decreased possibility of stroke, MI Adverse effects  29 - excessive bleeding, GI bleeds (less than Aspirin), flulike syndrome, H/A, diarrhea, dizziness, bruising, upper respiratory tract infection, rash or pruritus - When possible, clopidogrel should be discontinued at least 5 days prior to surgery to avoid excessive bleeding. Antiplatelets: Ticagrelor Nursing implications - Monitor signs of bleeding (e.g., hematuria, tarry stools) - Educate client that this drug is often used as adjunct therapy to anticoagulants - Stop the drug at least seven days prior to planned surgery Cyclooxygenase (COX) Inhibitors: Acetylsalicylic Acid Indications - antiplatelet (unique to this NSAID) - significant anticoagulant activity - secondary prevention of vascular events - risk reduction of recurrent vascular events (thrombosis) in those with hx of ACS, ischemic stroke, peripheral vascular disease - mild to moderate pain & inflammation, fever Mechanisms of Action - inhibits cyclooxygenase (COX) enzyme pathway preventing production of prostaglandin & synthesis of thromboxane A2 - COX irreversibly inhibited for lifespan of platelet (7-10 days) Desired effects - inhibits platelet aggregation (effect on platelets almost immediate) - secondary prevention of thrombotic events Adverse effects - gastric discomfort - Bleeding - ↑ clotting time - salicylism (can occur with high dosing)  30 - tinnitus, dizziness, headaches, sweating - No longer recommended for primary prevention as harms of daily use could outweigh benefits. Still strongly indicated for secondary prevention ASA Nursing Implications Monitor: - GI upset, tinnitus, ototoxicity - Platelet count - ASA is excreted in the urine and affects urine testing for glucose and other metabolites Safety: - Platelet aggregation inhibition caused by ASA is irreversible. ASA should be discontinued 1 week prior to elective surgery 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. Main Goal is Reperfusion! - Re-establish blood flow! - Early reperfusion can prevent necrosis and 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 Thrombolytics - Non-specific - dissolve existing intravascular clots in clients with MI, CVA, PE, DVT etc. - Narrow margin of safety - Example: tPA - alteplase Thrombolytics are not the same as anticoagulants. Thrombolytics break down existing clots Blockage & Reperfusion Following MI  31 Thrombolytics: Tissue Plasminogen Activator (tPA): Alteplase Indications - MI and CVA related to clots (thrombotic) - off-label use: restore IV catheter patency Mechanisms of action - identical to human tPA enzyme - mimics body’s process of clot destruction - converts plasminogen to plasmin (enzyme that breaks down fibrin in clot) → dissolves thrombi Desired effects - re-establishes bld flow to blood-starved tissues - limits or prevents cell death - causes clots to dissolve - coronary artery opens allowing perfusion of myocardium Adverse effects - severe risk of bleeding - spontaneous ecchymoses, hematomas, epistaxis, intracranial bleeding  32 - Do NOT give if risk of bleeding is greater than the potential benefit! Can you think of some examples when the risk may be greater than the benefit? - For maximum effectiveness: - Must be given within 6 hours of the onset of symptoms of MI and within 3 hours of thrombotic CVA 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? Anticoagulants & Antidotes Anticoagulants: Heparin  33 - Natural substance found in liver and lining of blood vessels. Its normal function is to prolong coagulation time, preventing excessive clotting within blood vessels. Nursing Implications 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 - signs of bleeding Administration Considerations: - Given sc or IV (intermittent or continuous) - 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 Antidote For Heparin Therapy: Protamine Sulfate Anticoagulants: Warfarin Indications - prophylaxis of thromboembolic events - DVT, PE, AF - prophylaxis of arterial thromboembolism - prevention of CVA/MI - prevents clotting in long-term indwelling catheters - can take several days to reach its maximum effect (overlapped with Heparin for a few days) Mechanisms of action  34 - inhibits action of vitamin K - without adequate vitamin K, synthesis of clotting factors II, VII, IX, and X is diminished - ↓ production of clotting factors including thrombin Desired effects - prevents intravascular clots/thrombosis Adverse effects - abnormal bleeding - 99% of the warfarin is bound to plasma proteins and is thus unavailable to produce its effect. - Anticoagulant activity of warfarin can take several days to reach its maximum effect. This is why heparin and warfarin therapy are overlapped. Nursing Implications 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 ineffective therapy and toxicity Monitor: - 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 Antidote for Warfarin Therapy: Vitamin K REVERSES ANTICOAGULANT ACTIVITY OF WARFARIN - vitamin K is essential for synthesis of bld coagulation factors Indications - when PT/INR indicates blood taking too long to clot Mechanisms of action - vitamin K overrides mechanism by which warfarin inhibits production of vitamin K-dependent clotting factors Desired effects - effective blood clotting Adverse effects - vitamin K is relatively nontoxic and thus causes minimal adverse effects - may have hypersensitivity reactions Warfarin: Dietary Requirements  35 Foods high in vitamin K may decrease warfarin’s ability to prevent clots - because…vitamin K is an antidote for warfarin! Warfarin maintenance dose can fluctuate significantly depending on amount of vitamin K in diet - Clients do not need to avoid dietary 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 Low-Molecular-Weight Heparins (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 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. Direct Thrombin Inhibitors: Dabigatran 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 replacement surgery Mechanisms of action - directly inhibits action of thrombin and prevents formation of fibrin Desired effects - prevents clot formation and reduce risk of thrombotic stroke & embolization - prevents intravascular thrombosis by ↓ blood coagulation Adverse effects - serious internal hemorrhage, hypersensitivity reactions, dyspepsia, gastritis Extensively excreted by kidneys, so dose is dependent on kidney function  36 Nursing Implications - Monitor for bleeding and allergic reaction - other considerations are similar to other anticoagulants 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? Loop Diuretics Thiazide Diuretics Potassium-Sparing Diuretics 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)  37 - electrolyte imbalances - tachycardia, dysrhythmias, nausea & vomiting - hypokalemia and metabolic alkalosis 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. Thiazide Diuretics: Hydrochlorothiazide Nursing Implications Monitor: - Serum lab values: - K+, Cl−, Na+, Ca+2, Mg+2, CBC, urea, creatinine Educate: - potassium is lost along with the sodium - clients must closely monitor their dietary potassium and are usually asked to increase their potassium intake as a precaution. 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:  38 - given early in the day to prevent nocturia Mineralocorticoid Receptor Antagonists: Spironolactone Indications - severe stages of HF - liver disease (aldosterone not metabolized) Mechanisms of action - blocks aldosterone receptors (distal convoluted tubules & collecting ducts); blocks sodium reabsorption Desired effects - sodium and water excretion is increased - ↓ cardiac preload - ↓ morbidity and mortality rates in severe HF when added to standard therapy Adverse effects - Hyperkalemia (Na+ is lost, and K+ is retained K+ sparing diuretic!) - muscle weakness, ventricular tachycardia, fibrillation - Activation of RAAS causes ↑ aldosterone → retention of Na+ and water → edema that can worsen HF! - Potassium-sparing diuretics - should not be used in clients with renal insufficiency or hyperkalemia, since potassium levels may rise to life-threatening levels Nursing Implications 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 may occur Education: - Clients should avoid excess potassium in their diet 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) WEEK 2: Complications of MI and Alterations of Cardiovascular Function A Quick Review! Cardiopulmonary Circulation Normal Blood Flow Through The Heart - What is the primary goal of normal heart function?