Cardiovascular System Drugs 2023-10-24 17_10_49.pdf

Cardiac Conditions • Hypertension • Angina • Heart Attack • Coronanry Artery Disease • Heart failure • Cardiomyopathy, cardiomegaly • Congenital heart disease, rheumatic heart disease • Cardiac arrest • Spontaneous coronary artery dissection (scad) • Valvular heart disease • Arrhyhmia, atrial fibrillation, heart block, long QT syndrome • Pericarditis, infective endocarditis • Vascular cognitive impairement Considerations • Incidence and prevalence of heart disease on the rise — Aging population — Comorbidities • Multifaceted variables impact disease process • Most conditions within heart disease can be manageable with adequate resources and education — Risk stratification — Phenotypes • Disease process understanding and Medicaiton education a huge part of therapy Adherence Vs. Compliance • Adherence is an active process in which a patient takes responsibility for their overall well-being, while compliance is a passive behavior in which a patient is following a list of recommendations from the doctors Medication Adherence in CVD • Multifaceted - health management behaviours • No simple one-fits-all strategy • Barriers • Complexity changing +/- evolving status • Patient understanding of stable vs unstable — warning signs • Reasons to seek healthcare • Family/social support Consideration For all Cardiac Classes Keep an open mind to understand these classes of medications individually but in light of their conditions they treat and how they may complement connected syndrome • Class • Diagnosis intended to treat + any other potential improvements to condition • Impact = expected/intended outcomes • Outcome = expected improvement of symptoms • Considerations = What potential side eﬀect/adverse outcomes possible Functions of Cardiac System Functions of blood and circulation • Circulates oxygen and removes carbon dioxide • Provides cells with nutrients • Removes the waste products of metabolism to the excretory organs for disposal • Protects the body against disease and infection • Clotting stops bleeding after injury • Transports Hormones to target cells and organs • Help regulate body temperature Factors that contribute to cardiac function Cardiac output = Heart rate x stroke volume • Myocardial contractility of the heart —- Heart rate • Overall amount of volume of blood within circulatory system — Filling volume = preload — Vascular resistance = After load (tone within blood vessels) • Diﬀerence between: — Systemic vascular resistance/pressure (SVR) — Pulmonary vascular resistance/ pressure (PVR) • Kidney function Blood Pressure = Cardiac output (strenght of heart) X Pressure within the blood vessels (SVR) (BP=Co x SVR) Antihypertensive Drug Categories • Adrenergic drugs • Angiotensin-converting enzyme (ACE) inhibtors • Angiotensin 2 receptor blockers (ARBs) • Calcium channel blockers (CCBs) (antidysrhythmic and antianginal) • Vasodilators • Diuretics Angiotensin-Converting Enzyme (ACE) Inhibitors “Prils” • Relaxing arteries and veins from inhibiting angiotensin 2 = reducing BP (main use) • Decreasing systemic volume to improve heart function when congestion present; usually in combination with other medications • Slowing progression of left ventricular hypertrophy after myocardial infraction (MI), thus it is cardioprotective • Renal protective eﬀects in patients with diabetes (and usually known CAD) • • • • • Captopri Enalapril Lisinopril Perindopril Ramipril Adverse Eﬀects • Fatigue, dizziness, headache • Hypotension • Hyperkalemia • Dry, nonproductive cough —-Reverses when therapy stops • Angioedema Contraindications • Reaction to ACE inhibitor —Angioedema — Introlerable dry cough • Baseline hyperkalmeia • Poor kidney function Angiotensin 2 Receptor Blocker (ARBs) • Newer class • “Sartans” • Well tolerated • Dry not cause a dry cough - usually first substitiue after and ACEi • Lower ortality after MI, better than ACE inhibitors Indications • Hypertension • Adjunctive drugs for the treatment of HF • • • • • Losartan potassium Valsartan Irbesartan Candesartan Telmisartan • Allow angiotensin 1 to be converted to angiotension 2 but block the receptors that recieve angiotensin 2 Block vasoconstriction and release of aldosterone • Adverse Eﬀects • Hypotension • Upper resipratory infections • Hyperrkalemia less likely than ACE inhibitors Calcium Channel Blockers (CCB) • Cause smooth muscle relaxation by blocking the binding of calcium to its receptors, thereby oreventing contraction = calcium blockade — CCbs allow blood vesselsto relax and open • • • Decreased peripheral smooth muscle tone (PVR) Decreased SVR Decreased BP • • • • Amlodipine Diltiazem Nifedipine Verapmil Diuretics • Act by diminishing sodium reabsorption at diﬀerent sites in the nephron, thereby increasing urinary sodium and water losses • Function to decrease the plasma and extracellular fluid volumes - by voided/urinating out volume • • • Decreased preload Decreased cardiac output Decreased peripheral vascular resistance (PVR) Overall eﬀect: • Decreased workload of the heart and decreased BP Thiazide diuretics: most comm. used diuretics for hypertension (hydrochlorothiazide) Vasodilators • Directly relax arteriolar or venous smooth muscle (or both) • Used for their ability to cause peripheral vasodilation — Severe refractory Hypertension — Malignant Hypertension — Hypertensive emergencies • • Decresed systemic vascular resistance (SVR) Not many common endings • • Hydralazine - PO/IM/IV (IV = hypertensive emergencies) Sodium nitroprusside (IV = “”/ Short half life) Antihypertensive nursing process • Thorough health history and physical exam ideal • Baseline VS- BP including orthostatic BP (in/out clinic) • Baseline bloodwork - CBD, extended electrolytes, renal function • Assess for any contraindications • Monitor BW overtime — Electrolyes K+ — Troponin levels MI — Kidney function - BUN, Cr, GFR Teaching Points • Educate on importance of not missing doses and abruptly stopping — If missed dose- never double — If stopped abruptly, can cause rebound HTN • Encourage self-monitoring of BP during therapy *journaling • Change position slowly to avoid syncope • Encourage patients to watch their diet, stress level, weight, exercise/ activity, and alcohol intake • Avoid eating foods high in sodium • Limit fluids, if necessary, and monitor urine consistency Heart Failure Drugs Heart Failure • Not a disease on its own, consequence of underlying conditions • Heart is unable to pump blood in suﬃcient amounts from the ventricles to meet bodys metabolic needs — Impairment of heart function — — Inability to pump - Systolic failure — — inability to fill - diastolic failure • Symptoms depend on cardiac area aﬀected — left ventriicular failure — right ventricular failure • Sequence of events result that further complicate body Symptoms depend on the cardiac area aﬀected. Left Sided Heart Failure Pulmonary Edema Coughing Shortness of Breath Dyspnea Right Sided Heart Failure Systemic Venous Congestion Pedal Edema Jugular Vein Distention Ascites Hepatic Congestion If you need more support on this topic and all meds, this is a longer video so only watch what you need - https://youtu.be/uuXJNJ9LvdM Causes Cardiac defect • Myocardial inraction • Valve defiency Defect outside the heart • Coronary artery disease • Pulmoary hypertension • Diabetes Supraventricular dysrhythmias • Atrial fibrillation • Atrial flutter Increased Workload • Volume overload (congestion) • Pressure Overload (HTN) • Decreased renal function • Angiotensin receptor – neprilysin inhibitor (ARNI) • ACE Inhibitors • Angiotensin II Receptor Blockers (ARBs) Diuretics (will be covered in more detail in GU section) Mineralocorticoid receptor antagonists (MRA) (will be covered in GU section) SGLT2 inhibitors (will also be covered in Endo section, Antidiabetics) Hydralazine with Nitrates ß-blockers Positive Inotropic Drugs / Cardiac glycosides Ivabradine +/- Warfarin Phenotype Treatment Cardiac phenotypes are useful clinical markers that guide diagnostic suspicion of a specific cause but may also be the first or major clinical manifestation that brings patients to medical attention and aﬀects disease evolution and prognosis Angiotensin Receptor - Neprilysin Inhibitor (ARNI) Entresto - Sacubitril valsartan • Blood pressure lowering drug while also getting rid of excess fluid to improve left ventricular ejection fraction (LVEF) • Combination drug — Sacubitril inhibits an enzyme called neprilysin, when blocked, it allows natriuretic peptides to linger in bloodstream which helps blood vessels relax, improving vascular tone, improving kidney filtering to remove fluid, thus improving heart function. — Valsartan is an ARB keeps blood vessels from narrowing , which lowers blood pressure and improve blood flow Side eﬀect: Hypotenstion SGLT-2 Inhibitors • Sodium-glucose co-transporter 2 (SGLT-2) are a pivotal therapy for heart failure improving LVEF. — improve fluid removal • With blood pressure control, is the only direct therapy recognized in the guidelines to reduce mortality in HEpEF (heart failure with preserved injection fraction) — Diabetic AND non-diabetiic • Benefits more significant if tx with SGLT2 is started early Works by: • Blocking the SGLT2 protein in the proximal tubule of the nephron, reducing the amount of reabsorbed glucose and sodium into the blood = glucose, sodium and water removed • (Glucose lvls fall as plasma levels fall, rarely causing hypoglycaemia alone) Ex. • empagliflozin • Canagliflozin Positive Inotropic Drugs Drugs that increase the force of myocardial contraction Used to treat heart muscle failure Include cardiac glycosides Digoxin (Lanoxin) Phosphodiesterase inhibitors IV forms in acute crisis/exacerbation +/- added cardiac support: Dobutamine (a synthetic catecholamine that acts on alpha-1, beta-1 and beta-2 adrenergic receptors). Milrinone (acts downstream from β-adrenergic receptor) Used in: Pulmonary HTN or chronic HF Support during cardiac surgeries (CABG/Transplant, etc.) Palliation due to bad CHF symptoms Cardiac Glycosides • Increase myocardial contractility = positive inotrope • Originally obtained from digitalis plant foxglove — Digoxin (lanoxin) is the prototype • Chnage electrical conduction properties of the heart • Decrease rate of electrical conduction • Prolong the refractory period = result in reduce/slower heart rate and improve cardiac eﬃency • • • Digoxin has a low therapeutic index - Monitor by: BW therapeuti drug monitoring Low K+ or magnesium levels may increase the potential for digitalis toxicity Digoxin toxicity: Bradycardia, headache, dizziness, confusion N/V Ivabradine - Rate Control • Selectively and specifically inhibits SA node via mixed sodium-potassium inward current that controls spntaenous diastole depolarizatio and hence regulates the heart rate • Tx: chronic HF to reduce risk of hospitalization for worsening heart failure. • Tx: 6 months + stable HF w/ symptoms cause by enlarged heart (dilated cardiomyopathy) Nursing Implications & Teaching for HF Medication • Take as prescribed: same time Q day. May need adjustments between meals • Monitor BP: change positions slowly if symptomatic. Report if persists • Track Weight daily: report weight gain 1kg in 24h or. 2.3kg 1 week • Track symptoms: fatigue, SOB, heavy limbs, finger indent, dizziness • Monitor BW: CBC, electrolytes, glucose • Encourage understanding of diagnosis and disease progression • Clear understanding of medications and for what reason —medication schedule/blister packs, dose adjustments normal When used in combination w/ other HF meds: • Increase age of mortality • Improve symptoms of HF • Reduce risk of hospitalization • Slow progression of HF Antianginal Drugs Supply of oxygen and nutrients in blood is insuﬃcient to meet the demands of the heart, and the heart muscle “aches” • Heart requires a large supply of oxygen to meet the demands placed on it Coronary Artery Disease • Oxygen supply is delivered through the coronary arteries. —RCA, LAD, LCs —Coronaru perfusion during diastole • Acute coronary syndrome (ACS) is a group of clinical symptoms compatible with acute myocardial ischemia —ST-elevation myocardial infarction (STEMI) —non-ST elevation myocardial infarction (NSTEMI) and unstable angina Ischemia Poor blood supply to an organ Ischemic heart disease • Poor blood supply • Causes: Atherosclerois, CAD Myocardial infarction (MI) “Heart Attack” • Caused by decreased/completed cessation of blood flow to a portion of the myocardium = necrosis • Acute result of CAD and ischemic heart disease • Disabling or fatal Types of Angina • Chronic Stable: Relieved w/ rest • Unstable angina (Pre-infarction or crescendo angina): Comes on during exertion or rest • Vasospastic angina (Prinzmetals or variant): Can be exertional and unpredictable Pharmacothearpy for Angina and Ischemic Heart Disease 1. Nitrates and Nitrires • Dilate all blood vessels • Used for prophylaxis and tx for angina and other heart problems Action: Vasodilation due to relaxation of smooth muscles • Potent dilating eﬀect on coronay arteris • Decresead afterload • Peripheral vasodilation • Increased oxygen to ischemic myocardial tissue Forms: Sublingual, PO, IV, Ointments, Transdermal, Translingual 2. B-Blockers • Reduce HR and reduce myocardial contractilitydecreases oxygen demand • Suppress renin production 3.Calcium channel blockers • Relaxes smooth muscles to dilate coronary arteries, which increases blood flow to the ischemic heart • PVR decreases-Heart works easier (demand is less) • Some impact SA nodes-slowing heart rate • Non-Dihydropyridine CCB act centrally to decreased HR (chronotropy) and contractility (inotropy) Verapamil Nifedipine Diltiazem Amoldipine Eﬀective at tx prinzmetal angina, supraventriuclar tachycardia (SVT), atrial fibrilation and flutter Nursing Considerations Contraindications • Drug allergy • Anemia • Baseline hypotension • Severe head injury • Glaucoma • Recent PDE5 use to treat erectile dysfunction, may lead to severe hypotension with nitrates Adverse Eﬀects • Hypotension • Headache • Reflex tachycardia • Tolerance may develop around the clock or long-acting forms • Overexpressions: Bradycardia, hypotension, heart block, dizziness, fatigue Nursing Consideration • alcohol consumption, hot tubs • Patterns of anginal attacks, precipitating factors, number of pills/sprays taken • Nitroglycerin: to reduce tolerance-follow schedule, monitor vs • Calcium channel blockers: constipation Teaching: • Nitro SL q5m when onset of CP —- if not relieved call EMS • sit or lie down when taking • Change positions slowly • Patch shouldn’t be applied to open skin • Ensure only 1 patch at a time Antidysrhythmic Drugs SA node determines HR, initiates all heartbeat, electrical impulses pass through the atrium and cause contraction AV node causes a delay to ensure equal conduction and therefore proper ventricular filling AV bundle of HIS – this bundle goes to left and right bundle branches Then go to the Purkinje fibers Dysrhythmia • Any deviation from the normal rhythm of the heart Anti-dysrhythmics • Drugs used for the treatment and prevention of disturbances in cardiac rhythm • Aim to re-establish normality within the hearts conduction system • Classification System commonly used to claddify antidysrhythmic drugs • Based on the ekectriohysiological eﬀect of particular drugs on the action potential Common dysrhythmias • Supraventricular dysrhythmia ——Originates above ventricles in atria ——Narrow QRS complex • Ventricular dysrhythmia ——Originates in ventricles ——Wide QRS complex • Atrial fibrillation or atrial flutter ——Irregularities of conduction in one or both artia Vaughan Williams Classification Class I - Sodium-channel blockers. Class II - Beta-blockers. Class III - Potassium-channel blockers. Class IV - Calcium-channel blockers. Miscellaneous Adenosine Electrolyte supplement magnesium and potassium salts) Digitalis compounds (cardiac glycosides) Electrophysiological eﬀect on the action potential Class I: Fast sodium channel blockers • Class Ia: procainamide, quinidine, and disopyramide • Block sodium (fast) channels to delay repolarization [Increase action potential duration (APD)] • Used for atrial fibrillation, premature atrial contractions, premature ventricular contractions, ventricular tachycardia, Wolﬀ-Parkinson-White syndrome • Class Ib: Lidocaine shortens repolarization Class II: ß-blockers • Reduce or block sympathetic nervous system stimulation, thus reducing transmission of impulses in the heart’s conduction system [Depress phase 4 depolarization] • General myocardial depressants for both supraventricular and ventricular dysrhythmias, also used as antianginal and antihypertensive drugs Class III: Increase APD • Prolong repolarization in phase 3 • Used for dysrhythmias that are diﬃcult to treat • Amiodarone, sotolol - Life-threatening ventricular tachycardia or fibrillation, atrial fibrillation or flutter that is resistant to other drugs Class IV: Calcium channel blockers • Inhibit slow channel (calcium-dependent) pathways • Depress phase 4 depolarization: Reduce atrioventricular node conduction • Diltiazem: Used for paroxysmal supraventricular tachycardia (PSVT); rate control for atrial fibrillation and flutter Amiodarone • • • used to treat life-threatening heart rhythm problems; ventricular arrhythmias. Markedly prolongs the action potential duration and the eﬀective refractory period in all cardiac tissues Blocks both the α- and ß-adrenergic receptors of the sympathetic nervous system Uses: one of the most eﬀective antidysrhythmic drugs for controlling supraventricular and ventricular dysrhythmias • Most serious eﬀect: pulmonary toxicity Can be given IV for acute onset Afib • Loading doses apply, pt must be monitored PO forms for maintenance • Sometimes doses change if they are being increased or tapered at all Miscellaneous/Unclassified Antidysrhythmic Drug Adenosine (Adenocard®) • Slows conduction through the atrioventricular node • Used to convert SVT to sinus rhythm • Very short half-life—less than 10 seconds • Only administered as fast intravenous (IV) push (2-person) • May cause asystole for a few seconds • Other adverse eﬀects are minimal. Adverse Eﬀects: All antidysrhythmics can cause dysrhythmias! Hypersensitivity reactions Nausea, vomiting, and diarrhea Dizziness Headache, and blurred vision Prolongation of the QT interval Constipation Prolongation of the QT interval Depression of sinus node function and/or AV conduction leading to severe bradycardia or asystole Nursing Implciations: • Baseline VS and ongoing VS, especially if changes felt/noticed on monitor • Instruct patients to not to skip doses or double up for missed doses. • Instruct patients not to crush or chew oral sustained-release preparations. • Teach patients taking cardiac meds when to seek help Consider 12-lead ECG as needed All antidysrhythmics can cause dysrhythmia Monitor for therapeutic response. Regular pulse rate Pulse rate without major irregularities Noticeable or not No increased heart block Improved regularity of rhythm Improved cardiac output Decreased blood pressure in hypertensive patients Decreased edema Decreased fatigue Coagulation Modifier Drugs Hemostasis • General term for any process that stops bleeding • Coagulation is hemostasis that occurs because of the physiological clotting of blood. Thrombus: technical term for a blood clot Embolus: thrombus that moves through blood vessels Reasons for drug use Given to people at a high risk of getting clots, to reduce their chances of developing serious conditions • Primary and secondary prevention for strokes and heart attacks • Prophylaxis & Treatment: Deep vein thrombosis (DVT), pulmonary embolism (PE) • Known thrombophilia • Arrhythmias: atrial fibrillation, aflutter, etc • Implanted valves • LV dysfunction • Pregnancy related clotting concerns • Surgeries and recovery, including immobility Etc. Thrombophilia’s factor V Leiden. protein C deficiency. protein S deficiency. antithrombin deficiency. antiphospholipid syndrome. Anticoagulants Adverse eﬀects Bleeding Minor – superficial like gums bleeding, nose bleeding, or it might take longer for superficial cuts to scab over (think men shaving) Severe – uncontrolled nose bleeds, intracranial, hematuria, or internal like GI bleeds (overt or occult). Internal Intracranial Superficial Risk increases with dosages “Blood thinners” prevent blood clots from forming. Do not break up clots that you already have. But they can stop those clots from getting bigger. Contraindications Drug Allergy Any acute bleeding process or high risk of such occurrence (need to know history) Some contraindicated in pregnancy Heparins • Action: inhibit clotting factors IIa (thrombin), Xa, and IX Factors XI and XII are also inactivated but do not play as important of a role as the other three factors. Unfractionated heparin: “heparin” Is obtained from sheep, cows, and pigs Low- molecular Weight Heparin LMWH is obtained by fractionation of polymeric heparin. LMWH diﬀers from unfractionated heparin in a number of ways: • average molecular weight; • the need for only once or twice daily dosing; • the absence of monitoring the aPTT; and • the lower risk of bleeding, osteoporosis, and HIT. Heparin • Is monitored by activated partial thromboplastin times (aPTTs) • Is available in parenteral form • Has a short half-life (1 to 2 hours); given IV and SC • Has as its antidote protamine sulfate Low-weight-molecular heparins (LMWH) • Include enoxaparin (Lovenox) and dalteparin (Fragmin) • Have a more predictable anticoagulant response • Do not require frequent laboratory monitoring • Are given subcutaneously Warfarin sodium (Coumadin) Action: inhibit vitamin K–dependent clotting factors II, VII, IX, and X which are normally synthesized in the liver. Final eﬀect is the prevention of clot formation Is given orally only Is monitored by prothrombin time (PT) and International Normalized Ratio (INR) (PT/INR) Normal INR 0.8-1.2 With Warfarin 2-3.5 Has as its antidote vitamin K Added vit K in diet needs to be avoided, or factored in Contraindicated in pregnancy Can take 24-72 hours to have eﬀect – so often first give heparin IV to keep blood thinned until warfarin eﬀective Antiplatelet Drugs • • Prevent platelet adhesion/sticking together Arterial thrombosis prevention Examples: *acetylsalicylic acid (Aspirin) [can bother the stomach, should be taken with food] *clopidogrel (Plavix) [OD] *Ticagelor (Brilinta) [BID, dyspnea-like sensation] pentoxifylline abciximab (Reopro) eptifibatide (Integrilin) Thrombolytic Drugs Drugs that break down, or lyse, preformed clots Older drugs Streptokinase and urokinase Newer drugs Alteplase (Activase or TPa) Tenecteplase (TNKase) Alteplase is a recombinant tissue plasminogen activator (rt-PA) used as a thrombolytic agent used commonly for strokes. Mechanism of Action useddown commonly infarctions Activate the fibrinolytic system TNK to break the clotforinmyocardial the blood vessel quickly Activate plasminogen and convert it to plasmin, which lyses the thrombus Plasmin is a proteolytic enzyme. = Mimics the body’s own process of clot destruction Indications Usually Urgent in nature and time sensitive Acute myocardial infarction Arterial thrombolysis DVT Occlusion of shunts or catheters Pulmonary embolism Acute ischemic stroke Adverse Eﬀects Bleeding Internal Intracranial Superficial Other eﬀects Nausea, vomiting, hypotension, hypersensitivity, anaphylactoid reactions Cardiac dysrhythmias; can be dangerous Antifibrinolytic Drugs Prevent the lysis of fibrin Result in promoting clot formation Used for prevention and treatment of excessive bleeding resulting from hyperfibrinolysis or surgical complications Example: Tranexamic acid (Cyklokapron) TXA IV doses need to monitor aPTT (activated partial thromboplastin time) q6h until within desired range, then daily Heparin-induced thrombocytopenia (HIT) is a life-threatening complication of exposure to heparin (ie, unfractionated heparin, low molecular weight [LMW] heparin) that occurs in up to 5% of patients exposed, regardless of the dose, schedule, or route of administration. Warfarin Takes a few days for full therapeutic eﬀect to be in eﬀect Pt may be on heparin and started on warfarin until therapeutic levels Monitor PT/INR daily, then when necessary Pt education on avoiding foods high in vit K Avoid ASA for aches/pains, Tylenol best Education Importance of bloodwork regularly Monitor for abnormal bleeding Monitor diet Assess Pt history Baseline VS Hx of abnormal bleeding conditions Thrombolytic Drugs: Monitor IV site Watch for signs of bleeding Antilipemic Drugs Triglycerides and Cholesterol Two primary forms of lipids in the blood Water-insoluble fats that must be bound to apolipoproteins, specialized lipidcarrying proteins Lipoprotein Very-low-density lipoprotein Produced by the liver Transports endogenous lipids to peripheral cells Intermediate-density lipoprotein Low-density lipoprotein (LDL) High-density lipoprotein (HDL) Responsible for “recycling” of cholesterol Ideals: LDL – want Low levels – also known as “bad cholesterol” HDL – want High levels - Also known as “good cholesterol” CCS Guidelines To Treat Dyslipidemia All reasonable nondrug means of controlling blood cholesterol levels (e.g., diet, exercise) Drug therapy based upon the specific lipid profile of the patient Antilipemic’s Four classes of drugs: Statins: Hydroxymethylglutaryl–coenzyme A (HMG–CoA) reductase inhibitors Bile acid sequestrants B vitamin niacin (vitamin B3, nicotinic acid) Fibrates: Fibric acid derivatives Miscellaneous agents Cholesterol absorption inhibitor (Ezetrol®) proprotein convertase subtilisin/kexin type 9 (PCSK9) inhibitors Statins First-line therapy for hypercholesterolemia Reduces plasma concentrations of LDL cholesterol by 30 to 40% Decrease in plasma triglycerides by 10 to 30% Increase in HDL cholesterol by 2 to 15% Dose dependent Dosed once daily, usually with the evening meal or at bedtime to correlate with diurnal rhythm E.g. simvastatin, atorvastatin (Lipitor®), rosuvastatin calcium (Crestor®) Proprotein convertase subtilisin/kexin type 9 inhibitors (PCSK9i) are a novel class of medications for patients with familial hypercholesterolemia or clinical atherosclerotic cardiovascular disease requiring additional lipid lowering beyond dietary measures and statin use Hydroxymethylglutaryl– coenzyme A (HMG–CoA) reductase inhibitors Most potent LDL reducers pravastatin sodium simvastatin (Zocor®) atorvastatin (Lipitor®) fluvastatin sodium (Lescol®) rosuvastatin calcium (Crestor®) lovastatin Action Inhibit HMG-CoA reductase, which is used by the liver to produce cholesterol Lower the rate of cholesterol production Adverse Eﬀects GI disturbances Myopathy (muscle pain) Could lead to rhabdomyolysis Do not use for patients with elevated liver enzymes or liver disease Rhabdomyolysis Breakdown of muscle protein Myoglobinuria: urinary elimination of the muscle protein myoglobin Can lead to acute kidney injury and even death When recognized reasonably early, rhabdomyolysis is usually reversible with discontinuation of the statin drug. Instruct patients to immediately report any signs of toxicity, including muscle soreness or changes in urine colour (teacoloured). Asian decent higher risk (flipino, Chinese, Japanese, Korean, veitnamese, or south Asian) Bile Acid Sequestrants Action: Prevent resorption of bile acids from small intestine Bile acids are necessary for absorption of cholesterol. Lowers LDL by 15-30% Increases HDL by 3-8% Adverse Eﬀects Constipation Heartburn, nausea, belching, bloating These adverse eﬀects tend to disappear over time. Also called bile acid–binding resins and ion-exchange resins Indicated for: Type II hyperlipoproteinemia and Relief of pruritus associated with partial biliary obstruction (cholestyramine) May be used along with statins Increase fiber when taking to help with constipation Considerations Overdose can cause obstruction because the bile acid sequestrants are not absorbed. Treatment of overdose includes restoring gut motility. Drug interactions All drugs must be taken at least 1 hour before or 4 to 6 hours after the administration of bile acid sequestrants. High doses of a bile acid sequestrant decrease the absorption of fat-soluble vitamins (A, D, E, and K). Contraindications: known hypersensitivity, phenylketonuria or complete biliary obstruction - Pregnancy and lactation considerations - Treatment of loose bowel movements - Caution when administering dry powder Niacin (Niaspan®, nicotinic acid) Action Vitamin B3 Lipid-lowering properties require much higher doses than when used as a vitamin. Eﬀective, inexpensive, often used in combination with other lipid-lowering drugs Eﬀective in lowering triglyceride, total serum cholesterol, and LDL cholesterol levels Increases HDL levels Adverse Eﬀects Flushing (caused by histamine release) Pruritus Gastrointestinal distress Fibric Acid Derivatives - fibrates Action Believed to work by activating lipoprotein lipase, which breaks down cholesterol Suppress the release of free fatty acid from adipose tissue Inhibit the synthesis of triglycerides in the liver, and increase the secretion of cholesterol in the bile Adverse eﬀects Abdominal discomfort, diarrhea, nausea Blurred vision, headache Increased risk of gallstones Prolonged prothrombin time Lower triglycerides but also total cholesterol and LDL levels and raise HDL levels Independent to their lipid changing profile they can change blood coagulation Decrease in platelet adhesion Can also increase plasma fibrinolysis – causes clots to be broken down Laboratory test reactions: Decreased hemoglobin level, hematocrit value, and white blood cell count Thought to inhibit lipolysis in adipose tissue, decrease esterification of triglycerides in the liver, and increase the activity of lipoprotein lipase Reduces the metabolism or catabolism of cholesterol and triglycerides Miscellaneous Cholesterol Absorption Inhibitor ezetimibe (Ezetrol) Inhibits absorption of cholesterol and related sterols from the small intestine Results in reduced total cholesterol, LDL cholesterol, apolipoprotein B, and triglyceride levels Also increases HDL cholesterol levels Often combined with a statin drug Can be used as monotherapy Proprotein convertase subtilisin/kexin type 9 (PCSK9) inhibitors By binding to hepatic LDL receptors PCSK9 inhibitors reduce the number of LDL receptors and reduces LDL uptake Examples: Alirocumab (Praluent®). Evolocumab (Repatha®). Most cases of familial hypercholesterolemia are due to mutations resulting in defective LDL receptors. Proprotein convertase subtilisin/kexin type 9 inhibitors (PCSK9i) are a novel class of medications for patients with familial hypercholesterolemia or clinical atherosclerotic cardiovascular disease requiring additional lipid lowering beyond dietary measures and statin use. Nursing Implications Assess dietary patterns, exercise level, weight, height, vital signs, tobacco and alcohol use, and family history. Assess for contraindications, conditions that require cautious use, and drug interactions. Contraindications include biliary obstruction, liver dysfunction, and active liver dysfunction. Monitor liver function studies, lipid profiles. Patients on long-term therapy may need supplemental fat-soluble vitamins (A, D, K). Teach patients when to take antilipemics Key words: assess, monitor, supplement (use these to guide your patient teaching) Questions to consider for Cardiac Pt c/o sudden and severe chest pain. You want to administer a medication that will give rapid relief – what would you give? You have a patient who complains of swelling to tongue, lips, and face. What medication would you suspect that they recently started? Your patient states that they used to be on Ramipril but developed a persistent dry cough so the medication was switched to something similar. What class of medication is the patient probably referring to? A patient tells you they were started on an IV blood thinner in hospital while their oral anticoagulation medication was getting into a “therapeutic range” and they had to have bloodwork every 6 hours, what drug were they likely on? And what blood measure was being checked? Your patient states that they have atrial fibrillation and take a medication to prevent stroke. They have regular bloodwork taken to determine the dose of the medication. What medication is the patient on? And what bloodwork measure is being checked frequently? What foods would the previous patient need to avoid, and why? Your patient states that they have heart failure, what drugs would be eﬀective for them to potentially be on? Your patient has high blood pressure, what reading is considered Hypertension? What are the most common complaints from taking statins? What organs are impacted and blood tests are required when taking antilepemics? What teaching do we want to provide our patients about taking antilepemics?

Cardiovascular System Drugs 2023-10-24 17_10_49.pdf

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