Cardiac Drugs 2024 PDF

MARIVIC E. ILARDE MAN, RN CARDIOVASCULAR SYSTEM  Learning Objectives: Af t e r the discussion, students are expected to: 1. Identify the diff erent classifi cations of cardiac drugs and their eff ects. 2. Understand the diff erent u...

MARIVIC E. ILARDE MAN, RN CARDIOVASCULAR SYSTEM  Learning Objectives: Af t e r the discussion, students are expected to: 1. Identify the diff erent classifi cations of cardiac drugs and their eff ects. 2. Understand the diff erent uses of Cardiac Drugs 3. Understand the pharmacokinetics and pharmacodynamics of cardiac drugs. 4. Identify the diff erent side eff ects of the cardiac drugs. 1.Inotropic (Inotrope) aff ects the force of contraction positive inotropic effect: = myocardial contraction, renal blood flow negative inotropic effect = myocardial contraction, renal blood 2.Chronotropic (Chronotrope) interferes with the rate of heart beat positive chronotropic effect: (sympathetic stimulation ) = heart rate & renal blood flow Negative chronotropic effect (Parasympathetic stimulation) = heart rate & renal blood 3. Dromotropic Effect (Dromotrope) pertains to conduction The heart conduction system is the network of nodes, cells and signals that controls your heartbeat positive dromotropic effect: speeds up conduction Negative dromotropic effect:  1.Hypertension 2.Angina Pectoris and Myocardial Infarction 3.Shock 4.Arrhythmia 5.CHF  pressure in your blood vessels is too high (140/90 mmHg or  Factors that Affect BP The contraction of Elasticity of the left the artery ventricle walls Peripheral Blood volume vascular resistance  mechanoreceptors located in the carotid sinus a n d in the aortic arch(near the heart that provide the brain with information pertaining to blood pressure and volume by detecting stretch on vascular walls).  sense pressure changes and respond to changes in the tension/stretch of the arterial wall, heart rate and contractility The baroreflex mechanism is a fast response to changes in blood pressure, it will increase or decrease BP Cardiac Output=SV(flow) X HR  BP decreases Baroreceptors send signal to the adrenal medulla catecholamine releases activate the Alpha and beta receptors increase in the sympathetic activity 1. Beta-1 receptors increase: increase heart rate, increase release of renin, increase contractility = increase BP 2. Alpha- 1 receptors increase: vasoconstriction and vascular peripheral resistance= increase BP BP 115/75 Normal No Response BP 140/90 High Parasympathetic BP 90/60 Low  Compensatory process that leads to increase or decrease BP and blood volume to ensure perfusion of the kidneys Vital in the continuous regulation of BP Renin Angiotensin Aldosterone System Juxtaglomerular cells  Goal: to decrease BP to normal CLASSIFICATIONS OF ANTIHYPERTENSIVE DRUGS: 1. ACE-INHIBITORS 2. ANGIOTENSIN II – RECEPTOR BLOCKERS (ARBs) 3. CALCIUM CHANNEL BLOCKERS (CCB) 4. VASODILATORS 5. DIURETICS 6. RENIN INHIBITORS 7. SYMPATHETIC NERVOUS SYSTEM BLOCKERS A. BETA BLOCKERS Mechanism of Action inhibit the production of the angiotensin converting enzyme in the lungs from converting angiotensin I to angiotensin II Decrease in BP Decrease in aldosterone production A small increase in serum potassium levels Increase sodium and fluid loss Captopril ( Capoten ) → 1st ACE inhibitor Benazepril ( Cibacen ) Perindopril ( Coversyl ) Enalapril ( Renitec, Vasopress ) Quinapril ( Accupril ) Fosinopril ( BPNorm ) Ramipril ( Tritace ) Lisinopril ( Zestril ) Trandolapril Moexipril ( Univasc )  also known as angiotensin II receptor antagonists Mechanism of Action: Selectively block the binding of All to specific tissue receptor found in the vascular smooth muscle and adrenal glands Block vasoconstriction a n d release of aldosterone associated with the renin-angiotensin-aldosterone system EXAMPLE: Losartan (Prototype) Candesartan Irbesartan Valsartan Telmisarta n AKA: Calcium antagonist/ Calcium Blockers Mechanism of Action slow the movement of calcium into the cells of the vascular smooth muscles: (heart and blood vessel walls) promoting vasodilation 2 CLASSIFICATIONS: 1.Dihydropyridines: Selectively inhibit the L type of calcium Channels in the vascular smooth muscle block the entry of Calcium into the vascular smooth muscle decreasing the contraction and decrease BP 2 CLASSIFICATIONS: 1. Dihydropyridines: Example: Amlodipine (Norvasc) Felodipine (Plendil) Nicardipine Nifedipine ( Calcibloc, Adalat) Long acting: used in older adults and low serum renin levels 2.Non-hydropyridines non selectively block the cardiac cells on the SA and AV node that decreases myocardial contractility , decrease the CO and HR Act on the arterioles and heart Used to treat chronic HPN, angina pectoris, cardiac dysrhythmia 2.Nonhydropyridines Example: Diltiazem  Verapamil ( isoptin)  Side Effects: 1. Flushing, headache, dizziness, edema, AV block 3. Verapamil inhibits CC in the smooth muscle of the GIT : constipation Mechanism of Action: a c t directly on vascular smooth muscle to cause vasodilation and drop of blood pressure Do not inhibit cardiovascular reflexes and tachycardia Renin is released Example: Hydralazine & Minoxidil : for moderate to severe hypertension (minimum dilation) Sodium Nitroprusside (Prototype): for acute hypertensive emergency : potent vasodilator: arterial and venous vessels Diazoxide (Hyperstat) Hydralazine (Apresoline) Tolazoline (Priscoline)  also called water pills increase the amount of water and sodium excretion from the body as urine.  first line agent in mild hypertension Mechanism of Action inhibit renin leading to decrease plasma renin activity Inhibit the conversion of AT to AT1 Result to decrease BP, aldosterone release, decrease decrease sodium reabsorption EXAMPLE: ALISKIREN (P) Enalliren Remikiren AKA beta-adrenergic agents Mechanism of Action: Compete with beta receptors (Beta 1 & Beta 2) of the sympathetic NS Result to vasoconstriction Decrease HR Negative inotropic eff ect Increase renal blood flow  Cardio selective Beta Blockers Non-Cardio Selective agents have a greater affi nity for β1- Have affi nity to β1-adrenergic adrenergic receptors located in the receptors and β2-adrenergic receptors heart located in bronchial musculature and smooth muscle M- etoprolol Propranolol A-tenolol Pindolol Sotalol N-ebivolol timolol B-etaxolol A-cebutolol B-isoprolol E-smolol Side eff ect: severe bronchospasm and fatalities, metabolic imbalances Cardiac Effects Decrease contractility (negative inotrophy) Decrease relaxation rate (negative lusitrophy) Decrease heart rate (negative chronotrophy) Decrease conduction velocity (negative dromotropy) Vascular Effects Smooth muscle contraction (mild vasoconstriction)  angioedema (swollen red tongue) cough ( dry/hacking cough) Electrolyte imbalance (hyponatremia/hyperkalemia)  radycardia: 60 or less don’t give the drug ottoms BP 80/60 reathing problems: asthma, COPD (constricts bronchi) lood sugar masking : hypoglycemia (monitor sugar) ecrease BP rain fluid ehydrate  ecrease BP ilate Vessels ecrease Vascular Resistance Caution: no erectile drugs like Viagra because it may drop the blood pressure too low  refers to a strangling or pressure-like pain caused by cardiac ischemia The pain is usually located substernally, sometimes with radiation to the neck, Left shoulder a n d arm, or epigastrium  DRUGS USED FOR 1. NITRATES: a. Nitroglycerin (P) ANGINA b. Isosorbide dinitrate c. Isosorbide Mononitrate 2. BETA BLOCKERS a. Metoprolol b. Nadolol c. Propranolol 3. CALCIUM CHANNEL BLOCKERS a. Diltiazem 4. PIPERAZINEACETAMIDE EXAMPLE Nitroglycerin Isosorbide dinitrate Isosorbide mononitrate Mechanism of Action: relaxes vascular smooth muscle with a resultant decrease in venous return and decrease in arterial blood pressure, reducing the left ventricular workload and decreasing myocardial oxygen Vasodilation-increase blood flow drug of choice for treating an acute angina at tack Forms: SL tablets, chewable, immediate release, sustained release, Patch Mechanism of Action Completely block beta-adrenergic receptors in the heart and kidneys, decreasing the influence of sympathetic NS and the excitability of the heart oDecrease CO which results in a lowered BP and decrease Cardiac workload Indication: oStable angina pectoris oPrevent MI oHeart Failure EX. Ditiazem (P) Mechanism of Action oInhibit the movement of calcium ions across the membrane of myocardial and arterial muscle orelieve the vasospasm of the coronary artery oIncrease blood flow to the muscle cells (Prinzmetal angina) Indication: oStable angina pectoris oPrevent MI oHeart Failure EX. Ranolazine Mechanism of Action o decrease myocardial workload, bringing the supply and demand for oxygen back to balance Indication: o first line treatment for angina in combination with nitrates, beta-blockers, and or amlodipine Nursing Considerations: o Grapefruit juice should b e avoided, increase level of the drug  AGENTS USED FOR HEART FAIL 1. Cardiotonic Drugs URE drugs) (inotropic Cardiac glycosides: digoxin 2. Vasodilators: decrease venous return 3.ACE inhibitors: dilate venules and arterioles – increase renal blood flow and decrease blood fluid volume 4.ARBs (Angiotensin 2 receptors antagonist): given if ACE is not tolerated 5.Diuretics (thiazides, furosemides spironolactone): reduce fluid volume 6. Beta blockers: improve cardiac performance  AGENTS USED FOR HEART FAIL(URE CARDIOTONIC DRUGS INOTROPIC DRUGS ) drugs that aff ect the intracellular calcium levels in the heart muscle that results in: o increase contractility, increase in contraction, increase cardiac output o increase renal blood flow, increase urine production, decrease renin release o interfere with the eff ects of the renin–angiotensin–aldosterone system o increase urine output o decrease blood volume o decrease in the heart’s workload o relieve HF CARDIAC GLYCOSIDES Example: Digoxin ( Lanoxin ) derived from digitalis plant most often used drug to treat HF, first line of treatment of acute HF increase the level of CALCIUM inside the cell by inhibiting the Sodium-Potassium pump More calcium will accumulate inside the cell during cellular depolarization Effects on the heart muscle: Positive inotropic action- increase contraction Negative chronotropic eff ect- decrease HR: Bradycardia Negative dromotropic action: decrease conduction of heart cell Nursing Considerations: 1. monitor apical pulse for 1 full minute before administering the drug to monitor for adverse effects. 2. hold the dose if the pulse is less than 60 beats/min in an adult or less than 90 beats/min in an infant; retake the pulse in 1 hour. If the pulse remains low, document it, withhold the drug, and notify the prescriber because the pulse rate could indicate digoxin toxicity 3. monitor the pulse for any change in quality or rhythm to detect arrhythmias or early signs of toxicity 4. monitor the patient for therapeutic digoxin level (0.5–2 ng/mL) 5. Patient teaching on the antidote in case of toxicity: DIGOXIN IMMUNE FAB (Digibind) 1. Ac e inhibitors 2.Nitrates: nitroglycerin Mechanism of Action: relax vascular smooth muscle that results in a decrease afterload a venous pooling: a decrease preload of the heart, decrease workload, (+) inotropic eff ect 3. Diuretics:  DRUGS FOR CIRCULATORY DISORDERS Five major groups: 1. Antilipidemics - hypolipidemics; antihyperlipidemia; decrease blood lipid concentration HMG CoA reductase inhibitors (statins), Bile acid sequestrant 2. Anticoagulants - prevent the formation of clots that inhibit the circulation 3.Thrombolytic - dissolve blood clots that have already formed 4. Antiplatelet (antithrombotic) - prevent platelet aggregation (clumping together of platelets to form a clot) 5. Peripheral vasodilators - promote dilation of blood vessels narrowed by vasospasm  ANTIHYPERLIPIDEMIC AGENTS 1. HMG CoA reductase inhibitors (statins) Action: block HMG CoA reductase  inhibits cholesterol biosynthesis in the liver ↓ total cholesterol, ↓ LDL, ↑ HDL Drugs: lovastatin fluvastatin(Lescol) pravastatin (Lipostat) atorvastatin(Lipitor) simvastatin (Zocor, Vidastat) Side effects: myopathy, increase liver enzymes Contraindication: active or chronic liver disease use in caution in patient taking cyclosporine, macrolide antibiotics, antifungal agents may increase statin serum level  2. BILE ACID SEQUESTRANTS Action: bind with bile acids in the intestine Drugs cholestyramine : cholestipol colesevelam hydrochloride: welchol Side effects:gastrointestinal distress, constipation, decreased absorption of other drugs Contraindication: cannot b e used in patients with elevated triglyceride (>400mg/dl)  PARENTERAL (SC OR IV) ANTICOAGULANT A. Heparin Combines with antithrombin III -> inactivates thrombin inhibits conversion of fibrinogen to fibrin (clot)  clot is prevented Poorly absorbed through Gl mucosa -> give SC or IV Can b e used to prevent clot from forming (SC) or to treat acute thrombosis (IV)  HEPARIN Side effects: Prolongs clotting time (monitor partial thromboplastin time or PTT and activated partial thromboplastin time or aPTT) Thrombocytopenia (decrease in platelet count) Bleeding  antidote: protamine sulfate Before discontinuing, oral therapy is begun (warfarin)  B. LOW MOLECULAR WEIGHT HEPARINS Lower risk of bleeding than heparin Use: to prevent thromboembolism Frequent laboratory is not required Drug examples: enoxaparin dalteparin sodium (Fragmin) sodium (Clexane) ardeparin nadroparin calcium (Fraxiparine) tinzaparin sodium (Innohep) average treatment duration : 7-14 days Side effects: bleeding is rare  antidote: protamine sulfate contraindicated for stroke (hemorrhagic), peptic ulcers a nd blood anomalies  ORAL ANTICOAGULANTS Drug examples: warfarin (Coumadin) →most prescribed dicumarol anisindione → more side eff ects noted Action: inhibit hepatic synthesis of vitamin K → aff ect vitamin K dependent clotting factors well absorbed in Gl mucosa but food will delay absorption long half-life and highly-protein bound →cumulative eff ect →bleeding and other side effects Side effects: bleeding: monitor prothrombin time (PT) and International Normalized Ratio (INR) antidote for side effects: parenteral vitamin K for severe bleeding may give fresh-frozen plasma or platelets  ANTIPLATELET AGGREGATION Action: used to prevent thrombosis in the arteries by suppressing platelet aggregation Indications: for prophylaxis against myocardial infarction and stroke Drugs:aspirin (Aspilet) dipyridamole (Persantin) ticlodipine (Ticlid) clopidogrel (Plavix) Platelet glycoprotein (GP) IIb/IIIa receptor antagonists abciximab – drug of choice for angioplasty eptifi tabide tirofiban (Aggrastat) dipyridamole + aspirin (Aggrenox)  PERIPHERAL VASODILATORS Peripheral Vascular Disease S/Sx: numbness and coolness of extremities, intermittent claudication, leg ulcers caused by arteriosclerosis and hyperlipidemia e.g. Raynaud’s disease, arteriosclerosis obliterans, cerebrovascular insuffi ciency Action of peripheral vasodilators: increase blood flow to the extremities acts directly on vascular smooth muscle (isoxsuprine) Drugs: tolazoline isoxsuprine (Duvadilan) nicotinyl alcohol papaverine prazosin (Minipress) nifedipine (Adalat, Calcibloc)