Chapter 20. Drugs Affecting Circulation: Antihypertensives, Antianginals, Antithrombotics
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1 Chapter 20 Drugs Affecting Circulation: Antihypertensives, Antianginals, Antithrombotics
2 Epidemiology and Etiology of Hypertension Primary: Unknown etiology Secondary: Due to known disease process Adversely affects numerous organs Termed cardiovascular disease (CVD) Diagnosis: Two or more seated BP taken on different days Increased risk of: Left ventricular (LV) hypertrophy, angina, myocardial infarction (MI), heart failure, stroke, peripheral arterial disease (PAD), retinopathy, and renal failure
3 Pathophysiology of Hypertension Arterial blood pressure Product of cardiac output (CO) and total resistance Preload is major factor in systolic blood pressure (SBP) Affects venous capacitance Afterload is major factor in diastolic blood pressure (DBP)
4 Hypertensive Crisis Patient with BP > 180/120 mmhg Hypertensive urgency No signs/symptoms of organ complication Hypertensive emergency Acute, chronic, or progressive organ injury
5 Hypertension Pharmacotherapy First-line agents: Angiotensin-converting enzyme inhibitors (ACEIs) Angiotensin II receptor blockers (ARBs) Calcium channel blockers (CCBs) β Blockers Thiazide-type diuretics
6 Hypertension Pharmacotherapy (cont d) Second-line agents Vasodilators α Blockers α 2 Agonists Antiadrenergics
7 Hypertension Pharmacotherapy (cont d) Angiotensin-converting enzyme inhibitors Suppress renin-angiotensin-aldosterone system Block conversion of angiotensin I to angiotensin II Hemodynamic effect Reduce peripheral arterial resistance (PAR) Increase CO Increase renal blood flow
8 Hypertension Pharmacotherapy (cont d) Indicated for: Hypertension (HTN), heart failure, systolic dysfunction, MI prevention, LV dysfunction, and diabetic neuropathy Generally decrease SBP and DBP 15-25% Most common side effect is dry cough Significant interaction with nonsteroidal antiinflammatory drugs (NSAIDs)
9 Hypertension Pharmacotherapy (cont d) Angiotensin II receptor blockers Angiotensin II type 1 receptor agonists Receptors found in vascular smooth muscle, myocardium, brain, kidney, liver, uterus, adrenal glands Indicated for HTN and treatment of heart failure Slightly weaker than ACEIs Side effects: Orthostatic hypotension, hyperkalemia, neutropenia, nephrotoxicity, and fetotoxicity
10 Hypertension Pharmacotherapy (cont d) Calcium channel blockers Cause coronary and peripheral vasodilation via L- channel blockade Verapamil and diltiazem Negative chronotropic and inotropic effects Long-acting formulations (target circadian rhythm) High incidence of constipation Side effects
11 Hypertension Pharmacotherapy β Blockers Method of action (cont d) Indications Essential HTN, angina, dysrhythmias, MI prevention, chronic heart failure Also: Migraine prophylaxis and alcohol withdrawal May induce bronchospasm and render β-agonist ineffective
12 Hypertension Pharmacotherapy Diuretics (cont d) Five classes Thiazide and thiazide-like agents Loop diuretics K-sparing agents Used for HTN Carbonic anhydrase inhibitors (CAIs) Osmotics Interact with NSAIDs
13 Hypertension Pharmacotherapy (cont d) Potassium-sparing diuretics Weak if used alone Additive effect with thiazides Amiloride (Midamor) and triamterene (Dyrenium) Side effects
14 Hypertension Pharmacotherapy (cont d) Thiazide and thiazide-like diuretics Increase Na and Cl excretion Dose-ceiling effect 2 to 4 weeks to elicit full effect Side effects
15 Hypertension Pharmacotherapy (cont d) Loop diuretics Decrease Na reabsorption at ascending limb of loop of Henle Indicated for chronic heart failure, ascites, renal failure, pulmonary edema, hypercalcemia, hypermagnesemia, syndrome of inappropriate antidiuretic hormone Second-line treatment for management of HTN Cause frequent urination
16 Hypertension Pharmacotherapy Aldosterone antagonists (cont d) Spironolactone (Aldactone) and Eplerenone (Inspra) Spironolactone is weak, often used with other antihypertensives Adverse effects: Impotence, gynecomastia, deep voice, menstrual irregularities, hirsutism, gastrointestinal upset, rash, drowsiness Eplerenone Indicated for HTN and post-mi heart failure Minimal adverse sexual side effects Higher risk of hyperkalemia
17 Hypertension Pharmacotherapy (cont d) Centrally acting adrenergic agents Affect CO and peripheral resistance Negative inotrope/negative chronotrope α 2 Agonists are effective, but riddled with side effects Clonidine transdermal is most effective and least toxic
18 Hypertension Pharmacotherapy (cont d) α 1 -Adrenergic antagonists Cause arterial and venous dilation Decrease preload and afterload First-dose phenomenon Initial doses low and at bedtime Indicated for HTN, benign prostatic hyperplasia, heart failure, and Raynaud s vasospasm
19 Hypertension Pharmacotherapy Antiadrenergic agents Second-line drugs (cont d) Reserpine Depletes postganglionic norepinephrine May cause: Sedation, depression, psychosis, peptic ulcers, nasal stuffiness Guanethidine (Ismelin) and Guanadrel (Hylorel) Substitute neurotransmitters May cause orthostatic hypotension, sexual dysfunction, explosive diarrhea
20 Hypertension Pharmacotherapy Vasodilators (cont d) Hydralazine (Apresoline) and minoxidil (Rogaine, Loniten) Second-line treatment for HTN because of side effects Act on vascular smooth muscle to decrease total peripheral resistance May cause reflex tachycardia, renin release, increased CO Often given with β blocker and loop diuretic
21 Epidemiology, Etiology, and Pathophysiology of Angina Chest pain Symptom of myocardial ischemia Imbalance of myocardial O 2 supply and demand May present as: Heavy weight or pressure on chest Burning sensation Shortness of breath (SOB) Pain over sternum, left shoulder, or lower jaw
22 Pharmacotherapy for Angina Nitrates Nitroglycerin dilates coronary arteries and collaterals (mostly venous effect) Indications: Angina, acute MI, HTN Formulations: Oral, IV, ointment, transdermal, translingual, sublingual Sublingual: Q 5 minutes x 3, then seek care Adverse effects: Tachycardia, palpitations, hypotension, dizziness, flushing, headache
23 Pharmacotherapy for Angina (cont d) Ranolazine (Ranexa) Indicated for chronic angina not responding to other medications Shifts energy production from fatty acid oxidation to glucose oxidation (uses less O 2 ) 500 mg BID (maximum, 1 g BID) Contraindicated in hepatic dysfunction
24 Antithrombotic Agents Formation and elimination of acute coronary thrombus Formation initiated by injury to endothelium Platelets adhere to site of injury, release chemicals that cause further aggregation, forming unstable thrombus Eventually forms insoluble fibrin clot Must be removed by fibrinolytic system for homeostasis to be maintained
25 Antithrombotic Agents (cont d) Anticoagulant agents Heparins: Unfractionated heparin and low molecular weight heparin Indicated for venous thromboembolism, pulmonary embolism, atrial fibrillation (AF), disseminated intravascular coagulation (DIC), and peripheral arterial embolism Extracted from porcine intestinal mucosa
26 Antithrombotic Agents (cont d) Anticoagulant agents (cont d) Heparins: Unfractionated heparin and low molecular weight heparin (cont d) Goal: Balance unwanted clotting with risk of hemorrhage Side effects: Bleeding, thrombocytopenia, hyperkalemia, osteoporosis, increased liver enzyme tests (LETs) Antidote: Protamine sulfate
27 Antithrombotic Agents (cont d) Anticoagulant agents (cont d) Direct thrombin inhibitors Desirudin (Iprivask): Indicated for deep vein thrombosis (DVT) Bivalirudin (Angiomax): Indicated for unstable angina Argatroban and lepirudin (Refludan): Used for anticoagulation of patients with heparin-induced thrombocytopenia type 2 (HIT-2) Common adverse side effect: Hemorrhage
28 Antithrombotic Agents (cont d) Anticoagulant agents (cont d) Warfarin (Coumadin) Oral anticoagulant for venous thrombosis, pulmonary embolism (PE), AF, valve replacement, coronary occlusion Daily dosing (delayed onset of 3-5 days) International normalized ratio (INR) is standard for monitoring therapy Hemorrhage is common side effect Many drugs may increase/decrease effects
29 Antithrombotic Agents (cont d) Antiplatelet agents Aspirin Reduces platelet aggregation by inhibition of prostaglandin production Antithrombotic indications: Reduce risk of thrombosis, transient ischemic attack (TIA), or stroke
30 Antithrombotic Agents (cont d) Antiplatelet agents (cont d) Aspirin (cont d) Side effects: Peptic ulcer, renal dysfunction, HTN, tinnitus, pulmonary dysfunction, and bleeding Ibuprofen inhibits pharmacological effect; concurrent NSAID use may cause fatal gastropathy
31 Antithrombotic Agents (cont d) Antiplatelet agents (cont d) Dipyridamole Vasodilator and platelet adhesion inhibitor Indicated as an adjunct to warfarin in prevention of postoperative thromboembolic complications of cardiac valve replacement May potentiate effect of adenosine
32 Antithrombotic Agents (cont d) Antiplatelet agents (cont d) Clopidogrel (Plavix) Platelet aggregation inhibitor Indications: History of MI, stroke, PAD, acute coronary syndrome Slightly more effective than aspirin (except for stroke prophylaxis) Metabolized by liver Steady state in 3 to 7 days 75 mg QD (plus aspirin) 300-mg loading dose for acute coronary syndrome (ACS)
33 Antithrombotic Agents (cont d) Antiplatelet agents (cont d) Ticlopidine Platelet aggregation inhibitor Indicated for stroke More effective than aspirin Steady state in 14 to 21 days Metabolized by liver Risk of life-threatening blood dyscrasias Use only if aspirin/clopidogrel are unacceptable
34 Antithrombotic Agents (cont d) Antiplatelet agents (cont d) Cilostazol and pentoxifylline Cause vasodilation and inhibition of platelet aggregation Indicated for PAD pain Clinical benefits may take up to 12 weeks Transient adverse effects: Headache, diarrhea, dizziness, palpitations 100 mg BID on an empty stomach
35 Antithrombotic Agents (cont d) Antiplatelet agents (cont d) Glycoprotein IIb/IIIa inhibitors Indicated for ACS Abciximab (ReoPro) is drug of choice Not available in oral formulation (ineffective) Bleeding is most common adverse side effect
36 Antithrombotic Agents (cont d) Thrombolytic agents Indicated for PE, ischemic stroke, and acute ST segment elevation MI Agents: Streptokinase (second line), alteplase, reteplase, and tenecteplase Therapy should begin within 12 hours of symptoms
37 Antithrombotic Agents (cont d) Thrombolytic agents (cont d) Contraindications: Internal bleeding, aortic dissection, head injury or stroke in last 3 months, HTN, anticoagulant use Bleeding is most common adverse effect Gastrointestinal, genitourinary, respiratory tract, retroperitoneal, intracranial
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