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1 Cardiovascular Agents Unit 7 2 Hypertension Risk Factors • Advancing age • Weight gain – esp. around the hips and thighs • Race – Most in blacks – Least in Mexican Americans • Males more than females • Heredity • Tobacco use • High-fat diets 3 Primary Factors Responsible for Blood Pressure • Cardiac output – volume of blood pumped per min. • Peripheral resistance – resistance in arteries increases due to constriction • Blood volume – increase in amount of blood 4 Classification of HTN in Adults • • • • 5 Non Pharmacological Methods for treating HTN • • • • • • 6 Normal - SBP < 120 and DBP < 80 Prehypertension - SBP 120–139 or DBP 80–89 Stage I hypertension - SBP 140–159 or DBP 90–99 Stage II hypertension - SBP > 160 or DBP >100 Weight reduction Stop tobacco use Limit salt intake Limit alcohol consumption Exercise Reduce stress HTN Therapy • Selection of antihypertensive drug depends on severity of disease • Trial period on med of about 2-4 weeks then recheck to evaluate • If hypertension not improved, may change drug, increase dose or implement stepped care. 7 “Stepped Care” Principles - Pertaining to Antihypertension Drugs • Use two drugs from different classes to control hypertension 1 • • • • Allows lower doses of each drug Lower doses produce fewer side effects Better patient compliance Combination drugs - patient can take one pill instead of 2 8 Renin-Angiotensin Pathway Modifiers Block the Renin-Angiotensin Pathway and Decrease Blood Pressure 9 ACE Inhibitors • ACE inhibitors “prils”- block angiotensin-converting enzyme (ACE) that blocks formation of angiotensin II resulting in vasodilation and decrease reabsorption of sodium by kidneys resulting in more urine excreted resulting in decreased blood volume which decrease BP • Primary uses – hypertension • Important side effects – persistent dry non productive cough, hypotension, Increased K+ 10 Nursing considerations 11 Angiotensin receptor blockers • Angiotensin receptor blockers “sartans” - block angiotensin receptors in arteriolar smooth muscle and adrenal glands- leading to arteriolar dilation and increase renal sodium excretion which decreases BP • Primary uses – hypertension • Side effects: - headache, hypotension 12 Nursing considerations • Monitor BP, I/O, daily wt. • Monitor serum K+ levels, renal function • Examples : Diovan (valsartan) 13 Beta Blockers • Beta Blockers- “olols” • Mechanism of action - bind to block b1 and b2 receptors, decreasing heart contractility, decrease SA node firing (heart rate) • Therapeutic effects: decrease HR, decrease angina, decrease angiotensin II formation. • Primary uses: hypertension, angina, cardiac arrhythmias , migraine headaches • Side effects: bradycardia, heart failure, bronchospasm, fatigue, depression, impotence 14 Nursing considerations • • • • Monitor BP, HR, I/O, daily wt Focused assessment : cardiac, pulmonary Contraindicated in some dysrhythmias, heart failure, some lung diseases Examples: inderal (propranolol), Lopressor (metoprolol), Tenormin (atenolol) 2 15 Calcium Channel Blockers • Mechanism of action - block calcium channels in plasma membrane which causes vasodilation of arteriole which decreases BP • Primary use - angina, hypertension • Important side effects – bradycardia, peripheral edema, headache, dizziness 16 Nursing considerations • Monitor BP, heart rate, I/O, daily weight and side effects • Focused assessment – cardiac and pulmonary • Examples – Calan (verapamil) – Cardiazem (diltazem) – Norvasc (amlodipine) 17 Diuretics • Mechanism of action - increase the amount of urine produced by the kidneys which increases excretion of water and electrolytes (Na, Ca, CL, K) which decreases blood volume which decreases BP • Primary use - mild to moderate hypertension • Important side effects - electrolyte imbalances (especially loss of K) • Example - hydrochlorothiazide (HydroDIURIL), furosemide (Lasix) 18 Types of Diuretics • Loop- Inhibit sodium and chloride reabsorption (Lasix) – Monitor K+ levels • Thiazide and Thiazide-like – inhibit sodium reabsorption (Hydrochlorothhiazide) – Monitor K+ levels • Potassium sparing – Inhibits sodium- potassium exchange in distal tubles (aldactone) 19 Nursing Considerations for Diuretics • • • • 20 Monitor I/O closely Monitor BP prior to dosing Monitor Electrolytes (especially K+) Monitor Kidney function Direct-Acting Vasodilators • Mechanism of action - direct relaxation of arteriolar smooth muscle leading to vasodilation which decreases BP • Primary use - severe hypertension, hypertensive crisis • Important side effects - reflex tachycardia, sodium and fluid retention, diziness • Examples: Apresoline (hydralazine) 3 • Nursing considerations: Monitor HR, BP 21 Angina Pectoris • Reduced blood flow to the heart muscle is called myocardial ischemia • Decreased blood flow in the coronary arteries results in decreased oxygen to the heart muscle • Lack of oxygen to the myocardium causes chest pain or angina pectoris 22 Classic Presentation of Angina Pectoris • • • • 23 Sharp pain in the heart region Moving to left side of neck and lower jaw and down left arm Preceded by physical exertion or emotional excitement Angina pain may closely mimic myocardial infarction (MI) Stable Angina • Subsides with rest • Predictable in frequency and duration 24 Unstable Angina • • • • 25 Lifestyle Changes • • • • • • • • 26 Can occur with rest Occurs more frequently or severely Signifies an increased risk of myocardial infarction (MI) Requires aggressive medical treatment Tobacco cessation Limit sodium intake and eat foods rich in potassium and magnesium Limit alcohol consumption Implement an exercise plan Reduce stress levels Reduce dietary saturated fats Keep weight at optimal level Treat hyperlipidemia and/or hypertension if present Surgical Procedures • Coronary artery bypass graft (CABG) • Percutaneous transluminal coronary angioplasty (PTCA) 27 Antianginal Drugs • • • • • • Reduce Myocardial Demand for Oxygen Slowing heart rate Reducing blood flow into the heart (reduce preload) by dilating veins Reducing contractility Lowering blood pressure (reducing afterload) Antianginal drugs only relieve symptoms, they do not cure the underlying disorder 4 28 Classes of Antianginal Drugs • Organic nitrates • Beta-adrenergic blockers • Calcium channel blockers 29 Organic Nitrates - Vasodilation • Relieve anginal pain by dilating both venous and arterial smooth muscle 30 Organic Nitrates - Decrease Workload of the Heart • Dilatation of the veins reduces preload - less blood in the heart • Less blood in the heart decreases afterload - decreased cardiac output 31 Organic Nitrates - Dilation of Coronary Arteries • Primary mechanism is to treat variant angina • Spasm of a coronary artery • Nitrates relax spasms 32 Two Types of Organic Nitrate • Short-acting is taken sublingually - nitroglycerin • Long-acting is taken orally or transdermally - isosorbide dinitrate – Tolerance often develops – Reduce symptoms of heart failure 33 Adverse Effects of Nitrates • • • • • 34 Reduction in blood pressure with possible dizziness Tachycardia and palpitations Headache Flushing of the skin Can cause life-threatening hypotension and cardiovascular collapse when used within 24 hours of taking Viagra Drug Profile - Organic Nitrate, Vasodilator • Nitroglycerin (Nitrostat, Nitrobid, Nitro-Dur), short-acting nitrate • Actions- vasodilation • Adverse effects-headache, hypotension 35 Beta-Adrenergic Blockers to Relieve Angina • Decrease oxygen demands on the heart – Slow heart rate and decrease contractility • Used for angina prophylaxis • Interactions: – Cardiac suppression when used with ca+channel blockers – Heart block when used with digitalis • Example : tenormin (atenolol) 36 Calcium Channel Blockers (CCBs) To Relieve Angina 5 • • • • 37 Left-Sided Heart Failure • • • • • 38 Relax arterial smooth muscle - lowers peripheral resistance and reduces blood pressure Decreases myocardial oxygen demand Useful in treating variant angina Example: cardizem (diltazem) Decrease Cardiac Output Skin cyanotic and clammy, which leads to decreased oxygen supply Anxiety/restlessness leads to decreased oxygen to the brain Upright posture/leaning forward/persistent cough leads to blood backing into the lungs Rapid breathing leads to decreased oxygen to the body Right-Sided Heart Failure • Decrease Blood to Lungs • Edema of lower limbs leads to blood backing up in venous circulation • Fast heart rate leads to the body not getting enough oxygen 39 Nonpharmacological Methods for Controlling Heart Failure • • • • • • • 40 Stop using tobacco Limit salt (sodium) intake and eat foods rich in potassium and magnesium Limit alcohol consumption Implement a medically supervised exercise plan Learn and use effective ways to deal with stress Reduce weight to an optimum level Limit caffeine consumption First-Choice Drugs for CHF • ACE Inhibitors and Diuretics • Given first • Reduce most symptoms of mild to moderate heart failure – Diuretics reduce volume – ACE inhibitors –unload (decrease afterload) • Fewer side effects 41 Second-Choice Drugs to Treat CHF • Phosphodiesterase inhibitors, vasodilators, and beta-adrenergic blockers • Used in severe heart failure • First-choice drugs not effective 42 Three Basic Steps to Hemostasis • Injured vessel constricts to slow blood flow • Platelets adhere to injured area and aggregate, plugging damaged vessel • Coagulation cascade occurs thus forming insoluble fibrin strands which slows blood flow more 43 Coagulation Cascade • Series of Complex Steps – Injured cells release prothrombin activator 6 – Prothrombin activator changes prothrombin to thrombin – Thrombin changes fibrinogen to fibrin – Fibrin forms an insoluble web over injured area which stops blood flow 44 Coagulation-Modifier Drugs • Anticoagulants • Thrombolytics • Hemostatics 45 Anticoagulants • • • • 46 Prevent the Formation of Clots and Enlargement of Clots Inhibiting specific clotting factors in the coagulation cascade Diminishing the clotting action of platelets Both ways increase the time to form clots Anticoagulants • Mechanism of action - inhibit specific clotting factors which interfere with coagulation cascade in order to prevent formation or enlargement of clot • Primary use - thromboembolic disease; prevent formation of clots in veins • Adverse effects - abnormal bleeding • Examples - heparin (Heplock), warfarin (Coumadin) 47 Antiplatelet Agents • Prolong Bleeding Time by Interfering with Platelet Aggregation • Mechanism of actions – Aspirin: inhibits thromboxane2, which prevents aggregation of platelets – ADP receptor blockers: interfere with platelet plasma membrane, which prevents platelet aggregation – Glycoprotein IIb/IIIa inhibitors: glycoprotein IIb/IIIa enzyme inhibited which prevents platelet aggregation • Example – Asprin (acetylsalicylic acid), dipyridamole (persantine) 48 Antiplatelet Agents • Primary uses - prevent clot formation in arteries • Adverse effects - abnormal bleeding; reduce number of neutrophils 49 Thrombolytics • Used to Dissolve Existing Clots • Given IV • Adverse effects - abnormal bleeding; contraindicated in patients with active bleeding or recent trauma • Example - alteplase (Activase) 50 Cardiac Glycosides • Positive inotropes • Increase the Force of Myocardial Contraction • Mechanism of action - 1) positive inotropic effect: more blood ejected per beat leads to increased cardiac output in order to meet, the metabolic demands of tissues; 2) slow 7 electrical conduction through the heart, which creates fewer beats per minute and decreases heart rate • Example - digoxin (Lanoxin) 51 Cardiac Glycosides (cont’d) • Primary use - heart failure • Administration: – Loading • Generally 1mg over 24 hrs in divided doses orally or IV – Maintenance • 0.125mg- 0.25mg orally daily • Monitor serum digoxin levels, K+ level • Important adverse effects –bradycardia, loss of appetite, vomiting, diarrhea, headache, drowsiness, confusion, visual disturbances (yellow halos) 52 Nursing considerations • Monitor HR – When would you hold a dose? • Monitor renal function – Cannot be dialyzed out • Client ed: teach signs of dig. Toxicity 53 Beta-Adrenergic Blockers • Used in Combination with Other Drugs to Slow Progression of Heart Failure and to Prolong Patient Survival • Mechanism of action - blocks beta1, beta2, and alpha1 receptors, which decreases heart rate and blood pressure, decreases afterload, and reduces the workload on the heart • Primary use - slow progression of heart failure and increased exercise tolerance when combined with other heart failure drugs • Important adverse effects - can worsen heart failure • Example - carvedilol (Coreg) 54 Natriuretic Peptides • First New Drugs to Treat Heart Failure in More than 10 Years • Mechanism of action - acts on kidney, which increases excretion of sodium and water, thereby lowering blood pressure; also causes vasodilation, which reduces preload • Primary use - severe heart failure • Important adverse effects - severe hypotension • Example - nesiritide (Natrecor) 55 Dysrhythmias • • • • 56 Heart chambers are not contracting in a synchronized manner Can Seriously Affect Cardiac Output Both atria contract simultaneously Followed by contraction of both ventricles Dysrhythmias Based on Location and Conduction Abnormality 8 • Atrial dysrhythmias – Premature atrial contractions lead to ectopic foci in atria, producing impulse – Atrial tachycardia - atria contracting at greater than 150 bpm – Atrial flutter and/or fibrillation - very rapid, uncoordinated contractions of atria • Sinus bradycardia - SA node producing impulses at less than 50 bpm 57 Dysrhythmias Based on Location and Conduction Abnormality (con’t) • Ventricular dysrhythmias – Premature ventricular contractions (PVC) - ectopic foci in ventricles producing impulses – Ventricular tachycardia - ventricles contract at greater than 150 bpm – Ventricular flutter and/or fibrillation - very rapid, uncoordinated contractions of ventricles • Heart block - area where impulse is prevented either partially or completely from passing through 58 Ion Channels in the Plasma Membrane of Myocardial Cells Open and Close • Sodium ion channels open, allowing sodium ions to rush into cell and produce depolarization • Calcium ion channels open, allowing calcium ions to enter the cell which are responsible for cardiac muscle contraction • Potassium ion channels open, allowing potassium ions to leave the cell, after which the cell is polarized • Cells in the SA and AV nodes result in calcium ions that produce the depolarization 59 Pharmacotherapy of Dysrhythmias • Block potassium, sodium, or calcium ion channels • Prolong the refractory period 60 Nonpharmacological Treatment of Dysrhythmias • Cardioversion (defibrillation) - for more serious types of dysrhythmias – Electrical shock momentarily stops all electrical impulses in the heart – Allows SA node to return conduction to normal sinus rhythm • Catheter ablation - identification and destruction of myocardial cells responsible for the abnormal conduction 61 Nonpharmacological Treatment of Dysrhythmias (con’t) • Insertion of cardiac pacemaker - for dysrhythmias that cause the heart to beat too slowly • Implantable cardioverter defibrillator (ICD) – Paces the heart to normal sinus rhythm or – Gives an electrical shock when dysrhythmia occurs – Stores information regarding heart rhythm 62 Basic Mechanisms of Antidysrhythmics • Block ion channel – Sodium ion channels – Potassium ion channels – Calcium ion channels 9 • Block beta-adrenergic receptors in the heart 63 Sodium Channel Blockers (Class I) • Mechanisms of action - blocks Na+ channels, slowing rate of impulse conduction through heart • Primary use - many types of dysrhythmias; some more specific - only for life-threatening ventricular dysrhythmias • Important adverse effects - creates new dysrhythmias or worsens existing ones, hypotension, dizziness, fainting • Example –Xylocaine (lidocaine), Quinidex (quinidine) 64 Beta-Adrenergic Blockers (Class II) • Mechanisms of action - block beta receptors in the heart, which slows the heart rate and decreases conduction velocity through the AV node • Primary use - atrial dysrhythmias associated with heart failure • Important adverse effects - bradycardia, hypotension with dizziness and fainting, bronchospasms if they block beta2 receptors • Example - propranolol (Inderal) 65 Potassium Channel Blockers (Class III) • Mechanism of action - block potassium ion channels in myocardial cells, prolonging the refractory period of the Heart • Primary use - resistant ventricular tachycardia, atrial dysrhythmias with heart failure • Important adverse effects - can worsen dysrhythmias, bradycardia, hypotension • Example –Cordarone (amiodarone) 66 Calcium Channel Blockers (Class IV) • Mechanisms of action - block calcium channels in myocardial cells, which leads to reduced automaticity in SA node and slows impulse conduction through the AV node, which prolongs the refractory period • Primary use - supraventricular tachycardia • Important adverse effects - bradycardia, hypotension • Monitor BP and HR prior to administering • Example – Calan (verapamil), Cardizem (diltiazem) 10