2014 cardio


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  • Craven, R. F. and C. J. Hirnle (2003). Fundamentals of nursing: Human health and function . Philadelphia, Lippincott Williams & Wilkins. High blood pressure is the most common manifestation of altered blood flow, affecting 25% of the adult population. It is the most common risk factor for cardiovascular disease in developed and developing countries (AHA, 2001a). Researchers have postulated that primary high BP results from an increased level of circulating vasoactive substances or increased sympathetic nervous system activity (Craven & Hirnle, 2003). William Phipps, Judith Sands, Jane Marek, Medical-Surgical Nursing: Concepts & Clinical Practice. 1999. St. Louis: Mosby, Inc. p. 747. Causes of secondary hypertension: Renal: Renal parenchymal disease (glomerulonephritis, renal failure) causes a renin or sodium-dependent hypertension Adrenal gland: Cushings syndrome causes increase in blood volume. Primary aldosteronism : increase in aldosterone, causing sodium and water retention that increases blood volume Pheochromocytoma: excess secretion of catecholamines (NE increases PVR). Coarctation of Aorta : causes marked elevated BP in upper extremities with decreased perfusion in lower extremities Head Trauma or Cranial tumor: increased ICP reduces cerebral blood flow, resultant ischemia stimulates medullary vasomotor center to raise BP. Pregnancy-induced hypertension : cause unknown. Generalized vasospasm may be a contributing factor. Degrees of hypertension: 1-4 range Stage 1: 140-159 Stage 2: 160-179 Stage 3: 180-209 Stage 4: greater than 210 Systolic or diastolic. Diastolic above 120-130 mm Hg is considered to be a hypertensive crisis that requires emergency medical treatment 64% of the US population aged 65-74 have primary hypertension. Danger is that it may have no overt symptoms so ‘silent killer.’ Incidence increases steadily with age.
  • Phillips, Sands & Sarek, 1999. p. 748 Blood flow: determined by the volume of blood ejected from the left ventricle with each contraction. PVR: size of peripheral blood vessels. More constricted the vessel, greater the resistance to flow. More dilated, less resistance. Dilation and constriction is controlled primarily by sympathetic nervous system and the renin-angiotension system . Sympathetic system : Catecholamines such as epinephrine and NE are released. These cause vasoconstriction. Renin-angiotension system : Angiotension causes vasoconstriction of blood vessels. Groups of drugs used to reduce BP DIURETICS : Thiazide Diuretics : Bendroflumethiazide, Benzthiazide, Chlorthiazide, Hydrochlorothiazide, hydroflumethiazide, etc. These act by blocking sodium reabsorption in cortical portion of ascending tubule, water excreted with sodium, producing decreased blood volume. Thiazides are ineffective in renal failure. Also, must monitor electrolytes (K+ especially) as they dump potassium. Need supplements. Loop Diuretics : Bumetanide, Ethacrynic acid (Edecrin), Frusemide (Lasix) Action: block sodium and water reabsorption in medullary portion of ascending tubule; cause rapid volume depletion. Potassium loss can be severe. Monitor daily weight to assess response to treatment. Monitor labs for increases in uric acid, glucose, BUN. Potassium-sparing diuretics : Amiloride (Midamor), Spironolactone (Aldactone), Triameterene (dyrenium) Action: inhibit aldosterone; sodium excreted in exchange for potassium Monitor labs for potassium excess. Weigh daily. Teach client to expect an increased volume of urine, avoid potassium-rich foods, report incidence of drowsiness or GI side effects. ADRENERGIC INHIBITORS : Beta-Adrenergic blockers : Acebutolol (Sectral), Atenolol (Tenormin), Betaxolol (Kerlone), Carteolol (Cartrol) Action : block beta-adrenergic receptors of sympathetic nervous system, decreaseing heart rate and blood pressure. Note: B-blockers should not be used in patients with asthma, COPD, CHF, and heart block; use with caution in diabetes and PVD. Nursing implications: establish baseline vitals and labs. Check BP and pulse before administration. Teach clients to change position slowly, take drug as prescribed, report decline in sexual responsiveness, report fatigue, drowsiness, or SOB. Centrally action Alpha-blockers : Clonidine (Catapres), Guanabenz (Wytensin), Guanfacine (Tenex), Methyldopa (Aldomet). Action : activate central receptors that supress vasomotor and cardiac centers, causing a decrease in peripheral resistance . Note: rebound hypertension may occur with abrupt discontinuation of drug (except with Aldomet). Nursing Implications : Check vitals before administer. Teach clients to change position slowly, avoid hot baths, steam rooms, saunas, use gum or hard candies to counteract dry mouth, be cautious driving machinery if drowsy, report decline in sexual response. Peripherally acting adrenergic antagonists : Guanadrel (Hylorel), Guanethidine (Ismelin), Rauwolfia Serpentina (Raudixin). Action : deplete catecholamines in peripheral sympathetic postganglionic Fibers. Block NE release from adrenergic nerve endings. Alpha-adrenergic blockers: Doxazosin mesylate (Cardura), Prazosin (Minipress), Terazosin (Vasocard, Hytrin). Action: block synaptic receptors that regulate vasomotor tone; reduce peripheral resistance by dilating arterioles and venules. Nursing implications: monitor closely at first dose for syncope occurring 30-90 minutes after first administration. Give first dose at bedtime, monitor BP and pulse, Syncope may be preceded by tachycardia. VASODILATORS: Hydralazine (Apresoline), Minoxidil (Loniten) Dilate peripheral blood vessels by directly relaxing vascular smooth muscle. Usually used in combination with other antihypertensives as they increase sodium and fluid retention and can cause reflex cardiac stimulation. Nursing implications: teach to change position slowly, avoid hot baths, take drug with meals, be prepared for nasal congestion and excess lacrimation, report incidence of constipation or peripheral edema. ACE INHIBITORS : Captopril (Capoten), Enalapril (Vasotec), HCTZ (Veseretic). Action: Inhibit conversion of angiotensin to angiotensin II, thus blocking the release of aldosterone, thereby reducing sodium and water retention. Nursing Implications : monitor for first-dose syncope in patients with CHF, change position slowly, report incidence of fatigue, skin rash, impaired taste, chronic cough. CALCIUM ANTAGONISTS : Diltiazen (Cardizem), Felodipine (Plendil), Nifedipine (Procardia), Verapamil (Calan) Action : inhibit influx of calcium into muscle cells; act on vascular smooth muscles (primary arteries) to reduce spasms and promote vasodilation. Nursing implications : check vitals before giving. Bradycardia is common. Monitor renal and liver functon tests. Take drugs before meals, change positions slowly.
  • suppress fast rhythms of the heart (cardiac arrhythmias), such as atrial fibrillation, atrial flutter, ventricular tachycardia, and ventricular fibrillation. It is important to stress that these medications do NOT cure the underlying cause of an arrhythmia Normal: depending on your age and physical conditioning 60-80 bpm Tachcarydia: 150-250 bpm Bradycardia: < 60 bpm Irregular heart beat due to extra beats or fibrillation
  • Antiarrhythmic drugs are grouped into 4 classes using the Vaughan Williams classification , introduced in 1970 Drugs are classfied based on its primary mechanism of its antiarrhythmic effect. However, one of the limitations of the VW classifcations, is that many antiarrhtmic agenst have MULTIPLE MOAs Arrythmias, hypertension, heart failure or myocardial infarctions
  • .
  • 2014 cardio

    1. 1. Cardiovascular Drugs Nelia B. Perez RN, MAEd, MSN PCU – MJCN Class 2014 - Pharmacology
    2. 2. Learning Objectives• Students will be able to: – Discuss the major categories of drugs as they relate to the treatment of Cardiac Disease. – Describe the major effects of various medications on cardiac function. – Discuss major nursing implications when administering above medications.
    3. 3. iv e n s r te pe y t ihAn
    4. 4. Hypertension• Defined as a consistent elevation of the systolic or diastolic blood pressure above 140/90mm Hg• On two elevated readings (sitting and supine) on separate office visits• Two types hypertension – Primary: no known cause – Secondary: consequence of underlying disease or condition
    5. 5. CLASSIFICATION OF HYPERTENSIONHypertension is classified as follows: • Prehypertension: BP 120 to 139 / 80 to 89 mm Hg • Hypertension, Stage 1: BP 140 to 159 / 90 to 99 mm Hg • Hypertension, Stage 2: systolic BP greater than or equal to 160 or diastolic BP greater than or equal to 100 mm Hg.
    6. 6. Goal with hypertension:• Two primary regulatory factors: – Blood flow (volume) – Peripheral Vascular Resistance (PVR)• Goal is to optimise these two in order to get pressure below 140/90 mm Hg
    7. 7. o
    8. 8. Pharmacotherapy•Primary: •Alternate:•Diuretics •Alpha1-blockers•ACE Inhibitors •Alpha2-blockers•ARBs •Direct-acting vasodilators•Beta-blockers •Peripheral adrenergic•Calcium channel antagonistblockers
    9. 9. DiureticsTherapeutic Effects (overall)• General site of action is the nephron structure in the kidney (exact area depends on drug)• Increases urine formation and output resulting in a net loss of H2O from the body and decreased BP
    10. 10. Loop DiureticsMechanism of action:• Inhibits Na+ and Cl- resorption in the loop of Henle and so H2O (water follows sodium)• Dilates blood vessels
    11. 11. Loop DiureticsTherapeutic effects:• Potent diuresis resulting in substantial fluid loss• Treats edema associated with CHF and hepatic or renal diseaseAdverse effects:• hypokalemia• metabolic alkalosis• dehydration (hypovolemia), leading to hypotension• dose-related hearing loss (ototoxicity)
    12. 12. Loop DiureticsSpecific Drugs• furosemide• Torsemide• bumetanideNursing actions:• Monitor I/O and BP• Monitor effects of Lanoxin (digoxin)• Baseline and close monitoring of K+• Assess for: • Dehydration • Hypotension • Hearing loss
    13. 13. ThiazideMechanism of action: – inhibit the sodium-chloride transporter in the distal tubule. Because this transporter normally only reabsorbs about 5% of filtered sodium, these diuretics are less efficacious than loop diuretics in producing diuresis and natriuresis.
    14. 14. ThiazideTherapeutic effects: – Excretion of Na+, Cl-, K+ and H2O without altering pH – Treatment of edema Side effects – Hypokalemia – Headache, dizziness
    15. 15. ThiazideSpecific Drug• Hydrodiuril (hydrochlorthiazide)• Zaroxolyn (Metolazone)
    16. 16. NCs: ThiazideNursing actions: • Monitor I/O, BP and K+ • Monitor effects of Lanoxin (digoxin) • Monitor electroytes • Adequate dietary K+ • Monitor uric acid • Crosses placenta and into breastmilk
    17. 17. Potassium Sparing DiureticsMechanism of action:• antagonize the actions of aldosterone (aldosterone receptor antagonists) at the distal segment of the distal tubule. This causes more sodium (and water) to pass into the collecting duct and be excreted in the urine.Therapeutics effects:• Diuresis• Decreased K+ excretion
    18. 18. Potassium Sparing Diuretics contAdverse effects:• Electrolyte imbalance with potential elevation in K+• Headache, dizzinessPrototype:• Aldactone (spironolactone)
    19. 19. NCs: Potassium Sparing DiureticsNursing actions: – Monitor I/O, BP and K+ – Monitor effects of Lanoxin (digoxin) – No salt substitutes or K+ rich foods – Contraindicated: • Pregnancy, lactation• Initial and follow-up uric acid levels• Monitor CBC• Watch for s/s of infection• Spironalactone • Gynecomastia • Testicular atrophy • Hirsutism
    20. 20. Calcium Channel BlockersMechanism of action:• Inhibits transport of calcium into myocardial and smooth muscle cells• Dilates peripheral arterioles, decreasing afterload• Decreases heart contractility (negative ionotrope)• Decreases SA node firing rate and conductivity of AV node (negative chronotrope)
    21. 21. Calcium Channel Blockers cont.Therapeutic Effects:• Lowers HR and BP- Depending on drug in class• Decreases myocardial O2 demand• Decreases coronary artery spasm• Decreases angina and rhythm disturbances
    22. 22. Calcium Channel Blockers cont.Side effects:• Bradycardia, reflex tachycardia• Peripheral edemaInteractions:• Other antihypertensives and diuretics (increased hypotensive effects)
    23. 23. Calcium Channel Blockers cont.Prototypes:• Calan (verapamil), Cardiazem (diltiazem) and Norvasc (amlodipine)Nursing considerations:• Monitor BP, HR, I/O, daily weight, side effects• Focus assessment-cardiac and pulmonary
    24. 24. NCs: Calcium Channel Blockers• Baseline ECG, HR, BP• Frequent assessment of VS• Contraindicated: • complete heart block• Pregnancy Category C• No grapefruit juice• May worsen Heart Failure• Evaluate any c/o chest pain
    25. 25. e
    26. 26. RENIN-ANGIOTENSIN-ALDOSTERONE SYSTEM (RAAS) Juxtaglomerular RENIN Angiotensinogen↓Serum Sodium↓Blood volume cells-kidney in plasma Angiotensin I Angiotensin- converting Via vasoconstriction of arterial smooth muscle enzyme ↑Sodium Angiotensin II resorption Kidney (H2O ALDOSTERONE tubules Adrenalresorbed with sodium); ↑ CortexBlood volume Intestine, sweat glands, Salivary glands
    27. 27. Angiotensin Converting Enzyme Inhibitors (ACE-I)- “prils”• Mechanism: Blocks interaction between Angiotensin I and Renin, preventing production of Angiotensin II• Angiotensin II not produce resulting in decreased vasoconstriction and decreased afterload• Decreased aldosterone production results in decreased Na and H2O reabsorption so decreased BP
    28. 28. Angiotensin Converting Enzyme Inhibitors (ACE-I)- “prils” cont.• Adverse Effects – Most common: dry, nonproductive cough – Dizziness, increased potassium levels• Interactions: Other antihypertensives and diuretics (increased hypotensive effects)• Prototypes:• Vasotec (enalapril) and Zestril (lisinopril)
    29. 29. te
    30. 30. NCs: ACE Inhibitors• Baseline VS• Captopril- oral dose 1 hour pc• First dose phenomenon• IV: monitor BP carefully• Monitor for Angioedema• Monitor K+, CBC• Assess for S/S infection• Pregnancy Category D• Assess for minor side effects
    31. 31. Angiotensin II Receptor Blockers (ARB’s)- “sartans”• Mechanism of action: Blocks binding of Angiotensin II to its receptor sites• Therapeutic effects – Decreased BP: Decreased vasoconstriction, decreased vascular resistance, decreased afterload – Major use is afterload reduction in CHF and MI – Frequently a second line treatment for patients who do not tolerate ACE-I
    32. 32. Angiotensin II Receptor Blockers (ARB’s)- “sartans” cont.• Adverse effects – Most common is headache• Interactions: Other antihypertensives and diuretics (increased hypotensive effects)• Prototype:• Cozaar (losartan) and Diovan (valsartan)
    33. 33. Angiotensin II Receptor Blockers (ARB’s)- “sartans” contNursing considerations• Monitor BP, I/O, daily weight, side effects• Monitor Potassium levels and renal function• Reinforce patient education• Contraindicated to pregnant women• Can be taken without regard to food• First Dose Phenomenon• Orthostatic BP checks• Monitor renal, hepatic, and electrolyte level
    34. 34. Beta Blockers- “ololsMechanism of action:• Cardioselective: Bind to and block B1 receptors on the hearts conduction system and throughout the myocardium• Nonselective: bind to, and block, B1 and B2 receptors (heart and lungs)• Decreases heart contractility (Negative ionotrope) reducing O2 requirements of myocardial cells• Decrease SA node firing rate (negative chronotrope)
    35. 35. Beta Blockers- “olols cont.Therapeutic Effects – Decreased heart rate and decreased myocardial oxygen demand – Decreased angina – Fewer rhythm disturbances – Decreased renin release
    36. 36. Beta Blockers- “olols cont.Adverse effects: – Dysrhythmias (bradycardia), heart failure – Bronchospasm / bronchoconstriction – Fatigue, depression, impotenceInteractions: – Other antihypertensives and diuretics (increased hypotensive effects)
    37. 37. Beta Blockers- “olols cont.Prototypes: – Inderal (propranolol), Lopressor (metoprolol) and Tenormin (atenolol)Nursing Actions: – Monitor BP, HR, I/O, daily weight, side effects – Focus assessment-cardiac and pulmonary – Contrindicated with some dysrhythmias, CHF and some lung diseases
    38. 38. NCs: Beta-adrenergic Blockers• May take two weeks for optimal therapeutic response• Check BP and pulse prior to dose• Monitor cardiac function• Assess for: • Respiratory distress • Bradycardia, heart block, fatigue, activity intolerance• DO NOT STOP SUDDENLY
    39. 39. y
    40. 40. Alpha1-adrenergic AntagonistsMechanism of action -selectively inhibits alpha-1 adrenergic receptors. Blockages of the alpha-1 adrenergic action on the vascular smooth muscles lead to a decrease in vascular resistance and antihypertensive activity.
    41. 41. NCs: Alpha1-adrenergic Blockers• First dose phenomenon• Assess BP prior to and during RX• Persistent orthostatic hypotension• Assess for: • Weakness, dizziness, headache, GI complaints• Closely monitor elderly
    42. 42. Direct Vasodilators• Relaxes smooth muscle in arterioles  < PVR• Highly effective but many side effects (some serious) • Reflex tachycardia • Sodium/water retention• Not a first choice drug• Primary use: emergency situations where immediate ↓ in BP is needed
    43. 43. NCs: Direct Vasodilators• Monitor: VS, ECG, SpO2 during RX• Assess for increased HR• BP q 5 min if not continuous monitor• Contraindicated: hypersensitivity, CAD, rheumatic mitral valve disease, CVA, renal insufficiency, SLE• Priapism- medical emergency
    44. 44. Direct Vasodilators• IV Nitroprusside (Nitropress): • Continuously monitored • Only dilute in D5W • Brown color; protect from light• Minoxidil (Loniten): • BP & pulse both arms, three positions • Assess for orthostatic hypotension• Diazoxide (Hyperstat): • For hypetensive crisis in L&D
    45. 45. ar di acC de s, ly co siG ngina ls, n t ia i csA yt hm
    46. 46. Cardiac Glycosides• AKA digitalis glycosides• Group of drugs that inhibit the sodium- potassium pump, thus increasing intracellular calcium which causes cardiac muscle fibers to contract more efficiently
    47. 47. Action Potential
    48. 48. Cardiac GlycosidesTherapeutic Effects1.Positive Inotropic action2.Negative Chronotropic action3.Negative Dromotropic effect
    49. 49. Inotropes
    50. 50. Inotropes• Agents that affect myocardial contraction• Positive Inotropes – Cardiac glycosides – Catecholamines• Negative Inotropes – BB – CCB – Class IA & IC anti-arrhythmics
    51. 51. Class ParticipationWhich of the following is an example of a positive inotrope?a) Docusateb) Digoxinc) HCTZd) Propranolole) Nitroglycerin
    52. 52. Class ParticipationWhich of the following is an example of a positive inotrope?a) Docusateb) Digoxinc) HCTZd) Propranolole) Nitroglycerin
    53. 53. Cardiac Glycosides• Prototype: Digoxin (Lanoxin®, Digitek®, Lanoxicaps®)
    54. 54. Digoxin MOA
    55. 55. Digoxin (cont’d) Nursing Responsibilities– Assess heart rate before administration; if below 60 bpm withhold the drug.– Monitor serum potassium– Assess for signs of Digitalis toxicity • Bradycardia • GI manifestations (anorexia, nausea, vomiting and diarrhea) • Dysrhythmias • Altered visual perceptions • In males: gynecomastia, decreased libido and impotence
    56. 56. Chronotropes
    57. 57. Chronotropes• Agents that change heart rate – affects the nerves controlling the heart – changes the rhythm produced by the SA node
    58. 58. Chronotropes (cont’d)• Positive Chronotropes • Negative Chronotropes – Atropine – Beta-blockers – Quinidine – Acetylcholine – Dopamine – Digoxin – Dobutamine – Diltiazem – Epinephrine – Verapamil – Isuprel – Ivabradine – Metoprolol
    59. 59. Positive ChronotropePrototype: Atropine• belladonna alkaloid• d,l-hyoscyamine• Anticholinergic• Uses – Symptomatic bradycardia – Aspiration prophylaxis – Produces mydriasis – Organophosphate toxicity – Adjunct nerve agent & insecticide poisoning
    60. 60. Atropine (cont’d)• MOA – competitive inhibitor at autonomic postganglionic cholinergic receptors• Clinical effects – “anti-SLUD” Salivation, Lacrimation, Urination, Digestion, Defecation – ↓ in salivary bronchial, & sweat gland secretions; mydriasis; changes in heart rate; contraction of the bladder detrusor muscle and of the GI smooth muscle; ↓ gastric secretion; and ↓ GI motility
    61. 61. Nursing Responsibilities• Monitor HR---note rhythm, quality, and rate• Monitor I&O• Assess for dryness or mucus membranes• Monitor GI function
    62. 62. Anti-anginal Drugs
    63. 63. Antianginal Drugs• Prototype: Nitrites & Nitrates• BB• Calcium Channel Blockers (CCBs)
    64. 64. Angina PectorisDefinition:Angina: Choking or suffocation.Pectoris: Chest. Angina pectoris, is the medical term used to describe acute chest pain or discomfort. Angina occurs when the heart’s need for oxygen increases beyond the level of oxygen available from the blood nourishing the heart.It has 3 types• Stable Angina• Un stable angina &• Variant Angina (Prinzmetal’s or resting angina) :
    65. 65. Types of Angina• Stable angina: – People with stable angina have episodes of chest discomfort that are usually predictable. That occur on exertion or under mental or emotional stress. Normally the chest discomfort is relieved with rest,  nitroglycerin (GTN) or both. – It has a stable pattern of onset, duration and intensity of symptoms.
    66. 66. • Unstable angina: – It is triggered by an un predictable degree of exertion or emotion. – (progressive), more severe than stable. Characterized by increasing frequency & severity. Provoked by less than usual effort, occurring at rest & – interferes with pt lifestyle.
    67. 67. • Variant Angina (Prinzmetal’s or resting angina) : occur spontaneously with no relationship to activity. Occurs at rest due to spasm. Pt discomfort that occurs rest usually of longer duration. Appears to by cyclic & often occurs at about the same time each day (usually at night). Thought to be caused by coronary artery spasm
    68. 68. Symptoms of Angina
    69. 69. Nitrites/Nitrates• Previously known as “coronary dilators”• Main effect: to produce general vasodilation of systemic vein & arteries – ↓preload & ↓afterload – ↓ cardiac work & oxygen consumption• 2 main uses – Angina attacks – Angina prophylaxis
    70. 70. Class ParticipationWhich is the PREFERRED route for nitroglycerin during angina attacks? a) Topical (ointment 2%) b) IV infusion c) Transdermal d) SL e) Extended release tablets/capsules
    71. 71. Class ParticipationWhich is the PREFFERED route for nitroglycerin during angina attacks? a) Topical (ointment 2%) b) IV infusion c) Transdermal d) SL e) Extended release tablets/capsules
    72. 72. Drug Common Onset Duration(Trade Name) DosageAmyl nitrate 0.3 ml 30-60 sec 10 min(Vaporole®) inhalationISDN 2.5 - 10 mg SL 2-5 min 2 - 4 hr(Isordil®) 5 - 30 mg po qidNitroglycerin(Nitro-bid®) 2% ointment 15 min 4 - 8 hr(Nitrostat®) 0.3 - 0.6 mg SL 1-3 min 10 - 45 min(Nitrogard®) 1,2,3 mg XR tab 30 min 8 - 12 hr(Transderm- 2.5 - 15 mg/day 30-60 min 24 hrNitro®) Transdermal patch
    73. 73. MOADirect relaxation of arterial and venous smooth muscle – Venodilation predominates at therapeutic doses which reduces preload – Arteriodilation at high doses (high therapeutic/toxic) which produces hypotension compensated by sympathetics (heart/vascular)to produce tachycardia
    74. 74. Nitroglycerin (NG)• Indications – Angina – Acute MI – HF – HTN – Hypertensive emergency – Hypotension induction – Peri/postoperative HTN – Pulmonary edema – Pulmonary HTN
    75. 75. NG (cont’d)• Dosing – 1 tablet (0.3 mg, 0.4 mg, or 0.6 mg strength) SL, dissolved under the tongue or in buccal pouch immediately following indication of anginal attack – During drug administration, the patient should rest, preferably in the sitting position – Symptoms typically improve within 5 minutes. If needed for immediate relief of stable angina symptoms, SL nitroglycerin may be repeated every 5 minutes as needed, up to 3 doses
    76. 76. NG (cont’d)• Adverse Effects • Contraindication: – dizziness or fainting – sildenafil (Viagra®) – flushing of the face or – tadalafil (Cialis®) neck – vardenafil (Levitra®) – headache, this is common after a dose, but usually only lasts • Lab monitoring not for a short time necessary – irregular heartbeat, palpitations – nausea, vomiting
    77. 77. AntidysrhythmicsAntiarrhythmics
    78. 78. What are Arrhythmias?• Cardiac disorder of – Rate – Rhythm – Impulse generation – Conduction of electrical impulses in the heart• Causes – May develop from a diseased heart – Consequence of chronic drug therapy• Symptoms – Mild palpitations  cardiac arrest• Treatment goal – Covert arrhythmia to a normal rhythm
    79. 79. Antidysrhythmics/Antiarrhythmics• Uses – restore normal cardiac rhythm – Successful conversion of an arrhythmia depends on the type of arrhythmia present
    80. 80. Antidysrhythmics/Antiarrhythmics• 4 major classes – Class I • Class IA • Class IB • Class IC – Class II – Class III – Class IV
    81. 81. Cardiac Action Potential 4: resting membrane potential; steady K+ flux 0: Na+ influx into cell 1: K+ efflux 2: K+ efflux & Ca+ influx 3: K+ efflux
    82. 82. Antiarrthymics: Class I• Na channel blockers• Common features – Local anesthetic activity – Interferes with movement of Na ions – Slow conduction velocity – Prolong refractory period – Decreases automaticity of the heart
    83. 83. Class IA• Quinidine (Quinidine sulfate®, Quinaglute®, Quinidex®, Cardioquin®)• Disopyramide (Norpace®)• Procainimide (Procainimide HCI®, Procan®, Procanabid®, Pronestyl®)
    84. 84. Class 1A – Quinidine• Derived from cinchona tree• Depresses both the myocardium & conduction system• Overall effect: slows heart rate• Pharmacokinetics – Well absorbed in GI tract after po administration – Metabolized to several active metabolites – Primarily excreted by urinary tract – Cardiac poison when large amounts are present in blood
    85. 85. Class 1A – Quinidine (cont’d)• Adverse Effects – N/V, diarrhea, weakness, fatigue, cinchonism• Drug Interactions – Hyperkalemia – Digitalis – propranolol• Monitoring – CBC – ECG – serum quinidine concentrations (target range 2-6 µg/ml or higher)• CI: AV block
    86. 86. Class IB• prototype: Lidocaine (Xylocaine®)• Tocainide (Tonocard®)• Mexiletene (Mexitel®)• Phenytoin (Dilantin®)
    87. 87. Lidocaine – Class IB• MOA: blocks influx of Na fast channel• Indication: ventricular arrhythmias
    88. 88. Lidocaine – Class IB (cont’d)• Common Adverse Effects – anxiety, nervousness – dizziness, drowsiness – feelings of coldness, heat, or numbness; or pain at the site of the injection – N/V• Monitoring – serum lidocaine concentrations (target range 2-6 µg/ml): parenteral use
    89. 89. Class IC• prototype: Flecainide (Tambocor®)• Propafenone (Rhythmol®)
    90. 90. Flecainide – Class IC• MOA – Blocks fast Na channels depresses the upstroke of the action potential, which is manifested as a decrease in the maximal rate of phase 0 depolarization. – significantly slow His-Purkinje conduction and cause QRS widening – shorten the action potential of Purkinje fibers without affecting the surrounding myocardial tissue.• Indications – Afib – Atrial flutter – Ventricular tachycardia prophylaxis
    91. 91. Flecainide – Class IC• Adverse Reactions – visual impairment, dizziness, asthenia, edema, abdominal pain, constipation, headache, fatigue, and tremor, N/V, arrhea, dyspepsia, anorexia, rash, diplopia, hypoesthesia, paresthesia, paresis, ataxia, flushing, increased sweating, vertigo, syncope, somnolence, tinnitus, anxiety, insomnia, and depression.• Avoid in – CHF – Acute MI – Hx of MI (LVEF < 30%)• Monitoring – ECG – serum creatinine/BUN: baseline
    92. 92. Class II – Beta Blockers• Propranolol (Inderal®)• Acebutolol (Sectral®)• Atenolol (Tenormin®)• Betaxolol (Kerlone®)• Bisoprolol (Zebeta®)• Carvedilol (Coreg®)• Esmolol (Brevibloc®)• Metoprolol(Toprol®, Lopressor®)• Nadolol (Corgard®)• Timolol (Blocadron®)
    93. 93. Propranolol Warning• 2 situations in which propranolol requires extreme caution – AV block – CHF – Asthma or emphysema
    94. 94. Class III• K+ channel blockers• Drugs: – Prototype: Amiodarone (Cordarone) – Bretylium (Bretylol) – Sotalol (Betapace)
    95. 95. Amiodarone – Class IIIMOA – noncompetitively inhibits alpha- and beta-receptors, – possesses both vagolytic and calcium-channel blocking properties – relaxes both smooth and cardiac muscle• Indications – Vfib – Vtach
    96. 96. Amiodarone – Class III (cont’d)• Monitoring – CBC – chest x-ray – ECG – ophthalmologic exam – thyroid function tests (TFTs)
    97. 97. Class IV• Ca channel blockers• Drugs – Adenosine (Adenocard ®) – Diltiazim (Cardizem®, Tiazac®) – Verapamil (Dovera®, Isoptin®, Calan®)• Clinical Effects – widen the blood vessels – may decrease the heart’s pumping strength
    98. 98. Sympathomimetics
    99. 99. Sympathomimetics• 2 classes: • SE: – α- agonist – hypertension, • Phenylephrine – excessive cardiac • Clonidine stimulation • Oxymetazoline – cardiac arrhythmias • Tetrahydralazine – Long-term use increases • Xylometazoline mortality in heart failure patients. – β-agonist • CI • Prototype: Epinephrine – CAD • Norepinephrine • Dopamine • Dobutamine • Isoproterenol
    100. 100. Epinephrine • “fight or flight “hormone • Aka “adrenaline” • increases heart rate and stroke volume • dilates the pupils • constricts arterioles in the skin and gastrointestinal tract while dilating arterioles in skeletal muscles
    101. 101. Epinephrine MOA
    102. 102. Epinephrine (cont’d)• Indications • IV Dosage – Vfib – IV: 1 mg (10 ml of a – Ventricular asystole 1:10,000 solution) IV; – Cardiac arrest may repeat every 3-5 minutes – Pulseless electrical – Each dose may be activity given by peripheral injection followed by a 20 ml flush of IV fluid.
    103. 103. Epinephrine• Common Adverse Effects – anxiety or nervousness – dry mouth – drowsiness or dizziness – headache – increased sweating – nausea – weakness or tiredness• Monitoring – ECG: in patients receiving IV therapy
    104. 104. Vasopressors
    105. 105. Vasopressors• Vasoconstrictors vs. Vasodilators• 2 Vasoconstrictor Classes – Sympathomimetics – Vasopressin Analogs• Vasodilators • Alpha-adrenoceptor antagonists (alpha-blockers) • Angiotensin converting enzyme (ACE) inhibitors • Angiotensin receptor blockers (ARBs) • Beta2-adrenoceptor agonists (b2-agonists) • Calcium-channel blockers (CCBs) • Centrally acting sympatholytics • Direct acting vasodilators • Endothelin receptor antagonists • Ganglionic blockers • Nitrodilators • Phosphodiesterase inhibitors • Potassium-channel openers • Renin inhibitors
    106. 106. Vasoconstrictor• any agent that produces vasoconstriction and a rise in blood pressure (usually understood as increased arterial pressure)• Drugs – Prototype: Vasopressin – Epinephrine – Dobutamine – Dopamine – Norepinephrine
    107. 107. Vasopressin• aka : “ADH”• MOA – ↑ the resorption of water at the renal collecting ducts – Vasoconstrictive property: stimulates the contraction of vascular smooth muscle in coronary, splanchnic, GI, pancreatic, skin, and muscular vascular beds
    108. 108. Vasopressin (cont’d)Indications: – Cardiac arrest – Cardiogenic shock – Cardiopulmonary resuscitation – Hypotension – Septic shock – Diabetes Insipidus
    109. 109. Vasopressin (cont’d)• Dosage for cardiac arrest including ventricular asystole and pulseless electrical activity (PEA) during cardiopulmonary resuscitation (CPR) – IV or intraosseous dosage: • Adults: A single dose of 40 units IV (or intraosseous) may be given one time to replace the first or second dose of epinephrine during cardiac arrest • Do not interrupt cardiopulmonary resuscitation to administer drug therapy.
    110. 110. Vasopressin (cont’d)• Adverse Effects – Cardiovascular: Cardiac arrest; circumoral pallor; arrhythmias; decreased cardiac output; angina; myocardial ischemia; peripheral vasoconstriction; and gangrene – CNS: Tremor; vertigo; “pounding” in head – Dermatologic: Sweating; urticaria; cutaneous gangrene – GI: Abdominal cramps; nausea; vomiting; passage of gas – Hypersensitivity: Anaphylaxis (cardiac arrest and/or shock) has been observed shortly after injection – Respiratory: Bronchial constriction.• Monitoring – serum osmolality – serum Na
    111. 111. Anticoagulants
    112. 112. Antiplatelets/Anticoagulants• Prevents/interferes with coagulation• Uses – deep vein thrombosis (DVTs), pulmonary embolism, myocardial infarctions & strokes in those who are predisposed
    113. 113. Types of Antiplatelets/Anticoagulants• Antiplatelets – Aspirin – Dipyridamole – Thienopyridines • Clopidogrel (Plavix) • Ticlopidine (Ticlid) – Glycoprotein IIb/IIIa antagonists • Abciximab (ReoPro) • Eptifibatide (Integrelin) • Tirofiban (Aggrastat)
    114. 114. Antiplatelets/Anticoagulants• Anticoagulants – Heparin – LMWH • Enoxaparin (Lovenox®) • Dalteparin (Fragmin®) • Tinzaarin (Innohep®) – Factor Xa inhibitors • Fondaparinux (Arixtra®) – Direct Thrombin Inhibitors • Argatroban • Lepirudin (Refludan®) – Oral Anticoagulants • Prototype: Warfarin
    115. 115. Coagulation Cascade
    116. 116. Warfarin – Oral Anticoagulant• MOA: Warfarin inhibits the synthesis of vitamin K-dependent coagulation factors II, VII, IX, and X and anticoagulant proteins C and S
    117. 117. Warfarin (cont’d)• Indications – Stroke – DVT – Post MI – Afib – Cardiomyopathy
    118. 118. Warfarin WarningsBleeding Risk!• Warfarin can cause major or fatal bleeding• Risk factors for bleeding – 65 years of age and older – history of GI bleeding – Hypertension – cerebrovascular disease – anemia, malignancy – Trauma – renal function impairment – long duration of warfarin therapy.• Pregnancy Category X
    119. 119. Warfarin (cont’d)• SE – Hemorrhage: Signs of severe bleeding resulting in the loss of large amounts of blood depend upon the location and extent of bleeding. Symptoms include: chest, abdomen, joint, muscle, or other pain; difficult breathing or swallowing; dizziness; headache; low blood pressure; numbness and tingling; paralysis; shortness of breath; unexplained shock; unexplained swelling; weakness Nursing responsibilities Patients should be instructed about prevention measures to minimize risk of bleeding and to report immediately to health care provider signs and symptoms of bleeding – prothrombin time (PT) – stool guaiac – bleeding – DDIs • NSAIDs • 3 G’s – Garlic – Ginger – Ginsing – Vitamin K intake
    120. 120. Class Participation Question #5:Which foods are high in vitamin K?
    121. 121. Class Participation Question #5:Which foods are high in vitamin K?
    122. 122. Fibrinolytic Enzymes
    123. 123. Fibrinolytic Enzymes• “clotbusters”• MOA: stimulate the synthesis of fibrinolysin which breaks the clot into soluble products• Drugs – Urokinase (Abbokinase®) – Anistreplase (Eminase®) – Alteplase (Activase®) – Reteplase (Retevase®) – Prototype: Streptokinase (Strepase®)
    124. 124. Streptokinase (cont’d)• Indications – Acute MI – Acute ischemic stroke – Pulmonary embolism – Lysis of DVT• Dose Administration – Parental infusion (usually IV) – Deep vein or arterial thrombosis • IV: 250,000 IU over 30 min followed by 100,000 IU per hour up to 72 hours
    125. 125. Streptokinase (cont’d)• Adverse Effects – Hemorrhage – Concomitant use of heparin, oral anticoagulants, NSAIDs is NOT recommended because of the increased risk of bleeding – Allergic reactions
    126. 126. Streptokinase (cont’d)
    127. 127. Antilipidemics
    128. 128. Antilipidemics• Drugs that lower down abnormal blood lipid levels.
    129. 129. Types of antilipidemics– Statin drugs work by inhibiting the synthesis of cholesterol in the liver. Liver enzymes must be regularly monitored. (ex. Simvastatin)– Niacin, a water-soluble B vitamin, is highly effective in lowering LDL and triglyceride levels by interfering with their synthesis. Niacin also increases HDL levels better than many other lipid-lowering drugs.(Ex. Niacin SR)– Fibric acid derivatives work by accelerating the elimination of VLDLs and increasing the production of apoproteins A-I and A-II. (ex. Lipofen, Tricor)– Bile-acid sequestrants increase conversion of cholesterol to bile acids and decrease hepatic cholesterol content. The primary effect is a decrease in total cholesterol and LDLs. (ex. Questran)
    130. 130. Side effects• Constipation• Peptic ulcer• Flushing• Headache
    131. 131. Nursing responsibilities• Monitor client’s lipid levels• Observe for signs of GI upset• Instruct to take with sufficient fluids or meals• Low fat diet• Instruct not to abruptly stop intake
    132. 132. Questions?