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    i am preparing for a report this Friday (July 23, 2010) on Cardiovascular medications. may i have these slides?? i need to have it in the soonest possible time. thank you!!
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  • Cardiodrugs

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