1. Drug Affecting Cardiovascular System ANTIDYSRHYTHMIC DRUGS Cardiac Glycosides Calcium Channel Blockers Diuretics Present by:Dr.Amira Yahia

2. Figure 48-1 Cardiac conduction pathways.

3. Electrical Properties of the Heart Impulse Conduction: pathways and timing – SA node—pacemaker of heart – AV node – Bundle of His-Purkinje system

4. Generation of Dysrhythmias Two fundamental causes Disturbances of automaticity Disturbances of conduction – Atrioventricular block – Reentry (recirculating activation)

5. Antidysrhythmic Drugs (cont’d) An abnormality in the rhythm of the heartbeat Two basic types of dysrhythmias – Tachydysrhythmias: heart rate is increased – Bradydysrhythmias: heart rate is slowed Dysrhythmias are also known as arrhythmias

6. Common Dysrhythmias and Their Treatment (cont’d) Ventricular – Sustained ventricular tachycardia – Ventricular fibrillation – Ventricular premature beats – Digoxin-induced ventricular dysrhythmias – Torsade's de pointes

7. Common Dysrhythmias and Their Treatment Supraventricular – Impulse arises above the ventricle – Atrial flutter – Atrial fibrillation – Sustained supraventricular tachycardia (SVT)

8. Classification of Antidysrhythmic Drugs Vaughan Williams classification – Class I: sodium channels blockers – Class II: beta blockers – Class III: potassium channel blockers – Class IV: calcium channel blockers – Other: adenosine, digoxin, and ibutilide

9. Class I: Sodium Channel Blockers Class IA agents Class IB agents Class IC agents Other class I: moricizine

10. Class IA Agents Quinidine Effects on the heart – Blocks sodium channels – Slows impulse conduction – Delays repolarization – Blocks vagal input to the heart Effects on the ECG – Widens the QRS complex – Prolongs the QT interval Therapeutic uses – Used against supraventricular and ventricular dysrhythmias

11. Class IA Agents (cont’d) Quinidine (cont’d) Adverse effects – Diarrhea – Cinchonism – Cardiotoxicity – Arterial embolism – Alpha-adrenergic blockade, resulting in hypotension – Hypersensitivity reactions Drug interactions – Digoxin

12. Class IB Agents Lidocaine [Xylocaine] Effects on the heart and ECG – Blocks cardiac sodium channels Slows conduction in the atria, ventricles, and His- Purkinje system – Reduces automaticity in the ventricles and His- Purkinje system – Accelerates repolarization Adverse Effects – CNS effects – Drowsiness – Confusion – Paresthesias

13. Class IC Agents Block cardiac sodium channels Delay ventricular repolarization All class IC agents can exacerbate existing dysrhythmias and create new ones Two class IC agents – Flecainide – Propafenone

14. Class II: Beta Blockers Propranolol [Inderal] – Nonselective beta-adrenergic antagonist Effects on the heart and ECG – Decreased automaticity of the SA node – Decreased velocity of conduction through the AV node – Decreased myocardial contractility Therapeutic use – Dysrhythmias caused by excessive sympathetic stimulation – Supraventricular tachydysrhythmias Suppression of excessive discharge Slowing of ventricular rate

15. Class II: Beta Blockers (cont’d) Adverse effects – Heart block – Heart failure – AV block – Sinus arrest – Hypotension – Bronchospasm (in asthma patients) Other class II: beta blockers – Acebutolol [Sectral] – Esmolol [Brevibloc]

16. Class III: Potassium Channel Blockers Bretylium Delay repolarization of fast potentials QT interval prolonged Adverse effect – Profound persistent hypertension Therapeutic use – Ventricular fibrillation – Ventricular tachycardia

17. Class III: Potassium Channel Blockers (cont’d) Amiodarone [Cordarone, Pacerone] Therapeutic use – For life-threatening ventricular dysrhythmias only – Recurrent ventricular fibrillation – Recurrent hemodynamically unstable ventricular tachycardia

18. Class III: Potassium Channel Blockers (cont’d) Amiodarone [Cordarone, Pacerone] (cont’d) Effects on the heart and ECG – Reduces automaticity in the SA node – Reduced contractility – Reduced conduction velocity – QRS widening – Prolongation of the PR and QT intervals

19. Class III: Potassium Channel Blockers (cont’d) Amiodarone [Cordarone, Pacerone] (cont’d) Adverse effects – Pulmonary toxicity – Cardiotoxicity – Toxicity in pregnancy and breastfeeding – Corneal microdeposits – Optic neuropathy

20. Class III: Potassium Channel Blockers (cont’d) Drug interactions – Quinidine – Diogoxin – Procainamide – Diltiazem – Phenytoin – Warfarin

21. Class IV: Calcium Channel Blockers Verapamil and diltiazem Reduces SA nodal automaticity Delays AV nodal conduction Reduces myocardial contractility Therapeutic uses – Slow ventricular rate (atrial fibrillation or atrial flutter) – Terminate SVT caused by an AV nodal reentrant circuit

22. Class IV: Calcium Channel Blockers (cont’d) Verapamil and diltiazem (cont’d) Adverse effects – Bradycardia – Hypotension – AV block – Heart failure – Peripheral edema – Constipation

23. Other Antidysrhythmic Drugs Adenosine Effects on the heart and ECG – Decreases automaticity in the SA node – Slows conduction through the AV node – Prolongation of PR interval Therapeutic use: termination of paroxysmal SVT

24. Other Antidysrhythmic Drugs (cont’d) Adenosine (cont’d) Adverse Effects – Sinus bradycardia – Dyspnea – Hypotension – Facial flushing Drug Interactions – Methylxanthines – Dipyridamole

25. NURSING INTERVENTIONS FOR PATIENTS RECEIVING ANTIDYSRHYTHMIC DRUGS Obtain a complete health history including previous dysrhythmias, hypertension, MI, HF. Obtain baseline weight, vital signs, ECG, cardiac monitoring & breath sounds. Assess for desired therapeutic effects. Continue frequent monitoring of ECG. Continue periodic monitoring of electrolytes specially potassium. Assess for adverse effects like dizziness, hypotension, nausea, vomiting, etc.

26. What are Cardiac Glycosides? Family of compounds derived from the Digitalis plant (Digitalis purpurea or Digitalis lanata)

27. What are Cardiac Glycosides? Contain a polysaccharide chain, a steroid portion and a lactone ring

28. Types Two main types: Bufadienolides and Cardenolides

29. What are they used for? Cardiac glycosides are cardiotonic drugs Used in the treatment of congestive heart failure and cardiac arrhythmia

30. Digoxin Also known as Lanoxin

31. DIGOXIN ACTION: Cause the heart to beat more forcefully (positive inotropic effect) & more slowly, thus improving cardiac output. USES: in heart failure and dysrhythmias DOSE: PO, 0.125 – 0.5 mg/ day ADVERSE EFFECTS: nausea, vomiting, headache, visual disturbances, AV block, dysrhythmia CONTRAINDICATIONS: patient with AV block or ventricular dysrhythmia.

32. NURSING INTERVENTIONS FOR PATIENTS RECEIVING DIGOXIN THERAPY Obtain a complete health history including previous MI, HF, renal dysfunction, dysrhythmias. Obtain baseline weight, vital signs, ECG, cardiac monitoring & breath sounds. Take the apical pulse for 1 full minute, noting rate, rhythm before administering. If the pulse is below 60 beats /min, withhold the dose and notify the provider. Check for recent serum digoxin level results before administering.

33. Use with caution in geriatric & pediatric patients. Report signs of possible digoxin toxicity immediately like bradycardia, nausea, visual disturbances, etc. Assess for desired therapeutic effects. Continue periodic monitoring of electrolytes specially potassium, renal function. Assess for adverse effects like bradycardia, pulse rate below 60 or above 100, palpitations, dizziness, fatigue, nausea, vomiting, etc. NURSING INTERVENTIONS FOR PATIENTS RECEIVING DIGOXIN THERAPY

34. NURSING INTERVENTIONS FOR PATIENTS RECEIVING CALCIUM CHANNEL BLOCKER THERAPY Obtain a complete health history including previous MI, HF, fatigue, muscle or joint pain. Obtain baseline weight, vital signs, ECG, cardiac monitoring & breath sounds. Assess for desired therapeutic effects. Continue periodic monitoring of electrolytes specially potassium. Assess for adverse effects like headache, dizziness, musculoskeletal fatigue, nausea, constipation, etc.

35. Calcium Channel Blocking Drugs

36. Chemical Type Chemical Names Brand Names Phenylalkylamines verapamil Calan, Calna SR, Isoptin SR, Verelan Benzothiazepines diltiazem Cardizem CD, Dilacor XR 1,4-DihydropyridinesNifedipine nicardipine isradipine felodipine amlodipine Adalat CC, Procardia XL Cardene DynaCirc Plendil Norvasc Three Classes of CCBs

37.  Angina pectoris  Hypertension  Treatment of supraventricular arrhythmias - Atrial Flutter - Atrial Fibrillation - Paroxysmal SVT Widespread use of CCBs

38.  Increase the time that Ca 2+ channels are closed  Relaxation of the arterial smooth muscle but not much effect on venous smooth muscle  Significant reduction in afterload but not preload CCBs – Mechanisms of Action

39. Myofibril Plasma membrane Transverse tubule Terminal cisterna of SR Tubules of SR Triad T SR Skeletal muscle relies on intracellular Ca 2+ for contraction

40. CCBs Act Selectively on Cardiovascular Tissues  Neurons rely on N-and P-type Ca 2+ channels  Skeletal muscle relies primarily on [Ca] i  Cardiac muscle requires Ca 2+ influx through L-type Ca 2+ channels - contraction (fast response cells) - upstroke of AP (slow response cells)  Vascular smooth muscle requires Ca 2+ influx through L-type Ca 2+ channels for contraction

41. Differential effects of different CCBs on CV cells AV SN AV SN Potential reflex increase in HR, myocardial contractility and O 2 demand Coronary VD Dihydropyridines: Selective vasodilatorsNon -dihydropyridines: equipotent for cardiac tissue and vasculature Heart rate moderating Peripheral and coronary vasodilation Reduced inotropism Peripheral vasodilation

42. EffectVerapamilDiltiazemNifedipine Peripheral vasodilatation  Coronary vasodilatation Preload000/ Afterload  Contractility 0/ / */ * Heart rate 0/  /0 AV conduction  0 Hemodynamic Effects of CCBs

43. DiltiazemVerapamilDihydropyridines Overall0-3%10-14%9-39% Hypotension++ +++ Headaches0++++ Peripheral Edema ++++++ Constipation0++0 CHF (Worsen)0+0 AV block++0 Caution w/beta blockers +++0 Comparative Adverse Effects

44.  heart rate  blood pressure  anginal symptoms  signs of CHF  adverse effects CCBs - Monitoring

45. ContraindicationVerapamilNifedipineDiltiazem Hypotension++++ Sinus bradycardia +0 AV conduction defects ++0 Severe cardiac failure ++++ Contradications for CCBs +

46. Drugs that accelerate the rate of urine formation In the nephron, where sodium goes, water follows – 20% to 25% of all sodium is reabsorbed into the bloodstream in the ascending loop of Henle – 5% to 10% in the distal convoluted tubules – 3% in collecting ducts If water is not absorbed, it is excreted as urine Result: removal of sodium and water Diuretics

48. Diuretic Drugs Classifications Carbonic anhydrase inhibitors Loop diuretics Osmotic diuretics Potassium-sparing diuretics Thiazide and thiazide-like diuretics

49. Carbonic Anhydrase Inhibitors (CAI) Mechanism of Action The enzyme carbonic anhydrase helps to make H + ions available for exchange with sodium and water in the proximal tubules CAIs – block the action of carbonic anhydrase, – thus preventing the exchange of H + ions with sodium and water – reduces H + ion concentration in renal tubules Result: – increased excretion of bicarbonate, sodium, water, & K+ – Reabsorption of water is decreased and urine volume is increased

50. Carbonic Anhydrase Inhibitors (CAIs) acetazolamide (Diamox) methazolamide dichlorphenamide

51. Carbonic Anhydrase Inhibitors Indications Adjunct drugs in the long-term management of open-angle glaucoma* Used with miotics to lower intraocular pressure before ocular surgery in certain cases Also useful in the treatment of: – Edema* – Epilepsy – High-altitude sickness Acetazolamide (Diamox) is used in the management of edema secondary to HF when other diuretics are not effective* CAIs are less potent diuretics than loop diuretics or thiazides—the metabolic acidosis they induce reduces their diuretic effect in 2-4 days

52. Carbonic Anhydrase Inhibitors: Adverse Effects Metabolic acidosis Anorexia Hematuria Photosensitivity Melena   Hypokalemia  Drowsiness  Paresthesias  Urticaria

53. Loop Diuretics Mechanism of Action Act directly on the ascending limb of the loop of Henle to inhibit chloride and sodium reabsorption Increase renal prostaglandins, resulting in the dilation of blood vessels and reduced peripheral vascular resistance bumetanide (Bumex) ethacrynic acid (Edecrin) furosemide (Lasix)

54. Loop Diuretics -- Drug Effects Potent diuresis and subsequent loss of fluid Decreased fluid volume causes: – Reduced BP – Reduced pulmonary vascular resistance – Reduced systemic vascular resistance – Reduced central venous pressure – Reduced left ventricular end-diastolic pressure Potassium and sodium depletion

55. Loop Diuretics -- Indications Edema associated with HF or hepatic or renal disease Control of hypertension Increase renal excretion of calcium in patients with hypercalcemia Certain cases of HF resulting from diastolic dysfunction

56. Loop Diuretics -- Adverse Effects Body SystemAdverse Effects CNSDizziness, headache, tinnitus, blurred vision GINausea, vomiting, diarrhea HematologicAgranulocytosis, neutropenia, thrombocytopenia MetabolicHypokalemia, hyperglycemia, hyper uric

57. Osmotic Diuretics Mechanism of Action Work mostly in the proximal tubule No absorbable, producing an osmotic effect Pull water into renal tubules from the surrounding tissues Inhibits tubular reabsorption of water and salts Increases glomerular filtration and renal plasma Reduces excessive intraocular pressure

58. Osmotic Diuretics -- Indications Used in the treatment of patients in the early, oliguric phase of ARF To promote the excretion of toxic substances Reduction of intracranial pressure Treatment of cerebral edema NOT indicated for peripheral edema

59. Osmotic Diuretics -- Adverse Effects Convulsions Thrombophlebitis Pulmonary congestion Also headaches, chest pains, tachycardia, blurred vision, chills, and fever

60. Osmotic Diuretics mannitol (Osmitrol) Intravenous infusion only May crystallize when exposed to low temperatures—use of a filter is required

61. Potassium-Sparing Diuretics Mechanism of Action Interfere with sodium-potassium exchange in collecting ducts and convoluted tubules Competitively bind to aldosterone receptors – Block the restoration of sodium and water Prevent potassium from being pumped into the tubule, thus preventing its secretion Competitively block the aldosterone receptors and inhibit its action Sodium and water are excreted

62. Potassium-Sparing Diuretics amiloride (Midamor) spironolactone (Aldactone) triamterene (Dyrenium) Also known as aldosterone-inhibiting diuretics

63. Potassium-Sparing Diuretics Indications spironolactone and triamterene – Hyperaldosteronism – Hypertension – Reversing the potassium loss caused by potassium-losing drugs – Certain cases of heart failure – Liver failure Amiloride – Treatment of HF

64. Potassium-Sparing Diuretics Adverse Effects Body SystemAdverse Effects CNSDizziness, headache GI Cramps, nausea, vomiting, diarrhea OtherUrinary frequency, weakness **hyperkalemia**

65. Potassium-Sparing Diuretics Adverse Effects Spironolactone Gynecomastia Amenorrhea Irregular menses Postmenopausal bleeding

66. Thiazide and Thiazide-like Diuretics Mechanism of Action Actions: Acts in the distal convoluted tubule – Inhibit tubular reabsorption of sodium, chloride, and potassium ions – Result: water, sodium, and chloride are excreted Potassium is also excreted to a lesser extent Dilate the arterioles by direct relaxation Results: – Lowered peripheral vascular resistance – Sodium, water, chloride and potassium are excreted

67. Thiazide and Thiazide-like Diuretics Thiazide diuretics – hydrochlorothiazide (Esidrix, HydroDIURIL) – chlorothiazide (Diuril) – trichlormethiazide (Metahydrin) Thiazide-like diuretics – chlorthalidone (Hygroton) – metolazone (Mykrox, Zaroxolyn)

68. Thiazide and Thiazide-like Diuretics Precautions Thiazides should not be used if creatinine clearance is less than 30 to 50 mL/min (normal is 125 mL/min) Metolazone (Zaroloxyn) remains effective to a creatinine clearance of 10 mL/min

69. Thiazide and Thiazide-like Diuretics Indications Hypertension – first line drug for HTN Edematous states Idiopathic hypercalciuria Diabetes insipidus Heart failure due to diastolic dysfunction Adjunct drugs in treatment of edema related to HF, hepatic cirrhosis, corticosteroid therapy

70. Thiazide and Thiazide-like Diuretics Adverse Effects Body SystemAdverse Effects CNSDizziness, headache, blurred vision, paresthesias, decreased libido GIAnorexia, nausea, vomiting, diarrhea GU Impotence Integumentary Urticaria, photosensitivity Metabolic Hypokalemia, glycosuria, hyperglycemia, hyperuricemia OTHER EFFECTS ALSO

71. Nursing Implications Thorough patient history and physical examination Assess baseline fluid volume status, intake and output, serum electrolyte values, weight, and vital signs—especially postural BPs/orthostatic BPs Assess for disorders that may contraindicate or necessitate cautious use of these drugs Monitor serum K+ levels during therapy – K+ supplements are usually recommended to maintain K+ levels at approximately 4 mEq/L

72. Patient Education Instruct patients to take in the morning as much as possible to avoid interference with sleep patterns Teach patients to maintain proper nutritional and fluid volume status Teach patients to eat more potassium-rich foods when taking any but the potassium-sparing drugs Foods high in potassium include bananas, oranges, dates, raisins, plums, fresh vegetables, potatoes, meat, and fish, apricots, whole grain cereals, legumes

73. Patients taking diuretics along with a digitalis preparation digoxin (Lanoxin) should be taught to monitor for digitalis toxicity Diabetic patients who are taking thiazide and/or loop diuretics should be told to monitor blood glucose and watch for elevated levels Change positions slowly, and to rise slowly after sitting or lying to prevent dizziness and possible fainting related to orthostatic hypotension Patient Education

74. Encourage patients to keep a log of their daily weight A weight gain of 2 or more pounds a day or 5 or more pounds a week should be reported immediately Encourage patients to return for follow-up visits and lab work Notify physician if you are ill with nausea, vomiting, and/or diarrhea because fluid loss may be dangerous Patient Education

75. Excessive consumption of licorice can lead to an additive hypokalemia in patients taking thiazides Signs and symptoms of hypokalemia include muscle weakness, constipation, irregular pulse rate, and overall feeling of lethargy Notify the physician immediately if rapid heart rate or syncope occurs (reflects hypotension or fluid loss) Patient Education