Download
slide1 n.
Skip this Video
Loading SlideShow in 5 Seconds..
DRUGS AFFECTING THE CARDIOVASCULAR and RENAL SYSTEMS PowerPoint Presentation
Download Presentation
DRUGS AFFECTING THE CARDIOVASCULAR and RENAL SYSTEMS

DRUGS AFFECTING THE CARDIOVASCULAR and RENAL SYSTEMS

329 Views Download Presentation
Download Presentation

DRUGS AFFECTING THE CARDIOVASCULAR and RENAL SYSTEMS

- - - - - - - - - - - - - - - - - - - - - - - - - - - E N D - - - - - - - - - - - - - - - - - - - - - - - - - - -
Presentation Transcript

  1. DRUGS AFFECTING THE CARDIOVASCULAR and RENAL SYSTEMS Winter 2013

  2. CARDIAC PROBLEM AREAS • PUMP • CIRCULATION TO MUSCLE • ELECTRICAL SYSTEM Winter 2013

  3. CARDIAC A&P REVIEW Winter 2013

  4. CARDIAC A&P REVIEW Winter 2013

  5. CARDIAC A&P REVIEW Winter 2013

  6. HEART FAILUREChapter 22 • LEFT SIDED HEART FAILURE (CHRONIC HEART FAILURE) • RESTLESS • ORTHOPNEA • SOB (SHORTNESS OF BREATH) • DOE (DYSPNEA ON EXERTION) Winter 2013

  7. Common Causes for Heart Failure • Inadequate Contractility • Myocardial Infarction • Inadequate Filling • Atrial fibrillation • Pressure Overload • Hypertension • Volume Overload • Hypervolemia • Complete list on pg. 336 Winter 2013

  8. DRUG CLASSES FOR HEART FAILURE • ANGIOTENSIN – CONVERTING ENZYME INHIBITORS • ANGIOTENSIN II RECEPTOR BLOCKERS • BETA-BLOCKERS • B-TYPE NATRIURETIC PEPTIDE • PHOSPHODIESTERASE INHIBITORS • CARDIAC GLYCOSIDES Winter 2013

  9. ANGIOTENSIN –CONVERTING ENZYME INHIBITORS • ACE Inhibitors • Prevents vasoconstriction, sodium and water resorption • Lisinopril • Indicated for heart failure, hypertension, acute Myocardial Infarction Winter 2013

  10. ANGIOTENSIN II RECEPTOR BLOCKERS • ARBs • valsartan (Diovan) • Potent vasodilating effects • Decreases systemic vascular resistance • Used in combination with diuretics to treat Heart Failure and Hypertension Winter 2013

  11. BETA-BLOCKERS • Block sympathetic nervous system stimulation of the heart • Reduce heart rate, delayed AV node conduction, reduced myocardial contractility and decreased myocardial automaticity. • metoprolol • Decreased workload of the heart Winter 2013

  12. Synthetic human B-type natriuretic peptide • Nesiritide (Natrecor) • Vasodilating effect on both arteries and veins • Treatment of patients with acutely decompensated CHF who have dyspnea at rest or with minimal activity. • Treatment for severe life-threatening heart failure • Causes diuresis, urine sodium loss and vasodilation Winter 2013

  13. PHOSPHODIESTERASE INHIBITORS • inamrinone and milrinone • Positive inotropic and vasodilating effects • Decrease cardiac work load • Parenteral only • Short-term management of CHF Winter 2013

  14. CARDIAC GLYCOSIDES(aka: digitalis glycosides) • INCREASE THE EFFICIENCY OF THE HEART BY IMPROVING THE CONTRACTION OF THE HEART MUSCLE • POSITIVE INOTROPIC ACTION • INCREASING THE FORCE OF MYOCARDIAL CONTRACTION • Negative chronotropic effect – reduced heart rate • Negative dromotropic effect – decreased automaticity at the SA note, AV node and bundle of HIS • digoxin (Lanoxin) • Not first line drug in Heart Failure Winter 2013

  15. WHY DO WE WANT TO INCREASE THE MYOCARDIAL CONTRACTILITY?? • INADEQUATE CONTRACTILITY • MI (MYOCARDIAL INFARCTION) • CORONARY ARTERY DISEASE • CARDIOMYOPATHY • INADEQUATE FILLING • ATRIAL FIBRILLATION Winter 2013

  16. Atrial Fibrillation • NORMAL SINUS RHYTHM (NSR) • A FIB Winter 2013

  17. WHY DO WE WANT TO INCREASE THE MYOCARDIAL CONTRACTILITY?? • PRESSURE OVERLOAD • HYPERTENSION • VOLUME OVERLOAD • HYPERVOLEMIA Winter 2013

  18. DIGOXIN (LANOXIN) • DIGITALIZATION • The administration of digitalis or one of its glycosides in a dosage schedule designed to produce and then maintain optimal therapeutic concentration • CARDIAC GLYCOSIDES HAVE BEEN USED TO TREAT HEART FAILURE FOR OVER 200 YEARS Winter 2013

  19. DIGOXIN (LANOXIN) • WHAT DOES IT DO??? • INCREASES CARDIAC CONTRACTILITY BY INHIBITING THE K+/Na+ PUMP AND INFLUENCING CALCIUM MOVEMENT • STIMULATES THE VAGUS NERVE = SLOWING THE HEART RATE NEGATIVE CHRONOTROPIC EFFECT • POSITIVE INOTROPIC EFFECT – Increases the squeeze! Winter 2013

  20. ADVERSE EFFECTS OF CARDIAC GLYCOSIDES MEDICATIONS • DYSRYTHMIAS • HEADACHE • FATIGUE • ANOREXIA • N, V, D Winter 2013

  21. NURSING CONSIDERATIONS • APICAL PULSE FOR ONE MINUTE PRIOR TO GIVING DIGOXIN “HOLD” IF <60 • ANTACIDS INTERFERE WITH ABSORPTION • AVOID GIVING DIGOXIN WITH HIGH-FIBER FOODS (FIBER BINDS WITH DIGITALIS) • TEACH S&S OF TOXICITY • TRACK BLOOD LEVELS FOR DIG AND ELECTROLYTES • DIGOXIN LEVELS MUST BE MONITORED • 0.5 TO 2 ng/ml Winter 2013

  22. DIGITALIS TOXICITY • SIGNS AND SYMPTOMS • N, V • ANOREXIA • VISUAL DISTURBANCES • MAY SEE YELLOW, GREEN, BLUE HALOS • CONFUSION • BRADYCARDIA • EKG CHANGES Winter 2013

  23. TREATMENT FOR DIG TOXICITY • STOP TAKING THE DRUG • DIGOXIN IMMUNE FAB (DIGIBIND) • WHAT CAUSED THE PROBLEM? • HYPOKALEMIA R/T DIURETIC DRUGS • LIVER FAILURE Winter 2013

  24. ANTIDYSRHYTHMIC DRUGSChapter 23 • DYSRHYTHMIA (ARRHYTHMIA) • ANY DEVIATION FROM THE “NORMAL” RHYTHM Winter 2013

  25. “NORMAL” ELECTRICAL PATTERN OF THE HEART Winter 2013

  26. Vaughan Williams Classification System commonly used to classify antidysrhythmic drugs Based on the electrophysiologic effect of particular drugs on the action potential Winter 2013

  27. Vaughan Williams Classification (cont’d) Class I Class Ia Class Ib Class Ic Class II Class III Class IV Other Winter 2013

  28. Vaughan Williams Classification:Mechanism of Action Class I Membrane-stabilizing drugs Fast sodium channel blockers Divided into Ia, Ib, and Ic drugs, according to effects Winter 2013

  29. Vaughan Williams Classification:Mechanism of Action and Indications Class I: moricizine General class I drug Has characteristics of all three subclasses Used for symptomatic ventricular and life-threatening dysrhythmias Winter 2013

  30. Vaughan Williams Classification:Mechanism of Action and Indications (cont’d) Class Ia: quinidine, procainamide, disopyramide Block sodium (fast) channels Delay repolarization Increase APD (action potential duration) Used for atrial fibrillation, premature atrial contractions, premature ventricular contractions, ventricular tachycardia, Wolff-Parkinson-White syndrome Winter 2013

  31. Winter 2013

  32. Winter 2013

  33. Vaughan Williams Classification:Mechanism of Action and Indications (cont’d) Class Ib: phenytoin, lidocaine Block sodium channels Accelerate repolarization Increase or decrease APD Used for ventricular dysrhythmias only Premature ventricular contractions, ventricular tachycardia, ventricular fibrillation Winter 2013

  34. Vaughan Williams Classification:Mechanism of Action and Indications (cont’d) Class Ic: flecainide, propafenone Block sodium channels (more pronounced effect) Little effect on APD or repolarization Used for severe ventricular dysrhythmias May be used in atrial fibrillation/flutter, Wolff-Parkinson-White syndrome, supraventricular tachycardia dysrhythmias Winter 2013

  35. Winter 2013

  36. Winter 2013

  37. Winter 2013

  38. Vaughan Williams Classification:Mechanism of Action and Indications (cont’d) Class II: beta-blockers: atenolol, esmolol, metaprolol, propranolol Reduce or block sympathetic nervous system stimulation, thus reducing transmission of impulses in the heart’s conduction system Depress phase 4 depolarization General myocardial depressants for both supraventricular and ventricular dysrhythmias Also used as antianginal and antihypertensive drugs Winter 2013

  39. Vaughan Williams Classification:Mechanism of Action and Indications (cont’d) Class III: amiodarone, sotalol*, ibutilide, others Increase APD Prolong repolarization in phase 3 Used for dysrhythmias that are difficult to treat Life-threatening ventricular tachycardia or fibrillation, atrial fibrillation or flutter—resistant to other drugs Sustained ventricular tachycardia *Sotalol also exhibits Class II properties Winter 2013

  40. Vaughan Williams Classification:Mechanism of Action and Indications (cont’d) Class IV: verapamil, diltiazem Calcium channel blockers Inhibit slow-channel (calcium-dependent) pathways Depress phase 4 depolarization Reduce AV node conduction Used for paroxysmal supraventricular tachycardia (PSVT); rate control for atrial fibrillation and flutter Winter 2013

  41. Winter 2013

  42. Vaughan Williams Classification: Other Antidysrhythmics Digoxin, adenosine Have properties of several classes and are not placed into one particular class Winter 2013

  43. UnclassifiedAntidysrhythmic adenosine (Adenocard) Slows conduction through the AV node Used to convert paroxysmal supraventricular tachycardia to sinus rhythm Very short half-life—less than 10 seconds Only administered as fast IV push May cause asystole for a few seconds Other adverse effects minimal Winter 2013

  44. ADVERSE REACTION TO ANTIDYSRHYTHMICS • N, V, D • DIZZINESS • HEADACHE • BLURRED VISION • CAN CAUSE DYSRHYTHMIAS !! Winter 2013

  45. NURSING CONSIDERATIONS • MONITOR PULSE RATE • IF SENDING PT HOME – TEACH THEM HOW TO MONITOR THEIR PULSE • ALWAYS CHECK ALL VS BEFORE ADMINISTERING THE MEDICATION Winter 2013

  46. NURSING CONSIDERATIONS • MONITOR FOR FLUID RETENTION • DO NOT STOP DRUGS ABRUPTLY • AVOID ALCOHOL Winter 2013

  47. CHAPTER 24Antianginal Drugs Winter 2013

  48. Angina Pectoris (Chest Pain) When the supply of oxygen and nutrients in the blood is insufficient to meet the demands of the heart, the heart muscle “aches” The heart requires a large supply of oxygen to meet the demands placed on it Winter 2013

  49. Ischemia Ischemia Poor blood supply to an organ Ischemic heart disease Poor blood supply to the heart muscle Atherosclerosis Coronary artery disease Myocardial infarction (MI) Necrosis, or death, of cardiac tissue Disabling or fatal Winter 2013

  50. Winter 2013