Heart Failure- Clinical Therapeutics

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CASE 3 HYPERTENSION AND CONGESTIVE HEART FAILURE DELA CRUZ, JUSAY, YANG, ZAGADA

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Heart Failure, Pharmacology, Clinical Therapeutics Report

Transcript of Heart Failure- Clinical Therapeutics

  • 1. HYPERTENSION AND CONGESTIVE HEART FAILURE DELA CRUZ, JUSAY, YANG, ZAGADA

2. Problem 1 Congestive Heart Failure (in acute exacerbation) 3. Basis: Chief Complaint: increased shortness of breath History of Present Illness: swolen legs malaise weakness weight gain paroxysmal nocturnal dyspnea ankle edema PMH: HF (LVEF of 15%) orthopnea HTN for 30 years CAD tachycardia Medications: Digoxin Furosemide Spirinolactone Carvedilol Amiodarone 4. Basis: Physical Examination: SOB weight gain of 7 kg hepatomegaly +S1, S2 jugular venous distention edema bibasal rales Laboratory Findings: 2+ protein BUN 32 SCr 1.9 5. Treatment Objectives To decrease fluid retention To decrease workload of the heart To increase myocardial contractility 6. Pharmacologic intervention 1. Decreasing fluid retention Drug of Choice: Loop Diuretics Action: dec. NaCl and KCl reabsorption in thick ascending limb of the loop of henle in the nephron Indication: antihypertensive, manifestation of fluid overload, swollen legs, edema, weight gain 7. Furosemide Drug interactions: Ace inhibitor can cause hyperkalemia Diuretics may cause hypokalemia Digoxin may inc. its effect or may reach toxicity 8. Pharmacologic intervention2. To decrease workload of the heart DRUGS EFFICACY SAFETY SUITABILITY COST ACE inhibitor ++++ +++ ++++ ++ ARB +++ +++ +++ +++ Vasodilators ++ + + + 9. Drug of Choice: ACE inhibitorPharmacologic intervention Alternative Drug: ARBs ACEIs and ARBs ACTION: Inhibits angiotensin converting enzyme, thus, aldosterone and ADH secretion is inhibited ACE inhibitor will also inhibit the inactivation of bradykinin, thus, prostaglandin synthesis will increase 10. Drug of Choice: ACE inhibitorPharmacologic intervention Alternative Drug: ARBs ACE inhibitors: Increase toxicity in patients with renal failure Interaction with : K-sparing diuretics Patient has ACEI-induced cough 11. Pharmacologic intervention To increase myocardial contractility DRUGS EFFICACY SAFETY SUITABILITY COST Cardiac Glycoside ++++ + ++ ++ Beta adrenoceptor agonist ++++ ++ ++ +++ Bipyridines ++ ++ ++ + 12. Dobutamine ACTION: directly binds to cardiac beta 1 receptors which increase force of contraction Pharmacologic interventionDrug of Choice: Beta Adrenoceptor Agonist 13. Pharmacologic intervention IF HEART FAILURE CONTINUES TO WORSEN: Add NITRATES or ALPHA BLOCKERS 14. Non - Pharmacologic intervention Diet Daily weight chart Sodium restriction Alcohol restriction Nutritional Supplements (vitamins) Other Smoking cessation Exercise Psychosocial services Intensive follow-up 15. Yang, Sheryl Ray B. 16. Hypertension One of the most common worldwide diseases afflicting human and is a major risk factor for stroke, myocardial infarction, vascular disease and CKD HPN is defined as a Systolic Blood Pressure (SBP) of > 140 mmHg, or a Diastolic Blood Pressure (DBP) of >90 mmHg, or taking antihypertensive medication 17. Types of HPN Types: 1. Primary (Essential) 90-95% Chronic High blood pressure without a source or associated with any other disease Most common form 2. Secondary 5-10% Elevation of BP associated with another disease such as kidney disease Causes include: CKD, D/o of adrenal gland, Pregnancy, Hyperparathyroidism 18. Classification of HPN 19. Risk factors Family History of High BP Family Hx of Premature CVD Diabetes Race (African American) Lifestyle Risk Factors: Weight (BMI >30) Stress Sedentary lifestyle Diet Smoking Alcohol (F:>1 Drink/day; M: >2 Drinks/day) Birth control pills Cant be changed Can be changed 20. Treatment Goals Use and Maximize nonpharmacologic therapies in combination with pharmacotherapy Individualize all therapies based on compelling indications and comorbid conditions Treat systolic BP to recommended goal as primary focus (esp. patients >50 yrs old) Ultimate treatment goal is the reduction of cardiovascular and renal morbidity & mortality 21. Basis of DiagnosisHistory: 59y/o, Male African American Hypertension for 30 years Diabetes Mellitus (DM) type 2 for 5 years Prior cigarette smoker 3-4 packs/week; quit 30 years ago Social drinker; 6 cans of beer/week Medications: Furosemide, 80mg PO QAM Spironolactone, 12.5mg PO QD Carvedilol, 25mg PO QAM, 12.5mg PO QPM Physical Examination: BP 153/91 mmHg BMI of 26.4 = Overweight 22. Choice of Anti-HPN drugs depend on: Stage of hypertension Physical factors( cardiac, renal complications) Individualized prescribed on a trial basis 23. Diuretics Sympathoplegi c agents Vasodilators Angiotensin antagonists Major Classes of Anti-Hypertensive Drugs 24. DRUG CLASSES EFFICACY SAFETY SUITABILITY COST Diuretics ++++ +++ +++ ++++ Vasodilators ++ ++ ++ + Calcium channel blockers ++++ ++ +++ ++ Beta Blockers ++++ ++ ++++ ++ ACE Inhibitor ++++ +++ +++ ++++ Angiotensin Receptor Blocker ++++ ++++ ++++ +++ Major Classes of Anti-Hypertensive Drugs 25. Angiotensin-Receptor Blockers Competitive angiotensin II receptor antagonists Effect same as ACEIs Vasodilatation and decreased sodium retention Do not block bradykinin metabolism Same efficacy with ACEIs; more expensive For those unable to tolerate ACEIs Losartan, Valsartan - first marketed AT1 receptor blocker 26. Angiotensin Receptor Blockers DRUG EFFICACY SAFETY SUITABILITY COST Losartan (Cozaar) +++ ++++ +++ +++ Valsartan (Diovar) +++ ++++ +++ +++ Olmesartan (Olmetec) ++++ ++++ ++++ +++ Candesartan (Atacand) ++++ ++++ +++ ++ Irbesartan ++++ ++++ +++ ++ Telmisartan (Micardis) ++++ ++++ ++++ ++++ 27. NONPHARMACOLOGIC THERAPY Appropriate lifestyle modifications are important therapies in both the prevention and treatment of hypertension. The prevalence of hypertension is 50% greater in overweight 28. PATIENT EDUCATION Immediate reporting of any adverse side effects, especially slow or irregular heartbeat, dizziness, weakness, breathing difficulty, gastric distress and numbness or swelling of extremities Taking medication on time as prescribed by the physician, not skipping a dose or doubling a dose, NOT discontinuing the medication, even, if the patient is feeling well, without consulting the physician first 29 29. PATIENT EDUCATION Rising slowly from reclining position to reduce lightheaded feeling, Taking care in driving a car or operating machinery if medication causes drowsiness. Potentiation of adverse side effects by alcohol, esp dizziness, weakness, sleepiness and confusion, Reduction or cessation of smoking to help lower blood pressure 30 PATIENT EDUCATION 30. PATIENT EDUCATION Importance of diet in control of blood pressure , following the physicians instructions regarding appropriate diet for the individual, which may include a low-salt diet or low sodium or weight reduction diet if indicated. Avoiding hot rubs and hot showers, which may cause weakness or fainting. Mild exercise on a regular basis as approved by the physician. 31 PATIENT EDUCATION 31. SHERYL RAY YANG, MD FEU-NRMF MEDICAL CENTER Fairview, Quezon City Tel no. 312-1234 Name:________________ Date: _______________ Age:_____ Sex:_____ Address: __________________ Telmisartan 40 mg tablet # 7 (Micardis) Sig. Take 1 tablet of Telmisartan daily for the control of Hypertension. Follow up after 7 days. Sheryl Ray B. Yang, M.D. Lic. No. 3333_________ PTR no. 101010_______ 32. JUSAY , ARKEE REYLO P. 33. Diabetes Diagnosed as DM type 2 for 5 years. Fasting glucose level of o f 210 mg/ dl (Normal is 126 mg/dL/ 7 mmol/L) HbA1C level of 7.2% (Normal for the patient is less than 7 %) 34. Treatment Goals 1. Lower the fasting glucose level less than 130 mg/dL. 2. Lower the HbA1c level to 6.5-6.9 % in 3 months. 3. Follow a versatile diet in relation to patient preference. 4. Maintain the therapeutic glucose level for a long term and educate the patient for glucose monitoring. 5. Develop a routine exercise for the patient. 35. Pharmacologic Intervention Management of hyperglycemia in type 2 Diabetes: A patient-centered Approach A position statement of the American Diabetes Association (ADA) and the European association for the study of Diabetes (EASD) PUBLISHED: APRIL 19, 2012 36. 1. Classify the patient if its type 1 DM or type 2 -DM type 2 2. FBS level and HbA1c level? - FBS- 210 mg/dL and HbA1c level of 7.2 % 3. Age of the patient and other pertinent data? -59 years old 37. DRUG/DRUG CLASS EFFICACY SAFETY SUITABILITY COST METFORMIN +++ + ++ ++++ SULFONYLUR EAS (GLYBURIDE) ++++ +++ +++ ++++ THIAZOLIDINED IONES (PIOGLITAZONE) ++ + + + MEGLITINIDES (REPAGLINIDE) +++ ++ ++ + a- GLUCOSIDASE INHIBITORS ++ +++ ++ ++ DPP-4 INHIBITORS ++++ ++ ++ + 38. ARKEE REYLO P. JUSAY, MD FEU-NRMF MEDICAL CENTER Sta Mesa, Manila Tel no. 312-1234 Name:________________ Date: _______________ Age:_____ Sex:_____ Address: __________________ Glyburide 5 mg tablet # 7 (Micardis) Sig. Take 1 tablet of Glyburide daily for the control of Hyperglycemia. Follow up after 7 days. ARKEE REYLO P. JUSAY, M.D. Lic. No. 3333_________ PTR no. 101010_______ 39. Non-pharmacologic intervention Diet modification. Develop a regular exercise. 40. DRUG CLASS MOA EFFECTS CLINICAL APPLICATIO NS Amiodarone Class III antiarrhythmi c K+ Channel blocker Beta adrenoreceptor and Ca Blocker Na channel blockage Prolongs atrial and ventricular repolarization slows heart rate and AV node conduction Slow intraventricula r conduction Ventricular arrhythmias, tachycardia, atrial fibrillation Furosemide Loop Diuretic Inhibition of the Na/K/2Cl transporter in the ascending limb of Henles loop Increased excretion of salt and water; reduces cardiac preload and afterload, reduces pulmonary and peripheral edema Acute & chronic heart failure, severe hypertension, edematous conditions 41. DRUG CLASS MOA EFFECTS CLINICAL APPLICATIO NS (Avandia) Rosiglitazon e thiazolidinedio ne (TZD) Bind and stimulate the nuclear hormone receptor peroxisome proliferator activated receptor- (PPAR) increasing insulin sensitivity in adipose tissue, liver, and muscle Diabetes Mellitus type 2 Spironolacto ne Aldosterone Antagonist (Potassium sparing) Blocks cytoplasmic aldosterone receptors in collecting tubules of nephron Decreased salt and water retention; reduces cardiac remodeling and mortality Chronic heart failure, aldosteronism , hypertension, adrenal tumor Carvedilol Sympatholytic mixed alpha- and beta-adrenergic blockers Prevents sympathetic cardiac stimulation, reduce renin secretion Hypertension, heart failure 42. DRUG CLASS MOA EFFECTS CLINICAL APPLICATIO NS (Coumadi n) Warfarin Oral Anticoagu lant inhibits synthesis of biologically active coagulation factors II, VII, IX, and X and anticoagulant proteins C and S Reduces formation of blood lots Prophylaxis for thrombosis and thrombo- embolism Digoxin Cardiac Glycoside Na+, K+ ATPase inhibition positive inotropy increase parasympathetic (vagal) tone prolong effective refractory period and slow conduction velocity Heart failure, Atrial fibrillation 43. DRUG INTERACTIO 44. Carvedilol Warfarin Furosemide Amiodarone Management: Additive effects of severe bradycardia, cardiac arrest, ventricular fibrillation Clinical monitoring of patient hemodynamic status and response is recommended. Increased effects of Warfarin 30% to 50% reduction in anticoagulant dosage has been recommended, in addition to frequent monitoring of the patient and the prothrombin time or INR. Additive arrythmogenic potential; Amiodarone causes dose-related prolongation of QT interval Coadministration of amiodarone with medications that can cause potassium and/or magnesium disturbances should generally be avoided 45. Amiodarone Carvedilol Furosemide Spironolacto ne Digoxin Manage ment may increase serum digoxin concentration s by up to 100% Empirical reduction of digitalis dosage by one-third to one-half should be considered decreases AV nodal conduction; increase the risk of developing bradycardia Serum digoxin levels, heart rate, and blood pressure should be monitored closely. diuretic-induced hypokalemia and hypomagnesemi a may predispose patients on digitalis to arrhythmias. Digoxin, potassium and magnesium levels should be followed closely. Spironolactone may reduce the tubular secretion of digoxin. patient should be monitored for signs and symptoms of digoxin toxicity 46. Spironolactone Furosemide Coumadin (Warfarin) Management Spironolactone may cause diuresis and hemoconcentration of clotting factors. The effects of some anticoagulants may be decreased. The INR or PT should be monitored, and oral coagulant dosage should be increased as needed. Loop diuretics may displace warfarin from plasma protein binding sites. Plasma warfarin concentrations and warfarin effects may be increased. Close monitoring of the INR is recommended, particularly if diuretic dosage must be high. 47. DRUG CLASS MOA EFFECTS CLINICAL APPLICATIO NS Amiodaron e Class III antiarrhythmi c K+ Channel blocker Beta adrenoreceptor and Ca Blocker Na channel blockage Prolongs atrial and ventricular repolarization slows heart rate and AV node conduction Slow intraventricula r conduction Ventricular arrhythmias, tachycardia, atrial fibrillation Furosemide Loop Diuretic Inhibition of the Na/K/2Cl transporter in the ascending limb of Henles loop Increased excretion of salt and water; reduces cardiac preload and afterload, reduces pulmonary and peripheral edema Acute & chronic heart failure, severe hypertension, edematous conditions 48. DRUG CLASS MOA EFFECTS CLINICAL APPLICATIO NS (Avandia) Rosiglitazon e thiazolidinedione (TZD) Bind and stimulate the nuclear hormone receptor peroxisome proliferator activated receptor- (PPAR) increasing insulin sensitivity in adipose tissue, liver, and muscle Diabetes Mellitus type 2 Spironolact one Aldosterone Antagonist (Potassium sparing) Blocks cytoplasmic aldosterone receptors in collecting tubules of nephron Decreased salt and water retention; reduces cardiac remodeling and mortality Chronic heart failure, aldosteronism , hypertension, adrenal tumor Carvedilol Sympatholytic mixed alpha- and beta-adrenergic blockers Prevents sympathetic cardiac stimulation, reduce renin secretion Hypertension, heart failure 49. DRUG CLASS MOA EFFECTS CLINICAL APPLICATIO NS (Coumadi n) Warfarin Oral Anticoagu lant inhibits synthesis of biologically active coagulation factors II, VII, IX, and X and anticoagulant proteins C and S Reduces formation of blood lots Prophylaxis for thrombosis and thrombo- embolism Digoxin Cardiac Glycoside Na+, K+ ATPase inhibition positive inotropy increase parasympathetic (vagal) tone prolong effective refractory period and slow conduction velocity Heart failure, Atrial fibrillation 50. DRUG INTERACTIO 51. Amiodarone Carvedilol Furosemide Spironolacto ne Digoxi n Manage ment may increase serum digoxin concentration s by up to 100% Empirical reduction of digitalis dosage by one-third to one-half should be considered decreases AV nodal conduction; increase the risk of developing bradycardia Serum digoxin levels, heart rate, and blood pressure should be monitored closely. diuretic-induced hypokalemia and hypomagnesemi a may predispose patients on digitalis to arrhythmias. Digoxin, potassium and magnesium levels should be followed closely. Spironolactone may reduce the tubular secretion of digoxin. patient should be monitored for signs and symptoms of digoxin toxicity 52. Spironolactone Furosemide Coumadin (Warfarin) Management Spironolactone may cause diuresis and hemoconcentration of clotting factors. The effects of some anticoagulants may be decreased. The INR or PT should be monitored, and oral coagulant dosage should be increased as needed. Loop diuretics may displace warfarin from plasma protein binding sites. Plasma warfarin concentrations and warfarin effects may be increased. Close monitoring of the INR is recommended, particularly if diuretic dosage must be high. 53. Warfarin Glyburide Management sulfonylureas may enhance or reduce the hypoprothrombinemic response to oral anticoagulants The patient should be monitored for altered anticoagulation (PT/INR) and altered glycemic effect spironolactone Telmisartan Management may increase the risk of hyperkalemia Caution is advised if angiotensin II receptor blockers must be used concurrently with potassium-sparing diuretics