Heart Failure Pharmacotherapy Course 1 PDF

Chronic Heart Failure (CHF) Pharmacotherapy Course 1 Updates in Therapeutics® 202 3 and pharmacotherapy handbook 11th : HEART FAILURE  Chapter Outline Definition Etiology Pathophysiology Clinical Manifestation Diagnosis HF classification system Treatment Learning Objec...

Chronic Heart Failure (CHF) Pharmacotherapy Course 1 Updates in Therapeutics® 202 3 and pharmacotherapy handbook 11th : HEART FAILURE  Chapter Outline Definition Etiology Pathophysiology Clinical Manifestation Diagnosis HF classification system Treatment Learning Objectives Recommend patient-specific pharmacologic therapy for the management of chronic heart failure, HFrEF Definition  Heart Failure Heart failure is a complex (progressive) clinical syndrome caused by any structural or functional cardiac disorder that impairs the ability of the ventricle to fill or eject blood -The term “heart failure” is preferred over “congestive heart failure” because not all the patients are presented with volume overload. Ejection fraction; EF EF is a measurement of the percentage of blood leaving your heart each time it contracts. EF is usually measured only in the left ventricle (LV). An LV ejection fraction of 55 percent or higher is considered normal. Heart failure with reduced ejection fraction  ’ (HFr EF). EF ≤ 40%. Previously known as systolic HF Heart failure with preserved ejection fraction ’ (HFp EF). EF ≥ 50%.  HFrEF etiology The leading causes of HF are coronary artery disease and hypertension. ACCP 2023 d. One third of cases are attributable to nonischemic cardiomyopathy. vi. Myocarditis vii. Idiopathic viii. Tachycardia ix. Peripartum  HFr EF; causes / etiology Heart failure with reduced ejection fraction (HFrEF)  LVEF < 40%  Etiology Any condition that place a great demand on the heart will result in Heart Failure, as: 1. Hypertension./ Obesity 2. Coronary Heart Disease. Two thirds of cases due to (CHD)/IHD 3. Aortic stenosis. / Stress (Takotsubo). 4. Hyperthyroidism. / Severe anemia. 5. Cardiotoxins, (a) Alcohol, (b) Cocaine (c) Chemotherapeutic agents HFrEF Pathophysiology Pathophysiology CO = HR(heart rate) ×SV CO: cardiac output: volume of blood ejected per unit time. SV: Stroke Volume: the volume of blood ejected with each systole. Causes of systolic dysfunction (decreased contractility) include HFrEF Clinical Presentation Patient presentation may range from asymptomatic to cardiogenic shock.  Clinical presentation Primary symptoms are ’ dyspnea (especially on exertion) and ’ fatigue, which lead to exercise intolerance. Other pulmonary symptoms include ’ orthopnea, paroxysmal nocturnal dyspnea (PND), tachypnea, and cough. ’ Fluid overload can result in pulmonary congestion and peripheral edema. 14  Clinical presentation Nonspecific symptoms may include ’ fatigue, ’ nocturia, ’ hemoptysis, ’ abdominal pain, ’ anorexia, nausea, bloating, ’ ascites, poor appetite or early ’ satiety, and weight gain or loss.. 15  HFrEF Diagnosis Assessment of fluid status. Assessment of ejection fraction (usually 50% (filling problem)  Same medications – none have shown mortality benefit  Control BP and volume overload  Case #1 Ms. L is a 75 years old with heart failure (NYHA III) and arterial fibrillation. Ms. L is on Captopril 100mg, Bisoprolol 10 mg and Furosemide 40 mg. The patient has orthopnea and cannot sleep at night (BP : 125/80 and HR : 57) , The best management for this patient is : Case #1 Which of the following is the best approach to maximize the management of her heart failure? Increase the dose of Bisoprolol to 25 mg Bid. Add Hydrochlorothiazide 12.5 mg. Add Digoxin 0.125 mg Add Ivabradine 5 md BID.  Case #2 Patient with cardiac disease that result in marked limitation to physical activity and less than Ordinary activity results in fatigue and palpitation. Case # 2 The patient’s heart failure classification is NYHA I and ACC\AHA B NYHA II and ACC\AHA B NYHA III and ACC\AHA C NYHA II and ACC\AHA C HF case 2 2. J.T. is a 62-year-old man (height 72 inches, weight 85 kg) with a history of CHD (MI 3 years ago), HTN, depression, chronic kidney disease (CKD; baseline SCr 2.8 mg/dL), PAD, osteoarthritis, hypothyroidism, and HF (LVEF of 25%). His medications include aspirin 81 mg/day, simvastatin 40 mg every night, enalapril 5 mg twice daily, metoprolol succinate 50 mg/day, furosemide 80 mg twice daily, cilostazol 100 mg twice daily, acetaminophen 650 mg four times daily, sertraline 100 mg/day, and levothyroxine 0.1 mg/day. His vital signs include BP 120/70 mm Hg and HR 72 beats/minute. Pertinent laboratory results include K 4.1 mEq/L, SCr 2.8 mg/dL, and a thyroid-stimulating hormone of 2.6 mIU/L. His HF is stable and considered NYHA class II. What is the best approach for maximizing the management of his HF? A. Discontinue metoprolol and begin carvedilol 12.5 mg twice daily. B. Increase enalapril to 10 mg twice daily. C. Add spironolactone 25 mg/day. D. Add digoxin 0.125 mg/day. Role in Heart Failure Self reading Diuretics Short-term benefits (days)  Decreased jugular venous distension  Decreased pulmonary congestion  Decreased peripheral edema Intermediate-term benefits (weeks to months)  Decreased daily symptoms  Improved cardiac function  Increased exercise tolerance Long-term benefits (months to years):  No affect on mortality  EVALUATION OF THERAPEUTIC OUTCOMES Self reading ’ Chronic Heart Failure 1. Ask patients about the presence and severity of symptoms and how sym ptoms affect daily activities. 2. Evaluate efficacy of diuretic treatment by disappearance of the signs an d symptoms of excess fluid retention. Focus the physical examination o n body weight, extent of JVD, presence of HJR, and presence and severit y of pulmonary congestion (crackles, dyspnea on exertion, orthopnea, and PND) and peripheral edema. 3. Other outcomes are improvement in exercise tolerance and fatigue, de creased nocturia, and decreased HR.  EVALUATION OF THERAPEUTIC OUTCOMES Self reading ’ Chronic Heart Failure 1. Monitor BP to ensure that symptomatic hypotension does not develop as a result of drug therapy. 2. Body weight is a sensitive marker of fluid loss or retention, and patients should weigh themselves daily and report changes of 3–5 lb (1.4– 2.3 kg) to their healthcare provider so adjustments can be made in diuretic doses. 3. Symptoms may worsen initially on β- blocker therapy, and it may take weeks to months before patients notic e symptomatic improvement. 4. Routine monitoring of serum electrolytes (especially potassium and ma gnesium) and renal function (BUN, serum creatinine, eGFR) is mandat ory in patients with HF Role in Heart Failure Self reading ACEI  Decreased mortality 25-50% RRR  Decreased hospitalizations ~ 30%  Improved symptoms  Improved quality of life Beta Blocker  Decreased mortality ~ 35% RRR  Decreased hospitalizations ~25% relative risk reduction  Symptom improvement  Improved ejection fraction RRR; relative risk reduction  Self reading ’ HR: is controlled via autonomic nervous system and stimulated via the β-adrenergic receptors. ’ SV: is determined via: - Preload: ventricular filling pressure or the volume of blood in the left ventricle. And it’s determined via: venous return and contractility. - Afterload: the resistance to ventricular ejection. Regulated via: ejection impedance, wall tension, regional wall geometry. - Contractility: influenced by: adrenergic activity and 67 circulating catecholamines.  Self reading Left-sided failure: The blood can not be adequately pumped from LV to periphery  accumulates within the LV  unable to accept further blood from LA and lungs  blood backs up into lungs (pulmonary alveoli)  pulmonary edema. Right-sided failure: The blood can not be pumped from RV to lungs accumulates in the RV  blood backs up throughout the body (veins, legs, bowels)  systemic edema. Self reading  HFrEF Algorithm; ACCP 2020 Figure 1. Algorithm for pharmacologic management of heart failure with reduced ejection fraction. Guideline directed treatment algorithm for patients with ACC/AHA stage C heart failure with reduced ejection fraction. o. Other medication therapies; treating HF i. Anticoagulation (a) Recommended for HF with permanent, persistent, or paroxysmal AF with an additional risk factor for stroke (no preference on agent) (b) Reasonable for patients with HF who have permanent, persistent, or paroxysmal AF without an additional risk factor for stroke (c) Not recommended in the absence of AF, prior stroke, or a cardioembolic source ii. Statins: Not recommended solely on the basis of HF diagnosis iii. Antiarrhythmics: Given the neutral effects on mortality, the preferred antiarrhythmics in patients with HFrEF are dofetilide (AF/atrial flutter) and amiodarone. iv. Nondihydropyridine (DHP) calcium channel blockers (CCBs) with negative inotropic effects can be harmful in patients with a low EF and should be avoided (class III recommendation: harm). v. DHP CCBs: DHP CCBs have no proven benefit on morbidity or mortality in HF. Use of amlodipine can be considered for HTN or ischemic heart disease management in HF patients because of its neutral effects on morbidity and mortality. p. Device therapy i. Implantable cardioverter defibrillator recommended for primary prevention of sudden cardiac death in the following patients with ischemic or nonischemic HFrEF: (a) Patients with ischemic or nonischemic HFrEF (LVEF of 35% of less) and NYHA class II or III symptoms on chronic optimal medical therapy. Life expectancy should be greater than 1 year, and patient must be at least 40 days post-MI (class I indication). (b) Patients with HFrEF (LVEF of 30% or less) resulting from previous MI and NYHA class I symptoms on chronic optimal medical therapy. Life expectancy should be greater than 1 year, and patient should be at least 40 days post-MI (class I indication). ii. Chronic resynchronization therapy recommended for those with an LVEF of 35% or less, in SR, and a left bundle branch block with a QRS of 150 milliseconds or greater on optimal medical therapy with NYHA class II–III symptoms or NYHA class IV with ambulation