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Heart Failure Lior Ness 19.2.2009 4th year Medical Student Sackler Medical School, Tel-Aviv University Internal Medicine Department Sheba Medical Center ISRAEL Definition Heart failure is a clinical syndrome that occurs in patients who develop a constellation of clinical symptoms (dyspnea and fatigue) and signs (edema and rales) that lead to frequent hospitalizations, a poor quality of life, and a shortened life expectancy. In other words… Heart failure is a condition in which the heart is unable to pump blood at an adequate rate or volume. Epidemiology Overall prevalence of HF in developed countries is 2%, with over 20 million people affected worldwide. Prevalence rising with age: 6-10% of people over 65. Although the relative incidence of HF is lower in women than in men, women constitute 50% of cases because of their longer life expectancy. Prognosis is poor: 30-40% of patients die within 1 year of diagnosis and 60-70% die within 5 years, mainly from worsening HF or as a sudden event. Pathogenesis Etiologies Any condition that leads to an alteration in LV structure or function can predispose a patients to developing HF. In most cases, patients remain asymptomatic following the initial decline in pumping capacity of the heart. LV dysfunction is necessary for the pathogenesis of HF, but not sufficient. Etiologies Pathogenesis- compensatory mechanisms (1) Renin-Angiotensin-Aldosterone (RAA) Adrenergic nervous system Increased myocardial contractility Vasodilatory molecules: ANP, BNP, prostaglandins, NO Pathogenesis- compensatory mechanisms (2) LV function is modulated so that the functional capacity of the patient is preserved. Patients may remain asymptomatic for a period of years. At some point, patients become overtly symptomatic, with a striking increase in morbidity and mortality. The exact mechanisms that are responsible for this transition are not fully understood, but involve activation of neurohormonal (NE, angiotensin II), adrenergic and cytokine systems that lead to a series of adaptive changes within the myocardium, known as LV remodeling. LV Remodeling Myocytes hypertrophy and alterations in the contractile properties and metabolism. Progressive loss of mycotes through necrosis and apoptosis. ß-adrenergic desensitization. Reorganization of the extracellular matrix. LV Remodeling may contribute independently to the progression of HF due to changes in LV geometry Clinical Manifestations Symptoms Fatigue – Mechanism: low cardiac output. Noncardiac comorbidities (e.g. anemia) also contribute. Dyspnea – Mechanism: pulmonary congestion with accumulation of interstitial or intra-alveolar fluid. – In early stages, observed only during exertion. Orthopnea is a later manifestation, often accompanied by nocturnal cough or paroxysmal nocturnal dyspnea (PND). – In advanced HF: Cheyne-Stokes respirations, acute pulmonary edema. Symptoms cont. Gastrointestinal symptoms: anorexia, nausea, and early satiety associated with abdominal pain and fullness. – May be related to edema of the bowel and/or congested liver. Cerebral symptoms (confusion, disorientation, sleep and mood disorders) in severe HF. Nocturia. Physical Examination General Appearance and Vital Signs – In mild to moderate HF: no distress at rest, but patient uncomfortable when lying flat for more than few minutes. In more severe HF, patient must sit upright and may have labored breathing. – Blood pressure usually reduced due to LV dysfunction (but can be normal/high in early stages). Pulse pressure may be diminished (reduction in stroke volume). – Adrenergic activity: sinus tachycardia, peripheral vasoconstriction and cyanosis. – With severe chronic HF, there may be marked cachexia and weight loss. Physical Examination cont. JVP – Increased. In early stages, JVP may be normal at rest but may become abnormally elevated with sustained pressure on the abdomen (positive abdominojugular reflux). Pulmonary Examination – When present in patients without concomitant lung disease, crepitations are specific to HF. – Pleural effusion. Physical Examination cont. Cardiac Examination – If cardiomegaly present, PMI displaced. – In some patients S3 is audible, most commonly in patients with volume overload. – S4 is not specific but usually present in patients with diastolic dysfunction. Abdomen – Hepatomegaly, ascites. Extremities – Peripheral edema (usually absent in patients treated adequately with diuretics). Edema is symmetric, dependent and pitting. Diagnosis of HF Diagnosis is relatively straightforward when the patient presents with classic signs and symptoms; however, the signs and symptoms of HF are neither specific nor sensitive. Diagnosis ECG – LV hypertrophy, prior MI. Chest X-ray – Cardiac size and shape. Assessment of LV function – Echocardiogram, MRI (gold standard). – The most useful index of LV function: Ejection Fraction (EF). Biomarkers – BNP, troponin, CRP Exercise Testing – Not routinely used for every patient, but useful for assessing the need for cardiac transplantation. – Measures peak oxygen uptake (VO2). Differential Diagnosis Conditions with circulatory congestion secondary to abnormal salt and water retention (e.g. renal failure). Noncardiac causes of pulmonary edema (e.g. ARDS). Treatment Progression of HF Stage A: Patients who are at risk for developing HF but without structural heart disease or symptoms (e.g. diabetic, hypertensive). Stage B: Patients who have structural heart disease but without symptoms of HF (e.g. previous MI). Stage C: Patients with structural heart disease and symptoms of HF (dyspnea and fatigue) Stage D: Patients with refractory HF requiring special interventions (e.g. cardiat transplantation). Every effort should be made to prevent HF by treating the preventable causes (hypertension). Patients in stages B and C should be treated with drugs that prevent disease progression. NYHA Classification Once patients have developed structural heart disease, their therapy depends on their NYHA functional classification. NYHA Classification – Strategies Class I (asymptomatic): Slow disease progression by blocking neurohormonal systems that lead to LV remodeling. Class II-IV (symptomatic): Alleviate fluid retention, lessen disability, and reduce risk of further disease progression. – Usually treated with diuretics and neurohormonal interventions. Treatment of HF with Depressed Ejection Fraction (<40%) Physical activity is beneficial for patients with NYHA class I-III. Diet: Sodium restriction is recommended in all patients with HF. Diuretics – Should be initiated in low doses and then carefully titrated upward to relieve symptoms of fluid overload. Once the congestion has been relieved, treatment with diuretics should be continued to prevent recurrence of fluid retention. – Drug of choice: loop diuretics (fusid). Thiazides less potent and lose effectiveness in renal insufficiency. – Adverse effects: electrolyte and volume depletion, azotemia, increased neurohormonal activation and disease progression. Treatment (EF<40%) Preventing Disease Progression ACE Inhibitors – Should be used in both symptomatic and asymptomatic patients with a depressed EF. – Stabilize LV remodeling, improve symptoms, reduce hospitalization and prolong life. – Adverse effects: Decreased blood pressure, azotemia, hyperkalemia, nonproductive cough, angioedema. Angiotensin Receptor Blockers – Well tolerated in patients who are intolerant of ACE inhibitors because of cough, skin rash and angioedema. – Should be used in symptomatic and asymptomatic patients with EF<40%. – Same benefits as ACEI: Improve LV remodeling and prolong life. – Adverse effects: Same as ACEI- low blood pressure, impairs renal function, potassium retention. ß-Blockers – Interfere with the harmful effects of sustained activation of the adrenergic nervous system. Most of the deleterious effect is related to ß1 receptor. – Indicated for both symptomatic and asymptomatic patients with EF<40%. Initiated in low doses, then titrated slowly if well tolerated. – Adverse effects: Bradycardia, heart blocks, hypotension (especially in agents that also block α1), bronchospasm. Aldosterone Antagonists – Classified as potassium-sparing diuretics, but have beneficial effects that are independent of sodium balance. – In chronic ACEI therapy, aldosterone levels may return to levels similar to those before therapy. – Recommended for patients with NHYA IV or III with EF<35%, who are receiving standard therapy (diuretics, ACEI, beta-blockers). – Adverse effects: hyperkalemia (therefore not recommended if creatinine>2.5 mg/dl or serum potassium>5 meq/L), painful gynecomastia in 1015% of patients (eplerenone may be substituted). Algorithm for Treatment of HF Anticoagulation and Antiplatelet Therapy Patients with HF have an increased risk for arterial or venous thromboembolic events. The rate of stroke ranges from 1.3 to 2.4% per year. Depressed LV function is believed to promote relative stasis of blood in dilated cardiac chambers with increased risk of thrombus formation. Treatment with warfarin (goal INR of 2.0-3.0) is recommended for patients with HF and CAF or PAF, or with a history of emboli (including stroke and TIA). Aspirin is recommended in HF patients with ischemic heart disease for the prevention of MI. Management of HF with a preserved EF (>40-50%) Pathogenesis of HF with preserved EF not fully understood. Suggested: diastolic dysfunction, vascular and ventricular stiffness. There are no proven pharmacologic or device therapies. Treatment should be focused on the underlying disease process (e.g. MI, hypertension). Precipitating factors (e.g. tachycardia, AF) should be treated as quickly as possible. Dyspnea may be treated by sodium restriction, nitrates, ACEI, ARBs, and/or beta-blockers. Acute HF Acute HF – Precipitating Factors Factors that may precipitate acute decompensation in patients with chronic HF: – – – – – – – – – – – Dietary indiscretion MI Arrhythmias (tachy/brady) Discontinuation of HF therapy Infection Anemia Medications: CCB, beta-blockers, NSAIDs, antiarrythmic agents (class I agents, sotalol), anti-TNF Abs. Alcohol consumption Pregnancy Worsening hypertension Acute valvular insufficiency Management of Acute HF Stabilizing the hemodynamic derangements that provoked the symptoms. Treating reversible factors that precipitated decompensation (e.g. infection, arrythmias, dietary indiscretion, PE, IE, environmental and/or emotional stress, etc.). Reestablish an effective outpatient medical regimen that will prevent disease progression and relapse. Hemodynamic Derangements in Acute HF The two primary hemodynamic determinants of acute HF are: – Elevated LV filling pressure (may have signs of fluid retention). – Depressed cardiac output (usually accompanied by an increase in systemic vascular resistance). These two hemodynamic derangements may occur singly or together. The therapeutic approach to treating patients with acute HF should be tailored to reflect the patient’s hemodynamic presentation. Pharmacologic Management of Acute HF Vasodilators: Exert dilating effect on arterial resistance and venous capacitance, which results in a lowering of LV filling pressure. Improve CO without increasing heart rate. Inotropic agents: Stimulate cardiac contractility as well as peripheral vasodilation. Improve CO and reduce LV filling pressure. Vasoconstrictors: Support systemic blood pressure. The End