Drug Topics - June 16, 2008 - (Page 45)

45 Etiology and pathophysiology Heart failure results from conditions that affect the heart’s ability to contract normally. These are primarily represented by ischemic and hypertensive diseases with a predominance of systolic HF (decreased contractility). The body typically responds to this problem via compensatory mechanisms. Symptoms do not typically develop until the compensation methods are no longer capable of maintaining adequate cardiac function. As function continues to decrease, a number of central and peripheral mechanisms attempt to preserve performance of the heart. Results of this compensation include enhanced neurohormonal stimulation, cardiac hypertrophy, and recruitment of preload reserve. Although initially helpful, these processes become unfavorable over time and contribute to further deterioration of cardiac function. Neurohormonal processes thought responsible for the damage of normal heart function include the reninangiotensin-aldosterone system (RAAS), sympathetic nervous system, natriuretic peptide system, vasopressin, endothelin, and various cytokines. Targeting these mechanisms helps slow the progression of HF and preserve cardiac function. GOAL To provide pharmacists with an overview of heart failure and optimal drug therapy management OBJECTIVES Upon completion of this article, the pharmacist should be able to: 1. Demonstrate an understanding of the pathophysiology, incidence, presentation, and diagnosis of heart failure (HF). 2. Exhibit an understanding of standard drug therapy and each drug’s role in the treatment of HF. 3. Evaluate and modify drug therapy regimens in patients with chronic HF and recognize symptoms of HF exacerbations. 4. Assess the significance of non-pharmacological options for optimizing control of the disease. To receive credit you must score 70% or higher on the quiz and complete the evaluation. Upon successful completion, the University of Florida College of Pharmacy will mail Statements of Credit for written quizzes within 10 working days. Participants completing the program online may print a Statement of Credit after successfully completing the program. Clinical presentation, diagnosis, and classification Patients with HF present with symptoms ranging from cardiogenic shock in an acute decompensation state to completely asymptomatic, depending on the severity of the HF. In general, however, many patients initially present with fatigue and dys- and family history. Laboratory tests help rule out other causes of pnea. This can then lead to exercise intolerance and fluid over- symptoms. For example, a complete blood count may identify load, possibly resulting in peripheral edema and/or pulmonary anemia or infection; a cardiac injury panel differentiates HF congestion. Other symptoms reported include orthopnea (in- from ischemic injury; and B-type natriuretic peptide (BNP), creased pillow use) and paroxysmal nocturnal dyspnea (sudden a hormone marker commonly seen in HF, may help confirm and severe shortness of breath while sleeping). Symptoms vary the presence of HF. Chest x-rays and EKGs additionally help in each individual patient over rule out infection and ischemic or dysrhythmia causes respectively. time depending on how well the Table 1 underlying causes are managed. Echocardiograms assess left venNYHA functional classes for HF As exercise intolerance and dystricular ejection fraction (LVEF) to NYHA Class Patient symptoms pnea occur for a variety of reasons, determine systolic versus diastolic diagnosis of HF presents many dysfunction (or HF with a preClass I No limitations in physical activity challenges. In patients with wellserved LVEF). due to HF Classification is based on padocumented risk factors and heart Class II With ordinary exertion tient severity and progression of disease, diagnosis of HF is often Class III With less than ordinary exertion the underlying disease. Two difsuspected and evaluated sooner Class IV At rest ferent systems are currently used. than those without known risk The New York Heart Association factors. No single test determines the presence of HF creating additional challenges for proper (NYHA) evaluates the functional status based on patient sympdiagnosis. Physical examination and patient history comprise toms and activity level. Classes range from I-IV, with IV being the initial evaluation of patients suspected to have HF. Initial the most symptomatic (Table 1). The NYHA designation does laboratory tests, echocardiograms, chest x-rays, and electrocar- not change, however, based on ejection fraction or response to diograms (EKGs) further assist with diagnosis. Physical exami- therapy. As this is based on symptoms, patients do not continue nation may be used to detect peripheral and pulmonary edema, to progress from one class to another, but fluctuate between jugular venous distention (JVD), hepatojugular reflux, and classes. In 2001, the ACC/AHA recognized the limitations of hepatomegaly, all possible signs of HF. Patient history becomes using this classification system and developed a staging system important to assess risk factors, symptoms, past medication use, based on risk factors as well as progression of the disease. Pa-

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Drug Topics - June 16, 2008 Contents Latebreakers Letters Latebreakers in Depth Pharmacists Lose in Final ESRD Rule New Drug Helps Palliative Patients on Opioids Take Care of Business Oral Treatment Reduces Multiple Sclerosis Flare-ups Beware of Inflammatory Masses From Implantable Infusion Systems Safer Therapeutic Options Emerging for Atrial Fibrillation Congressional Committee Chair Calls for Action Against Hospital Infections This Software System Helps Hospitals Manage Anticoagulation Therapy Rx Care Community Practice JP at Large Self-Care Cover Story Long-Term Care Chains and Business Technology Technology Update Continuing Education New Products Advertisers Index Classified Viewpoint

Drug Topics - June 16, 2008

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