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Beyond the Four Quadrants: The Critical and Emerging Role of Impedance Cardiography in Heart Failure
Author(s) -
Strobeck John E.,
Silver Marc A.
Publication year - 2004
Publication title -
congestive heart failure
Language(s) - English
Resource type - Journals
eISSN - 1751-7133
pISSN - 1527-5299
DOI - 10.1111/j.1527-5299.2004.03405.x
Subject(s) - medicine , hemodynamics , heart failure , cardiology , impedance cardiography , aldosterone , pulmonary artery , endothelial dysfunction , stroke volume , ejection fraction
John E. Strobeck, MD, PhD;1 Marc A. Silver, MD,2 Co-Editors in Chief From the Heart-Lung Center, Hawthorne, NJ;1 and the Department of Medicine and the Heart Failure Institute, Advocate Christ Medical Center, Oak Lawn, IL2 Address for correspondence: Marc A. Silver, MD, Advocate Christ Medical Center, 4440 West 95th Street, Suite 428 South, Oak Lawn, IL 60453-2600 E-mail: marc.silver@advocatehealth.com Heart failure (HF) is a disorder characterized by hemodynamic abnormalities including a reduction in the heart’s ability to deliver oxygenated blood to the body. HF is also associated with important neurohormonal abnormalities, including activation of the renin-angiotensin-aldosterone and sympathetic nervous systems and their resulting effects on the heart and vascular endothelium. Our understanding of the neurohormonal role in the progression of HF has greatly improved in the past 10 years,1 and many of the therapies that significantly improve the symptoms and prognosis of patients with HF now target the underlying neurohormonal abnormalities. As shown in Figure 1, neurohormonal activation can lead to progression of hemodynamic abnormalities resulting in reduced cardiac output (CO); increased filling pressures; and ultimately worsening symptoms of fatigue, dyspnea, and decreased exercise tolerance. Although the neurohormonal mechanisms may cause progression of the disease process, nearly all medications used in HF treatment have demonstrable effects on hemodynamics. Current acute HF treatment is aimed directly at stabilizing and improving a patient’s short-term hemodynamic condition; chronic HF treatments can alter short-term and improve long-term hemodynamics. Specific hemodynamic measurements such as CO and systemic vascular resistance are generally obtained for only the most critically ill HF patients, in large part due to the risk, discomfort, and cost of invasive procedures such as pulmonary artery catheterization.2 Nonetheless, understanding and measuring the factors that affect CO are central to the assessment, prognosis, and treatment of patients with HF. The four determinants of CO are the rate of the pump (heart rate), the volume of blood available to pump (preload), the pumping strength (contractility), and the force the heart must overcome to pump (afterload, generally approximated by systemic vascular resistance). Symptoms— physical findings like vital signs—and laboratory findings such as blood tests and chest radiographs are imprecise measures of hemodynamic function. Unfortunately, they are the only data many clinicians have at their disposal when making important decisions in the care of patients with HF. The direct cost of treating HF is estimated to be $56 billion per year in the United States3 and the number of HF patients in this country may reach 10 million by 2010.4 A significant portion of the cost of HF care is the high cost of hospitalizations for patients with acute decompensation. Through careful surveillance of patients with chronic HF using improved methods for measuring hemodynamic and neurohormonal www.lejacq.com ID:3405

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