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CHAPTER • 21



                               Fluid and Diuretic Therapy in

                               Heart Failure



                               John D. Bonagura, Linda B. Lehmkuhl, and Helio Autran de Morais







            Congestive heart failure (CHF) is a clinical syndrome  THE NORMAL CIRCULATION
            characterized by cardiac dysfunction, abnormal hemody-
            namics, neurohormonal activation, release of cytokines,  The central circulation is regulated largely by a need to
            and renal retention of sodium and water. A cardiac or vas-  maintain plasma volume, mean ABP, and tissue perfusion.
            cular lesion that limits cardiac output and decreases arte-  Of prime importance is the maintenance of normal effec-
            rial blood pressure (ABP) triggers heart failure, leading to  tive plasma volume and ABP in the central circula-
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            a homeostatic state that is characterized by vasoconstric-  tion.  These two variables depend on cardiac
            tion and renal sodium retention. The stereotypical com-  output, systemic vascular impedance, and renal regula-
            pensatory responses to heart failure support ABP but also  tion of sodium and water excretion. The reflexes that con-
            promote a maladaptive state that leads to substantial mor-  trol the circulation have evolved so that blood pressure
            bidity and mortality.                                and plasma volume are maintained within a narrow range
               Advanced CHF, as well as the therapy of this syndrome,  even in the presence of sudden physiologic stresses, such
            often is associated with alterations in renal function and a  as exercise, hypotension, or hemorrhage. Blood pressure
            variety of fluid, electrolyte, and serum biochemical  and plasma volume are monitored by different mechanor-
            abnormalities. Some of these disturbances are mild and  eceptors and osmoreceptors located in the arteries, veins,
            seemingly well tolerated, but others, such as hyponatremia  heart, kidney, and central nervous system. Ultimately,
            and acute renal failure, indicate severe circulatory dysfunc-  two factors—cardiac output and systemic vascular resis-
            tion and a need for urgent therapy. 75  There are    tance (more precisely, vascular resistance and arterial
            circumstances in which cardiac patients actually require  impedance)—determine ABP (Figure 21-1). A change
            fluidtherapytomaintainoptimalventricular fillingandpre-  in either one of these two variables causes a parallel
            vent deterioration of renal function. However, it is more  change in blood pressure. Numerous physiologic
            common for fluid therapy to produce edema or effusions  variables can affect cardiac output and vascular impedance
            inapreviouslycompensatedcardiacpatient.Saferestoration  (Box 21-1), and many of these factors are perturbed in
            of fluidandelectrolytebalanceinthepatientwithcardiovas-  CHF. Of particular relevance in this chapter are
            cular disease is challenging. To orchestrate such treatment,  determinants of plasma volume in health and disease
            the clinician must appreciate the pathophysiology of heart  (Box 21-2). Plasma volume is a major contributor to
            failure and the compensatory changes that develop. This  venous pressure and cardiac filling. The serum sodium
            chapter addresses some of the clinically relevant pathophys-  concentration, as described more fully in Chapter 3, plays
            iologic and therapeutic aspects of heart failure.    a central role in determining plasma volume. Renal tubu-
               Much of our understanding of hemodynamics, renal  lar activity, vascular dynamics, hormones, and other vaso-
            function, and neurohumoral activity in heart failure stems  active factors regulate sodium balance. Abnormalities of
            from many experimental studies in dogs and from a lim-  sodium excretion are pivotal to the development of CHF.
            ited number of clinical investigations of dogs and cats  Attention also must be directed to the microcircula-
            with spontaneous heart disease. However, studies of fluid  tion and factors controlling fluid movement across
            therapy in spontaneous CHF in dogs and cats are largely  capillaries. Tissue perfusion is crucial for organ functions
            unavailable. Accordingly, the recommendations offered  such as the formation of urine, muscle contraction, and
            here represent our interpretation of relevant animal stud-  exchange of oxygen and carbon dioxide. Assuming the
            ies and personal experience with the treatment of dogs  maintenance of adequate mean ABP, regional vascular
            and cats with CHF.                                   resistance largely governs tissue perfusion across the



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