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Inpatient Management of Patients with Volume Overload and High Filling Pressures

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Inpatient Management of Patients with Volume Overload and High Filling Pressures REVIEW Inpatient Management of Patients with Volume Overload and High Filling Pressures Tariq Khan, MD The majority of patients with acute decompensated heart failure are admitted J. Thomas Heywood, MD with symptoms of congestion. The classic symptoms of ‘‘congestive’’ heart failure reflect fluid overload, that is, orthopnea, paroxysmal nocturnal dyspnea, and pe- Scripps Clinic, La Jolla, California. ripheral edema; these symptoms can be so dramatic that it is not surprising that patients seek hospitalization. Activation of the renin angiotensin system coupled with sympathetic hyperactivity results in marked sodium retention and high fill- ing pressures that ultimately bring about these congestive symptoms. The treat- ment goal of patients hospitalized with volume overload and high filling pressures is to improve symptoms by normalizing the filling pressure and volume status without worsening renal function. The current use of diuretics, vasodila- tors, and ultrafiltration, as well as potential future use of investigational agents such as oral vasopressin antagonists and adenosine A1-receptor antagonists, is surrounded by the important issues of when to stop intravenous therapy in hos- pitalized patients and the exact mechanism by which the filling pressures are normalized. New data from evidence-based clinical trials and optimal strategies for monitoring fluid overload will help define this issue and ultimately reduce mortality in these patients. Journal of Hospital Medicine 2008;3(Suppl 6):S25– S32. VC 2008 Society of Hospital Medicine. KEYWORDS: acute decompensated heart failure, ADHF, filling pressure, renal function, volume overload. lthough patients with left ventricular dysfunction may pres- A ent with low-output syndrome and even cardiogenic shock, the majority are admitted with symptoms of congestion.1 The classic symptoms of ‘‘congestive’’ heart failure reflect fluid over- load, that is, orthopnea, paroxysmal nocturnal dyspnea, and pe- ripheral edema; these symptoms can be so dramatic that it is not surprising that patients seek hospitalization.2 Activation of the renin angiotensin system coupled with sympathetic hyperac- tivity results in marked sodium retention and increased filling pressures in the right and left ventricle that ultimately bring about these congestive symptoms of dyspnea and orthopnea.3 Increased filling pressure precedes admission to the hospital, and filling pressure falls during successful therapy.4,5 Indeed, Tariq Khan did not receive an honorarium in sup- normalization of the left ventricular filling pressure much better 6 port of this work. predicts survival than improved cardiac output. However, de- spite the many advances in the evidence-based armamentarium J. Thomas Heywood received research support for heart failure, the one great deficiency in the evidence base is and editorial assistance from OptumHealth Edu- the lack of data on modalities that can reduce or normalize left cation through an educational grant from Otsuka American Pharmaceuticals and an honorarium ventricular filling pressures. This is not as unexpected as it from OptumHealth Education, in support of this seems because the symptoms of congestion are so dramatic work. and, until recently, the tools to mitigate were so few that rando- ª 2008 Society of Hospital Medicine S25 DOI 10.1002/jhm.396 Published online in Wiley InterScience (www.interscience.wiley.com). mized trials were difficult to conceive. However, aldosterone axis.20 Unfortunately, severe hyperka- the treatment paradigms for acute decompensated lemia remains a significant side effect and can heart failure (ADHF) management are changing, limit their use.21 and evidence-based mortality trials for filling pres- Despite the obvious beneficial effects of loop sure reduction and congestion relief continue to diuretics in the treatment of ADHF, we lack key evolve.7–10 fundamental information about these most fre- quently used drugs. For example, what is the cor- rect dose? Escalating the dose of diuretics has DIURETICS been associated with increased mortality in heart Mercurial diuretics were introduced in the 1920s failure even when corrected for the severity of the as the mainstay of therapy for ADHF; the loop illness.22,23 Proposed explanations for the diuretics became the foundation of therapy in the increased morality in patients with heart failure 1960s.11,12 In the Acute Decompensated Heart include activation of the renin-angiotensin-aldo- Failure National Registry database (ADHERE), 88% sterone system and sympathetic nervous system, of patients received intravenous loop diuretics decreases in the glomerular filtration rate (GFR) during their hospitalization.13 Loop diuretics act contributing to cardiorenal syndrome, and intra- in the thick ascending limb of the loop of Henle vascular volume contraction and decreased left to inhibit reabsorption of sodium and chloride by ventricular filling pressure worsening cardiac per- inhibiting the sodium, potassium, and chloride formance in patients without significant fluid 1 1 2 (Na /K /2Cl ) pump. This blockade causes retention.22,23 It is now recognized that kidney dys- increased delivery of these solutes to the distal function plays a vital role in the progress of convoluted tubule and collecting duct, resulting in patients with heart failure, and increases in serum a shift in the balance of osmotic forces toward creatinine or blood urea nitrogen are known pre- fluid secretion into the collecting system. Through dictors of mortality.24 Thus, larger doses of diure- this mechanism, loop diuretics increase natriuresis tics may result in unfavorable outcomes in heart and diuresis (Figure 1).14 failure patients because of adverse effects on renal Less commonly used are the thiazide diuretics, function. In the Evaluation Study of Congestive which act on the distal convoluted tubule to block Heart Failure and Pulmonary Artery Catheteriza- 1 1 Na ,K -ATPase and thereby NaCl transport in the tion Effectiveness (ESCAPE), there was a clear distal convoluted tubule.15 Thiazide diuretics are increase in mortality with escalating loop diuretic much less powerful than loop diuretics and are doses, especially above 300 mg/day of furosemide rarely used intravenously in the hospital. These do (or an equivalent dose of another loop diuretic).25 possess a synergistic effect when used with loop Although patients with renal dysfunction may diuretics in that sodium reabsorption is blocked in require higher doses, prudence would dictate using 2 sections of the nephron.16 Extreme care must be the lowest dose to gain a reasonable urine output. taken to avoid overdiuresis, but this combination How should loop diuretics be given: as a bolus can be helpful to treat diuretic resistance.17 or continuous infusion? Although diuretics have The third class of agents are the so-called been typically given as a bolus, there are signifi- potassium-sparing diuretics, which block sodium cant theoretical concerns about this method. reuptake in the final portion of the nephron (the Furosemide, for example, has a half-life of collecting ducts), resulting in an obligatory reup- approximately 2 hours; when it is given once or take of potassium. These agents include the aldo- twice a day, a breaking phenomenon is seen in sterone receptor blocker spironolactone and which the kidneys start to retain sodium and the eplerenone, which act primarily through competi- effectiveness of the bolus is reduced.26 A Cochrane tive binding of receptors at the aldosterone-de- review has found evidence that a continuous infu- pendent sodium-potassium exchange site in the sion of diuretics produces more diuresis, although distal convoluted renal tubule. Although weak the same article suggests that more titration is diuretics, they are the only class of diuretics needed to support this observation.27 shown to improve mortality in moderate to severe Several loop diuretics are used clinically, heart failure,18,19 presumably by modulating the including furosemide, torsemide, and bumetanide. abnormal neurohormonal activation of the sympa- Which one should be chosen? Furosemide is the thetic nervous system and the renin-angiotensin- least expensive and most widely used, but 2 S26 Journal of Hospital Medicine Vol 3 / Issue 6 / Supplement 6 / November/December 2008 FIGURE 1. Single juxtamedullary nephron. Adapted with permission from Patel et al.14 animal models suggest more favorable cardiac caused natriuresis in some studies.34,35 Natriuresis effects (less fibrosis) with torsemide and even and augmentation of diuresis has not been consis- mortality benefit.28,29 There are no comparable tently demonstrated in published reports, how- human data to guide the clinician, unfortunately. ever.36,37 In addition, B-type natriuretic peptide, On a milligram per milligram basis, bumetanide when given therapeutically, does suppress aldoste- produces more natriuresis than either torsemide rone.38 or furosemide, but again, the clinical significance The largest clinical experience to date with of this is not known. nesiritide came in the Vasodilation in the Manage- ment of Acute Congestive Heart Failure (VMAC) 39 VASODILATORS trial. In this study, nesiritide was compared with Nitrates intravenous nitroglycerin and placebo when added to standard care for 3 hours in a double-blind, Nitrates, including nitroglycerin and nitroprusside, randomized protocol. Nesiritide reduced filling have been used in therapy for ADHF primarily as pressures in comparison with nitroglycerin and venodilators.30 Thus,
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