acute decompensated heart

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outcomes. In this article, we discuss the role, in theacute setting, of diuretics, ultrafiltration, vasodi-lator therapy, neurohormonal blockade, inotropes,and mechanical support for treatment of ADHF.Just as importantly, we need to consider prog-nosis, discharge planning and optimization of

outpatient care.

THE ROLE OF DIURETICS

Diuresis provides a reduction of intracardiac fillingpressures, thereby reducing pulmonary pressuresand improving patients symptoms. They havenever been shown in the long-term to improvemorbidity or mortality, and, in fact, some datasuggest that diuretics may be deleterious whenused long term. Nevertheless, adequate diuresisis clearly essential for acute improvement in symp-toms. Loop diuretics are the most commonly usedin ADHF because of their superior efficacy andrapid onset compared with other diuretics. Intra-venous diuretics are usually given initially, aspatients with significant volume overload mayhave intestinal edema delaying their oral absorp-tion. It is recommended that the lowest possibledose of diuretic thought to be effective be givenfirst, as the goal is to precipitate symptom relief while minimizing potential side effects, such aselectrolyte disturbances, hypotension, and hypo-

kalemia. Bolus doses have been the historicalstandard of care. If optimal results are not seen,the dosage, as well as the frequency, can beincreased until goal diuresis is met. Continuousintravenous infusion can also be administered.Studies comparing intermittent intravenous ad-ministration of furosemide compared with contin-uous infusion suggest that either regimen works,with the total dose being most important. 2 Never-theless, inadequate diuresis and fear of usingnecessary high doses are common problems in

clinical practice.Individual loop diuretics differ in their pharmacoki-netic properties. Furosemides bioavailability afteroral administration is variable and approximately50%, whereas bumetanide and torsemide bothhave bioavailabilities closer to 90%. In patients withdecompensated heart failureandsimultaneousrenalinsufficiency, higher doses of diuretics are oftenneeded to provoke a therapeutic response. Dosesof 200 mg of intravenous furosemide may be neces-sary. Combination of diureticsmayalso be helpful. Insome patients, renal insufficiency may improve withdiuresis because of decreased intra-abdominalpressure. Often, however, increased diuresis mayworsen the renal insufficiency without eliciting theneeded diuretic response. Such patients may needmore aggressive therapy.

Another challenging question in the hospitalsetting is when to transition to oral diuretics. Thisis usually done when the symptoms of fluid over-load have resolved and the patient is close to a eu-volemic state. Too often patients are transitionedto oral diuretics and discharged when they are still

considerably volume overloaded; this is likely onereason for the high rehospitalization rate in thispatient population. When a patient is approachingeuvolemia, it is appropriate to consider switchingto oral diuretics, but the dosage must be carefullyconsidered. Patients should be monitored for atleast 24 hours after the transition to demonstrateeffective response to the oral regimen beforedischarge, and close follow-up should be ar-ranged to ensure rapid fluid accumulation doesnot occur.

ULTRAFILTRATION

When diuretic resistance develops, ultrafiltration isan alternative approach for effective fluid removal.In the Ultrafiltration vs IV Diuretics for PatientsHospitalized for Acute Decompensated CHF(UNLOAD) trial, 200 patients hospitalized with ADHF were randomly assigned to receive ultra-filtration or standard care (including intravenousdiuretics). 3 At 48 hours, patients assigned to ultrafil-tration hadsignificantly greater fluid loss than those

in the standard care arm; however, the change inrenal function was no better, with patients oftendemonstrating increased creatinine when goodfluid loss was achieved. At 90 days, patients as-signed to ultrafiltration had significantly fewer heartfailure rehospitalizations than patients assigned tostandard care, perhaps because of the larger fluidloss. Whether increased diuretic doses in the stan-dard of care group would have achieved the sameresults is unknown. Ultrafiltration is reserved forpatients who do not achieve an adequate response

to an aggressive diuretic regimen. The sickestpatients, however, may develop renal dysfunctionwith the necessary fluid removal.

VASODILATOR THERAPY

In the setting of decompensated heart failure, theremay be a role for vasodilator therapy to aid withdecongestion. Vasodilators result in decreasedafterload, decreased preload, and a reducedpulmonary capillary wedge pressure. Vasodilatorsmay be given orally or intravenously. In the acutesetting, intravenous agents, such as nitroglycerin,nitroprusside, or nesiritide, are often used. Oralagents, such as the combination of hydralazineand isosorbide mononitrate or isosorbide dinitrate,may also be used.

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Intravenous nitroglycerin is primarily a venodila-tor and therefore results in decreased preload anddecreased left-sided filling pressures. It may alsolower blood pressure. It is an effective agent forthe acute reduction in symptoms in the setting of ADHF; however, dose escalation is often limited

by hypotension and headache.Nitroprusside is another option for intravenous

vasodilation, and, in particular, should be consid-ered when reduced afterload is needed. For thisreason, nitroprusside can be particularly useful inthe setting of ADHF secondary to hypertensiveemergency, acute aortic or mitral regurgitation, oracuteseptal rupture.Nitroprusside requirescontin-uous blood pressure monitoring, usually with anarterial line and should not be used for more than48 to 72 hours, as thiocyanate toxicity maydevelop. Additionally, nitroprusside should beused with extreme caution, if at all, in patientswith liver or renal disease.

Nesiritide is a third option for intravenous vasodi-lator therapy in ADHF. Nesiritide is recombinant B-type natriuretic peptide (BNP), andhas been shownto decrease the pulmonary capillary wedge pres-sure and perhaps improve acute symptoms inpatients with decompensated heart failure. 4 Nesiri-tide has been shown to have no long-term benefit.The Acute Study of Clinical Effectiveness of Nesiritide in Decompensated Heart Failure Trial

(ASCEND-HF) randomized patients with ADHF toreceive standard therapy and either a continuousintravenous infusion of nesiritide or placebo. Theresults showed no significant difference in the pre-specified end point of dyspnea, and at 1 monththe rate of death and hospital readmission for heartfailure was not statistically different 5 ; however, the

investigators also found no evidence of an increasein mortality or renal injury.

Careful consideration must be taken beforestarting these agents and, in particular, closeattention to blood pressure is needed. Hypoten-sion must be avoided to ensure that adequate

renal perfusion is maintained. The effects of a vasodilator on blood pressure are unpredictable,with increased cardiac output often minimizing theblood pressure effects. Although vasodilatorsimprove hemodynamics in the short term, thereis no good evidence to suggest they provide anylong-term benefit. Retrospective studies suggestimproved outcomes in patients who receive vaso-dilators as compared with inotropes, but this maybe because of selection bias or adverse effects of inotropes.

INOTROPIC THERAPY

Inotropic agents increase cardiac contractility,thereby improving cardiac output and may be indi-cated in ADHF when low output and poor organperfusion are suspected; however, whereas ino-tropes may be beneficial in improving hemo-dynamics in ADHF, the use of inotropes isassociated with a number of adverse cardiovas-cular events, and may worsen patient outcomesin the long term ( Fig. 1 ).6 Limitations and adverse

effects of inotropic therapy include tachyarrhyth-mias, ischemia, hypotension, and, with chronicuse, increased pathologic ventricular remodeling.

Intravenous inotropes should therefore beconsidered only in the management of ADHFwhen other therapies, such as diuretics and vaso-dilators, have been ineffective. Whenever possible,

Fig. 1. In OPTIME-HF, patients receiving milrinone were found to have a significantly increased adverse event rateby 48 hours as compared withplacebo. ( Data from Cuffe MS, Califf RM, Adams KF Jr, et al. Outcomes of a ProspectiveTrial of Intravenous Milrinone for Exacerbations of Chronic Heart Failure (OPTIME-CHF) Investigators. Short-termintravenous milrinone for acute exacerbation of chronic heart failure: a randomized controlled trial. JAMA2002;287(12):15417.)

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inotropic support should be short term, althoughinotropes may need to be continued in patientswith severe advanced heart failure who are await-ing heart transplantation or are being consideredfor mechanical circulatory support. Despite theirlimitations and no controlled studies, inotropes still

play an essential role in the resuscitation of a selectpatient population.

NEUROHORMONAL BLOCKADE

A decline in cardiac output leads to activationof various neurohormonal cascades as compen-satory processes. This includes activation of thesympathetic nervous system and the renin-angiotensin-aldosterone axis. Increased concentra-tionsof catecholamines,angiotensinII, vasopressin,atrial/brain natriuretic peptides, and endothelin areseen. Although the short-term results of theseprocesses often are helpful, the long-term conse-quences are more problematic. The proper use of neurohormonal blocking agents in the acute settingis thus difficult, with need to consider both short-term and long-term consequences.

There are minimal data about how to managebeta-blockers in patients with ADHF. Discontinuingbeta-blockers in these patientsmay improvehemo-dynamics in the short term, but the withdrawalof beta-blocker therapy may permit more rapid

ventricular remodeling and worsen long-termprognosis. Thegoal should thereforebe to continueas much beta-blocker as possible while stabilizingthe patient as rapidly as possible.

Thus, patients who come into the hospital with ADHF should remain on some dosage of beta-blocker if they are not in cardiogenic shock. If theexacerbation is mild, with fluid overload beingthe main issue, the home dosage of beta blockercan be maintained. (However, make sure that thepatient is truly taking the prescribed dosage at

home!) If the exacerbation is more severe, then itis reasonable to consider cutting the dosage inhalf until perfusion is improved. The sickestpatients may need withdrawal of beta blockade.Patients with ADHF, who have either not been onbeta-blocker therapy or who have not beencompliant with beta-blockers, should not be re-started on beta-blocker therapy acutely. Low-dose initiation may be considered just beforedischarge in stable reliable patients.

Long-term use of any medication is improved if started in the hospital. For this reason, once thepatient has been optimized from a hemodynamicstandpoint, beta-blockers can be started at a lowdose and titrated up very slowly (usually every 2weeks), as an outpatient. Obviously more cautionshould be used in patients requiring inotropic

therapy, and those with symptomatic hypotension,bradycardia, or recent cardiogenic shock.

ACE inhibitors were the first drugs shown toimprove outcomes in patients with advanced heartfailure. They have been shown to improve survivalwhenstarted in patientshospitalized with refractory

heart failure. 7 The Cooperative North ScandinavianEnalapril Survival Study provides the basis for initi-ating therapy with ACE inhibitors during initial treat-ment of advanced heart failure while thepatient is inthe hospital. Angiotensin receptor blockers (ARB)can be used in patients who develop a cough orangioedema with ACE inhibitors.

Agents should be initiated at a low dose inpatients with low blood pressure. In patients whoare being aggressively diuresed, there is a risk of renal dysfunction and therefore the initiation of an ACE inhibitor can be delayed until the patient is eu-volemic. It is also important to remember wheninitiating these medications thatpatientsmayexpe-rience an early rise in creatinine levels, to approxi-mately 25% above their baseline. The serumcreatinine concentration is likely to stabilize after4 weeks of therapy, and this rise is expected andshould not be a reason for discontinuing the drug.Renal dysfunction may be acutely impaired in thesetting of aggressive diuresis, and if ACE inhibitorsor ARBs are held acutely, they should be restartedwhen the creatinine returns to baseline.

Patients with advanced heart failure should alsobe treated with aldosterone antagonists becausethese agents have been shown to improve survivalin patients receiving ACE inhibitors or ARBs. 8 Theyhave little acute hemodynamic effect, and cansafely be started early in most patients. In clinicalpractice, early treatment may aid with diuresis,prevent hypokalemia, and permit the long-termeffects to occur sooner.

Mechanical Circulatory Support

In the sickest patients, usually those presenting incardiogenic shock, adequate perfusion cannot bemaintained with the previously described thera-pies and mechanical circulatory support isneeded. Occasionally patients will present to thehospital very unstable and in need of emergentcardiopulmonary resuscitation. In these selectpatients, an initial period of support with extracor-poreal membrane oxygenation is an effectivestrategy to allow triage and stabilization. As thesepatients are stabilized, and the medical team getsto know the patient a little better, the patientsprognosis can be assessed and long-term support(such as an LV assist device) can be consideredif medical therapy is not successful. On theother hand, patients who present in more chronic

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hospitalization. 13,14 Negative studies are oftenassociated with close medical follow-up in allpatients (including the comparison group). 15

Although the most important attributes of closefollow-up care are not known, there is no doubtthat close and knowledgeable follow-up care is

essential.When seen in the outpatient setting, a continuing

effort has to be placed on medical optimization.Patients drug regimens should be pushed toreach target dosages. Medical care providersmay be too concerned about asymptomatichypotension and not titrate to proven dosages.Similarly, patients who appear to be stable areoften not given effective dosages of medicinesthat improve long-term prognosis.

These patients need to be seen frequently, sothat aggressive diuresis can continue in the outpa-tient setting and so that they can continue toreceive much-needed dietary counseling. It hasclearly been shown that frequent communicationbetween the patient and the caretaker improvesoutcomes. Additionally, the patients need tounderstand that if their regimens are adjusted byphysicians outside of their cardiology team, theyneed to notify their cardiologist right away.

It is also very important to realize, both in theacute setting and chronically, that patients whoare difficult to manage should be considered for

referral to a tertiary care center. There are manyoptions for patients with advanced heart failure,including mechanical assist devices and transplan-tation, which have dramatically improved theoutcomes in these patients in the long term. Thesepatients should be referred before damage to thekidneys or other organs has been prolonged. Renalinsufficiency and prolonged hepatic congestion,leading to cirrhosis, increase the risk of mechanicalsupport and transplantation, so it is better to err onthe side of referring too early.

SUMMARY

Congestive heart failure is themost commoncauseof cardiovascular hospital admission. Not only ischronic heart failure a major cause of morbidityand mortality in the general population, but it alsoconsumes 1% to 2% of the total health careresources. 16 The total costs for congestive heartfailure care have increased considerably over thepast 10 years. The most effective approach for pre-venting heart failure hospitalizations is a combina-tion of improvement in management of thesepatients while they are in the hospital and compre-hensive post hospitalization care. Decreasing thelength of hospitalization can increase readmissionrate, so optimization of inpatient and outpatient

care is essential. This should include ensuringadequate diuresis before discharge, optimizationof medical treatment for heart failure during thehospitalization, thorough patient education beforedischarge, and close outpatient follow-up.

REFERENCES

1. Ross JS, Chen J, Lin ZQ, et al. Recent nationaltrends in readmission rates after heart failure hospi-talization. Circ Heart Fail 2010;3(1):97103.

2. Felker MG, Lee KL, Bull DA, et al. Diuretic strategiesin patients with acute decompensated heart failure.N Engl J Med 2011;364:797805.

3. Costanzo MR, Guglin ME, Saltzberg MT, et al,UNLOAD Trial Investigators. Ultrafiltration versusintravenous diuretics for patients hospitalized foracute decompensated heart failure. J Am Coll Cardi-ol 2007;49:67583.

4. Young JB, Abraham WT, Warner-Stevenson L, et al.Results of the VMAC trial: vasodilation in themanagement of acute congestive heart failure.Circulation 2000;102:2794.

5. OConnor CM, Starling RC, Hernandez AF, et al.Effect of nesiritide in patients with acute decom-pensated heart failure. N Engl J Med 2011;365:3243.

6. Cuffe MS, Califf RM, Adams KF Jr, et al, Outcomes ofa Prospective Trial of Intravenous Milrinone for Exac-

erbations of Chronic Heart Failure (OPTIME-CHF)Investigators. Short-term intravenous milrinone foracute exacerbationof chronicheart failure: a random-ized controlled trial. JAMA 2002;287(12):15417.

7. The CONSENSUS Trial Study Group. Effects of ena-lapril on mortality in severe congestive heart failure:results of the Cooperative North Scandinavian Ena-lapril Survival Study (CONSENSUS). N Engl J Med1987;316:142935.

8. Zannad F, McMurray JJ, Krum H, et al. Eplerenone inpatients with systolic heart failure and mild symp-toms. N Engl J Med 2011;364:1121.

9. Levy D, Kenchaiah S, Larson MG, et al. Long-termtrends in the incidence of and survival with heartfailure. N Engl J Med 2002;347:1397.

10. Tsuyuki RT, Shibata MC, Nilsson C, et al. Contempo-rary burden of illness of congestive heart failure inCanada. Can J Cardiol 2003;19:4368.

11. Horwich TB, Patel J, MacLellan WR, et al. Cardiactroponin I is associated with impaired hemody-namics, progressive left ventricular dysfunction,and increased mortality rates in advanced heartfailure. Circulation 2003;108:8338.

12. McAlister F, Stewart S, Ferrua S, et al. Multidisci-plinary strategies for the management of heartfailure patients at high risk for admission. A system-atic review of randomized trials. J Am Coll Cardiol2004;44:8109.

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13. Cleland JG, Louis AA, Rigby AS, et al. Noninvasivehome telemonitoring for patients with heart failureat high risk of recurrent admission and death.J Am Coll Cardiol 2005;45:165464.

14. Goldberg L, Piette J, Walsh M, et al. Randomizedtrial of a daily electronic home monitoring system

in patients with advanced heart failure: the WeightMonitoring in Heart Failure (WHARF) trial. Am HeartJ 2003;146:70512.

15. Jaarsma T, van der Wal M, Lesman-Leegte I, et al.Effect of moderate or intensive disease manage-ment program on outcome in patients with heartfailure. Coordinating Study Evaluating Outcomes ofAdvising and Counseling in Heart Failure (COACH).Arch Intern Med 2008;168:31624.

16. Berry C, Murdoch DR, McMurray JJ. Economics ofchronic heart failure. Eur J Heart Fail 2001;3(3):28391.

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