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• W2895852028 abstract "Heart failure (HF) is extremely prevalent and for those with end-stage (stage D) disease, 1-year survival is only 25-50%. Several studies have captured the mortality impact of kidney disease on patients with HF, and measures of kidney function are a component of many HF risk stratification scores. The management of advanced HF complicated by cardiorenal syndrome (CRS) is challenging, and irreversible kidney failure often limits patient candidacy for advanced HF therapies, such as transplant or left ventricular assist device therapy. Thus, prompt institution of aggressive therapy is warranted in stage D HF patients with CRS to prevent irreversible kidney failure. In this chapter, we discuss the assessment and management of patients with CRS with end-stage HF. In addition to discussing medical therapy aimed at decongestion and increased cardiac inotropy, we provide a summary of temporary circulatory support devices that can be considered for those whom hospice is not desired. In all circumstances, a close collaboration between the advanced HF specialist and nephrologist is needed to achieve the best patient outcomes. Heart failure (HF) is extremely prevalent and for those with end-stage (stage D) disease, 1-year survival is only 25-50%. Several studies have captured the mortality impact of kidney disease on patients with HF, and measures of kidney function are a component of many HF risk stratification scores. The management of advanced HF complicated by cardiorenal syndrome (CRS) is challenging, and irreversible kidney failure often limits patient candidacy for advanced HF therapies, such as transplant or left ventricular assist device therapy. Thus, prompt institution of aggressive therapy is warranted in stage D HF patients with CRS to prevent irreversible kidney failure. In this chapter, we discuss the assessment and management of patients with CRS with end-stage HF. In addition to discussing medical therapy aimed at decongestion and increased cardiac inotropy, we provide a summary of temporary circulatory support devices that can be considered for those whom hospice is not desired. In all circumstances, a close collaboration between the advanced HF specialist and nephrologist is needed to achieve the best patient outcomes. Clinical Summary•Acute or chronic kidney failure correlates with worse survival in patients with heart failure, irrespective of patient ejection fraction.•In heart failure patients with cardiorenal syndrome without evidence of shock, vasodilators and diuretics, but not inotropes, are first-line therapies.•Cardiogenic shock phenotypes often differ based on cardiomyopathy etiology; patients with shock warrant urgent stabilization with inotropes, vasopressors, and/or temporary mechanical circulatory support.•Patients with evidence of shock often have concomitant systemic inflammatory response syndrome with microcirculatory dysfunction and improvements in kidney function can lag behind gains achieved in cardiac output with shock management. •Acute or chronic kidney failure correlates with worse survival in patients with heart failure, irrespective of patient ejection fraction.•In heart failure patients with cardiorenal syndrome without evidence of shock, vasodilators and diuretics, but not inotropes, are first-line therapies.•Cardiogenic shock phenotypes often differ based on cardiomyopathy etiology; patients with shock warrant urgent stabilization with inotropes, vasopressors, and/or temporary mechanical circulatory support.•Patients with evidence of shock often have concomitant systemic inflammatory response syndrome with microcirculatory dysfunction and improvements in kidney function can lag behind gains achieved in cardiac output with shock management. Heart failure (HF) affects over 6.5 million Americans over the age of 19 years, and the prevalence of HF is expected to increase 46% by 2030.1Benjamin E.J. Blaha M.J. Chiuve S.E. et al.Heart disease and stroke statistics-2017 update: a report from the American Heart Association.Circulation. 2017; 135: e146-e603Crossref PubMed Scopus (6298) Google Scholar, 2Yancy C.W. Jessup M. Bozkurt B. et al.2017 ACC/AHA/HFSA focused update of the 2013 ACCF/AHA guideline for the management of heart failure: a report of the American College of Cardiology/American Heart Association task force on clinical practice guidelines and the heart failure Society of America.Circulation. 2017; 136: e137-e161Crossref PubMed Scopus (1685) Google Scholar Several population and cohort studies have demonstrated the mortality impact of concomitant kidney dysfunction (acute and/or chronic) in HF patients with preserved ejection fraction and reduced ejection fraction.3Al-Ahmad A. Rand W.M. Manjunath G. et al.Reduced kidney function and anemia as risk factors for mortality in patients with left ventricular dysfunction.J Am Coll Cardiol. 2001; 38: 955-962Crossref PubMed Scopus (621) Google Scholar, 4Colombo G.L. Caruggi M. Ottolini C. Maggioni A.P. Candesartan in heart failure: assessment of reduction in mortality and morbidity (CHARM) and resource utilization and costs in Italy.Vasc Health Risk Manag. 2008; 4: 223-234Google Scholar, 5Lee D.S. Austin P.C. Rouleau J.L. Liu P.P. Naimark D. Tu J.V. Predicting mortality among patients hospitalized for heart failure: derivation and validation of a clinical model.JAMA. 2003; 290: 2581-2587Crossref PubMed Scopus (1123) Google Scholar, 6Levy W.C. Dardas T.F. Comparison of cardiopulmonary-based risk models with a clinical heart failure risk model.Eur J Heart Fail. 2018; 20: 711-714Google Scholar, 7Pocock S.J. Ariti C.A. McMurray J.J. et al.Predicting survival in heart failure: a risk score based on 39 372 patients from 30 studies.Eur Heart J. 2013; 34: 1404-1413Crossref PubMed Scopus (698) Google Scholar, 8Thorvaldsen T. Claggett B.L. Shah A. et al.Predicting risk in patients hospitalized for acute decompensated heart failure and preserved ejection fraction: the atherosclerosis risk in communities study heart failure community surveillance.Circ Heart Fail. 2017; 10: e003992https://doi.org/10.1161/CIRCHEARTFAILURE.117.003992Crossref Scopus (14) Google Scholar, 9Wessler B.S. Ruthazer R. Udelson J.E. et al.Regional validation and recalibration of clinical predictive models for patients with acute heart failure.J Am Heart Assoc. 2017; 6: e006121https://doi.org/10.1161/JAHA.117.006121Crossref Scopus (12) Google Scholar, 10Yancy C.W. Lopatin M. Stevenson L.W. De Marco T. Fonarow G.C. Clinical presentation, management, and in-hospital outcomes of patients admitted with acute decompensated heart failure with preserved systolic function: a report from the Acute Decompensated Heart Failure National Registry (ADHERE) Database.J Am Coll Cardiol. 2006; 47: 76-84Crossref PubMed Scopus (805) Google Scholar In the subpopulation of patients with the most extreme stage of HF (stage D), the presence of kidney dysfunction often limits candidacy for advanced HF therapies, including cardiac transplant and surgically implanted mechanical circulatory support. Building on the concepts detailed in prior chapters on the pathophysiology and management of cardiorenal syndrome (CRS), this section will focus on those with advanced HF with or without various degrees of cardiogenic shock. We will review the importance of medical therapies aimed at decongestion, perfusion, and stabilizing the patient with advanced HF, as well as mechanical circulatory support options for carefully selected patients with CRS and HF. The American Heart Association and American College of Cardiology devised a classification for patients with HF, ranging from stage A (at risk for HF without structural or clinical HF) to stage D (end-stage HF)11Hunt S.A. Baker D.W. Chin M.H. et al.ACC/AHA guidelines for the evaluation and management of chronic heart failure in the adult: executive summary. A report of the American College of Cardiology/American Heart Association task force on practice guidelines (Committee to revise the 1995 guidelines for the evaluation and management of heart failure).J Am Coll Cardiol. 2001; 38: 2101-2113Crossref PubMed Scopus (1213) Google Scholar (Fig 1). Those with past or current clinical HF symptoms fall into the American College of Cardiology/American Heart Association stage C HF category, while patients with recalcitrant HF despite guideline-directed therapy, biventricular pacing, and adherence to therapy fall into stage D. Kidney dysfunction is an important contributor to morbidity and mortality in those with symptomatic (stage C and D) HF, regardless of ejection fraction. HF registries, secondary analyses of clinical trials, and cohort studies have demonstrated the important contribution of acute and/or chronic kidney dysfunction on HF mortality. The Acute Decompensated Heart Failure National Registry (ADHERE) evaluated 33,046 patient hospitalizations for HF to identify predictors of inpatient mortality.10Yancy C.W. Lopatin M. Stevenson L.W. De Marco T. Fonarow G.C. Clinical presentation, management, and in-hospital outcomes of patients admitted with acute decompensated heart failure with preserved systolic function: a report from the Acute Decompensated Heart Failure National Registry (ADHERE) Database.J Am Coll Cardiol. 2006; 47: 76-84Crossref PubMed Scopus (805) Google Scholar The left ventricular ejection fraction (LVEF) was preserved in 46% of patients and inpatient mortality was 4.2%. A systolic blood pressure <115 mmHg, serum blood urea nitrogen (BUN) > 43 mg/dL, and/or a creatinine (Cr) > 2.75 mg/dL were found to be the strongest correlates of inpatient mortality, regardless of LVEF.12Fonarow G.C. Adams Jr., K.F. Abraham W.T. Yancy C.W. Boscardin W.J. Risk stratification for in-hospital mortality in acutely decompensated heart failure: classification and regression tree analysis.JAMA. 2005; 293: 572-580Crossref PubMed Scopus (1317) Google Scholar Patients with a BUN >43 mg/dL had a 9% mortality compared with 2.7% in those with a BUN ≤43 mg/dL. If all 3 of the aforementioned risk factors were simultaneously present in a patient, inpatient mortality averaged 22%.12Fonarow G.C. Adams Jr., K.F. Abraham W.T. Yancy C.W. Boscardin W.J. Risk stratification for in-hospital mortality in acutely decompensated heart failure: classification and regression tree analysis.JAMA. 2005; 293: 572-580Crossref PubMed Scopus (1317) Google Scholar The Studies of Left Ventricular Dysfunction (SOLVD) was a multicenter, randomized, double-blind, placebo-controlled trial evaluating the effect of the angiotensin-converting enzyme inhibitor (ACEI) enalapril on survival in patient with an LVEF <35%.13Yusuf S. Pitt B. Davis C.E. Hood W.B. Cohn J.N. Effect of enalapril on survival in patients with reduced left ventricular ejection fractions and congestive heart failure.N Engl J Med. 1991; 325: 293-302Crossref PubMed Scopus (6682) Google Scholar Ahmad and colleagues performed a retrospective analysis of SOLVD to further characterize the interaction between the level of kidney dysfunction and all-cause mortality in patients.3Al-Ahmad A. Rand W.M. Manjunath G. et al.Reduced kidney function and anemia as risk factors for mortality in patients with left ventricular dysfunction.J Am Coll Cardiol. 2001; 38: 955-962Crossref PubMed Scopus (621) Google Scholar On multivariable analysis, reduced kidney function independently predicted death in HF (adjusted hazard ratio 1.06 per 10 mL/min/1.73 m2 decrease in estimated glomerular filtration rate [eGFR]). Similar findings were observed in the Candesartan in Heart Failure: Assessment of Reduction in Mortality and Morbidity trial which examined the impact of the angiotensin receptor blocker (ARB) candesartan in 3 different symptomatic HF (New York Heart Association II-IV) populations: those with preserved LVEF (LVEF >40%), those with a low LVEF (LVEF <40%), and those with a low LVEF already on ACEI therapy.14Hillege H.L. Nitsch D. Pfeffer M.A. et al.Renal function as a predictor of outcome in a broad spectrum of patients with heart failure.Circulation. 2006; 113: 671-678Crossref PubMed Scopus (757) Google Scholar Hillege and colleagues performed a secondary analysis of the combined cohorts (2680 North American patients) to further assess the prognostic value of the eGFR. Compared with HF patients with an eGFR >60 mL/min per 1.73 m2, the adjusted risk of death was 50% and 91% higher in those with an eGFR of 45-60 and < 45 mL/min per 1.73 m2, respectively. The prognostic value of eGFR for predicting mortality was noted in both the preserved and reduced LVEF groups. Finally, the Evaluation Study of Congestive Heart Failure and Pulmonary Artery Catheterization Effectiveness trial15Binanay C. Califf R.M. Hasselblad V. et al.Evaluation study of congestive heart failure and pulmonary artery catheterization effectiveness: the ESCAPE trial.JAMA. 2005; 294: 1625-1633Crossref PubMed Scopus (1004) Google Scholar, 16Shah M.R. O'Connor C.M. Sopko G. Hasselblad V. Califf R.M. Stevenson L.W. Evaluation study of congestive heart failure and pulmonary artery catheterization effectiveness (ESCAPE): design and rationale.Am Heart J. 2001; 141: 528-535Crossref PubMed Scopus (91) Google Scholar was a prospective, randomized study comparing the use of pulmonary artery (PA) catheter-guided therapy to clinical assessment alone in 433 patients with an LVEF ≤30% and advanced HF symptoms. A post hoc analysis of the Evaluation Study of Congestive Heart Failure and Pulmonary Artery Catheterization Effectiveness trial was performed to further characterize the cardiorenal interactions in the HF population.17Nohria A. Hasselblad V. Stebbins A. et al.Cardiorenal interactions: insights from the ESCAPE trial.J Am Coll Cardiol. 2008; 51: 1268-1274Crossref PubMed Scopus (446) Google Scholar On adjusted analysis, impaired baseline (hazard ratio 1.25) and discharge (hazard ratio 1.28) eGFR, but not worsening kidney function, were associated with worse outcomes (death and/or rehospitalization) at 6 months. PA catheter-guided therapy did not impact 6-month survival, rehospitalization, length of stay, or the development of worsening kidney function in either those with (eGFR <60 mL/min) or without baseline kidney dysfunction. While a previous history of hypertension and diabetes predicted the development of worsening kidney function while inpatient, the use of intravenous vasodilator and loop diuretic dosage did not, suggesting that intrinsic kidney disease may have played a larger role in the negative prognosis.17Nohria A. Hasselblad V. Stebbins A. et al.Cardiorenal interactions: insights from the ESCAPE trial.J Am Coll Cardiol. 2008; 51: 1268-1274Crossref PubMed Scopus (446) Google Scholar In addition to the clinical trials outlined previously, several risk models have been developed for prognostication of mortality in HF patients with preserved ejection fraction and preserved ejection fraction.5Lee D.S. Austin P.C. Rouleau J.L. Liu P.P. Naimark D. Tu J.V. Predicting mortality among patients hospitalized for heart failure: derivation and validation of a clinical model.JAMA. 2003; 290: 2581-2587Crossref PubMed Scopus (1123) Google Scholar, 6Levy W.C. Dardas T.F. Comparison of cardiopulmonary-based risk models with a clinical heart failure risk model.Eur J Heart Fail. 2018; 20: 711-714Google Scholar, 7Pocock S.J. Ariti C.A. McMurray J.J. et al.Predicting survival in heart failure: a risk score based on 39 372 patients from 30 studies.Eur Heart J. 2013; 34: 1404-1413Crossref PubMed Scopus (698) Google Scholar, 8Thorvaldsen T. Claggett B.L. Shah A. et al.Predicting risk in patients hospitalized for acute decompensated heart failure and preserved ejection fraction: the atherosclerosis risk in communities study heart failure community surveillance.Circ Heart Fail. 2017; 10: e003992https://doi.org/10.1161/CIRCHEARTFAILURE.117.003992Crossref Scopus (14) Google Scholar, 9Wessler B.S. Ruthazer R. Udelson J.E. et al.Regional validation and recalibration of clinical predictive models for patients with acute heart failure.J Am Heart Assoc. 2017; 6: e006121https://doi.org/10.1161/JAHA.117.006121Crossref Scopus (12) Google Scholar The Meta-Analysis Global Group in Chronic Heart Failure (MAGGIC) score is one of the more robust HF risk scores.7Pocock S.J. Ariti C.A. McMurray J.J. et al.Predicting survival in heart failure: a risk score based on 39 372 patients from 30 studies.Eur Heart J. 2013; 34: 1404-1413Crossref PubMed Scopus (698) Google Scholar The MAGGIC model was devised using data from 39,372 patients enrolled into 30 different cohort studies, and it can be used to estimate an individual's probability of dying within 1 and 3 years. Patients in the MAGGIC cohort had both reduced and preserved LVEF, and average mortality was 40% over a median follow-up of 2.5 years. The MAGGIC cohort is composed of 13 predictors of mortality (including age, LVEF, HF medication use, blood pressure), and serum creatinine is one of the strongest predictors (rate ratio for mortality 1.039 per 10 μmol/L Cr). The model has also been independently validated and demonstrated very good accuracy (C index 0.74) for mortality discrimination in HF.18Sartipy U. Dahlstrom U. Edner M. Lund L.H. Predicting survival in heart failure: validation of the MAGGIC heart failure risk score in 51,043 patients from the Swedish heart failure registry.Eur J Heart Fail. 2014; 16: 173-179Crossref PubMed Scopus (104) Google Scholar In the subpopulation of patients with stage D HF, there are 4 options for management: medical therapy with diuretics and/or inotropes, mechanical circulatory support, transplant, or hospice. For many, especially those who are older or with major comorbidities including end-stage kidney failure, palliative care and/or hospice care may be the best care recommendation. However, the decision on the optimal HF management strategy for some is often unclear until appropriate cardiac support and decongestion are achieved to demonstrate if improvements in end-organ function can be achieved. This is particularly true of those patients with acute kidney dysfunction from HF (CRS type I) and those with acute worsening of chronic kidney disease due to cardiac insufficiency (CRS type II). Categorization of patients based on volume and perfusion statuses is critical. Some patients may suffer mainly from volume overload without severe reductions in cardiac output (“warm and wet”) and others may be more profoundly “low flow” with (“cold and wet”) or without volume elevation (“cold and dry”). While LVEF can provide an estimate of cardiac function, LVEF is not synonymous with cardiac output, and cardiac output is not always synonymous with end-organ perfusion. Thus, even patients with preserved LVEF can have reduced cardiac output because of reduced stroke volumes in the setting of a small left ventricular (LV) chamber or restrictive filling. These features can be seen in patients with advanced hypertrophic cardiomyopathy, critical aortic stenosis, cardiac amyloidosis, and other restrictive or constrictive myopathies. In addition, elevated right-sided cardiac filling pressures can lead to renal venous congestion and reduced kidney perfusion. Patients with pulmonary hypertension, congenital heart disease, and other maladies provoking right ventricular (RV) failure can display this phenotype. When volume status and cardiac output are in doubt, right heart catheterization should be performed. Cardiac congestion increases myocardial wall stress, which increases cardiac oxygen consumption and reduces cardiac efficiency. In the normal heart, the LV is capable of increasing contractile force and stroke volume when exposed to increased preload, a principle described by the Frank-Starling curve (Fig 2A).19Klabunde R. Cardiovascular Physiology Concepts: Frank-Starling Mechanism. http://www.cvphysiology.com/Cardiac%20Function/CF003. Published July 3, 2015. Accessed May 10, 2018.Google Scholar, 20Klabunde R. Cardiovascular Physiology Concepts: Ventricular systolic dysfunction. http://www.cvphysiology.com/Heart%20Failure/HF005. Published December 20, 2017. Accessed May 10, 2018.Google Scholar, 21Muslin A. The pathophysiology of heart failure.in: Hill J.A. Olson E.N. Muscle: Fundamental Biology and Mechanisms of Disease. Academic Press, Cambridge, MA2012Google Scholar In patients with HF, the Frank-Starling curve flattens, and more preload is required to increase contractility and stroke volume (Fig 2B),19Klabunde R. Cardiovascular Physiology Concepts: Frank-Starling Mechanism. http://www.cvphysiology.com/Cardiac%20Function/CF003. Published July 3, 2015. Accessed May 10, 2018.Google Scholar promoting patient fluid retention through activation of the renin-angiotensin-aldosterone system.21Muslin A. The pathophysiology of heart failure.in: Hill J.A. Olson E.N. Muscle: Fundamental Biology and Mechanisms of Disease. Academic Press, Cambridge, MA2012Google Scholar In addition, as venous return and preload rise, myocyte stretching occurs. According to the Law of Laplace, the increase in ventricular pressure (P) and dilation of the ventricular chamber (r, radius) increases wall tension (Tension α P*r), thereby increasing myocardial oxygen consumption.22Hoffman J.I. Buckberg G.D. The myocardial oxygen supply:demand index revisited.J Am Heart Assoc. 2014; 3: e000285https://doi.org/10.1161/JAHA.113.000285Crossref Scopus (84) Google Scholar Depletion of myocardial calcium and adenosine triphosphate can lead to reduced myocardial contractility, reduced lusitropy (relaxation), and cardiac systolic and diastolic failure, respectively. In patients with acutely decompensated chronic cardiomyopathies who are “warm and wet” (intravascular volume overload without shock), a reduction in cardiac filling pressures though diuresis, ultrafiltration, and/or afterload reduction, can improve cardiac stroke volumes, leading to an improvement in kidney function in patients with type 1 or type 2 CRS. In this patient group, high-dose parenteral diuretics with a dietary sodium and fluid restriction are often required to achieve kidney threshold and successful decongestion. Short-acting diuretics such as furosemide result in natriuresis as long as renal tubular fluid diuretic concentrations are high enough to block the renal Na+/K+/2Cl− cotransporter in the loop of Henle.23De Bruyne L.K. Mechanisms and management of diuretic resistance in congestive heart failure.Postgrad Med J. 2003; 79: 268-271Crossref PubMed Scopus (85) Google Scholar When urinary concentrations decline below the diuretic threshold, compensatory sodium retention occurs during the rest of the day, leading to postdiuretic salt retention. Thus, dietary sodium restrictions are important during acute decompensated HF because postdiuretic salt retention from a high-sodium diet can completely negate the prior beneficial effect of the loop diuretic. Chronic administration of loop diuretics in HF can lead to the phenomena of diuretic resistance. Diuretic resistance is likely multifactorial and related to renal tubular hypertrophy and kidney hypoperfusion in the setting of elevated sympathetic nerve system–induced renal vasoconstriction.24Schrier R.W. Abraham W.T. Hormones and hemodynamics in heart failure.N Engl J Med. 1999; 341: 577-585Crossref PubMed Scopus (970) Google Scholar In addition, patients with kidney insufficiency often have reduced active secretion of furosemide into the loop of Henle because endogenous organic anions compete for the secretory binding sites. This leads to higher diuretic dose requirements to overcome competitive inhibition of the transport.23De Bruyne L.K. Mechanisms and management of diuretic resistance in congestive heart failure.Postgrad Med J. 2003; 79: 268-271Crossref PubMed Scopus (85) Google Scholar In addition to diuretics, the addition of vasodilator therapy to the medical regimen of patients with HF without severe hypotension is an important armamentarium in HF management. Patients with chronic HF have stroke volumes that are very afterload-dependent, such that reductions in pulmonary (RV afterload) and/or systemic blood pressure (LV afterload) have a more pronounced effect on cardiac output than that of a normal heart.21Muslin A. The pathophysiology of heart failure.in: Hill J.A. Olson E.N. Muscle: Fundamental Biology and Mechanisms of Disease. Academic Press, Cambridge, MA2012Google Scholar The optimal agent for afterload reduction is guided by patient clinical status. Table 1 outlines considerations to be had for the various medications.25Yancy C.W. Jessup M. Bozkurt B. et al.2013 ACCF/AHA guideline for the management of heart failure: executive summary: a report of the American College of Cardiology Foundation/American Heart Association task force on practice guidelines.Circulation. 2013; 128: 1810-1852Crossref PubMed Scopus (1647) Google Scholar In addition to pharmacotherapy, clinical trials are underway examining various support technologies for those with congestive HF without evidence of shock. The Aortix device (Procyrion, Houston, TX) is a percutaneous heart pump that is placed into the descending aorta. In animal and pilot in vivo human studies, the pump demonstrated the ability to decouple the heart and the kidneys, improving kidney flow and cardiac output while reducing afterload and cardiac work. In the next phase of the Aortix clinical trial, investigators will be examining the use of the Aortix in stage C patients with either systolic or diastolic HF who are “wet and warm” admitted with worsening kidney function to see if the device improves congestion and kidney function.Table 1Vasodilator Agents Used in the Medical Management of Heart Failure (HF) Without Evidence of ShockBased on data from Yancy and colleagues.25Yancy C.W. Jessup M. Bozkurt B. et al.2013 ACCF/AHA guideline for the management of heart failure: executive summary: a report of the American College of Cardiology Foundation/American Heart Association task force on practice guidelines.Circulation. 2013; 128: 1810-1852Crossref PubMed Scopus (1647) Google ScholarVasodilator AgentsMain RouteDose RangeConsiderations∗All listed agents can cause hypotension. Please read product inserts for full explanation of side-effect profiles and dosing recommendations.Beta-blockersOralCarvedilol 3.125 to 50 mg twice dayAvoid in severely decompensated HF Carvedilol Bisoprolol Metoprolol succinateHydralazineIV or oralIV: 10 mgOral: 10-100 mg every 6-8 hoursDrug-induced lupus reaction. Can cause reactive tachycardia.Oral nitratesOralISDN 10 mg-40 mg every 6-8 hoursAvoid in patients with PDE inhibitor use. May cause headaches. Should be dosed with HYD to avoid nitrate tolerance. Isosorbide dinitrate (ISDN) Isosorbide mononitrateACE inhibitors (ACEI)OralCaptopril 3.125-50 mg every 8 hours. Can be converted to a long-acting agent when the patient is stableAvoid in AKI, severe CKD, or hyperkalemia. Side-effects include cough, angioedema, hyperkalemia, worsening kidney function Captopril Enalapril Lisinopril Fosinopril Quinapril Ramipril TrandolaprilAngiotensin receptor blockers (ARB)OralLosartan 25-150 mg dailyAvoid in AKI, severe CKD, or hyperkalemia. Side effects include angioedema, hyperkalemia, worsening kidney function Losartan Candesartan ValsartanSacubitril/valsartanoral24/26 mg–97/103 mg twice daily.Not tested in stage D heart failure. Contraindicated in patients with angioedema. Should not be used with ACEI or ARBs.Dihydropyridine calcium channel blockersOralAmlodipine 2.5-10 mg dailyNot used for acute hypertension management due to slow-steady state. Side effects include lower extremity edema (venous insufficiency) and constipation. No proven mortality benefit in heart failure. Felodipine amlodipine NifedipineNitroprussideIV0.05-3.0 mcg/kg/minRequires arterial line monitoring for titration. Monitor for thiocyanate toxicity, especially at doses >2 mcg/kg/min. Avoid prolonged use in AKI or CKD and in patients with PDE inhibitor use.NitroglycerinIV5-100 mcg/minSide effects include headaches and tachyphylaxis. Avoid in patients with PDE inhibitor use.Abbreviations: AKI, acute kidney injury; CKD, chronic kidney disease; HYD, hydralazine; IV, intravenous; PDE, phosphodiesterase inhibitor.∗ All listed agents can cause hypotension. Please read product inserts for full explanation of side-effect profiles and dosing recommendations. Open table in a new tab Abbreviations: AKI, acute kidney injury; CKD, chronic kidney disease; HYD, hydralazine; IV, intravenous; PDE, phosphodiesterase inhibitor. Finally, the use of inotrope agents in those “wet and warm” HF patients with CRS should generally be avoided, as outlined in the 2013 American College of Cardiology/American Heart Association joint HF management guidelines.26Dworzynski K. Roberts E. Ludman A. Mant J. Diagnosing and managing acute heart failure in adults: summary of NICE guidance.BMJ (Clinical research ed). 2014; 349: g5695https://doi.org/10.1136/bmj.g5695Crossref PubMed Scopus (21) Google Scholar Inotropes can be proarrhythmic and have shown no benefit or the potential for increased mortality when compared with vasodilator therapy.27Burger A.J. Elkayam U. Neibaur M.T. et al.Comparison of the occurrence of ventricular arrhythmias in patients with acutely decompensated congestive heart failure receiving dobutamine versus nesiritide therapy.Am J Cardiol. 2001; 88: 35-39Abstract Full Text Full Text PDF PubMed Scopus (111) Google Scholar, 28Abraham W.T. Adams K.F. Fonarow G.C. et al.In-hospital mortality in patients with acute decompensated heart failure requiring intravenous vasoactive medications: an analysis from the Acute Decompensated Heart Failure National Registry (ADHERE).J Am Coll Cardiol. 2005; 46: 57-64Crossref PubMed Scopus (579) Google Scholar, 29Cuffe M.S. Califf R.M. Adams Jr., K.F. et al.Short-term intravenous milrinone for acute exacerbation of chronic heart failure: a randomize" @default.
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• W2895852028 date "2018-09-01" @default.
• W2895852028 modified "2023-09-24" @default.
• W2895852028 title "Advanced Heart Failure Therapies and Cardiorenal Syndrome" @default.
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