Indexed in PubMed and Scopus
pISSN 2636-154X  eISSN 2636-1558
Open Access, Peer-reviewed
    Int J Heart Fail. 2023 Jul;5(3):111-126. English.
    Published online Jul 13, 2023.
    https://doi.org/10.36628/ijhf.2023.0019
    Copyright © 2023. Korean Society of Heart Failure
    Review

    Korean Society of Heart Failure Guidelines for the Management of Heart Failure: Advanced and Acute Heart Failure

    Junho Hyun, MD, MSc,1 Jae Yeong Cho, MD, PhD,2 Jong-Chan Youn, MD, PhD,3 Darae Kim, MD, PhD,4 Dong-Hyuk Cho, MD, PhD,5 Sang Min Park, MD, PhD,6 Mi-Hyang Jung, MD, PhD,3 Hyun-Jai Cho, MD, PhD,7 Seong-Mi Park, MD, PhD,5 Jin-Oh Choi, MD, PhD,4 Wook-Jin Chung, MD, PhD,8 Byung-Su Yoo, MD, PhD,9 Seok-Min Kang, MD, PhD,10 and on behalf of Committee of Clinical Practice Guidelines, Korean Society of Heart Failure
      • 1Division of Cardiology, Department of Internal Medicine, Asan Medical Center, University of Ulsan College of Medicine, Seoul, Korea.
      • 2Department of Cardiovascular Medicine, Chonnam National University Medical School, Gwangju, Korea.
      • 3Division of Cardiology, Department of Internal Medicine, Seoul St. Mary’s Hospital, Catholic Research Institute for Intractable Cardiovascular Disease, College of Medicine, The Catholic University of Korea, Seoul, Korea.
      • 4Division of Cardiology, Department of Medicine, Heart Vascular Stroke Institute, Samsung Medical Center, Sungkyunkwan University School of Medicine, Seoul, Korea.
      • 5Division of Cardiology, Department of Internal Medicine, Korea University Anam Hospital, Korea University College of Medicine, Seoul, Korea.
      • 6Department of Cardiology, Nowon Eulji Medical Center, Eulji University, Seoul, Korea.
      • 7Department of Internal Medicine, Seoul National University Hospital, Seoul, Korea.
      • 8Division of Cardiology, Department of Internal Medicine, Gil Medical Center, Gachon University College of Medicine, Incheon, Korea.
      • 9Division of Cardiology, Department of Internal Medicine, Yonsei University Wonju College of Medicine, Wonju, Korea.
      • 10Division of Cardiology, Department of Internal Medicine, Severance Hospital, Yonsei University College of Medicine, Seoul, Korea.
    • Correspondence to Seok-Min Kang, MD, PhD. Division of Cardiology, Department of Internal Medicine, Heart Failure Center, Severance Hospital, Yonsei University, 50-1 Yonsei-ro, Seodaemun-gu, Seoul 03722, Korea. Email: smkang@yuhs.ac
    Received March 23, 2023; Revised June 14, 2023; Accepted June 28, 2023.

    This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (https://creativecommons.org/licenses/by-nc/4.0) which permits unrestricted noncommercial use, distribution, and reproduction in any medium, provided the original work is properly cited.

    Abstract

    The Korean Society of Heart Failure (KSHF) Guidelines provide evidence-based recommendations based on Korean and international data to guide adequate diagnosis and management of heart failure (HF). Since introduction of 2017 edition of the guidelines, management of advanced HF has considerably improved, especially with advances in mechanical circulatory support and devices. The current guidelines addressed these improvements. In addition, we have included recently updated evidence-based recommendations regarding acute HF in these guidelines. In summary, Part IV of the KSHF Guidelines covers the appropriate diagnosis and optimized management of advanced and acute HF.

    Keywords
    Heart failure; Cardiogenic shock; Heart-assist devices; Heart transplantation

    INTRODUCTION

    Globally, heart failure (HF) is a major cause of morbidity and mortality.1, 2) Patients presenting with acute HF are especially at a high risk of adverse outcomes, which necessitates prompt and accurate diagnosis and timely management. Moreover, progressive HF leads to an advanced stage of HF, which is characterized by a devastating clinical course and poor prognosis. Therefore, advanced HF requires timely assessment and management with specialized therapy. In Korea, the introduction of left ventricular assist device (LVAD) improved the management strategy of advanced HF. The Korean Society of Heart Failure (KSHF) had introduced guidelines for the management of acute and chronic HF.3, 4) Subsequently, rapid advances improved clinical outcomes remarkably for acute and advanced HF, which indicated the need for updated guidelines. Herein, we have appended latest evidence to the updated guidelines with a focus on acute and advanced HF.

    ADVANCED HF

    • Timely referral of patients with advanced HF to an appropriate center is recommended to assess risk stratification and provide appropriate therapy for advanced HF. (Class I, Level of Evidence C)

    Definition

    Some patients with HF do not respond to medical therapy and progress to the advanced stage. In advanced HF, symptoms or signs of HF are not improved and worsen even with guideline-directed medical therapy (GDMT); specialized therapy such as mechanical circulatory assist (MCS) devices, heart transplantation, or palliative care are often required.5, 6, 7) Patients with advanced HF have persistent severe symptoms that limits activities of daily living, impairs the quality of life, and requires frequent administration of intravenous agents for symptom relief. The inclusion criteria for defining the stage of advanced HF is listed in Table 1.7) Left ventricular ejection fraction (LVEF) is not the only mandatory defining factor of HF; in addition, symptom burden and anticipated prognosis of HF are more crucial factors to define this stage. Therefore, HF with preserved LVEF can be classified as advanced HF.

    Table 1
    European Society of Cardiology criteria defining stage of advanced HF

    Classification

    Conventionally, the Interagency Registry for Mechanically Assisted Circulatory Support (INTERMACS) profiles are used to classify patients with advanced HF who require mechanical support such as left ventricular assistive devices and total artificial hearts. The INTERMACS classification ranges from 1–7 profiles; the lower profiles indicate a more urgent requirement for additional circulatory adjuvant treatment (Table 2).8) Patients with severe HF symptoms and/or signs despite GDMT should be referred to a medical center to receive prompt and specialized treatment for HF. Furthermore, medical staff of the primary or secondary hospitals that treat patients with HF should suspect advanced HF and assess whether the findings correspond to the patients’ symptoms (Table 3).

    Table 2
    Interagency for Mechanically Assisted Circulatory Support profiles

    Table 3
    Clinical criteria of referral for advanced HF

    CARDIOGENIC SHOCK

    • 1. For patients with cardiogenic shock, the Society for Cardiovascular Angiography and Interventions classification may be used to assess individual risk and predict prognosis. (Class IIb, Level of Evidence C)

    • 2. Supplemental oxygen is recommended for patients with cardiogenic shock and hypoxemia. (Class I, Level of Evidence C)

    • 3. Mechanical ventilation should be considered for patients with cardiogenic shock and persistent respiratory failure despite supplemental oxygen or non-invasive ventilation. (Class IIa, Level of Evidence C)

    • 4. Adequate support with vasoactive agents may be considered for patients with cardiogenic shock to maintain end-organ perfusion. (Class IIb, Level of Evidence C)

    Cardiogenic shock is a severe impairment of cardiac performance that results in inadequate end-organ perfusion and causes life-threatening consequences such as multi-organ failure or mortality. Decline of cardiac function can occur suddenly due to myocardial infarction and myocarditis or gradually due to exacerbation of chronic HF. Identifying tissue hypoxia and alteration of cellular metabolism as indicated by evidence of hypoperfusion on physical examination (including oliguria, altered consciousness, and low pulse pressure) and biochemical studies (including renal dysfunction, metabolic acidosis, and elevated serum lactate) is vital. The Society for Cardiovascular Angiography and Interventions classifies cardiogenic shock into five stages according to the types and intensity of treatment; it is effective in mortality risk stratification (Figure 1).9, 10) Treatment for cardiogenic shock should be promptly initiated to restore hemodynamic stability and prevent organ failure; however, early identification and treatment of the causative disease are equally important (Figure 2).6)

    Figure 1
    Stages of cardiogenic shock. Adapted from Baran et al.9) with the permission of the Society for Cardiovascular Angiography & Interventions.
    CPR = cardiopulmonary resuscitation; ECMO = extracorporeal membrane oxygenation.

    Figure 2
    Treatment algorithm for cardiogenic shock.
    ACS = acute coronary syndrome; PCI = percutaneous coronary intervention; MCS = mechanical circulatory support; RRT = renal replacement therapy.

    TEMPORARY CIRCULATORY SUPPORT DEVICES

    • 1. Routine use of intraaortic balloon pump (IABP) is not recommended for cardiogenic shock. (Class III, Level of Evidence B)

    • 2. Use of IABP can be considered for cardiogenic shock resulting from acute mitral regurgitation or ventricular septal defect. (Class IIa, Level of Evidence C)

    • 3. Use of extracorporeal membrane oxygenation (ECMO) should be considered for cardiogenic shock refractory to medical therapy. (Class IIa, Level of Evidence C)

    • 4. Extracorporeal cardiopulmonary resuscitation using ECMO is not recommended for patients with unwitnessed, out-of-hospital cardiac arrest, and signs of irreversible neurologic impairment. (Class III, Level of Evidence C)

    • 5. Evaluation of cardiac function recovery to determine adequacy for weaning from ECMO should be assessed by echocardiography, hemodynamic (e.g., CVP, mean arterial blood pressure [BP]), and biochemical parameters (e.g., lactate). (Class IIa, Level of Evidence C)

    The use of temporary MCS devices should be considered for patients with acute HF who are refractory to fluid and vasoactive/inotropic therapy. The application of specific type of devices should be individualized based on the mechanical characteristics and amount of hemodynamic support required (Figure 3). Current United States and European practice guidelines do not recommend the routine use of intra-aortic balloon pumps; however, these may be helpful for acute MR or VSD, which result from mechanical complication of acute myocardial infarction.5, 6) In Korea, the Impella device (Abiomed, Danvers, MA, USA) is unavailable; hence, ECMO is widely used as a bridge to recovery or bridge to LVAD/heart transplantation (HT).

    Figure 3
    Temporary circulatory support for drug-refractory cardiogenic shock.
    MR = mitral regurgitation; VSD = ventricular septal defect; MI = myocardial infarction; IABP = intra-aortic balloon counterpulsation; ECMO = extracorporeal membrane oxygenation.

    Although clear criteria are yet to be established, weaning from ECMO can be considered in those exhibiting stable hemodynamics with minimal support level of ECMO (<1–1.5 L/min) and vasoactive agents (Figure 4).11) Moreover, the use of echocardiographic parameters may help guide weaning decisions.12, 13)

    Figure 4
    Weaning of percutaneous ECMO.
    ECMO = extracorporeal membrane oxygenation; MAP = mean arterial pressure; SvO2 = mixed venous oxygen saturation; RV = right ventricular; S’ = tissue Doppler tricuspid lateral peak systolic velocity; CVP = central venous pressure; LVOT = left ventricular outflow tract; VTI = velocity time integral; LVEF = left ventricular ejection fraction; SFA = superficial femoral artery; PAOD = peripheral arterial occlusive disease; MCS = mechanical circulatory support

    *Low level of vasopressor/inotropes refers to norepinephrine ≤0.03 μg/min/kg and dobutamine ≤5 μg/min/kg.

    LVAD

    A LVAD improve survival and the quality of life for patients with advanced HF. The LVAD can be used in following clinical situations: as a bridge to transplantation, bridge to candidacy to determine adequacy of transplantation, and destination therapy. It can be used in patients with refractory cardiogenic shock who are dependent on temporary MCS as well. The LVAD can be implanted in patients with INTERMACS profiles 2–4 and 5, especially those with a potential risk of sudden cardiac death or irreversible organ failure (Figure 5). The outcomes after durable, centrifugal-flow LVAD implantation as a bridge to transplantation is comparable with HT.14) In Korea, hemorrhagic stroke is a leading cause of mortality and bleeding is most common complication during the first year after LVAD implantation.15)

    Figure 5
    Treatment strategy according to the INTERMACS profile.
    NYHA = New York Heart Association; INTERMACS = Interagency Registry for Mechanically Assisted Circulatory Support; LVAD = left ventricular assist device; MCS = mechanical circulatory support; ECMO = extracorporeal membrane oxygenation.

    HT

    • 1. HT is recommended to improve survival and quality of life for selected patients with advanced HF. (Class I, Level of Evidence C)

    • 2. Cardiopulmonary exercise test is recommended in patients with advanced HF to guide HT listing. (Class I, Level of Evidence B)

    • 3. Annual evaluation of right heart catheterization is recommended to evaluate hemodynamic status in patients listed for HT. (Class I, Level of Evidence C)

    HT is gold standard therapy for patients with advanced HF; it helps improve survival, exercise capacity, and the quality of life.16) In Korea, nearly 200 heart transplants are performed annually and this number has been gradually increasing since 2000.1, 17) However, donor shortage is a major limitation of HT18); hence, appropriate recipient selection is important to maximize post-transplant outcome (Table 4). In Korea, the one-year survival after transplantation was reported to reach 90%19) and the International Society for Heart and Lung Transplantation reported a median survival of 12.5 years.20) Cardiopulmonary exercise test helps guide listing for evaluating the candidacy for HT.16, 21) HT can be considered if peak oxygen consumption is <14 mL/kg/min for non-beta-blocker (BB) users and <12 mL/kg/min for BB users, achieved during maximal exercise workload represented by a respiratory exchange ratio >1.05.16) Annual right heart catheterizations should be performed to evaluate hemodynamic status in patients who have been listed for HT.16)

    Table 4
    Common indications and contraindications of heart transplantation

    PALLIATIVE AND END-OF-LIFE CARE

    • 1. Patients with advanced HF refractory to medical therapy and not indicated for HT or LVAD can benefit from palliative and end-of-life care. (Class IIa, Level of Evidence C)

    • 2. Morphine, antiemetics, diuretics, and oxygen therapy may be considered for palliative care in patients with severe pain and congestive symptoms; GDMT, which lower BP without immediate effect, prescribed for long-term benefit may be continued at a reduced dose or discontinued. (Class Iib, Level of Evidence C)

    • 3. Physician Orders for Life Sustaining Treatment may be prepared after multidisciplinary discussion and review. (Class Iia, Level of Evidence C)

    Palliative and end-of-life care can be considered for patients with advanced HF who are not indicated for LVAD implantation or HT, those who are unable to maintain independent daily activities, and those with deteriorating symptoms despite appropriate therapy. Palliative care mainly focuses on providing symptomatic relief to maintain the quality of life and offers psychological support through a multidisciplinary approach that includes the patient, physician, nurse, and other specialists.22, 23)

    Morphine can reduce breathing difficulty, pain, and anxiety; however, patients should be informed of the following side effects: constipation, nausea, and altered mental status.24, 25) Supplemental oxygen and diuretics can help reduce dyspnea or congestive symptoms. BP lowering HF medications with a well-proven efficacy in improving long-term survival can be reduced or withdrawn based on the patient’s condition, thereby reducing risk of falls. A special care plan needs to be established for some patients including desired place for death and deactivation of implanted devices such as pacemakers or implantable cardioverter defibrillators (ICDs); it should consider the legal policies in the country.

    ACUTE HF

    Definition and aggravating factors

    Acute HF, characterized by the rapid onset and deterioration of the symptoms or signs of HF, requires prompt medical attention and often leads to emergency room visits or unexpected hospitalization. If acute HF is suspected, diagnostic tests should be performed immediately and adequate therapy initiated simultaneously. In Korea, among patients with acute HF, approximately 52% were newly-diagnosed with HF and 48% had acute decompensation of pre-existing chronic HF.26) The aggravating factors of HF, albeit not as a cause that leads to worsening events, are diverse (Table 5).

    Table 5
    Common aggravating factors of acute HF

    Prognosis

    Patients presenting with acute HF are at a high risk of in-hospital mortality, which is substantially lowered once they are stabilized and discharged. The Korean Acute Heart Failure (KorAHF) Registry study reported an in-hospital mortality rate of 4.8%.26) The rates of mortality and re-hospitalization of Korean HF population are presented in Table 6.

    Table 6
    The rates of mortality and re-hospitalization of acute heart failure in Korea

    Diagnosis

    Acute HF should be immediately diagnosed during the hospital visit. The diagnosis should aim to assess the hemodynamic profile and investigate reversible causes and aggravating factors, which require prompt treatment (Figure 6). In addition, natriuretic peptides (NPs) measurement and echocardiography should be performed to confirm the diagnosis. NPs measurement can help rule out HF in patients who have symptoms or signs suggestive of HF; although elevated NP levels support a diagnosis of HF, they are not essentially diagnostic because other non-cardiac medical conditions can cause elevated NP levels as well.27, 28) Chest radiography and lung ultrasound may help assess acute HF, especially when NP levels cannot be measured. In patients with acute HF, measurement of serum creatinine, blood urea nitrogen, and electrolytes levels is useful for therapeutic management. Elevated liver enzymes suggest poor prognosis.29, 30) Hypothyroidism or hyperthyroidism may precipitate HF; hence, thyroid-stimulating hormone levels should be measured. Lactate and hydrogen ion concentration, obtained via arterial blood gas analysis, may help assess hemodynamic condition and predict prognosis. Troponin elevation can be observed in the absence of definite myocardial ischemia or stenotic coronary artery disease in patients with acute HF and provide clinical evidence of acute coronary syndrome as a possible etiology of acute HF.31)

    Figure 6
    Diagnostic approach to suspected acute HF.
    HF = heart failure; US = ultrasound; CAG = coronary angiography; CT = computed tomography; BNP = brain natriuretic peptide; NT-pro-BNP = N-terminal pro-B-type natriuretic peptide.

    *Blood tests include troponin, serum creatinine, electrolytes, blood urea nitrogen, thyroid stimulating hormone, liver function test, d-dimer, procalcitonin, arterial blood gas analysis, lactate.

    †Coronary angiography can be performed if acute coronary syndrome is suspected, and chest CT if pulmonary embolism is suspected.

    Classification

    According to clinical status, acute HF can be classified into four subgroups that may overlap with each other (Table 7). Each subgroup is distinguished based on the status of congestion and tissue perfusion, thereby necessitating appropriate management for each group (Figure 7).

    Table 7
    Subtypes of acute HF

    Figure 7
    Therapeutic algorithm of acute HF.
    HF = heart failure; SBP = systolic blood pressure; RRT = renal replacement therapy; MCS = mechanical circulatory support.

    MONITORING ACUTE HF

    • 1. Vital signs and oxygen saturation should be continuously monitored in patients with acute HF. (Class I, Level of Evidence C)

    • 2. Volume status and fluid balance should be assessed by symptoms (orthopnea) and signs (jugular venous distention, peripheral edema, and body weight gain). (Class I, Level of Evidence C)

    • 3. Renal function and serum electrolytes should be assessed frequently when initiating treatment with intravenous diuretics or renin-angiotensin-aldosterone system blockers. (Class I, Level of Evidence C)

    • 4. Hemodynamic assessment using pulmonary artery catheter can be considered for refractory symptoms despite standard therapy with uncertainty of volume or perfusion status, low systolic BP, worsening renal function, and need for inotropes or MCS or HT. (Class Iia, Level of Evidence C)

    • 5. Measurement of brain natriuretic peptide (BNP) or N-terminal pro-B-type natriuretic peptide (NT-pro-BNP) and/or cardiac troponin levels is recommended to predict prognosis and assess HF severity. (Class I, Level of Evidence A)

    More than 90% of patients presenting with acute HF have dyspnea; it is an important surrogate to evaluate treatment efficacy. Orthopnea predicts elevated pulmonary capillary wedge pressure (PCWP) with approximately 90% sensitivity.32) Along with symptom improvement, measurement of body weight, jugular venous pressure (JVP), pulmonary rales on auscultation, and assessment of peripheral edema provide important evidence for treatment effect.33) Daily measurement of body weight with a standardized scale at a certain time is recommended. Since JVP reflects right atrial pressure, PCWP can be indirectly assessed by JVP measurement, which is an efficient method to evaluate volume status.32, 33, 34, 35) Pulmonary congestion can be evaluated via auscultation and chest radiography. Loop diuretics and renin-angiotensin-aldosterone system blockers can reduce glomerular filtration rate and result in electrolyte imbalance; hence, assessment of renal function and serum electrolyte levels are important. Routine use of pulmonary artery catheter is not recommended for patients with acute HF36, 37); however, it may help guide management of patients with HF with uncertain hemodynamic and/or volume status, refractoriness of initial therapy, persistent hypotension, progressively worsening renal function, and those considering MCS or HT. The CHAMPION (CardioMEMS Heart Sensor Allows Monitoring of Pressure to Improve Outcomes in NYHA Class III HF Patients) trial reported that individualized adjustment of diuretics doses through pulmonary artery pressure monitoring may reduce the risk of HF-related hospitalization by 28% in patients with New York Heart Association functional class III symptom.38, 39) The subsequent GUIDE-HF (haemodynamic-GUIDEd management of Heart Failure) study did not report significant benefits of pulmonary artery pressure monitoring in HF with mild symptoms; hence, further studies are needed to clarify the merits of pulmonary artery pressure monitoring.40)

    DIURETICS

    • 1. Intravenous loop diuretics should be used to improve symptoms for all patients admitted for acute HF with symptoms or signs of volume overload. (Class I, Level of Evidence C)

    • 2. The recommended initial doses of intravenous loop diuretics are 20–40 mg of furosemide for non-users of diuretics and an equivalent dose or more for those already on diuretics for acute exacerbation of pre-existing HF. (Class I, Level of Evidence B)

    • 3. Measurement of urine sodium and urine output can be helpful to assess diuretic response. (Class Iia, Level of Evidence C)

    • 4. Combination therapy of loop diuretics and thiazides can be considered for those with inadequate response to loop diuretics. (Class IIa, Level of Evidence C)

    Diuretics prevent the renal absorption of salt and water and consequently, promote their excretion, thereby relieving fluid accumulation and congestion. Diuretics should be administered in the early course of management of acute HF in all patients presenting with symptoms or signs of congestion and volume overload, regardless of LVEF. Although the level of evidence for mortality was low because of the lack of randomized controlled trials, most HF trials were conducted on the basis of sufficient diuretic usage. Diuretic therapy is targeted at achieving and maintaining euvolemic status at the lowest dose. Reduced dose or treatment withdrawal should be considered after achievement of euvolemic or hypovolemic status because excessive diuretics can cause hypotension and renal dysfunction.41)

    Loop diuretics are first-line agents because of their rapid action and strong diuretic effect, especially via the intravenous route, which is beneficial in the early presentation of acute HF. These diuretics can be initiated at a low dose and gradually increased if the diuretic effect is insufficient, while monitoring the response. An initial dose of 20–40 mg of furosemide or 10–20 mg of torsemide may be intravenously administered for patients with de novo acute HF. Furosemide can be administered as a twice or three times daily bolus injection or as a continuous infusion. If the patient is on oral diuretics before exacerbation, intravenous administration of an equivalent or twice the dose of the total daily oral dose can be administered.

    Diuretic responses are targeted at a weight loss of 0.75–1.0 kg/day with sufficient urine output. The response should be assessed by estimating the spot urine sodium excretion (>50–79 mEq/L at after 2 or 6 hours) and hourly urine output (>100–150 mL during first 6 hours) after initiation of diuretic therapy.41, 42, 43) In case of insufficient response, the diuretic dose can be doubled until it reaches the maximal dose. If diuretic response remains unsatisfactory (hourly urine volume <100 mL) despite the doubled dose, a combination therapy of other diuretic classes including acetazolamide and thiazides may be considered.44, 45, 46) Diuretic doses should gradually be reduced upon achieving euvolemia, while maintaining the lowest dose of diuretics that can prevent congestion. Concomitant therapy with angiotensin receptor-neprilysin inhibitors (ARNIs), mineralocorticoid receptor antagonists (MRAs) and sodium-glucose cotransporter-2 inhibitors should be monitored for excessive diuresis as these agents also have diuretic properties.47, 48)

    VASODILATORS AND OTHER DRUGS

    • 1. Intravenous nitroglycerin or nitroprusside may be considered in patients with acute HF and systolic BP >110 mmHg to help improve symptoms and congestion. (Class Iib, Level of Evidence B)

    • 2. Prophylactic anticoagulation therapy is recommended to prevent deep vein thrombosis and pulmonary thromboembolism in patients not on anticoagulants and where it is not contraindicated. (Class I, Level of Evidence A)

    • 3. Routine use of opiates is not recommended to control symptoms except in selected patients with severe pain or anxiety. (Class III, Level of Evidence C)

    Intravenous vasodilators

    Intravenous vasodilators, nitrates or nitroprusside, induce arterial and venous dilation, reduce preload and afterload, and subsequently, lead to increased stroke volume, decreased congestion, and symptom relief. Although evidence supporting the use of these agents is lacking, certain patients with acute HF may be considered suitable for receiving intravenous vasodilators especially those with acute pulmonary edema and increased afterload manifested as high BP, coronary ischemia, or significant MR.49, 50) However, vasodilators may increase the risk of hypotension, tachyphylaxis; therefore, adequate hemodynamic monitoring is essential. The criterion for systolic BP of 110 mmHg to initiate vasodilator therapy lacks robust evidence and is primarily based on expert opinion derived from large-scale randomized trials.

    Venous thromboprophylaxis

    Anticoagulation therapy is recommended for patients hospitalized for worsening HF and other medical problems in pre-existing HF to decrease the risk of deep vein thrombosis and pulmonary embolism for those who do not have contraindications to and are not already on anticoagulant therapy. Unfractionated heparin, low-molecular-weight heparins, warfarin, or approved direct oral anticoagulants can be used.

    Opiates

    Opiates reduce dyspnea and anxiety and can be used as sedatives in patients with non-invasive positive pressure ventilation. However, routine use of opiates for acute HF is not recommended because some retrospective studies have reported that morphine increased the risk of mechanical ventilation, prolonged the length of hospital stay, increased admissions to intensive care units, and increased mortality.51, 52)

    Digoxin

    Digoxin can be considered in patients with atrial fibrillation intolerable to BBs and a higher heart rate (>110 beats/min) despite BB use. However, since the metabolism of digoxin can be influenced by multiple factors including other drugs or renal function, serum level of digoxin should be measured.

    INOTROPES AND VASOPRESSORS

    • 1. Inotropes may be considered to maintain systemic perfusion in patients with hypotension and evidence of end-organ hypoperfusion despite standard therapy and adequate fluid resuscitation. (Class Iib, Level of Evidence C)

    • 2. Routine administration of inotropes is not recommended unless symptomatic hypotension and evidence of systemic hypoperfusion are observed. (Class III, Level of Evidence C)

    • 3. Vasopressors may be used to maintain hemodynamics and end-organ perfusion for patients with cardiogenic shock. (Class Iib, Level of Evidence B)

    In some patients, acute HF can be accompanied by a decrease in end-organ perfusion due to low cardiac output and systemic BP. In such patients, inotropes and/or vasopressors may be necessary to maintain adequate hemodynamics and restore systemic perfusion. Each agent has different properties or mechanism of action; hence, they should be used accordingly (Table 8).53) Inotropes/vasopressors should be initiated at low doses and gradually increased, and the hemodynamic response should be monitored to maintain adequate blood pressure (mean BP 65–70 mmHg). Results from the KorAHF registry study suggested that use of inotropes/vasopressors in patients with systolic BP >90 mmHg was associated with poor prognosis.54) Since these agents may increase the risk of arrhythmia and myocardial ischemia, they should be used in minimal doses and for a short-term, if possible, until end-organ perfusion improvement.55)

    Table 8
    Hemodynamic properties of common inotropes and vasopressors

    Inotropes

    Dobutamine mainly acts on β1 receptors to increase myocardial contractility and consequently, cardiac output. However, dobutamine increases the risk of arrhythmia and myocardial ischemia.56, 57) Dobutamine acts on β2 receptor of peripheral vessels causes vasodilation and subsequent reduction of BP, which require hemodynamic monitoring. Milrinone, a type-3-phosphodiesterase inhibitor, increases myocardial contractility and reduces pulmonary vascular resistance. Since milrinone does not act on β1 receptors, it can be used with BBs. However, milrinone decreases systemic BP and should be cautiously used especially in patients with shock.

    Vasopressors

    Norepinephrine, epinephrine, and dopamine are commonly used vasopressors, which increase both myocardial contractility and systemic vascular resistance. Vasopressors are often combined with inotropes for patients with cardiogenic shock and hypotension. Evidence supporting the superiority of one specific agent over another is lacking. In the SOAP (Sepsis Occurrence in Acutely Ill Patients) II trial, dopamine use significantly increased the risk of arrhythmia in patients with shock and norepinephrine was reportedly favorable in terms of mortality for a subgroup of patients with cardiogenic shock.58) Another study reported that norepinephrine was favorable over epinephrine regarding heart rate and lactic acidosis, without differences in hemodynamic profiles in patients with myocardial infarction-induced cardiogenic shock.59) Therefore, based on available evidence, norepinephrine may be prioritized over various vasopressors for cardiogenic shock necessitating vasoactive agents.

    PRE- AND POST-DISCHARGE MANAGEMENT

    • 1. Patients admitted for HF should be evaluated for the achievement of adequate decongestion before discharge. (Class I, Level of Evidence C)

    • 2. GDMT should be initiated and preferably optimized before discharge. (Class I, Level of Evidence C)

    • 3. Early follow-up evaluation within 1–2 weeks after discharge is recommended to assess volume status and drug tolerance. (Class I, Level of Evidence C)

    The early period of post-hospitalization discharge for worsening HF refers a vulnerable period that demonstrates a high risk of mortality and readmission.60) Therefore, it is necessary to ensure that the precipitating factors are appropriately corrected and symptoms and/or signs of HF are improved before discharge. Approximately 30% of patients discharged from HF hospitalization have residual congestion and a higher risk of first-year mortality compared with those without congestion.61) Therefore, appropriate decongestion before discharge through diuretic therapy is mandatory.

    Furthermore, optimization of medical therapy, evaluation for clinical need of device therapy (e.g. ICD), and appropriate patient education for diet and physical exercise are important.62) Patients admitted for acute HF should be initiated on evidence-based medical therapy prior to discharge unless it is contraindicated.63) In Korea, the at-discharge prescription rates of renin-angiotensin system blockers, BBs, and MRAs were 68.8%, 52.2%, and 46.6%, respectively,26) which is suboptimal. Medical therapy with these agents at discharge is reported to improve clinical outcomes; hence, physicians should check whether these medications are prescribed.63, 64) Furthermore, in-hospital initiation of ARNI can reduce NT-pro-BNP levels and reduce the risk of HF-related adverse clinical outcomes.65) Therefore, early initiation of ARNI should be considered.

    CONCLUSION

    The diagnosis and management of acute and advanced HF is rapidly advancing recently. Early diagnosis and optimization of therapy is cornerstone for acute HF, and adequate assessment and management in accordance with the patient’s profile is crucial in patients with advanced HF. This Part 4 of the HF guidelines adapted latest evidence and provided optimal approach focused on the patients with acute or advanced HF.

    Notes

    Conflict of Interest:The authors have no financial conflicts of interest.

    Author Contributions:

    • Conceptualization: Cho JH, Kang SM.

    • Funding acquisition: Cho JH, Yoo BS, Kang SM.

    • Supervision: Cho JH, Kang SM.

    • Writing - original draft: Hyun J.

    • Writing - review & editing: Cho JY, Youn JC, Kim D, Cho DH, Park SM, Jung MH, Cho JH, Park SM, Choi JO, Chung WJ, Yoo BS, Kang SM.

    ACKNOWLEDGMENTS

    This article has been published jointly, with consent, in both Korean Circulation Journal and International Journal of Heart Failure.

    Also, the final version of this guideline was endorsed by Korean Society of Cardiology, Korean Society of Lipid and Atherosclerosis, Korean Association of Clinical Cardiology, Korean Society of Hypertension, Korean Society of Heart Failure, Korean Society of Echocardiography, Korean Society of Interventional Cardiology, Korean Heart Rhythm Society, and Korean Society of CardioMetabolic Syndrome.

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    MeSH Terms
    Diagnosis
    Heart Failure*
    Heart Transplantation
    Heart*
    Heart-Assist Devices
    Shock, Cardiogenic
    Metrics
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