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Acute Decompensated Heart Failure Guidelines

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Esc Clinical Practice Guidelines

Acute Decompensated Heart Failure and Cardiogenic Shock (Arvind Bhimaraj, MD)

The aim of this ESC guideline is to help health professionals manage people with heart failure according to the best available evidence. Fortunately, we now have a wealth of clinical trials to help us select the best management to improve the outcomes for people with HF for many, it is now both preventable and treatable. This guideline provides practical, evidence-based recommendations. The format of the previous 2016 ESC HF Guidelines was revised to make each phenotype of HF stand-alone in terms of its diagnosis and management. The therapy recommendations mention the treatment effect supported by the class and level of evidence and are presented in tables. In this guideline, we have decided to focus on the diagnosis and treatment of HF, not on its prevention.

Guidelines and related materials are for use by individuals for personal or educational purposes. No commercial use is allowed. Re-use permission must be correctly obtained .

Description Of The Problem

Acute heart failure is a complex clinical syndrome that results from the inability of the heart to meet the metabolic demands of the body. This disease is quite prevalent: over 5 million people have heart failure in the United States alone. There are nearly 300,000 deaths from heart failure annually, and well over 1 million hospitalizations for heart failure each year.Patients often present to their clinician with a variety of signs and symptoms. Most of these are related either to vascular congestion or impaired perfusion. Common signs and symptoms include dyspnea, orthopnea, paroxysmal nocturnal dyspnea , peripheral edema, nausea/vomiting, weight gain or weight loss, elevated jugular venous pressure, hepatomegaly, pulmonary rales, cardiac gallops , and pleural effusions, to name a few.The goal for managing a patient with acute decompensated heart failure is several-fold: 1) Identify an etiology for the decompensation, 2) Decongest the patient , 3) Ensure adequate perfusion to vital organs, and 4) Preserve hemodynamic stability.

Congestion And Organ Dysfunction

In the heart, elevated ventricular filling pressures lead to increased ventricular wall tension, myocardial stretch and remodelling, contributing to a progressive worsening in cardiac contractility, valvular regurgitation and systemic congestion. In response to the increased wall tension, circulating natriuretic peptides are physiologically released by atrial and ventricular cardiomyocytes as a compensatory mechanism, and often high-sensitivity cardiac troponins are detectable in a large proportion of patients with AHF, revealing nonischaemic myocyte injury or necrosis. Increases in left atrial pressure and mitral valve regurgitation will increase the hydrostatic pressure in the pulmonary capillaries, thereby increasing fluid filtration rate from the capillaries to the pulmonary interstitium, causing lung stiffness and dyspnoea. Notably, the relationship between hydrostatic pressure and interstitial fluid content is rather complex, as other mechanisms are involved in fluid homeostasis. For example, the lymphangiogenic factor VEGF-D has been found to regulate and mitigate pulmonary and systemic congestion in patients with HF or renal failure,,. Indeed, in the early stage of lung congestion, the lymphatic system can cope with the large volume of interstitial fluid, but eventually, the drainage capacity is exceeded. Hence, fluid moves to pleural and intra-alveolar spaces causing pleural effusion and pulmonary oedema.

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Identifying Precipitating Causes Of Acute Hf Decompensation

Acute Decompensated Heart Failure in the Observation Unit: Treatment ...
Coronary artery disease
Mechanical complications of AMI
Valvular disease
Mitral regurgitation: worsening chronic or acute
Progressive aortic stenosis
Progression of underlying cardiac dysfunction
Physical, emotional or environmental stress
Cardiac toxins alcohol, cocaine, methamphetamines, chemotherapy
RV pacing
Excessive salt and water intake
Medication nonadherence
Bradycardia-sinus node dysfunction, heart block, AF with slow ventricular response
Recent onset LBBB
Systemic infection: sepsis, pneumonia, URI, UTI, viral infection
Renal insufficiency
Depression, dementia, and cognitive impairment
Recent addition of medications with negative inotropic effects:
Calcium channel blockers: especially the non-dihydropyridines verapamil and diltiazem
Class Ia, Ic and III antiarrhythmic medications:
Quinidine, procainamide, disopyramide, flecainide, sotalol, propafenone, dronedarone
-adrenergic blocking agents
Non-cardiac medications that promote sodium retention:
Nonsteroidal anti-inflammatory drugs
Monoclonal antibodies Trastuzumab and Bevacizumab
Taxanes paclitaxel and docetaxel
Cyclophosphamide
Small tyrosine kinase inhibitors Sunitinib, sorafenib, imatinib

ACS Complicated by Heart Failure

Pneumonia or Other Pulmonary Processes

Medications

Right Ventricular Pacing

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Diagnosis Assessment And Monitoring

1.2.1 Take a history, perform a clinical examination and undertake standard investigations for example, electrocardiography, chest Xray and blood tests in line with the NICE guideline on chronic heart failure.

1.2.2 In people presenting with new suspected acute heart failure, use a single measurement of serum natriuretic peptides and the following thresholds to rule out the diagnosis of heart failure:

  • BNP less than 100 ng/litre

  • NTproBNP less than 300 ng/litre.

1.2.3 In people presenting with new suspected acute heart failure with raised natriuretic peptide levels , perform transthoracic Doppler 2D echocardiography to establish the presence or absence of cardiac abnormalities.

1.2.4 In people presenting with new suspected acute heart failure, consider performing transthoracic Doppler 2D echocardiography within 48 hours of admission to guide early specialist management.

1.2.5 Do not routinely offer pulmonary artery catheterisation to people with acute heart failure.

Acute Decompensated Heart Failure: History And Biologic Markers

However, although NT-proBNP performs well in an unselected population with dyspnea, the marker may have limited utility to distinguish increased pressure from increased permeability edema. In a prospective cohort study of patients with ARDS or ARDS risk factors, NT-proBNP was reported at a median value greater than 3000 pg/mL, well above the value to exclude heart failure only one-third of ARDS subjects had normal NT-proBNP values.129 Furthermore, although the NT-proBNP values observed in ARDS were numerically lower than those observed in the ADHF subjects from the PRIDE study, the difference between them was not statistically significant.127,129 A few smaller studies have assessed the ability of BNP to distinguish ARDS from cardiogenic pulmonary edema, using clinician judgment as the gold standard to determine edema type, and reported limited discriminative utility.130132

Nicholas Ioannou, … David Treacher, in, 2014

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Definition: What Is Acute Heart Failure Why Does The Definition Matter

AHF is a clinical diagnosis. No single test or physical exam feature definitively rules in or rules out AHF. Thus there is no diagnostic gold standard. Perhaps unsurprisingly, there is neither a universal, well-accepted definition of AHF, nor a nomenclature to describe the various AHF syndromes.11 Various names have been used, including acute decompensated heart failure , hospitalization for heart failure , and acute heart failure syndromes . Currently, AHF is the most widely used and is the current terminology in several consensus guidelines.12,13

Agreement upon a definition is not an academic exercise it has significant clinical implications. Describing AHF in an 85-year-old female with no past history of HF and a systolic blood pressure at presentation of 210/120 mm Hg does not appropriately describe the 65-year-old male with known ischemic heart disease, EF of 10%, on maximal guideline recommended HF therapies awaiting transplantation. Such heterogeneity of the AHF presentation broadens when comorbid conditions and precipitants of AHF are considered. Lack of consensus on a definition hinders both policy and research the slow rate of progress to reduce morbidity and mortality may be directly related to the inability to define exactly what problem we are addressing.

Unfortunately, no universal definition is proposed. For the purposes of this chapter, AHF is defined as signs of symptoms of heart failure requiring urgent or emergent therapy.11

Initial And Ongoing Monitoring And Disposition Decisions

Acute Decompensated Heart Failure (Jessica Brown, MD)

The extent of monitoring will depend on the disease severity and the response to therapy.4 Vital signs should be measured on a regular basis until stabilization. Laboratory tests should be repeated regularly : electrolytes, creatinine, and complete blood count, if abnormal. Electrolyte abnormalities, especially hypokalemia which has been linked to ventricular arrhythmias,52 should be prevented or corrected promptly. There is limited evidence to support measurement or replacement of magnesium in patients with AHF. Significant renal impairment might require more frequent laboratory testing.

Table 28: Should the patient be admitted to hospital or discharged home?

Variable

Vital signs resolved and stable for > 24 hrs, especially blood pressure & heart rate

Clear discharge plan for labs, follow-up and other testing

Chronic oral HF therapy initiated, titrated and optimized

Greater than 30% decrease in natriuretic peptide level from time of admission and relatively free from congestion

Education initiated, understood by patient, continued education planned

Recommendation 141: We recommend that a pulmonary artery catheter not be used routinely in patients with AHF .

Practical tips:

  • Tailored hemodynamic therapy with a pulmonary artery catheter under experienced supervision may be clinically useful in highly selected cases, such as ongoing heart failure accompanied by cardiorenal syndrome, poor response to therapy or systemic hypotension or as evaluation for advanced therapies .

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Acute Decompensated Heart Failure National Registry Algorithm

Inpatients with acute decompensated heart failure.

  • The ADHERE Algorithm estimates in-hospital mortality in admitted patients with acute decompensated HF.
  • This model uses 3 variables to classify patients, but it does not allow more precise characterization of individual risk.
  • The ADHERE Algorithm can NOT predict intermediate- and long-term mortality risks.
  • The analysis of the ADHERE cohort also identified heart rate and age as significant independent predictors of risk according to the regression model, but these variables were omitted from the algorithm in order to simplify the model as a bedside tool.
  • The data used reflect individual hospitalization episodes, not individual patients, and multiple hospitalizations of the same patient may be entered into the registry as separate records.
  • Study results were based on a registry, the accuracy of which can be influenced by differences in disease assessment, treatment, and documentation patterns at participating institutions.

Risk stratification, triage and optimization of medical management.

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Dr. Gregg Fonarow

Pathophysiological Mechanisms Of Ahf

An underlying structural or functional cardiac condition is a prerequisite for AHF and includes a multitude of different acute or chronic cardiac pathologies. The underlying cardiac disease leads to the activation of several pathophysiological pathways that counter the negative effects of HF on oxygen delivery to the peripheral tissues, but such pathways can also eventually cause systemic congestion, ventricular remodelling and organ dysfunction. Furthermore, some acute diseases can act as precipitating factors and trigger AHF either by directly impairing cardiac diastolic and/or systolic function or by further promoting systemic congestion. Systemic congestion has a major effect on the clinical presentation in the majority of patients with AHF and is a relevant determinant of multi-organ dysfunction occurring in AHF . The pathophysiology of AHF is heterogeneous, as it is greatly affected by the nature of the underlying cardiac disease. It is perhaps not surprising, therefore, that the responses to treatment may vary and that different patients may respond best to distinct treatment strategies that depend on the underlying pathophysiology.

Fig. 1: Schematic representation of possible pathophysiological mechanisms in AHF.

LV systolic and diastolic dysfunction

Fluid retention

Fluid redistribution

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Esc Guidelines For Acute And Chronic Heart Failure: Key Points

Aug 29, 2021 | Supriya Shore, MD

McDonagh TA, Metra M, Adamo M, et al.
Citation:
2021 ESC Guidelines for the Diagnosis and Treatment of Acute and Chronic Heart Failure: Developed by the Task Force for the Diagnosis and Treatment of Acute and Chronic Heart Failure of the European Society of Cardiology With the Special Contribution of the Heart Failure Association of the ESC. Eur Heart J 2021 Aug 27:.

The following are key points to remember from the 2021 European Society of Cardiology Guidelines for the Diagnosis and Treatment of Acute and Chronic Heart Failure :

  • The nomenclature for HF with left ventricular ejection fraction of 41-49% has been revised to HF with mildly reduced EF . HF with LVEF 40% remains HF with reduced EF , and HF with LVEF 50% remains HF with preserved EF .
  • All patients with suspected HF should have an electrocardiogm, transthoracic echocardiogram, chest X-ray, blood tests including cell count, urea and electrolytes, thyroid function, glycated hemoglobin , lipid, iron studies, and B-type natriuretic peptide . Cardiac magnetic resonance imaging is recommended in those with poor acoustic windows with an echo or in patients with suspected infiltrative cardiomyopathy, hemochromatosis, LV noncompaction, or myocarditis.
  • For HFpEF patients, diagnosis and treatment of contributing factors and use of diuretics are recommended. No specific therapies have been proven to reduce mortality in HFpEF.
  • Acute Decompensated Heart Failure

    Acute Decompensated Heart Failure

    Diuretic kinetics are impaired in decompensated HF.325,326 The bioavailability of furosemide, unlike that of bumetanide or torsemide, is erratic in HF.327 This feature, and a longer duration of action, may account for the finding of a 50% reduction in the requirement for readmission to hospital in patients with HF randomly assigned to receive torsemide rather than furosemide.98 There is decreased plasma clearance in decompensated HF because of a decreased RBF.325 Together, these effects can limit the peak diuretic concentration in the tubular fluid to the foot of the dose-response curve and thereby diminish the response .

    G. Michael Felker, Marat Fudim, in, 2018

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    What Is Acute Decompensated Heart Failure Isnt It Just A Worsening Of Chronic Heart Failure

    Acute decompensated heart failure is a clinical syndrome of worsening signs or symptoms of heart failure requiring hospitalization or other unscheduled medical care. For many years, ADHF was viewed as simply an exacerbation of chronic HF as a result of volume overload, with few implications beyond a short-term need to intensify diuretic therapy . Recent decades have seen an explosion of research into the epidemiology, pathophysiology, outcomes, and treatment of ADHF. Although some controversy persists, multiple lines of evidence now support the concept that ADHF is a unique clinical syndrome with its own epidemiology and underlying mechanisms and that there is a need for specific therapies. This viewpoint suggests that ADHF is not just a worsening of chronic HF any more than an acute myocardial infarction is just a worsening of chronic angina.

    Outcome data from a variety of studies now support the concept that hospitalization for ADHF can often signal a dramatic change in the natural history of the HF syndrome. Rates of rehospitalization or death are as high as 50% within 6 months of the initial ADHF event, which is a much higher event rate than is seen with acute MI.

    A schematic representation of the pathophysiology of acute HF is given in Fig. 26.1.

    V. Courtney Broaddus MD, inMurray & Nadel’s Textbook of Respiratory Medicine, 2022

    Precipitating Factors Of Ahf

    The onset and increase in systemic congestion that precede AHF may develop over hours up to days, and can be triggered by several factors, either directly through stimulation of pathophysiological mechanisms leading to fluid accumulation or redistribution or indirectly through a worsening of cardiac diastolic or systolic function. The understanding of the pathophysiology involved in the development of AHF is important for providing the appropriate treatment. Although in many patients a progressive increase in body weight and pulmonary pressures may be observed as early as several days before hospital admission, in a relevant proportion of patients AHF is associated with only a minimal increase in body weight,. Several registries, including the North American OPTIMIZE-HF registry and the Euro-Asian registry of the GREAT network, have investigated the presence of precipitants in patients with AHF,. Acute coronary syndromes, arrhythmias , infections , uncontrolled hypertension and non-compliance with dietary recommendations and drug prescriptions are the most common identified precipitants,. Of note, in a relevant proportion of patients , no precipitants could be identified, whereas a combination of multiple factors were present in ~520% of patients,.

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    How Do We Maximize Diuresis In Acute Decompensated Heart Failure

    • Release date: October 1, 2022
    • Expiration date: September 30, 2023

    In patients with acute decompensated heart failure , the initial diuretic regimen should maximize intravenous loop diuretics based on urine output or spot urine sodium. Combination therapy can be used if diuretic resistance occurs.

    ADHF accounts for more than 1 million hospitalizations per year in the United States, and inadequate diuresis is a common cause of readmissions and higher mortality. In the absence of cardiogenic shock, ADHF manifestations are driven primarily by expansion of extracellular fluid volume, leading to elevated cardiac filling pressures and congestion ., Despite the evidence supporting guideline-directed medical therapy, studies guiding diuresis are limited.

    Classification Of Acute Heart Failure

    Acute Decompensated Heart Failure (Laurie Letarte, MD) Saturday, August 20, 2016

    The definition of AHF presented here is broad and there have been many attempts to stratify this further . Although characterised by a distinctive set of signs and symptoms, a major challenge in classifying AHF as a single entity is that the patient population is not uniform. Patients admitted with HF exhibit a wide spectrum of disease and range from those with severe LV systolic dysfunction and low cardiac output to those with severe hypertension and normal or near-normal LV systolic function. The majority of patients with AHF lie between these extremes and therefore also demonstrate a distribution of underlying pathology and precipitants, leading to the common endpoint of fluid overload.

    This is a neat classification system and focusses the treating physician towards the management of the underlying cause of AHF. However, given patients often present with a range of co-morbidities, the reasons for decompensation may not be apparent at initial presentation or indeed, there may be multiple contributing factors. Practically speaking, therefore, it may be more prudent to stratify patients with AHF based on their initial clinical presentation. This allows the attending physician to identify those most at risk in order to direct specific interventions such as instituting ionotropic agents and/or mechanical circulatory support.

    Fig. 1

    Sameer Kurmani and Iain Squire reports personal fees from NOVARTIS.

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