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    Acute exacerbation of congestive heart failureHighlights

    SummaryOverview

    BasicsDefinition

    Epidemiology AetiologyPathophysiologyClassification

    PreventionPrimaryScreeningSecondary

    DiagnosisHistory & examinationTestsDifferential

    Step-by-stepCriteriaGuidelinesCase history

    TreatmentDetailsStep-by-stepEmergingGuidelinesEvidence

    Follow UpRecommendations

    ComplicationsPrognosis

    ResourcesReferencesImagesOnline resourcesPatient leafletsCredits

    EmailPrintFeedbackShare

    Add to PortfolioBookmark Add notes

    History & exam

    Key factors presence of risk factors (previous cardiovascular disease, age >70 years)

    dyspnoea

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    pulmonary crepitations

    peripheral oedema

    cool peripheries

    chest pain

    third heart sound (S3)

    Other diagnostic factors fatigue and weakness

    hypotension

    tachycardia

    elevated jugular venous pressure

    displaced apex beat (point of maximal impulse)

    dullness to percussion and decreased air entry in lung bases

    wheezing

    palpitations

    cough

    fever

    syncope

    murmur

    ascites

    hepatomegaly

    central cyanosisHistory & exam details

    Diagnostic tests

    1st tests to order ECG

    CXR

    Hb

    TFT

    troponin

    B-type natriuretic peptide (BNP)

    Tests to consider echocardiography

    cardiac catheterisation

    endomyocardial biopsy

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    Diagnostic tests details

    Treatment details

    Acute

    haemodynamically stable

    oxygen therapy morphine

    loop diuretics

    vasodilators

    supportive care

    ventilation

    inadequate response to loop diuretics

    o non-loop diuretics

    due to cardiac ischaemia

    o aspirin revascularisation

    due to valvular disease

    o nitroprusside

    due to acute right heart failure

    o treatment of underlying cause

    due to acute myocarditis

    o supportive care or immunosuppressant therapy

    inadequate response to combination diuretics

    o ultrafiltration

    hypotensive (systolic BP

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    oxygen therapy

    IV beta-blockers and glyceryl trinitrate

    nitroprusside

    supportive care

    ventilation

    Ongoing

    acute episode stabilised: LVEF 100 mmHg

    ACE inhibitor or angiotensin-II receptor antagonist

    beta-blocker

    aldosterone receptor antagonist

    vasodilators

    diuretics

    supportive care

    acute episode stabilised: LVEF

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    Diuretics and oxygen are initial treatments for symptom relief. Cardiogenic shock may require pressor

    support or mechanical ventilation. If acute myocardial infarction (MI) is present, early revascularisation is essential.

    Other related conditions Chronic congestive heart failure

    ST-elevation myocardial infarction

    Non-ST-elevation myocardial infarction

    Assessment of cardiomyopathy

    Myocarditis

    Aortic stenosis

    Mitral regurgitation

    Pulmonary embolism

    Acute respiratory distress syndrome

    COPD

    Acute asthma exacerbation in adults

    Hypertensive emergencies Email Print Feedback Share Add to Portfolio Bookmark Add notes

    CXR of acute pulmonary oedema showing increased alveolar markings, fluid in the horizontal fissure,and blunting of the costophrenic angles

    From the private collections of Syed W. Yusuf, MBBS, MRCPI, and Daniel Lenihan, MD

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    Left ventricular hypertrophy with sinus tachycardia

    From the private collections of Syed W. Yusuf, MBBS, MRCPI, and Daniel Lenihan, MD

    Systolic image of dilated left ventricle (arrow); note there is no change from diastolic image

    From the private collections of Syed W. Yusuf, MBBS, MRCPI, and Daniel Lenihan, MD

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    Diastolic image of dilated left ventricle

    From the private collections of Syed W. Yusuf, MBBS, MRCPI, and Daniel Lenihan, MD

    CXR of acute pulmonary oedema showing increased alveolar markings and bilateral pleural effusions

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    From the private collections of Syed W. Yusuf, MBBS, MRCPI, and Daniel Lenihan, MD

    Definition Acute congestive heart failure (CHF) is the rapid onset of symptoms andsigns due to abnormal cardiac function. It may be due to cardiac or extra-cardiac causes and results in reduced cardiac output, tissue hypoperfusion,increased pulmonary capillary wedge pressure, and tissue congestion. [1]

    EpidemiologyBoth the incidence and prevalence of heart failure increase with age. [3] Inthe UK there were 60,480 cases of CHF in the 1-year period between 2006and 2007, with just more than 42,000 cases occurring in people over the ageof 75 years. [NHS. Hospital episode statistics] (external link) Studies of heartfailure in the US and Europe found that the annual incidence in people under 65 years of age is 1/1000 for men and 0.4/1000 for women. Over 65 years of age, the annual incidence is 11/1000 for men and 5/1000 for women. Under 65 years of age, the prevalence of heart failure is 1/1000 for men and 1/1000for women; over age 65 years the prevalence is 40/1000 for men and30/1000 for women. [3] Heart failure is the most common indication for hospitalisation in the US, andacute decompensated heart failure is the most common cause for hospitalisation among patients over 65 years. [4] The prevalence of heart failure in the US in 2004 was an estimated 5.2 millionpeople. It has significant public health implications and the estimated cost of heart failure in the US is $33.2 billion for the year 2007. The incidence of heart failure is around 10/1000 people over 65 years per year. [5] In the US,the mean age of people with heart failure is 74 years, with 52% being womenand mostly white people affected (73% to 78%). [6] [7] The average age of people with heart failure in studies conducted in Europe is also older than 70years, with slight predominance of men. [4] Heart failure is a global epidemic with a prevalence ranging from 11,000 to19,000 per million population among other countries. [8]

    AetiologyCauses and precipitating factors in acute CHF are: [1]

    Decompensation of pre-existing chronic heart failure

    Acute coronary syndrome

    Hypertensive crisis

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    Acute arrhythmia

    Valvular regurgitation

    Severe aortic valve stenosis

    Acute severe myocarditis

    Cardiac tamponade

    Aortic dissection

    Post-partum cardiomyopathy

    Non-cardiovascular precipitating factors

    o Lack of compliance with medical treatment

    o Volume overload

    o Infections

    o Severe brain insult

    o After major surgery

    o Reduction of renal function

    o Asthma

    o Drug abuse

    o Phaeochromocytoma

    High output syndromes

    o Septicaemia

    o Thyrotoxic crisis

    o Anaemia

    o Shunt syndromes.

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    The most common concurrent conditions present in patients with acute CHFare CAD, HTN, DM, atrial fibrillation, and renal insufficiency. [4] [9] Causes of right heart failure include: [10]

    Secondary to LV failure

    Secondary to pulmonary arterial hypertension

    Secondary to right ventricle (RV) myopathic process

    RV infarction

    Arrythmogenic RV cardiomyopathy

    Restrictive cardiomyopathy

    Pericardial disease

    Right-sided valvular disease

    Congenital heart disease.

    PathophysiologyDuring an episode of acute CHF, the majority of patients will have evidenceof volume overload with pulmonary and/or venous congestion.Haemodynamic measurements in these cases usually show increased right-and left-sided ventricular filling pressures with depressed cardiac index andcardiac output. However, if there is associated infection, the cardiac outputmay be normal or, in some cases, increased.

    Activation of the sympathetic nervous system causes tachycardia, increasedmyocardial contractility, increased myocardial oxygen consumption,peripheral vasoconstriction, and activation of renin-angiotensin system withsalt and water retention. There is also activation of vasoconstrictor neurohormones, which leads to sodium and fluid retention, increasedmyocardial wall stress, and decreased renal perfusion. [11] If the condition is not treated effectively, the myocardium becomes unable tomaintain a cardiac output sufficient to meet the demands of the peripheralcirculation. In order for patients with acute CHF to respond quickly totreatment, the increased myocardial stress must be reversed; for example,correction of acute severe HTN. This is particularly important in acute CHF

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    caused by ischaemia, as a dysfunctional myocardium can return to normalwhen appropriately treated.

    ClassificationClinical presentations [1]

    Acute CHF has been classified by the European Society of Cardiology intofollowing clinical groups:

    1. Acute decompensated heart failure (ADHF)

    De novo or as decompensation of chronic CHF with signs and symptoms of ADHF, which are mild and

    do not fulfil criteria for cardiogenic shock, pulmonary oedema, or hypertensive crisis.

    2. Hypertensive acute CHF

    Signs and symptoms of heart failure are accompanied by high blood pressure (BP) and relatively

    preserved left ventricular (LV) function, with a CXR compatible with acute pulmonary oedema.

    3. Pulmonary oedema (verified by CXR) View image View image Severe respiratory distress with associated crackles on lung examination, orthopnoea, and reduced

    oxygen saturation, usually below 90% on room air before treatment.

    4. Cardiogenic shock

    Defined as evidence of tissue hypoperfusion induced by heart failure after correction of preload.

    Usually characterised by reduced BP (systolic BP 30

    mmHg) and/or low urine output (60 bpm, with or without evidence of organ

    congestion.

    There is a continuum from low cardiac output syndrome to cardiogenic shock.

    5. High output failure

    Characterised by high cardiac output, usually with high heart rate (caused by arrhythmias,thyrotoxicosis, anaemia, Paget's disease, iatrogenic, or other mechanisms), with warm peripheries, pulmonary

    congestion, and, sometimes, with low BP such as in septic shock.

    6. Right heart failure

    Characterised by low output syndrome with increased jugular venous pressure, increased liver size, and

    hypotension.

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    Clinical classification of acute heart failure (AHF) [2] For simplification these patients can be classified into 3 main groups:

    1. Hypertensive AHF (acute de novo heart failure or vascular failure)

    Symptoms develop rapidly against a background of hypertension (HTN) with increased sympathetic tone

    and neurohormonal activations.

    Left ventricular ejection fraction (LVEF) is usually preserved and there are clinical and radiological

    findings of pulmonary congestion, usually without signs of systemic congestion; for example, peripheral oedema.

    Response to therapy is rapid.

    2. Normotensive AHF (acutely decompensated chronic heart failure)

    History of progressive worsening of chronic heart failure.

    BP is usually normal and symptoms and signs develop gradually with both systemic and pulmonary

    congestion.

    LVEF is usually reduced.

    3. Hypotensive AHF

    Presents with symptoms and signs of hypotension, organ hypoperfusion, and cardiogenic shock.

    Types of heart failureSystolic

    Associated with LV dysfunction and characterised by cardiomegaly, third heart sound, and volume

    overload with pulmonary congestion. LVEF is decreased.

    Diastolic

    Typically associated with normal cardiac size, hypertension, pulmonary congestion, and a fourth heart

    sound. LVEF is preserved.

    Primary prevention Aggressive control and treatment of risk factors should be considered in order to prevent acute heart failure: CAD is managed with aspirin, beta-blockers,statins, and ACE inhibitors.

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    Optimising treatment of HTN, smoking cessation, and lipid control providessubstantial benefit in patients with CAD.

    Optional control of HTN may require more than one antihypertensivemedication.

    In asymptomatic patients with reduced LVEF, ACE inhibitors arecardioprotective and reduce further decline in LVEF. [19] Beta-blockers mayalso be considered in this group of patients.

    All patients with diabetes mellitus (DM), in addition to metabolic control, needaggressive control of lipids, BP (target 70 years) (common)

    Key risk factors include age over 70 years, previous cardiovascular disease, diabetes, and poor

    compliance with medication for chronic CHF.dyspnoea (common) Predominant symptom and is present in the majority of patients with acute CHF. [9]

    pulmonary crepitations (common)

    Key finding on chest examination. [9] peripheral oedema (common)

    Present in the majority of patients (around 65% of cases). [6] [9] cool peripheries (common)

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    is a key diagnostic factor chest pain (uncommon)

    If underlying cardiac ischaemia.third heart sound (S3) (uncommon)

    is a key diagnostic factor

    Other diagnostic factorshide all

    fatigue and weakness (common)

    is a diagnostic factor hypotension (common)

    is a diagnostic factor tachycardia (common)

    Due to activation of the sympathetic nervous system or underlying arrhythmia.elevated jugular venous pressure (common)

    is a diagnostic factor displaced apex beat (point of maximal impulse) (common)

    is a diagnostic factor dullness to percussion and decreased air entry in lung bases (common)

    Suggestive of pleural effusion.wheezing (common)

    Suggests cardiac asthma.palpitations (uncommon)

    If underlying arrhythmia.cough (uncommon)

    Due to pulmonary congestion.fever (uncommon)

    Suggestive of precipitating underlying infection.syncope (uncommon)

    Suggestive of underlying cause, such as significant aortic stenosis or pulmonary embolism.murmur (uncommon)

    Both significant stenotic and regurgitate lesions can lead to heart failure.ascites (uncommon)

    is a diagnostic factor hepatomegaly (uncommon)

    is a diagnostic factor central cyanosis (uncommon)

    is a diagnostic factor Risk factors hide all

    Strongage >70 years

    A typical patient with acute heart failure is older than 70 years. [6] prior episode of congestive heart failure

    In patients hospitalised for acute CHF, around 75% have a history of prior heart failure. [6]

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    coronary artery disease

    CAD accounts for around 50% of all patients with acute HF. [6] [7] [12] [13] Chronic myocardial

    ischaemia results in myocardial damage with progressive decline in left ventricular (LV) systolic

    function. Subendocardial ischaemia also causes increase in left ventricular end diastolic pressure

    (LVEDP) leading to pulmonary oedema in the presence of normal LV systolic function. Acute coronary ischaemia can lead to acute CHF either due to pump failure or papillary muscle

    destruction/rupture. In the case of pump failure, the LV function is depressed, but in cases of heart

    failure associated with papillary muscle rupture, the measured LV function may appear preserved.hypertension

    A history of HTN is present in 72% of patients in the US and 60% of patients from

    Europe . [6] [12] [13] HTN predisposes to the development of heart failure by increasing the after-load on the ventricles,

    which induces LVH, which in turn leads to LV dysfunction, an increased risk of MI, and significant

    arrhythmias. In patients with non-compliant ventricles, an abrupt or significant increase in BP increases the

    LVEDP, precipitating acute CHF.valvular heart disease

    About 23% of patients in the US and 34% in Europe have valvular disease as an associated

    condition. [6] [13] Both significant stenotic and regurgitate lesions can lead to heart failure. Although rheumatic valvular disease is now rarely found in western countries, calcific valvular heart

    disease, in particular aortic stenosis, is commonly encountered. In patients with significant valvular disease, the heart failure will not improve until the underlying

    valvular disease has been corrected.pericardial disease

    A large pericardial effusion can present with symptoms or signs of acute CHF. Pericardial constriction, such as tuberculosis pericarditis or the effects of radiotherapy, can also

    present with acute CHF.myocarditis

    There are many causes of myocarditis, of which a viral aetiology appears to be the most common.

    There is usually a prodrome of a non-specific illness characterised by fatigue, mild dyspnoea, and

    myalgias.atrial fibrillation

    Present in 31% of cases. [6] diabetes mellitus

    Related directly to ischaemia and renal failure.non-compliance with medications

    Precipitating factor in patients with chronic CHF.

    Weak

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    excessive salt intake

    Present in 22% of cases. [14] excessive catecholamine stimulation

    Can be caused by phaeochromocytoma or subarachnoid haemorrhage. [15] abnormal thyroid function

    Both hypothyroidism and thyrotoxicosis can be associated with heart failure. [16] [17] excessive alcohol intake

    Excessive drinking is associated with heart failure (>3 drinks/day). [18]

    Diagnostic tests1st tests to order hide allTest

    ECG

    The ECG analysis in acute CHF shows atrial fibrillation in 20% of cases and other abnormal rhythms in 26% of t

    cases. [6]

    ECG abnormality is found in almost all cases of heart failure. If the ECG is completely normal then alternate diashould be considered. [31] View image

    CXR

    Pulmonary congestion on CXR is present in up to 76% of patients with acute CHF. [6] View image View i

    Hb

    Suggests anaemia as a precipitating cause.

    TFT

    Hypo- or hyperthyroidism can cause acute CHF.

    troponin

    Elevated in acute cardiac ischaemia.

    Also elevated in over 50% of cases of acute CHF without evidence of infarction. [25]

    B-type natriuretic peptide (BNP)

    If above 500 nanograms/L (>500 picograms/mL), dyspnoea likely to be due to CHF.

    If below 100 nanograms/L (

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    echocardiography

    Left ventricular ejection fraction (LVEF) 40% is transient systolic dysfunction or diagnostic dysfunction. [1]

    Preserved LVEF (45%) is observed in 34% of patients with acute CHF. [13]

    Guidelines from the European Association of Echocardiography state an LVEF of >55% is considered as normal

    LVEF of 45% to 54% is mildly abnormal, LVEF of 30% to 44% is moderately abnormal, and an LVEF of 50% as normal.

    cardiac catheterisation

    Also detects haemodynamic derangements, valvular disease, and shunts.

    endomyocardial biopsy

    Only indicated if myocarditis is clinically suspected.

    Differential diagnosisCondition

    Differentiatingsigns/symptoms Differentiating tests

    Pneumonia Fever, cough,

    productive sputum.

    Focal signs of

    consolidation -

    increased vocalfremitus and

    bronchial

    breathing.

    WCC: elevated.

    Blood cultures: positive for organism.

    CXR: consolidation.

    Pulmonary embolism Haemoptysis and

    sharp, pleuritic

    chest pain.

    Risk factors of thromboembolism

    (TE) include

    personal history of TE, family history,

    recent trauma,

    prolonged

    CT pulmonary angiography: clot in pulmonary artery

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    immobilisation,

    smoker, or OCPuse.

    Asthma

    Wheezing onphysical

    examination.

    Reduced peak flow.

    Spirometry: obstructive pattern, reversibility with be

    Interstitial lung disease Progressively

    increasingdyspnoea.

    Oxygen

    desaturation withexercise.

    Fine bibasal

    crepitations with

    no other signs of

    heart failure.

    CXR: reticular infiltrate in the late stages of disease.

    High-resolution CT scan: ground-glass appearance, r

    honeycombing, and architectural distortion.

    Spirometry: restrictive pattern.

    Adult respiratory distresssyndrome

    Severe hypoxia,

    fine crepitations.

    CXR: diffuse infiltrates

    Pulmonary artery wedge pressure:

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    and pulmonary embolism, and precipitating factors causing exacerbation of chronic CHF such as dietary indiscretion with excessive salt intake, non-compliance with medications, and excessive alcohol or drug intake.

    SymptomsHeart failure presents with dyspnoea, decreased exercise tolerance, swellingof the legs, fatigue, and generalised weakness. Sometimes the patient maypresent with predominant symptoms of the underlying condition, such aschest pain, syncope, palpitations, or viral prodrome.

    SignsCommon signs include central cyanosis, tachycardia, elevated jugular venouspressure (JVP), displaced apex beat, S3, crepitations or pleural effusion,hepatomegaly, ascites, and oedema. The presence of these signs dependsupon the duration, acuity, and the underlying cause of heart failure. Patientswith end-stage heart failure may exhibit most of these clinical signs, whereasthose in the early phase of the illness may have minimal signs.

    Patients with acute CHF can be classified clinically into 4 haemodynamicprofiles. [24] These profiles, which are based on haemodynamic principles of presence or absence of elevated filling pressure (wet or dry) and perfusionthat is adequate or critically limited (warm or cold), include:

    Warm and dry

    Warm and wet

    Cold and dry

    Cold and wet.

    Patients with pulmonary oedema present with severe respiratory distress withreduced oxygen saturation (usually 60 bpm and/or low urine output (

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    An ECG and CXR should be performed immediately in all patients withsuspected acute CHF. ECG findings are commonly related to the underlyingpathologies and include presence of Q waves, ST-T changes, left ventricular hypertrophy (LVH), left bundle branch block, and atrial fibrillation. View imageCXR may show cardiac enlargement (cardiothoracic ratio >50%); however,

    there is poor correlation between the cardiothoracic ratio (CTR) and presenceof heart failure, as the heart size may be normal in patients with diastolicdysfunction, acute valvular regurgitation as part of infective endocarditis, or acute MI. An enlarged CTR may also be seen in the absence of heart failure(e.g., pericardial effusion and LVH).

    Evaluation of the lung fields will show signs of pulmonary congestion, initiallyin the upper zones, then in the horizontal fissures followed by pulmonaryoedema and pleural effusion. View image View image The x-ray findings have

    to be taken in the context of clinical picture, as pulmonary infiltrates andcongestion, in some cases, may be due to non-cardiac cause such as ARDSor alveolar haemorrhage.CXRs rarely may show pericardial calcification, prosthetic valves, or valvular calcification. In these situations, it is helpful in identifying the possibleunderlying aetiology for heart failure.

    The following blood tests should be requested when patients present withsuspected acute CHF: [22]

    Hb: may identify anaemia as a contributing factor.

    TFTs: both hypothyroidism and hyperthyroidism can cause heart failure.

    Cardiac enzymes: >50% of patients with cardiogenic pulmonary oedema (but without evidence for MI)

    have elevated troponin T levels. [25] Elevated troponin T levels in patients with acute CHF may reflect

    subendocardial ischaemia due to elevated left ventricular end diastolic pressure. In patients with acute

    cardiogenic pulmonary oedema, a troponin T level of 0.1 g/L (0.1 ng/mL) is a powerful independent predictor

    and is associated with poor long-term survival. [25] BNP: measurement of serum BNP level in patients with symptoms of heart failure is now routinely

    carried out in most centres. The addition of BNP or N-terminal pro-brain natriuretic peptide (NT-proBNP) levelsto clinical assessment significantly enhances the accuracy of diagnosis and effectiveness of acute

    management. [26] [27] BNP is also helpful in differentiating a cardiac from a pulmonary cause of

    dyspnoea. [28] An elevated BNP level is a predictor of in-hospital mortality in patients with acute decompensated

    heart failure. [29] However, an elevated BNP level should only be taken in the context of clinical picture as it may

    be increased in a variety of other condition, such as atrial fibrillation, pulmonary embolism, or sepsis. [30]

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    Subsequent investigationsEchocardiogram is an integral part of the evaluation in a patient with acuteCHF and should be performed as soon as possible to presentation. It isrequired to assess chamber size, ventricular function (systolic and diastolic),ventricular wall thickness, valvular function, and the pericardium. Viewimage View imageCardiac catheterisation is needed in cases where significant CAD is thoughtto be the contributing factor, and is also indicated in cases where the causeof acute CHF can not be determined from other tests.

    Endomyocardial biopsy is not recommended for routine evaluation of acuteCHF, but is indicated in patients whose clinical findings suggest acutemyocarditis.

    Click to view diagnostic guideline references. Diagnostic criteriaFramingham criteria for CHF [33] The Framingham criteria are the most widely accepted clinical criteria for diagnosing heart failure. For establishing a definite diagnosis of CHF, 2 major criteria or 1 major and 2 minor criteria must be present.

    Major criteria are:

    Paroxysmal nocturnal dyspnoea or orthopnoea

    Neck-vein distention

    Rales

    Cardiomegaly

    Acute pulmonary oedema

    S3 gallop

    Increased venous pressure >16 cm of water

    Circulation time 25 seconds or longer

    Hepatojugular reflux.

    Minor criteria are:

    http://bestpractice.bmj.com/best-practice/monograph/62/resources/images/print/3.htmlhttp://bestpractice.bmj.com/best-practice/monograph/62/resources/images/print/3.htmlhttp://bestpractice.bmj.com/best-practice/monograph/62/resources/images/print/4.htmlhttp://bestpractice.bmj.com/best-practice/monograph/62/diagnosis/guidelines.htmlhttp://bestpractice.bmj.com/best-practice/monograph/62/resources/references.html#ref-33http://bestpractice.bmj.com/best-practice/monograph/62/resources/references.html#ref-33http://bestpractice.bmj.com/best-practice/monograph/62/resources/references.html#ref-33http://bestpractice.bmj.com/best-practice/monograph/62/resources/images/print/3.htmlhttp://bestpractice.bmj.com/best-practice/monograph/62/resources/images/print/3.htmlhttp://bestpractice.bmj.com/best-practice/monograph/62/resources/images/print/4.htmlhttp://bestpractice.bmj.com/best-practice/monograph/62/diagnosis/guidelines.htmlhttp://bestpractice.bmj.com/best-practice/monograph/62/resources/references.html#ref-33
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    Ankle oedema

    Night cough

    Dyspnoea on exertion

    Hepatomegaly

    Pleural effusion

    Vital capacity reduced one third from maximum

    Tachycardia (120 bpm).

    Major or minor criteria are:

    Weight loss of 4.5 kg or more in 5 days in response to treatment.

    New York Heart Association (NYHA) clinical classificationof heart failure [34]

    Class I: asymptomatic

    Class II: mild symptoms with moderate exertion

    Class III: symptoms with minimal activity

    Class IV: symptoms at rest.

    Case history #1 A 70-year-old woman complains of increasing exertional dyspnoea for thelast 2 days and now has dyspnoea at rest. She has a history of hypertensionfor the last 5 years and a 35 pack-year smoking history, but no other established illnesses. Current medications are hydrochlorothiazide daily for the last 3 years. She has been prescribed lisinopril but failed to fill the

    prescription. On examination her BP is 190/90 mmHg, heart rate 104 bpm.There is an audible S4 and the jugular venous pressure (JVP) is elevated 2cm above normal. Lung examination reveals fine bibasal crepitations. Thereis no ankle oedema.

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    Case history #2 A 73-year-old woman presents to the emergency department havingcollapsed. She is breathless and finding it difficult to talk in full sentences. Onexamination she is centrally cyanosed with cool extremities. Her pulse is 110

    bpm and systolic BP only just recordable at 80 mmHg. Jugular venouspressure (JVP) is elevated 3 cm above normal and the cardiac apex beat isdisplaced. Respiratory rate is increased and she has widespread cracklesand wheezes on chest examination.

    Other presentationsPatients may present with predominant symptoms of the underlying conditionsuch as chest pain with acute MI, syncope with significant valvular stenosis,palpitations with arrhythmias, and viral prodrome with myocarditis.

    Treatment Options

    Patient group

    Treatment

    line Treatment hide all

    haemodynamically stable 1st oxygen therapy Oxygen saturation should ideally be maintained

    between 95% and 98% to maximise tissue

    oxygenation.

    adjunct

    [?]morphine

    Morphine results in mild vasodilatation and slows

    the heart rate. It is particularly useful if the patient is

    restless and significantly dyspnoeic. [1]

    Primary Options

    morphine sulphate : 2.5 to 10 mg intravenously

    every 2-6 hours when required

    plus

    [?]loop diuretics

    Indicated in patients with a systolic BP >85

    mmHg. [1]

    Primary Options

    furosemide : 40-160 mg/dose orally/intravenously

    initially, increase by 20-40 mg/dose every 6-12

    http://bestpractice.bmj.com/best-practice/monograph/62/resources/references.html#ref-1http://bestpractice.bmj.com/best-practice/monograph/62/resources/references.html#ref-1http://bestpractice.bmj.com/best-practice/monograph/62/resources/references.html#ref-1http://bestpractice.bmj.com/best-practice/druglink.html?component-id=179025-68&optionId=expsec-637860&dd=MARTINDALEhttp://bestpractice.bmj.com/best-practice/monograph/62/resources/references.html#ref-1http://bestpractice.bmj.com/best-practice/monograph/62/resources/references.html#ref-1http://bestpractice.bmj.com/best-practice/monograph/62/resources/references.html#ref-1http://bestpractice.bmj.com/best-practice/druglink.html?component-id=179025-69&optionId=expsec-637863&dd=MARTINDALEhttp://bestpractice.bmj.com/best-practice/druglink.html?component-id=179025-69&optionId=expsec-637863&dd=MARTINDALEhttp://bestpractice.bmj.com/best-practice/monograph/62/resources/references.html#ref-1http://bestpractice.bmj.com/best-practice/druglink.html?component-id=179025-68&optionId=expsec-637860&dd=MARTINDALEhttp://bestpractice.bmj.com/best-practice/monograph/62/resources/references.html#ref-1http://bestpractice.bmj.com/best-practice/druglink.html?component-id=179025-69&optionId=expsec-637863&dd=MARTINDALE
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    Patient group

    Treatment

    line Treatment hide all

    haemodynamically stable 1st oxygen therapy Oxygen saturation should ideally be maintained

    between 95% and 98% to maximise tissue

    oxygenation.

    hours according to response, maximum 600

    mg/day

    OR

    bumetanide : 0.5 to 2 mg orally/intravenously once

    or twice daily initially, increase dose according to

    response, maximum 10 mg/day

    OR

    torasemide : 5-20 mg orally once daily initially,increase dose according to response, maximum 40

    mg/day

    plus

    [?]vasodilators

    Indicated in patients with pulmonary

    congestion/oedema and a systolic BP >90

    mmHg. [39] [56] Both IV nitroglycerin and nesiritide lower left

    ventricular filling pressure and provide symptomatic

    improvement. [57] Nitroglycerin is the preferred agent with nesiritide

    considered less preferred, as there is some

    concern about worsening in renal function with

    nesiritide and increased mortality. [40] [58] [59] However, a recent retrospective observational

    analysis from the ADHERE study showed that both

    nesiritide and nitroglycerin are equally safe in thetreatment of acute CHF. [12]

    Primary Options

    glyceryl trinitrate : 5 micrograms/min intravenously

    initially, increase by 5-20 micrograms/min

    increments every 3-5 minutes according to

    http://bestpractice.bmj.com/best-practice/druglink.html?component-id=179025-70&optionId=expsec-637863&dd=MARTINDALEhttp://bestpractice.bmj.com/best-practice/druglink.html?component-id=179025-70&optionId=expsec-637863&dd=MARTINDALEhttp://bestpractice.bmj.com/best-practice/druglink.html?component-id=179025-71&optionId=expsec-637863&dd=MARTINDALEhttp://bestpractice.bmj.com/best-practice/druglink.html?component-id=179025-71&optionId=expsec-637863&dd=MARTINDALEhttp://bestpractice.bmj.com/best-practice/monograph/62/resources/references.html#ref-39http://bestpractice.bmj.com/best-practice/monograph/62/resources/references.html#ref-39http://bestpractice.bmj.com/best-practice/monograph/62/resources/references.html#ref-39http://bestpractice.bmj.com/best-practice/monograph/62/resources/references.html#ref-56http://bestpractice.bmj.com/best-practice/monograph/62/resources/references.html#ref-56http://bestpractice.bmj.com/best-practice/monograph/62/resources/references.html#ref-57http://bestpractice.bmj.com/best-practice/monograph/62/resources/references.html#ref-57http://bestpractice.bmj.com/best-practice/monograph/62/resources/references.html#ref-57http://bestpractice.bmj.com/best-practice/monograph/62/resources/references.html#ref-40http://bestpractice.bmj.com/best-practice/monograph/62/resources/references.html#ref-40http://bestpractice.bmj.com/best-practice/monograph/62/resources/references.html#ref-40http://bestpractice.bmj.com/best-practice/monograph/62/resources/references.html#ref-58http://bestpractice.bmj.com/best-practice/monograph/62/resources/references.html#ref-58http://bestpractice.bmj.com/best-practice/monograph/62/resources/references.html#ref-59http://bestpractice.bmj.com/best-practice/monograph/62/resources/references.html#ref-59http://bestpractice.bmj.com/best-practice/monograph/62/resources/references.html#ref-12http://bestpractice.bmj.com/best-practice/monograph/62/resources/references.html#ref-12http://bestpractice.bmj.com/best-practice/monograph/62/resources/references.html#ref-12http://bestpractice.bmj.com/best-practice/druglink.html?component-id=179025-72&optionId=expsec-637866&dd=MARTINDALEhttp://bestpractice.bmj.com/best-practice/druglink.html?component-id=179025-70&optionId=expsec-637863&dd=MARTINDALEhttp://bestpractice.bmj.com/best-practice/druglink.html?component-id=179025-71&optionId=expsec-637863&dd=MARTINDALEhttp://bestpractice.bmj.com/best-practice/monograph/62/resources/references.html#ref-39http://bestpractice.bmj.com/best-practice/monograph/62/resources/references.html#ref-56http://bestpractice.bmj.com/best-practice/monograph/62/resources/references.html#ref-57http://bestpractice.bmj.com/best-practice/monograph/62/resources/references.html#ref-40http://bestpractice.bmj.com/best-practice/monograph/62/resources/references.html#ref-58http://bestpractice.bmj.com/best-practice/monograph/62/resources/references.html#ref-59http://bestpractice.bmj.com/best-practice/monograph/62/resources/references.html#ref-12http://bestpractice.bmj.com/best-practice/druglink.html?component-id=179025-72&optionId=expsec-637866&dd=MARTINDALE
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    Patient group

    Treatment

    line Treatment hide all

    haemodynamically stable 1st oxygen therapy Oxygen saturation should ideally be maintained

    between 95% and 98% to maximise tissue

    oxygenation.

    response, maximum 200 micrograms/min

    Secondary Options

    nesiritide : 2 micrograms/kg/dose intravenous bolusinitially, followed by 0.01 micrograms/kg/min

    infusion

    plus

    [?]supportive care

    Continued supportive care includes maintenance of

    adequate oxygenation (ideally maintained between

    95% and 98% to maximise tissue oxygenation),

    patent airways, a low salt diet, and restriction of

    daily fluid intake.

    adjunct

    [?]ventilation

    Required if oxygen saturation cannot be maintained

    with oxygenation alone. [1] Non-invasive positive pressure ventilation (NIPPV)

    or CPAP should be tried first. Mechanical

    ventilation is only used when other treatmentsincluding NIPPV fail.

    inadequate response to loop

    diuretics

    adjunct

    [?]non-loop diuretics

    Indicated in patients with a systolic BP >85

    mmHg. [1] Non-loop diuretics are commonly used in

    combination with loop diuretics to improve diuresis.

    Primary Options

    spironolactone : 25-100 mg orally once daily

    OR

    eplerenone : 25-50 mg orally once daily

    OR

    http://bestpractice.bmj.com/best-practice/druglink.html?component-id=179025-73&optionId=expsec-637866&dd=MARTINDALEhttp://bestpractice.bmj.com/best-practice/druglink.html?component-id=179025-73&optionId=expsec-637866&dd=MARTINDALEhttp://bestpractice.bmj.com/best-practice/monograph/62/resources/references.html#ref-1http://bestpractice.bmj.com/best-practice/monograph/62/resources/references.html#ref-1http://bestpractice.bmj.com/best-practice/monograph/62/resources/references.html#ref-1http://bestpractice.bmj.com/best-practice/monograph/62/resources/references.html#ref-1http://bestpractice.bmj.com/best-practice/druglink.html?component-id=179025-37&optionId=expsec-637890&dd=MARTINDALEhttp://bestpractice.bmj.com/best-practice/druglink.html?component-id=179025-38&optionId=expsec-637890&dd=MARTINDALEhttp://bestpractice.bmj.com/best-practice/druglink.html?component-id=179025-73&optionId=expsec-637866&dd=MARTINDALEhttp://bestpractice.bmj.com/best-practice/monograph/62/resources/references.html#ref-1http://bestpractice.bmj.com/best-practice/monograph/62/resources/references.html#ref-1http://bestpractice.bmj.com/best-practice/druglink.html?component-id=179025-37&optionId=expsec-637890&dd=MARTINDALEhttp://bestpractice.bmj.com/best-practice/druglink.html?component-id=179025-38&optionId=expsec-637890&dd=MARTINDALE
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    Patient group

    Treatment

    line Treatment hide all

    haemodynamically stable 1st oxygen therapy Oxygen saturation should ideally be maintained

    between 95% and 98% to maximise tissue

    oxygenation.

    metolazone : 2.5 to 10 mg orally once daily

    due to cardiac ischaemia plus

    [?]aspirin revascularisation

    Aspirin is given to all patients (in the absence of

    contra-indication) with coronary ischaemia and

    those undergoing revascularisation. Revascularisation may be achieved with

    percutaneous revasculatisation or, in selected

    cases, with coronary artery bypass grafting.

    Primary Options

    aspirin : 300 mg orally as a single dose, followed by

    75 mg once daily thereafter

    due to valvular disease adjunct

    [?]

    nitroprusside

    Indicated in patients with aortic stenosis, aorticregurgitation, mitral stenosis, or mitral regurgitation

    who are not hypotensive. Dose of nitroprusside exceeding 400

    micrograms/minute generally does not produce

    added benefit and may increase the risk of

    thiocyanate toxicity. [55]

    Primary Options

    nitroprusside : 0.3 micrograms/kg/min intravenouslyinitially, increase by 0.5 micrograms/kg/min

    increments according to response, usual dose is 5

    micrograms/kg/min

    due to acute right heart failure plus

    [?]treatment of underlying cause

    Therapy is centred around treatment of the

    underlying pathology; e.g., pulmonary embolism

    http://bestpractice.bmj.com/best-practice/druglink.html?component-id=179025-39&optionId=expsec-637890&dd=MARTINDALEhttp://bestpractice.bmj.com/best-practice/druglink.html?component-id=179025-40&optionId=expsec-637887&dd=MARTINDALEhttp://bestpractice.bmj.com/best-practice/druglink.html?component-id=179025-40&optionId=expsec-637887&dd=MARTINDALEhttp://bestpractice.bmj.com/best-practice/monograph/62/resources/references.html#ref-55http://bestpractice.bmj.com/best-practice/monograph/62/resources/references.html#ref-55http://bestpractice.bmj.com/best-practice/monograph/62/resources/references.html#ref-55http://bestpractice.bmj.com/best-practice/druglink.html?component-id=179025-41&optionId=expsec-637884&dd=MARTINDALEhttp://bestpractice.bmj.com/best-practice/druglink.html?component-id=179025-39&optionId=expsec-637890&dd=MARTINDALEhttp://bestpractice.bmj.com/best-practice/druglink.html?component-id=179025-40&optionId=expsec-637887&dd=MARTINDALEhttp://bestpractice.bmj.com/best-practice/monograph/62/resources/references.html#ref-55http://bestpractice.bmj.com/best-practice/druglink.html?component-id=179025-41&optionId=expsec-637884&dd=MARTINDALE
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    Patient group

    Treatment

    line Treatment hide all

    haemodynamically stable 1st oxygen therapy Oxygen saturation should ideally be maintained

    between 95% and 98% to maximise tissue

    oxygenation.

    (anticoagulation, thrombolytics, catheterisation, or

    surgically directed thrombectomy), right ventricular

    infarction (PCI or thrombolytics), and chronic

    thromboembolic pulmonary hypertension

    (thromboendarterectomy). [49]

    due to acute myocarditis plus

    [?]supportive care or immunosuppressant therapy

    Giant cell myocarditis is treated with single or

    combination immunosuppressant therapy including

    corticosteroids, azathioprine, cyclosporine, andmuromonab-CD3 (OKT3). [50]

    Treatment of other forms of myocarditis is limited to

    supportive care. [51]

    inadequate response to

    combination diuretics

    adjunct

    [?]ultrafiltration

    For patients with volume overload who do not

    respond to medical therapy.

    hypotensive (systolic BP

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    Patient group

    Treatment

    line Treatment hide all

    haemodynamically stable 1st oxygen therapy Oxygen saturation should ideally be maintained

    between 95% and 98% to maximise tissue

    oxygenation.

    Evidence] [B Evidence] The infusion rate is modified according to

    symptoms, diuretic response, or haemodynamicmonitoring.

    Choice of inotrope depends on clinical findings. Dobutamine or milrinone are recommended for

    patients with systolic BP 85 to 100 mmHg and noclear clinical evidence of shock (such as cold

    extremities and low urine output). [1] Levosimendan, a calcium sensitiser, is a new drug

    that is sometimes recommended as an alternative

    to dobutamine or milrinone; however, it is not

    commonly used in practice, and may not be

    available in some countries (including the

    US) . [44] [45] [46] [47] Avoid if the patient is very

    hypotensive (systolic BP

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    Patient group

    Treatment

    line Treatment hide all

    haemodynamically stable 1st oxygen therapy Oxygen saturation should ideally be maintained

    between 95% and 98% to maximise tissue

    oxygenation.

    dobutamine : 2-20 micrograms/kg/min

    intravenously

    OR

    dopamine : 5-15 micrograms/kg/min intravenously

    OR

    norepinephrine : 0.5 to 30 micrograms/minintravenously

    plus

    [?]supportive care

    Continued supportive care includes maintenance of

    adequate oxygenation (ideally maintained between

    95% and 98% to maximise tissue oxygenation),

    patent airways, a low salt diet, and restriction of

    daily fluid intake.

    adjunct

    [?]ventilation

    Required if oxygen saturation cannot be maintained

    with oxygenation alone. [1] Non-invasive positive pressure ventilation (NIPPV)

    or CPAP should be tried first. Mechanical

    ventilation is only used when other treatments

    including NIPPV fail.

    2nd intra-aortic balloon pump Required in patients with persistent cardiogenic

    shock, despite inotropic therapy.3rd left ventricular assist device (LVAD)

    The use of LVADs has evolved significantly over

    the past 25 years and various types of LVAD now

    exist. Extracorporeal devices, the most common of

    which are the extracorporeal membrane

    oxygenators (ECMOs), require full heparinisation

    http://bestpractice.bmj.com/best-practice/druglink.html?component-id=179025-75&optionId=expsec-637896&dd=MARTINDALEhttp://bestpractice.bmj.com/best-practice/druglink.html?component-id=179025-75&optionId=expsec-637896&dd=MARTINDALEhttp://bestpractice.bmj.com/best-practice/druglink.html?component-id=179025-76&optionId=expsec-637896&dd=MARTINDALEhttp://bestpractice.bmj.com/best-practice/druglink.html?component-id=179025-77&optionId=expsec-637896&dd=MARTINDALEhttp://bestpractice.bmj.com/best-practice/monograph/62/resources/references.html#ref-1http://bestpractice.bmj.com/best-practice/druglink.html?component-id=179025-75&optionId=expsec-637896&dd=MARTINDALEhttp://bestpractice.bmj.com/best-practice/druglink.html?component-id=179025-76&optionId=expsec-637896&dd=MARTINDALEhttp://bestpractice.bmj.com/best-practice/druglink.html?component-id=179025-77&optionId=expsec-637896&dd=MARTINDALEhttp://bestpractice.bmj.com/best-practice/monograph/62/resources/references.html#ref-1
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    Patient group

    Treatment

    line Treatment hide all

    haemodynamically stable 1st oxygen therapy Oxygen saturation should ideally be maintained

    between 95% and 98% to maximise tissue

    oxygenation.

    and are typically used for days or weeks as a

    bridge for patients who are expected to recover

    within days. Percutaneous short-term devices (e.g.,

    Tandem Heart) are inserted through the femoral

    artery and advanced into the left ventricle. Longer-term assist devices are divided into first generation

    (e.g., Heart Mate I), second generation (e.g., HeartMate II), and third generation (e.g., HVAD and Dura

    Heart) devices. The third generation pumps are

    thought to last as long as 5 to 10 years and arecurrently being evaluated in several phase 1

    studies . [53]

    due to cardiac ischaemia plus

    [?]aspirin revascularisation

    Aspirin is given to all patients (in the absence of

    contra-indication) with coronary ischemia and those

    undergoing revascularisation. Revascularisation may be achieved with

    percutaneous revasculatisation or, as second-line

    therapy, coronary artery bypass.

    Primary Options

    aspirin : 300 mg orally as a single dose, followed by

    75 mg once daily thereafter

    due to valve stenosis adjunct[?]

    percutaneous valvotomy Used as a bridge to aortic valve replacement. May

    be considered for mitral stenosis if no thrombuspresent on trans-oesophageal echocardiogram.

    hypertensive crisis 1st oxygen therapy Oxygen saturation should ideally be maintained

    http://bestpractice.bmj.com/best-practice/monograph/62/resources/references.html#ref-53http://bestpractice.bmj.com/best-practice/monograph/62/resources/references.html#ref-53http://bestpractice.bmj.com/best-practice/monograph/62/resources/references.html#ref-53http://bestpractice.bmj.com/best-practice/monograph/62/resources/references.html#ref-53http://bestpractice.bmj.com/best-practice/druglink.html?component-id=179025-42&optionId=expsec-637926&dd=MARTINDALEhttp://bestpractice.bmj.com/best-practice/druglink.html?component-id=179025-42&optionId=expsec-637926&dd=MARTINDALEhttp://bestpractice.bmj.com/best-practice/monograph/62/resources/references.html#ref-53http://bestpractice.bmj.com/best-practice/druglink.html?component-id=179025-42&optionId=expsec-637926&dd=MARTINDALE
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    Patient group

    Treatment

    line Treatment hide all

    haemodynamically stable 1st oxygen therapy Oxygen saturation should ideally be maintained

    between 95% and 98% to maximise tissue

    oxygenation.

    between 95% and 98% to maximise tissueoxygenation.

    plus

    [?]IV beta-blockers and glyceryl trinitrate

    Primary Options

    metoprolol : 5-10 mg intravenously every 4-6 hoursor

    esmolol : 250-500 micrograms/kg/dose

    intravenously over 1 minute initially, followed by 50-

    100 micrograms/kg/min infusion for 4 minutes, may

    repeat loading dose and increase infusion up to200 micrograms/kg/min according to response,

    consult specialist for further guidance on dose

    -- AND --

    glyceryl trinitrate : 5 micrograms/min intravenously

    initially, increase by 5-20 micrograms/minincrements every 3-5 minutes according to

    response, maximum 200 micrograms/min

    adjunct

    [?]nitroprusside

    Dose of nitroprusside exceeding 400

    micrograms/minute generally does not produce

    added benefit and may increase the risk of

    thiocyanate toxicity. [55]

    Primary Options

    nitroprusside : 0.3 micrograms/kg/min intravenously

    initially, increase by 0.5 micrograms/kg/min

    increments according to response, usual dose is 5

    micrograms/kg/min

    http://bestpractice.bmj.com/best-practice/druglink.html?component-id=179025-14&optionId=expsec-15&dd=MARTINDALEhttp://bestpractice.bmj.com/best-practice/druglink.html?component-id=179025-14&optionId=expsec-15&dd=MARTINDALEhttp://bestpractice.bmj.com/best-practice/druglink.html?component-id=179025-15&optionId=expsec-15&dd=MARTINDALEhttp://bestpractice.bmj.com/best-practice/druglink.html?component-id=179025-16&optionId=expsec-15&dd=MARTINDALEhttp://bestpractice.bmj.com/best-practice/monograph/62/resources/references.html#ref-55http://bestpractice.bmj.com/best-practice/monograph/62/resources/references.html#ref-55http://bestpractice.bmj.com/best-practice/monograph/62/resources/references.html#ref-55http://bestpractice.bmj.com/best-practice/druglink.html?component-id=179025-1&optionId=expsec-16&dd=MARTINDALEhttp://bestpractice.bmj.com/best-practice/druglink.html?component-id=179025-14&optionId=expsec-15&dd=MARTINDALEhttp://bestpractice.bmj.com/best-practice/druglink.html?component-id=179025-15&optionId=expsec-15&dd=MARTINDALEhttp://bestpractice.bmj.com/best-practice/druglink.html?component-id=179025-16&optionId=expsec-15&dd=MARTINDALEhttp://bestpractice.bmj.com/best-practice/monograph/62/resources/references.html#ref-55http://bestpractice.bmj.com/best-practice/druglink.html?component-id=179025-1&optionId=expsec-16&dd=MARTINDALE
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    Patient group

    Treatment

    line Treatment hide all

    haemodynamically stable 1st oxygen therapy Oxygen saturation should ideally be maintained

    between 95% and 98% to maximise tissue

    oxygenation.

    plus

    [?]supportive care

    Continued supportive care includes maintenance of

    adequate oxygenation (ideally maintained between

    95% and 98% to maximse tissue oxygenation),

    patent airways, a low salt diet, and restriction of daily fluid intake.

    Precipitating factors such as pain and agitationshould be also be controlled.

    adjunct

    [?]ventilation

    Required if oxygen saturation cannot be maintained

    with oxygenation alone. [1] Non-invasive positive pressure ventilation (NIPPV)

    or CPAP should be tried first. Mechanical

    ventilation is only used when other treatmentsincluding NIPPV fail.

    Acute

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    Patient group

    Treatment

    line Treatment hide all

    acute episode stabilised:

    LVEF 100 mmHg

    1st ACE inhibitor or angiotensin-II receptor antagonist An ACE inhibitor is the preferred agent. An

    angiotensin-II receptor antagonist is only used in

    patients who are intolerant of ACE inhibitors. A

    combination of an ACE inhibitor and angiotensin-II

    receptor blocker should be avoided because of therisk of renal dysfunction and hyperkalaemia.

    Dose should be started low and increased according

    to response. Treatment is targeted to maximum dosetolerated.

    Primary Options

    captopril : 6.25 to 50 mg orally three times daily

    OR

    lisinopril : 2.5 to 40 mg orally once daily

    OR

    ramipril : 1.25 to 10 mg orally once daily

    OR

    enalapril : 2.5 to 20 mg orally twice daily

    Secondary Options

    candesartan : 4-32 mg orally once daily

    OR

    losartan : 25-150 mg orally once daily

    OR

    valsartan : 40-160 mg orally twice daily

    plus

    [?]

    beta-blocker

    The pivotal trials with beta-blockers were conductedin patients with continuing symptoms and a

    persistently low EF, despite treatment with an ACE

    inhibitor and, in most cases, a diuretic. Despite this,there is consensus that these treatments are

    complementary and that a beta-blocker and an ACE

    inhibitor should both be started as soon as possible

    after diagnosis of heart failure with reduced ejection

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    Patient group

    Treatment

    line Treatment hide all

    acute episode stabilised:

    LVEF 100 mmHg

    1st ACE inhibitor or angiotensin-II receptor antagonist An ACE inhibitor is the preferred agent. An

    angiotensin-II receptor antagonist is only used in

    patients who are intolerant of ACE inhibitors. A

    combination of an ACE inhibitor and angiotensin-II

    receptor blocker should be avoided because of therisk of renal dysfunction and hyperkalaemia.

    Dose should be started low and increased according

    to response. Treatment is targeted to maximum dosetolerated.

    Primary Options

    captopril : 6.25 to 50 mg orally three times daily

    OR

    lisinopril : 2.5 to 40 mg orally once daily

    OR

    ramipril : 1.25 to 10 mg orally once daily

    OR

    enalapril : 2.5 to 20 mg orally twice daily

    Secondary Options

    candesartan : 4-32 mg orally once daily

    OR

    losartan : 25-150 mg orally once daily

    OR

    valsartan : 40-160 mg orally twice daily

    fraction (HF-REF). [37] Typically, beta-blockers are started only after the

    patient has been stabilised and is in compensated

    heart failure. Treatment is targeted to maximum dose tolerated.

    Primary Options

    bisoprolol : 1.25 mg orally once daily initially, increase

    http://bestpractice.bmj.com/best-practice/druglink.html?component-id=179025-61&optionId=expsec-637920&dd=MARTINDALEhttp://bestpractice.bmj.com/best-practice/druglink.html?component-id=179025-61&optionId=expsec-637920&dd=MARTINDALEhttp://bestpractice.bmj.com/best-practice/druglink.html?component-id=179025-62&optionId=expsec-637920&dd=MARTINDALEhttp://bestpractice.bmj.com/best-practice/druglink.html?component-id=179025-63&optionId=expsec-637920&dd=MARTINDALEhttp://bestpractice.bmj.com/best-practice/druglink.html?component-id=179025-64&optionId=expsec-637920&dd=MARTINDALEhttp://bestpractice.bmj.com/best-practice/druglink.html?component-id=179025-64&optionId=expsec-637920&dd=MARTINDALEhttp://bestpractice.bmj.com/best-practice/druglink.html?component-id=179025-65&optionId=expsec-637920&dd=MARTINDALEhttp://bestpractice.bmj.com/best-practice/druglink.html?component-id=179025-65&optionId=expsec-637920&dd=MARTINDALEhttp://bestpractice.bmj.com/best-practice/druglink.html?component-id=179025-66&optionId=expsec-637920&dd=MARTINDALEhttp://bestpractice.bmj.com/best-practice/druglink.html?component-id=179025-67&optionId=expsec-637920&dd=MARTINDALEhttp://bestpractice.bmj.com/best-practice/druglink.html?component-id=179025-67&optionId=expsec-637920&dd=MARTINDALEhttp://bestpractice.bmj.com/best-practice/monograph/62/resources/references.html#ref-37http://bestpractice.bmj.com/best-practice/monograph/62/resources/references.html#ref-37http://bestpractice.bmj.com/best-practice/monograph/62/resources/references.html#ref-37http://bestpractice.bmj.com/best-practice/druglink.html?component-id=179025-86&optionId=expsec-682508&dd=MARTINDALEhttp://bestpractice.bmj.com/best-practice/druglink.html?component-id=179025-61&optionId=expsec-637920&dd=MARTINDALEhttp://bestpractice.bmj.com/best-practice/druglink.html?component-id=179025-62&optionId=expsec-637920&dd=MARTINDALEhttp://bestpractice.bmj.com/best-practice/druglink.html?component-id=179025-63&optionId=expsec-637920&dd=MARTINDALEhttp://bestpractice.bmj.com/best-practice/druglink.html?component-id=179025-64&optionId=expsec-637920&dd=MARTINDALEhttp://bestpractice.bmj.com/best-practice/druglink.html?component-id=179025-65&optionId=expsec-637920&dd=MARTINDALEhttp://bestpractice.bmj.com/best-practice/druglink.html?component-id=179025-66&optionId=expsec-637920&dd=MARTINDALEhttp://bestpractice.bmj.com/best-practice/druglink.html?component-id=179025-67&optionId=expsec-637920&dd=MARTINDALEhttp://bestpractice.bmj.com/best-practice/monograph/62/resources/references.html#ref-37http://bestpractice.bmj.com/best-practice/druglink.html?component-id=179025-86&optionId=expsec-682508&dd=MARTINDALE
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    35/76

    Patient group

    Treatment

    line Treatment hide all

    acute episode stabilised:

    LVEF 100 mmHg

    1st ACE inhibitor or angiotensin-II receptor antagonist An ACE inhibitor is the preferred agent. An

    angiotensin-II receptor antagonist is only used in

    patients who are intolerant of ACE inhibitors. A

    combination of an ACE inhibitor and angiotensin-II

    receptor blocker should be avoided because of therisk of renal dysfunction and hyperkalaemia.

    Dose should be started low and increased according

    to response. Treatment is targeted to maximum dosetolerated.

    Primary Options

    captopril : 6.25 to 50 mg orally three times daily

    OR

    lisinopril : 2.5 to 40 mg orally once daily

    OR

    ramipril : 1.25 to 10 mg orally once daily

    OR

    enalapril : 2.5 to 20 mg orally twice daily

    Secondary Options

    candesartan : 4-32 mg orally once daily

    OR

    losartan : 25-150 mg orally once daily

    OR

    valsartan : 40-160 mg orally twice daily

    according to response, maximum 10 mg/day

    OR carvedilol : 3.125 mg orally (immediate-release) twice

    daily initially, increase according to response,

    maximum 50 mg/day

    OR

    metoprolol : 12.5 to 200 mg orally (extended-release)

    once daily

    http://bestpractice.bmj.com/best-practice/druglink.html?component-id=179025-87&optionId=expsec-682508&dd=MARTINDALEhttp://bestpractice.bmj.com/best-practice/druglink.html?component-id=179025-88&optionId=expsec-682508&dd=MARTINDALEhttp://bestpractice.bmj.com/best-practice/druglink.html?component-id=179025-87&optionId=expsec-682508&dd=MARTINDALEhttp://bestpractice.bmj.com/best-practice/druglink.html?component-id=179025-88&optionId=expsec-682508&dd=MARTINDALE
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    36/76

    Patient group

    Treatment

    line Treatment hide all

    acute episode stabilised:

    LVEF 100 mmHg

    1st ACE inhibitor or angiotensin-II receptor antagonist An ACE inhibitor is the preferred agent. An

    angiotensin-II receptor antagonist is only used in

    patients who are intolerant of ACE inhibitors. A

    combination of an ACE inhibitor and angiotensin-II

    receptor blocker should be avoided because of therisk of renal dysfunction and hyperkalaemia.

    Dose should be started low and increased according

    to response. Treatment is targeted to maximum dose