Acute Exacerbation of Congestive Heart Failure: History & Exam

Acute exacerbation of congestive heart failure
Highlights
Summary Overview
Basics
Definition Epidemiology Aetiology Pathophysiology Classification
Prevention
Primary Screening Secondary
Diagnosis
History & examination Tests Differential Step-by-step Criteria Guidelines Case history
Treatment
Details Step-by-step Emerging Guidelines Evidence
Follow Up
Recommendations Complications Prognosis
Resources
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History & exam

Key factors
presence of risk factors (previous cardiovascular disease, age >70 years) dyspnoea
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 cyanosis History & 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
Diagnostic tests details
Treatment details
Acute
haemodynamically stable o o o o o o oxygen therapy morphine loop diuretics vasodilators supportive care ventilation inadequate response to loop diuretics non-loop diuretics due to cardiac ischaemia aspirin revascularisation due to valvular disease nitroprusside due to acute right heart failure treatment of underlying cause due to acute myocarditis supportive care or immunosuppressant therapy inadequate response to combination diuretics ultrafiltration hypotensive (systolic BP <90 mmHg) o o oxygen therapy inotropes supportive care ventilation intra-aortic balloon pump left ventricular assist device (LVAD) due to cardiac ischaemia aspirin revascularisation due to valve stenosis percutaneous valvotomy hypertensive crisis
oxygen therapy IV beta-blockers and glyceryl trinitrate nitroprusside supportive care ventilation
Ongoing
acute episode stabilised: LVEF <50% and systolic BP >100 mmHg ACE inhibitor or angiotensin-II receptor antagonist beta-blocker aldosterone receptor antagonist vasodilators diuretics supportive care acute episode stabilised: LVEF <50% and systolic BP 90-100 mmHg ACE inhibitor beta-blocker aldosterone receptor antagonist vasodilators diuretics supportive care acute episode stabilised: LVEF 50% ACE inhibitor or beta-blocker diuretic supportive care Treatment details
Summary
Clinical syndrome of reduced cardiac output, tissue hypoperfusion, increased pulmonary pressure, and tissue congestion. Presents with dyspnoea, decreased exercise tolerance, swelling of the legs, fatigue, and generalised weakness. Clinical diagnosis is supported by ancillary tests such as echocardiogram (ECG), chest x-ray (CXR), and B-type natriuretic peptide (BNP).
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
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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
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
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
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 and signs due to abnormal cardiac function. It may be due to cardiac or extracardiac causes and results in reduced cardiac output, tissue hypoperfusion, increased pulmonary capillary wedge pressure, and tissue congestion. [1]
Epidemiology
Both the incidence and prevalence of heart failure increase with age. [3] In the UK there were 60,480 cases of CHF in the 1-year period between 2006 and 2007, with just more than 42,000 cases occurring in people over the age of 75 years. [NHS. Hospital episode statistics] (external link) Studies of heart failure 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 1/1000 for women; over age 65 years the prevalence is 40/1000 for men and 30/1000 for women. [3] Heart failure is the most common indication for hospitalisation in the US, and acute 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 million people. 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 women and 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 70 years, with slight predominance of men. [4] Heart failure is a global epidemic with a prevalence ranging from 11,000 to 19,000 per million population among other countries. [8]
Aetiology
Causes and precipitating factors in acute CHF are: [1]
Decompensation of pre-existing chronic heart failure Acute coronary syndrome Hypertensive crisis
o o o o o o o o o o o o o
Acute arrhythmia Valvular regurgitation Severe aortic valve stenosis Acute severe myocarditis Cardiac tamponade Aortic dissection Post-partum cardiomyopathy Non-cardiovascular precipitating factors Lack of compliance with medical treatment Volume overload Infections Severe brain insult After major surgery Reduction of renal function Asthma Drug abuse Phaeochromocytoma High output syndromes Septicaemia Thyrotoxic crisis Anaemia Shunt syndromes.
The most common concurrent conditions present in patients with acute CHF are 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.
Pathophysiology
During an episode of acute CHF, the majority of patients will have evidence of volume overload with pulmonary and/or venous congestion. Haemodynamic measurements in these cases usually show increased rightand left-sided ventricular filling pressures with depressed cardiac index and cardiac output. However, if there is associated infection, the cardiac output may be normal or, in some cases, increased. Activation of the sympathetic nervous system causes tachycardia, increased myocardial contractility, increased myocardial oxygen consumption, peripheral vasoconstriction, and activation of renin-angiotensin system with salt and water retention. There is also activation of vasoconstrictor neurohormones, which leads to sodium and fluid retention, increased myocardial wall stress, and decreased renal perfusion. [11] If the condition is not treated effectively, the myocardium becomes unable to maintain a cardiac output sufficient to meet the demands of the peripheral circulation. In order for patients with acute CHF to respond quickly to treatment, the increased myocardial stress must be reversed; for example, correction of acute severe HTN. This is particularly important in acute CHF
caused by ischaemia, as a dysfunctional myocardium can return to normal when appropriately treated.
Classification
Clinical presentations [1] Acute CHF has been classified by the European Society of Cardiology into following 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 imageView 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 <90 mmHg or a drop of mean arterial pressure >30 mmHg) and/or low urine output (<0.5 mL/kg/hour), with a pulse rate >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.
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 failure Systolic

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.
Optimising treatment of HTN, smoking cessation, and lipid control provides substantial benefit in patients with CAD. Optional control of HTN may require more than one antihypertensive medication. In asymptomatic patients with reduced LVEF, ACE inhibitors are cardioprotective and reduce further decline in LVEF. [19] Beta-blockers may also be considered in this group of patients. All patients with diabetes mellitus (DM), in addition to metabolic control, need aggressive control of lipids, BP (target <135/80 mmHg) and should be treated with an ACE inhibitor, regardless of the level of the LV dysfunction, when other cardiovascular risk factors are present.[20] [21] Alcohol consumption and excessive salt and fluid intake should be discouraged in patients with known LV dysfunction. [22]
Screening
There is no consensus on the optimal and cost-effective screening method for the detection of asymptomatic ventricular dysfunction. Various modalities, including ECG, echocardiogram, and cardiac biomarkers, have been suggested as screening tools, but none are practically applicable for screening purposes in the general community. [35] Some have suggested selective screening of patients who are identified at higher risk for asymptomatic ventricular dysfunction. [36]
Secondary prevention
All patients with heart failure are recommended to have pneumococcal vaccination and annual influenza vaccine.
History & examination

Key diagnostic factorshide all
presence of risk factors (previous cardiovascular disease, age >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)
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)
Risk
is a diagnostic factor factorshide all
Strong age >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]
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 Weak
Precipitating factor in patients with chronic CHF.
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 tests
1st tests to orderhide all
Test
ECG cases. [6] should be considered. [31] View image CXR Pulmonary congestion on CXR is present in up to 76% of patients with acute CHF. [6] View imageView image
The ECG analysis in acute CHF shows atrial fibrillation in 20% of cases and other abnormal rhythms in 26% of th
ECG abnormality is found in almost all cases of heart failure. If the ECG is completely normal then alternate diag
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 (<100 picograms/mL), unlikely to be caused by CHF. If 100 to 500 nanograms/L (100-500 picograms/mL), further investigations are required. [27]
Tests to considerhide all

Test
echocardiography Left ventricular ejection fraction (LVEF) <40% is consistent with systolic LV dysfunction.View imageView image LVEF >40% is transient systolic dysfunction or diagnostic dysfunction.[1] Preserved LVEF (45%) is observed in 34% of patients with acute CHF. [13] LVEF of 45% to 54% is mildly abnormal, LVEF of 30% to 44% is moderately abnormal, and an LVEF of <30% is abnormal. [32] In clinical practice, many centres consider an LVEF of >50% as normal. cardiac catheterisation Also detects haemodynamic derangements, valvular disease, and shunts.
Guidelines from the European Association of Echocardiography state an LVEF of >55% is considered as normal
endomyocardial biopsy Only indicated if myocarditis is clinically suspected.
Differential diagnosis
Condition Differentiating signs/symptoms Differentiating tests
Pneumonia
Fever, cough, productive sputum.
WCC: elevated. Blood cultures: positive for organism. CXR: consolidation.
Focal signs of consolidation increased vocal fremitus and bronchial breathing.
Pulmonary embolism
Haemoptysis and sharp, pleuritic chest pain.
CT pulmonary angiography: clot in pulmonary artery.
Risk factors of thromboembolism (TE) include personal history of TE, family history, recent trauma, prolonged
immobilisation, smoker, or OCP use. Asthma
Wheezing on physical examination.
Reduced peak flow.
Spirometry: obstructive pattern, reversibility with beta-ag
Interstitial lung disease
Progressively increasing dyspnoea.
CXR: reticular infiltrate in the late stages of disease.
High-resolution CT scan: ground-glass appearance, reti honeycombing, and architectural distortion.
Oxygen desaturation with exercise.
Spirometry: restrictive pattern.
Fine bibasal crepitations with no other signs of heart failure.
Adult respiratory distress syndrome
Severe hypoxia, fine crepitations.
CXR: diffuse infiltrates Pulmonary artery wedge pressure: <18 mmHg
Step-by-step diagnostic approach

Despite advances in technology, the diagnosis of acute CHF is primarily clinically based, supported by ancillary tests such as ECG, CXR, B-type natriuretic peptide (BNP), and echocardiogram. [1] [22] The sensitivity of clinical assessment in identifying left ventricular (LV) systolic dysfunction is approximately 81% but the specificity is only 47%. The specificity of this diagnosis is improved to 69% by addition of ECG and to 92% by addition of CXR. [23]
History and risk factors

A careful history should be taken for causes of acute CHF, such as myocardial ischaemia, uncontrolled HTN, significant valvular disease (both stenosis and regurgitation), arrhythmias, infection, anaemia, thyrotoxicosis,
and pulmonary embolism, and precipitating factors causing exacerbation of chronic CHF such as dietary indiscretion with excessive salt intake, noncompliance with medications, and excessive alcohol or drug intake.
Symptoms
Heart failure presents with dyspnoea, decreased exercise tolerance, swelling of the legs, fatigue, and generalised weakness. Sometimes the patient may present with predominant symptoms of the underlying condition, such as chest pain, syncope, palpitations, or viral prodrome.
Signs
Common signs include central cyanosis, tachycardia, elevated jugular venous pressure (JVP), displaced apex beat, S3, crepitations or pleural effusion, hepatomegaly, ascites, and oedema. The presence of these signs depends upon the duration, acuity, and the underlying cause of heart failure. Patients with end-stage heart failure may exhibit most of these clinical signs, whereas those in the early phase of the illness may have minimal signs. Patients with acute CHF can be classified clinically into 4 haemodynamic profiles. [24] These profiles, which are based on haemodynamic principles of presence or absence of elevated filling pressure (wet or dry) and perfusion that 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 with reduced oxygen saturation (usually <90% on room air) and crackles or wheezes on lung examination. Patients with haemodynamic compromise, systolic BP <90 mmHg, or a drop of mean arterial pressure of >30 mmHg with a pulse rate >60 bpm and/or low urine output (<0.5 mL/kg/hour), with or without evidence of organ congestion, are considered to be in cardiogenic shock.
Immediate investigations
An ECG and CXR should be performed immediately in all patients with suspected acute CHF. ECG findings are commonly related to the underlying pathologies and include presence of Q waves, ST-T changes, left ventricular hypertrophy (LVH), left bundle branch block, and atrial fibrillation.View image CXR may show cardiac enlargement (cardiothoracic ratio >50%); however, there is poor correlation between the cardiothoracic ratio (CTR) and presence of heart failure, as the heart size may be normal in patients with diastolic dysfunction, 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, initially in the upper zones, then in the horizontal fissures followed by pulmonary oedema and pleural effusion.View imageView image The x-ray findings have to be taken in the context of clinical picture, as pulmonary infiltrates and congestion, in some cases, may be due to non-cardiac cause such as ARDS or alveolar haemorrhage. CXRs rarely may show pericardial calcification, prosthetic valves, or valvular calcification. In these situations, it is helpful in identifying the possible underlying aetiology for heart failure. The following blood tests should be requested when patients present with suspected 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) levels to 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]
Subsequent investigations
Echocardiogram is an integral part of the evaluation in a patient with acute CHF and should be performed as soon as possible to presentation. It is required to assess chamber size, ventricular function (systolic and diastolic), ventricular wall thickness, valvular function, and the pericardium.View imageView image Cardiac catheterisation is needed in cases where significant CAD is thought to be the contributing factor, and is also indicated in cases where the cause of acute CHF can not be determined from other tests. Endomyocardial biopsy is not recommended for routine evaluation of acute CHF, but is indicated in patients whose clinical findings suggest acute myocarditis.
Click to view diagnostic guideline references.
Diagnostic criteria
Framingham 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:
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 classification of 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 the last 2 days and now has dyspnoea at rest. She has a history of hypertension for 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 2 cm above normal. Lung examination reveals fine bibasal crepitations. There is no ankle oedema.
Case history #2
A 73-year-old woman presents to the emergency department having collapsed. She is breathless and finding it difficult to talk in full sentences. On examination she is centrally cyanosed with cool extremities. Her pulse is 110 bpm and systolic BP only just recordable at 80 mmHg. Jugular venous pressure (JVP) is elevated 3 cm above normal and the cardiac apex beat is displaced. Respiratory rate is increased and she has widespread crackles and wheezes on chest examination.
Other presentations
Patients may present with predominant symptoms of the underlying condition such as chest pain with acute MI, syncope with significant valvular stenosis, palpitations with arrhythmias, and viral prodrome with myocarditis.
Treatment Options
Treatment Patient group haemodynamically stable line 1st Treatmenthide all
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
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 the treatment 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
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 bolus initially, 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 treatments including 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
oxygen therapy
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, aortic regurgitation, 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 intravenously initially, 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
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, and muromonab-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 <90 mmHg)
1st
oxygen therapy
plus [?]
inotropes
Patients with hypotension (systolic BP <90 mmHg) or hypoperfusion (i.e., cold and dry, cold and wet profiles) should be commenced on inotropic support because they may help stabilise haemodynamics. [43]
However, positive inotropes should be used with caution because there is evidence that they result in increased mortality and can cause arrhythmias and worsening of coronary ischaemia. [12] [60] [B
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 haemodynamic monitoring.
Choice of inotrope depends on clinical findings. Dobutamine or milrinone are recommended for patients with systolic BP 85 to 100 mmHg and no clear 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 <85 mmHg). Levosimendan or milrinone may be considered to reverse the effect of beta-blockade if beta-blocker is thought to be contributing to hypotension.
Dopamine is recommended for patients with systolic BP <85 mmHg with clinical evidence of shock. [1]
Norepinephrine (noradrenaline) is recommended for patients with systolic BP <85 mmHg and persistent signs of shock. [1] Primary Options milrinone : 25-50 micrograms/kg/dose intravenously over 10-20 minutes, followed by 0.375 to 0.75 micrograms/kg/min infusion OR
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/min intravenously
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

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
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. Longerterm assist devices are divided into first generation (e.g., Heart Mate I), second generation (e.g., Heart Mate 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 are currently 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 thrombus present on trans-oesophageal echocardiogram.
hypertensive crisis
1st
oxygen therapy
Oxygen saturation should ideally be maintained
oxygen therapy
between 95% and 98% to maximise tissue oxygenation. plus [?] IV beta-blockers and glyceryl trinitrate Primary Options metoprolol : 5-10 mg intravenously every 4-6 hours or esmolol : 250-500 micrograms/kg/dose intravenously over 1 minute initially, followed by 50100 micrograms/kg/min infusion for 4 minutes, may repeat loading dose and increase infusion up to 200 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/min increments 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
oxygen therapy
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 agitation should be also be controlled.
adjunct [?]
ventilation

Acute
Treatment Patient group acute episode stabilised: LVEF <50% and systolic BP >100 mmHg line 1st Treatmenthide all
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 the risk of renal dysfunction and hyperkalaemia.
Dose should be started low and increased according to response. Treatment is targeted to maximum dose tolerated. 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 conducted in 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
Dose should be started low and increased according to response. Treatment is targeted to maximum dose tolerated. 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
Dose should be started low and increased according to response. Treatment is targeted to maximum dose tolerated. 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
Dose should be started low and increased according to response. Treatment is targeted to maximum dose tolerated. 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 OR nebivolol : 1.25 mg orally once daily initially, increase according to response, maximum 10 mg/day
plus [?]
aldosterone receptor antagonist

Spironolactone and eplerenone block receptors that bind aldosterone and other corticosteroids. These agents can cause hyperkalemia and worsening
Dose should be started low and increased according to response. Treatment is targeted to maximum dose tolerated. 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 renal function, especially in older people. Both should only be used in patients with adequate renal function and a normal serum-potassium concentration.
Serial monitoring of serum electrolytes and renal function are mandatory. Primary Options eplerenone : 25 mg orally once daily initially, increase
Dose should be started low and increased according to response. Treatment is targeted to maximum dose tolerated. 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 50 mg/day OR spironolactone : 25 mg orally once daily initially, increase according to response, maximum 50 mg/day
adjunct [?]
vasodilators
Hydralazine/isosorbide dinitrate can be used as a second line treatment in addition to ACE inhibitors or
Dose should be started low and increased according to response. Treatment is targeted to maximum dose tolerated. 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 angiotensin-II receptor antagonists. It can also be used as an alternative to ACE inhibitors if these are contra-indicated. Black people, in particular, have been shown to gain benefit from this combination of drugs. Primary Options hydralazine/isosorbide dinitrate : 37.5/20 mg orally
three times daily initially, increase according to response, maximum 75/40 mg three times daily adjunct [?] diuretics
Patients who have evidence of volume overload or pulmonary congestion are continued on loop diuretics.
Most patients with decreased LV function will need
Dose should be started low and increased according to response. Treatment is targeted to maximum dose tolerated. 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 long-term diuretics, whereas those with primary diastolic heart failure will usually not need to be kept on maintenance diuretics. Primary Options furosemide : 40-160 mg/dose orally/intravenously initially, increase by 20-40 mg/dose every 6-12 hours according to response, maximum 600 mg/day
Dose should be started low and increased according to response. Treatment is targeted to maximum dose tolerated. 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 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 [?] 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
Dose should be started low and increased according to response. Treatment is targeted to maximum dose tolerated. 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 fluid intake.
acute episode stabilised: LVEF <50% and systolic BP 90-100 mmHg
1st
ACE inhibitor
Patients with a systolic BP <100 mmHg are generally not able to tolerate vasodilators or beta-blockers. However, in clinical practice, hospitalised patients with a systolic BP >90 mmHg and no symptoms of
hypotension can be started on the minimum starting dose of an ACE inhibitor with close blood pressure monitoring. A beta-blocker can be used if ACE inhibitors are contraindicated or not tolerated. Primary Options captopril : 6.25 to 12.5 mg orally three times daily initially, increase according to response, maximum
Dose should be started low and increased according to response. Treatment is targeted to maximum dose tolerated. 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 450 mg/day OR lisinopril : 2.5 to 5 mg orally once daily initially, increase according to response, maximum 40 mg/day OR ramipril : 1.25 mg orally once daily initially, increase according to response, maximum 10 mg/day
OR enalapril : 2.5 mg orally once daily initially, increase according to response, maximum 40 mg/day adjunct [?] beta-blocker
Patients with a systolic BP <100 mmHg are generally not able to tolerate beta-blockers or vasodilators.
Dose should be started low and increased according to response. Treatment is targeted to maximum dose tolerated. 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 However, if BP improves on an ACE inhibitor and the patient is able to tolerate it, then a beta-blocker can be introduced at a low dose and cautiously titrated upwards.
If ACE inhibitors are contraindicated or not tolerated, beta-blockers can also be used first line. Primary Options
Dose should be started low and increased according to response. Treatment is targeted to maximum dose tolerated. 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 bisoprolol : 1.25 mg orally once daily initially, increase 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)
Dose should be started low and increased according to response. Treatment is targeted to maximum dose tolerated. 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 once daily OR nebivolol : 1.25 mg orally once daily initially, increase according to response, maximum 10 mg/day
adjunct [?]
aldosterone receptor antagonist
Spironolactone and eplerenone block receptors that bind aldosterone and other corticosteroids.
These agents can cause hyperkalemia and worsening renal function, especially in older people. Both should only be used in patients with adequate renal function and a normal serum potassium concentration.
Serial monitoring of serum electrolytes and renal function are mandatory. Primary Options
Dose should be started low and increased according to response. Treatment is targeted to maximum dose tolerated. 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 eplerenone : 25 mg orally once daily initially, increase according to response, maximum 50 mg/day OR spironolactone : 25 mg orally once daily initially, increase according to response, maximum 50 mg/day
adjunct [?]
vasodilators
Hydralazine/isosorbide dinitrate can be used as a
Dose should be started low and increased according to response. Treatment is targeted to maximum dose tolerated. 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 second line treatment in addition to ACE inhibitors or beta-blockers. It can also be used as an alternative to ACE inhibitors if these are contra-indicated. Black people, in particular, have been shown to gain benefit from this combination of drugs. Primary Options hydralazine/isosorbide dinitrate : 37.5/20 mg orally
three times daily initially, increase according to response, maximum 75/40 mg three times daily adjunct [?] diuretics

Most patients require diuretics, depending upon volume status and left ventricular systolic function. Patients who have evidence of volume overload or pulmonary congestion are continued on loop
Dose should be started low and increased according to response. Treatment is targeted to maximum dose tolerated. 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 diuretics.
Most patients with decreased LV function will need long-term diuretics, whereas those with primary diastolic heart failure will usually not need to be kept on maintenance diuretics.
Diuretics should be started at the minimum starting dose with close blood pressure monitoring.
Dose should be started low and increased according to response. Treatment is targeted to maximum dose tolerated. 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 Primary Options furosemide : 40-160 mg/dose orally/intravenously initially, increase by 20-40 mg/dose every 6-12 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
Dose should be started low and increased according to response. Treatment is targeted to maximum dose tolerated. 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 OR torasemide : 5-20 mg orally once daily initially, increase dose according to response, maximum 40 mg/day
plus [?]
supportive care
Continued supportive care includes maintenance of
Dose should be started low and increased according to response. Treatment is targeted to maximum dose tolerated. 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 adequate oxygenation (ideally maintained between 95% and 98% to maximise tissue oxygenation), patent airways, a low salt diet, and restriction of daily fluid intake.
acute episode stabilised: LVEF 50%
1st
ACE inhibitor or beta-blocker
For patients with normal or preserved EF (diastolic
heart failure), good control of blood pressure, arrhythmias, and underlying ischaemia are essential. No treatment has been convincingly shown to reduce mortality in this subset of patients.
An ACE inhibtor is the first-line choice for patients with hypertension in this category of patient. A betablocker is the first-line choice for patients with
ischaemia or arrhythmia. Primary Options captopril : 6.25 to 12.5 mg orally three times daily initially, increase according to response, maximum 450 mg/day OR lisinopril : 2.5 to 5 mg orally once daily initially,
Dose should be started low and increased according to response. Treatment is targeted to maximum dose tolerated. 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 increase according to response, maximum 40 mg/day OR ramipril : 1.25 mg orally once daily initially, increase according to response, maximum 10 mg/day OR enalapril : 2.5 mg orally once daily initially, increase according to response, maximum 40 mg/day
OR bisoprolol : 1.25 mg orally once daily initially, increase 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 OR nebivolol : 1.25 mg orally once daily initially, increase according to response, maximum 10 mg/day
adjunct [?]
diuretic
The aim of using diuretics is to achieve and maintain euvolaemia (the patient's 'dry weight') with the lowest achievable dose. Once 'dry' body weight is achieved, reduction in diuretic dose is often required to avoid dehydration, hypotension, and renal dysfunction. Some patients can be trained to self-adjust their diuretic dose based on monitoring of symptoms and signs of congestion as well as daily weight
Dose should be started low and increased according to response. Treatment is targeted to maximum dose tolerated. 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 measurements. [37]
Patients with primary diastolic heart failure (i.e., HF with 'preserved' EF) will usually not need to be kept on maintenance diuretics.
Diuretics should be started at the minimum starting dose with close blood pressure monitoring. Primary Options
Dose should be started low and increased according to response. Treatment is targeted to maximum dose tolerated. 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 furosemide : 40-160 mg/dose orally/intravenously initially, increase by 20-40 mg/dose every 6-12 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 [?] supportive care
Continued supportive care includes maintenance of adequate oxygenation (ideally maintained between 95% and 98% to maximise tissue oxygenation),
Dose should be started low and increased according to response. Treatment is targeted to maximum dose tolerated. 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 patent airways, a low salt diet, and restriction of daily fluid intake.
Ongoing
Treatment approach
The main goal of the treatment of acute CHF is to provide symptomatic relief.
Initial management options include a combination of oxygen, morphine, diuretics, ultra-filtration, vasodilators, inotropes, and vasopressors. [37] Morphine causes mild vasodilatation and slows the heart rate. It is particularly useful if the patient is restless and significantly dyspneic. [1] Other possible therapies include ultra-filtration; ventilation (non-invasive and endotracheal intubation); and mechanical support (intra-aortic balloon pump, ventricular assist devices). [37] All patients should be admitted to the hospital. If the patient responds adequately to initial treatment, telemetry monitoring is acceptable. Those who are hypotensive or fail to respond to initial therapy require admission to the ICU and may need invasive monitoring if tissue perfusion is compromised. [36] If cardiogenic shock is present, invasive evaluation is required. Patients with acute CHF should undergo evaluation for potential precipitating factors, including myocardial ischaemia, arrhythmias (commonly atrial fibrillation), underlying valvular disease, exacerbation of hypertension, anaemia, thyroid disorders, and drug interactions. Other concomitant conditions, such as pneumonia and pulmonary embolism, may also be contributing factors. Venous thrombo-embolism prophylaxis is recommended in all patients. Low molecular weight heparin, low-dose unfractionated heparin, or fondaparinux can be used. In patients with contraindication to anticoagulation, a mechanical device (intermittent compression devices or graded compression stockings) should be used.
Maintenance of oxygen saturation

Oxygen therapy should be given to all patients to maintain oxygen saturation between 95% to 98%, to maximise tissue oxygenation. Ventilation with non-invasive positive pressure ventilation (NIPPV) or CPAP may be required if oxygen saturation cannot be maintained by oxygenation alone, and is associated with a decreased requirement for intubation and mechanical ventilation. [1] Mechanical ventilation is only used when other treatments, including noninvasive ventilation methods, fail.
Haemodynamically stable
Diuretics and vasodilators
Loop diuretics are the mainstay of treatment and are effective in relieving symptoms. [38]Non-loop diuretics, such as spironolactone and metolazone, may be added if there is an inadequate response to loop diuretics alone. Intravenous diuretics are indicated in patients with a systolic BP >85 mmHg. [1]
Vasodilators (glyceryl trinitrate, nitroprusside, neseritide) are indicated in patients with pulmonary congestion/oedema and a systolic BP >90 mmHg. [39] Glyceryl trinitrate is the first-line agent, with nesiritide considered second-line. [40]
Although there are no large-scale studies comparing diuretics alone with glyceryl trinitrate in patients with acute CHF, some have suggested that nitrates alone may be a better alternative in patients with acute CHF. [41] In clinical practice, both these agents are used in combination.[B Evidence]
In patients who do not respond to initial therapy, extra-corporeal ultra-filtration is used to reduce volume overload. [42] [A Evidence]
Haemodynamically unstable
Patients with hypotension or hypoperfusion (i.e., cold and dry, cold and wet profiles) should be commenced on inotropic support as this may improve hemodynamics. [43] [B Evidence]However, positive inotropes should be used with caution because there is evidence that they result in increased mortality and can cause arrhythmias and worsening of coronary ischaemia.[12] [B Evidence] The occurrence of sustained arrhythmias should lead to their discontinuation. Concomitant use of amiodarone may be advisable, although there are no large-scale data on the use of anti-arrhythmics in this setting. If the patient has symptomatic coronary ischaemia, inotropes should be discontinued. Patients with a systolic BP below 90 mmHg or a drop of mean arterial pressure of more than 30 mmHg with a pulse rate above 60 bpm and/or low urine output (<0.5 mL/kg/hour) are defined as being in cardiogenic shock. Insertion of an intra-aortic balloon pump is indicated in patients with persistent cardiogenic shock, despite inotropic therapy. However, patients with significant aortic regurgitation or aortic dissection are not candidates. Choice of inotrope depends on clinical findings. [1] Dobutamine or milrinone are recommended for patients with a systolic BP of 85 to 100 mmHg and no clear 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] Dopamine is recommended for patients with systolic BP <85 mmHg with clinical evidence of shock. [1] Norepinephrine (noradrenaline) is recommended for patients
with systolic BP <85 mmHg and persistent signs of shock. [1]Continuous monitoring of cardiac rhythm is recommended during infusion of inotropes.
Specific treatment of underlying cause

Coronary artery disease
further. In cases of significant CAD causing acute CHF, percutaneous revascularisation or coronary artery bypass should be carried out. Aspirin is given to all patients with coronary ischaemia and those undergoing revascularisation. In the case of cardiogenic shock with acute MI, revascularisation is recommended. Thrombolysis in this setting is not effective. [43] IV glyceryl trinitrate is first-line treatment. The common adverse effect of glyceryl trinitrate is headache and hypotension. The dose of nitrates should be reduced if systolic BP decreases below 90 to 100 mmHg, and discontinued permanently if BP drops
Hypertensive emergency
Use of IV beta-blockers and glyceryl trinitrate is recommended. If additional medicines are needed, nitroprusside is recommended in addition to other choices.
Valvular heart disease

In cases of severe aortic stenosis with heart failure, nitroprusside can be used, provided the patient is not hypotensive. [48] The definitive treatment for aortic stenosis or mitral stenosis is valve replacement, but in resistant heart failure a percutaneous valvotomy may be used as temporary measure until definitive valve replacement is carried out. In mitral stenosis, percutaneous valvuloplasty may be done if no thrombus is present on transoesophageal echocardiogram (TOE). Similarly in heart failure associated with mitral regurgitation or aortic regurgitation, a vasodilating drug such as nitroprusside should be used. A decrease in the peripheral arterial resistance results in an increase in the cardiac output and a decrease in regurgitant volume, which, in turn, is associated with a reduction in left ventricular end-diastolic volume and an augmentation of the ejection fraction.
Acute right heart failure
Therapy is centred around treatment of the underlying pathology; e.g. pulmonary embolism (anticoagulation, thrombolytics, catheterisation, or surgically directed thrombectomy), right ventricular infarction (PCI or thrombolytics), and chronic thromboembolic pulmonary hypertension (thromboendarterectomy). [49]
Acute myocarditis
Giant cell myocarditis is treated with single or combination immunosuppressant therapy including corticosteroids, azathioprine, cyclosporine, and muromonab-CD3 (OKT3). [50] Treatment of other forms of myocarditis is limited to supportive care. [51]
Resistance to maximal medical therapy

In cases resistant to maximal medical therapy, a left ventricular assist device (LVAD) should be inserted. In some cases of non-ischaemic cardiomyopathy, sustained reversal of severe heart failure is seen with implantation of an LVAD. [52] 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 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., Heart Mate 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 are currently being evaluated in several phase 1 studies. [53]
Ongoing therapy
Once the patient is stabilised, definitive medical therapy for heart failure should be commenced. Usually an ACE inhibitor[A Evidence] (or an angiotensin-II receptor antagonist if ACE inhibitors are not tolerated)[B Evidence] is started first, followed by the addition of beta-blockers.[A Evidence] The dose of ACE inhibitors and beta-blockers should be increased to the maximum tolerated dose depending upon BP and heart rate. Patients who have persistent signs of fluid overload will need ongoing diuretics. Patients with ongoing symptoms, despite this therapy, should be treated as having chronic CHF. In patients with reduced LVEF, an aldosterone receptor antagonist should be prescribed. In patients with low LVEF, combination of an ACE inhibitor, beta-blocker and an aldosterone receptor antagonist should be commenced and continued
long-term. For black patients with low LVEF, a combination of hydralazine and isosorbide dinitrate can be particularly beneficial. For patients with normal or preserved EF (diastolic heart failure), good control of blood pressure, arrhythmias, and underlying ischaemia is essential. No treatment has been convincingly shown to reduce mortality in this subset of patients. A meta-analysis of 6 prospective randomised controlled trials, evaluating the use of a number of renin-angiotensin inhibitors (e.g., perindopril, enalapril, ramipril, valsartan, candesartan, and irbesartan) was done on patients with heart failure and preserved EF. It found that treatment with renin-angiotensin inhibitors leads to an improvement in 6-minute walk distance and quality of life, and reduction in worsening heart failure events. However, it did not reduce total or cardiovascular mortality. [54]
Emerging treatments
Tolvaptan A vasopressin antagonist that may relieve symptoms of acute CHF, but may not reduce morbidity or mortality. [61] Levosimendan May be used as an alternative to dobutamine or milrinone for patients with an acute exacerbation of CHF with a systolic BP 85 to 100 mmHg and no clear clinical evidence of shock (such as cold extremities and low urine output). [1] Levosimendan is a calcium sensitiser. [44][45] [46] It may not be available in some countries. A multinational, randomised, double-blind, phase IV study of 60 patients with acutely decompensated chronic New York Heart Association class III-IV heart failure receiving optimal oral therapy (including a beta-blocker) investigated and compared the effects of IV infusions of levosimendan and dobutamin. This study found that both levosimendan and dobutamine led to a significant increase in cardiac index and decrease in pulmonary capillary wedge pressure at 24 and 48 hours but, although the haemodynamic and neurohormonal improvement achieved by both drugs was comparable at 24 hours, levosimendan had a superior effect on cardiac index at 48 hours. Clinical assessment revealed that dobutamine resulted in a greater improvement in fatigue and dyspnoea, and that hypotension was observed more frequently with levosimendan. [47] A meta-analysis has shown reduction in mortality with levosimendan. [62] Length of hospital stay was reduced in the levosimendan group but a higher percentage of patients experienced hypotension compared to the control group. [62]
Other investigational medications These include ularitide, tezosentan, istaroxime, perhexiline, relaxin, and cardiac myosin activators. These agents are investigational and not routinely used to treat acute heart failure.[63] [64] [65] [66] Adenosine A1- receptor antagonists (e.g., tonapofylline and rolofylline) have failed to show any clinical benefit in initial studies. [67] [68] When compared to placebo, rolofylline did not show any benefit in patients with acute heart failure and impaired renal function. [68]
Monitoring
During the acute phase all patients require cardiac monitoring. Once stabilised, they can be transferred to a non-cardiac monitoring ward. After discharge, a telephone follow-up is recommended within 3 days and patients should be reviewed in the clinic within 7 to 10 days. [22]
Patient Instructions
Patients should be advised on measures to prevent further episodes:
Fluid intake restricted to 1 to 1.5 L a day. Salt intake restricted: 1 teaspoon of salt equals 2.2 g of sodium. Therefore, patients are advised not to exceed 1 teaspoon of salt a day. They should lower salt intake as much as possible, ideally to 65 mmols/day of sodium (corresponding to 1.5 g/day of sodium). Alcohol intake limited to 2 drinks a day for men and 1 drink a day or less for woman. Importance of continuing medication as prescribed by doctor should be stressed. Weight should be checked daily.
If patients notice more than 0.9 kg (>2 pounds) weight gain in 24 hours, 2 days in a row, or develop symptoms of shortness of breath, chest pain, palpitations, increased tiredness, dizziness. or lightheadedness, or increasing swelling of the legs or abdomen, they should seek medical attention.
Complications
Complicationhide all
arrhythmias see our comprehensive coverage of Overview of dysrhythmias (cardiac)
Acute CHF is frequently precipitated by arrhythmias, in particular AF, but acute CHF may also cause arrhythmias.[71] [72] complications of glyceryl trinitrate Commonly causes headache and hypotension. The headache is usually mild to moderate in severity and either resolves or diminishes in intensity with continued nitrate therapy. If hypotension occurs then the infusion rate should be decreased. If hypotension persists then the infusion should be discontinued and re-started when patient is haemodynamically stable. complications of treatment: nesiritide Causes headache and hypotension. If hypotension occurs than the infusion rate should be decreased. If hypotension persists than the infusion should be discontinued and re-started when patient is haemodynamically stable. complications of treatment: diuretics Over-diuresis leads to worsening of renal function, hypotension, and hypokalaemia, and also activation of neurohormones including renin-angiotensin system and the sympathetic system. It may potentiate the toxicity of other agents like digoxin, either by causing hypokalaemia or by decreasing the glomerular filtration. In cases of worsening renal impairment due to over-diuresis, the dose of diuretics should be decreased. In case of severe renal impairment the diuretic can be withheld and the patients assessed daily, with re-introduction of diuretic at lower doses. complications of treatment: inotropes Dobutamine and milrinone can cause arrhythmias and worsening of coronary ischaemia. The occurrence of sustained arrhythmias should lead to discontinuation. In cases where these medications are absolutely needed, concomitant use of amiodarone may be advisable, although there are no large-scale data on the use of anti-arrhythmics in this setting. If patient has symptomatic coronary ischaemia, these infusions should be discontinued.
Prognosis
In hospital, mortality ranges from 2% to 20% depending on clinical factors found on admission.[69] Predictors of adverse outcomes include: hypotension, renal dysfunction, older age, male sex, ischaemic CHF, previous CHF, respiratory rate on admission >30/minute, anaemia, hyponatraemia, elevated troponin, elevated B-type natriuretic peptide (BNP), and other comorbidities such as cancer. [70]

Acute Exacerbation of Congestive Heart Failure: History & Exam

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Acute Exacerbation of Congestive Heart Failure: History & Exam

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Acute exacerbation of congestive heart failure

History & exam

Other diagnostic factors

Diagnostic tests details

If acute myocardial infarction (MI) is present, early revascularisation is essential.

Other related conditions

2. Hypertensive acute CHF

3. Pulmonary oedema (verified by CXR)View imageView image

5. High output failure

6. Right heart failure

2. Normotensive AHF (acutely decompensated chronic heart failure)

Types of heart failure Systolic

History & examination

is a diagnostic factor factorshide all

coronary artery disease

valvular heart disease

Precipitating factor in patients with chronic CHF.

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

Tests to considerhide all

endomyocardial biopsy Only indicated if myocarditis is clinically suspected.

Fever, cough, productive sputum.

WCC: elevated. Blood cultures: positive for organism. CXR: consolidation.

Focal signs of consolidation increased vocal fremitus and bronchial breathing.

Haemoptysis and sharp, pleuritic chest pain.

CT pulmonary angiography: clot in pulmonary artery.

immobilisation, smoker, or OCP use. Asthma

Wheezing on physical examination.

Reduced peak flow.

Spirometry: obstructive pattern, reversibility with beta-ag

Interstitial lung disease

Progressively increasing dyspnoea.

CXR: reticular infiltrate in the late stages of disease.

High-resolution CT scan: ground-glass appearance, reti honeycombing, and architectural distortion.

Oxygen desaturation with exercise.

Spirometry: restrictive pattern.

Fine bibasal crepitations with no other signs of heart failure.

Adult respiratory distress syndrome

Severe hypoxia, fine crepitations.

CXR: diffuse infiltrates Pulmonary artery wedge pressure: <18 mmHg

Step-by-step diagnostic approach

History and risk factors

Framingham criteria for CHF [33]

Minor criteria are:

Major or minor criteria are:

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

Treatment Patient group haemodynamically stable line 1st Treatmenthide all

Treatment Patient group haemodynamically stable line 1st Treatmenthide all

inadequate response to loop diuretics

Treatment Patient group haemodynamically stable line 1st Treatmenthide all

metolazone : 2.5 to 10 mg orally once daily

due to valvular disease

due to acute right heart failure

treatment of underlying cause

Treatment Patient group haemodynamically stable line 1st Treatmenthide all

due to acute myocarditis

supportive care or immunosuppressant therapy

Treatment of other forms of myocarditis is limited to supportive care. [51]

inadequate response to combination diuretics

hypotensive (systolic BP <90 mmHg)

Treatment Patient group haemodynamically stable line 1st Treatmenthide all

Treatment Patient group haemodynamically stable line 1st Treatmenthide all

intra-aortic balloon pump

Required in patients with persistent cardiogenic shock, despite inotropic therapy.