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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:
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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
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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
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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
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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
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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
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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
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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
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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=MARTINDALE7/27/2019 akut.si
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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
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
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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