1 de Novo Heart Failure
Transcript of 1 de Novo Heart Failure
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DEPARTEMEN KARDIOLOGI FK USU MEDAN
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ACUTE LEFT VENTRICULAR
FAILURE
Acute LV failure can either occur de novo
or on a background of chronic cardiacfailure, i.e. acute-on-chronic cardiac
failure. This is important because the
aetiologies, clinical presentation and
management are quite distinct.
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CLASSIFICATION
Most cases of cardiac failure are
associated with reduced systolic function
and sometimes a low-output state.Diastolic dysfunction may also contribute
to cardiac failure in patients with large
infarct zones, cardiomyopathies,pericardial disease or mitral stenosis.
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AETIOLOGY
Acute ‘de novo’ cardiac failure
Acute MI Acute native valve failure (e.g.chordal
rupture, endocarditis) or acute VSD
Acute myocarditisHypertensive crisis
accelerated hypertension with background
essential hypertensionrenovascular disease (e.g.renal arterystenosis)
phaeochromocytoma
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Cardiac tamponade
Profound bradycardia or tachycardia
Myocardial depression due to drug toxicity
tricyclic antidepressants
β –blockers
calcium channel antagonists
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Acute-on-chronic cardiac failure
Non – compliance with or reduction in
cardiac failure drug therapy (e.g.diuretic,
ACE inhibitor) a common precipitant
Myocardial depressant drug or drugs that
promote sodium / water retention(e.g.corticosteroids, NSAIDs)
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Intercurrent non-cardiac illness in a patients with
chronic cardiac failure
Progression of underlying cardiac disease
Myocardial ischaemia/infarction
Arrhythmias, especially atrial fibrillation
Increased metabolic demand : anaemia,pregnancy, thyrotoxicosis
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CLINICAL PRESENTATION
Acute de novo LV failure usually presents with
rapidly worsening fatigue, dyspnoea and
limitation of effort tolerance. Orthopnoea,
paroxysmal nocturnal dyspnoea and acuterespiratory distress may supervene. There may
also be prodormal symptoms which suggest an
underlying aetiology, e.g.chest pain or
palpitation. Physical signs of cardiac failure and
underlying cardiac diseases are described more
comprehensively.
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INVESTIGATION
Laboratory tests
U & Es - renal failure (predisposes to fluid retention)
- High or low K+ predisposes to arrhythmias ABGs - systemic hypoxia
- Acidosis (may be metabolic due to poortissue perfusion, or mixed due toadditional CO2 retention)
Virology - If viral myocarditis suspected(e.g.antecedentHx of flu-like illness), serology may helpidentify the culprit organism
TFTs
FBC - anaemia (exacerbates cardiac failure),
↑ WCC(infection) ECG
acute or previous MI
ischaemic features
arrhythmia, e.g.atrial fibrillation
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CXR
pulmonary oedema
Pleural effusions, fluid in horizontal fissure
Septal (Kerley B) linesPulmonary pathology
Cardiac size
Echo
- LV function
- LVH (suggests hypertension, aortic stenosis
or hypertrophic cardiomyopathy)-associated with
diastolic dysfunction
- valve disease, e.g.mitral regurgitation, aortic stenosis
- pericardial effusion
- endocarditis
Right heart catheterization
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Key points : examination General - usually distressed or agitated
- tachypnoea
- semiconscious or unconscious insevere/protracted cases
- signs of sympathetic activation/lowcardiac output
pallorsweating
Cool peripheries
Peripheral cyanosis
- Cutaneous stigmata of endocarditis- Signs of non-cardiac ilness
clinical anaemia
Fever
Thyroid signs
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JVP - often elevated, but notinvariably so
Precordium - apex usually not displaced in de
novo cardiac failure; may bedyskinetic in anterior MI
- apex often displaced in chronicheart failure
- murmur (may suggest valvepathology or acute VSD)
- ‘gallop’ rhythm :S3 ± S4
- inspiratory crepitations
- pleural effusions in chroniccardiac failure
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Other - peripheral/sacral oedema,pulsatile hepatomegaly,
ascites, right parasternal lift
most often accompanychronic right-sided cardiac
failure, but are uncommon
in de novo cardiac failure
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MANAGEMENT
Acute cardiac failure should be managed in a high-
dependency or coronary care unit. Patients who are
unable to maintain adequate systemic oxygenation or
acid-base balance despite initial therapy need to be
managed in an intensive care unit with ventilationfacilities. ECG, blood pressure and O2 saturation
monitoring are mandatory.
Initial management
IV access
High-low O2 (60-100%)
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Nitrates - this is at least as important as diureticRX.
- buccal GTN 2-5 mg OR- IVI GTN 0.6-12 mg min-1 OR
- IVI isosorbide dinitrate 2-10 mg h-1
- IVI sodium nitroprusside 10-200 μg
min-1
Opiate - IV morphine 5-20 mg
Loop - IV frusemide 50-100 mg bolus OR
diuretic - IVI frusemide 5-20 mg h-1
The acute effect of loop diuretic isvenodilation;intravascular volume reductionoccurs later
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Digoxin - useful for rate control in atrial
fibrillation; role in cardiacfailure in sinus rhythm controversial
- oral dose:0.5 mg, repeated after 6
hours
- IVI:0.5 mg over 20 min, repeated after
6 hours
Treat identifiable triggers, e.g.aspirin andthrombolysis for acute MI.
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An additional agent (e.g. ACE inhibitor) may be
needed if nitrate therapy fails to controlhypertension. Arrhythmias are often poorly
tolerated. Atrial fibrillation can cause
catastrophic haemodynamic collapse because of
the loss of atrial contribution to ventricular filling.
In these cases DC cardioversion ± IVI
amiodarone via a central venous catheter (300
mg over 30 min, followed by 900 mg over 24 h)may be needed.
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Management of resistant cardiac failure
Advanced haemodynamic support
Hypotensive patients with cardiac failuremay benefit from inotropes
Dobutamine 5-20 μg kg-1 min-1
Dopamine 2.5-5 μg kg-1 min-1
Adrenaline 1-12 μg min-1
Noradrenaline 1-12 μg min-1
Intra-aortic balloon pumping
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Renal failure
Patients with fluid overload in whom diuresis isnot achieved may require extracorporealhaemofiltration.
Respiratory failure
If, despite medical management, the patientsremains in a state of repiratory compromise,mechanical ventilation should be considered.
Intubation, paralysis and intermittent positive-
pressure ventilationMask continuous positive airway pressure
ventilation