1 de Novo Heart Failure

20
DEPAR TEMEN KARDIOLOGI FK USU MEDAN

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