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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.
AETIOLOGY
Acute de novo cardiac failure Acute MI Acute native valve failure (e.g.chordal rupture, endocarditis) or acute VSD Acute myocarditis Hypertensive crisis accelerated hypertension with background essential hypertension renovascular disease (e.g.renal artery stenosis) phaeochromocytoma
Cardiac tamponade Profound bradycardia or tachycardia Myocardial depression due to drug toxicity tricyclic antidepressants blockers calcium channel antagonists
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 pregnancy, thyrotoxicosis : anaemia,
CLINICAL PRESENTATION
Acute de novo LV failure usually presents with rapidly worsening fatigue, dyspnoea and limitation of effort tolerance. Orthopnoea, paroxysmal nocturnal dyspnoea and acute respiratory 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.
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 poor tissue perfusion, or mixed due to additional CO2 retention) Virology - If viral myocarditis suspected(e.g.antecedent Hx of flu-like illness), serology may help identify the culprit organism TFTs FBC - anaemia (exacerbates cardiac failure), WCC(infection) ECG acute or previous MI ischaemic features arrhythmia, e.g.atrial fibrillation
CXR pulmonary oedema Pleural effusions, fluid in horizontal fissure Septal (Kerley B) lines Pulmonary 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
Pulse
- usually tachycardic. Relative bradycardia can worsen cardiac failure by limiting cardiac output - may be irregular; suggests atrial fibrillation - may be low ( output) or normal pulse volume
Blood pressure - hypotension heralds poor prognosis - hypertension may aggravate cardiac failure - check for pulsus paradoxus
JVP
- often elevated, but not invariably so - apex usually not displaced in de novo cardiac failure; may be dyskinetic in anterior MI - apex often displaced in chronic heart failure - murmur (may suggest valve pathology or acute VSD) - gallop rhythm :S3 S4 - inspiratory crepitations - pleural effusions in chronic cardiac failure
Precordium
Other
- peripheral/sacral oedema, pulsatile hepatomegaly, ascites, right parasternal lift most often accompany chronic right-sided cardiac failure, but are uncommon in de novo cardiac failure
MANAGEMENT
Acute cardiac failure should be managed in a highdependency 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 ventilation facilities. ECG, blood pressure and O2 saturation monitoring are mandatory.
Initial management
IV access High-low O2 (60-100%)
Nitrates - this is at least as important as diuretic RX. - 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 g min-1 Opiate - IV morphine 5-20 mg Loop - IV frusemide 50-100 mg bolus OR diuretic - IVI frusemide 5-20 mg h-1
Digoxin - useful for rate control in atrial fibrillation; role in cardiac failure 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 and thrombolysis for acute MI.
An additional agent (e.g. ACE inhibitor) may be needed if nitrate therapy fails to control hypertension. 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.
Renal failure
Patients with fluid overload in whom diuresis is not achieved may require extracorporeal haemofiltration.
Respiratory failure
If, despite medical management, the patients remains in a state of repiratory compromise, mechanical ventilation should be considered. Intubation, paralysis and intermittent positivepressure ventilation Mask continuous positive airway pressure ventilation