Aetiology
Causes and precipitating factors are:
Acute coronary syndrome (ACS)
Hypertensive emergency
Rapid arrhythmias or severe bradycardia/conduction disturbance
An acute mechanical cause (e.g., myocardial rupture as a complication of ACS [such as free wall rupture], ventricular septal defect or acute mitral regurgitation, chest trauma)
Acute pulmonary embolism
Valve disease
Myocarditis
Decompensation of pre-existing chronic heart failure
Cardiac tamponade
Aortic dissection
Postpartum cardiomyopathy
Lack of adherence with medical treatment
Volume overload
Infections
Severe brain insult
After major surgery
Reduction of renal function
Drug abuse
Phaeochromocytoma
High output syndromes
Septicaemia
Thyrotoxic crisis
Anaemia
Shunt syndromes.
The most common concurrent conditions present in patients with acute heart failure are coronary artery disease, hypertension, diabetes mellitus, atrial fibrillation, and renal insufficiency.[7][8]
Pathophysiology
During an episode of acute heart failure, the majority of patients will have evidence of 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 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.[9]
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 heart failure to respond quickly to treatment, the increased myocardial stress must be reversed: for example, correction of acute severe hypertension. This is particularly important in acute heart failure caused by ischaemia, as a dysfunctional myocardium can return to normal when appropriately treated.
Classification
There have been several attempts to classify acute heart failure based on different criteria. The European Society of Cardiology supports a classification of acute heart failure based on clinical presentation. This allows the rapid identification and management of potentially reversible causes, precipitants, and coexisting life threatening conditions.[1]
Clinical presentation
The European Society of Cardiology describes four major clinical presentations of acute heart failure based on the presence of signs of congestion and/or peripheral hypoperfusion. While these presentations may overlap, each requires different treatment:[1]
Acute decompensated heart failure
symptoms associated with peripheral fluid accumulation, increased intraventricular pressure
gradual onset (days)
normal or low systolic blood pressure
Acute pulmonary oedema
symptoms associated with fluid redistribution to the lungs and acute respiratory failure
rapid onset (hours)
Isolated right ventricular failure
symptoms from increased central venous pressure and often systemic hypoperfusion
gradual or rapid onset
low systolic blood pressure
Cardiogenic shock
symptoms from systemic hypoperfusion (severe cardiac dysfunction)
gradual or rapid onset
low systolic blood pressure
Precipitants
An alternative approach is to classify patients according to the presence of factors leading to decompensation (which need to be treated urgently):[1]
Acute coronary syndrome
Hypertensive emergency
Rapid arrhythmias or severe bradycardia/conduction disturbance
Acute mechanical cause underlying acute heart failure
Acute pulmonary embolism
Infection (including myocarditis)
Tamponade.
Types of heart failure
Traditionally heart failure is classified as:
Systolic - associated with left ventricular dysfunction and characterised by cardiomegaly, third heart sound, and volume overload with pulmonary congestion. Left ventricular ejection fraction (LVEF) is decreased
Diastolic - typically associated with normal cardiac size, hypertension, pulmonary congestion, and a fourth heart sound. LVEF is preserved.
Based on measurement of LVEF, heart failure is classified as:[1]
Heart failure with reduced ejection fraction (HFrEF) - symptoms and signs and LVEF ≤40%
A subgroup of HFrEF can be further classified as heart failure with improved ejection fraction (HFimpEF) if a previous ejection fraction ≤40% has improved to >40% after follow-up measurement[2]
Heart failure with mildly reduced ejection fraction (HFmrEF) - symptoms and signs and LVEF 41% to 49%
Heart failure with preserved ejection fraction (HFpEF) - symptoms and signs and LVEF ≥50%
Evidence of structural heart disease may be used to further support the diagnosis of HFpEF.[2]
The diagnosis of HFmrEF and HFpEF requires evidence of spontaneous (at rest) or provokable (e.g., during exercise, fluid challenge) increased LV filling pressures.[1][2] This may be fulfilled by elevated natriuretic peptides, non-invasive measures (e.g., echocardiographic diastolic parameters), or invasive haemodynamic measurement.[2]
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