Molecular structure pattern

Heart Failure - Acute Disease Background

Last updated: 07 September 2026

Introduction

Heart failure is a clinical syndrome that is due to a structural and/or functional cardiac abnormality that impairs the ability of the ventricle to fill with or eject blood in order to deliver oxygen (O2) at a rate commensurate with the requirements of the metabolizing tissues in spite of normal filling pressures or only at the expense of elevated filling pressures. This is corroborated by objective evidence of cardiogenic, pulmonary, and/or systemic congestion and/or elevated levels of natriuretic peptides. This is characterized by either left ventricular hypertrophy or dilation or both.

Acute Heart Failure1  

Acute heart failure is a life-threatening condition that needs immediate medical attention and treatment initiation or intensification. Notably, indications for hospital admission include a new diagnosis of heart failure with rapidly progressive symptoms, severe congestion (eg ascites, marked leg edema, perineal or scrotal edema) or higher complexity of disease. It involves rapid or gradual onset of new or worsening signs and/or symptoms of heart failure. It may occur as acute decompensation of previously diagnosed, persistent heart failure (worsening of pre-existing heart failure) or may also be the first presentation of heart failure (de novo heart failure). Cardiac dysfunction may be related to ischemia, arrhythmia, valvular abnormalities, pericardial disease, myocarditis, cardiomyopathy, volume overload, increased filling pressure or elevated systemic resistance.  

Acute heart failure arising from decompensation of chronic heart failure is a slow and progressive deterioration and is associated with arrhythmia, uncontrolled hypertension, infection and non-compliance with therapy and diet. Worsening heart failure involves a deterioration of heart failure symptoms and/or signs and reflects disease progression, whereas decompensated heart failure is defined specifically by the need to modify treatment. Worsening heart failure can include progression to decompensated heart failure. However, decompensated heart failure can occur at any time in the heart failure disease course and is not limited to those with worsening heart failure.  

1In the 2026 European Society of Cardiology (ESC) guidelines, decompensated heart failure replaces acute heart failure, but acute heart failure is retained in this disease management chart to maintain consistency with other international guidelines and published clinical literature.

Epidemiology

Heart failure affects more than 60 million individuals globally. The prevalence ranges between 1-2% in the general adult population. The incidence of heart failure increases with age and is higher in males than in females.

The prevalence estimates of heart failure in Asia range between 1.3% and 6.7%. In Asia, the prevalence of heart failure with preserved ejection fraction is higher compared with the Western countries and may be due to enhanced treatment and prevention of ischemic heart disease. In Southeast Asia, the lean diabetic phenotype makes up 20% of all heart failure cases and is associated with higher rates of all-cause mortality and hospitalization. The age-standardized prevalence of heart failure per 100,000 population was highest in East Asia and lowest in South Asia.

 

Pathophysiology

Heart failure is a clinical syndrome caused by structural and/or functional cardiac abnormalities that impair ventricular filling and/or ejection, resulting from systolic dysfunction (impaired contractility) and/or diastolic dysfunction (impaired relaxation and reduced compliance).

Cardiac injury and chronic hemodynamic stress trigger cellular, structural, and neurohumoral modulations, including the activation of the sympathoadrenergic system and renin-angiotensin-aldosterone system (RAAS), which are initially adaptive but become maladaptive, causing vasoconstriction, sodium and water retention, volume overload, tachycardia, congestion and dyspnea.

Chronic catecholamine and neurohormonal activation increase intracellular calcium and myocardial O2 demand predisposing to arrhythmias, while promoting hypertrophy, fibrosis, cell death, altered gene expression, and adverse ventricular remodeling, leading to progressive deterioration of cardiac function.

Etiology

The causes of heart failure include acute coronary syndrome or its complications (eg rupture of interventricular septum, right ventricular infarction, valvular heart disease, mitral valve chordal rupture, acute mitral regurgitation), arrhythmias, aortic dissection, cardiomyopathic states (eg peripartum, hypertrophic, tachycardia-mediated or stress-related cardiomyopathy), poorly controlled hypertension (eg bilateral renal artery stenosis), and infection (eg infective endocarditis, viral myocarditis).

Precipitants of heart failure include hypertensive crisis or severe and uncontrolled hypertension; tachyarrhythmia (eg atrial fibrillation, atrial flutter, ventricular tachycardia), severe bradycardia or conduction abnormalities; pulmonary embolism; pericardial or cardiac tamponade; infection (eg pneumonia, sepsis); chronic obstructive pulmonary disease (COPD) exacerbation; cerebrovascular insult; worsening renal failure; electrolyte disturbances; high output states (eg severe anemia, thyrotoxicosis, large atrioventricular shunts/malformations, obesity, advanced liver failure, chronic lung disease, Paget’s disease); surgery and perioperative problems; non-compliance to diet or drug therapy; medications (non-steroidal anti-inflammatory drugs [NSAIDs], steroids, cardiotoxic chemotherapeutics, negative inotropic agents, drugs that increase fluid retention, Clozapine); fluid overload (eg volume overload causing pulmonary edema in acute kidney injury, iatrogenic causes); and toxic substances (recreational drugs, alcohol, radiotherapy).

Risk Factors

The risk factors for heart failure are increasing age, male sex, coronary artery disease, atherosclerotic disease, hypertension, diabetes mellitus (DM), metabolic syndrome, obesity, smoking, alcohol use, and exposure to drugs (eg cancer chemotherapies) or toxins with cardiotoxicity.  Inflammation also plays a key role in the development of heart failure. Socioeconomic status is also a risk factor for heart failure due to poor diet, smoking, physical inactivity, and non-adherence to medications.

Classification

Classification of Acute Heart Failure

Clinical Conditions


Patients with acute heart failure may present in one of several categories, which are not mutually exclusive and may overlap (eg a patient with hypertensive crisis or cardiogenic shock may also develop severe pulmonary edema).

Worsening or Decompensated Left Heart Failure  

Worsening or decompensated heart failure is usually seen in patients with new-onset heart failure or acute decompensation of chronic heart failure. Usually, there is a gradual onset with progressive worsening despite treatment. This is characterized primarily by progressive fluid retention, increased intraventricular pressure, and pulmonary and systemic congestion. It can occur across the full range of left ventricular ejection fraction and, in advanced disease, may result in right ventricular dysfunction and decompensated right-sided heart failure, causing both pulmonary and peripheral congestion. Hypotension on admission is associated with a poor prognosis. Treatment primarily focuses on relieving congestion through diuretic therapy.

Acute Pulmonary Edema


Heart Failure - Acute_Disease BackgroundHeart Failure - Acute_Disease Background




Patients with acute pulmonary edema present with severe respiratory distress (dyspnea with orthopnea, tachypnea, increased work of breathing, respiratory failure) and bilateral coarse airway sounds (eg rhonchi, wheeze and rales) over the lung fields caused by massive pulmonary congestion which develops over a short period of time. Arterial O2 saturation is usually <90% on room air prior to O2 therapy. This diagnosis is confirmed by chest radiography. Cardiogenic pulmonary edema shows perihilar infiltrates while non-cardiogenic pulmonary edema shows peripheral infiltrates. Treatment objectives are to relieve pulmonary congestion with diuretics and vasodilators, treat respiratory insufficiency and ensure peripheral perfusion with carefully titrated vasodilators.

Decompensated Isolated Right Heart Failure

Decompensated isolated right heart failure is characterized by elevated right ventricular and right atrial pressures resulting in systemic congestion and, in advanced stages, tissue hypoperfusion. Patients present with symptoms and signs of right-sided volume overload, including elevated jugular venous pressure, with or without hepatomegaly. This may present as a low-output syndrome without pulmonary congestion accompanied by low left ventricular filling pressures, low systolic blood pressure (SBP) and cardiac output, and increased right ventricular end-diastolic pressure. Fluid overload, elevated central venous pressure and multiorgan dysfunction are common features, and in the most severe cases, the condition may progress to refractory shock. Management includes fluid optimization, diuretics, appropriate use of inotropes and vasopressors, and mechanical circulatory support when indicated. 

Cardiogenic Shock  

Cardiogenic shock is defined as a state of sustained, critical end-organ and tissue hypoperfusion caused by primary cardiac dysfunction, despite adequate correction of preload and major arrhythmias, and evidenced by clinical and biochemical abnormalities. It is characterized by hypotension (SBP <90 mmHg, mean arterial pressure <60 mmHg, or a decrease of >30 mmHg from baseline SBP), diminished pulse pressure, cutaneous pallor, mental confusion, and absent or low urine output of <0.5 mL/kg/hr. Rhythm disturbance is common. Pulmonary congestion and organ hypoperfusion develop rapidly. There is a continuum from low cardiac output syndrome to cardiogenic shock. One may check lactic acid level (>2 mmol/L) in patients with decompensated end-stage heart failure who present with marked weakness and/or uncertain peripheral perfusion to help identify occult shock. Management includes the use of inotropes and vasopressors, mechanical circulatory support when indicated, and diuretics if needed.

Hypertensive Heart Failure  

There are signs and symptoms of heart failure accompanied by high BP and preserved left ventricular function (heart failure with a preserved ejection fraction). There is evidence of increased sympathetic tone with tachycardia and vasoconstriction. They may be mildly hypervolemic or euvolemic with signs of pulmonary congestion without signs of systemic congestion. There is a rapid response to appropriate treatment and a low hospital mortality.  

Acute Coronary Syndrome and Heart Failure  

Some patients with acute coronary syndrome present with symptoms and signs of heart failure. The episodes of heart failure are associated with or precipitated by arrhythmia. Patients are managed according to the acute coronary syndrome (ACS) guidelines.  

Please see Acute Coronary Syndrome without Persistent ST-Segment Elevation disease management chart for further information.

Acute Mechanical Causes  

Acute mechanical causes are conditions that include acute incompetence of the native or prosthetic valve due to endocarditis, aortic dissection or thrombosis, cardiac intervention, chest trauma, or acute coronary syndrome complicated by the rupture of the myocardium such as acute mitral regurgitation, free wall rupture, or ventricular septal defect.