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 BackgroundPatients 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.
