Heart Failure | Causes, Symptoms, Treatment

Heart Failure | Causes, Symptoms, Treatment

Medically reviewed by MyHSN Editorial Team – last updated May 2026

Heart failure – also known as congestive (or chronic) cardiac (or heart) failure (CCF/CHF) – does not mean the heart has stopped beating.

Instead, it means the heart muscle is unable to pump blood efficiently enough to meet the body’s needs for blood and oxygen. This leads to a backup of fluids in the lungs and extremities.

1. Definitions

• Progressive Efficiency Loss: Heart failure is a chronic condition where the heart muscle cannot pump blood efficiently enough to meet the body’s metabolic demands for oxygen and nutrients.

• Systolic Dysfunction (HFrEF): Heart Failure with Reduced Ejection Fraction (<40%). The ventricular walls become thin and stretched, losing their contractility and ability to squeeze blood forward.

• Diastolic Dysfunction (HFpEF): Heart Failure with Preserved Ejection Fraction (>50%). The ventricle becomes thick and rigid, preventing the heart muscle from relaxing and filling properly between beats.

2. Primary Cause

• Coronary Artery Disease (CAD): The leading driver of heart failure. Atherosclerotic plaques narrow the coronary arteries, restricting blood flow and starving the myocardium of oxygen.

• Myocardial Infarction (Heart Attack): A sudden arterial blockage causing localized tissue necrosis. The dead muscle is replaced by rigid, non-contractile scar tissue.

3. Other Causes

• Hypertension (High Blood Pressure): Elevated systemic vascular resistance increases ventricular afterload. The heart must pump against intense resistance, forcing the muscle walls to thicken, stiffen, and eventually fail.

• Valvular Heart Disease: Stenotic (narrowed) or regurgitant (leaking) valves disrupt one-way hemodynamics, forcing the heart chambers to work twice as hard to maintain forward circulation.

• Cardiomyopathy: Intrinsic structural diseases of the heart muscle, which can be genetic or acquired through toxins, heavy alcohol use, or specific chemotherapy agents.

• Myocarditis: Acute inflammation of the myocardium, typically triggered by a viral infection (e.g., influenza or COVID-19), which directly weakens cardiomyocyte function.

4. Left-Sided Heart Failure

• Pulmonary Venous Hypertension: When the left ventricle fails to empty effectively, pressure backs up into the left atrium and pulmonary veins, driving fluid into the lung tissue.

• Exertional Dyspnoea: Shortness of breath during basic physical tasks (e.g., climbing stairs) caused by early interstitial fluid accumulation in the lungs.

• Orthopnoea: Breathlessness when lying flat. Gravitational shifts redistribute fluid from the abdomen and legs into the thoracic cavity, forcing the patient to use multiple pillows to sleep.

• Paroxysmal Nocturnal Dyspnoea (PND): Sudden, severe gasping for air that wakes a patient from sleep, caused by the gradual reabsorption of peripheral edema back into the central circulation during prolonged rest.

5. Right-Sided Heart Failure

• Peripheral Pitting Oedema: Elevated venous pressures force fluid out of capillaries into dependent interstitial spaces, causing visible swelling in the feet, ankles, and lower legs.

• Splanchnic Congestion: Fluid backup into the hepatic veins and digestive tract, resulting in a bloated abdomen (ascites), hepatomegaly, loss of appetite, and nausea.

• Acute Weight Fluctuation: Rapid weight gain—such as 0.5kg in 24 hours—is a direct indicator of rapid intravascular fluid retention rather than tissue mass.

6. Investigation

• Echocardiogram (TTE): The primary diagnostic tool. This cardiac ultrasound evaluates chamber dimensions, valve anatomy, and calculates the Ejection Fraction (EF).

• Natriuretic Peptide Biomarkers (BNP / NT-proBNP): Blood tests measuring proteins secreted by cardiomyocytes under high wall tension or stretch, used to confirm active cardiac stress.

• Electrocardiogram (ECG): Tracks electrical conduction to detect arrhythmias, left bundle branch blocks, left ventricular hypertrophy, or signs of past silent heart attacks.

• Chest X-Ray: Provides a visual of the thoracic cavity to identify cardiomegaly (enlarged heart) and pulmonary edema (fluid in the lungs).

7. Stages

• NYHA Functional Classification: A bidirectional scale measuring current symptomatic capacity:

  • Class I: No physical limitations; ordinary exertion does not cause symptoms.

  • Class II: Mild limitations; comfortable at rest, but ordinary activity causes dyspnea.

  • Class III: Marked limitations; comfortable at rest, but minimal activity triggers symptoms.

  • Class IV: Inability to perform any physical activity; symptoms may be present even at rest.

8. Treatment

• Loop Diuretics (e.g., Furosemide): Used strictly for volume titration to flush out excess salt and fluid, relieving physical congestion without altering long-term mortality.

• ARNI (Sacubitril/Valsartan): Replaces traditional ACE inhibitors. It dilates blood vessels while inhibiting neprilysin to protect beneficial, native natriuretic peptides.

• Beta-Blockers (e.g. Metoprolol Succinate, Carvedilol): Block sympathetic overactivation to lower resting heart rate, maximise diastolic filling time, and protect against ventricular arrhythmias.

• Mineralocorticoid Receptor Antagonists (MRAs): Medications like Spironolactone block aldosterone to prevent fluid retention and limit myocardial fibrosis (scarring).

• SGLT2 Inhibitors (e.g. Dapagliflozin, Empagliflozin): Promote glucose and sodium filtration through the kidneys, reducing preload, afterload, and overall cardiac strain.

9. Surgical and Device-Based Therapies

• Cardiac Resynchronization Therapy (CRT): A specialized biventricular pacemaker that corrects conduction delays (like Left Bundle Branch Block) to ensure both ventricles contract in harmony.

• Implantable Cardioverter-Defibrillators (ICDs): Continuously monitors cardiac rhythms to deliver immediate anti-tachycardia pacing or electrical shocks during fatal ventricular arrhythmias.

• Structural Repair: Surgical or percutaneous options, including Transcatheter Edge-to-Edge Repair (TEER) for leaking valves or bypass surgery (CABG) to revascularize ischemic tissue.

• Mechanical Support & Transplantation: For Stage D patients, a Left Ventricular Assist Device (LVAD) can mechanically take over pumping duties, either as a bridge to a heart transplant or as permanent destination therapy.

10. Self-Management

• Daily Weights: Weighing every morning before eating detects subclinical fluid retention (0.5kg in 24 hours), allowing for proactive diuretic adjustments before physical symptoms develop.

• Dietary Sodium Restriction: Restricting dietary salt stops osmotic water retention, keeping intravascular volumes stable and preventing sudden fluid overloads.

• Cardiac Rehabilitation: Supervised exercise conditioning down-regulates resting sympathetic tone, improves peripheral oxygen extraction, and increases functional capacity.

• Implantable Haemodynamic Sensors: Wireless devices (e.g. CardioMEMS) track heart pressures, warning doctors of a problem days before clinical decompensation occurs.