Heart Failure Definition and Causes (2021)

A clinical syndrome, with current or prior symptoms and/or signs that result from a functional cardiac abnormality
The heart's ventricles have a problem filling with and/or ejecting blood.
Confirmed by at least one of the following: increased natriuretic peptide levels or objective evidence of cardiogenic pulmonary or systemic congestion.

Pressure overload: LVF (Left Ventricular Failure) - systemic hypertension, valvular disease (aortic stenosis, pulmonary hypertension, valvular disease - pulmonic stenosis), congenital diseases (coarctation of the aorta, patent ductus arteriosus) and hyperdynamic circulation (valvular disease - aortic regurgitation, mitral regurgitation, pulmonic regurgitation, tricuspid regurgitation). RVF - (Right Ventricular Failure) pulmonary hypertension (e.g. COPD), valvular disease (pulmonic stenosis).
Volume overload: IHD (ischemic heart disease), renal failure, Iatrogenic fluid overload.
Contractility: IHD (myocardial infarction), cardiomyopathy (DCM), myocarditis, global affection, pericardial disease (pericardial effusion, constrictive pericarditis), arrhythmias, toxic damage (heavy metals, alcohol, cocaine).
Relaxation/Filling: cardiac diseases, including hypertrophic cardiomyopathy (HCM).

Infections: infective endocarditis, rheumatic activity, chest infections;
Iatrogenic: corticosteroids, calcium channel blockers (except amlodipine & felodipine), discontinuation of anti-failure treatment, excessive salt intake, IV fluids, anemia, thyrotoxicosis, hyperdynamic circulation;
Acute coronary syndrome (ACS): myocardial infarction;
Sudden increase in systemic blood pressure (hypertensive emergency);
Arrhythmias: atrial fibrillation (AF) or bradyarrhythmias;
Acute mechanical causes: acute mitral regurgitation secondary to endocarditis,acute pulmonary embolism;
Pregnancy and late labor, physical and emotional stress.

Forward failure: Inability of the heart to eject sufficient cardiac output resulting in low CO (cardiac output)
Backward failure: Difficulty of the heart to adapt incoming blood flow (VR), thus causing pulmonary or systemic congestion.
Compensatory mechanisms (Cardiac reserve): short-term adaptations to restore cardiac output include tachycardia, redistribution of blood flow (from less vital organs to more vital organs), hypertrophy (concentric hypertrophy in pressure overload, eccentric hypertrophy in volume overload), and dilation. However, long-term these mechanisms can become maladaptive.

RAAS (Renin-angiotensin-aldosterone system): plays a role in increasing blood volume and pressure leading to preload and afterload increase.
SNS (Sympathetic Nervous System): activated in response to low CO, producing vasoconstriction and increases in HR and SV, leading to a higher preload and afterload.
Natriuretic peptides: are released in response to increased blood volume and pressure, opposing the actions of the RAAS and SNS. Increase in natriuretic peptides may have adverse impacts such as fluid loss, electrolyte imbalance and vasoconstriction.
ADH (antidiuretic hormone): retains water in the body, increasing preload.
Endothelin: increases vasoconstriction leading to a higher afterload.

Biventricular HF: LVEF and RVEF are impaired.
Acute vs Chronic: Acute HF presents symptoms unexpectedly and acutely or worsens quickly; Chronic HF develop gradually over time.
Ejection Fraction (EF): Percentage of blood ejected from the ventricle (LV and RV) with each stroke.
HFpEF (HF with preserved EF): EF is intact(>50%);
HFrEF (HF with reduced EF): EF is reduced (<40%);
HFmrEF (HF with mildly reduced EF): EF is between 41-49%.
Stages (A, B, C, D) of heart failure: determined by symptoms, presence of cardiac dysfunction, and structural damage.
Functional Classification (NYHA Classes): determined by symptom severity and physical activities.

CLASS I: No limitation of ordinary physical activity;
CLASS II: Slight limitation;
CLASS III: Marked limitation;
CLASS IV: Unable to carry out any physical activity without discomfort, symptoms present at rest.

Compensatory mechanisms: useful in short-term; may become maladaptive in the long-term
Triggers and precipitating factors: may worsen HF symptoms.
Treatment modalities: including diuretics (thiazide-like, loop, potassium sparing), vasodilators, inotropes, and digitalis;
Assessment of HF: using physical examination (signs and symptoms), imaging (CXR, Echo), blood tests (BNP, cardiac enzyme), and electrocardiogram (ECG).