Congestive Heart Failure

Updated on November 18, 2025

Table Of Contents

Overview
NYHA Heart Failure Classification
Definitions
Etiology
Pathophysiology
Systolic HF (HFrEF)
Diastolic HF (HFpEF)
Congestive Heart Failure Exacerbations
HFrEF vs HFpEF

Overview

Congestive Heart Failure (CHF) is a disorder of the pumping or filling ability of the heart. The most common cause is coronary artery disease (Systolic) and chronic hypertension (diastolic). It is a significant morbidity of myocardial infarction (MI) (watch the patient like a hawk, especially within 1y post-MI). Commonly presents with symptoms suggesting volume overload hence why diuretics are an important part of the treatment of CHF.

The common presentation of CHF
- Shortness of Breath
- Dyspnea
- Easy fatiguability
- Peripheral oedema
- Orthopnea
Differentials for CHF picture
- Deconditioning: the patient is out of shape, which happens with age (SOB, dyspnea, easy fatiguability)
- Isolated valvular lesions: get echo (Shortness of breath (SOB), dyspnea, easy fatiguability, orthopnea)
- Primary Lung disease: COPD etc. (SOB, dyspnea, easy fatiguability but no volume overload -peripheral edema). Get Chest X-ray
- Renal disease: Nephrotic syndrome etc. (edema, dyspnea if severe) get U/E/Cs

NYHA Heart Failure Classification

The New York Heart Association HF classification assesses the patient’s functional capacities and has prognostic value

NYHA Class	Limitation to physical activity	Signs and symptoms
Class I	No limitation of physical activity	Ordinary physical activity does not cause symptoms
Class II	Slight limitation of physical activity	Comfortable at rest. Ordinary physical activity causes symptoms
Class III	Marked limitation of physical activity	Comfortable at rest. Less than ordinary activity causes symptoms
Class IV	Severe limitation of physical activity	Symptoms are present even at rest

Definitions

According to the American College of Cardiology Foundation (ACCF)/ American Heart Association (AHA), heart failure is defined as a constellation of signs and symptoms caused by structural or functional impairment of ventricular filling and/or ejection of blood leading to the cardinal symptoms (dyspnea and fatigue), and signs (edema and rales) of heart failure.

Term	Definition
Congestive Heart Failure (CHF)	Clinical syndrome in which the heart is unable to pump enough blood to meet the metabolic needs of the body
Heart Failure with Reduced Ejection Fraction (HFrEF)	Formerly systolic Heart failure. CHF with reduced stroke volume, reduced ejection fraction (Left Ventricular Ejection Fraction ≤ 35-40%)
Heart Failure with Preserved Ejection Fraction (HFpEF)	Formerly diastolic Heart failure. CHF with reduced stroke volume, normal or reduced end-diastolic volume, and preserved ejection fraction (Left Ventricular Ejection Fraction 50-70%)
Borderline HFpEF	has a Left Ventricular Ejection Fraction of 40-49%
Right Heart Failure (RHF)	CHF due to right ventricular dysfunction resulting in congestion of blood in the vena cava and peripheral veins, which increases venous hydrostatic pressure and results in peripheral edema, increased jugular venous pressure, ascites, and hepatomegaly
Left Heart Failure (LHF)	CHF due to ventricular dysfunction resulting in tissue hypoperfusion and increased pulmonary capillary pressure.
Biventricular or Global CHFC	CHF in which both the left and right ventricles are affected resulting in the development of both RHF and LHF symptoms
Chronic compensated CHF	CHF on echo but the patient is asymptomatic, or symptomatic and stable
Acute Decompensated CHF	Sudden deterioration of CHF or new onset CHF due to an acute cardiac condition such as Myocardial infarction

Etiology

Systolic heart failure is the most common form of CHF. Over 20 million individuals worldwide are affected. The incidence of CHF increases with age. Approximately 6-10% of people aged >65 are affected. The relative incidence of HF is lower in women than in men, but women constitute half the cases of HF because they have a longer life expectancy. Overall prevalence of HF is increasing in part due to improved therapies for cardiac disorders leading to longer patient survival. Approximately half of patients who develop HF have normal or preserved ejection fraction. Data are currently inadequate for Heart Failure in the Kenyan population.

Causes of Systolic Heart Failure (HFrEF, <40%)
- Coronary artery disease
- Hypertension
- Dilated Cardiomyopathy
- Obstructive valvular disease (aortic stenosis)
- Regurgitant valvular disease (mitral regurgitation)
- Cor pulmonale
- Chronic bradyarrhythmia
- Chronic tachyarrhythmias
Causes of diastolic heart failure (HFpEF >40-50%)
- Hypertrophic cardiomyopathy (HHD)
- Restrictive cardiomyopathy
High-output states that cause heart failure
- Hyperthyroidism
- Beriberi
- Arteriovenous shunting
- Chronic anemia
Causes of CHF exacerbation
- Non-compliance or cessation of therapy
- Non-compliance to dietary recommendations
- Uncontrolled hypertension
- Cardiac arrhythmias especially A-fib and A-flutter
- New or worsening myocardial ischemia or infarction
- Intercurrent infective illness
- Anemia
- Hyperthyroidism
- Pregnancy
- Pulmonary embolism
- Renal failure
- Worsening underlying heart disease e.g. further narrowing of a stenotic aortic or mitral valve
- Alcohol excess
- Medications: NSAIDs, corticosteroids, Calcium channel blockers, Antiarrhythmics, Anti-TNF antibodies, Thiazolidinediones

Pathophysiology

Underlying mechanisms
- HFrEF
  - Reduced contractility → systolic ventricular dysfunction → decreased LVEF → decreased CO
- HFpEF
  - Decreased ventricular compliance → diastolic ventricular dysfunction → reduced ventricular filling and increased diastolic pressure → decreased CO while LVEF remains normal
- Left-sided heart failure
  - Increased left ventricular afterload due to arterial hypertension (increased mean aortic pressure) or aortic stenosis (outflow obstruction)
  - Increased left ventricular preload in aortic insufficiency (left ventricular volume overload)
- Right-sided heart failure
  - Increased right ventricular afterload in pulmonary hypertension (increased pulmonary artery pressure)
  - Increased right ventricular preload in tricuspid valve regurgitation or left-to-right shunt (right ventricular volume overload)
Compensatory mechanisms
- Structural changes in the myocardium
  - Structural changes include myocardial hypertrophy and dilation
  - In volume overload there is increased diastolic pressure → increased diastolic wall stress → series addition of new sarcomeres and chamber enlargement
  - In pressure overload there is increased systolic pressure → increased systolic wall stress → parallel addition of new myofibrils and wall thickening
- Neurohumoral mechanisms
  - RAAS
    - Activation of the renin-angiotensin aldosterone system increases total peripheral resistance, increases water retention leading to increased blood volume, preload and stroke volume.
  - Increased sympathetic outflow
    - Decreased cardiac output reduced perfusion pressure sensed by carotid and aortic arch baroreceptors. There is decreased parasympathetic afferents which causes a reflexive increase in sympathetic outflow with the release of Epinephrine, Norepinephrine and ADH. Increased sympathetic outflow to the heart and peripheral circulation causes increased heart rate, increased myocardial contractility, increased peripheral venous resistance and increased venous return. ****
  - Release of natriuretic peptides
    - Increased right and left atrial pressure in heart failure causes increased secretion of ANP which increases natriuresis and water excretion in the kidneys. This is to help prevent congestive symptoms during cardiac failure
  - Compensation through the frank starling mechanism
    - Decreased stroke volume causes reduced chamber emptying and increased end diastolic volume. This corresponds to an increase in preload, ventricular wall stretching and contractility thus increasing stroke volume to compensate.
Effects of compensation
- Adrenergic desensitization – Continuous sympathetic activation = decreased sensitivity to circulating catecholamines and reduced ionotropic response
- Loss of myocardiocytes- Increased heart rate and myocardial contractility – increased myocardial cell death
- Worsened pulmonary vascular congestion- Increased circulating volume and preload = overwhelmed Frank-staring mechanism, thus worsening pulmonary vascular congestion
- Reduced cardiac output- Increase in total peripheral resistance = increased afterload, reduced left ventricular stroke volume, and reduced cardiac output
- Chronically elevated angiotensin II and aldosterone = cytokine production and adverse cardiac remodeling, including myocyte hypertrophy, alterations in the contractile properties of the myocyte, progressive loss of myocytes through necrosis, apoptosis, and autophagy

Framingham’s diagnostic criteria for heart failure

Category	Criteria
Major criteria	Acute pulmonary oedema, cardiomegaly, hepatojugular reflux, neck vein distension, PND or orthopnea, rales, third heart sound gallop
Minor criteria	Ankle edema, dyspnea on exertion, hepatomegaly, nocturnal cough, pleural effusion, tachycardia (>120)

Systolic HF (HFrEF)

The heart “relaxes but can’t contract”. The heart muscles have lost their “strength”. The treatment goals in HFrEF are rate control and afterload reduction. Rate control is to allow the heart to fill better (recall Frank-Starling law).

Causes
- Ischemic Heart disease
- Long-standing Hypertension (though more of a problem with diastolic heart failure)
- Dilated cardiomyopathy (Alcoholism)
- Viral or Idiopathic cardiomyopathy (In younger pts)
Pathophysiology
- LVEF is decreased due to reduced pumping ability
- Back pressure causes increased pressure in pulmonary vasculature (increased PCWP)
- Increased hydrostatic pressure causes fluid extravasation (pulmonary edema)
- High ESV in LV causes eccentric hypertrophy of the left ventricle
- The blood remaining in the ventricle causes S3 sound (”Kentucky murmur” – same cadence as “Kentucky”)
- Pressure in atria increases later in the course causing atrial hypertrophy which messes with conduction causing A-Fib → Mural thrombi → Stroke
Signs and symptoms
- Symptoms
  - Poor exercise tolerance (Easy fatiguability) – the first clue to CHF
  - Dyspnea on exertion
  - Orthopnea
  - Paroxysmal Nocturnal Dyspnea
- Signs
  - Increased Respiratory rate
  - Adventitious lung sounds (Rales, Rhonchi, Wheezing)
  - Jugular venous distention
  - S3 gallop
  - Displaced Apex Beat
  - Cyanosis/Hypoxic signs (clubbing)
  - Peripheral edema
Investigations
- Vitals: Increased respiratory rate, Decreased O2 saturation
- CXR: Left ventricular hypertrophy, Late atrial hypertrophy, Pulmonary edema, effusions, consolidations, cephalization of flow, Kerley B lines
- EKG: Atrial fibrillation later in the course (indiscernible P waves, Irregularly irregular rhythm)
- Echo: reduced ejection fraction, <40% is diagnostic; eccentric hypertrophy
Treatment
- Rate control: Beta Blockers (carvedilol, metoprolol, bisoprolol)
- Afterload reduction: ACEi or ARB
- Others:
  - Diuretics (Spironolactone if K is normal – best for maintenance therapy as it reduces mortality)
  - Digoxin (symptomatic relief) Or Dobutamine
- Exacerbation (Acute management): Loop diuretic (Furosemide) to reduce volume overload
- Automatic implantable Cardioverter defibrillator (if Ejection Fraction < 35%)
- Treat underlying cause (Coronary artery disease – statins, stenting, etc.)

Diastolic HF (HFpEF)

The heart “contracts but can’t relax”. The heart muscles have lost their “ability to fill properly”. The best way to differentiate between HFrEF and HFpEF is echo, though it will often be apparent with clinical exam and Chest X-ray. **The treatment goal in HFpEF is blood pressure control. Administer diuretics judiciously so u don’t cause SCD.

Causes
- Long-standing hypertension with LVH (Hypertensive heart disease)
- Aortic stenosis (increases afterload)
- Hypertrophic Cardiomyopathy (young pts, congenital predisposition – see young people dropping dead [SCD] in football pitches, basketball courts, etc. because of dehydration…)
- Restrictive cardiomyopathy
- Sarcoidosis
- Systemic scleroderma
- Amyloidosis, hemochromatosis, fibrosis from radiation or surgery
The signs and symptoms of HFpEF are similar to HFrEF. However, what different signs would you expect to elicit in a patient with HFpEF?
- No jugular vein distension
- S4 heart sound: stiff ventricle (”Tennessee murmur”)
Investigations
- Chest X-ray
- EKG
- Echo: normal (preserved) ejection fraction, concentric hypertrophy
Treatment
- Maintenance therapy: Blood pressure control
- Exacerbations (acute management): cautious administration of diuretics to reduce volume overload (it can reduce the amount of blood “feeding” the myocardium, reducing stroke volume. Patient may develop syncope or sudden cardiac death)
- Treat underlying cause