Heart Failure (Congestive Heart Failure - CHF) Summary

Definition & Significance

 Heart failure is the final stage of many heart diseases and has a poor prognosis.

 Affects over 5 million people in the U.S., leading to 1+ million hospitalizations annually
and a $32+ billion economic burden.

 50% of patients die within 5 years of diagnosis; 1 in 9 deaths in the U.S. is linked to CHF.

Causes & Mechanisms

 Occurs when the heart fails to meet metabolic demands or does so only at high filling
pressures.

 May result from:

o Systolic dysfunction (poor contraction) → caused by ischemic heart disease or

hypertension.

o Diastolic dysfunction (poor relaxation/filling) → seen in left ventricular

hypertrophy, myocardial fibrosis, amyloidosis, or constrictive pericarditis.

 Other causes include valvular disease, rapid blood volume increases, or high-output
conditions (e.g., hyperthyroidism, anemia).

Types of Failure

 Forward failure → inadequate cardiac output to tissues.

 Backward failure → increased venous pressure leading to congestion.

 Most CHF cases involve both forward & backward failure, eventually affecting all
organs.

Compensatory Mechanisms (Short-Term Help, Long-Term Harm)

1. Frank-Starling Mechanism → More ventricular filling leads to stronger contraction, but

excessive stretching eventually worsens heart failure.

2. Neurohumoral Activation →

o Norepinephrine release increases heart rate & contractility.

o Renin-angiotensin-aldosterone system retains water & salt, increasing blood

volume.
 o Atrial natriuretic peptide (ANP) counteracts fluid retention via diuresis &
vasodilation.

3. Myocardial Hypertrophy (Heart Growth)

o Pressure overload (e.g., hypertension) → concentric hypertrophy (thicker walls,

smaller chamber).

o Volume overload (e.g., valve disease) → eccentric hypertrophy (larger chamber,

normal or thinner walls).

o Downside: Increased oxygen demand, ischemia risk, and altered gene expression
leading to worsened heart function over time.

Types of Heart Failure

1. Left-Sided Heart Failure (Most Common)

o Causes: Ischemic heart disease, hypertension, mitral/aortic valve disease,

cardiomyopathy.

o Symptoms:

pulmonary Symptoms: Why Does Breathlessness Occur?

The left ventricle fails to push blood forward effectively, causing blood to back up into the lungs
(pulmonary circulation). This increases pressure in the pulmonary capillaries, leading to fluid
leakage into the alveoli (air sacs).

 Dyspnea (shortness of breath) on exertion

o Why? The lungs become congested with fluid, making it difficult for oxygen to
pass into the bloodstream.

o Earliest symptom because physical activity increases oxygen demand, which the
failing heart cannot meet.

 Cough

o Why? Fluid leakage into the airways (pulmonary edema) can irritate lung
receptors, triggering a reflex cough.

o Worsens at night because lying down increases blood flow to the lungs,
worsening congestion.

 Orthopnea (difficulty breathing when lying flat)

o Why?
  Lying down increases venous return from the lower body to the heart,
further overloading the left ventricle.

 The diaphragm shifts upward, reducing lung capacity, making breathing

even harder.

o Patients sleep in a semi-seated position to relieve symptoms.

 Paroxysmal Nocturnal Dyspnea (PND)

o Why? A more severe form of orthopnea, where sudden fluid redistribution

during sleep causes severe breathlessness.

o Patients wake up gasping for air, sometimes feeling like they are suffocating.

 Pulmonary rales (crackles in the lungs)

o Why? The sound comes from fluid-filled alveoli popping open during breathing.

o Best heard at the lung bases, where fluid accumulates due to gravity.

2. Cardiac Symptoms and Complications

As the heart struggles to maintain circulation, structural and electrical changes develop:

 Enlarged heart (Cardiomegaly)

o The left ventricle dilates and thickens in response to increased pressure.

o Why? The heart tries to compensate by growing larger, but this eventually
increases oxygen demand, worsening failure.

 Tachycardia (fast heart rate)

o Why?

 The sympathetic nervous system releases norepinephrine to increase

heart rate and maintain circulation.

 However, this compensatory mechanism increases heart strain over time.

 Third Heart Sound (S3)

o Why? Rapid filling of a dilated, weak ventricle causes abnormal vibrations.

o Indicates heart failure when heard in adults.

 Mitral Regurgitation (MR) and Systolic Murmur

 o Why? The left ventricle dilates, pulling the mitral valve apart, preventing it from
closing properly.

o Effect: Blood leaks back into the left atrium, worsening congestion.

 Atrial Fibrillation (AFib)

o Why? Left atrial dilation stretches electrical pathways, disrupting normal

conduction.

o Effects:

 Irregularly irregular heartbeat due to chaotic atrial contractions.

 Reduces ventricular filling, further lowering cardiac output.

 Increases stroke risk because stagnant blood in the atria can form clots.

3. Systemic Effects Due to Reduced Cardiac Output

As heart failure worsens, other organs suffer from reduced blood flow:

 Kidney Dysfunction (Prerenal Azotemia)

o Why? Reduced heart output → Decreased kidney perfusion → Activates the

renin-angiotensin-aldosterone system (RAAS).

o Effects:

 Water and salt retention increases blood volume, worsening lung

congestion.

 Waste products (e.g., nitrogenous compounds) build up in the blood,

impairing kidney function.

 Brain Hypoxia (Hypoxic Encephalopathy)

o Why? Reduced cardiac output leads to decreased oxygen delivery to the brain.

o Effects:

 Mild cases → Confusion, irritability, poor concentration

 Severe cases → Stupor, coma

4. Treatment Strategies for CHF (Congestive Heart Failure)

Since heart failure has multiple causes, treatment aims to:
✔ Reduce fluid overload
✔ Improve heart function
✔ Lower workload on the heart

A. Addressing the Underlying Cause

 Fixing valve problems (e.g., surgery for mitral regurgitation)

 Revascularization (if caused by blocked coronary arteries)

B. Symptom Management

 Salt restriction & diuretics

o Reduces fluid overload, improving symptoms of pulmonary congestion and

swelling.

 Positive inotropes (e.g., digoxin, dobutamine)

o Increase myocardial contractility, improving cardiac output.

 Afterload reducers (e.g., ACE inhibitors, beta-blockers)

o ACE inhibitors (e.g., lisinopril):

 Reduce vasoconstriction and fluid retention by blocking the RAAS

system.

 Prevent harmful cardiac remodeling.

o Beta-blockers (e.g., metoprolol):

 Reduce heart rate and oxygen demand, improving heart efficiency.

C. Advanced Therapies

 Cardiac Resynchronization Therapy (CRT)

o Pacemakers that stimulate both ventricles to beat in sync, improving pumping

efficiency.

 Cardiac Contractility Modulation (CCM)

o Electrical stimulation of heart muscle to enhance contraction strength.

Despite these treatments, CHF remains a leading cause of death and disability worldwide.
Right-Sided Heart Failure (RHF)

Right-sided heart failure (RHF) occurs when the right ventricle fails to pump blood effectively
into the pulmonary circulation, leading to systemic venous congestion. While RHF can occur in
isolation (e.g., due to lung disease), it is most commonly a consequence of left-sided heart
failure (LHF).

1. Why Does Right-Sided Heart Failure Occur?

A. Secondary to Left-Sided Heart Failure

 LHF causes blood to back up into the pulmonary circulation, increasing pressure in the
lungs.

 The right ventricle must pump against this increased resistance, leading to
hypertrophy, dilation, and eventual failure.

B. Isolated Right-Sided Heart Failure (Cor Pulmonale)

In rare cases, RHF occurs independently due to lung or pulmonary vascular diseases:

 Chronic lung diseases (e.g., COPD, interstitial fibrosis, cystic fibrosis) → increase
pulmonary resistance.

 Pulmonary hypertension (high blood pressure in lung arteries) → forces the right
ventricle to work harder.

 Recurrent pulmonary emboli (blood clots in lung arteries) → block blood flow, raising
pulmonary pressure.

 Obstructive sleep apnea → leads to chronic pulmonary vasoconstriction.

C. Myocardial Changes in Right-Sided Heart Failure

 Hypertrophy (muscle thickening) of the right ventricle occurs in response to the

increased workload.

 Chronic dilation (enlargement of the right heart chambers) eventually weakens the
ventricle.

 Ventricular septal bulging into the left ventricle → decreases left ventricular output by
obstructing blood flow.
2. Symptoms of Right-Sided Heart Failure: Why Do They Occur?

Unlike LHF, which causes pulmonary congestion, RHF primarily leads to systemic venous
congestion because blood returning from the body cannot enter the failing right heart
efficiently.

A. Systemic Venous Congestion

 Hepatic congestion (Congestive Hepatomegaly or "Nutmeg Liver")

o Why? Blood backs up into the hepatic veins, causing liver enlargement.

o Effects:

 Painful liver swelling (especially in the upper right abdomen).

 Liver dysfunction (elevated liver enzymes).

 Severe cases → Cardiac cirrhosis (scarring of the liver).

 Splenic congestion (Congestive Splenomegaly)

o Why? Blood backup into the portal vein increases pressure in the spleen.

o Effects:

 Enlarged spleen → Can cause low platelet counts (thrombocytopenia).

 Jugular Venous Distention (JVD)

o Why? Blood backs up in the superior vena cava, causing distension of the jugular
veins in the neck.

 Peripheral edema (Leg & Ankle Swelling)

o Why? Increased venous pressure forces fluid into the interstitial spaces of the
lower extremities.

o Effects:

 Pitting edema in the ankles and legs (worse when standing for long
periods).

 Ascites (Fluid buildup in the abdomen)

o Why? Increased pressure in the portal vein leads to fluid leakage into the
abdominal cavity.

o Effects:
  Swollen abdomen with discomfort.

 Possible breathing difficulties (if fluid pushes on the diaphragm).

 Pleural Effusion (Fluid around the lungs)

o Why? Systemic congestion forces fluid out of the pleural blood vessels into the
pleural space.

o Effects:

 Shortness of breath (fluid compresses the lungs).

B. Organ Hypoxia Due to Poor Circulation

Similar to LHF, RHF results in reduced oxygen delivery to organs, causing dysfunction:

 Kidney Dysfunction (Prerenal Azotemia)

o Why? Poor blood flow to the kidneys reduces filtration, leading to fluid and
waste buildup.

o Effects:

 Worsened fluid retention, exacerbating edema and ascites.

 Brain Hypoxia (Cognitive Impairment, Fatigue, Confusion)

o Why? Reduced cardiac output leads to poor cerebral blood flow.

o Effects:

 Mental fog, poor concentration, restlessness, dizziness.

 Severe cases → Stupor, coma (especially in advanced CHF).

3. The Progression to Biventricular Heart Failure

Over time, RHF and LHF often coexist, leading to biventricular congestive heart failure (CHF).

 Left-sided failure causes pulmonary congestion, which in turn leads to right-sided

failure and systemic congestion.

 In advanced CHF, tissue perfusion is severely compromised, causing cyanosis (bluish

skin) and metabolic acidosis (due to tissue oxygen deprivation).
4. Treatment of Right-Sided Heart Failure

Since RHF is usually secondary to LHF or lung disease, treatment is directed at the underlying
cause:

A. Treat Left-Sided Heart Failure (if present)

 ACE inhibitors & Beta-blockers → Improve left ventricular function.

 Diuretics → Reduce pulmonary and systemic congestion.

B. Reduce Pulmonary Hypertension (in Cor Pulmonale)

 Oxygen therapy → Reduces pulmonary vasoconstriction.

 Pulmonary vasodilators (e.g., sildenafil, bosentan) → Lower pulmonary artery pressure.

C. Manage Venous Congestion & Organ Dysfunction

 Diuretics (e.g., furosemide, spironolactone) → Reduce leg swelling, ascites, pleural

effusions.

 Salt restriction → Helps control fluid retention.

 Inotropes (e.g., digoxin) → Increase right ventricular contraction (for severe cases).

D. Advanced Therapies for Severe RHF

 Right ventricular assist devices (RVADs) → For end-stage cases.

 Heart-lung transplant → For severe cor pulmonale or biventricular failure