CHF Definition & Overview:

• A condition where the heart cannot pump enough blood to meet the metabolic demands of the body.
• Usually chronic, but can be acute in severe cases.
• Primarily caused by weakened heart muscle or valvular defects that reduce contractility.

Causes & Contributing Factors:

• Cardiopulmonary conditions such as:
  • Previous myocardial infarction.
  • Valve diseases.
  • High blood pressure (hypertension): often leads to left-sided heart failure.
  • Lung diseases (e.g., COPD) causing cor pulmonale (right-sided failure).
• Increased workload, e.g., from hypertension or lung disease, strains the heart and leads to failure over time.

Types of Congestive Heart Failure:

1. Left-Sided Heart Failure:

• Most common type.
• Usually results from damage to the left ventricle, often due to myocardial infarction or chronic hypertension.
• Damage decreases left ventricle contractility, leading to both reduced stroke volume and cardiac output.
• Features:
  • Blood backs up into the lungs.
  • Causes pulmonary congestion and edema.
  • Symptoms: shortness of breath, orthopnea, pulmonary edema.

2. Right-Sided Heart Failure:

• Often caused by left-sided failure or pulmonary disease.
• Blood backs up into systemic circulation, leading to peripheral edema.
• Commonly involves decreased blood flow to the lungs (cor pulmonale).
• Symptoms: jugular venous distension, peripheral edema, ascites.

Clinical Manifestations:

• Patients may manage daily activities fine initially, but exercise intolerance develops.
• Struggle with climbing stairs or performing vigorous activity.
• Compensation mechanisms are activated to maintain organ perfusion:
  • These include increased heart rate and stroke volume.
  • Neurohormonal responses like activating the renin-angiotensin-aldosterone system.

Body’s Compensation of Left-Sided CHF:

1.  Neural response:

• • Brain detects low blood pressure and low oxygen.
    • Baroreceptors detect low blood pressure, sending the information to the
    • Medulla oblongata which activates the sympathetic nervous system (SNS) which:
      • Increases heart rate and force of contraction.
      • Causes vasoconstriction (↑ afterload).
    • Activates sympathetic nervous system.
  • Increases heart rate, force of contraction, and induces vasoconstriction.
  • Outcome: Maintains perfusion but increases afterload, making it harder for the heart to eject blood.

2.  Hormonal response (RAAASE):

• • Renin-Angiotensin II-ADH-Aldosterone Sympathetic Erythropoietin System:
  • Kidneys sense low blood flow/pressure.
  • Kidneys release Renin in response to ↓ blood flow.
  • Renin converts inactive angiotensinogen into angiotensin I.
  • ACE (released from lungs) converts angiotensin I into active form, Angiotensin II which:
    • Causes vasoconstriction → ↑ blood pressure and afterload.
    • Stimulates ADH release from posterior pituitary gland
    • Stimulates Aldosterone release from adrenal glands, both ADH and aldosterone:
      • Increase salt and water retention.
      • Elevate blood volume and BP, further increasing workload.
  • Angiotensin II causes vasoconstriction, increasing resistance (blood pressure).
  • Increased blood volume (preload), aiming to improve tissue perfusion.
  • Secretes Erythropoietin, leading to polycythemia (more red blood cells for oxygen transport).

3.  Heart Remodeling & Progressive Deterioration:

• Increased workload causes pathologic hypertrophy of the left ventricle:
  • Heart wall thickens, becoming spherical (cardiomegaly).
  • Excessive hypertrophy diminishes efficiency; the heart becomes less effective.
  • Hypertrophied heart muscle requires more oxygen, but blood supply may not keep pace.
  • Insufficient blood supply causes myocardial hypoxia, weakening the heart further.
• Outcome: The weakened heart cannot sustain a high stroke volume; cardiac output declines.

4.  Pulmonary Consequences:

• Blood backs up into pulmonary circulation:
  • Engorged pulmonary vessels.
  • Causes pulmonary congestion and edema (including fluid in alveoli).
    • Impaired gas exchange → dyspnea and hypoxia.
    • Shortness of breath (dyspnea): Especially orthopnea (difficulty breathing when lying flat).
      • Paroxysmal nocturnal dyspnea: Sudden nighttime breathlessness.
      • Cough: Often dry, irritant response; may cough up blood (hemoptysis).
      • Physical signs: pulmonary crackles, wet sounds, cyanosis.
  • Reduced cardiac output leads to organ hypoxia, dizziness, confusion.
  • Cells switch to anaerobic respiration, produce lactic acid → acidosis.
  • The brain stimulates increased respiration rate to compensate.

• Chronic pulmonary edema visible on chest X-ray as white, opaque lungs.

5.  Progression to Right-Sided Failure:

• The pulmonary circuit becomes congested and increased pressure (pulmonary hypertension) develops.
• Elevated pressure in pulmonary vessels makes it harder for the right ventricle to eject blood.
• The right ventricle hypertrophies and weakens.
• Blood backs up into systemic circulation:
  • Engorged blood vessels.
  • Edema in feet, legs, and abdominal cavity.
  • Impaired function of digestive organs.
• Progression: Left-sided failure often progresses to right-sided failure.
• Progressive worsening of cardiac function and eventual heart failure.

End-Stage & Worsening:

• Persistent volume overload and pressure lead to worsening hypertrophy and heart deterioration.
• Increased atrial stretch raises atrial natriuretic peptide (ANP) secretion.
• An increased ANP:
  • Opposes aldosterone and ADH.
  • Promotes natriuresis (salt and water excretion).
  • Attempts to reduce blood volume and pressure, but is a sign of advanced disease.
  • • Eventually decreased urine output (oliguria) due to reduced kidney perfusion.

Right-Sided Congestive Heart Failure (CHF) – Comparison to Left-Sided CHF, Pathophysiology and Causes:

1.  Predisposing Factors of Right-Sided CHF:

• Primary cause: Damage to the right ventricle, often due to myocardial infarction or valvular issues.
  • A weakened right ventricle can’t effectively empty, leading to decreased blood flow through the pulmonary circulation.
  • Consequence: Less blood reaches the left side of the heart, reducing stroke volume and cardiac output overall.

• Two Secondary causes (most common):
  • • Left-sided failure → Pulmonary congestion → Pulmonary hypertension → Right ventricle hypertrophy and failure.
    • Lung disease (cor pulmonale): Conditions like emphysema cause damage to alveolar capillaries which increases pulmonary vessel narrowing and pulmonary resistance (pulmonary hypertension).
      • Pulmonary Hypertension & Cor Pulmonale:
      • Lung damage (from smoking, infection, or other lung disease) leads to:
        • Capillary damage → scars and narrowing of vessels.
        • Increased pulmonary vascular resistance → pulmonary hypertension.
        • Right ventricle hypertrophies in response to increased afterload.
        • Over time, the right ventricle weakens and fails.

2.  Hemodynamic Changes of Right-Sided CHF:

• Blood backs up into systemic circulation:
  • Vena cavae (superior and inferior) become engorged.
  • Increased pressure causes leakage of exudate into tissues.
• Edema formation:
  • • Peripheral edema: Legs, feet, ankles, and abdomen (ascites).
    • Jugular venous distension: Swollen neck veins.
    • Hepatosplenomegaly: Enlarged liver and spleen due to vascular congestion (engorgement and pressure).
    • Digestive disturbances: Loss of appetite, nausea, and abdominal discomfort.
  • Signs of systemic congestion: Cyanosis, fatigue, and signs of hypoxia affecting organs.

3.  Cerebral & Organ Effects of Right-Sided CHF:

• Brain:
  • Increased intracranial pressure from edema.
  • Reduced blood flow causes hypoxia, confusion, and potential neurological damage.
• Other tissues:
  • Impaired organ perfusion causes fatigue, weakness, and tissue hypoxia.
  • Signs include pale skin, cold extremities, and slow healing wounds.

4. Body’s Compensation of Right-Sided CHF:

• Exactly the same as Body’s Compensation of Left-Sided CHF

CHF Treatment Strategies:

• Vasodilators:
  • Alpha blockers and vasodilators reduce systemic resistance.
  • Calcium channel blockers: Promote vasodilation and decrease afterload.
• Beta blockers: Slow heart rate and decrease force of contraction, reducing workload.
• Digoxin: Increases contractility, helping the heart maintain stroke volume while reducing workload.
• ACE inhibitors: Block the formation of angiotensin II, reducing vasoconstriction and lowering blood pressure.
• Diuretics: Reduce blood volume and preload, easing the load on the heart.

These treatments aim to reduce workload, improve heart efficiency, and slow disease progression.

CHF Compensation & Deterioration:

• While initially beneficial, compensatory responses increase workload on the heart.
• Over time, these lead to worsening heart failure and progressive deterioration.
• Long-term management involves addressing root causes, reducing workload, and preventing compound damage.

Summary:

Congestive heart failure involves inadequate cardiac output, leading to fluid retention, pulmonary congestion, or systemic edema depending on the side affected. The body’s compensatory mechanisms support life temporarily but can accelerate disease progression. Management aims to optimize cardiac function, reduce workload, and prevent complications.

Left-sided CHF begins with weakened left ventricle function, leading to pulmonary congestion and edema. Compensation mechanisms initially preserve perfusion but eventually worsen heart strain, promote hypertrophy, and cause systemic and pulmonary circulatory failure, often progressing to right-sided failure and widespread edema. Early detection and management are essential to interrupt this vicious cycle.  Treatment aims to reduce preload, afterload, and myocardial workload, preventing progression and improving quality of life.

Right-sided CHF results from primary right ventricular failure or secondary to left-sided failure or lung disease. It causes systemic venous congestion, peripheral edema, and organ hypoperfusion. The body compensates through neurohormonal activation, but long-term, this worsens cardiac hypertrophy and deteriorates heart function. Early detection and intervention are crucial to prevent progression to biventricular failure.

CHF affects both sides of the heart, leading to pulmonary congestion or systemic edema depending on the failure side. The body’s compensatory mechanisms initially support organ perfusion but ultimately contribute to worsening heart failure. Monitoring blood volume and pressures, along with managing symptoms and underlying causes, is crucial in treatment. An increase in atrial natriuretic peptide signifies severe or progressing heart failure.