Heart Failure and Congestive Heart Failure Review

Overview and Etiology of Heart Failure

  • Heart failure is defined as a complex syndrome resulting from any functional or structural disorder of the heart.
  • The condition results in, or increases the risk of developing, manifestations of low cardiac output and/or pulmonary or systemic congestion.
  • Common causes of heart failure include:
    • Coronary Artery Disease (CAD).
    • Hypertension (HTN).
    • Dilated cardiomyopathy.
    • Valvular heart disease.

Cardiovascular Anatomy and Physiological Review

  • Right Side of the Heart: Accepts deoxygenated blood from the venous system and pumps it to the lungs via the pulmonary artery.
  • Left Side of the Heart: Accepts oxygenated blood from the lungs via the pulmonary veins and pumps it into the systematic circulation to supply the body.
  • Cardiac Cycle Phases:
    • Systole: The period when the ventricles contract forcefully to expel blood into the outflow vessels.
    • Diastole: The period when the ventricles relax and fill with blood from the atria.
  • Major Cardiac Structures (Wolters Kluwer, 2015):
    • Superior and inferior vena cava.
    • Right and left pulmonary arteries and pulmonary veins.
    • Right and left atria; Right and left ventricles.
    • Valves: Pulmonic valve, Tricuspid valve, Mitral valve, and Aortic valve.
    • Mechanical supports: Papillary muscles and Chordae tendineae.
    • Main outflow: Descending aorta.

Cardiac Performance and Dynamics

  • Cardiac Output (CO): Determined by the amount of blood the heart ejects each minute. The formula is expressed as: CO=SV×HRCO = SV \times HR
  • Regulation: The heart is regulated by a balance between the Sympathetic Nervous System (SNS) and the Parasympathetic Nervous System (PNS).
  • Cardiac Reserve: This is the ability of the heart to increase its output during periods of increased activity. Persons with heart failure are distinct in that they use their cardiac reserve even while at rest.

Determinants of the Heart as a Pump

  • Preload:
    • Definition: The volume of blood in the ventricle at the end of diastole.
    • Physiological indicator: The blood pressure in the left ventricle at the end of diastole immediately before contraction.
    • Origin: Pressure originating from the venous system.
  • Afterload:
    • Definition: The force that the contracting heart muscle must generate to eject blood.
    • Resistance: Represents the resistance that the heart faces during systole.
    • Structural Origin: Systemic vascular resistance created by the arteries which the heart must overcome.
  • Contractility:
    • Definition: The inherent ability of the heart muscle to contract.
    • Characteristics: Increases cardiac output independently of preload and afterload.
    • Requirements: Utilizes energy from Adenosine Triphosphate (ATP) and requires the presence of Calcium ions (Ca++Ca^{++}).

Classifications and Types of Heart Failure

  • Output Capacity: Differentiation between high-output versus low-output failure.
  • Functional Impairment:
    • Systolic Failure: The heart fails to pump out enough blood.
    • Diastolic Failure: The heart fails to accept enough blood from the body and lungs.
  • Location of Failure:
    • Left-sided heart failure: Characterized by the inability of the left ventricle to pump enough blood, leading to fluid backup into the lungs.
    • Right-sided heart failure: Characterized by inefficient pumping of the right side of the heart, leading to fluid buildup in the abdomen, legs, and feet.

Pathophysiology of Systolic and Diastolic Dysfunction

  • Systolic Dysfunction:
    • Results from impaired (decreased ↓\downarrow) myocardial contractility.
    • Clinical marker: Decreased ejection fraction (EF<40%EF < 40\%).
    • Consequences: Increased preload and ventricular pressures leading to volume overload. Blood accumulates in the atria and the pulmonary venous system, eventually leading to pulmonary or peripheral edema.
  • Diastolic Dysfunction:
    • Results from the inability of the left ventricle to fill sufficiently during diastole.
    • Contributing conditions: Conditions preventing ventricle expansion, such as myocardial hypertrophy, ischemic heart disease, and aging.
    • Consequences: Increased ventricular pressures at any given volume and decreased (↓\downarrow) CO due to decreased filling.
    • Manifestations: Pulmonary congestion, increased work of breathing (WOB), and dyspnea.

Left-Sided vs. Right-Sided Heart Failure Detail

  • Left-Sided Heart Failure:
    • Causes: Hypertension (HTN), acute Myocardial Infarction (MI), and valvular defects.
    • Pathophysiology: Increased left ventricular and left atrial pressures; progressive accumulation of blood within pulmonary circulation.
    • Outcomes: Diminished CO with decreased peripheral blood flow and pulmonary edema.
  • Right-Sided Heart Failure:
    • Causes: Left-sided heart failure, Chronic Obstructive Pulmonary Disease (COPD), and pulmonary hypertension.
    • Pathophysiology: The right ventricle is unable to move blood from the systemic venous circulation to the pulmonary circulation.
    • Outcomes: Edema to lower extremities, systemic and hepatic venous system congestion, and visceral congestion (e.g., hepatomegaly).

Compensatory Mechanisms in Heart Failure

  • The body utilizes six primary mechanisms to attempt to fix system failure:
    1. Frank-Starling Mechanism: Increases stroke volume (SVSV). As preload (end diastolic volume) increases, cardiac muscle fibers stretch, triggering a more forceful contraction. This allows for increased SVSV at a lower Heart Rate (HRHR).
    2. Sympathetic Nervous System (SNS) Activity.
    3. Renin-Angiotensin-Aldosterone (RAAS) Mechanism.
    4. Natriuretic Peptides.
    5. Endothelins.
    6. Myocardial Hypertrophy and Remodeling.

Clinical Manifestations and Symptoms

  • General Concepts of Heart Failure:
    1. Effects of impaired pumping.
    2. Effects of decreased renal blood flow.
    3. Effects of the sympathetic nervous system.
  • Specific Symptoms:
    • Respiratory: Dyspnea, exertional dyspnea, and cyanosis (associated with desaturated Hemoglobin/Hgb).
    • Fluid Balance: Fluid retention and edema.
    • Systemic: Fatigue, weakness, and mental confusion.
    • Nutritional: Cachexia and malnutrition.
    • Electrical: Atrial and ventricular arrhythmias; risk of sudden cardiac death.

Acute Pulmonary Edema

  • This is a life-threatening condition where capillary fluid moves into the alveoli.
  • It is caused by severe pulmonary edema due to elevated left ventricular filling pressures (with or without low cardiac output).
  • Clinical Signs:
    • Decreased oxygen supply to the brain causing confusion.
    • Dyspnea and "air hunger."
    • Productive cough with frothy, blood-tinged sputum.
    • Auscultation reveals crackles.

Diagnostics and Treatment

  • Diagnostics:
    • Physical Examination: Monitoring Heart Rate (HR), heart sounds, Blood Pressure (BP), jugular vein distention (JVD), edema in extremities, breath sounds, and pulse oximetry.
    • Labs: Complete Blood Count (CBC) to assess for anemia; Electrolytes.
    • Imaging/Monitoring: Echocardiography; In acute emergencies, measurement of central venous pressure and central artery pressure.
  • Non-Pharmacologic Treatment:
    • Exercise.
    • Sodium and fluid restriction.
    • Weight management.
  • Pharmacologic Treatment:
    • Diuretics.
    • Digoxin.
    • ACE inhibitors.
    • Beta-blockers.
    • Note: Medication choice is determined by the specific cause of the failure.
  • Advanced Interventions:
    • Oxygen therapy.
    • Cardiac re-synchronization and implants for those with abnormal intraventricular conduction.
    • Mechanical support via Ventricular Assist Devices (e.g., Left Ventricular Assistive Device or LVAD).