Heart Disease Manifestations and Heart Failure

Heart Failure

• The heart strives to maintain adequate cardiac output for oxygen and nutrient transport to support cellular metabolism.
• Heart failure (HF) occurs when perfusion is inadequate and/or there's increased diastolic filling pressure in the left ventricle.
• While typically involving the left ventricle, HF can affect the right ventricle, especially with lung disease.

Risk Factors

• Leading factors: hypertension and ischemic heart disease.
• Other factors:
  • Advanced age
  • Smoking
  • Obesity
  • Anemia
  • Renal insufficiency
  • Electrolyte imbalances
  • Dysrhythmias
  • Polypharmacy
  • Hypernatremia
  • Hypercholesterolemia
• Genetic polymorphisms that code for myocyte contractility, cardiomyopathies, and neurohumoral receptors contribute to HF.

Left Heart Failure (Congestive Heart Failure)

• Heart failure with reduced ejection fraction (HFrEF) (systolic):
  • Ejection fraction (EF) < 40% with inadequate cardiac output to perfuse vital tissues.
• Heart failure with preserved ejection fraction (HFpEF) (diastolic):
  • Pulmonary congestion despite normal cardiac output and stroke volume.
• Both HFrEF and HFpEF can occur.

Heart Failure and Ejection Fraction (EF)

• Normal EF: 55-70%.
• HFrEF:
  • EF ≤ 40%, leading to inadequate perfusion of vital tissues.
  • Means 40% or less of the total blood volume in the left ventricle at the end of diastole is ejected with each systolic contraction.
• HFpEF:
  • Signs/symptoms of HF with left ventricular EF ≥ 50%.

Hemodynamics – Mechanics of Blood Flow

• Cardiac output is central to heart's effectiveness.
• Cardiac output is the product of heart rate and stroke volume.
  • Adult Normal: ~5 Liters/minute.
  • Mathematically: Cardiac\ Output = Heart\ Rate \times Stroke \ Volume
• Stroke volume is the amount of blood that leaves the heart with each contraction.
  • Adult Normal: ~70ml/beat.
• Stroke volume is determined by preload, afterload, and cardiac contractility.

Hemodynamics: Preload, Afterload, and Contractility

• Preload:
  • Volume of blood inside the ventricle at the end of diastole.
  • Amount of venous blood returning to the ventricle at the end of diastole.
  • Amount of blood remaining in the ventricle after systole.
• Afterload:
  • Increased resistance to blood flow as it is ejected from the heart and circulates through the vessels.
• Contractility:
  • Shortening of cardiac muscle cells in response to electrical current within the cardiac conduction system.
  • Myocardial infarction is the most common cause of decreased contractility.
  • Other factors influencing contractility:
    • Heart rate
    • Cardiac muscle length, shortening velocity, and force
    • Availability of calcium necessary to trigger electrical conduction

Frank-Starling Law

• Provides a basis for understanding heart failure.
• Cardiac contractility is increased or enhanced by stretch in the length of the resting muscle fiber.
• Effective as a mechanism to optimize contractility.
• Reaches a tipping point where increasing myocardial fiber length is no longer effective.
• Prolonged compensatory mechanism leads to decline of contractility, resulting in clinical consequences of heart failure.

Left Heart Failure Pathophysiology and Manifestations

• Ineffective pumping of the left ventricle.
• Blood backs up into the left atrium and pulmonary vasculature, potentially leading to pulmonary edema.
  • Pulmonary edema is a life-threatening complication of acute decompensated heart failure.
• Clinical manifestations:
  • Pulmonary congestion – inspiratory crackles
  • Orthopnea
  • Exertional dyspnea
  • Cyanosis
  • Edema
  • Pleural effusion
  • Cough with blood-tinged sputum
• Left heart failure is categorized as having reduced ejection fraction or preserved ejection fraction.

Ventricular Remodeling and Neurohumoral Mediation

• Widespread heart failure characteristics are mediated by neurohumoral, inflammatory, and metabolic reactions.
• Ventricular remodeling is a compensatory response to decreased myocardial contractility.
• Altered extracellular structure of the heart produces myocardial dilation and progressive decline of contractility.
• Decreased contractility leads to decreased stroke volume and increased left ventricular end-diastolic volume.
• Dilation of the heart allows for increased preload.

Right Heart Failure Pathophysiology

• Right ventricle unable to move adequate blood into pulmonary circulation at normal venous pressure.
• Leading cause: severe left heart failure.
• In the absence of left heart failure, etiology is often hypoxic forms of pulmonary disease such as COPD or cystic fibrosis.
• Right ventricle hypertrophy occurs due to increased myocardial workload.

Right Heart Failure Clinical Manifestations

• Ineffective pumping of the right ventricle.
• Blood backs up into the right atrium and retrogradely, into the jugular vein and then into the venous circulation.
• Clinical manifestations:
  • Jugular venous distention
  • Peripheral/dependent edema
  • Organ edema (liver, spleen)
  • Ascites
  • Intestinal malabsorption
  • Anorexia

Dysrhythmias

• Disturbance of the heart rhythm, altering cardiac output.
• Variations:
  • Rapid, slow, or occasional “missed” beat.
  • Severe disturbances affecting the pumping ability.
• Cause:
  • Abnormal rate of impulse generation or impulse conduction.
  • The impulse won't conduct normally through ischemic tissue and not at all through infarcted tissue.
• Important considerations:
  • Normal pumping involves synchrony between the atria and ventricles and the right side to left side. Any variation can result in decreased cardiac output.
  • Higher heart rate means increased oxygen demand (consumption).
• Examples:
  • Tachycardia, flutter, fibrillation, bradycardia, premature ventricular contractions (PVCs), premature atrial contractions (PACs), asystole.