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Heart Failure: Pathophysiology




General Features and Pathophysiology

  • Heart failure (HF)­ is defined as the inability of the heart to provide sufficient output to meet the metabolic demands of the body.
  • Most often a chronic condition, but may also be acute.
  • Heart failure leads to tissue hypoperfusion, as well as pulmonary and systemic venous congestion.
  • There are many possible etiologies. Low output failure occurs with conditions associated with impaired cardiac contractility, impaired cardiac filling, excess afterload, or arrhythmias. High output failure describes a condition in which the signs and symptoms of heart failure occur in the setting of increased cardiac output, reduced systemic vascular resistance, and increased metabolic demand.
  • Examples of conditions that cause low output heart failure include coronary artery disease, hypertension, cardiomyopathy, pericardial disease, arrhythmias, and valvular disease.
  • Examples of conditions that cause high output heart failure include severe anemia, thyrotoxicosis, Paget’s disease of bone, sepsis, systemic arteriovenous shunts, and beriberi.
  • Compensatory mechanisms develop to improve cardiac output, but in time these responses only serve to exacerbate the underlying cardiac problem. Examples of compensatory mechanisms include:
  • Neurohormonal activation
  • Increased sympathetic nervous system activity causes increased myocardial contractility and peripheral vasoconstriction.
  • Activation of the renin-angiotensin-aldosterone system leads to sodium and water retention.
  • Vasopressin/ADH secretion causes peripheral vasoconstriction and water retention.
  • Neurohormonal activation helps maintain systemic arterial pressures, but also contributes to an increased workload on the heart.
  • Cardiac dilation and hypertrophy

Flash Cards: Heart Failure Pathophysiology