chapter 37

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  1. What are compensatory mechanisms?
    • SNS stimulation
    • Renin-angiotensin system activation
    • Other chemical responses
    • Myocardial hypertrophy
  2. What is left-sided heart (ventricular) failure
    • Decreased tissue perfusion from poor CO and pulmonary congestion from increased pressure in the pulmonary vessels
    • Causes:
    • Hypertensive disease
    • Coronary artery disease
    • Valvular disease involving mitral or aortic valve
  3. What is systolic heart failure?
    • When the heart cannot contract forcefully enough during systole to eject adequate amounts of blood into the circulation
    • Preload increases with decreased contractility
    • Afterload increases as a result of increased peripheral resistance
    • Tissue perfusion diminishes and blood accumulates in the pulmonary vessels
    • CO is decreased and fluid backs up into the pulmonary system
  4. What is diastolic heart failure?
    • Left ventricle cannot relax adequately during diastole
    • Inadequate relaxation prevents the ventricle from filling with sufficient blood to ensure an adequate CO
    • Ventricle becomes less compliant over time because more pressure is needed to move the same amount of volume as compared with a healthy heart
  5. What is right-sided (ventricular) failure?
    • Right ventricle cannot empty completely
    • Increased volume and pressure develope in the venous system, and peripheral edema results
    • May be caused by:
    • Left ventricular failure
    • Right ventricular MI
    • Pulmonary hypertension
  6. What is high-output heart failure?
    • Can occur when CO remains normal or above normal
    • Caused by increased metabolic needs or hyperkinetic conditions-septicemia, anemia, hyperthyroidism
  7. Stimulation of the SNS
    • Increasing catecholamines as a result of tissue hypoxia represents the most immediate compensatory mechanism
    • Stimulation of the adrenergic receptors causes an increase in heart rate (beta adrenergic)and BP from vasoconstriction (alpha adrenergic)
    • CO is the product of HR and SV so an increase in HR results in an immediate increase in CO
    • HR is limited in its ability to compensate for decreased CO-if it becomes too rapid, diastolic filling time is limited and CO may start to decline
    • An increase in HR also significantly increases oxygen demand by the myocardium-if heart is poorly perfused because of arteriosclerosis, HF may worsen
    • Sympathetic stimulation also results in arterial vasoconstriction and has the benefit of maintaining BP and improving tissue perfusion in low-output states
    • Constriction of the arteries increases afterload, the resistance against which the heart must pump
    • As afterload increases, the left ventricle requires more energy to eject its contents and SV may decline
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chapter 37

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