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What are compensatory mechanisms?
- SNS stimulation
- Renin-angiotensin system activation
- Other chemical responses
- Myocardial hypertrophy
What is left-sided heart (ventricular) failure
- Decreased tissue perfusion from poor CO and pulmonary congestion from increased pressure in the pulmonary vessels
- Hypertensive disease
- Coronary artery disease
- Valvular disease involving mitral or aortic valve
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
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
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
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
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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