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8 Cards in this Set
- Front
- Back
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CHF
Therapeutic Goals |
1. Elimination of precipitating cause of symptoms
2. Management of heart failure 3. Increased cardiac output and enhanced tissue and organ profusion 4. Modulation of neurohumoral response |
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CHF
Compensatory Mechanism (Increased Sympathetic Activity) |
Activation of BETA-adrenergic receptor in the heart
LEADS TO Increase in heart rate and cardiac output LEADS TO Vasoconstriction LEADS TO Enhanced venous return and increased cardiac output |
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CHF
Compensatory Mechanism (Fluid Retention) |
Decreased cardiac output
LEADS TO Decreased blood flow to kidney LEADS TO Increased renin, angiotensin II, and aldosterone LEADS TO Increased peripheral resistance and retention of Na+ and water LEADS TO Increased blood volume |
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CHF
Compensatory Mechanism (Myocardial and Cardiac Remodeling) |
Ventricular hypertrophy
Myocardial structural and functional alterations Change in cardiac size, shape, and composition |
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CHF
Compensatory Mechanism (Neurohormonal) |
Increase in Angiotensin II
Increase in Aldosterone Increase in Norepinephrine Increase in Endothelin Increase in Vasopressin |
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CHF Risk Factors
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Age
Coronary Artery Disease Hypertension Smoking Alcohol Thyroid Disease Rheumatic Heart Disease Cardiotoxic Drugs |
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4 Categories of HF
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Stage A: Patients at high risk of developing HF due to conditions present that are strongly associated with development of HF
Stage B: Patients with structural heart disease highly associated with development of HF, but who have not had signs or symptoms of HF Stage C: Patients with current or past symptoms of HF with underlying structural heart disease Stage D: Patients with progressive structural heart disease and marked symptoms of HF at rest |
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Diuretic Resistance
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Dx: Patient that does not respond to loop diuretics alone
Tx: Furosimide and Metolazone (Lowers the chances of resistance and is the only time that metolazone is used as a diuretic) |
