Class I: Cardiac disease WITHOUT ANY physical limitations.

Class II: Cardiac disease w/ SLIGHT limitation in phys. activity.

Class III: Cardiac disease with MARKED limitations in phys. activity.

Class IV: Cardiac disease with INABILITY to carry on phys. activity without discomfort.

NOREPI--positive effect acutely, then incr. work of heart and fibrosis.

ANGIOTENSIN II--fibrotic change, also H2O, Na retention.

NATRIURETIC PROTEINS: Oppose kidney by promoting urination.

Aldosterone: Incr. pre- and after-load.

Endothelin: Incr. pre- and after-load.

Vasopressin: Incr. pre- and after-load.

Cytokines

ALL adversely affect structure and fxn. of heart (remodeling).

MECH: Arterovenous dilation with NO change in HR or contractility.

BENEFIT: Alleviate sympt., improve clinical status, REDUCE RISK OF DEATH AND HOSPITALIZATION. NO NEUROHORMONAL ACTIVATION, REFLEX TACHY OR TOLERANCE DEVELOPED. ALSO, INHIBIT CARDIAC AND VASCULAR REMODELING.

USE: Replace ACE inhibitor when cough is an issue.

AE: Can cause angioedema. Decrease GFR, Incr. potassium, hypotension.

USE: Replace ACE inhibitor when cough is an issue.

AE: Can cause angioedema. Decrease GFR, Incr. potassium, hypotension.

USE: Replace ACE inhibitor when cough is an issue.

AE: Can cause angioedema. Decrease GFR, Incr. potassium, hypotension.

USE: Replace ACE inhibitor when cough is an issue.

AE: Can cause angioedema. Decrease GFR, Incr. potassium, hypotension.

USE: Replace ACE inhibitor when cough is an issue.

AE: Can cause angioedema. Decrease GFR, Incr. potassium, hypotension.

USE: Replace ACE inhibitor when cough is an issue.

AE: Can cause angioedema. Decrease GFR, Incr. potassium, hypotension.

USE: Decr. volume and preload. No direct affect on CO. NEUROHORMONAL ACTIVATION--therefore, use sparingly and only when volume expanded.

CONTRA: Hypovolemia.

SE: Volume contraction, hypokalemia, hyponatremia.

USE: LOW DOSE--improved Class 3 and 4 HF patients by 30% reduced mortality.

CONTRA: Poor renal fxn. and CO--prone to hyperkalemia. Spironolactone will increase this to fatal end.

SE: Hyperkalemia, metabolic acidosis, gynecomastia, gastric upset, thinning hair (sex hormone effects).

USE: LOW DOSE--Mortality decr. from 13.6 to 11.8% in patients who had a LVEF <40%, evidence of HF or diabetes within 14 days of MI.

CONTRA: Poor renal fxn. and CO--prone to hyperkalemia. Spironolactone will increase this to fatal end.

SE: Hyperkalemia, metabolic acidosis, gynecomastia, gastric upset, thinning hair (sex hormone effects).

MECH: HF is a high catacholamine state, beta-blockers block the effects of these agents.

USE: ONLY 3 beta blockers (Bisoprolol, metoprolol, carvedilol) show reduced risk of death. Initiate at LOW DOSE and GRADUALLY increase.

MECH: Inhibition of Na/K ATPase causing increased intracellular Na reducing effectiveness of membrane Na/Ca exchanger's clearance of Ca from cell resulting in sustained contraction. ALSO, increases vagal efferent activity to heart--reduces SA firing rate, conduction to AV.

EFFECTS: INCREASED CO, LVEF, exercise tolerance, natriuresis. DECREASED LVEDP, neurohormonal activation (decr. norepi, RAAS activity).

CAUTION: Has a narrow therapeutic-toxic window. Causes Atrial tachycardia AND AV block. Needs to be KIDNEY DOSED. Improves quality BUT NOT QUANTITY OF LIFE

MECH: Inhibits phosphodiesterase IIIa--breakdown of cAMP increases contractility and HR.

USE: Indicated when treatment with vasodilators and diuretics is insufficient.

MECH: Beta-1 selective agonist. Positive ionotrope and chronotrope.

USE: Great for acute, decompensated HF. Take patient off quickly--no positive long-term effects.

Recombinant BNP

MECH: REDUCE catecholamines, aldosterone, renin. INCR. perfusion.

PROVEN INEFFECTIVE!!