1. increase myocardial contractility
2. decrease afterload
3. prevent/reverse remodeling of heart

1. Length-tension - based on preload, if too great then decline in contractility
2. Intracellular calcium - if low, then decreased contractility

• Loop diuretics (furosmide) preferred
• spionolactone - aldosterone antagonist

• Beta blocker
• reduce heart rate and improve cardiac performance
• α1 (↓afterload), β1 (↓heart), β2 (↓vascular)
• titrate dose to identify max improvement w/ minimal side effects

• cardiac glycoside - steroid-like w/ a sugar
• anti-arrhythmic and inotropic agent
• blocks Na/K ATPase
• incrased intracellular Ca --> increased contractility
• SE: depletion of K, too much Na and CA --> trigger arrhythmias

1. therapeutic - inhibits enzyme on cardiac and vagal--> inc contractility and vagal tone
2. toxic range - inhibits sympathetic and vascular smooth muscle --> arrhythmias, HTN
3. extreme toxic range - inibits skeletal muscles --> hyperkalemia

Indirect effects - inhibition of SA node and delayed conduction through AV node

In CHF, treat patients who are symptomatic after optimal therapy.  Reduces symptoms but does not improve survival.

1. general malaise is common
2. GI symptoms in half of patients (partially due to direct activation of chemo-emetic trigger zone)

arrhythmias

bradycardias (due to inc vagal tone)

inc myocardial excitability and symp tone:

• supraventricular and ventricular tacharrhythmias
• blocks and excitatory arrhythmias

1. monitor serum drug levels w/ immunoassay
2. t1/2 1.6days, slow clearance
3. correct electrolyte abnormalities
4. anti-arrhythmics

• IV or ORAL
• cleared lsowly by kidneys
• need to use loading dose to reach steady-state rapidly

• diuretics - loop and thiazide diuretics cause hypokalemia
• Ca channel, B blockers - interfere w/ aV node conduction

for hypotension: give inotropic agents plus pressor agents

for pulmonary edema give diuretics and vasodilators plus inotropic agents

ANP, BNP

• secreted by cardiac myocytes in response to atrial/ventricular stretch
• BNP as indicator for heart failure
• when they bind to receptors increase NO
• vasodilation and diuresis
• Can by administered IV foractue heart failure
• SE: hypotension and renal failure

treat acute LV failure

• dobutamine - B-1 agonist to increase CO
• dopamine - B-1 agonist that also has pressor activity (less selective)
• dopamine also produces reno-vasodilation and prevents acute tubular necrosis

B1 receptor agonists, that increase cAMP

incrases intracellular Ca

increases HR and conduction

1. in poorly perfused tissue causes ischemia
2. preisposes patients to arrhythmias

continuous IV infusion

• restricted to critically ill patients w/ adequate monitoring
• prolonged use results in desensitization (so just for 2-3 days)

IV digitalis

rapid onset of action, long half-life, and does not show desensitization