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Cardiac Output (CO)
- - CO= SVxHR
- -if the SV decreases, the HR must increase to sustain CO
- -if the HR decreases, SV musct increase to sustain Co
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Preload
amount of blood that has filled the ventricles by the end of diastole
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Contractility
force of squeezing achieved by ventricles
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Afterload
Amount of pressure ventricles must overcome to eject blood
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CHF
- systemic and pulmonayr congestion aren't always present in chronic CHF
- progressive changes that result in declining pumping ability
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Cardiac Remodeling
- ventricles get bigger and walls get thicker b/c its working harder, pump out more volume, increased HR
- fibrosis
- the heart gets round instead of cone shape
- makes it harder to contract causing increased preload
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Increased Sympathetic Tone
- everything is constricted/tense increasing afterload
- affects rate, contractility, venous and arterial tone
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Naturetic Peptides
- two peptides in blood get released trying to get rid of sodium, but they are not effective
- ANP and BNP- check serum levels to measure degree of failure
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Thiazide Diuretics
- Moderate Diuresis
- not effective if CO or GFR is low
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Loop Diuretics
- profound diuresis
- effective even when CO is low
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Potassium Sparing Diuretics
- very mild diuresis
- risk for hyperkalemia
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ACE Inhibitors
- Angiotensin Converting Enzyme inhibitor
- Block production of angiotensin II
- dilate arterioles and veins
- Decrease release of aldosterone reducing sodium and water retention effecting preload and afterload
- prevents cardiac remodeling because they affect SV
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ARBs
- Angiotensin Receptor Blockers
- reserved fir yse when patients cannot tolerate ACE inhibitors
- Should NOT be used together with ACE because of hyperkalemia potential
- prevents cardiac remodeling b/c affects SV
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Aldosterone Receptor Blockers
- Aldosterone contributes to volume overload, myocardial and vascular fibrosis
- Spironlactone blocks receptors in heart and blood vessels, helps to decrease remodeling, adverse effects->hyperkalemia and gynecomastia
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Beta Adrenergic Blocking Agents
- possible negative effects because of beta 1 blocking
- dose is started small and gradually increased
- increased vasodialtion and decreased peripheral resistance
- beneficial effects may take up to 3 months
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Carvedilol
- beta blocker used as an adjunct in treating mild to moderate CHF
- non selective- decreases force of contraction and CO (Can make HF worse initially)
- alpha 1 blocking activity- increases casodilation and decreases peripheral resistance
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Metoprolol XL
- SELECTIVE bata 1 blocking agains
- is also approved for HF
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Inamrinone
- drug for HF
- for short term, inpatient use
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Milrinone
- outpatient use for HF in patietns who are not responding to other drug therapy for acute HF
- Can't stop taking it or actions get reversed
- produces inotropic action (increaced contractility)
- vasodilation by relaxing vascular smooth muscle
- IV adminsitration only
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Phoshpoidestrase Inhibitors
- produce ionotropic action
- (increase contractility)
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Nesitritide
- IV vasodilatore for HF
- Human B-type natriuretic pepetide- it tries to get rid of sodium
- direct dilation of cascular smooth muscle
- supression of sympathetic outflow (supressing vasoconstriction)
- Supresses renin secretion
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Nitroglycerin
- ACUTE SITUATIONS- IV vasodilator for HF
- Venous Dilation- decreases venous return decreasing preload and O2 demand
- Arteriolar Dilation- reduces systemic vascular resistance and arterial pressure, reduces afterload
- decreases overall myocardial oxygen consumption
- reduces pulmonary edema (frothy pink sputum)
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Dopamine
- Sympathomimetic druc
- used short term for SEVERE failure, so heart doesn't stop
- catecholamine and a precursosr to NE
- stimulation of alpha 1 and beta 1 and dopamine receptors
- the higher the dose, the more vasoconstriction
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Dobutamine
- Sympathomymetic Drugs
- short term in SEVERE failure
- Stimulation of beta 1 receptors ONLY
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Digoxin
- Manage symptoms of HF
- therapeutic range: 0.5-0.8 mg/ml
- treat atrial fibrillation (irregular, no p-wave)
- treat atrial flutter (regular, but not effective, over 300 bpm)
- slows heart rate and regulates rhythym
- strengthems contraction (positive inotropic)
- slows conduction (negative dromotropic)
- slows HR (negative chronotropic)
- need anticoagulate to prevent clotting in Afib**
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Digoxin Toxicity
- caused by hypokalemia- b/c K+ and digozin compete for the same receptors, so if there is not enough K+, too much digoxin binds
- keep K+ within normal range
- watch out for with loop and thiazide diuretics
- also alcohol has effect
- 0.5-0.8 mg/ml
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Antidote fore Digoxin overdose
- Digoxin immune FAB (DigiBind)
- activated cahrcoal (not supposed to mix it with anything, usually given with lexative)
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