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Albany College of Pharmacy
test 4 #1
test 4 #1
Albany College of Pharmacy
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what is heart failure?
heart is not able to pump enough blood to meet bodies demand.
what is heart failure caused by?
coronary artery disease and hypertension
what is more common in men? women?
men=coronary artery disease
is incidence of heart failure going up? why?
yes it is people are living longer and greater mi survival
what is the 5 year mortality of hf?
what is the normal heart blood flow internally?
right atrium fills (unoxygenated), right ventricle fills and pumps to lungs, left atrium fills (oxygenated), left ventricle fills and pumps blood to body
what type of dysfunction does coronary heart disease lead to? how does it get there?
leads to an MI, decrease in muscle mass, contractility impaired, less left ventricle pump fraction(systolic dysfunction)
what type of dysfunction does hypertension lead to? hows it get there?
hypertension leads to pressure overload, heart walls stiffen, relaxation impaired (dyostolic dysfunction), partial filling of the heart
What are the two major consequences of hf?
edema, and tissue hypoperfusion not enough stuff to tissues.
what is systolic hf?
reduced contractility and reduced ejection fraction.
what is dyostolic hf?
stiffening of the heart, less filling and reduced cardiac output, ejection fraction may be normal, stroke volume reduced.
ejection fraction? stroke fraction?
RV to lungs,
LV to body
signs and symptoms of hf?
periods of acute decompensation, teachycardia, decreased excersis tolerance, dyspnea, fatigue, tachypenia, edema
what type of condition is systolic?
what type of condition is ADHF? treatment goals?
relieve acute symptoms, edema, o2 trans, tissue perfusion, reduce cardiac damamge
what is preload?
ventricle wall tension at the end of diastolye, measured by LV filling pressure.
What is afterload?
ventricular wall tension during contraction, ventrical ejection resistance, measured by systolic pressure
what is contractility?
inotropic state, property of heart muscle to control force velocity of contraction.
what is Co dependent on?
heart rate and stroke volume
stroke volume depends on?
preload, afterload, contractility
what is MAP?
mean arteriole pressure
what is formula for MAP?
CO x systemic vascular resistance
what are maladaptive responses body makes against hf?
increased hr, increased preload, vasoconstriction, ventricular hypertrophy and remodeling
maladaptive short and long term?
short term maintains homeostasis.
long term complex functional, structural, biochemical and molecular changes.
do these conpensatory responses help hf?
negative of compensatory reponse of increasing contractility?
diastolic filling compromised, higher intracellular ca+ more tension, diastolic and systolic dysfunction.
how does compensatory response increase contractility?
sympathetic system stimulation
how does compensatory response increase preload?
activate renin angiotensin system, renin-angiotensin 1, ace=angiotensin 2, increase volume via NA and water retention
bad of increased preload compensatory response?
increase contractions only so much, pulmonary or systemic congestion
normal cardiac function at a preload?
as tension/pressure increases in LV cardiac performance increases.
increased contractility at a preload?
cardiac output increases at any level of preload
heart failure cardiac function at preload?
cardic output is less with same preload
compensatory response of vasocontriction bad?
impedes ejection of blood, CO down
what causes compensatory response of vasoconstriction?
regulated by nuero hormones, up in peripheral resistance.
what makes compensatory responses maladaptive?
What are the 4 non ionotropic drugs and function of them?
diuretics, anti-angiotensin, vasodialators, b-rec antagonists
they decrease maladaptive compensatory responses
what are the 3 ionotropic drugs and their function?
digitalis glycosides, bipyridines, b-rec agonists
Diuretics mec of action?
decrease extracellular volume, decrease blood volume, down in edema preload and afterload
diuretics effect on CO and contractility?
no effect on contractility, CO up
Ang 2 mec of action?
decrease preload, aftgerload, and edema. resulting in increased CO
What do beta blockers reduce in heart? bad?
reduce contractility and heart rate
can be bad cause lowers hr and stops sympathetic activation
what are used for vasodialators in heart?
verapamil, nifedipine, diltiazem
verapamil vs dilitazem vs nifedipine
verpamil effective in vasodialtion, decreasing heart force, and decreasing heart rate.
diltiazem vasodialates, small decrease in heart force, effective decrease in heart rate.
nifedipine effect in vasodialation not HR or HF
digitalis glycosides when used where absorbed?
in advanced hf, in Gi
mech of action of glycolysides?
inhibits NA/K atpase, increases NA, less NCX activity, increases intracellular ca conc, decreases ap duration
how much contractility gotten back with glycolosides?
about half of what was lost
glycolosides adverse effects?
disrupts electrical impulses, ca overload, tachycardia
b receptor agonists how gotten into body when used?
IV, advanced hf
beta receptor adverse effects?
bipyridines when used where absorbed 2 agents?
iv, advanced hf, inamrinone, milrinone
bipyridines mec of action?
inhibit pde-3, increase camp, increase ca and increase contraction
bipyridines affect on preload after and CO
down in afterload up in CO
bipyridines adverse effects?
naseau and vomiting, arrhythmias, thrombocytopenia, hepatotoxicity
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