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64 Cards in this Set
- Front
- Back
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What is the chain of events in CHF that begins with increased sympathetic activity in attempt to increase contractility? (4)
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activation of beta-receptors in the heart --> increase in HR and CO --> vasoconstriction --> enhanced venous return and CO
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Chain of events in CHF leading to fluid retention (5)
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decreaed CO --> decreased blood flow to kidney --> increased renin, aldosterone, agtII --> peripheral resistance, retention of Na and water --> increased blood volume
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What do renin and aldosterone directly cause and how?
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cardiofibrosis via oxidative damage
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chain of events leading to cardiac remodeling (4)
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ventricular hypertrophy --> cardiofibrosis --> myocardial structural and functional alterations --> change in cardiac shape, size, and composition
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systolic dysfunction
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declining myocardial contractility
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diastolic dysfunction
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left ventricular ejection and contractility
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chain of events leading to concentric remodeling (2)
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cardiofibrosis, increased fibroblast proliferation, increased cytokines --> concentric hypertrophy of the left ventricular wall (this worsens the left ventricular ejection fraction)
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at what level of LVEF will a patient become symptomatic
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0.4
normal = 0.58 |
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neurohormonal changes of CHF (5)
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increased AgtII
increased aldosterone increased norepi increased endothelin increased vasopressin |
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Stage A CHF patients
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patients at very high risk with no structural defects
treat with risk factor reduction and education |
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Stage B patients in CHF
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patients who do have structural defects that remain asymptomatic
treat with ACE inhibitors or ARBs in all patients beta blockers for selected patients |
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Stage C patients in CHF
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patients who are symptomatic and require treatment
ACE inhibitors and beta-blockers in all patients |
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Stage D patients in CHF
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patients who become decompensated despite treatment
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Actions of ACE inhibitors (6)
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decrease agtII
decrease bradykinin inactivation (which will lead to vasodilation) decrease aldosterone secretion decrease vascular resistance decrease venous tone decrease BP |
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ACE inhibitor indications (5)
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all patients with LV systolic HF
diabetic patients post-MI patients slows progression of renal disease reduces mortality rates |
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which ACE inhibitor will you initiate therapy with and why?
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captopril because it has a shorter half life and is fast acting
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which ACE inhibitor will you switch to for long-term therapy
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enalapril
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What do you need to evaluate with ACE inhibitor administration
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renal function and serum potassium because declining renal function will only exacerbate symptoms
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absolute contraindications of ACE inhibitors (3)
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angioedema
bilateral renal artery stenosis pregnancy |
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relative contraindications of ACE inhibitors (5)
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unilateral renal artery stenosis
cough renal insufficiency hypotension hyperkalemia |
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what type of drug is captopril
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ACE inhibitor
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what type of drug is enalapril
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ACE inhibitor
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Why would you used an angiotensin receptor blocker
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when an ACE inhibitor causes an uncomfortable dry cough
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3 angiotensin receptor blockers
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candersartan
losartan valsartan |
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what type of drug is candersartan
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ARB
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what type of drug is losartan
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ARB
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what type of drug is valsartan
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ARB
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What type of drug is spironolactone
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aldosterone antagonist
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what type of drug is eplerenone
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aldosterone antagonist
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two aldosterone antagonists
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spironololactone
eplernone |
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side effects of spironolactone (2)
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anti-androgen effects
can result in hyperkalemia because it is a big calcium sparing agent |
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side effects of eplerenon (2)
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does not have the adverse side effects of spironolactone
a strong CYP3A4 substrate (thus it can't be on macrolides, can't have grapefruit, etc) |
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what drugs can aldosterone antagonists be combined with?
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always combined with a beta-blocker and ACE inhibitor
can add a loop diuretic and digoxin |
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when are aldosterone antagonists indicated
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advanced heart failure
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contraindications of aldosterone antagonists
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loop diuretics may precipitate digoxin toxicity through hypokalemia
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when should you begin digoxin administration
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is a patient remains symptomatic and CO goes down; also indicated in atrial fibrillation because of its ability to slow ventricular rate
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MOA of digoxin
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inhibits Na/K ATPase, specifically the K component which drives the Na/Ca++ exchanger and increases the calcium which thus increased contractility
digoxin is also able to blunt sympathetic activation |
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digoxin results in (4)
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increased intracellular sodium
increased cardiac contractility reduced sympathetic activation reduced renin-agt-aldosterone activation |
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what can digoxin be given in combination with (3)
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ACE inhibitors, diuretics, and beta blockers (although must switch off the beta-blockers if patient becomes exacerbated)
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what precipitates digoxin intoxication
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a depletion of serum K caused by diuretics; this reduces the effectiveness of digoxin because without K, digoxin has nothing to bind to and flows freely in plasma
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what predisposes to digoxin toxicity (2)
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decreased renal function
hypokalemia |
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when do signs of digoxin toxicity appear?
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when plasma concentrations are >2ng
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what are the symptoms of digoxin toxicity (5)
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anorexia
nausea, vomiting headache, delirium visual disturbances (yellow-green halos = TELL TALE SIGN) ventricular tachycardia |
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treatment of digoxin toxicity (5)
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discontinue digoxin
maintain K concentrations between 4-5mmol treat ventricular arrhythmias with lidocaine treat AV block with atropine antidigoxin antibodies for an overdose (digibind) |
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metabolism of digoxin
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1/2 life = 36-48 hours (allows for once-a-day dosing)
renal elimination, mostly unchanged half-life is increased to 4 days+ in renal failure, thus renal failure can increase digoxin toxicity |
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dosage of digoxin
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loading dose administered over 24 hours
target plasma levels = 0.5-1ng |
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Loop diuretics (3)
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furosimide
bumetanide tosemide |
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what type of drug is furosimide
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loop diuretic
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what type of drug is bumetanide
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loop diuretic
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what type of drug is tosemide
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loop diuretic
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dosage of loop diuretics
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dosage adjustment based on symptomatic improvement and daily body weight
begin therapy on a low dose target weight loss = 2lb/day cautious tapering and withdrawal |
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how does loop diuretic resistance occur?
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may develop because the Na/K cotransported becomes resistant
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how do you treat loop diuretic resistant patients?
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instead of increasing the dose of the loop diuretic you should add a thiazide diuretic which increases the effectiveness of the loop diuretic
combination of furosimide and metolazone via continuous IV produces the best effects |
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why are beta-blockers used in CHF?
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even though they will reduce contractility, they are used in order to reduce sympathetic remodeling, reduce cardiac oxidative damage and ischemia
because it is used in such a low dose, it will not reduce contractility to a dangerous extent |
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in what CHF patients are beta-blockers used?
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class B and C, not class D
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what is the only vasodilator shown to improve CHF survival?
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hydralazine-isosorbide dinitrate
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MOA of venous vasodilators (3)
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increase venous capacitance
decrease venous return to the heart reduce preload |
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what are the venous vasodilators used for CHF?
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nitrates
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MOA of arteriolar vasodilators (2)
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reduces systemic vascular resistance and therefore afterload
useful increasing forward cardiac output |
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what are the arteriorlar vasodilators used for CHF?
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hydralazine
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when is B-natriuretic peptide released?
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when the atrium is released
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what is nesiritide
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a recombinant form of BNP
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what does nesiritide do?
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activates cGMP and guanylcyclase and causes vasodilation
increases naturesis and diuresis to decreased volume overload rapid vasodilator increases CO |
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how is nesiritide administered?
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IV in hospitalized patients
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