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37 Cards in this Set
- Front
- Back
Role of compensatory mechanisms in HF
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contribute to the problem
increase sympathetic tone--increase release of Norepi decreased perfusion--RAAS activation |
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What did the V-HEFT 1 study find?
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Mortality dramatically incrased w/increasing plasma norepi levels.
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Valsartan
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Angiotensin receptor blocker use when pt. is intolerated of ACEi.
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What did the Val-Heft study find?
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w/combination of ACEi and beta blocker, and ARB pts. did worse than those getting only two.
Excess (-) of the SNS is undesirable |
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What is the cardinal symptom of HF?
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Effort intolerance
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NYHA Classification for HF
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Class 1- no symptoms
Class 2- Symptoms w/normal activity Class 3- Symptoms w/less than ordinary activity Class 4- Symptoms @ rest |
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Which drugs improve effort intolerance but don't prolong life? Which does both?
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Vesnarinone and + inotropes
Digoxin |
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What is fluid retention caused by?
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Na and H2O retention due to RAAS activation
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What does increased pulmonary venous pressure (as in edema) cause?
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Dyspnea on exertion, orthopnea, paroxysmal nocturnal dyspnea
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Treatment for HF associated edema?
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Early- ACEi
Later- digoxin |
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Loop diuretic commonly used? Why use caustion when using it to treat HF?
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Furosemide
Hypokalemia can develop |
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Why avoid K supplements w/ACEi?
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Lethal hyperkalemia (ck pts. for salt-substitue use)
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Drugs used in end-stage HF for edema
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1)low dose DA (increase renal perfusion)
2) Morphine (vasodilation) |
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How many people does HF affect/yr? What is the 5 year mortality rate?
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500,000
60% in men 45% in women |
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Does sudden arrythmic death happen more to class 2 or class 4 people
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Careful! Class 2 people
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What signs are worrisome in HF pts?
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Syncope or near syncope
ventricular ectopy on EKG |
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What did the MADIT-2 study show?
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Pts with EF <30% and hx of MI have 30% lower death rate @ one year if they recieve a defribillator
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What drugs reduce the risk of sudden death?
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ACEi
Spironolactone Beta-blockers |
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Which drugs reduce risk of progressive pump failure?
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ACEi
Beta blockers ARAS (possibly) |
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The approach to HF pts.
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Prevent
Prove prescence of Lft. Ventricular dysfxn Classify dysfxn as sys. or dias. *must have echo, nucleotide study, or angiogram Seek correctable cause Treat (try to prolong life) |
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Standard of care used to classify LV dysfxn
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Echo
Nucleotide study Angiogram |
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Name 5 causes of correctable HF
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Sarcoid
Hemochromatosis Hyper/hypothyroidism SLE Beri Beri |
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What treatment goal is essential for systolic dysfxn?
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Afterload reduction
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Recommendations for pts. w/sys dysfxn.
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Normalize BP
Reduce EtOH Increase K intake AVOID unnecessary NSAIDS |
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Class 1 Drugs
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ACEi
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Therapeutic Goal for Class 1
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Reduce BP (prevent LV dilation, supress RAAS)
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Toxicities of Class 1 drugs
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Cough
Allergic Pneumonia |
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Class 2 drugs
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ACEi
ARB (if ACEi not tolerated) Na restriction Beta blockers* Consider digoxin (nitrates) |
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Therapeutic Goal of Class 2
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Treat ischemia
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Toxicities of Class 2 drugs
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Bradycardia*
Arrhytmias (increase in hypoK and renal failure) |
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Class 3 drugs
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ACEi
ARB Beta Blocker* Digoxin* (nitrates) Na restriction Diuretics |
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Therapeutic guidelines for Class 3 drugs
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Titrate upwards
Spironolactone is first line for diuretics |
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Toxicities of Class 3 drugs
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Can worsen sys. dysfxn at first
Watch serum K+!! |
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Class 4 drugs
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ACEi
ARB Consider Beta blockers Digoxin (Nitrates) Na/H2O restricion Diuretics Periodic ionotropes |
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Most common error in mangement of HF
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Inducing bradycardia w/xs Beta blockade
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Four other errors in managing HF
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Hypokalemia (xs diuretics)
Hyperkalemia (K+ sparing diuretics + ACEi) Acute renal failure (NSAIDS + ACEi) Digoxin toxicity |
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What level of digoxin should you aim for?
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O.5-0.8 ng/ml
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