Block 3: CHF 2
Terms
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- 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 - What did the V-HEFT 1 study find?
- Mortality dramatically incrased w/increasing plasma norepi levels.
- Valsartan
- Angiotensin receptor blocker use when pt. is intolerated of ACEi.
- 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 - What is the cardinal symptom of HF?
- Effort intolerance
- Which drugs improve effort intolerance but don't prolong life? Which does both?
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Vesnarinone and + inotropes
Digoxin - What is fluid retention caused by?
- Na and H2O retention due to RAAS activation
- What does increased pulmonary venous pressure (as in edema) cause?
- Dyspnea on exertion, orthopnea, paroxysmal nocturnal dyspnea
- Treatment for HF associated edema?
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Early- ACEi
Later- digoxin - Loop diuretic commonly used? Why use caustion when using it to treat HF?
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Furosemide
Hypokalemia can develop - Why avoid K supplements w/ACEi?
- Lethal hyperkalemia (ck pts. for salt-substitue use)
- Drugs used in end-stage HF for edema
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1)low dose DA (increase renal perfusion)
2) Morphine (vasodilation) - 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 - Does sudden arrythmic death happen more to class 2 or class 4 people
- Careful! Class 2 people
- What signs are worrisome in HF pts?
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Syncope or near syncope
ventricular ectopy on EKG - What drugs reduce the risk of sudden death?
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ACEi
Spironolactone
Beta-blockers - Which drugs reduce risk of progressive pump failure?
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ACEi
Beta blockers
ARAS (possibly) - The approach to HF pts.
-
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) - Standard of care used to classify LV dysfxn
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Echo
Nucleotide study
Angiogram - Name 5 causes of correctable HF
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Sarcoid
Hemochromatosis
Hyper/hypothyroidism
SLE
Beri Beri - What treatment goal is essential for systolic dysfxn?
- Afterload reduction
- Recommendations for pts. w/sys dysfxn.
-
Normalize BP
Reduce EtOH
Increase K intake
AVOID unnecessary NSAIDS - Class 1 Drugs
- ACEi
- Therapeutic Goal for Class 1
- Reduce BP (prevent LV dilation, supress RAAS)
- Toxicities of Class 1 drugs
-
Cough
Allergic
Pneumonia - Class 2 drugs
-
ACEi
ARB (if ACEi not tolerated)
Na restriction
Beta blockers*
Consider digoxin
(nitrates) - Therapeutic Goal of Class 2
- Treat ischemia
- Toxicities of Class 2 drugs
-
Bradycardia*
Arrhytmias (increase in hypoK and renal failure) - Class 3 drugs
-
ACEi
ARB
Beta Blocker*
Digoxin*
(nitrates)
Na restriction
Diuretics - Therapeutic guidelines for Class 3 drugs
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Titrate upwards
Spironolactone is first line for diuretics - Toxicities of Class 3 drugs
-
Can worsen sys. dysfxn at first
Watch serum K+!! - Class 4 drugs
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ACEi
ARB
Consider Beta blockers
Digoxin
(Nitrates)
Na/H2O restricion
Diuretics
Periodic ionotropes - Most common error in mangement of HF
- Inducing bradycardia w/xs Beta blockade
- 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 - What level of digoxin should you aim for?
- O.5-0.8 ng/ml