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37 Cards in this Set

  • Front
  • Back
Role of compensatory mechanisms in HF
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?
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
NYHA Classification for HF
Class 1- no symptoms

Class 2- Symptoms w/normal activity

Class 3- Symptoms w/less than ordinary activity

Class 4- Symptoms @ rest
Which drugs improve effort intolerance but don't prolong life? Which does both?
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?
Early- ACEi
Later- digoxin
Loop diuretic commonly used? Why use caustion when using it to treat HF?
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
1)low dose DA (increase renal perfusion)

2) Morphine (vasodilation)
How many people does HF affect/yr? What is the 5 year mortality rate?
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?
Syncope or near syncope
ventricular ectopy on EKG
What did the MADIT-2 study show?
Pts with EF <30% and hx of MI have 30% lower death rate @ one year if they recieve a defribillator
What drugs reduce the risk of sudden death?
ACEi
Spironolactone
Beta-blockers
Which drugs reduce risk of progressive pump failure?
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
Echo
Nucleotide study
Angiogram
Name 5 causes of correctable HF
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
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
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
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