Heart Failure Flashcards Preview

Uncategorized > Heart Failure > Flashcards

Flashcards in Heart Failure Deck (14):

Normal Cardiac Function

CO = HR x SV --> can increase HR or SV to increase CO
BP = CO x TPR --> can increase CO or TPR to maintain BP



marker of volume at end of diastole
stretch of the myocytes
dependent on venous blood volume returned to heart
primary compensatory mechanism to inc CO in normal hearts is to inc this


Frank Starling Law

as preload inc so does stroke volume, in a failing heart this is not nearly as effective, at some point the SV levels off no matter how high preload is



it is the resistance against which ventricle must pump in order to eject blood (the TPR) depends on BP and ventricular wall tension
inc TPR leads to dec SV this is not effective in failing hearts


Classification Heart Failure (General)

Systolic (impaired ventricle contraction, dec ejection fraction [<40%])
Diastolic (impaired ventricle relaxation, normal ejection fraction)


New York Heart Association Classification

I. Cardiac Disease without signs or symptoms
II. Symptoms w/ exertion; slight limitation activity
III. Symptoms w/ less than ordinary activity; marked limitation activity
IV. Symptoms at rest and with any activity


American College of Cardiology and American Heart Association Staging of Heart Failure

A. No structural heart disease, but pt is at risk
B. Structural heart disease, but no signs/symptoms
C. Structural heart disease with PRIOR or current symptoms of heart failure (most fall here, once in stage C cannot leave it)
D. Structural Heart Disease w/ refractory symptoms; end stage disease


Compensatory Mechanisms (general)

1. Inc Preload
2. Tachycardia
3. Vasoconstriction
4. Ventricular Remodeling
5. Neurochemical activation


Increased Preload

1. dec CO
2. dec renal profusion
3. kidney perceives as ineffective blood vol
4. Na and H2O retention, activation RAAS


Consequences Inc Preload

inc sarcomere stretch (GOOD)
pulmonary/systemic congestion (BAD)
inc wall tension, inc myocardial O2 needs (BAD)
leads to impaired contractile function (BAD)



Mediated by: AT2, norepinephrine, endothelin, vasopressin
Maintains BP (GOOD)
Increases Afterload (BAD)



Inc HR to inc the CO in order to maintain BP
Maintains BP (GOOD)
Increases O2 demand (BAD)
Inc risk arrhythmia (BAD)


Ventricular Remodeling

Hypertrophy and Fibrosis (necrotic myocytes replaced with fibrotic tissue)
initially helps maintain CO (GOOD)
Inc stiffness (BAD)
Myocyte death, wall thinning (BAD)
dec contractility, systolic dysfunction (BAD)
arrhythmias due to fibrotic tissue (BAD)


Neurohormonal Activation

activation of vasoconstrictors in order to regulate BP has many risks