heart failure pathophys Flashcards
4 broad pathophys causes of HF
impaired CTY (ischemic or dilated CM) increased afterload (HTN or AS) increased volume (valve insufficiency), impaired filling (LVH)
most common cause of HF
MI, causes damage secondary to coronary problems
compensation for reduced CTY and SV
increased EDV (Frank starling) and hypertrophy
both initially help but eventually increase atrial pressure and cause HF
how to increase SV when CTY is impaired, potential problems
increase preload, help via frank starling
helps to a point then maladaptive (flat part of frank starling curve), increases in preload eventually just cause pulm congestion
3 factors to regulate preload
venous tone (SNS), blood volume, body position (more when laying down, less standing up)
SNS effect on CV system
increased HR and CTY (B1), increaed venous return (a1 venoconstriction), increased renin release from kidneys and fluid retention
RAAS connection to HF
causes fluid retention in response to low CO, causes many of the signs and Sx of HF w/ excess preload
BNP and ANP role
counteract neurohormones- block renin, cause vasodilation, cause Na excretion
what processes drive transition from injury to HF
SNS activation, RAAS activation- cause the evnetual remodeling
determinants of afterload
SVR (systolic BP), aortic compliance, Aortic valve resistance
compensation from chronic high afterload
concentric hypertrophy- becomes failure with added dilation and fibrosis, dysfn, myocyte death
why does dilation of the ventricle signal a worsening for HF
increased volume causes more afterload via laplace mechanism
SVR response to HF
will increase to preserve MAP and perfusion
ATII, aldosterone, and NE effect on afterload
ATII causes vasoconstriction, aldo causes cardiac fibrosis, NE causes vasoconstriction, fibrosis, and cardiomyocyte death
effect of diastolic dysfn on pressure volume curve
passive curve is shifted up to reflect a higher pressure at the same volume, this decreases SV
