Heart failure physiology Flashcards
1
Q
HF definition
A
- A syndrome caused by cardiac dysfunction (from myocardial muscle dysfxn or loss) and characterized by either LV dilation, hypertrophy, or both
- HF leads to neurohormonal and circulatory abnormalities including fluid retention, SOB, fatigue and DOE
- Beneficial heart remodeling can be result of therapy or spontaneously
- HF is usually accompanied by pulmonary or systemic venous congestion, or both
- Also often accompanied by inadequate O2 delivery (at rest or stress) due to cardiac dysfxn
2
Q
Components of HF
A
- Abnormal LV function (systolic, diastolic, or both)
- Abnormal hemodynamic profile
- Activation of neurohormonal systems
- Activation of inflammatory markers, endothelial dysfxn
- Signs and Sx (edema, hepatomegaly, pulm edema, tachycardia)
3
Q
Heart dysfxns
A
- Ventricular remodeling
- Wall motion abnormalities (desynchrony)
- Endothelial dysfxn
- Electrical abnormalities (arrhythmias)
- Reduced longevity
4
Q
Relevant heart terms
A
- Contractility (independent of preload and after load)
- SV, CO (based on SV and HR)
- Preload: based on venous pressure (return), approximated as EDV
- Afterload: based on TPR
- Ejection fraction (EF): SV/EDV (the fraction of the EDV that is ejected)
- Normal EF is 55-75%
- Compliance: change in pressure/ change in volume (how easily it changes volume)
5
Q
HF ventricular function curve
A
- In VF curves, SV (y axis) is compared to preload (EDV, x axis)
- Normal curves are at the top, w/ HF curves down and to the right (+ inotropes up and to left)
- Increasing EDV will increase SV to a point, but after that it has little effect on increasing SV
- But lowering EDV by decreasing blood volume will move a point on a curve down/left on the same curve
6
Q
HF force-tension curves
A
- In FT curves, SV (y axis) is compared to afterload (TPR, x-axis)
- Normal curves at the tope, w/ HF curves down and to left
- Lower TPR means a larger SV, but during HF there is smaller SV at the same TPR as a normal heart
- However, lowering TPR (after load) in HF can increase SV (positive inotropic effect)
- This moves the curve up one curve
7
Q
Changing the ventricular function curve 1
A
- Want to move the curve up and to the left (increasing SV while decreasing EDV)
- This is b/c want to decrease EDV to reduce work the heart must do, but also want to increase SV instead of losing SV to increase CO
- In order to accomplish this, certain drugs are required
- Drugs that decrease EDV move the point on a curve down (to the left) the same curve, and drugs that decrease TPR move the point directly up to a new curve (those that do both move the point up and to the left
8
Q
Changing the ventricular function curve 2
A
- Diuretics: decrease blood volume (thus decreasing EDV), so they move a point on a curve to the left
- Positive-inotropic effects (anything that vasodilates arteries: hydralazine, ACEIs, nitroprusside) moves the point up to a new curve
- Vasodilators can move the curves variably, based on where they vasodilate
9
Q
Changing the ventricular function curve 3
A
- Isorbide dinitrate (venous only) moves the point down the curve, nitroprusside (both) moves the point up and to the left (also ACEIs, b/c they cause arteriole dilation and decrease EDV), and hydralazine (arteries only) moves the point up
- Combining drugs also can achieve the desired effect, as in giving a diuretic and hydralazine (moves the curve up and to the left)
10
Q
Systolic dysfxn
A
- Diminished capacity of the ventricle to eject blood due to impaired myocardial contractility or volume overload
- There is reduced SV and increased EDV in return (leads to larger ventricle w/ limited capacity to generate force), therefore EF goes down
- Usually seen w/ dilated ventricle remodeling (LV systolic function impaired)
11
Q
Diastolic dysfxn
A
- Impaired early diastolic relaxation, increased stiffness of ventricular wall (reduced compliance)
- But LV retains normal systolic function
- There is reduced EDV and reduced SV, thus EF doesn’t change
- Lower compliance leads to increased ED pressure, thus the low EDV/SV
- Hypertrophy usually due to pressure overload (HTN)
- Heart must work more to generate same CO so there is often LV hypertrophy remodeling, exacerbating the low compliance of the ventricle and HF
12
Q
Risk factors for HF
A
- CAD or Hx of MI
- HTN, diabetes
- EtOH, drugs (coke, meth)
- Age, obesity, smoking, etc
13
Q
Right sided HF
A
- Cardiac causes: L sided HF, RV infarction, pulm stenosis
- Pulmonary diseases: pulm HTN (often from L sided HF), pulm embolism, COPD, chronic lung infection, etc
14
Q
Compensatory mechanisms
A
- Frank starling: decrease in SV leads to increase in EDV to increase SV back to normal (leads to dilated LV b/c of constantly large EDV)
- Laplace law: when after load increases the ventricle must compensate by increasing wall thickness (which also decreases radius of ventricle) to maintain normal wall stress (leads to LVH)
15
Q
Myocardial hypertrophy
A
- First stage of HF, can be either concentric (small ventricle) or eccentric (larger ventricle)
- Concentric hypertrophy is due to pressure overload leading to increased systolic wall stress and remodeling to thick walls
- Sarcomeres in parallel
- Eccentric hypertrophy due to volume overload leading to increased diastolic wall stress and remodeling to dilated walls (same thickness)
- Sarcomeres in series
