Heart Failure Flashcards
1
Q
general facts
A
- 5.8 million americans
- 670,000 new per year
- 3.5 million hospitalizations per year
- 5 year mortality of 50%
- costs 34.8 billion per year
- prognosis of life is improving and mortality increasing
- longevity, more cases
2
Q
definition
A
- inability of the heart to meet the metabolic needs of the body
- different from cardiac dysfunction with successful adaptation
- when adaptation fails and becomes part of the problem
- clinical diagnosis is a complex of findings
3
Q
causes of heart failure
A
- decreased circulatory supply to the body
- CAD, MI, ischemic cardiomyopathy
- valvular heart disease
- cardiomyopathy - increased circulatory demand from the body
- HTN
- thyrotoxicosis
- anemia
- AV fistula - Heart failure-final common pathway
4
Q
adaptive mechanisms
A
- compensations that maintain pump function in the presence of heart disease or increased demand
1. Frank Starling (short term)
2. Neruo-hormonal (intermediate)- renal
3. Hypertrophy
5
Q
starling
A
- improved ventricular performance when end diastolic volume increases
- normal curve moves up and to the left with increased SNS or exercise
- curve moves down and right with impaired ventricular function
- progressive reaction until you can’t compensate anymore then shock
6
Q
increased plasma NE
A
- increased release from neurohumoral nerve endings
- decreased uptake by neurohumoral nerve endings
- decreased rate of degradation
- eventually leads to B1 receptor exhaustion due to chronic stim and decrease in B1 receptor synthesis
- increase in coronary sinus NE output
- increased PNE associated with decreasing length of survival
7
Q
Neurohormonal sympathetic stim
A
- redistribution of CO
- maintains flow to brain and heart
- at expense of skin, skeletal muscle and kidneys
- much less to skeletal muscle
- total output goes down with severe CHF
8
Q
renal mechanisms
A
- stimulated by dec GFR, dec RBF, inc aldosterone
- response is increases Na and water retention, increased plasma volume, increased venous return, increased venous pressure
9
Q
beta receptor density
A
- decreases in patients with failing hearts because they are over stimulated
- only B1
- response to IV epi goes down in failing patients
10
Q
renin-angiotensin
A
- activated by adrenergic stimulation of J-G apparatus and decreased renal blood flow
- angiotensin II has various affects all over the body that lead to increased Na and water retention
- increases thirst
- vasoconstricts
- can lead to myocardial hypertrophy and increased NE, vessel hypertrophy
- increases aldosterone
- increases AVP
11
Q
ANP
A
- counter regulatory
- promotes vasodilation, natriuresus, suppresses RAS
12
Q
brain natriuretic factor
A
- from ventricles
- counter regulatory, actions similar to ANP
13
Q
endothelin
A
-powerful vasoconstrictor
14
Q
IF cytokines
A
-TNF alpha promotes cell hypertrophy and apoptosis
15
Q
in heart failiure
A
- plasma NE increases
- renin increases
- Aldosterone increases
- ANP increase
- Endothelin increases
16
Q
clinical hypertrophy
A
- increase in myocardial mass, remodeling
- if abnormality can be corrected, hypertrophy will regress
- if not corrected, myocardial dysfunction will worsen and become permanent
- pressure vs volume overload
- maintain or increase contractility
- ejection fraction
17
Q
length vs tension and force velocity
A
- heart isn’t as contractile when hypertrophied
- doesn’t contract as fast
18
Q
pressure vs volume overload
A
- effort to return wall stress toward normal
- individual muscles show reduced contractility however
- maintains pump function by keeping wall stress near normal
19
Q
pressure overload
A
- concentric hypertrophy
- increases systolic wall stress
- parallel sarcomeres
20
Q
volume overload
A
- eccentric hypertrophy
- increases diastolic wall stress
- series sarcomeres
21
Q
LVMI
A
- mass index
- increases about the same
22
Q
LV thickness
A
-increases more with pressure overload (concentric)
23
Q
LV volume
A
increases more with volume overload (eccentric)
24
Q
starling disad
A
-high LVEDP leads to pulm edema
25
Q
neuro-humoral problesm
A
- increased heart oxygen consumption
- arrhythmias
- diminished response to SNS
- blunted baroreceptor function
- increased systemic vascular resistance
26
Q
renal problems
A
- peripheral/organ edema
- decreased renal function
27
Q
myocardial hypertrophy problems
A
- decreased contractility
- necrosis and apoptosis
- decreased coronary reserve
- changes in matrix (diastole)
28
Q
failure maladaption
A
- worsening LV function
- fluid retention and pulm edema
- excessive increase in vascular resistance
- renal failure
29
Q
Right vs Left
A
- Right-PE, cor pulmonale, mitral stenosis
- Left- mitral insufficiency, aortic stenosis and insufficiency, HTN, cardiomyopathy
- ventricular interdependence
30
Q
acute vs chronic
A
acute: MI, endocarditis
chronic- cardiomyopathy, HTN
31
Q
low vs high CO
A
low- cardiomyopathy, CAD
high-thyrotoxicosis, anemia, AV fistula
32
Q
forward vs backward
A
- forward-effect of low CO
- backward- effects of high venous pressure
33
Q
systolic vs diastolic
A
- systolic- MI, etc
- diastolic- preserved ejection fraction 40-50% of pts
- delayed relaxation elderly, HTN, early ischemia
- increased stiffness, rare infiltrative disease, amyloidosis
- some pts have both systolic and diastolic
34
Q
therapies
A
- treat underlying cause
- inotropic agents-digitalis, dobutamine
- diuretics- loop, furosemide, thiazide, distal tubule
- venodilator-reduce preload, nitrates, BNP
- arterial vasodilation-reduce afterload, ACE inhibitors, angiotensin receptor blockers
- B blockers- blunt SNS
- aldosterone antagonists
- resynchronization- bi or uni-ventricular pacing
- internal cardiac defibrillator
- left ventricular assist device (LVAD)
- transplantation
