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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

causes of heart failure

A
  1. decreased circulatory supply to the body
    - CAD, MI, ischemic cardiomyopathy
    - valvular heart disease
    - cardiomyopathy
  2. increased circulatory demand from the body
    - HTN
    - thyrotoxicosis
    - anemia
    - AV fistula
  3. Heart failure-final common pathway
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

ANP

A
  • counter regulatory

- promotes vasodilation, natriuresus, suppresses RAS

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

brain natriuretic factor

A
  • from ventricles

- counter regulatory, actions similar to ANP

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

endothelin

A

-powerful vasoconstrictor

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

IF cytokines

A

-TNF alpha promotes cell hypertrophy and apoptosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

in heart failiure

A
  • plasma NE increases
  • renin increases
  • Aldosterone increases
  • ANP increase
  • Endothelin increases
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
  1. treat underlying cause
  2. inotropic agents-digitalis, dobutamine
  3. diuretics- loop, furosemide, thiazide, distal tubule
  4. venodilator-reduce preload, nitrates, BNP
  5. arterial vasodilation-reduce afterload, ACE inhibitors, angiotensin receptor blockers
  6. B blockers- blunt SNS
  7. aldosterone antagonists
  8. resynchronization- bi or uni-ventricular pacing
  9. internal cardiac defibrillator
  10. left ventricular assist device (LVAD)
  11. transplantation