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MS 1- Physiology > Heart Failure > Flashcards

Heart Failure Flashcards

1
Q

General factors

A
  • 5.8 million Americas have it
  • 670,000 new cases per year
  • 3.5 million hospitalization per year
  • mortality 50%
  • $34.6 billion/year
  • prognosis improving- mortality increasing
  • the more we increase longevity, the more cases there are
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2
Q

Definition of heart failure

A
  • inability of the heart to meet the metabolic needs of the body
  • to be distinguished from cardiac dysfunction with successful adaptation
  • when adaptation fails and becomes part of the problem
  • clinical: no single one finding,a complex of findings
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3
Q

Causes of heart failure

A
  1. Decreased circulatory supply to the body: coronary heart disease (MI, ischemic cardiomyopathy), valvular heart disease, cardiomyopathy
  2. Increased circulatory demand from the body: hypertension, thyrotoxicosis, anemia, A-V fistula
  3. Heart failure- final common pathway
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4
Q

Adaptive mechanisms of heart failure

A

1) Frank-Starling (short term)
2) Neuro-hormonal (intermediate) - Renal
3) Hypertrophy

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5
Q

Frank Starling Mechanism

A

Normal curve- shows improved ventricular performance when the EDV is increased (increased preload or venous return)

  • normal curve moves upward and to the left with exercise or increased sympathetic stimulation
  • heart failure: down and to the right with impaired ventricular performance: you can still increase EDV but the ventricular performance isn’t getting much better
  • short term adaptation
  • with increasing severe LV dysfunction the LV filling pressure reaches 25 mm Hg where the oncotic pressure of the plasma is exceeded and fluid crosses the alveolar membrane and enters the pulmonary alveoli
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6
Q

Neurohumeral Sympathetic Stimulation

A

Increased plasma NE:

  • increase release from neurohumoral nerve endings
  • decrease uptake by those endings
  • decrease rate of degradation
  • increase B1 receptor exhaustion due to chronic stimulation
  • decrease B1 receptor synthesis (low levels of B1 in CHF patients)
  • increase coronary sinus NE output

-increasing levels of PNE are associated with decreasing length of survival in heart failure

  • redistribution of cardiac output
  • maintain flow to brain, heart at expense to the skin, skeletal muscle and kidneys
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7
Q

Adaptive Mechanisms: Renal

A
  • Stimuli:
  • Decrease GFR, RBF
  • Increase aldosterone

Response:

  • increase Na and H2O retention
  • increase plasma volume
  • increase venous return and pressure
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8
Q

Effects of Angiotensin II

A
  • activated by adrenergic stimulation of J-G Apparatus and decrease renal blood flow
  • increase vasoconstriction and blood pressure
  • increase aldosterone release
  • vessel hypertrophy, mycocardial hypertrophy, increased NE release, Na+ retention, CNS dypsogenia, efferent constriction
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9
Q

Atrial natiretic factor

A
  • counter- regulatory

- promotes vasodilation, natriuresis, suppresses RAS

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10
Q

Brain Natiretic factor

A
  • from ventricle
  • counter-regulatory
  • similar to ANP- promotes vasodilation, natriuresis, suppresses RAS
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11
Q

Endothelin

A
  • from endothelial cells

- potent vasoconstrictor

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12
Q

Inflammatory cytokines

A
  • TNF alpha

- promotes cell hypertrophy- apoptossi

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13
Q

Neurohormal stimulation in heart failure

A

-norepinephrine, plasma renin, arginine vasopressin, atrial natriuretic factor and endothelin are all much higher in patients with heart failure

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14
Q

Adaptive Mechanism: Hypertrophy

A
  • increase in myocardial mass- remodeling
  • if abnormality is not corrected, myocardial dysfunction will worse and become permanent
  • when? pressure vs. volume overload
  • maintain or increase contractility
  • Ejection fraction= (EDV-ESV)/EDV x 100
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15
Q

Effects of hypertrophy

A
  • poor contracile function despite hypertrophy

- force velocity relationship- much lower for CHF

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16
Q

Clinical Hypertrophy

A
  • Two types: pressure( aortic stenosis) or volume overload(mitral insufficiency)
  • effort to return wall stress toward normal
  • though individial muscles show reduced contractility
  • hypertrophy maintains pump function (cardiac output) by keeping wall stress near normal
17
Q

Concentric/ Eccentric hypertrophy

A
  • pressure overload -> increase systolic wall stress -> mechanical transducers -> extracellular and intracellular signals -> ventricular remodeling -> parallel sarcomeres -> concentric hypertrophy (LV thickness greater)
  • volume overload -> increase diastolic wall stress -> mechanical transducers ->extracellular and intracellular signals -> ventricular remodeling -> series sarcometers -> eccentric hypertrophy (LV volume greater)
18
Q

Adaptation Disadvantages

A

1) Frank Starling- high LVEDP- pulmonary edema
2) Neuro-humoral
- increases myocardial O2 consumption
- arrhymias
- diminished response to sympathetic stimulation
- blunted baroreceptor function
- increased systemic vascular resistance
3) Renal
- perpherial/organ edema
- decreased renal function
4) Myocardial hypertrophy- remodeling
- decreased contractility
- necrosis and apoptosis
- decreased coronary reserve
- changes in matrix (diastole)

19
Q

Failure Mal adaptation

A
  • worsening LV function
  • fluid retention- Pulmonary edema
  • excessive increase in vascular resistance
  • renal failure
20
Q

Right vs Left heart failure

A
  • Right: Pulmonary embolism, cor pulmonale, mitral stenosis

- Left: mitral insufficiency, aortic stenosis and insufficiency, hypertension, cardiomyopathy

21
Q

Acute vs chronic CHF

A
  • acute: MI, endocarditis

- chronic: cardiomyopathy, hypertension

22
Q

Low vs High Cardiac Output

A
  • Low: cardiomyopathy, coronary heart disease

- High: Thyrotoxicosis, Anemioa, AV fistula

23
Q

Forward vs. Backward

A
  • Forward: effect of low cardiac output

- Backward: effects of high venous pressure

24
Q

Systole vs. Diastole

A
  • Systolic: MI etc
  • Diastolic:preserved ejection fraction 40-50% of patients
    a) Delayed relaxation, elderly, hypertension, early ischemia
    b) increased stiffness- rare, infiltrative disease, amlyoidosis

Can be both

25
Q

Therapy for CHF

A

1) Treat underlying cause
2) Inotropic agents- digitalis, dobutamine
3) Diuretics- Loop (Furosemide {lassix}), distal tubule (Thiazide)
4) Venodilator- reduce pre load- Nitrates, BNP
5) Arterial vasodilation- reduce afterload, angiotensin converting enzyme inhibitors, angiotensin receptor blockers
6) Beta blockers- blunt sympathetic stimulation
7) Aldosterone antagonist (good for diastolic CHF)
8) Pace maker
9) Internal Cardiac Defribrillator
10) Left ventricular assist device (LVAD)
11) Transplantation

MS 1- Physiology (32 decks)

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