Lecture 10: Heart Failure Flashcards

1
Q

Define heart failure

A
  • Failure of the heart to pump enough blood to satisfy the body’s requirements.
    • Acute or chronic
  • Characterized by a clinical syndrome involving a characteristic pattern of hemodynamic, renal, neural, and hormonal responses. Heart failure is considered a multisystem disorder.
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2
Q

Causes of heart failure

A
  • Diminished coronary blood flow (ischemic heart disease)
  • Damaged heart valves
  • thyrotoxicosis
  • Vitamin B deficiency
  • Cardiac muscle disease
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3
Q

What are the acute effects of moderate heart failure?

A
  • Sudden damage (MI)
  • Reduced cardiac output → fatigue
  • Fall in arterial pressure
  • Damming of blood in veins → congestion
  • RESULT: compensation
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4
Q

What is the role of sympathetic reflexes in heart failure compensation?

A
  • Baroreceptor that measure arterial pressure
    • Detect fall in BP
    • NET EFFECT
      • Sympathetic nervous system activated
      • Parasympathetic nervous system inhibited
    • TLDR: fall in CO, body compensates by increase CO n BP
  • Direct effect on the heart
    • SNS speeds up the heart n contractility of the heart (positive ionotropic effect)
    • Positive ionotropic n chronotropic
  • Increases venous return [causes blood vessel constriction] → more blood cmng to the heart → increases cardiac output → raises filling pressure
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5
Q

What is the effect of heart failure on the Starling curve?

A
  • Increase filling pressure → bigger CO
    • Stretching the muscles fibers of the myocardium
    • When they contract, they push out more blood
    • More preload (blood cmng back to the heart in the vein) → shift along the curve
  • Sudden fall in BP [lack of CO] → curve shift to the right [more filling pressure bc constricting the vein]
  • Sympathetic nervous system increases contractility → efficiency of pumping increased
    • For given pressure, more CO
    • Direct effect of sympathetic nervous system by beta receptors
    • Pushes the curve upwards
  • Fall in CO → body compensates in short term by shifting along the curve n shifting curve up
    • Result net increase in CO for increase filling pressure
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6
Q

How does the baroreceptor reflex compensate for a decrease in BP?

A
  • Decrease in BP [fall in CO] detected by baroreceptors in carotid sinus n aortic arch
  • Reduces number of nerve impulses in vasomotor centers in medulla
  • Inhibits parasympathetic nervous system
  • Activates SNS
  • Increase heart rate n contractility
  • Increase vasomotor tone (constricts blood vessels) -> increases TPR n venous return
    • More pressure for the heart to push against can help compensate in short term but may be damaging in the long term
  • When the heart fails, makes the heart work harder -> can be damaging
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7
Q

What is the role of fluid retention in heart failure compensation?

A
  • Long term try n increase fluid retention
  • Retention of fluid by kidneys -> reduced urine output via release of aldosterone n ADH
  • Effects of aldosterone n ADH
  • Increased blood volume -> increased venous return ->

increased systemic filling pressure

  • Reduces venous resistance which eases flow of blood to the heart
  • Moderate fluid retention is beneficial
  • Large amt of fluid retention is not beneficial
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8
Q

What are the causes of reduced renal urine output?

A
  • Decreased glomerular filtration
    • Caused by a fall in arterial pressure
  • Renin-angiotensin system
  • Aldosterone secretion
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9
Q

What are the aims of treating CHF?

A
  • Relieve symptoms
  • Improvise exercise tolerance
  • Reduce acute exacerbations
  • Reduce mortality
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10
Q

What are some first line treatments of chronic CHF?

A
  • ACE inhibitors
  • Angiotensin II receptor antagonists
  • β-adrenoreceptor blockers
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11
Q

What are some second line treatments of chronic CHF?

A
  • Aldosterone antagonist (spironolactone)
  • Cardiac glycosides (digoxin)
    • Increase heart contractility
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12
Q

What do ACE inhibitors and angiotensin II receptor antagonists do and what are some examples?

A
  • ACE inhibitor: enalapril
  • Angiotensin II receptor antagonists: candersarta
  • FUNCTION
    • Reduce peripheral resistance (afterload)
      • Stop angiotensin II vasoconstriction
    • Reduce blood volume (preload) via reducing aldosterone release
    • Increase K+ concentration counteracting loss via diuretics
    • Helps to prevent cardiac remodeling
      • Increase in size
    • Strong evidence that they increase survival
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13
Q

What do β-adrenoreceptor blockers do and what are some examples?

A
  • EXAMPLES: bisoprolol n carvedilol
  • Reduce the work of the heart n slow disease progression
  • Reduce renin-angiotension-aldosterone
  • Some also block α receptors on blood vessels leading to vasodilation
  • Start at low dose n slowly titrate
  • Only use in stable heart failure
    • Can shift along the curve w/o changing CO
    • Reducing work of the heart
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14
Q

What do cardiac glycosides do?

A
  • Block Na+/K+ exchange → greater Ca2+ influx via Na+/Ca2+ exchanger → increases myocardium contractility
  • Suitable for patients w CHF n atrial fibrillation
  • Worsening or severe heart failure due to left ventricular systolic dysfunction despite ACE inhibitor, β-blocker n diuretic therapy
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15
Q

What is ivabradine?

A
  • Used to treat angina
  • Slows heart by direct action on SA node
  • Probably blocks pacemaker current (If)
  • Increases filling time n CO
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16
Q

How to treat intractable heart failure?

A
  • Transplantation
  • Ventricular assist device (VAD)
    • Mechanical pump that pumps blood thru the body