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IC 1.0 > Heart Failure > Flashcards

Heart Failure Flashcards

1
Q

How is heart failure defined?

A

as the inability to pump blood at a rate adequate to meet the metabolic demands of the body

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2
Q

How is the degree of heart failure often estimated in clinic?

A

by the degree to which it limits physical activity

  • Class I: no limitation
  • Class II: slight limitation, ordinary physical activity will result in symptoms
  • Class III: marked limitation of physical activity, symptoms at less than normal activity
  • Class IV: symptoms present even at rest
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3
Q

The etiologies of heart failure fall into what three categories?

A

those that impair contractility, increase after load, or impair ventricular filling

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4
Q

List several etiologies for left-sided heart failure.

A
  • increased afterload (aortic stenosis, hypertension)
  • impaired contractility (MI, chronic volume overload, transient myocardial ischemia)
  • impaired filing (hypertrophy, restrictive cardiomyopathy, mitral stenosis, pericaridal tamponade)
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5
Q

What ECG leads are used to asses the axis deviation of a patient’s heart?

A

lead I is the x-axis while lead aVF is the y-axis

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6
Q

Describe the appearance of a left shift on an ECG.

A
  • lead I is still positive
  • lead aVF is negative
  • on the axis deviation graph, the vector is up and to the right (negative aVF is an upward vector, positive I is a rightward vector)
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7
Q

How does atrial hypertrophy affect the axis deviation?

A

it doesn’t because the axis of deviation is based on the QRS complex, which is a measure of ventricular activity

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8
Q

What would cause a left axis deviation?

A
  • pregnancy

- left ventricular hypertrophy (secondary to hypertension, aortic stenosis, or aortic insufficiency)

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9
Q

What would cause a right axis deviation?

A
  • an infarct in the left ventricle
  • right ventricular hypertrophy (secondary to pulmonic stenosis, pulmonic insufficiency, mitral stenosis, or living at altitude for months)
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10
Q

Mitral valve stenosis will cause hypertrophy of which heart chamber?

A

both the left atrium and right ventricle (secondary to pulmonary hypertension)

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11
Q

Why does hypertrophy of ventricular myocytes pose a risk to the patient?

A
  • because larger cells increase the diffusion distance for movement of oxygen and hypertrophied cells require more oxygen than normal
  • as a result, myocardial ischemia is more likely to occur
  • especially upon increased effort because cardiac reserve is minimal
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12
Q

What is the most dangerous type of arrhythmia? Why?

A

ventricular fibrillation because it results in zero cardiac output

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13
Q

What induces ventricular hypertrophy?

A

conditions which result in pressure and/or volume overload and subsequently increase cardiac work

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14
Q

Describe the positive feedback loop responsible for accelerating heart failure.

A
  • as heart failure develops, cardiac output decreases, which results in a lower MAP
  • this prompts a compensatory response (tachycardia, increased TPR, blood volume increase, etc.), which ultimately demands more work from and places more stress on the heart
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15
Q

What is systolic dysfunction?

A

a diminished capacity to eject blood from the affected ventricle due to either impaired myocardial contractility or increased afterload

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16
Q

What is a sign of past MI and myocardial cell death?

A

pathologic Q waves (more negative) in two or more leads

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17
Q

How does breathing affect the stroke volume of the right and left ventricles?

A
  • inspiration increases preload of the RV

- expiration increases preload of the LV

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18
Q

Define end-diastolic volume?

A

the maximal ventricular volume at the end of filling

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19
Q

Define stroke volume?

A

the volume of blood ejected during a single ventricular contraction

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20
Q

How is ejection fraction calculated? What is a normal value?

A

EF = stroke volume/end-diastolic volume = 0.5-0.7

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21
Q

How can ejection fraction be used to asses heart failure?

A
  • the ejection fraction is typically lower in those with systolic dysfunction
  • the ejection fraction is typically normal in those with diastolic dysfunction
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22
Q

Review the lines and points on a ventricular pressure-volume loop

A

see slide 19 of the heart failure lecture

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23
Q

On a ventricular pressure-volume loops, what initiates the change form isovolumic contraction to ejection?

A
  • during isovolumic contraction, pressure in the ventricle rises until it exceeds diastolic aortic pressure
  • when this occurs, the aortic valve is pushed open and ejection begins
  • ejection ends when ventricular pressure falls below aortic pressure again
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24
Q

How does systolic dysfunction change a ventricular pressure-volume loop?

A
  • it flattens the line representing force of contraction (Po)
  • the passive filling curve is the same but the graph is shifted on to the right along that curve, revealing an increased EDV (due to low ejection fraction and residual blood volume building)
  • there is a decrease in arterial systolic pressure
  • the aortic valve closes at a higher end systolic volume than normal, contributing to lower the stroke volume
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25
Q

How is diastolic dysfunction defined?

A

an impaired ventricular filling due to either stiffness of the ventricular wall or reduced ventricular relaxation during diastole (excessive Ca remaining in ventricular myocytes)

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26
Q

How does diastolic dysfunction change a ventricular pressure-volume loop?

A
  • the force of contraction curve remains in place
  • the passive filling curve is elevated
  • there is decreased end diastolic volume, stroke volume, arterial systolic pressure, and mean arterial pressure
  • end diastolic pressure pressure is increased
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27
Q

Describe the pulse in someone with heart failure.

A

it will feel weaker than normal because whether it is diastolic or systolic dysfunction, stroke volume, and thus pulse pressure, is reduced

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28
Q

What are the common signs and symptoms of left-sided heart failure?

A
  • dyspnea, orthopnea, paroxysmal nocturnal dyspnea, and fatigue
  • diaphoresis, tachycardia, pulmonary rales, and pulmonary edema
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29
Q

Why is heart failure accompanied by sweating?

A

because the drop in mean arterial pressure induces a reflexive increase in sympathetic tone

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30
Q

What are the common signs and symptoms of right-sided heart failure?

A
  • right upper quadrant discomfort (hepatic enlargement) and fatigue
  • JVD, peripheral edema, sweating, tachycardia
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31
Q

JVD is a sign of heart failure on which side?

A

right-sided HF

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32
Q

What sort of edema is characteristic of left-sided heart failure? Right-sided?

A
  • left: pulmonary edema

- right: peripheral edema

33
Q

Why is edema a significant problem?

A
  • the additional fluid impairs oxygen diffusion
  • it also compresses small vessels
  • the effect is ischemia
34
Q

How do pulmonary arterioles respond to hypoxia? Why does this occur and why is it problematic?

A
  • unlike most tissues, they vasoconstrict in an effort to reduce blood flow to poorly oxygenated alveoli and rout it to well-oxygenated ones instead
  • this is fine when oxygen diffuse out of some alveoli is unaffected, but in the setting of pulmonary edema, all pulmonary vessels will constrict as oxygen diffuse is poor
  • the result is pulmonary hypertension and systemic hypoxia
35
Q

Through what mechanism does left-sided heart failure lead to pulmonary hypertension?

A
  • left-sided heart failure causes pulmonary edema, which induces vasoconstriction, increasing TPR
  • it also increases the pressure for the forward flow of blood in the pulmonary veins
36
Q

Why does left-sided heart failure often present with orthopnea and paroxysmal nocturnal dyspnea?

A
  • they struggle to breath at night because they are laying down, same as orthopnea
  • in both cases, laying down, increases venous return because gravity is no longer fighting return
  • this increases volume and pressure in the heart, exacerbating pulmonary edema
37
Q

What is Starling’s Law?

A

stroke volume increases when preload is increased

38
Q

Describe the baroreflex response to decreased mean arterial pressure.

A
  • reduced parasympathetic and increased B1-adrenergic firing to the SA node increase heart rate and therefore cardiac output
  • B1 activity also increases the inotropic state of the heart, increasing stroke volume
  • an increase in a1-adrenergic activity causes arteriolar and venous constriction, increasing TPR and venous return, respectively
  • release of angiotensin II stimulates vasoconstriction, ventricular hypertrophy, and release of aldosterone
  • aldosterone increases blood volume by promoting sodium and water reabsorption
  • release of ADH also serves to increase blood volume and, to a lesser extent, constrict systemic arterioles
39
Q

What is the primary manner in which reduced cardiac output is corrected for in the baroreflex? Why is this paradoxical?

A

an increase in TPR, which increases afterload and accelerates failure

40
Q

In patients with worsening heart failure, chronic sympathetic activation of the heart is common. Why is this problematic?

A
  • because chronic stimulation results in down regulation of cardiac beta-1 receptors, decreasing the inotropic state of the heart
  • repeated B1 stimulation can also result in caspase activation and contribute to myocyte death and systolic dysfunction
  • additionally, repeated B1 stimulation can increase oxidative stress within myocytes which results in calcium leakage from the sarcoplasmic reticulum; this increases cytosolic calcium during diastole, impairing relaxation and contributing to diastolic dysfunction
41
Q

Why are heart failure patients insensitive to catecholamines?

A

because they experience chronic B1-adrenergic activity in response to low MAP due to heart failure and this chronic stimulation results in down regulation of B1 receptors

42
Q

What danger do diuretics pose to those in heart failure?

A
  • those in heart failure already have reduced MAP
  • the danger of using diuretics to reduce blood volume and treat edema is that you could potentially send a patient into shock
43
Q

What three variables affect stroke volume?

A
  • preload
  • afterload
  • inotropic state
44
Q

Why are ACE inhibitors a better treatment for heart failure than diuretics?

A
  • although diuretics are likely to improve the edema by reducing preload, they pose a risk for inducing shock
  • ACE inhibitors on the other hand decrease blood volume but they also decrease afterload, which improves stroke volume and helps reduce the risk of reducing MAP to far
45
Q

When during the cardiac cycle is coronary blood flow to the left ventricle highest?

A

during diastole

46
Q

What is the disadvantage of using ACE inhibitors to treat heart failure?

A
  • ACE inhibitors may decrease aortic diastolic pressure to a significant degree
  • ventricular coronary blood flow occurs mostly during diastole
  • if the decrease in aortic diastolic pressure is too great, myocardial ischemia could become more severe
47
Q

What is the five year survival rate in those with CHF?

A

about 50%

48
Q

How does “high output” CHF differ from “low output” CHF?

A
  • high output is due to a healthy heart exhausted by working too hard (excess need of tissues)
  • low output is due to the heart being unable to pump enough to meet tissue needs
  • high output likely won’t respond to inotropic drugs
49
Q

What might cause high output CHF?

A
  • anemia
  • AV shunts
  • hyperthyroidism
  • thiamine deficiency
50
Q

How does angiotensin II contribute to heart failure?

A

it serves to increase preload and afterload while also promoting tissue remodeling within the heart

51
Q

In someone with CHF, what does increasing the preload cause?

A

increased pulmonary or peripheral edema

52
Q

Which heart failure medications are used to decrease preload?

A
  • venodilators (nitroglycerine)

- diuretics

53
Q

Which heart failure medications are used to decrease afterload?

A

arteriodilators

54
Q

What lifestyle changes are recommended in the treatment of CHF?

A
  • check weight daily and report gains of more than 2 lbs for several days in a row
  • limit sodium to less than 1500 mg/day
  • limit alcohol to less than one drink per day
  • exercise
55
Q

Describe the algorithm used to guide treatment of CHF and layering of drugs.

A
  • begin with a diuretic if the patient has fluid retention
  • then initiate an ACE inhibitor; B-blocker as well if patient is stable (SBP > 100 and pulse > 60 otherwise you could send into shock) and experiencing systolic dysfunction
  • if symptoms persist, add an aldosterone antagonist
  • finally, add digoxin or an ARB or hydralazine/isosorbide denigrate for AA patients
56
Q

How does the treatment of African Americans with CHF differ from the treatment of others with CHF?

A

African Americans don’t respond as well to inhibition of the renin-angiotensin system, so hydrazine/isosorbide denigrate is often used in place of an ARB

57
Q

What limitation do purely inotropic drugs have in the treatment of CHF?

A

they are helpful in managing acute failure but long-term use is actually associated with increased mortality

58
Q

Which diuretic is most commonly used to treat patients CHF?

A

furosemide

59
Q

Why aren’t thiazides typically used in those with CHF?

A

because if used alongside a vasodilator, it is likely to reduce renal blood flow and thus inhibit the diuretics efficacy

60
Q

For a normal, healthy individual, what is the daily recommendation for sodium intake?

A

less than 2,300 mg/day

61
Q

Why do CHF patients typically have an increase in renin-angiotensin system activity?

A
  • reduced renal perfusion increases renin release
  • an increase in sympathetic activity stimulates JG granular cells, evoking renin release
  • antihypertensive drugs used in treatment also tend to elevate the renin-angiotensin system
62
Q

How are ACE inhibitors and ARBs effective in treating CHF?

A
  • they decrease preload by reducing aldosterone release
  • they also decrease afterload by inhibiting ATII mediated vasoconstriction (which ensures that even with the decrease in preload, stroke volume does not diminish)
63
Q

How do ARBs compare to ACE inhibitors?

A
  • ARBs have more complete inhibition of the angiotensin system
  • ARBs are also more specific and therefore don’t pose a risk for cough or angioedema
64
Q

What is sodium nitroprusside? What is it’s most common adverse effect?

A
  • a balanced vasodilator acting on both veins and arteries, thereby reducing both preload and afterload
  • may cause excessive hypotension
65
Q

Describe the mechanism by which oral nitroglycerine acts and why it isn’t used long-term in the treatment of CHF.

A
  • it dilates veins more than arteries
  • therefore it decreases preload without simultaneously decreasing afterload and poses a risk for shock if stroke volume decreases too much
  • furthermore, long-term use is precluded because tolerance builds quickly
66
Q

What is hydralazine + isosorbide dinitrate?

A

a vasodilator primarily used in the treatment of African Americans with CHF

67
Q

Which calcium channel blockers are used to treat CHF? What is there mechanism of action? Why are others not used for CHF?

A
  • amlodipine and felodipine are used because they relax arteriolar smooth muscle
  • others aren’t used because they inhibit cardiac contraction, SA node impulse generation, and AV node conduction
68
Q

Which beta-blockers are commonly used in the treatment of CHF?

A

bisoprolol, carvedilol, and metoprolol have all be shown to reduce mortality in stable, severe HF

69
Q

Through what mechanism do beta-blockers help those with CHF?

A

they decrease cardiac work by reducing heart rate and contractile force

70
Q

Which aldosterone antagonists have been demonstrated to improve survival in CHF patients?

A
  • spironolactone

- epleronone

71
Q

What are the side effects of using aldosterone antagonists in CHF patients?

A
  • often induce hyperkalemia
  • spironolactone induces gynecomastia in some men
  • renal insufficiency may result if combined with thiazides
72
Q

What is digoxin? What is it’s mechanism of action? What are it’s primary uses?

A
  • it is glycoside used mainly for treatment of CHF and afib
  • it inhibits the Na/K-ATPase thus indirectly inhibiting the Na/Ca antiporter to elevate intracellular Ca
  • high intracellular calcium increases cardiac contractility
73
Q

Why is digoxin use declining? Which drugs affect it’s absorption and toxicity?

A
  • because there is a narrow therapeutic window before doses become toxic
  • quinidine, amiodarone, captopril, verapamil, cyclosporine all enhance it’s toxicity
  • many antibiotics increase absorption
74
Q

Describe Digoxin toxicity.

A
  • narrow therapeutic window
  • earliest signs of toxicity are GI (anorexia, vomiting, diarrhea, discomfort)
  • most dangerous effects are cardiac as they can stimulate almost every arrhythmia (including Vfib)
75
Q

Digoxin competes with which electrolyte?

A

potassium, which shares a binding site with digoxin on the Na/K-ATPase

76
Q

How is digoxin toxicity treated?

A
  • discontinuation of drug
  • correction of hypokalemia and hypomagnesemia
  • lidocaine if arrhythmic
  • digoxin antibodies
77
Q

What are milrinone and inamrinone? How are they effective in the treatment of CHF?

A
  • they are PDE inhibitors
  • they sustain cAMP levels and are therefore inotropic and vasodilate smooth muscle
  • they have often intolerable adverse effects and minimal long-term efficacy
  • they increase CHF mortality and are only used for acute heart failure
78
Q

How are dopamine and dopamine agonists used in the treatment of CHF?

A

they increase myocardial contractility in those with acute CHF

79
Q

List nine classes of drugs used in the treatment of CHF.

A
  • diuretics
  • ACE inhibitors
  • ARBs
  • vasodilators
  • calcium channel blockers
  • beta blockers
  • aldosterone antagonist
  • inotropic drugs (acute HF only)
  • B2 and DA agonists

IC 1.0 (24 decks)

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