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951 Block 3 > 7. Heart Failure > Flashcards

7. Heart Failure Flashcards

1
Q

Chronic heart failure is more prevalent in women. (T/F)

A

False: men

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2
Q

What disorders cause HF?

A
  • ischemic heart disease
  • HTN
  • valvular heart disease
  • other cardiomyopathies (less freqeunt)
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3
Q

Why does valvular dysfunction cause HF?

A

leaky valves over stress the heart muscle

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4
Q

What is the diagnostic criteria called for HF?

A

Framingham criteria

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5
Q

What are the major criteria of the Framingham criteria?

A
  • nocturnal dyspnea
  • neck vein distension
  • pulmonary edema
  • radiographic cardiomegaly
  • hepatojugular reflux
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6
Q

What are the minor criteria of the Framingham criteria?

A
  • bilateral ankle edema
  • nocturnal cough
  • dyspnea on ordinary exertion
  • hepatomegaly
  • tachycardia
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7
Q

Relaxation of the cardiac muscle cells is a passive process. (T/F)

A

False: active process

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8
Q

What are the major contractile proteins?

A
  • thin actin

- thick myosin

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9
Q

Ca interacts with ________ to initiate muscle cell contraction.

A

troponin C

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10
Q

Ca enters cardiac myocyte through __________ channels.

A

voltage sensitive L-type

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11
Q

The entrance of Ca into cardiac myocyte triggers what?

A

release of Ca from sarcoplasmic reticulum

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12
Q

What uncovers sites on actin that bind myosin heads?

A

tropomyosin

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13
Q

What phase of the cardiac cycle occurs when the myosin heads flex?

A

systole

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14
Q

What happens when Ca is removed from troponin C binding sites?

A
  • ends systole

- begins the diastolic phase of cardiac cycle

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15
Q

What factors strengthen muscle cell contraction?

A
  • Ca concentration

- length of muscle fiber at end of diastole

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16
Q

Describe the pressure difference during systole.

A

Left ventricular pressure exceeds the atrial pressure

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17
Q

What valve closes during systole?

A

mitral

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18
Q

During what phase of the cardiac cycle is Ca taken up by the SR?

A

diastole

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19
Q

What is the preload?

A

load (blood) present before contraction

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20
Q

What occurs when preload is increased?

A
  • ventricle distends during diastole

- HR ↑ because atrial mechanoreceptors ↑ the rate of SA node discharge

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21
Q

What is afterload?

A

systolic load on the left ventricle after it has started to contract

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22
Q

Where is afterload produced?

A

in te artery leaving the ventricle

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23
Q

What is the primary determinate of afterload?

A

total peripheral resistance

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24
Q

Why is an increased afterload detrimental?

A

It makes the heart work harder to push the blood out into the body

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25
Q

What is end systolic volume?

A

Blood volume remaining in the left ventricle at the end of systole

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26
Q

What is end diastolic volume?

A

volume of blood in the ventricle at the end of diastole

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27
Q

How do you find stroke volume?

A

EDV – ESV = SV

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28
Q

What is stroke volume?

A

Volume of blood ejected from the ventricle during systole

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29
Q

What is ejection fraction?

A

The percentage of ventricular volume expelled during systole

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30
Q

Systolic HF is an impaired _______ state.

A

inotropic

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31
Q

What characterizes systolic HF?

A
  • inadequate cardiac output

- diminished expulsion of blood

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32
Q

What are the symptoms of systolic HF?

A
  • cardiomegaly
  • edema
  • jugular venous distention
  • left ventricular dilation
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33
Q

What is diastolic heart failure?

A

the reduced ability of the ventricles to accept blood

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34
Q

What characterizes diastolic HF?

A
  • slowed or incomplete ventricular relaxation
  • resting pressure in ventricle is ↑ : LV stiffness keeps the ventricle from filling properly
  • SV is ↓ since filling volume is ↓
  • ejection fraction may be normal
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35
Q

Left ventricular hypertrophy is greater with ______ HF.

A

systolic

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36
Q

Why does the heart remodel itself?

A

LV hypertrophy initially helps to maintain CO

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37
Q

Why is LV hypertrophy detrimental?

A

eventually the heart cells get so large and swollen that the contractile proteins do not overlap efficiently and over time, loses contractile function

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38
Q

Eventually, an enlarged heart cannot ____ properly and leads to _______ dysfunction.

A
  • fill

- diastolic

39
Q

What is the ryanodine receptor?

A

Ca release channel from sarcoplasmic reticulum

40
Q

How is Ca actively taken up into the sarcoplasmic reticulum?

A

SERCA: sarcoendoplasmic reticulum Ca ATPase

41
Q

In HF, Ca uptake by _______ is depressed.

A

SERCA

42
Q

Right side HF is more common than left side HF. (T/F)

A

False: left is more common

43
Q

What is right side HF?

A

Right ventricle cannot accept or eject the returning blood volume from the periphery.

44
Q

What is the result of right side HF?

A

Blood backs up into the periphery

  • capillary pressure in the periphery ↑
  • results in loss of fluids to the tissues
45
Q

In right side HF, edema is in response to stimulation of the _______.

A

RAAS

46
Q

What is the primary characteristic of right side HF?

A

peripheral edema

47
Q

In left side HF, the right side pumps normally so blood continues to go out to the lungs. (T/F)

A

True

48
Q

Left side HF results in ______ blood volume in the lungs.

A

increased

49
Q

What is the pulmonary impact of left side HF?

A
  • ↑ pulmonary capillary pressure
  • fluid filters out into lung interstitial space
  • pulmonary edema (serious enough to cause death)
50
Q

What are the pulmonary symptoms of left side HF?

A
  • dyspnea
  • orthopnea
  • cough from pulmonary congestion
51
Q

What are the 3 methods that the heart may use to adapt to maintain CO?

A
  • Frank-Starling mechanism
  • activation of neurohumoral systems
  • myocardial remodeling
52
Q

What is the Frank-Starling method?

A

an increased preload helps to sustain cardiac performance

53
Q

What is the activation of neurohumoral systems?

A
  • release of norepinephrine by adrenergic cardiac nerves

- activation of RAAS to maintain arterial pressure and perfusion to vital organs

54
Q

What is myocardial remodeling?

A

mass of contractile tissue is increased

55
Q

Which 2 cardiac adaptations occur rapidly?

A
  • Frank-Starling mechanism

- activation of neurohumoral systems

56
Q

What is Starling’s Law of the Heart?

A

Greater the heart is stretched during filling, the greater the force of contraction.

57
Q

In a non-failing heart, an increased blood volume in, results in a normal volume pumped out. (T/F)

A

False: increased blood volume in, results in an increased volume pumped out

58
Q

What is the compensation mechanism that leads to Na/water retention?

A
  • ↓ renal perfusion

- aldosterone release

59
Q

What is the compensation mechanism that leads to vasoconstriction?

A

↑ SNS activity
↑ Ang II
↑ vasopressin

60
Q

What is the compensation mechanism that leads to tachycardia?

A
  • ↑ SNS activity

- baroreceptor response to ↓ BP

61
Q

What is the compensation mechanism that leads to ventricular hypertrophy?

A

↑ afterload
↓ CO
↑ preload

62
Q

What is the compensatory benefit of Na/water retention?

A

↑ blood volume

↑ venous return, results in FS mech.

63
Q

What is the compensatory benefit of vasoconstriction?

A

helps maintain BP when CO is reduced

64
Q

What is the compensatory benefit of tachycardia?

A

helps maintain CO

65
Q

What is the compensatory benefit of ventricular hypertrophy?

A
  • helps maintain CO

- reduced myocardial wall stress

66
Q

What is the adverse effect of Na/water retention?

A

pulmonary and systemic edema

67
Q

What is the adverse effect of vasoconstriction?

A

↑ afterload

↑ myocardial oxygen demand

68
Q

What is the adverse effect of tachycardia?

A
  • ↑ myocardial oxygen demand
  • arrhythmias
  • β1 receptor down regulation
69
Q

What is the adverse effect of ventricular hypertrophy?

A
  • diastolic dysfunction
  • hypertrophied ventricles - valve dysfunction
  • arrhythmias
70
Q

Why is maintaining arterial pressure an effective compensatory mechanism of ↓ CO?

A

allows limited CO to be most useful for survival

71
Q

In HF, where does compensatory vasoconstriction mostly occur?

A

areas not vital for immediate survival

  • skin
  • skeletal muscle
  • gut
  • kidney
72
Q

What vasoconstrictor systems increase in compensatory mechanism?

A
  • SNS
  • RAAS
  • endothelin
73
Q

Redistribution of blood maintains delivery of oxygen to what organs?

A

brain and heart

74
Q

What is the primary stimulus to hypertrophy?

A

pressure overload

75
Q

Increased ventricular wall stress leads to:

A
  • thickening and elongation of individual myocytes
  • replication of sarcomeres
  • ventricular dilation
76
Q

With chronic volume overload, ventricle becomes more _______ and causes _____ ______ defects.

A
  • spherical

- mitral valve

77
Q

A normal heart has a ______ force-frequency relationship.

A

positive

78
Q

What is a positive force-frequency relationship?

A

the force of contraction and rate of tension development rise with ↑ stimulation frequency

79
Q

cAMP __(↑/↓) activity of the Ca ATPase of the SERCA.

A

increases ↑

80
Q

↑ Ca reuptake into the SR accelerates _______ _______.

A

diastolic relaxation

81
Q

Heart failure creates a ______ force-frequecy relationship.

A

negative

82
Q

In HF, disturbances in Ca concentrations __ (↑/↓) contractile function during myocardial failure.

A

reduce ↓

83
Q

The Na/Ca exchanger in the cell membrane _______ Ca from the cytoplasm during diastole.

A

removes

84
Q

In what way is the Na/Ca exchanger abnormal in HF?

A

expression is increased

85
Q

Expression of the Na/Ca exchanger correlates ______ with the decrease in SERCA.

A

inversely

86
Q

Why does Na/Ca exchanger increase as SERCA decreases?

A

compensatory response to the reduction in Ca reuptake by a decrease in SERCA

87
Q

What is the benefit of increasing Na/Ca exchanger expression?

A

facilitates diastolic Ca removal

88
Q

What is the adverse reaction of increasing Na/Ca exchanger expression?

A

increased potential for arrhythmias

89
Q

Why does increasing Na/Ca exchanger expression increase potential for arrhythmias?

A

Ca efflux is associated with an influx of Na that prolongs depolarization and causes after-depolarization

90
Q

What is NYHA Class I heart failure?

A

No limitation: ordinary physical activity does not cause undue fatigue, dyspnea, or palpitation

91
Q

What is NYHA Class II heart failure?

A
  • Slight limitation of physical activity: ordinary physical activity results in fatigue, palpitation, dyspnea, or angina
  • comfortable at rest
92
Q

What is NYHA Class III heart failure?

A
  • Marked limitation of physical activity: less than ordinary physical activity results in symptoms
  • comfortable at rest
93
Q

What is NYHA Class IV heart failure?

A
  • inability to carry out any physical activity without discomfort
  • symptoms present at rest

951 Block 3 (10 decks)

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