Heart Failure Flashcards

1
Q

In terms of volume, central venous pressure increases with ____ and decreases with _____.

A

volume overload

volume depletion

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2
Q

What is the range of normal central venous pressure?

A

about 2 mm Hg to about 8 mm Hg

You can think of 6 mm Hg as an average normal CVP

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3
Q

How do you measure CVP?

A

from the tip of a central venous catheter in the superior vena cava.

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4
Q

How to you test to see if a patient in heart failure is volume depleted?

A

Give the patient a bolus of fluid via the central line. If the CVP goes up and
stays up, volume depletion is not the problem. If CVP goes up transiently and then falls back down, the patient may have both heart failure and volume depletion.

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5
Q

What is the equation for left ventricular end systolic volume?

A

LVESV = LVEDV – SV

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6
Q

What is normal left ventricular end diastolic pressure ?

A

4 mm Hg to about 12 mm Hg.

10 mm Hg as an average normal LVEDP

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7
Q

What is the normal LVEDV?

A

65 ml to around 240 ml.

120 ml as an average normal LVEDV

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8
Q

What is a normal stroke volume?

A

55 ml to about 100 ml.

70 ml as an average normal SV

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9
Q

What is a normal ejection fraction?

A

50% to about 75%

60% as an average normal EF

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10
Q

What is normal LVESV?

A

15 ml to about 145 ml

50 ml as average normal LVESV

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11
Q

Does a failing heart have higher or lower LVEDP than normal?

A

higher (4X)

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12
Q

Does a failing heart have higher or lower LVEDV than normal?

A

higher (2X)

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13
Q

Does a failing heart have higher or lower SV than normal?

A

lower (2X)

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14
Q

Does a failing heart have higher or lower EF than normal?

A

lower (50% points)

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15
Q

Does a failing heart have higher or lower LVESV than normal?

A

higher (5X)

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16
Q

When and what is the initial symptom of heart failure?

A

exertional dyspnea

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17
Q

True or false: most heart failure patients have isolated left failure.

A

FALSE: Most heart failure patients have both left and right heart failure.

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18
Q

What is the level of stroke volume reduction that stands as the threshold for heart failure? Why is it set at this number?

A

25% reduction in stroke volume is when patients begin to have symptoms

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19
Q

Is mitral valve regurgitation a cause or effect of heart failure?

A

BOTH- it can be either

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20
Q

Mitral regurgitation causes a heart murmur when?

A

systole (blowing holosytolic murmur)

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21
Q

MItral stenosis causes a heart murmur when?

A

diastole

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22
Q

Aortic regurgitation causes a heart murmur when?

A

diastole

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23
Q

Aortic stenosis causes a heart murmur when?

A

systole

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24
Q

List the top 4 left heart failure symptoms.

A

1) Dyspnea on exertion progressing to dyspnea at rest
2) Orthopnea
3) PND (paroxysmal nocturnal dyspnea)
4) Fatigue

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25
Q

List the top 2 right heart failure symptoms.

A
  1. Edema of feet, ankles, then legs

2. Abdominal distention

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26
Q

List the top 4 left heart failure signs.

A
  1. Bibasilar pulmonary crackles
  2. Tachycardia
  3. S3 (third heart sound)
  4. Pedal, ankle or leg edema (from backup of venous pressure)
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27
Q

List the top 4 right heart failure signs.

A
  1. Pedal, ankle or leg edema
  2. Jugular venous distention
  3. Hepatomegaly
  4. Ascites
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28
Q

How do you get edema in left heart failure patients?

A

Heart damage leads to decreased CO which causes decreased renal perfusion. This incresases Na retention, increases osmotic pressure, increases ADH and leads to an increase in fluid volume that can cause edema.

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29
Q

How does left heart failure lead to interstitial pulmonary edema?

A

Buildup of pressure in the left ventricle, left atrium, pulmonary veins and eventually pulmonary capillaries will reach such a high pressure (around 20 mmHg) that fluid will start to transudate out of them and into the interstitium.

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30
Q

At what pulmonary capillary pressure do you see alveolar pulmonary edema?

A

25 mmHg

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31
Q

What sign of left heart failure is related to alveolar pulmonary edema?

A

pulmonary crackles

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32
Q

What can cause acute lung injury and pulmonary edema with normal pulmonary capillary pressure?

A

septic shock

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33
Q

What can cause acute lung injury and pulmonary edema with low pulmonary capillary pressure?

A

hemorrhagic shock

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34
Q

How can you differentiate between pulmonary edema due to septic versus hemorrhagic shock?

A

Swan-Ganz Catheterization: Passing a catheter with a pressure monitor through the SVC, right atrium, right ventricle and pulmonary artery until it is wedged into the smallest artery it will fit into allows measurement of capillary pressure

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35
Q

The pulmonary capillary wedge pressure measured by the Swan-Ganz Catheter is approximately the same as what 2 pressures?

A

left atrial pressure and left ventricular end-diastolic pressure.

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36
Q

What else can you measure with a Swan-Ganz Catheter?

A

mixed venous O2 saturation and cardiac output

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37
Q

What is it called when a patient has noncompliant stiff left ventricles with impaired diastolic function and filling but a near-normal ejection fraction?

A

diastolic heart failure or heart failure with preserved ejection fraction.

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38
Q

Why do heart failure patients get tachycardia?

A
  1. Sympathetic nervous stimulation

2. Epinephrine and norepinephrine from the adrenal

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39
Q

What counterregulatory chemical is also elevated in heart failure patients?

A

B-type natriuretic peptide

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40
Q

When is B-type natriuretic peptide released?

A

at stretch or increase in cardiac chamber volume

41
Q

What does B-type natriuretic peptide do?

A

vasodilation

increased urinary sodium excretion

42
Q

What is the most common clinical scenario for heart failure with preserved ejection fraction?

A

elderly patient with long-standing hypertension, often obesity, and concentric left ventricular hypertrophy (now with impaired compliance)

43
Q

What leads to “compensated heart failure”?

A

Frank Starling mechanism- increased EDV dilate the heart and cause increased sarcomere stretching. The increased length allows for a more forceful contraction→ increasing cardiac output!

44
Q

How does a compensated heart become a decompensated heart?

A

The compensated (dilated) heart requires more oxygen and eventually the heart cannot propel sufficient blood to the body and the patient is said to be in “decompensated heart failure.”

45
Q

What is the state between compensation and decompensation called?

A

Diastolic dysfunction; heart failure with preserved ejection fraction

46
Q

Decompensation leads to what?

A

Systolic dysfunction

Heart failure with decreased ejection

47
Q

Do patients with large MI go into heart failure with preserved ejection fraction?

A

NO, go straight into systolic dysfunction and decreased ejection fraction

48
Q

Acute heart failure patients at the low end of perfusion are called?

A

cold

49
Q

Acute heart failure patients at the high end of congestion are called?

A

wet

50
Q

What are the 4 hemodynamic profiles of acute heart failure?

A

Warm and dry (10% die)
Warm and wet
Cold and dry
Cold and wet (40% die)

51
Q

How do you increase the adequacy of perfusion in a cold acute heart failure?

A

Vasodilators

Inotropes

52
Q

How do you decrease congestion in a wet acute heart failure?

A

diuresis

ultrafiltration

53
Q

True or False: Morbid obesity can cause heart failure by itself.

A

TRUE

54
Q

True or False: heart failure can be defined by a number.

A

FALSE: Like shock, heart failure is not defined by a number.

55
Q

What do you call shock with diffuse vasodilation, making the capacitance of the vascular system too big for the amount of blood volume available?

A

distributive shock

56
Q

What causes distributive shock?

A

sepsis
anaphylaxis
cytokine storm of TSS

57
Q

What do you call shock that blocks pulmonary circulation?

A

obstructive shock

58
Q

What causes obstructive shock?

A

thromboembolus
cardiogenic shock
hemopericardium causing cardiac tamponade

59
Q

What is the most common type of shock?

A

distributive (sepsis)

60
Q

The clinical signs of shock are observed through what 3 windows of the body?

A

behavior
skin
urine

61
Q

What is the biochemical sign of shock? Why?

A

elevated serum lactate from anaerobic metabolism required because the body is inadequately perfused.

62
Q

What is the behavior of someone in shock?

A

disorientation
confusion
obtundation

63
Q

What does the skin look like of someone in shock?

A

mottled
cold
clammy
pale/cyanotic

64
Q

What is the urine output of someone in shock?

A

reduced

65
Q

What two types of shock will have an elevated CVP?

A

cardiogenic

obstructive

66
Q

What will the LVEDP/ LVEDV/SV/EF/LVESV look like in someone with heart failure?

A

40/250/65/26/185

increase in everything but EF and SV which decrease

67
Q

What will the LVEDP/ LVEDV/SV/EF/LVESV look like in someone with compensated heart failure?

A

12/200/100/50/100

LVEDP slightly increases, and LVEDV really increases. Normal SV and EF.

68
Q

What will the LVEDP/ LVEDV/SV/EF/LVESV look like in someone with hypovolumia?

A

2/100/75/75/25

Low diastolic pressure and volume, because less blood, increased CO due to decreased BP will increase SV and EF.

69
Q

What will the LVEDP/ LVEDV/SV/EF/LVESV look like in someone with hypertrophy of their left ventricle?

A

40/100/65/65/35

increased pressure but decreased volume in left ventricle in diastole, because smaller space. EF remains the same.

70
Q

How can you determine if there is left ventricular hypertrophy? (what number?)

A

Anything thicker than 1.5 cm (1.2 cm is normal) will mean hypertophy.

71
Q

What is the most common cause of right heart failure?

A

left heart failure

72
Q

Why do patients with left heart failure get orthopnea?

A

exacerbation of left heart failure from the increase in venous return from lying on back

73
Q

Why do patients with right heart failure NOT get orthopnea?

A

failure of the right heart decreases the venous return that can go back to left heart

74
Q

What is the characteristic murmur of mitral stenosis?

A

diastolic rumble with opening snap (sometimes)

75
Q

What symptoms of mitral stenosis and heart failure overlap?

A

DOE, fatigue, palpitations

76
Q

Where is the best place to hear mitral valve murmurs?

A

cardiac apex (bottom of heart)

77
Q

What is SIADH?

A

syndorme of inappropriate antidiuretic hormone. Where you retain more water than sodium, so your sodium levels are low

78
Q

What percentage of heart failure patients have SIADH?

A

25%

79
Q

Why would a young woman go into heart failure soon after pregnancy?

A

PPCM (Peripartum cardiomyopathy)

80
Q

What is the cause of PPCM?

A

unknown, but cardiac angiogenic imbalances resulting from complex pregnancy-related immune system and hormonal changes play a key role

81
Q

Does heart failure lead to a pro-inflammatory cytokine profile?

A

YES

TNF, IL-1, and IL-6 are sometimes elevated

82
Q

Why is severe acute uncompensated aortic regurgiation so important?

A

it is a surgical emergency!

83
Q

How does the heart cope with chronic mitral valve regurgitation?

A

1) increases SV
2) increases EDV
3) Left ventricular dilation

84
Q

Does doubling SV (200) and increasing EDV to 240 prevent heart failure in a patient with chronic mitral regurgitation of 95 mL?

A

YES. you are still getting 105 mL of blood going forward

85
Q

How does the heart cope with acute mitral valve regurgitation?

A

1) increases SV

2) increases EDV

86
Q

Does increasing SV to 140 and EDV to 170 prevent heart failure in someone with acute mitral regurgitation of 70 mL?

A

NO. Only 70 mL is going forward, and baseline is 100 mL. This is a 30% reduction and heart failure occurs at 25%.

87
Q

BNP is similar to what medicaiton?

A

ACE inhibitor or diuretic

88
Q

Blood levels of what are very good for diagnosing heart failure?

A

BNP is 5-10 times higher in heart failure patients

89
Q

True or false: aortic stenosis is a “male disease”.

A

TRUE!

90
Q

True or false: there are NO innocent systolic murmurs.

A

FALSE there are NO innocent diastolic heart murmurs–it is characteristic of valve disease

91
Q

What will the LVEDP/ LVEDV/SV/EF/LVESV look like in someone with aortic regurgitation?

A

LVEDP, LEVDV, LVESV and SV increase

EF lowers

92
Q

What is one genetic cause of aortic regurgitation?

A

Marfan’s syndrome

93
Q

What type of histology is seen in the aorta of someone with Marfan’s syndrome?

A

“cystic” medial degeneration= fragmentation and loss of elastic fibers, leaving “cystic” areas of bluish myxoid matrix

94
Q

How does Marfan syndrome lead to cystic medial degeneration?

A

defective synthesis of the scaffolding protein “fibrillin” leads to abnormal sequestration of TGF-beta in aortic wall with dilation and loss of elastic tissue–no true cysts are actually formed but there is increase in amorphous proteoglycans

95
Q

How can someone get papillary muscle rupture?

A

acute myocardial infarction

96
Q

How can someone have an MI with no chest pain?

A

“silent MI”–seen in 1 in 4 patients with suspected CAD

97
Q

Who is 50% more likely to have a silent MI?

A

diabetics

98
Q

What will the LVEDP/ LVEDV/SV/EF/LVESV look like in someone with mitral regurgitation leading to heart failure?

A

high LAP, high LVEDV, FSV that is 25% decreased, decreased LVESV

99
Q

What will the LVEDP/ LVEDV/SV/EF/LVESV look like in someone with mitral regurgitation leading to COMPENSATED heart failure?

A

less elevated LAP, more elevated EDV but higher ESV