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Nurs 6413 Physiology & Pathophysiology > Heart Valves > Flashcards

Heart Valves Flashcards

1
Q

What is the most common form of valvular heart disease in Western countries?

A

Degenerative valve disease

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2
Q

Which disease accounts for the majority of valvular pathology in developing countries?

A

Rheumatic heart disease

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3
Q

What are the most commonly encountered valvular lesions in western countries?

A

Aortic stenosis and Mitral regurgitation

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4
Q

Why are MR and AS the most prevalent in western countries?

A

AS -> d/t calcific disease
MR -> d/t primary causes like degenerative disease
2ndary cause = ischemic heart disease

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5
Q

How do valvular lesions change the normal physiology of the heart?

A

Cause pressure and/or volume overload causes concentric and/or eccentric hypertrophy

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6
Q

Stenosis of which valves will be affected during systole?

A

Aortic and pulmonic

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7
Q

Stenosis of which valves will be affected during diastole?

A

Mitral and tricuspid

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8
Q

Valvular obstruction can be classified as either fixed or dynamic. Describe the difference between the two.

A

Fixed: Constant degree of obstruction to blood flow throughout the cardiac cycle (AS)

Dynamic: Variable degree of obstruction dependent on the phase of the cardiac cycle (hypertrophic obstructive cardiomyopathy)

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9
Q

Stenotic lesions cause increased pressure proximal to the affected valve (T/F)

A

True

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10
Q

Regurgitant lesions cause pressure overload (T/F)

A

False
Volume overload

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11
Q

Volume overload leads to what type of physiological changes?

A

Chamber dilation and eccentric hypertrophy

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12
Q

List the 3 ways the LV can respond to changes in pressure/volume

A
  1. Activation of the Frank-Starling mechanism
  2. Use of the adrenergic neurohormonal systems
  3. Chamber remodeling
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13
Q

As cardiac function declines the Frank-Starling curve is shifted to the _____ & _______

A

right & flattened

Further increases in left heart filling pressures lead to minimal increases in CO

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14
Q

Explain how activation of neurohormonal system effects CO

A

Increased fluid retention -> activating the Frank Starling law which increases both sarcomere length and contractility

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15
Q

Explain the pathophysiology of ventricular remodeling

A

Concentric LV remodeling enables ventricle to beat harder.
Eccentric hypertrophy enables ventricles to hold more volume.

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16
Q

Explain a New York Heart Association (NYHA) score of 1

A

Asymptomatic

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17
Q

Explain a New York Heart Association (NYHA) score of 2

A

Symptoms with ordinary activity but comfortable at rest

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18
Q

Explain a New York Heart Association (NYHA) score of 3

A

Symptoms with minimal activity but comfortable at rest

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19
Q

Explain a New York Heart Association (NYHA) score of 4

A

Symptoms at rest

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20
Q

List the physical exam findings associated with LHF

A

Pulmonary edema
Dyspnea
Pink-frothy sputum

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21
Q

List the physical exam findings associated with RHF

A

Dependent edema
ascites
JVD
hepatomegaly

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22
Q

What are the 4 unstable clinical risk factors that may require delay of sx?

A
  1. Unstable angina
  2. Dysrhythmias
  3. Severe valvular disease
  4. Decompensated HF
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23
Q

If patient needs emergency sx, you must delay for a full work up to determine extent of valvular disease (T/F)

A

False
Emergency sx takes precedence

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24
Q

Explain the steps for systematic evaluation of primary valvular dysfunction

A
  1. Category of valvular dysfunction (stenosis/insufficiency/mixed)
  2. Status of LV loading (filling problem or no?)
  3. Acute vs. chronic
  4. Cardiac rhythm & effects on diastolic filling time
  5. LV function (HFrEF vs. HFpEF)
  6. Secondary effects on pulmonary vasculature & RV function (Pulm HTN)
  7. HR
  8. Perioperative anti coagulation
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25
Q

How does bradycardia with Regurgitant lesions effect the RF and SV

A

Increase RF and decrease SV

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26
Q

How does tachycardia with stenotic lesions affect SV and myocardial oxygen demand?

A

Shortens ejection time, decreases SV and increases myocardial oxygen demand

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27
Q

The LV is subject to volume overload as a result of which 2 valvular lesions?

A

MR & AR

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28
Q

The LV is subject to pressure overload from which valvular lesion?

A

AS

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29
Q

The LV is subject to volume under load from which valvular lesion?

A

MS

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30
Q

In chronic valvular dysfunction the heart __________ over time, while acute valvular dysfunction causes severe _____________ ____________

A

Compensates
Hemodynamic consequences

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31
Q

What is a normal aortic valve area?

A

2.5 - 3.5 cm2

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32
Q

What is a normal aortic minimal gradient pressure?

A

2-4mmHg

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33
Q

What is a normal aortic flow rate?

A

250ml/min

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34
Q

Symptoms at rest occur when the aortic valve is stenosed by how much percentage?

A

50%

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35
Q

Aortic valve area <1cm2 indicates what level of disease?

A

Severe aortic stenosis & is associated with increase in peri operative mortality

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36
Q

Aortic valve area <1cm2 produces which triad of symptoms?

A
  1. Angina
  2. Syncope
  3. CHF
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37
Q

An aortic valve flow velocity of >4m/sec indicates good prognosis (T/F)

A

False
Indicates poor prognosis

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38
Q

A mean aortic valve gradient pressure >40mmHg indicates poor prognosis (T/F)

A

True

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39
Q

Describe murmur of AS and where you’ll hear it

A

Crescendo-decrescendo systolic ejection murmur heard best at RSB 2nd ICS

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40
Q

AS causes what type of hypertrophy?

A

Concentric
Increased pressure is needed to overcome impedance

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41
Q

The consequence of LVH in AS is a:

  1. __________ in ventricular compliance
  2. ___________ remodeling
  3. ___________ in intrinsic contractility of the myocardium
A

Decrease
Hypertrophic
Decrease

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42
Q

True or false
Reduction in ventricular compliance from AS leads to higher filling pressures required to produce the same amount of ventricular work

A

True

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43
Q

The cardiac rhythm does not matter to achieve adequate LV filling
True or false

A

False
NSR is required to ensure adequate LVEDV from the atrial kick

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44
Q

Concentric ventricular hypertrophy _________ myocardial O2 demand

A

INCREASES

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45
Q

Why does concentric ventricular hypertrophy increase myocardial O2 demand?

A
  1. Myocardial Mass increased
  2. Isovolumetric contraction uses more energy than ventricular ejection (high intracavitary pressure must be generated to Maintain CO
  3. EF phase prolonged (diastole shortened)
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46
Q

Why does concentric ventricular hypertrophy decrease O2 supply?

A
  1. CPP is decreased d/t increased LVEDP
  2. Systolic coronary flow is absent
  3. Prolonged systolic ejection reduces the coronary perfusion interval
  4. Subendocardial capillaries are compressed d/t myocardial hypertrophy
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47
Q

What changes to the pressure volume loop would you expect in AS?

A

Shifted up

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48
Q

What ECG changes would you expect from AS?

A

Lateral leads show increased voltage, T wave inversion

49
Q

Based on the Aortic stenosis classification system, stage 0 would show what manifestations?

A

No cardiac damage, no echo changes

50
Q

Based on the Aortic stenosis classification system, Stage 1 would show what manifestations?

A

LV damage
Increased LV mass index
LVEF <50%

51
Q

Based on the Aortic stenosis classification system, stage 2 would show what manifestations?

A

LA or Mitral damage
Moderate-severe mitral regurgitation on echo
AF

52
Q

Based on the Aortic stenosis classification system, stage 3 would show what manifestations?

A

Pulmonary vasculature or tricuspid damage
Systolic pulm HTN on echo >60mmHg
Moderate-severe tricuspid regurgitation

53
Q

Based on the Aortic stenosis classification system, stage 4 would show what manifestations?

A

RV damage
Moderate-severe RV dysfunction

54
Q

Anesthetic considerations for AS?

A

MAINTAIN

*NSR
*HR 70-80
*Maintain preload (LVEDV) to maintain CO
*Adequate CPP (maintain DBP)
*Avoid myocardial depression
*Maintain or increase afterload
*GA preferred

Use neuraxial with extreme caution

55
Q

Define Aortic insufficiency (aortic regurgitation)

A

Incomplete coaptation of the aortic valve leaflets in diastole and may be caused by disease processes that affect the aortic valve leaflets, aortic root, or both.

Causes portion of blood ejected from LV into the aorta regurgitated back into ventricle because of incomplete closure of aortic valve

56
Q

What type of murmur will be auscultated with AI? And where will you hear it?

A

Diastolic murmur, blowing or swishing best heard over the LV

57
Q

Does the intensity of the AR murmur correlate with the severity of the murmur

A

No

58
Q

List the cause of Primary acute AI

A

Infective endocarditis - resulting in direct damage to aortic valve cusps

59
Q

List the cause of primary chronic AI?

A

Rheumatic valvular disease (almost always involves mitral valve)

60
Q

List the cause of secondary acute AI?

A

Aortic root dissection caused by trauma or aneurysm

61
Q

Chronic overload of LV leads to _________ ventricular hypertrophy and chamber dilation

A

Eccentric
Dilation

62
Q

The degree of aortic regurgitation depends on
1. _________ time available for regurgitation to occur
2. Diastolic __________ _________ between aorta and LV
3. Degree of ________ of aortic valve

A

Diastolic
Pressure gradient
Incompetence

63
Q

AS murmur is a _______ pitched, ________ decrescendo murmur, loudest along the left sternal border

A

High
Blowing
Left sternal border

64
Q

End stage AR is characterized by (4)

A

Myocardial Failure
Decreased CO
Elevation of LVEDV
Evidence of pulmonary Congestion

65
Q

Causes of leaflet abnormalities that cause AR (5)

A
  1. Congenital abnormalities of aortic valve
  2. Rheumatic disease
  3. Infective endocarditis
  4. Calcific degeneration
  5. Myxomatosis degeneration
66
Q

Etiologies of aortic root abnormalities (AR)

A

Idiopathic aortic root dilation
HTN induced annuloaortic ectasia
Aortic dissection
Marfan syndrome
Ehler-danlos syndrome
Aortic is (syphilitic)
Rheumatoid arthritis
Ankylosis spondylitis

67
Q

Mortality rate for patients is asymptomatic AI is ______% per year
Mortality rate for patients who are symptomatic _____% per year

A

0.2
10

68
Q

At what point is Aortic valve replacement recommended in AR?

A

When evidence suggests that increase in LV volume result in left ventricular dysfunction

69
Q

In AR, _______ may occur in absence of CAD, often at night, d/t bradycardia with subsequent fall in diastolic pressure and _______ Regurgitant volume.

A

Angina
Increase

70
Q

Anesthesia and sx is an added stress to body & can push asymptomatic pt’s to point of decompensation due to anesthesia-induced ____________ _____________

A

myocardial depression

71
Q

What are hemodynamic goals during anesthesia for pt’s with AI?

A

FAST, FWD, FULL
HR maintained between 80-100 (FAST)
afterload decreased (FWD)
Preload increased or maintained (FULL)
myocardial depression avoided
NSR

72
Q

Normal Mitral valve area

A

4-6cm2

73
Q

At what size area does MS generally develop?

A

<2cm2

74
Q

Mitral stenosis (MS) occurs after _________ _____ _______ & results from profressive fusion & calcification of valve leaflets

A

rheumatic heart disease

75
Q

Which valvular lesions are more common in developing countries

A

MS and AR

76
Q

MS less common in western countries d/t early _________ and treatment of _____________ ___________.

A

detection
streptococcus pharyngitis

77
Q

Symptoms of MS usually occur ______ to ______ years after RHD

A

20 - 30

78
Q

______% of patients with RHD will have some form of mitral valve involvement

A

90

79
Q

List the etiologies of MS

A

rheumatic heart disease
severe mitral annular calcification
radiation associated valve disease
carcinoid syndrome
LA myxoma
rheumatoid arthritis
SLE
iatrogenic MS after MV repair sx

80
Q

Changes to MV with MS include fusion, thickening, calcification, of the ____________ & ____________ ____________

A

Leaflets & chordae tendinae

81
Q

In MS, chronic stress of the turbulent flow through the deformed valve leads to a _________ at the apex of a narrow-shaped, fish-mouth valve

A

narrowing

82
Q

Hemodynamic consequences of MS include
__________ LA volume & pressure is dependent of the ________ of MS, CO, & HR

A

Increased, severity

83
Q

In mild-mod MS - LA pressure only minimally elevated @ rest but _______ w/exercise, conditions that increase HR, like ________.

A

increases, AFIB

84
Q

In severe MS - LA pressure significantly elevated at rest leading to _____________ _________, RHF, & symptoms at rest

A

pulmonary HTN

85
Q

In MS, LV function is ________ ________

A

generally preserved

86
Q

Clinical presentation of MS

A

RHF
SVT/AFIB
dypnea on exertion
pulm HTN
hemoptysis
CP
ascites
BLE Edema
Ortner syndrome

87
Q

What is Ortner’s syndrome?

A

Horseness d/t LA compressing the RLN

88
Q

MS murmur is characterized by an opening snap early in ________, best heard during expiration, followed by a ______-pitched rumbling diastolic murmur. Best heart at apex w/pt in Left lateral decubitus position

A

diastole
high-pitched
apex

89
Q

What type of ECG abnormality might you find in lead II in a patient with MS

A

P-mitrale

(M shaped P wave)

90
Q

Anesthesia consideration for pt’s with MS

A

Neuraxial anesthesia - epidural > spinal
Focus on preventing & treating events that decrease CO or produce pulm edema
Treat dysrhythmias promptly
Avoid Ketamine & N2O
Avoid hypoxia & hypercarbia
HR 60-80
Maintain preload
Limit Trendelenburg (prevent dependent edema)

91
Q

What is MR

A

backward flow of blood into LA during systole with compensation via LV dilation & increasing EDV

92
Q

Acute Etiology of MR:

A

Papillary muscle dysfunction or rupture of chordae tendinae from MI & ischemia
Acute rheumatic fever
Endocarditis
Balloon Valvuloplasty
Penetrating chest wound

93
Q

Chronic etiology of MR:

Primary abnormality of one or more components of the ___________ _________, or 2ndary to another ________ disease

A

valvular apparatus
cardiac

94
Q

Degree of MV regurgitation (regurgitant fraction) is related to (4):

  1. size of the regurgitant valve _________
  2. _________-_________ between LA & LV
  3. Time available for _______
  4. Aortic ________ _______ (SVR)
A
  1. orifice
  2. pressure-gradient
  3. regurgitation (systole)
  4. outflow impedance
95
Q

In MR, increase LA volume = high risk for development of _______ & __________ ________

A

AFIB
thrombus formation

96
Q

Clinical presentation of pt’s with MR

A

asymptomatic until LA enlargement causes:
Pulm HTN or AFIB

Severe acute/chronic MR: symptomatic HF with pulm edema

97
Q

List symptoms of MR

A

exertional dyspnea
fatigue
palpitations
Pulm HTN
Afib
Hoarseness - Ortner’s syndrome

98
Q

Anesthetic considerations for patient’s with MR

A

FAST, FWD, not FULL

Avoid bradycardia
Avoid increases in systematic vascular resistance
Minimus myocardial depression
Maintain fwd SV and CO

99
Q

What is Mitral valve prolapse

A

bulging of one or moth mitral valve flaps into LA during contraction of the heart. May progress to MR or cause emoli or infective endocarditis

100
Q

MVP woman are _____ times more likely than men to develop

A

3

101
Q

Primary MVP is characterized by

*thickening, and fibrosis of the ________

*Thinning/lengthening of the ______ ____________

*frequently associated with __________ ________

A

Leaflets

chordae tendineae

marfan’s syndrome

102
Q

2ndary MVP is characterized by:

____________ damage to papillary muscles attached to chordae tendineae

Damage to________ themselves during MI, RHD, hypertrophic cardiomyopathy

A

Ischemic

valves

103
Q

MVP pathophysiological changes primariy effect the _____ & _______ _______

A

cusps & chordae tendineae

104
Q

CLinical presentation of pt’s with MVP

A

Undiagnosed in majoity of pt’s
PVCs
Prolonged V-tach

105
Q

Symptoms of MVP

A

weakness
dizziness
syncope
atypical CP
Palpitations

106
Q

Anesthetic considerations for MVP

A

Full
FWD
Decrease contractility
Low HOB

107
Q

Normal Tricuspid valve area

A

7-9cm2

108
Q

What is Tricuspid stenosis?

A

Persistent diastolic pressure gradient between RA & RV. Typically leaflets thickened with limited mobility, reduced separation of leaflet tips & diastolic doming of the valve

109
Q

Etiology of TS

A

RHD
Carcinoid syndrome
Infection endocarditis
Hypereosinophillic syndromes
RA tumors causing functional stenosis
Congenital causes

110
Q

Symptoms of TS

A

Systemic venous congestion

JVD
Ascites
Peripheral edema

Hepatomegaly
Hepatic pulsations
Anasarca

111
Q

What area indicates severe TS?

A

<1cm2

112
Q

What ECG abnormalities would you anticipate with TS?

A

Tall peaked p-waves in leads II, III, aVF (RA enlargement)

113
Q

TS murmur is a soft ________ heard loudest of the 3rd & 4th ICS near the _______

A

Mid-diastolic

LSB

114
Q

Tricuspid regurgitation is more commonly a 2ndary lesion with or without ________ tethering

A

Leaflet

115
Q

TR etiology

A

RV ischemia
Severe pulmonary HTN
Dilated cardiomyopathy (leads to RV pressure & volume overload)
Infective endocarditis
Carcinoid syndrome
RDH
Tricuspid valve prolapse
Epstein anomaly
Implantable devices leads that cross the RV

116
Q

TR symptoms

A

Usually not present until advanced stages

RHF - fatigue, edema, ascites, painful hepatosplenomegaly

May have sensations of pulsations in the neck w/severe disease

117
Q

TR murmur is a ________ murmur along the LSB that _______ with inspiration

A

Holosystolic
Intensifies

118
Q

Diagnostic findings with TR

A

ECG - R axis deviation

CXR - enlarged R heart border & obliteration of the retrosternal window

Echo - diagnostic of choice for evaluation of TR
Evaluation of the severity, valve morphology, R chamber size, RV function
Pulm pressures can be est.

119
Q

Anesthetic mgmt of TR

A

Maintain Intravascular fluid volume
CPS in high-normal range to facilitate adequate RV preload & ventricular filling
HR normal - high
Inotropic support

Avoid: hypeercarbia, hypoxia, hypotension, myocardial depression, N2O (increased PVR)

Techniques to blunt sympathetic response to laryngoscope

Consider peripheral nerve blocks

Nurs 6413 Physiology & Pathophysiology (1 decks)

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