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APEX > Unit 3 - Valvular Heart Disease > Flashcards

Unit 3 - Valvular Heart Disease Flashcards

1
Q

where is the best area to auscultate for aortic stenosis

A

2nd ICS at RSB

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2
Q

what do heart sounds coincide with

A

heart valve closure

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3
Q

what causes heart sounds

A
  • closure of valve leaflets causes valve, intracardiac blood, and heart’s walls to vibrate
  • mechanical energy transmitted throughout the chest, producing an audible sound
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4
Q

can valve opening be heard with a stethoscoepe?

A

nope

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5
Q

what does S3 suggest

A

heart failure (flaccid and inelastic heart)

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6
Q

what does S4 suggest

A

decreased ventricular compliance

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7
Q

S1 correlates with closure of which valves

A

mitral & tricuspid

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8
Q

which heart sound marks the onset of systole

A

S1

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9
Q

with S1, volume is proportionate to:

A

force of contraction

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10
Q

when is S1 louder or softer than normal

A
  • louder: vigorously contracting ventricle
  • softer: poorly contracting ventricle
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11
Q

S2 is caused by closure of what valves

A

aortic & pulmonary

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12
Q

which heart sound marks the onset of diastole

A

S2

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13
Q

heart sound that marks the end of LV ejection and beginning of isovolumetric relaxation

A

S2

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14
Q

in S2, volume is proportionate to:

A

LV pressure decrease at the end of systole

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15
Q

what makes S2 softer or louder

A
  • softer: hypotension
  • louder: HTN
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16
Q

when is S3 heard

A

during the middle 1/3 of diastole, after S2

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17
Q

which heart sound is described as a “gallop rhythm” or rumbling sound

A

S3

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18
Q

what is S4 caused by and when is it heard

A
  • caused by atrial systole
  • heard before S1
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19
Q

where is the aortic area located

A

right of sternal border at 2nd ICS

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20
Q

where is the pulmonic area

A

left sternal border at 2nd ICS

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21
Q

where is the tricuspid area

A

left sternal border 4th ICS (apex)

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22
Q

where is the mitral area located

A

left MCL 5th ICS (apex)

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23
Q

valvular diseases associated with eccentric hypertrophy

A

regurgitant lesions (mitral and aortic regurgitation)

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24
Q

valvular lesions associated with concentric hypertrophy

A

stenotic lesions (tend to produce pressure overload, compensates with thick wall + smaller chamber)

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25
Q

separates atria from ventricles

A

atrioventricular valves (mitral & tricuspid)

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26
Q

what anchors valve leaflets

A

chordae tendinae and papillary muscles anchor to interior of ventricles

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27
Q

what prevents AV collapse during ventricular systole

A

chordae tendinae and papillary muscles

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28
Q

valves that open to let blood exit ventricles

A

semilunar valves (aortic and pulmonary)

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29
Q

which valves are not anchored by chordae tendinae or papillary muscles

A

aortic & pulmonary

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30
Q

what propels blood forward when a valve opens

A

a pressure gradient created inside the cardiac chamber

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31
Q

what prevents blood from moving backward

A

valve closure

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32
Q

how do valves look on TEE

A

“mercedes benz” sign appearance

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33
Q

2 ways a valve can fail

A
  1. stenosis
  2. regurgitation
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34
Q

what causes stenotic valve failure

A

fixed obstruction to forward flow during systole

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35
Q

how does the heart overcome stenotic obstruction

A

requires higher transvalvular pressure gradient to push past stenotic valve

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36
Q

primary vs. secondary valve lesion

A
  • primary: due to problem with valve itself
  • secondary: due to supporting structures, such as ventricular dilation or papillary muscle infarction
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37
Q

how does the heart compensate for stenotic lesions

A
  • adding sarcomeres in parallel
  • chamber wall becomes thicker
  • reduces chamber radius
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38
Q

velocity of blood traveling through stenotic lesion

A

increased

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39
Q

quantities of blood entering the chamber during diastole with regurgitant lesion

A
  • blood returning from lesion
  • regurgitant fraction
  • results in volume overload
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40
Q

do stenotic lesions result in pressure or volume overload

A

pressure

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41
Q

how does the heart compensate for valvular regurgitation

A
  • adding sarcomeres in series
  • to accept a larger volume, chamber radius increases (dilates)
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42
Q

type of heart failure associated with stenotic valvular lesions

A

HF with normal EF

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43
Q

type of heart failure associated with regurgitant valvular lesions

A

HF with reduced EF

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44
Q

what happens to LVEDV following aortic valve replacement for aortic stenosis

A

decreased due to a reduction in impedence to ventricular ejection

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45
Q

where is afterload set in a patient with aortic stenosis

A

at the valve itself

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46
Q

primary regulator of afterload in a normal heart vs. a pt with aortic stenosis

A
  • normal: SVR
  • AS: valve itself
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47
Q

why does a patient with aortic stenosis who undergoes a valve replacement have a lower LVEDV

A

the new valve reduces impedence to LV ejection (afterload) and the heart naturally ejects a larger amount of blood with each beat (increased SV)

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48
Q

normal aortic valve orifice

A

2.5 - 3.5 cm2

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49
Q

aortic valve orifice in severe aortic stenosis

A

less than/equal to 0.8 cm2

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50
Q

mean transvalvular pressure gradient (Lv to aorta) diagnostic for severe AS

A

> 40 mmHg

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51
Q

4 etiologies of aortic stenosis

which is most common?

A
  1. bicuspid aortic valve
  2. calcification of valve leaflets
  3. rheumatic fever
  4. infective endocarditis

1&2 most common

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52
Q

why does a patient with aortic stenosis suffer from pressure overload and increased wall tension

A

the heart must generate more force to eject SV

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53
Q

what is CO dependent on in pts with aortic stenosis

A

HR
also preload dependent???

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54
Q

how does the pressure volume loop change in pt with AS?

A
  • increased ventricular pressure increases the height of PV loop
  • EDV and ESV also increase (shift to right)
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55
Q

law that explains why LV compensates with concentric hypertrophy

A

law of Laplace

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56
Q

key changes in the LV in pts with AS

A
  • thicker LV wall
  • decreased compliance
  • smaller chamber radius
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57
Q

how does compensatory concentric hypertrophy with AS become maladaptive over time

A
  • reduces myocardial O2 supply (subendocardial compression)
  • increases MvO2 (increased heart mass)
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58
Q

what will pt with AS experience as concentric hypertrophy becomes maladaptive

A
  • myocardial ischemia
  • LV failure
  • pulmonary edema
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59
Q

benefits of replacing a stenotic aortic valve

A
  • decreased afterload
  • decreased LV-Ao gradient
  • decreased LVESV
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60
Q

classic triad of severe aortic stenosis

A
  • syncope
  • angina
  • dyspnea
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61
Q

50% survival for the classic triad of AS symptoms

A

syncope = 3 years
angina = 5 years
dyspnea = 2 years

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62
Q

when do pts with aortic stenosis typically develop symptoms

A

when LV dysfunction develops

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63
Q

why is a spinal anesthetic contraindicated with severe AS

A

sympathectomy can cause CV collapse

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64
Q

associated disease in up to 90% of aortic stenosis patients

why

A

acquired von Willebrand disease - because von Willebrand molecule is damaged when it passes through stenotic valve

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65
Q

anesthetic management of which valve lesion is “full, slow, and constricted”

A

aortic stenosis

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66
Q

desired HR in aortic stenosis pt

A

slower side of normal with NSR

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67
Q

why is tachycardia dangerous in aortic stenosis

A
  • decreased time for ventricular filling
  • decreased LVEDV

= decreased SV, CO, ischemia

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68
Q

at a HR of ___ in a pt with aortic stenosis, further HR decrease should be avoided

A

70-80

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69
Q

why does a junctional rhythm or a fib require immediate treatment in a pt with aortic stenosis

A

properly timed atrial kick is required to prime non-compliant ventricle

loss of kick = decreased ventricular filling and SV

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70
Q

how does bradycardia affect pts with aortic stenosis

A
  • decreased CO
  • LV overdistention with compression of subendocardium
  • decreased myocardial o2 supply
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71
Q

why is adequate intravascular volume important in a pt with aortic stenosis

A
  • want increased preload
  • adequate LVEDP required to fill non-compliant LV
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72
Q

LVEDP and PAOP in pts with aortic stenosis

A

overestimate LVEDV

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73
Q

treatment for LV dysfunction in pt with aortic stenosis

A

inotropes

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74
Q

consequences of hypotension in pts with aortic stenosis

A
  • decreased aortic root pressure
  • decreased coronary perfusion pressure
  • myocardial ischemia
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75
Q

how should hypotension be treated in a pt with aortic stenosis

A

alpha-1 agonist - will increase SVR and coronary perfusion pressure without increasing HR

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76
Q

why is CPR ineffective in severe aortic stenosis

A

chest compressions won’t generate a sufficient intracardiac pressure to overcome stenotic aortic valve

SV and CO will be inadequate

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77
Q

results of diastolic failure in advanced aortic stenosis

A
  • increased LAP
  • pulmonary congestion and dyspnea
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78
Q

which neuraxial technique is preferred in aortic stenosis

A

epidural - slower LA onset, more gradual sympathectomy

lower block height is less likely to create HD instability

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79
Q

arterial tracing of aortic stenosis

A
  • vs. normal, has a slower systolic upstroke (pulsus tardus) with delayed peak
  • SV reduced, creates a narrow pulse pressure with waveform of small amplitude (pulsus parvus)
  • dicrotic notch may not be present
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80
Q

valvular lesion associated with pulsus tardus

A

aortic stenosis

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81
Q

valvular lesion associated with pulsus parvus

A

aortic stenosis

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82
Q

why is CO reduced in aortic regurgitation

A

a portion of the SV returns to LV

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83
Q

etiologies of aortic regurgitation

A

incompetent valve or dilation of aortic root or supporting structures

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84
Q

why does the ESV get bigger during isovolumetric relaxation in aortic regurgitation

A

the regurgitant volume is added to the blood volume entering from LA

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85
Q

what happens to the pressure volume loop in aortic regurgitation

A
  • wider (increased ESV)
  • loop for acute is smaller than chronic
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86
Q

3 conditions that increase regurgitant volume (things to avoid)

A
  1. bradycardia (longer diastolic filling time)
  2. increased SVR (increased aorta-LV pressure gradient)
  3. large valve orifice (larger area for blood to return through)
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87
Q

will a pt with aortic regurgitation have pulmonary symptoms?

A

not if the mitral valve is intact

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88
Q

where should cardioplegia be injected into aorta when pt has aortic regurgitation

A

retrograde (throuh coronary sinus) or directly into each coronary ostia

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89
Q

how must cardioplegia be injected in aortic regurg

A

retrograde through coronary sinus or directly into each corornary ostia

(injection into aorta requires functional aortic valve)

90
Q

causes of acute aortic regurgitation

A
  • usually from endocarditis
  • may be from aortic root dissection, aneurysm, trauma
91
Q

why does acute aortic regurgitation lead to rapid CV instabiliy

A

LV becomes acutely dilated with increased wall tension and impaired contractility

may develop LV failure

92
Q

how does LV compensate in chronic aortic regurgitation

A
  • dilates (eccentric hypertrophy)
  • chamber increases to greater degree than wall thickens
  • normalizes wall tension, preserves SV and contractility
93
Q

coronary perfusion pressure in chronic aortic regurgitation

A

reduced because of decreased aortic DBP and rise in LVEDP

94
Q

what happens as LV continues to dilate beyond range of compensatory mechanisms in chronic aortic regurgitation

A
  • wall tension and cardiac mass increase
  • results in decreased compliance, contractility
  • ultimately LV failure
95
Q

why is the volume overloaded ventricle better able to compensate for chronic vs. acute aortic regurgitation

A

chronic develops slowly - can compensate for progressively increasing regurgitant fraction

96
Q

conditions associated with chronic aortic regurgitation

A
  • valvular calcification
  • Marfan syndrome
  • Ehler Danlos syndrome
  • ankylosing spondylitis
97
Q

anesthetic management of which valvular lesion is “full, fast, forward”

A

regurgitant lesions

98
Q

preload goal in aortic regurgitation

A

maintain or increase

some SV is lost to LV, avoid hypotension

99
Q

HR goal in aortic regurgitation

A
  • increased with NSR
  • faster HR reduces regurgitant volume and increases AoDBP and CPP
100
Q

why is a slower HR not desired in aortic regurgitation

A
  • gives more time for SV to flow back into LV instead of moving forward
  • reduces CO, aortic root pressure, and can compromise CPP
101
Q

treatment of LV failure in aortic regurgitation

A

inotrope and vasodilator

102
Q

how does SVR affect aortic regurgitation

A
  • increased afterload increases regurgitant volume
  • lower afterload promotes forward flow into systemic circulation
103
Q

why is phenylephrine not an ideal choice in aortic regurgitation

A

increased afterload increases regurgitant volume

104
Q

PVR goal in aortic regurgitation

A

maintain
- acute LV dilation stretches mitral annnulus
- LV pressure will reflect to LA and pulm circulation
- pulmonary congestion will result

105
Q

why is neuraxial anesthesia beneficial in pts with aortic regurgitation

A

sympathectomy reduces afterload and reduces regurgitant fraction

106
Q

arterial waveform in aortic regurgitation

A
  • sharp upstroke
  • low diastolic pressure
  • wide pulse pressure
  • may have biphasic systolic peaks (bisferiens pulse)
107
Q

valvular lesion associated with bisferiens pulse and why

A

aortic regurgitation - becuase of an additional reflective wave from the periphery

108
Q

anesthetic goals for which valvular lesion - “full, slow, and constricted”

A

mitral stenosis

109
Q

what causes increased LAP in pts with mitral stenosis

A

any condition that increases CO or HR

110
Q

why should N2O be avoided in mitral stenosis

A

increases PVR, increasing workload of right ventricle

111
Q

use of furosemide in pts with aortic regurgitation

A

minimizes pulmonary congestion by reducing preload and LA volume

112
Q

normal area of mitral valve orifice

113
Q

valve orifice in severe mitral stenosis

114
Q

transvalvular pressure gradient and PA SBP in severe mitral stenosis

A
  • LA to LV pressure gradient: > 10 mmHg
  • PA SBP > 50 mmHg
115
Q

most common cause of mitral stenosis

A
  • in developing nations: rheumatic fever
  • in the US: endocarditis and calcification of mitral annulus 2/2 atherosclerosis
116
Q

6 etiologies of mitral stenosis (besides rheumatic fever and atherosclerosis)

A
  1. rheumatoid arthritis
  2. lupus
  3. congenital
  4. left atrial myxoma
  5. carcinoid syndrome
  6. iatrogenic following mitral valve repair
117
Q

how is LV filling maintained in early mitral stenosis

A

increased LAP provides a sufficient pressure to maintain

118
Q

what happens to the LV as mitral stenosis progresses

A
  • pressure gradient (LA-LV) increases
  • LV becomes chronically underfilled
  • net result: overfilled LA, underfilled LV
  • leads to lower EDV, SV, CO
119
Q

how does the body compensate for chronic LV underfilling as mitral stenosis progresses

A

by increasing SVR to maintain BP

120
Q

why can pts with mitral stenosis have pulmonary fluid overload

A
  • increased LAP creates back pressure & contributes to increased pulmonary venous pressure
  • promotes fluid movement into pulmonary interstituim, reduces pulm compliance, increased WOB
121
Q

results of chronic pulmonary fluid overload in mitral stenosis

A
  • causes anatomical changes in pulmonary vasculature, leading to pHTN
  • increases workload of RV, eventually causing cor pulmonale
122
Q

consequences of increased LA pressure and volume in mitral stenosis

A
  • alters anatomy of atrial conduction system
  • can precipitate A-fib (loss of atrial kick = reduced ventricular filling, CO)
123
Q

surgical options for treating A-fib

A
  • Maze procedure
  • pulmonary vein isolation
124
Q

why is tachycardia bad in mitral stenosis

A
  • decreased diastolic filling time
  • decreased time for blood to pass stenotic valve
  • increased LAP
125
Q

treatment of tachyarrythmias in mitral stenosis

A
  • amiodarone
  • beta blockers
  • CCBs
  • digoxin
  • cardioversion
126
Q

drugs to avoid in mitral stenosis

A

drugs that increase HR (anticholinergics, ketamine, atracurium)

127
Q

clinical examples of conditions that increase CO or HR and may increase LAP/lead to pulmonary edema in a pt with mitral stenosis

A
  • thyrotoxicosis
  • infection
  • autotransfusion during uterine contraction
128
Q

effects of hypervolemia in pt with mitral stenosis

A

increases LAP, may cause pulmonary congestion

129
Q

meds to decrease LAP in mitral stenosis

130
Q

what happens to the LA in mitral stenosis

A

undergoes concentric hypertrophy

131
Q

PAOP measurement in mitral stenosis

A

overestimates LVEDV

132
Q

PAOP waveform in mitral stenosis

A
  • prominent a wave
  • decreased y descent
133
Q

effects of systemic vasoconstriction in the setting of low SV and CO in pt with mitral stenosis

A

increases SVR, preserves BP

134
Q

why should a rapid increase in SVR be avoided with mitral stenosis

A

elicits a baroreceptor-mediated rise in HR

135
Q

hypotension treatment in pt with mitral stenosis

A

vasoconstrictor such as phenylephrine or vasopressin (not ephedrine)

136
Q

PVR goals in mitral stenosis

A

avoid conditions that increase (increases RV workload):
- acidosis
- hypercarbia
- hypoxia
- lung hyperinflation
- N2O
- Trendelenburg

137
Q

considerations for neuraxial anesthesia in mitral stenosis patients

A

if the pt has Afib, likely anticoagulated and should not receive a neuraxial block

138
Q

neuraxial is a safe option if INR is ?

139
Q

why is ephedrine not a good choice for hypotension with mitral stenosis

A

it will increase HR

140
Q

3 things that make regurgitant volume worse

A
  • bradycardia
  • increased LV to LA pressure gradient
  • increased SVR
141
Q

etiologies of mitral regurgitation

A
  • rheumatic fever
  • ischemic heart disease
  • papillary muscle function
  • ruptured chordae tendinae
  • endocarditis
  • mitral valve prolapse
  • LVH
  • lupus
  • rheumatoid arthritis
  • carcinoid syndrome
142
Q

patho of mitral regurgitation

A

SV goes in 2 directions - towards the aorta and through the incompetent mitral valve towards LA

leads to volume overload of LA & LV

143
Q

pressure volume loop of mitral regurgitation

A
  • ventricular volume gets smaller during isovolumetric contraction
  • acute loop always smaller than chronic
144
Q

4 conditions that increase regurgitant volume of mitral regurgitation (things to avoid):

A
  1. slower HR
  2. increased pressure gradient between LV and LA
  3. increased SVR
  4. increased size of valve orifice
145
Q

when does regurgitation occur with mitral insufficiency

A

during systole (isovolumetric contraction)

146
Q

how does HR affect mitral regurgitation

A

faster HR reduces time spent in systole (when regurgitation happens) and reduces regurgitant fraction

147
Q

why is a higher preload better in mitral regurgitation

A

helps compensate for SV lost to LA

148
Q

is PAOP a reliable measure of LV filling pressure with mitral regurgitation?

A

no - overestimates LVEDP

149
Q

PAOP waveform in mitral regurgitation

A

enlarged v wave (represents regurgitant volume passing through incompetent mitral valve)

150
Q

how does SVR affect mitral regurgitation

A
  • systemic vasodilation promotes forward flow
  • systemic vasoconstriction increases regurgitant volume
151
Q

risk after mitral valve repair

A

systolic anterior motion (SAM) of anterior leaflet - obstructs LV outflow tract during systole

152
Q

treatment if SAM is suspected or verified with TEE

A
  • increasing intravascular volume
  • increasing afterload with alpha agonist
153
Q

SAM is very similar to what other cardiac disease

A

hypertrophic cardiomyopathy

154
Q

PVR considerations in pt with mitral regurgitation

A

avoid conditions that increase PVR (increases workload of RV)
- acidosis
- hypercarbia
- hypoxia
- lung hyperinflation
- N2O
- Trendelenburg

155
Q

how can sympathectomy compromise coronary perfusion pressure in mitral regurgitation

A

if AoDBP is drastically reduced

156
Q

valvular disorders assoc. with systolic murmur

A
  • mitral regurgitation
  • aortic stenosis
157
Q

what phase of cardiac cycle is mitral regurgitation an issue

A

during isovolumetric contraction during systole

158
Q

what phase of cardiac cycle is aortic regurg an issue

A

isovolumetric relaxation of LV during diastole

159
Q

during what phase of cardiac cycle is mitral stenosis problematic

A

during atrial systole (atrial kick), which occurs during ventricular diastole

160
Q

mnemonic for aortic stenosis murmur

A

ASSS
Aortic Stenosis is a Systolic murmur heard at right Sternal border

161
Q

LV pressure in aortic stenosis

A

can exceed 350 mmHg

162
Q

why might aortic stenosis murmur be confused with carotid bruit

A

sound is transmitted through upper aorta and carotid arteries

163
Q

valvular disease with a systolic murmur that may be palpated as a thrill

A

aortic stenosis

164
Q

murmur in severe AS

A

may decrease in intensity - not enough flow passes to make a sound

165
Q

mnemonic for aortic regurgitation murmur

A

ARDS
Aortic Regurgitation is a Diastolic murmur heard at right Sternal border

166
Q

high pitched “blowing” murmur

A

aortic regurgitation

167
Q

which is louder - aortic stenosis or aortic regurgitation

A

aortic stenosis - less pressure gradient with regurg

168
Q

mnemonic for mitral stenosis murmur

A

MSDA
Mitral Stenosis is a Diastolic murmur heard at the Apex and left Axilla

169
Q

which murmur is an opening snap followed by low intensity rumbling murmur

A

mitral stenosis

170
Q

holosystolic murmur characterized by loud “swishing” sound

A

mitral regurgitation

171
Q

mnemonic for mitral regurgitation

A

MRSA
Mitral Regurg is a Systolic murmur heard at Apex and left Axilla

172
Q

most common valves used in TAVR

A
  • Edwards SAPIAN
  • Medtroinc CoreValve
173
Q

why are TAVR pts at risk for allergic reaction and renal injury

A

radiocontrast dye used

174
Q

3 surgical approaches to TAVR

A
  1. transfemoral
  2. transaortic
  3. transapical (antegrade)
175
Q

benefits of TAVR

A

sternotomy and CPB not required

176
Q

aortic valve replacement that requires balloon valvuloplasty prior to deploying replacement valve

A

SAPIAN valve

177
Q

unique feature of SAPIAN valve

A

need for rapid ventricular pacing

178
Q

why is rapid ventricular pacing used in SAPIAN TAVR

A

promotes cardiac standstill during valvuloplasty and valve deployment (reduces motion caused by ventricular ejection, makes it easier to get the valve into correct position)

179
Q

when should profound hypotension be anticipated with SAPIAN TAVR

A

rapid ventricular pacing (CO will be near 0 during this time)

180
Q

anesthetic considerations for SAPIAN TAVR

A
  • ensure MAP > 75 before rapid ventricular pacing helps patient restore BP after valve deployment
  • consider prophylactic vasopressors before rapid ventricular pacing
  • apnea required during valve deployment
181
Q

why should radiotranslucent pads be placed prior to drapes in SAPIAN TAVR

A

if pt doesn’t resume NSR after rapid ventricular pacing, defibrillation may be required

182
Q

CoreValve vs SAPIAN valve for TAVR

A

corevalve does not require valvuloplasty (the valve is self-expanding) or rapid ventricular pacing

183
Q

methods to assess new valve function after a TAVR

A

TEE and fluoro

184
Q

what are TEE and fluoro used to assess after TAVR

A
  • valve function
  • presence of aortic regurgitation
  • perivalvular leak
  • vascular injury
185
Q

feared complication of TAVR

A
  • mispositioned valve
  • if the valve doesn’t deploy properly, patient will develop aortic regurgitation
186
Q

treatment of a SAPIAN valve that doesn’t deploy correctly

A

another valve must be replaced through mispositioned valve

“valve-in-valve” procedure

187
Q

treatment of a CoreValve TAVR that doesn’t deploy properly

A

can be retrieved and redeployed

188
Q

complication to suspect with acute HD instability with TAVR

A

vascular injury

189
Q

complication to rule out if pt has s/s myocardial ischemia after TAVR

A

coronary occlusion from native valve folds or mispositioned new valve obstructing coronary artery

190
Q

complication of TAVR that may require aortic root repair or replacement

A

valvuloplasty can cause annular rupture (tamponade and CV collapse)

191
Q

9 complications of TAVR

A
  • malpositioned valve, acute aortic regurg
  • vascular injury
  • coronary occlusion
  • annular rupture
  • stroke
  • perivalvular leak
  • pericardial tamponade
  • AV block
  • LBBB
192
Q

what is a critical acute complication of an improperly placed valve during TAVR

A

wide open aortic regurgitation

193
Q

what are 2 unique needs when deploying a SAPIAN valve

A
  1. cardiac standstill via rapid ventricular pacing (160-200 bpm)
  2. balloon valvuloplasty
194
Q

why might a pt have LV dilation after a TAVR

A

a malpositioned valve can cause acute aortic insufficiency - can cause LV dilation as a function of increased pressure and volume

195
Q

what heart sounds are best using the bell of the stethoscope

A

S3, S4
(lower pitched sounds)

196
Q

what heart sounds are best heard with the diaphragm

A

higher-pitched heart sounds such as S1 and S2

197
Q

are diastolic murmurs best heard with diaphragm or bell

198
Q

the presence of an S1 murmur at MCL 5th ICS most likely suggests:

A

mitral regurgitation

199
Q

hallmark of HFrEF

A

decreased ejection fraction with increased EDV

200
Q

what hypertrophies in mitral stenosis

A

the LA - must generate a higher pressure to push past stenotic mitral valve

201
Q

how does the heart compensate for pressure overload in mitral stenosis

A

concentric hypertrophy of LA (parallel replication of sarcomeres)

202
Q

CVP and PAOP goals in aortic stenosis

A

high/normal

203
Q

why is it necessary to keep SVR high in pts with aortic stenosis

A

to help perfuse coronary arteries (afterload set by stenotic valve, CPP = AoDBP - LVEDP)

204
Q

when is the risk of SAM after mitral valve replacement increased

A

when the anterior leaflet is longer than the posterior leaflet or when there is a narrow angle between mitral annulus and aortic annulus

205
Q

pharmacologic treatment of SAM

A

(same as hypertrophic cardiomyopathy)

  • made worse by vasodilators and inotropes
  • improved by vasoconstrictors and volume expansion
206
Q

best treatment for hypotensive patient with mitral stenosis

A

phenylephrine or vasopressin - want to avoid meds that increase HR

207
Q

primary management goal of mitral valve prolapse

why

A

prevent excessive cardiac emptying

  • large ventricle tends to reduce MVP
  • small ventricle tends to increase MVP
208
Q

things to avoid to keep the heart full in MVP

A
  • SNS stimulation
  • decreased SVR
  • hypovolemia
  • reverse Trendelenburg, sitting
209
Q

why is ketamine avoided in mitral valve prolapse

A

activates SNS, increases contractility, augments LV emptying

210
Q

consequence of increased LAP in severe mitral stenosis

A

pulmonary edema

211
Q

which valve disease does this represent

A

aortic stenosis

212
Q

which valve disease is seen

A

aortic stenosis

213
Q
A

aortic regurg

214
Q
A

mitral stenosis

215
Q
A

mitral regurg

216
Q

anesthetic goal for pts with mitral valve prolapse

A

prevent excesive cardiac emptying

217
Q

things to avoid in pts with MVP

A
  • SNS stimulation
  • upright position
  • hypovolemia
  • decreased SVR
218
Q

why should ketamine be avoided in pts with MVP

A

activates SNS, ↑ contractility, augments LV emptying

219
Q

which valve disorder is assoc. with parallel replication of sarcomeres in left atrium

A

mitral stenosis

220
Q

most common dysrhythmia assoc. with mitral stenosis

APEX (54 decks)

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