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Medicine II > Valvular Heart Disease > Flashcards

Valvular Heart Disease Flashcards

1
Q

doppler effect

A

as the police siren travels towards you, the frequency of the wave (pitch) appears to be higher than if it was stationary; as the siren travels away, the pitch appears to be lower.

change in pitch coming off the red cells

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2
Q

aliasing effect

A

when the velocity gets higher than the maximum velocity of blood flow away

seen as yellow
aliasing is an effect that causes different signals to become indistinguishable (or aliases of one another) when sampled

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3
Q

two most common valvular dzs

A

aortic stenosis and mitral regurg are the two most common valve disease

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4
Q

what should you be weary of in a pt with a bicuspid aorta

A

strong correlation between bicuspid valve and marfans syndrome which results in an aneurysm and rupture

if you hear that there is a bicupid valve in the aorta it is essential to do an echo to look for aneurysm

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5
Q

congenital types of aortic stenosis

A

” Bicuspid AS: MC of these (usually aortic valve is TRIcuspid)
“ Membranous subvalvar
“ Fused leaflets w/ doming

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6
Q

acquired degenerative types of aortic stenosis

A

Calcific AS: MC type you will see (RF: smoking, HTN, hyperlipidemia, DM - same RF as CAD)
Thickening & calcification develops @ 40-60yo

Hypertrophic subaortic: need an echocardiogram to distinguish

Rheumatic heart dz - caused by AS but affects mitral valve more than aortic

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7
Q

what % of the population has aortic stenosis

A

1% of population w/ M>W;

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8
Q

what is th epathophysiology of AS

A

aortic leaflets do not oppen and pressure in the LV increases in order to compensate with increased

results in muscle hyeprtrophy

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9
Q

early phase of aortic stenosis is seen as

A

diastolic dysfunction - heart stiffens/can’t relax, smaller chamber, reducing amnt of blood it can receive

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10
Q

late phased of AS

A

” Late Phase: systolic de-compensation - muscles can’t keep up w/ pressure

reduced EF

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11
Q

What type of pulse pressures do we see at the end stage of AS

A

b/c fall of ejection fraction; drop in amount of blood w/ each beat (difference in systol/diast pressures narrows) –> HYPOTENSION

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12
Q

classic triad of AS

A

Angina - d/t supply/demand mismatch when O2 demand of hypertrophied LV (& CAD) exceeds supply –>5yr survival AVR

CHF (diastolic & systolic) - bad if present –> 2yrs

Stokes-Adams attacks - exertional (pre-syncope + syncope); from reduced stroke volume & inadequate cerebral perfusion —>3yr AVR

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13
Q

why do we see angina in AS

A

NO obstruction in the coronary artery

the muscle needs a certain amt of oxygen and the coronary flow can not keep up

the result of this is exertion angina

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14
Q

most common presentation of AS

A

diastolic HF

LA pressure rises in order to fill LVE and backup leads to the lungs

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15
Q

Stokes-Adams attacks

A

(pre-syncope + syncope); from reduced stroke volume & inadequate cerebral perfusion –>3yr AVR

classically seen on the end of exertion when the peripheral vasculature is still dialated

person slows done and sympathetic tone falls

dip in blood pressure followed by a loss of consciousness

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16
Q

murmur we hear with AS

A

SYSTOLIC (harsh) ejection murmur

thrill (palpable murmur), over aortic area radiating to carotids; high enough energy sound can be felt

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17
Q

when do you hear the murmur with AS and what does it sound like

A

” Mid-systolic crescendo decrescendo mumur

which peaks later in systole w/ worsening severity

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18
Q

if you can feel the artery filling through your finger tips which could happen with AS what is this indicative of

A

Delayed arterial upstroke - reduction in stroke volume (hypertrophy = small chamber)

felt as a quick tap

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19
Q

pulse pressure with AS

A

” Narrow pulse pressure - brisk, weakened, delayed = pulsus parvis

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20
Q

what heart sounds do we hear with AS (describe S2)

A

” Soft S2 - leaflets snapping, S4 present if LVH

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21
Q

prognosis of AS

A

Long interval of compensation as stenosis develops; once sxs occur (angina, CHF, syncope) –> Pt is DOOMED!

When HF starts to occur í RAPID deterioration w/ poor prognosis at the point of decompensating, especially if patient is symptomatic

very

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22
Q

1 diagnostic test used for diagnosing AS

A

red cells have to really speed up and you can measure this velocity with an echocardiogram

o ↑ leaflet thickness (don’t open well) & echodensity w/ ↓ excursion on structural views
o ↑ systolic velocity of blood flow w/ reduced valve area on Doppler measured
o Aortic valve calcif

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23
Q

Echo aortic valve area and continuity equation

A

Echo aortic valve area: flow rate is constant regardless of where it’s measured.

things don’t pile up

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24
Q

place of cardiac catheterization

A

Cardiac catheterization primarily to evaluate coronaries b/c CAD frequently

can be used to measure the gradient across the valve

first measuring the pressure in the LV

210 in the LV
130 in the aorta

that is the gradient

you can calculate the valve area and the restriction

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25
Q

Tx of aortic stenosis in a pt with sxs of diastolic dysfunction

A

CHF from diastolic dysfunction: Diuretics

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26
Q

Tx of aortic stenosis in pt

A

For classical triad of angina, CHF (systolic dysfxn), Stokes-Adam attack, mechanical intervention: valve replacement or balloon valvuloplasty

increase the valve a little bit but you see restenosis in a good portion of this pt

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27
Q

conventional surgical valve replacement : advantages and disadvantages of mechanical

A

mechanical: indefinite durability advantage but requires chronic anticoagulation

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28
Q

conventional surgical valve replacement : advantages and disadvantages of Heterograft (tissue)

A

good for AS at young age; anticoag NOT necessary in absence of Afib; durability finite but w/ the modern ways of treating the tissue before the valve is put in durability is longer

often times pt die before the end of the valve

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29
Q

what is the most common surgical tx of AS

A

heterograft from bovines

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30
Q

human valve replacement

what is it called and what are the advantages and disadvantages

A

Homograft - at one time more durable; rarely used

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31
Q

TAVR

A

Transcatheter Aortic Valve Replace

tissue valve is sewn into a metallic stent

balloon is inserted in the femoral artery, threaded up to the heart and placed in the aortic valve

32
Q

where would we find the PMI in a pt with AS

A

” Medially displaced PMI (should be at 5th intercostal space, mid-clavicularly)

33
Q

where is the murmur of AS best heard

A

” Systolic “ejection” crescendo-decrescendo @ RUSB

34
Q

other than cardio findings what would we see in the PE of a pt with AS

A

” Rales & other CHF signs

35
Q

pulsus parvis et tardus

A

slow-rising pulse and anacrotic pulse, is a sign where, upon palpation, the pulse is weak/small (parvus), and late (tardus) relative to its expected characteristics. It is seen in aortic valve stenosis.

36
Q

chronic I causes of Aortic Regurgitation

A

HTN (& other root dilation)

Atherosclerosis

Aortic Stenosis:
so stiff that they don’t come together well

Prosthesis (leaflet vs. perivalvular)
in a mechanical leaflet if not on anticoagulants you can have soft tissue growth into the valve region or leaflet develops a tear

Endocarditis: causes both leaflet and perivalvular

CT Dz - Marfan’s (dilation of aortic root)

Inflamm dz - Lupus, RA

37
Q

Chronic II causes of aortic regurg

A

Congenital dz (Bicuspid, vent septal defect)

Sinus of valsalva Aneurysm
most common rupture is the one adjacent to the right side of the heart

Aortitis
Rheumatic: doesn’t affect the aortic valves but can stiffen leaflets

3˚ Syphilis

38
Q

potential etiologies of acute aortic regurgitation

A 
rapid brkdown: 
aortic dissection (MC reason - infection chews through valve & leaflet ruptures), 
endocarditis
trauma
rheumatic fever
valve prosthesis
rupture of sinus of Valsalva aneurysm
39
Q

pathophysiology of aortic rugurg

A

Opposite problem of AS. No restriction of opening í instead, leaflets do NOT come together in diastole í so blood regurgitates from aorta back to LV d/t dilation of aorta í MC d/t HTN

Blood regurg into LV in diastole 2˚ widening/aneurysmal ∆ of aortic annulus

LV dilates and increase stroke volume to maintain CO

40
Q

acute decompensation of aortic regurg causes

A

diastolic pressure rises so high

pulmonary congestion

41
Q

chronic decompensation of aortic regurg causes

A

LV systolic failure

42
Q

what type of pulse pressure would we see with aortic regurg

A

diastolic pressure falls and systolic pressure increases resulting in a wide pulse pressue

43
Q

Common presentation with aortic regurg

A

” CHF - dyspnea on exertion, orthopnea, fatigue
“ Palpitation - awareness of heartbeat
í increased SV + arrhythmia (↑HR)

44
Q

water hammer pulse refers to

A

” LRG Stroke Volume (bounding pulse):

Rapid upstroke

45
Q

what type of heart sounds would you hear with aortic regurg

A

Systolic flow murmur louder than diastolic
you really need to play close attention for the diastolic murmur

Diastolic decrescendo (blowing) murmur after S2, radiating to LSB & apex - high pitch!

46
Q

” Severe AR is heard as what heart sound

A

AUSTIN FLINT Murmur/ mitral valve rumble

47
Q

why is the diagnosis of aortic regurg so difficult to make?

A

decomposition is severe
severe SOB w/in 30min

CXR is white
severe pulm edema
but you see a NORMAL HEART SIZE

most people with congestive heart failure you would see enlargement of at least one chamber of the heart

(pulmonary problem= right side enlargement)

Inaudible murmur (low output, wide open valve, noisy respiration)

diastolic pressure may not be low

you should be able to hear the first heart sound in someone BUT the mitral leaflets are already touching each other and don’t hit each other

S1 is MISSING because the mitral valves are closed due to high pressure

48
Q

why do you not hear a murmur with Acute severe AR

A

sudden severe rupture of a leaflet and you need turbulence for a murmur but if it is wide open there is no turbulent flow

49
Q

why is the diastolic pressure normal with acute severe AR

A

left ventricle is so small that it can’t accept much flow

back flow causes pressure to rise

periphery is clamped down with low CO

diastolic pressure doesn’t drop very much

50
Q

diagnostic of AR

A

” ECHO-Doppler - 1st Tx of Choice

REGURGITATION WITH DOPPLER

” Regurgitation by Doppler
“ Abnormal structures - vegetation, dialted root
“ LV size and Function

51
Q

indications of cardiac cath for diagnosis of AR?

A

: not needed for dx - but can evaluate if pt has other valvular lesions or check for CAD

52
Q

Transesophageal can be used to see what with AR

A

abscess vegetation, aortic dissection

53
Q

prognosis of pt with chronic AR

A

” Long period of compensation w/o sxs
“ Gradual LV ENLARGEMENT w/ norm systolic fxn

Sxs and/or LV dysfxn assoc w/ RAPID deterioration
LV systolic dysfxn w/o sxs = RARE!

if the person has sxsx you usually see reduced EF

54
Q

Tx of aortic regurgitation

A

Tx of Choice: Afterload reduction (vasodilators) to encourage forward flw

Abx prophylaxis pre-procedure

CHF treatment: diuretics

55
Q

when is surgical tx of AR indicated for acute?

when is indicated for chronic?

A

Surgical Valve Replacement

o Acute, severe AR is emergency

oChronic AR: sxs, sys dysfxn, progressive LV dilation (>55cm)

AVR w/ endocarditis is often successful

56
Q

Mitral Regurgitation common chronic causes

A 
"	MCC coronary dz (papillary muscle malfunction)
"	LV dilatation, any cause
"	Endocarditis
"	Myxomatous degeneration/prolapse
"	Rheumatic
"	Other CT dz
"	Congenital - lupus, Marfans
57
Q

common causes of acute mitral regurg

A

Acute:
“ Chordal rupture: myxomatous, endocard, trauma
“ Papillary rupture: infarction, trauma
“ Acute papillary ischemia (usually circumflex - REVERSIBLE!)
“ Valve perforation: endocarditis

Dilation = regurgitation

58
Q

what myocardial changes will we see in MR

A

” Blood regurg into LA in SYSTOLE –> LVH comps by enlarging

Chronic MR: LV systolic failure, LV becomes weak
- Regurg unloads LV in systole reducing LVES volume

59
Q

what do we see as the result of acute MR

A

Acute MR: congestion, can cause pulmonary edema

60
Q

what type of HF do we see with MR

A

” 1st L then 2nd R CHF

61
Q

murmur seen with MR

A

Mid-systolic click and late systolic murmur (usually from S1-S2)

–>

Typically holosystolic murmur

  • Papillary dysfxn
  • Prolapse after click
62
Q

PMI in MR

A

LV enlargement if chronic (PMI)

displaced

63
Q

sxs of chronic MR decompensation

A

” Typical CHF signs - dyspnea, orthopnea, paroxysmal nocturnal dyspnea, fatigue

64
Q

EKF of MR

A

non-specific findings, tell you nothing abt etiology
“ LVH
“ LAA - left atrial abnorm
“ A-Fib

65
Q

CXR finding with MR

A

” LA enlargement - splaying of bronchi
“ LV enlargement
“ CHF

66
Q

MR echocardiogram how to diagnose (2 ways)

A

Semi-quantitative MR estimation
(depth/width of jet, vol of LA filled)

Quantitative (orifice area, analogous to aortic

can see moicardial infarction hx
Lv function an ot

67
Q

indications of cardiac cath for MR

A

Cardiac catheterization
“ Etiology &/or other dz (CAD)
“ Large V wave in pulmonary wedge pressure, LV size & contractility confirmed
Hemodynamic effects: output & RH pressures

68
Q

TX for MR

A

Medical:

Analogous to AR; vasodilator (afterload reduction - ACE-I) so less backflow

  • Tx underlying dz
  • Endocarditis prophylaxis
  • Pther tx for CHF & arrhythmias PRN
69
Q

when is surgery indicated for MR

A

Timing was hardest issue, easy now b/c adv tech

  • Perform when symptomatic despite Rx
  • Before LV deteriorates: post-op afterload is higher

if the EF if abnormal before mitral valve replacement it would be worse than before

70
Q

surgical tx for MR

A

Valve repair is INCREASINGLY COMMON

  • Shorten or reattach chords
  • Tuck leaflets
  • Reduce annular diameter w/ ring

Catheter based

Repeat w/ clips and/or annular rings (mitraclip approved)
Replace valve (valves that are delivered on a cather are developing)
71
Q

causes of Tricuspid regurgitation

A

anything that causes failure to the right ventricle
dilation of the tricuspid ring can be caused by pulmonary HTN

RV failure or dilatation - not structural abnormality:
“ Pulm HTN–> RV dilation + tricuspid regurg d/t:
o Primary = RARE
o 2ndary: COPD, intracardiac shunts, LV failure, mitral dz, Eisenmenger synd (End stage vol overload: atrial/ventricular septal defect)

Endocarditis: IVDU -tricuspid is the valve of choice for this population
Rheumatic: very rare as primary lesion

72
Q

what fo we see in the neck tricuspid regurgitation

A

” Large V waves in jugular veins (JVD)

venus pulsations

73
Q

murmur heard with tricuspid regurg

A

no murmur because of the low pressure

74
Q

sxs of tricuspid regurg

A

” peripheral edema
“ ascities
“ ↓exercise tolerance

75
Q

tx of tricuspid regurg

A

Medical TX of CHOICE: diuretics (usually all you need)

–>Tx underlying condition

76
Q

surgical tx for tricuspid regurg

A

Surgical:
MUST Tx primary lesion (ex: mitral) - sometimes that is enough
Tricuspid annuloplasty w/ ring

Valve Replacement = UNCOMMON!

Medicine II (21 decks)

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