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CSI > valvular heart disease > Flashcards

valvular heart disease Flashcards

1
Q

heart sounds

A

S1: closure of AV valves at start of ventricular systole
S2: closure of semilunar valves at start of ventricular diastole
S3: sound of rapid filling of ventricles during early diastole
S4: sound of late filling from atrial kick in late diastole
Valve opening normally not heard

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2
Q

abnormalities

A

slide 4-6

esp fixed splitting of S2
myxomas and pericardial knot (S3) may mimic valvular disease

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3
Q

causes of high frequency sound in early diastole

A

slide 7

more 8,9

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4
Q

how to approach pt with VHD

most important question to ask about valvular condition ??

A

Correctly diagnosing the affected valve
Estimating severity
Judging its effect on the myocardium
Deciding on antibiotic prophylaxis (not necessary for mitral valve prolapse)
Deciding on timing of surgery or catheter-based intervention

what is the condition’s effect on the cardiac muscle?? esp. LV

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5
Q

5 finger approach

A

H/P, labs, EKG, XR, cardiac testing (i.e. ECHO)

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6
Q

Aortic Stenosis:

etiology
hx

A

Etiology
Senile calcific
bicuspid: more turbulent flow, have symptoms younger (think associated with aortipathies (coarctation, etc) if with coarctations and headache, think: berry aneurysm
rheumatic HD (more mitral)
congenital (uni/quad cuspid valves, present early–>respond to valvuplasty)
Paget’s, ESRD

History
long latent period
Angina, Syncope (fixed obstruction and cannot augment CO under conditions of low SVR; ie: meds, vasovagal), CHF

FA: syncope, angina, dyspnea on exertion (SAD)

angina: 50% 5 yr mortality
syncope: 50% 3 yr mortality
CHF: 50% 2 yr mortality
no meds shown to reduce progression of aortic stenosis

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7
Q

aortic stenosis exam:

A 
Harsh, late-peaking SEM (sys. ejection murmur) radiating to the neck, palpable systolic thrill, sustained LV impulse, pulsus parvus et tardus, 
S2 single (A2 is absent), paradoxical split S2 (A2 closure takes longer), S4 gallop (heard when diastolic dysfunction)
Prolongation of LV ejection due to severe outflow obstruction
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8
Q 
aortic stenosis 
EKG??
CXR??
more dx
sx?
A

EKG: LVH, LBBB

CXR
AV calcification, cardiomegaly, LV prominent without dilation

Echo (test of choice): measure doppler gradients,
severe AS if valvular area:

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9
Q

hypertrophic cardiomyopathy

A

biphasic: old and young
ddx from aortic stenosis

provocative maneuver:
valsalva: gets louder

small LV cavity bc wall is enlarged–>turbulence
make cavity smaller–>lower
dec. venous return into right heart->less blood in LV–>smaller cavity–>louder

softer with squatting: pushing more blood into heart–>larger LV–>less turbulence–>softer murmur

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10
Q

hypertrophic cardiomyopathy

ddx from aortic stenosis

A

after PVC: same PP in AS

PP gets smaller in hypertrophic myopathy

Brockenbrough phenomenon

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11
Q

Aortic stenosis time course charts

A

slide 12

long latent period

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12
Q

valve replacement

A

bioprosthetic (for oldies: last 10-15 yrs) don’t need anticoagulation

mechanical: for younger pts (need anticoagulation)

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13
Q

TAVR

A

transaortic valve replacement

access from groin
transapical
typically transferal

valve placed on stent and expanded, “crushing” old bad valves, open/closed based on heart pressure gradients
no opening of chest, good for old ppl

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14
Q

aortic stenosis parameters

A

slide 15

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15
Q

criteria for sx

A

EF falls below 50

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16
Q

LV outflow tract obstruction

A

supravalvar AS

congenital, assoc. with William’s syndrome

narrowing above valve

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17
Q

Subvalvular membrane:

subvalvular AS

A

congenital flap of tissue obstructing valve (before it) and may be a/w coarctation as part of *Shone’s syndrome mitral stenosis due to supravalvular MV membrane, LVOT obstruction, coarctation

needs sx

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18
Q

mean gradient of 40

A

get measurement from echo

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19
Q

using doppler probe (ECHO) measure velocity and convert velocity into pressure

A

Bernule formula

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20
Q

if CAD (3 vessel disease) along with AS

A

might as well replace AS w/ angioplasty

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21
Q

Aortic Regurgitation/insufficiency (Chronic) etiology

A

Aortic root dilation from HTN (–>dissection, aneurysm), CMN, bicuspid valve, ankylosing spondylitis, syphilis, RA
(secondary: something stretching leaflets open)

(primary: problem with leaflets)

FA: endocarditis, RF

long latent period
can have combo AI/AS

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22
Q

Aortic Regurgitation (Chronic) Hx

A

Dyspnea, Angina, Fatigue, CHF

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23
Q

Aortic Regurgitation (Chronic) exam

A

Wide pulse pressure, low diastolic pressure, bounding pulses (quick rising), laterally displaced PMI, long decrescendo diastolic murmur along LSB if valvular or RSB if aortic root etiology, Austin-flint murmur at apex (diastolic MR; MV struck by regurgitant jet–>you will not hear loud S1 or OS which is c/w mitral stenosis), S3 gallop (with dilated ventricle)

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24
Q

Aortic Regurgitation (Chronic) eponyms (FYI?)

A

Quinckes pulse, DeMusset’s sign (head bobbing from such strong pulse, uvula can vibrate) duroziez sign, bisferiens

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25
Q

AR (AI)
EKG?
imaging?

A

ECG: LVH

CXR
Cardiomegaly, boot-shaped heart, LV enlargement

Echo, cath: can see how much blood flowing backwards

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26
Q

AI: timing of sx

A

Symptoms, EF 55

EDD >75

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27
Q

chronic AI tx

A

Vasodilator therapy (ACE-Inh/ARB/Nifedipine)

don’t use B-blocker, will prolong diastole??

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28
Q

Remember, in chronic AI, the LV has time to adapt with ?? and ?? with each contraction without increasing LVEDP…eventually, this compensatory mechanism ??

A

eccentric myocyte hypertrophy
and larger SV

fails
then forward CO will diminish and will have higher LVEDP (back flow) and pulmonary congestion

29
Q 
Aortic Regurgitation (Acute)	
etiology??

hx?

A

Etiology
*Endocarditis, *Aortic dissection, ruptured sinus of Valsalva aneurysm

History
Acute pulmonary edema

severe! goes straight back into longs

30
Q

Aortic Regurgitation (Acute) exam

A

Short diastolic murmur, faint S1
(brief but severe)
may not hear murmur

31
Q 
Aortic Regurgitation (Acute) EKG?
imaging?
A

ECG: Not helpful

CXR
Normal heart size, pulmonary edema

*ECHO
TEE (look for dissection)
cath (no time)

doppler probe: see diastolic flow

32
Q

AI acute timing of sx

A

urgent

33
Q

causes of AI

A

slide 23

34
Q

Mitral Regurgitation (Chronic) etiology

A

primary (leaflet problem) MVP (mitral valve prolapse), mitral myxomatous disease, rheumatic (more likely MS)

FA: LV dilatation

secondary (pulls annulus open: ischemic (dysfunctional papillary muscles), dilated cardiomyopathy)

35
Q

Mitral Regurgitation (Chronic) hx

A

Late-onset of CHF, later R-heart failure

long latent period

36
Q

C MR: exam

A

Apical holosystolic murmur radiating to axilla, S3 gallop and wide-split S2

37
Q

C MR: EKG

A

LAE, LVH, afib (if LA dilates enough)

LV dysfunction from overloaded state

38
Q

C MR: imaging

A

CXR: Cardiomegaly, LV/LA enlargement, pulmonary venous redistribution

Echo, cath

EF should be >65 (supra-normal)

39
Q

C MR: timing of sx

A

Symptoms,
EF40

almost never for secondary MR

40
Q 
Mitral Regurgitation (Acute)
etiology

hx??

A

post-MI complication -
papillary muscle rupture in setting of MI
(supplied by RCA: posterior-medial supply)

Endocarditis
Acute pulmonary edema

41
Q

Mitral Regurgitation (Acute) exam

A

Decrescendo systolic murmur radiates to neck if posterior leaflet and back if anterior leaflet, loud P2, widely split S2
(may be soft, happens rapidly)
FA: holosystolic, high-pitched “blowing”

42
Q

Mitral Regurgitation (Acute) EKG

A

Sinus tachy, AMI changes

43
Q

Mitral Regurgitation (Acute) imaging

A

CXR
Pulmonary edema, normal heart size, cardiomegaly, LA, LV enlargement

Echo, cath
Flail leaflet, large v waves

44
Q

Mitral Regurgitation (Acute) timing of sx

A

Urgent, can temporize with vasodilators or IABP

put in balloon pump
decrease afterload (not if AI)

does not prolong life for secondary MR unless refractory symps or doing sx anyways

“mitral clip”

45
Q

MVP click changes with maneuvers

A

Squatting:
The click moves closer to S2 (more blood in R and L heart->more filling–>longer time before click happens–>closer to S2)

Standing:
The click moves closer to S1
(less blood–>valve clicks earlier, closer to S1)

46
Q

MVP in who

A

thought to be female, palpitations, anxiety

actually equally men as well: serious progression (also with oldies)

mid-systolic opening click
late systolic crescendo murmur

predispose to inf. endocarditis
etiology: myxomatous degeneration (often 2nd to Marfan/Ehlers-Danlos syndrome), RF, chordae rupture

47
Q

Mitral Stenosis etiology

A

RHEUMATIC esp. immigrants
calcific
FA: can result in LA dilatation

48
Q

Mitral Stenosis hx

A

Late-onset of CHF, later R-heart failure, a fib, dyspnea (criteria for sx)

(LV is protected?? eventually doesn’t fill, low CO)

49
Q

Mitral Stenosis exam

A

Diastolic rumble at apex, short S2-OS (opening snap) interval, loud P2, RV heave

The longer the murmur and the shorter the time from S2-OS-more severe* , high pressure
(if no longer hear OS: no longer pliable, end stage)

Anything that increases the gradient will increase the murmur intensity
(diff to hear)

increase HR–>higher the diastolic gradient -(should be zero), louder the murmur

50
Q

MS EKG

A

LAE, afib

51
Q

MS imaging

A

CXR
Pulmonary vein congestion, LAE, huge LA, compression of esophagus and recurrent laryngeal nerve (hoarse voice)

Echo, cath

52
Q

MS timing of sx

A

depends on MVA, pressure gradient

tx with balloon valvatomy; need favorable valves
-know if meet criteria via ECHO

if primary MR: try to repair valve
MS: can’t repair, have to replace

53
Q

Tricuspid Regurgitation etiology

A

could be rheumatic (would have MR, AR before)
*functional from RV failure (TR secondary to pulmonary HTN)

**Ebstein’s anomaly: congenital displacement of ant. tricuspid leaflet–>atrialization of RV–>sev. TR (assoc. with WPW, ASD)

  • *carcinoid tumor against liver–>release of vasoactive substances; serotonin–>glistening appearance “smoldering” of tricuspid valve
  • may have pulmonic valve involvement but lung filters out

FA: RV dilitation, endocarditis

54
Q

Tricuspid Regurgitation hx

A

R-sided CHF predominates

55
Q

TR exam

A

Holosystolic murmur at LLSB, louder with inspiration (Carvallo’s sign), prominent cv waves and rapid y descent

56
Q

TR EKG

A

nothing?

57
Q

TR: imaging

A

ECHO

58
Q

TR tx

A

Tx underlying condition,
-sx if carcinoid or Ebsteins
annuloplasty can be considered

59
Q

normal JVD

JVP estimation

A

8 cm H2O

should be same as LVEDP

60
Q

ACVXY for JVP

see chart

A

A: atrial contraction (end of ventr. diastole: A-wave (S4)
C: closure of TV in early ventricular systole raises pressure in RA (FA: RV contraction)
X: atrial relaXation (descent)
V: ventricular systole nearly over (RA filling occurs and pressure rise in RA) big V wave if backwards flow (TR, MR)
Y: opening of TV (FA: RA emptying into RV, descent)

61
Q

2 types TR

A

Secondary (Functional)
Left-sided CHF, MS, MR, primary pulmonary disease, L to R shunt, pulmonic valve stenosis, PA stentosis

Primary
Carcinoid, due to pacemaker, endocarditis, rheumatic fever, marantic, drug-induced, Ebsteins

62
Q

Tricuspid stenosis (rare)

A

Rheumatic, carcinoid (once metastatic carcinoid to liver, the neuroendocrine tumor releases serotonin and other vasoactive substances which directly affect R-sided valves and these substances are usually cleared by lungs so L-sided vlave typically not affected)

Prolonged y descent, prominent a wave

Diastolic murmur, LLSB; increases with inspiration

63
Q

Pulmonic stenosis

A

Noonan’s, TOF, congenital rubella, acquired form carcinoid

Valvular, subvalvular, supravalvular

Indication for balloon valvuloplasty
Symptoms: > 30 mmHg peak
Asymptomatic: > 40 mmHg peak

64
Q

Pulmonic regurgitation

A

Secondary to TOF(tetralogy of fallot) tx of RVOT obstruction

Carcinoid; endocarditis

Graham Steell murmur:
High-pitched blowing murmur louder with inspiration (not in isolation)

65
Q

Drug-induced valve disease

A 
Ergot alkaloids (for migraines)
Fen-fen
Pergolide 
MDMA (ecstasy)
IVDA (endocarditis)
66
Q

cannon a waves in

A 
heart block
atria contract (have p wave) but valves can't open-->pressure transmitted backwards
67
Q

VSD (FA) murmur

A

holosystolic, harsh-sounding

loudest @ tricuspid area

68
Q

PDA (FA) murmur

A

continuous machine-like murmur
loudest at S2, best heard @ left infraclavicular area
often due to congenital rubella or prematurity

CSI (75 decks)

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