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Cardio 2 > Valvular Heart Disease > Flashcards

Valvular Heart Disease Flashcards

1
Q

Mitral stenosis causes

A

Rheumatic fever is more common cause

Other less common - calcifcation, masses

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2
Q

RF

A

Involves heart, skin and conn tissue

Follows URI vause by GAS

Mainly in childre nadn adolescents

2-3 weeks adter initial (if acute)

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3
Q

Cardiac comps of RF

A

Autoimmiune cross reactivity between pacterial and cardiac antigens

Affects all 3 layers of the ehart

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4
Q

Pathology of RF

A

Aschoff body - focal fibrinoid necrosis surroundedb y infalmatory cells that resolves to fibrous scar tissue

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5
Q

Rheumatic fever path (non-histo)

A

Damage to valvular endocardium leads to chronic RHD characterized by permanent deformity

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6
Q

Jones criteria

A 
Carditis/valvulitis
Arthritis
CNS involvement (chorea)
Subq nodules
Erthemia marginatum

Minor - arthrlagia, fever, ESR/CRP, prolonged PR

2 major or 1 major and 2 minor

Also need pos culture of ASO

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7
Q

Tx fo acute epsiodes of RF

A

Aspirin, peniccilin, supportive care

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8
Q

mitral stensosi featurees

A

Fibrous thickening and calcification of valve leaflets
Fusion of commissures
Thickening and shortening of the chardae tendinae

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9
Q

Pathophys of mitral stenossi

A

More obstruction to BF…empyting is empeded and abnormal pressure gradient created bt La and LV….dec preload

Backpressure inc and blood moves into LV at higher gradient…LA enlargement, LA pressure inc, puml HTN

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10
Q

Chronic LA pressure elevation

A

Pulm HTN with rupture of bronchial veins and hemoptysis

LA enlargement - stretching of atrial tissue and afib…stagnation of blood flow and intra-arterial thrombus formation

Turbulent BF across the valve

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11
Q

Presnet of mitral stensosi

A

Depend on CSA of the valve

Earliest are dyspnea and exerciwse intole

Inc HR and inc FLow….dec diasotlic filling time…inc LA presure

Long stading pulm HTN induces RHF

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12
Q

Loud S1

A

Mitral stensosi

High pressure connection slams the leflets together…may dec as progresses

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13
Q

Opening snap

A

Sudden tensing of stenotic leaflets on opening of the valve

Interval bt S2 and OS relate INVERSELY to the severity of MS…more severe means higher LA pressure and earlier the valve is forced to open in diastole

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14
Q

Diastolic rumble

A

Turbulent blood flow across the stenotic valve

Relate to severity

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15
Q

Pre-systolic accentuation

A

Contraction of LA cuases pressure gradient between La and LV to rise again

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16
Q

Physical findings of mitral stensosi

A

Mitral “facies”
Loud S1 and opening snap
Diastolic rumble at apex
Systolic MR (holo)

LA impulse in axilla
RV life due to RVH
Loud P2

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17
Q

Mitral stenosis test of choice

A

Echo - look for MR, calcification and LA thrombus

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18
Q

Severity of MS

A

MPG - under 5, 5-10, over 10

MVA - over 1.5, 1-1.5, under 1

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19
Q

Tx of MS

A

Sx control - HR control with beta blocker and CCB…relief of HF with diuretics…anticoag if afib

If sx persist - need mech correction

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20
Q

Percutaenous balloon mitral valvuloplasy

A

Bloon catheter inserted into RA and crosses the IAS into the LA and is inflated to open stenotic mitral valve

21
Q

Other options of MS tx

A

Open mitral commussuroomy

Mitral valve replacement

22
Q

Mitral regurg physiology

A

Valve is no longer competent and blood ejected into both aorta and LA

LA pressure rises and pulm edema develops

Gap between LA and LV decreases during systole

23
Q

Chronic MR

A

Overitme the LA dilates to accommodate the inc volume

Decreases the LA pressure

LV also dilates because of the increased volume load…regurged blood goes through LV repetitively

24
Q

Clinical MR

A

Acute - LA pressure rapdily inc and pulm edema ensures

Chronic - LA dilates and is abkle to accomodate more BV
LA pressure rises but less so than acute
Fatigue and weakness
Once LV dysfxn occurs - dyspnea, orthopnea and PND
If RV failure, then ascities/LE edema may develop

25
Q

Exam of mitral regurg

A

Apical holosystolic murmur
Radiate to axilla
Can radaite to aortic area

Handgrip will inc murmur of MR but no change to AS

26
Q

Midsystolic click of MVP

A

Sooner after sudden standing bc dec preload

Later after sudden squatting bc inc preload

27
Q

Acute MR exam

A

Very difficult to hear

28
Q

Tx of MR

A

Augment formward flow and reduce backward with vasodilators

Diuretics for pulm edema

Valve surgery (repair is b etter)

29
Q

Severe MR pathophys

A

LV remodeling - dec contractility

Before surgery…dec afterload=falsely inc EF

After surgery - inc afterload will dec EF (true)

30
Q

LVOT obstruction

A

Aortic stenosis is most common

Supravalvular in Williams syndrome (elfin facies with hypercalcemia)

31
Q

Pathophys of aortic stenossis

A

inc pressure in LV leads to concentric hypertrophy

Diastolic dyfunction relaed to LV relaxation and compliance…passive filling becomes reduced so depend on preload from atrial contribution

32
Q

Presentation of aortic stensosi

A

Angina
Syncope
Heart failure

33
Q

Angina of AS

A

Supply demand mismathc

Demand - hypertrophied muscle and stress inc

SUpply - Elevated LVEDP dec coronary artery perfusion

34
Q

Syncope of AS

A

Exertional syncope

Ventricle cannot inc CO due to high afterload

Exercise leads to muscular vasodilation which dec preload

35
Q

HF of AS

A

Hypertrophied ventricle needs higher filling pressure - inc LA pressure

Inc workload leads to systolic failure

36
Q

Clinical exam of AS

A

Systolic ejection murmur radiates to carotids

Volume does not correlate with serverity but rather severe peaks later

Soft S2 in severe

S3 and S4 common

Systolic ejection click at bicuspid valve

37
Q

Path of congenital bicuspid valve

A

1-2% of people with a male predominance

38
Q

Clinical exam of AS

A

Pulsus parvus et tardus…less common in elderly

HTN can coexist

Apical impulse sustained and nondisplaced

39
Q

Managment of AS

A

Asx are treated conservatively

Surgery if develop sx

NO med therapy

Evolution and mod of cardiac risk factors is important

40
Q

Take home points of AS

A

Severe = velocity over 4, gradient over 40, valve area under 1

Angina, syncope, HF

Pathophy role of hypertropy

Fix valve if sx or LV dysfunction (related to valve)

41
Q

AI pathophys

A

Chornic - inc in LV EDV and wall tension,….eccentric hypertrophy (fibrosis)…chronic volume overload and dilation

Acute AI - hypotension and cardiogenic shock

42
Q

AI exam

A

Early diastolic mumur

Soft S1 with long PR interval

S3 common

More prominnet with severity then soften as LVEDP and diastolic pressure equalize

43
Q

Tricuspid dz

A

Regurg is more common…mostly due to pulm HTN

Prominent jug veins, RV heave, edema

44
Q

Pulomniic dz

A

Both rare…insuff from pulm HTN

45
Q

Infective endo

A

High risk if abnormal valves of IVDU

Typically staph or strep

46
Q

IE exam

A

Infection signs

Janeway lesions (non-tender)
Osler nodes (painful)
Roth spots
47
Q

Embolic infarcts vs. spetic emboli

A

Embolic inf - from mitral or aortic

Setpic - from tricupsid or pulm

48
Q

Tx of IE

A

Prolonged IV ABs or surgery

49
Q

Valve replacements

A

Mech - more need for AC (use warfarin)

All pts post valve surgeyr should get aspirin and endocarditis prophylaxis (penicillin/clindamycin)

Cardio 2 (23 decks)

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