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Cardiology > Valvular disorders > Flashcards

Valvular disorders Flashcards

1
Q

What is the problem and the result of cardiac valve disease? pathophys?

A
  • problem: structural and/or functional abnormalitiy of the cardiac valve
  • the result of this is altered blood flow across the valve
  • pathophys: pressure and volume changes of atria and ventricles (hypertrophy, dilation and failure)
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2
Q

What are teh 2 types of valvular lesions?

A
  • stenosis: scarring and blockage

- regurg: insufficiency, incompetence (leaky)

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3
Q

Etiology of valvular disease?

A
  • rheumatic fever (used to be most common etiology)
  • infective endocarditis
  • functional
  • congenital malformations (pediatric/bicsupid)
  • aging valve tissue (calcification)
  • rupture/dysfxn of papillary muscles (MI)
  • collagen vascular disease
  • aortic dissection
  • syphilis: tertiary
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4
Q

Pathology of tricuspid valve?

A
  • regurg
  • stenosis
  • endocarditis
  • carcinoid syndrome (frequently in small bowel - secretes serotonin, can met to liver and if met from there it could get to R side of heart and affect collagen tissue on R side valves, if it gets to lungs can even affect L side)
  • traumatic rupture
  • ebstein’s anamoly
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5
Q

Annular dilation (most commoni right sided valve disease in the adult) will cause what pathology of the tricuspid?

A
  • TR
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6
Q

Rheumatic fever can lead to what pathology of tricuspid?

A
  • TR and TS
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7
Q

How can carcinoid syndrome affect Tricuspid?

A
  • TR, TS
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8
Q

How does endocarditis affect Tricuspid?

A
  • TR (flail leaflet)
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9
Q

How does ebstein anomaly affect tricuspid?

A
  • TR
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10
Q

Affects of carcinoid syndrome on the body?

A
  • heart: P and T valve thickening and stenosis, endocardial fibrosis
  • liver: hepatomegaly
  • GI: diarrhea, cramps, N/V
  • retroperitoneal and pelvic fibrosis
  • respiratory: cough, wheezing, dyspnea
  • skin: cutaneous flushes, and apparent cyanosis
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11
Q

Pathophys of TR?

A
  • the most common presentation of TR is functional (tricuspid annulas dilates) rather than organic (MS, MR, AS, AI or LSHF)
  • pulm HTN develops leading to right ventricular dilation - tricuspid annulus dialates
  • ## as the annular and ventricular dilation progresses, the chordal papillary muscle complex becomes functionally shortened. This combo prevents leaflet apposition, resulting in valvular incompetence. The pre-load, afterload and RV function also contribute.
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12
Q

Clinical presentation of TR?

A
  • usually need pulm HTN*
  • fatigue and weakness related to reduction of CO
  • DOE and SOB
  • RHF lead to ascites, venous engorgement, and hepatosplenomegaly, pulsatile liver, pleural effusions and peripheral edema
  • in late stage: cachexia (hard to breathe and because of oncotic pressure drop, not absorbing protein) cyanosis, jaundice and A fib
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13
Q

What will you see on PE if pt has TR?

A
  • RSHF
  • abnorm pulse in jugular vein (pulsatile liver)
  • high pitched systolic murmur
  • EKG: RAE
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14
Q

Causes of TS? Present with what sxs? Pathophys? EKG presentation?

A
  • most commonly rheumatic, rare isolated stenosis
  • fatigue, anorexia, and malaise related to reduction of CO
  • as right atrial pressure increases, venous congestion leads to distension of jugular veins, edema, hepatomegaly, ascites, pleural effusion, and peripheral edema
  • anatomic features similar to mitral stenosis with fusion and shortening of chordae and leaflet thickening
  • RA wall thickens and chamber dilates
  • systolic murmur at LLSB, tall P waves, RAE on EKG
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15
Q

Why are tricuspid valve lesions on the rise?

A
  • infective endocarditis (usually staph)
  • increasing due to rising incidence of IV drug abuse
  • regurg, conduction abnorm, embolic events, and sepsis
  • intensive medical tx (abx) and maybe valve replacement
  • horrible mortality
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16
Q

What is ebstein’s anomaly?

A
  • atrialization of RV - sail like TV, TR: tricuspid is incompletely formed, not at annulus - WPW rhythm
  • 50% ASD/PFO
  • age at presentation varies from childhood - to adulthood and depends on factors such as severity of TR, pulm vascular resistance in newborn and assoc abnorm such as ASD
  • CXR: massive cardiomegaly this is mainly due to RAE (displaces the rest of the heart)
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17
Q

Medical management of tricuspid disease?

A
  • fluid restrction
  • diuretics
  • tx complications (rhythm disturbances)
  • surgery end option
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18
Q

etiology of pulm regurg?

A
  • congenital: abnormal cusp number, abnormal cusp development, no valve (pulm atresia)
  • acquired: (rare, little clinical significance): pulm HTN (need to tx this), annular dilation, and structural distortion
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19
Q

Etiology of pulmonary stenosis?

A
  • congenital (more common)

- acquired (rare): rheumatic heart disease, carcinoid, and infective endocarditis

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20
Q

Make up of a normal mitral valve?

A
  • anterior and posterior leaflet

- anterior makes up 1/3 of the annulus and posterior takes up 2/3, more elongated

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21
Q

Etiology of mitral stenosis?

A
  • primarily: result of rheumatic fever
  • scarring and fusion of valve apparatus
  • pure or predominant MS occurs in approx 40% of all pts with rheumatic heart disease
  • 2/3 of all pts with MS are female
  • also can be congenital
  • more rare etiologies:
    carcinoid, SLE, RA, amyloid
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22
Q

mitral stenosis - valve area and associated sx?

A
  • normal valve area: 4-5 cm2
  • mild mitral stenosis: MVA 1.5-2.5 cm2, mean gradient less than 5, minimal sxs
  • mod mitral stenosis: MVA 1-1.5 cm2, 5-10 mean gradient, usually no sxs at rest
  • severe mitral stenosis: MVA less than 1 cm2, gradient greater than 10
  • sxs begin when less than 2.5 cm
  • pressure difference
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23
Q

Natural history of mitral stenosis?

A
  • progressive, lifelong disease
  • usually slow and stable in early years
  • progressive acceleration in the later years
  • 20-40 yr latency from rheumatic fever to sx onset
  • add 10 yrs before disabling sxs
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24
Q

sx of mitral stenosis?

A
  • fatigue
  • palpitations
  • cough
  • SOB (DOE)
  • left sided failure: orthopnea, PND
  • palpitation
  • hoarseness: L recurrent laryngeal nerve affected from LAE
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25
Q

Recognizing MS on exam?

A
  • palpitation: small volume pulse, tapping apex- palpable S1, palpable pulmonic component of S2
  • CXR: pulm congestion and large LA, if severe RHD can see ring of Ca (annulus)
  • auscultation: loud S1, as loud as S2 in pulm area
  • diastolic murmur: length proportional to severity
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26
Q

Complications of MS?

A
  • atrial dysrhythmias
  • systemic embolization (10-25%)
    risk of embolization is related to age, pressence of afib, previous embolic events - L atrium dilated, not contracting in afib
  • CHF (right sided)
  • hemoptysis: massive secondary to ruptured bronchial veins (pulm HTN)
  • streaking/pink froth: pulmonary edema, or infections (recurrent bronchitis pt)
    -endocarditis (more common in MR)
  • pulm infections
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27
Q

Pathophys of MS

A

LA HTN: pulm interstitial edema, pulm HTN: passive = obligatory to preserve forward flow, reactive= vascular changes in 40% (protects interstitium from edema, leads to RHF)
- LA stretch and afib: increased HR thus decreased LV filling, decreased atrial kick thus decreased LV filling
atrial thrombus formation and embolus
- limited LV filling and CO

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28
Q

What will you see on EKG that pts ot MS?

A
  • LAE (wider P wave, biphasic hump in lead 2, more depressed p wave in V1)
  • RVH
  • PVCs
  • aflutter and/or fibrillation: increased frequency in pts with mod-severe MS for several years
  • afib develops in 30-40% of pts with sxs
  • USE your stethoscope!!!
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29
Q

Therapy for MS?

A 
- medical: diuretics for LHF/RHF
digitalis/BBs/CCB: rate control in Afib
anticoagulation: afib
endocarditis prophylaxis
- balloon valvuloplasty: effective long term improvement
- surgery:
mitral commissurotomy 
mitral valve replacement
mitral valve repair usually not possible
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30
Q

Etiology of MR?

A
  • valvular-leaflets: rheumatic, endocarditis, congenital
  • chordae: fused, ruptured, degenerative, and IE
  • annulus: calcification, IE (abscess)
  • papillary muscles: CAD (ischemia, infarction, rupture)
  • LV dilation and functional regurg
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31
Q

Most common causes of MR?

A
  • MVP (chordae ruptured): 20-70%
  • ischemia (papillary): 40%
  • RHD (valvular): 40%
  • infectious endocarditis (chordae): 10%
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32
Q

How can RHD manifest as MR?

A
  • annular dilatation and leaflet thickening
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33
Q

How can MVP manifest as MR?

A
  • leaflet redundany and thickening
34
Q

How can ischemia manifest as MR?

A
  • papillary muscle dysfunction or chordal rupture
35
Q

How can IE manifest as MR?

A
  • perforation or destruction of cusps or chordae
36
Q

MR pathophys?

A
  • chronic LV volume overload leads to compensatory LVH intially maintaining CO
  • decompensation (increased LV wall tension) - this leads to CHF
  • LVH - leads to annulus dilation - this leads to increased MR
  • backflow - leads to LAE, afib, and pulm HTN
37
Q

Sxs of MR?

A
  • similar to MS
  • dyspnea, orthopnea, PND
  • fatigue
  • pulm HTN, RSHF
  • systemic embolization in A fib
38
Q

Recognizing chronic MR on exam? (pulse and murmurs)

A
  • pulse: brisk, low volume
  • apex: hyperdynamic, laterally displaced, palpable S3 +/- thrill, late parasternal lift secondary to LA filling
  • S1 will be soft or normal, S2 wide split (early A2) unless LBBB
  • murmur fixed MR: pansystolic, louded apex to axilla
  • murmur-dynamic MR (MVP): mid-systolic, +/- click (prolapsing valve causes the click), upright
  • S3 flow rumble if severe
39
Q

Dx tests for MR?

A
  • EKG: LAE, Afib, LVH (50% pts with severe MR)
    RVH (15%)
    combined hypertrophy (5%)
  • CXR: increased LV, increased LA dilation, increased pulm vascularity, CHF
  • echo: flail leaflets (chordae/papillary rupture), thick (RHD), post movement of leaflets (MVP), vegetations (IE)
    severity: regurg volume/fraction/orifice area, LV systolic fxn, increased LV/LA size, EF
40
Q

MVP etiology?

A
  • congenital
  • marfan’s syndrome
  • RHD
  • sequelae of cardiomyopathy or MI
41
Q

Pathophys of MVP?

A
  • valve leaflet has redundant tissue, extra tissue balloons into LA, click sound
42
Q

Incidence of MVP?

A
  • 10-20% of pop

- affects females more than males

43
Q

Clinical presentation of MVP?

A
  • asx
  • sx:
    palpitations
    arrhythmias
    atypical CP
  • thin, young females more commonly affected
  • abnormalities: skeletal and heart
  • auscultation: hear a mid-systolic click
44
Q

dx tests of MVP

A
  • EKG: normal
    abnormal: arrythmias: SVT, NSST-T changes, WPW
  • echo: confirm dx
  • R/O other abnormalities
45
Q

Tx of MVP?

A
  • reassurance
  • SBE prophyalxis
  • BBs
46
Q

Prognosis in MV prolapse

A
  • often benign
  • rare complications: endocarditis, progressive MR: acute, chronic
  • thromboembolism
  • atrial and ventricular arrhythmias
47
Q

Medical therapy for chronic mitral regurg?

A
  • no generally accepted rx in asx pts
  • no long term studies suggesting benefit of afterload reduction in absence of HTN
  • ACEi if HTN
  • AF requires rate control, anticoa, and attempt at restoration of SR
  • low Na diet
  • preload reduction: diuretics
  • aferload reductions: vasodilators: ACEI, hydralazine
  • digoxin
  • SBE prophylaxis
48
Q

Mitral valve surgery? Optimal timing?

A
  • only effective tx is valve repair/replacement
  • reduces morbidity and mortality from severe MR but exposes pt to risk of surgery and prosthetic valve
  • optimal timing determined:
    presence/absence of sxs
    functional state of ventricle
    feasability of valve repair
    presence of Afib/PHTN
  • should be performed before onset of severe sxs or development of LV contractile dysfunction

** repair is preferred over replacement (want to replace if IE)

49
Q

Sxs that indicate surgery?

A
  • class III or IV sxs (even if transient) always indicate need for surgery
  • class II indicate need for surgery in pts with repairable valves or if increasing ESD (echo systolic dimensions)
50
Q

MV repair vs replacement?

A
  • lower operative mortality
  • better late outcome
  • preserves sub-valvular apparatus
  • curative
  • avoids anticoag unless afib
51
Q

What is occuring in acute mitral regurg?

A
  • abrupt volume load - no time for adaptation - this leads to sudden decrease in forward SV
  • this leads to sudden increase in LA volume/pressure - leads to increased PV pressure (pulmonary edema) , decrease in forward CO, cardiogenic shock
  • call the surgeon!!!
  • rapidly fatal if severe
52
Q

How do you recognize acute severe mitral regurg?

A
  • acute severe dyspnea, CHF and hypotension
  • LV size is normal
  • LV may or may not be hyperdynamic
  • loud S1
  • systolic murmur
  • S3 present, may be only abnormality
  • TEE for dx:
    chordal or papillary muscle rupture/tear, infarction with papillary muscle ischemia or tear, IE with leaflet perforation
53
Q

pathophys of aortic stenosis?

A

LV outflow obstruction: when LV systolic pressure is greater than aortic pressure

  • concentric LVH: sustains high LV pressures, normalizes wall stress (radiusxpressure/wall thickness)
  • eventually results in impaired LV diastolic compliance and progressive LV dilation and contractile failure leads to systolic dysfunction (at the end)
  • LAH and enlargement
  • severe stenosis: limits the ability to increase stroke volume on demand
    • exercise is dangerous in these pts - lead to syncope
54
Q

Ventricular compensation in aortic stenosis?

A
  • concentric hypertrophy: reduces wall stress, reduces ventricular compliance, LVEDp increases, LAp increases
55
Q

Etiology of aortic stenosis?

A
  • congenital bicuspid aortic valve
  • rheumatic aortic valve disease
  • calcific (senile) aortic stenosis: most common
56
Q

Natural hx of aortic stenosis?

A
  • long asx latent period
  • cardinal sxs of severe aortic stenosis: dyspnea, angina, syncope
  • sudden death: most common cause (exerting themselves, not enough reserve)
  • left ventricular dilation and contractile failure
  • endocarditis
  • arrhythmias: V tach, conduction system disease, a fib
57
Q

PP of angina in aortic stenosis

A
  • increased wall stress: increased myocardial O2 demand, exceeds ability to coronary flow to meet demand
58
Q

PP of syncope in aortic stenosis?

A
  • fixed CO: vasodilation (exercise, vagal stimulation, drug induced), inability to augment CO, drop in cerebral perfusion pressure
  • heart block: Ca deposits in aortic ring encroach upon conduction tissue (bundle of His)
  • ventricular arrhythmias (LVH)
59
Q

What are key physical findings in severe aortic stenosis?

A
  • carotids: may hear transmitted murmur (bruits)
  • heart: SEM
  • lungs: rales (failure)
  • extremities: cold and decreased pulses
60
Q

Dx studies in aortic stenosis?

A
  • EKG: LVH with repolarization changes “strain pattern”
  • CXR: aortic root dilation and failure
  • echo: aortic valve thickening and restricted motion
  • doppler: gradient across aortic valve and aortic valve area can be est from increased flow velocity across aortic valve
  • cath: measure gradient (pressure gradient) across aortic valve and calculate valve area (less than 1 cm is critical AS), also look at coronaries
61
Q

Normal aortic valve area and indications of mild, moderate and severe changes in valve area?

A
  • normal: 3-4 cm2
  • circulation affected when valve area reduced by 75% (0.75-1 cm2)
  • mild: greater than 1.5, gradient less than 25 mm HG
  • mod: 1-1.5, gradient 25-50
  • severe: less than 1, greater than 50 (need to replace the valve at this pt)
62
Q

Tx of aortic stenosis?

A
  • mild to moderate asx aortic stenosis
  • close f/u: H and P, serial echos
  • endocarditis proph
  • severe sx aortic stenosis: (1 yr survival rate of 57%)
    aortic valve replacement with either mechanical or bioprosthetic valve
  • 10 year survival rate is around 75%
63
Q

Aortic Valve disease is assoc with what other problems and diseases?

A
  • SOB, swelling of abdomen
  • hx of rheumatic fever
  • hx of laennec’s cirrhosis (secondary to CHF)
  • congenital icthyosis
64
Q

Majority of pts with aortic valve disease have what sort of etiology?

A
  • majority of aortic regurg pts had no obvious recognized etiology
65
Q

What is aortic insufficiency?

A
  • failure of the aortic valve to close tightly causing back flow of blood into the left ventricle
66
Q

Major causes of aortic regurg?

A
  • leaflet dysfunction: rheumatic fever, endocarditis, trauma, bicuspid aortic valve, RA, myxomatous degen, ankylosing spondylitis, marfan’s syndrome, fenfluramine-phentermine (wt loss drug), annulo-aortic ectasia
  • aortic root dilation: systemic HTN, dissecting aneurysm, aortitis (syphilis), reiters syndrome, ankylosing spondylitis (bamboo spine), ehlers-danlos, osteogenesis imperfecta, pseudoxanthoma elasticum, marfan’s syndrome
67
Q

pathophys of aortic regurg?

A
  • LV faces combined pressure and volume load
  • primary adaption is dilation (eccentric hypertrophy)
  • since this adaption takes time, AR classified as acute or chronic
  • acute AR results in sudden increase in LVEDP - pulmonary edema and cardiogenic shock
68
Q

What occurs in acute aortic regurg?

A
  • sudden diastolic volume overload without LV dilation - acute elevation in LVDP - leads to pulmonary edema, acute LV systolic failure - leads to hypotension
  • provide inotropic support, vasodilator therapy if tolerated, urgent valve replacement
69
Q

Pathophys of chronic aortic regurg?

A
  • slowly progressive diastolic volume overload
  • augmented SV with rapid runoff increased systolic pressure with low diastolic pressure: wide puls epressure
  • progressive LV dilation, some hypertrophy
  • increased diastolic compliance with maintenance of normal diastolic pressures initially
  • late systolic failure with reduced ejection fraction and CHF
70
Q

Phases of aortic regurg?

A
  • latent phase of AR, like AS, may last decades
  • decompensation when:
    LV systolic fxn begins to fail
    progressive LV dilation occurs
  • initially this is reversible, LV systolic function and ESD are the most impt predictors of survival after surgery
71
Q

What are sxs of aortic insufficiency?

A
  • angina, palpitations, CHF sxs
  • fatigue (poor CO)
  • poor exercise tolerance
  • vital signs: wide pulse pressure
72
Q

Physical findings in AR?

A
  • wide pulse pressure
  • bounding pulses
  • early diastolic murmur: upper RSB with root dilation, mid to lower LSB with leaflet dysfunction
  • systolic murmur at base (sim to aortic stenosis)
  • austin flint murmur: mid to late diastolic rumble at apex (due to vibration of anterior leaflet of mitral valve as it is buffetted simultaneous;y by the blood jets from LA and the aorta.
73
Q

Physical findings in severe chronic aortic regurg?

A
  • deMussets sign: head bob with each systolic pulsation
  • corrigans pulses: pistol shot pulses over femoral artery (b/c of wide pulse pressure)
  • muellers sign: pulsation of uvula
  • duroziez sign: systolic/diastolci bruit over femoral artery
  • quincke’s pulses: capillary pulsations are seen in the nailbeds
  • beckers sign: pulsation of retinal arteries and pupils
  • Hill’s sign: popliteal BP exceeds brachial BP by more than 60 mmHg
74
Q

Natural Hx of chronic aortic regurg?

A
  • long asx phase, may be decades long
  • LVSD: decline in EF
  • sxs assoc with LV dysfunction: exercise intolerance, dyspnea on exertion
  • angina (rare)
  • sudden death (rare)
75
Q

Dx aortic regurg?

A
  • ekg: LAE, LVH
  • echo 2d/color doppler - test of choice
  • cardiac cath: confirmatory: grades 1-4+ (like MR)
76
Q

Management of chronic aortic regurg?

A
  • close f/u of LV size and fxn with serial echo (q few years with mild AR, q 6-12 months with severe AR)
  • endocarditis prophylaxis
  • medical therapy: vasodilators: reduces blood pressure - reduces regurg fraction, digoxin (enhances systolic function), and diuretics (reduce LA pressure),, DONT slow the heart rate!!
  • aortic valve replacement with mecahnical or bioprsthetic valve (don’t wait until it’s too late)
77
Q

What are valve replacement issues?

A
  • mechanical valve: thromboembolism, bleed from anticoag (coumadin…rest of your life)
  • bioprosthetic valve: limited durability with degen (back in 7-10 years)
  • homografts, ross procedure
  • age, activity level, and compliance all come into play
  • chordal/subvalvular appartatus preservation with the mitral is impt
78
Q

Systolic murmurs?

A
  • aortic stenosis
  • mitral insufficiency
  • MVP
  • tricuspid insufficiency
79
Q

Diastolic murmurs?

A
  • aortic insufficiency

- mitral stenosis

80
Q

If the ventricle is enlarging with MR/AI what should you do?

A
  • call someone!!!

Cardiology (20 decks)

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