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

- 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)


What are teh 2 types of valvular lesions?

- stenosis: scarring and blockage
- regurg: insufficiency, incompetence (leaky)


Etiology of valvular disease?

- 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


Pathology of tricuspid valve?

- 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


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

- TR


Rheumatic fever can lead to what pathology of tricuspid?

- TR and TS


How can carcinoid syndrome affect Tricuspid?

- TR, TS


How does endocarditis affect Tricuspid?

- TR (flail leaflet)


How does ebstein anomaly affect tricuspid?

- TR


Affects of carcinoid syndrome on the body?

- 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


Pathophys of TR?

- 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.


Clinical presentation of TR?

- 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


What will you see on PE if pt has TR?

- abnorm pulse in jugular vein (pulsatile liver)
- high pitched systolic murmur


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

- 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


Why are tricuspid valve lesions on the rise?

- 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


What is ebstein's anomaly?

- 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)


Medical management of tricuspid disease?

- fluid restrction
- diuretics
- tx complications (rhythm disturbances)
- surgery end option


etiology of pulm regurg?

- 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


Etiology of pulmonary stenosis?

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


Make up of a normal mitral valve?

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


Etiology of mitral stenosis?

- 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


mitral stenosis - valve area and associated sx?

- 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


Natural history of mitral stenosis?

- 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


sx of mitral stenosis?

- fatigue
- palpitations
- cough
- left sided failure: orthopnea, PND
- palpitation
- hoarseness: L recurrent laryngeal nerve affected from LAE


Recognizing MS on exam?

- 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


Complications of MS?

- 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


Pathophys of MS

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


What will you see on EKG that pts ot MS?

- LAE (wider P wave, biphasic hump in lead 2, more depressed p wave in V1)
- 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!!!


Therapy for MS?

- 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


Etiology of MR?

- 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


Most common causes of MR?

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


How can RHD manifest as MR?

- annular dilatation and leaflet thickening


How can MVP manifest as MR?

- leaflet redundany and thickening


How can ischemia manifest as MR?

- papillary muscle dysfunction or chordal rupture


How can IE manifest as MR?

- perforation or destruction of cusps or chordae


MR pathophys?

- 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


Sxs of MR?

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


Recognizing chronic MR on exam? (pulse and murmurs)

- 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


Dx tests for MR?

- 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


MVP etiology?

- congenital
- marfan's syndrome
- sequelae of cardiomyopathy or MI


Pathophys of MVP?

- valve leaflet has redundant tissue, extra tissue balloons into LA, click sound


Incidence of MVP?

- 10-20% of pop
- affects females more than males


Clinical presentation of MVP?

- asx
- sx:
atypical CP
- thin, young females more commonly affected
- abnormalities: skeletal and heart
- auscultation: hear a mid-systolic click


dx tests of MVP

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


Tx of MVP?

- reassurance
- SBE prophyalxis
- BBs


Prognosis in MV prolapse

- often benign
- rare complications: endocarditis, progressive MR: acute, chronic
- thromboembolism
- atrial and ventricular arrhythmias


Medical therapy for chronic mitral regurg?

- 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


Mitral valve surgery? Optimal timing?

- 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)


Sxs that indicate surgery?

- 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)


MV repair vs replacement?

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


What is occuring in acute mitral regurg?

- 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


How do you recognize acute severe mitral regurg?

- 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


pathophys of aortic stenosis?

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


Ventricular compensation in aortic stenosis?

- concentric hypertrophy: reduces wall stress, reduces ventricular compliance, LVEDp increases, LAp increases


Etiology of aortic stenosis?

- congenital bicuspid aortic valve
- rheumatic aortic valve disease
- calcific (senile) aortic stenosis: most common


Natural hx of aortic stenosis?

- 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


PP of angina in aortic stenosis

- increased wall stress: increased myocardial O2 demand, exceeds ability to coronary flow to meet demand


PP of syncope in aortic stenosis?

- 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)


What are key physical findings in severe aortic stenosis?

- carotids: may hear transmitted murmur (bruits)
- heart: SEM
- lungs: rales (failure)
- extremities: cold and decreased pulses


Dx studies in aortic stenosis?

- 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


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

- 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)


Tx of aortic stenosis?

- 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%


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

- SOB, swelling of abdomen
- hx of rheumatic fever
- hx of laennec's cirrhosis (secondary to CHF)
- congenital icthyosis


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

- majority of aortic regurg pts had no obvious recognized etiology


What is aortic insufficiency?

- failure of the aortic valve to close tightly causing back flow of blood into the left ventricle


Major causes of aortic regurg?

- 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


pathophys of aortic regurg?

- 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


What occurs in acute aortic regurg?

- 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


Pathophys of chronic aortic regurg?

- 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


Phases of aortic regurg?

- 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


What are sxs of aortic insufficiency?

- angina, palpitations, CHF sxs
- fatigue (poor CO)
- poor exercise tolerance
- vital signs: wide pulse pressure


Physical findings in AR?

- 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.


Physical findings in severe chronic aortic regurg?

- 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


Natural Hx of chronic aortic regurg?

- 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)


Dx aortic regurg?

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


Management of chronic aortic regurg?

- 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)


What are valve replacement issues?

- mechanical valve: thromboembolism, bleed from anticoag ( 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


Systolic murmurs?

- aortic stenosis
- mitral insufficiency
- tricuspid insufficiency


Diastolic murmurs?

- aortic insufficiency
- mitral stenosis


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

- call someone!!!