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Flashcards in Valvular disorders Deck (80)
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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