Valvular Disease heart

Valvular Heart Disease

Disease/Disorder Pathophysiology/Etiology Pathology History and Clinical Signs

Investigation & Findings Treatment

Mitral Stenosis

normal mitral valve size 4-6 cm2

MnemonicsSequence of FlowTRIPS BIAS:TRIcuspidPulmonarySemilunarBIcuspidAorticSemilunar

Complications PASTRIPulm ↑BP, A fib, Systemic embolism, Tricuspid regurg, Right heart failure, Infectiveendocarditis

MS-more common in females

*Narrowing of mitral valve, causing obstruction of blood flow into LVLV getting less blood because of narrowingcausing PRESSURE difference

*diastole

Scarring/infection injury causes/congenital defects/rheumatic fever damage mitral valve2 main ways: commissures thicken/fuse (can’t open much if at all) & chordae tendonae shorten and fusevalve cusps become rigidvalve calcification also occurs over time, making valve more narrowimpeding blood flow

Backward EffectLA pressure risespulmonary pressure risespulmonary compliance falls (bc of defective mitral valve)exertional dyspnea developscausing pulmonary edema bc lack of fluid from the pulmonary capillaries getting into the pulmonary interstitium and alveolileading to pulmonary arterial hypertension (blood vessels also affected—overworked, stiff over time—further increases BP w/in lungs & impedes blood flow)Pulmonary HTN causes RHF

FORWARD EFFECTSCO falls because of stenosisexercise tolerance low because heart cant pump fast enoughtired (most energy exerted in heart)

*Stenotic mitral valve (<2cm2) causes impediment/impairment of blood flowpressure gradient across mitral valve increasesLV fill time increases eventually LV requires atrial kick to fill with bloodas HR increases the amount of time the ventricle is in diastole filling period decreases

When HR goes above certain point diastolic fill time is insufficient to fill ventricle with blood and pressure builds in LA

*Rheumatic fever most common cause*Congenital defect rare*chronic renal disease*can be associated with mitral regurg or aortic disease

**Symptoms can be a guide for when surgery needed*** develop over 20-30 years*fatigue*exertional dyspnea*w/onset of a-fib symptoms increase/intensify rapidly*hemoptysis (coughing up blood)*pulmonary edema

Thrombic Complications

*occurs esp in a-fib*form in atria, esp atrial appendages*more in elderly*may be main complaint from pt (woman with cold leg)

*opening snap (valve stiff/rigid)*can hear 1st heart sound*diastolic murmur- low pitched -apex and lateral decubitus position -exercise may increase noise*signs of RH failure (shortness of breath, edema, frequent night peeing, pronounced neck veins)*other murmursEKG: Broad notched p-wave in II*p mitrale (double hump) in LAE (v1-v2, v5-v6)*Signs of RVH*A-fib=bad=need surgeryChest X-ray*straightening L heart border, then bulges*prominent pulmonary arteries (eventually causing HTN)*enlarged heart posteriorly on esophagus (when barium swallowed)*LV doesn’t enlarge; LA does*pericardial calcification (more so in TB)Cardiac Catherization*evaluate other valvular lesions & associated CAD (men over 45/women over 55*measure gradient across mitral valve (wedge pressure-LVEDP)

*physical exam and echo determine whether surgery is needed*

*antibiotic prophylaxis for further strep infection

*A-fib- control ventricular rate w/ warfarin/anticoag

Surgical treatment*balloon valvulotomy*surgical valvulotomy-open*valve repair or replacement

Valve Repair vs Replacement

Valve*Better hemodynamics*No anticoagulantsReplacement*For severe MR/severe *valve distortion*Anticaog required using mechanical device or atrial fib

*if in a-fib, always have them on anticoagulants

Disease/Disorder Pathophysiology/Etilogy Pathology History and Clinical Signs


Mitral Regurgitation

MnemonicsSequence of FlowTRIPS BIAS:TRIcuspid

*Mitral valve doesn’t close properlyas LV contracts there is some blood pumped back into the atriumLV VOLUME OVERLOAD*SystoleAcuteSudden volume overload of LA & LV

*Mitral Valve Prolapse (MVP) caused by myxomatous degeneration (pathological weakening of

**Symptoms NOT guide for when surgery needed*** acute severe MR will present symptoms within hours/days (send to

*PMI of LVH-lateral, enlarged, brisk*systolic thrill at apex*S1 soft/absent*holosystolic murmur grade III or more in severe MR at apex (may radiate to base pr

*vasodilators*ACE inhibitors*treat a-fib as w/ MS*usual measures for CHF


Disease/Disorder Pathophysiology/Etiology Pathology History and Clinical Signs


Aortic Stenosis

*25% of all valvular heart disease patients

*80% male


Symptoms of aortic stenosis ASDAngina 2 years }Syncope 1 year } prognosisDyspnoea 6/12 }

*Narrowing of aortic valve, causing obstruction of blood flow into bodycausing PRESSURE OVERLOAD ON LV

*diastole

Aortic valve becomes narrowedblood isn’t pumped adequatelypressure in LV increasesinitially LV compensates by thickening walls (myocardial hypertrophy/concentric hypertrophy-LV walls evenly enlarged) to maintain adequate pumping pressuremaintain CO without LV dilation for many years

Severe ASLater stagesLV dilates, wall things, diastolic function deterioratesturbulent blood flow causing inflammation & degeneration

*Mean gradient >50mm Hg (use gradient to determine extent of damage)*Valve area <1cm2 or valve area index <.6cm2/m2

*Ejection velocity > 4m/sec on Doppler*CO doesn’t increase normally with exercise*Late in course resting CO, gradient & murmur decreases (bc LV failure)*Increased wall tension compresses CAsflow reduced

*age-related progressive calcification of aortic valve- USA/Western Europe*rheumatic fever- usually associated with MV disease (usually have both)*congenital bicuspid aortic valve (most common congenital heart defect 1-1.5%of population (males more so)

Aortic Sclerosis- can lead to stenosis*Irregular leaflet thickening and focal increased echogenicity (calcification) are the hallmarks*present in 30% people over 65*may have a murmur, NO STENOSIS*risk factors: HTN, smoking, elevated LDL*no treatment needed- normal aging

**Symptoms guide for when surgery needed*** severe AS can be asymptomatic for years bc LVH maintains output*usually symptomatic 6-8 decade*Cardinal symptoms-exertional dyspnea -angina-due to AS or associated CAD-Syncope-associated w/ arrhythmias or vasodilation*orthopnea, fatigue, pulmonary edema occur late

*Rhythm regular until late in course (afib suggests MV disease or advances severe AS with failing LV)*delayed upstroke to carotids & brachial pulses*reduced volume pulses*displaced, sustained LV pulse*Systolic thrill at base & neck*S4 (atrial gallop)common- due to LVH & increased LVEDP*S2 diminished (scarred, not going to close)Murmurs*crescendo-decrescendo*rough & raspy*primary aortic radiating to neck, occasionally to apex, NOT AXILLA*with severe, usually grade 3 or greater*late stages, murmur softerEKG: most severe AS have LVH; absence of severe LVH doesn’t exclude severe ASChest X-ray*early/late stage may be normal (LVH concentric w/smaller chamber)*dilated ascending aorta*late stage, heart size increased with LV contour (boot)Echo*thickened immobile leaflets with bright echoes (calcification)*small orifice visible*LVH*Doppler demonstrates gradient by measuring velocity of flow in systolic across AV

*early-none needed*late-valve replacement-balloon valvulotomy-temporary (6 months)-transcatheter AV replacement-femoral, apical, transaortic-stoke and severe AR are the major complications but may be the best choice in old person w/comorbidity


Disease/Disorder Pathophysiology/Etiology Pathology History and Clinical Signs Investigation & Findings

Treatment

Aortic Insufficiency (AI)*also known as aortic regurgitation (AR)

¾ AI pts male2/3 AI pts rheumatic


* aortic valve can’t close causing blood flow from aortic valve back into LVcausing VOLUME OVERLOAD

*has two inflows in diastole (from LA and aortic valve)

*annuloaortic ectasiaproximal ascending aorta & aortic annulus are dilateddilation can causes valve to be incompetentcausing obstruction of blood flow into LVcausing PRESSURE difference

*rheumatic AI frequently associated with*can be caused by primary valve or aortic disease

Hemodynamic issues are dependent upon rate of onset of AI

*Marfans*Congenital*Valvular abnormality

Secondary CausesInfectious endocarditisTraumaAortic dissection or aneurysmMarfansSyphilisankylosing spondylitis (long term arthritis)

MnemonicsCREAM- CausesCongenitalRheumatic damageEndocarditisAortic dissection/ Aortic root dilatationMarfan's

Signs/SymptomsDyspnea on exertion, orthopnea, paroxysmal nocturnal dyspneaBounding pulseAcute AI*LV cant dilate increase in SV*LVEDP rises rapidly*Pulmonary edema or shock

Chronic AI*Stroke volume increases (dilation & LVH)*left ventricular end diastolic pressure slows in late diastole*As LV dilates more forward flow decreases*significant LV deterioration occurs before symptoms

Severe AI*Bobbing of head, body shakes*pulse rises rapidly*quickne pulse (when squeeze fingers you see red white red white)*wide pulse pressure (increased systolic & decreased diastolic) 160/40*Point Maximum Impact (PMI) heaving & displaced laterally*diastolic thrill*decrescendo diastolic murmur LSB-valvular AI*decrescendo diastolic murmur RSB- dialted aortic root*may have short, softer murmur

EKG: LVH w/ ST-T changesChest X-ray*LVH & LAEEcho*early increased EF*Serial exams to assess for failing LF function*EDD (end diastolic diameter) > 55mm*Size of jet to estimate AICath*to evaluate LF function, confirm amount of AI, & assess associated CAD

*Nifedipine, diuretic, ACE inhibitors

Surgical treatment*Rarely repair:2 degree infectious endocarditis, traumatic damage*AVR usually necessary in chronic, rheumatic AI*AI second degree dilated root frequently requires a valve conduit*prognosis dependent on LV function @time of surgery









Disease/Disorder

Pathophysiology/Etiology History and Clinical Signs

Investigation & Findings

Treatment

Tricuspid Regurg- usually secondary to marked dilation of tricuspid annulus from RV enlargement

*seen in late HF due to rheumatic or CHF*usually functional dilation of annulus & right heart**endocarditis secondary to IV drug use

Systemic venous congestion, reduction of CO*neck veins distended*pulse weak

Marked hepatomegaly, , jaundice, ascites

ECG: inferior Q wave MI or RVH

Chest X-ray: prominence of RA & superior vena cava

Echo: shows RV dilation and prolapse

Well tolerated normallySurgery eventually needed

Disease/Disorder

Pathophysiology/Etiology History and Clinical Signs

Investigation & Findings

Treatment

Tricuspid Stenosis*Rare, generally rheumatic in origin

*diastolic pressure gradient b/w RA and RV defines TS*augmented by trasnvalvular blood flow

Dyspnea, pulmonary congestion, and fatigue

Marked hepatic congestion, cirrhosis, jaundice, anasarca, ascites

ECG: RA enlargement, tall peaked P waves

Chest X-ray: prominence of RA & superior vena cava

Echo: tricuspid valve usually thickened, domes in diastole

Salt restrictionBed restDiuretic therapy

Surgery needed

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Valvular Disease heart