VALVULAR DISORDER

Etiology/Natural hx Pathophysiology Clinical sxs Eval Therapy

Aortic
Stenosis
Rheumatic 1. Congenital uni- or bicuspid valve fxns
Calcific/degenerative normally for decades until turbulence
Congential bicuspid m/c induces calcification
Post-endocarditis 2. Degenerative calcification occurs similarly
but from yrs of wear n tear esp in
Natural hx: HTN
Very predictable course if not 3. Hi outflow resistance causes concentric
corrected LVH
1. from onset of angina mortality 4. Hi LV filling pressure
in 5 yrs 5. LV filling pressure reflected to atrium
2. from onset of syncope 6. Systolic fxn preserved till late
mortality in 3yrs 7. Hypertrophied ventricle becomes less
3. from onset of CHF mortality compliant stiff
in 18 months 8. Atrial contraction provides proportionally
Congenital bicuspid valve may be more LV filling vol as opposed to passive
filling
asymptomatic for decades
9. As gradient increases peak ejection
delayed later in systole
10.Pulse volume
11.Ventricular hypertrophy & hi filling
pressures lead to subendocardial ischemia
Regurg
Triad of sxs occur sequentially:
1. chest pain
2. exertional syncope or near syncope
3. dyspnea/orthopnea - CHF
Delayed & weakened carotid upstroke
(pulsus tardis et parvis)
Late peaking crescendo/decrescendo
murmur at base w/ radiation to
carotids
Soft or absent S2
Hyperdynamic apical impulse
S4 at apex
Murmur may decrease w/ standing
Significant systolic HTN rare (over
180mm)
Paradoxic split S2
Palpable thrill over base common in
severe AS
Rare assoc w/ colonic angiodysplasia
& lower GI bleed
CXR normal or slightly
enlarged LV
Echo structure &
mobility of valve leaflets
thickeness & fxn of
ventricular walls
Doppler quantify gradient
& calculate valve area (most
diagnostic)
Cardiac cath
ECG LVH
Not a medical illness no medical
therapy can significantly alter
prognosis or sxs
Surgery
Most appropriate intervention
Successful even in severly impaired
ventricle, w/ improvement in sxs &
mortality
Critical valve area for intervention is
0.75 cm2
Surgery should not be delayed till
CHF occurs, but must be planned
after grandient established
Balloon vulvaloplasty
Initial success rate excellent
Rapid/profound restenosis, most
w/in 6 months
Present indication only for bridge
to surgery in patients w/ other
transient lo-morbid illness

Endocarditis Hi pressure leak increases LV filling vol, Bounding cental pulses (Corrigans Hx focus on functional Afterload reduction
Rheumatic raises LVEDP causes dilation or water hammer) capacity Inotropes, late
Calcific degeneration Hi pressure leak also causes LV hypertrophy Diastolic descrescendo murmur at 2nd Careful P.E. Preload reduction only in presence of
Trauma Cor bovinum large, thick walled heavy interspace right radiates to apex, Echo LV chamber pulm edema
Aortic root dz hearts heard best in end expiration, learning dimension, wall thickness, & Limit strenuous exercises
Cystic medial necrosis Well tolerated for yrs till myocardial forward motion Maintain sinus rhythm
Marfans compensation outstrips vascular supply Laterally displaced PMI, w/ Doppler quantification of Antibiotic prophylaxis
Annulo-ectasia Systolic fxn preserved hyperdynamia & enlargement regurgitant flow Surgery:
Hi SV causes most peripheral physical Anterior heave L. heart cath
Indicated at onset of sxs or if
Aortic aneurysm/ dissection
findings of AI Wide pulse pressure CXR cardiomegaly functional capacity falls
Syphilitic aortitis
Normal to low SVR Austin Flint murmur prominent
LV end systolic dimension 5cm or
Seronegative arthropathies Quinckes pulses (nailbed capillary ECG: LVH
Wide pulse pressure (>60mmHg) common diastolic dimension 7cm need
Natural hx: pulsations) surgery
Chronic regurg tolerated well for Durozierz sign
If root aneursysmal, need combo
yrs till dilation exceeds metabolic Pulsus bisferiens valve/root replacement
accommodation
Severity correlates w/ duration of
Sxs commonly appear after
murmur
development of irrev LV dysfxn
Acute AR poorly tolerated
leads to pulm edema & death if
not corrected
Mitral
Stenosis

Rheumatic fever m/c 2 to 10 yrs
after acute infxn
Degenrative calcific dz in elderly
Connective tissue disorders (SLE,
RA)
Congenital
Natural hx:
5 yrs to progress from mild to
severe disability
80% 5 yr survival after surgery
Surgical risk 6%, higher in elderly
Valvuloplasty restenosis rate 80% in
10 yrs
Rheumatic fusion at tips calcific fusion Exertional dyspnea/orthopnea CXR large RV, pulm vasc Diuresis for acute pulm edema
from cusps Hemoptysis w/ pulm HTN engorgement, no LV Maintain sinus rhythm anti-
Normal orifice 4-6 cm sq, critical stenosis Palpitations dilation, large L atrium arrhythmics where indicated
<1 cm sq Thromboembolism Echo thick fused leaflets Prevent tachycardia -blockers
Gradient develops raising atrial pressure Endocarditis ECG atrial abn, RVH Digoxin control rate in a-fib
Pulm HTN long standing Diastolic low pitched apical murmur Doppler gradient & valve Oral anticoags
Atrial dilation leads to a-fib Opening snap after S2, before area Abx prophylaxis
Normal LV pressure & LV contraction murmur R & L heart cath Balloon valvuoplasty
Tachycardia decreases LV filling pressure & S1 loud w/ rheumatic & soft w/ Open commissurotomy
cardiac output calcific Valvular replacement
Rising pulm artery pressure can impair RV RV heave Surgery timed to prevent irreversible
fxn Normal PMI & fxn pulm HTN
 MItral Regurg
Leaflet destruction Leak unloads LV into low pressure atrium Sxs depend on severity of leak & CXR LV/LA dilation, Preload reduction for acute HF
Infection (SBE) Leak worsened by systemic afterload time frame pulm vasc engorgement Afterload reduction to improve
Calcific degeneration L atrial pressure & pulm wedge pressure rise Exertional dyspnea/orthopnea are late Echo LV/LA forward flow
Connective tissue disorder Atrium dilates findings enlargement, wall motion Inotrope to maintain contractility
trauma LV dilates to accommodate filling volume Palpitations w/ arrhythmia normal till late Antiarrhythmics to control ectopy &
Contractility eventually decreases A-fib tolerated better than in MS Doppler ID & quantify maintain sinus
Myxomatous degeneration (MVP,
Pulm HTN & edema ensues R heart failure at end-stage regurgitant jet Abx prophylaxis
Marfans
Acute MR is tolerated very poorly than Fatigue, weakness due to C.O ECG LVH, LAA, RVH, Surgery
Papillary muscle dysfxn
chronic due to insufficient time for atrial & Laterally displaced PMI w/ A-fib Annuloplasty
Ischemia/infarction
ventricular adaptation enlargement Ejection fraction normaly Valvuloplasty
Myxomatous degeneration
S3 common early, reduced late Valve replacement
Spontaneous rupture Cardiac cath
Holosystolic murmur at apex Coronary revascularization
Dilated cardiomyopathy
Murmur radiates to back, L axilla Surgery timed to prevent irreversible
Hypertrophic cadiomyopathic
most common can radiate to base LV dysfxn
Natural hx:
Pulse upstrokes full
Small leaks tolerated for normal life
S2 normal
span
Marker for significant LV dyxfxn LV heave
indicating need for surgery is end- Does not substantially vary w/
diastolic LV dimension of 7cm, or maneuvers
end-systolic dimension of 5cm
LVEF <40% indicates severe,
possibly inoperable LV dysfxn
eprolapsvalveMitral

Myxomatous degeneration of valve
Genetically mediated
Assoc w/ other dyscollagenoses
(Marfans, osteogenesis imperfecta)
Frequency 4 times higher in females
Natural hx:
Generally benign
Can progress to symptomatic MR in
older age
Men progress more often & more
rapidly than women
Small increased risk for SBE,
embolus, & arrhythmia
Stenosis
Pulmonic
Leaflets reductant & bulge into atrium Chest pain Echo for prolapse Reassurance
during systole Palpitations Doppler for MR -blocker may alleviate some sxs
Occasionally regurgitant Exertional dyspnea Holter for arrhythmia Ascultory f/u for progression
Can continue to degenerate & cause severe Occasional syncope Abx prophylaxis if murmur present
MR Usually in 2nd 3rd decade
High circulating catecholamines Early to mid systolic click at apex
Mid to late systolic murmur if MR
present
No other findings
Click/murmur prolong and increase
w/ maneuvers this decrease LV
filling volume (standing, valsava,
nitrates)

Congenital Increase outflow gradient Exertional fatigue Surgery

Endocarditis RV hypertrophy Dyspnea Judiciuos preload reduction
RV HTN Signs of RV HTN
RV pressure overload Systolic murmur 2nd L interspace
Reduced LV filling RV heave
Peripheral venous congestion RVD
Peripheral edema
Insufficiency

Endocarditis Presentation Preload reduction

Congenital Similar to PS Tx for pulm HTN
Pulm HTN Clinical signs Surgery rarely necessary
Drescendo diastolic murmur 2nd L
interspace
Signs of RV olume/pressure overload
Tricuspid Regurg
Pulm HTN Exertional fatigue Diuresis
Endocarditis Anorexia/bloating Preload reduction and valve
Acute PE Peripheral edema replacement
RV infarction Sleep disturbance
JVD
RV heave
Epigastric systolic murmur
Hepatomegaly
Peripheral edema
Abn LFT