Aortic stenosis

Pathogenesis LV pressure increase, causing pressure hypertrophy, angina, CCF, causes

hypertension.

Concentric hypertrophy, sustained heaving apex, area is the same

Normal dia. 4cm2 symptoms at 1cm2

Stenosis can be valvular: subvalvular: supravalvular

Etiology congenital congenital AS or bicuspid arotic valve

rheumatic, degenerative, pagets disease, SLE, RA, post radiation.

Symptoms: dyspnea (1st symptom with 5 year survival), syncope, angina, sudden death.

Signs: tardeus and parveous pulse, high bp, soft and split 2nd heart sound, s4 gallop

Systolic ejection murmur, crescendo-decrescendo,

Sv1+ Rv5 > 35mm means LVH

Severity of AS mild >1.5 moderate 1.5-1 severe <1

Aortic regurgitation

Causes: bicuspid valve, RHD, syphilis, dissecting aneurysms, IE, SLE, traumatic aortic
stenosis.

Symptoms: mild to moderate- asymptomatic to palpitation,

Severe AR – breathlessness, angina nocturnal angina.

Signs: all peripheral signs of AR

 Head light sign: alternate blanching and de-blanching of forehead.

 Landolfi’s sign: Systolic contraction and diastolic dilation of the pupil.

 Becker’s sign: Visible pulsation of the retinal arterioles

 De Musset’s sign: Bobbing of the head with each heartbeat (like a bird walking)

 Muller’s sign: Visible pulsations of the uvula

 Quincke’s sign: Capillary pulsations seen on light compression of the nail bed.

 Corrigan’s pulse: A rapid and forceful distension of the arterial pulse with a quick
collapse.

 Mayne’s sign: A decrease in diastolic blood pressure of 15 mmHg when the arm is held
above the head (very non-specific)

 Shelly’s sign: Pulsation of the cervix

 Rosenbach’s sign: Hepatic pulsations

 Gerhardt’s sign (aka Sailer’s sign): Pulsation of the spleen in the presence of
splenomegaly

 Traube’s sign: Systolic and diastolic sounds heard over the femoral artery (“pistol
shots”)

 Duroziez’s sign: Gradual pressure over the femoral artery leads to a systolic and
diastolic bruit

 Hill’s sign: Popliteal systolic blood pressure exceed brachial systolic blood pressure by ≥
60 mmHg (most sensitive sign for aortic regurgitation)

Murmur: Austin flint a mid diastolic murmur heard paradoxically in AR.

Mitral stenosis:

Valve size 4cm2, stenosis at 1.5cm2

Causes: RHD, mitral valve degeneration.

LA pressure increases – LA hypertrophy – pulmonary venous HTN – hemoptysis

Can cause winter bronchitis, streaks of blood

Dyspnea and cough due to J cell exudates, pulmonary arterial HTN takes time, JVP increases,
hepatomegaly, pedal edema, palpitation – atrial fibrillation

Symptoms – dyspnea, palpitation, hemoptysis, cough, edema, syncope, embolism.

Sign – low volume pulse, less mean arterial pressure, increase JVP a wave absent, tapping apex
LOUD S1, mid diastolic murmur, opening snap, shift correlate the severity.

Pre-systolic accentuation, s2 OS interval inversely relates with severity.

Mitral regurgitation:

Causes: Mitral annulus Annular calcification

Leaflets Myxomatous degeneration, Rheumatic disease, Endocarditis, SAM (hypertrophic

cardiomyopathy)

Chordae tendineae Rupture (idiopathic),Endocarditis

Papillary muscles Dysfunction or rupture

Left ventricle Cavity dilatation

Symptoms: Dyspnea on exertion, Fatigue, Palpitation, RV failure symptoms

Signs: soft s1, s3 gallop, murmur systolic.

Severity of MR

 Apical displacement and size

 Palpable S3

 Longer/louder MR murmur

 S3 intensity

 length of diastolic flow rumble

 Wider split S2 (earlier A2)

Hypertrophic cardiomyopathy (great masquerder)

 Myocardial hypertrophy
 Non-dialated hyperdynamic chambers
 Absence of any other cardiac disease
 Independent of obstruction
Description by teare, brock myomectomy, marrow popularized myomectomy, sigwart PTSMA

Beta-myosin heavy mutation 14q12 MISSENCE MUTATION,

Malignant mutation – associated with sudden cardiac death, B- MHC and tropomyosin
mutation, cTnT mutation have only mild hypertrophy but worst prognosis and increase SCD.

Other genetic disorder- Noonan, fredrechich ataxia, hunter-hurler, aceyl CoA def.

Mitral vlave abnormalities – elongation of leaflet, anterior displacement of papillary muscle,

very short choridae, Systolic anterior movement

DIASTOLIC DYSFUNCTION- HALLMARK when systolic dysfunction occurs its called

burned out HCM

Nt- pr BNP increases in diastolic dysfunction

Normal EF with less CO

LVOT mainly occurs due to SAM which occurs due to 2 phenomenon

Venturi effect and drag effect MR occurs with posterior jets 80%

20% intrinsic defect and jets directed anteriorly

Autonomic dysfunction – very poor prognosis, 25% will have abnormal pressure.

C/f – dyspnea, angina, presyncope, syncope, sudden death

Risk list

Conventional Potentially high risk Potential arbitrator

Family h/o of SCD
Unexplained syncope
Repetitive non-sustained VT
Hypotensive
Massive LV hypertrophy
Late gadolinium enhancement
End stage phase
LV apical aneurysm with scar
Substantial LVOT
Diffuse gadlolinium enchan.
Transmural scar
Multiple Sacrcomere mutation
Intensive sports
Athersosclerotic plaque
Examination –

 JVP with prominent a wave

 Pulses bigeminus
 Double apical impulse / triple apical impulse
 S2 paradoxical split
 S3 in decompensate LV
 S4 atrial systole
 Murmur – MR murmur is heard, LVOT murmur at apex and b/w apex and sternum
increases on standing, valsalva, amyl nitrate.
 Harsh crescendo- decrescendo murmur, ejection systolic murmur
 Brockenbrough-Braunwald-Morrow sign decrease pulse pressure after ectopic beat