MITRAL STENOSIS

Diastol :
FISH MOUTH Symetrical fussion ot commisure, the
shape anterior leaflet not it right position
LUTENBACHER SYNDROME  ASD + MS
Rheumatic Fever (20 yr)
Congenital End stagerigid can’t open or shutcombined MS,MR
Inhomogenous refractory
Rheumatic mitral Valve : period, reentry
1. Fibrous thickening and calcification
2. Fussion ot commissures Chronic  LA enlgmn streach cond. Fibre  AF  rapid :
3. Thickening & shortening chordae tendinea shortened diastolic time  filling ↓CO↓  LA press ↑
Dominan MR
Normal : negligible pressure difference LA/LV early diastole
MS : OBSTRUCTION Abnormal Pressure gradien between LA & LV  LA press ↑ (necessery for blood to flow)  transmitted
to pulmonary vein and capiler hidrostatik press ↑transudation fluid to lung interstitium and alveolidyspnoe,CHF symtom

 PH : Passive or reactive (30-60mmHg)

Passive : 60%, ok Backward transmission to pulmonal vein
Reactive : 40% vasocontriction, Remodeling PA  medial hypertrophy, intimal fibrosis  protecting capillary(ok
resistensi ↓, flow↓ ,↓hidrostatic pressure) RV press ↑  RV Failure

 Severe case  Collateral to bronchial Vein RupturHemoptysis

Impaired filling LV  SV and CO ↓
Stagnation blood flow(dilated LA)
Tromboemboli antikoagulan
AF

INCREASE FLOW (takikardi) INCREASE LA PRESSERE ?  increase LA pressure : increase flow.

MVA : 4-6 cm2,< 2  haemodinamic significans
AF rapid
exercise
Fever
Increase flow LA pressure CONGESTI
Anemia
Increase HR ↑ DYSPNOE
Pregnancy
Tiroid CO↓
AF rapid
Emosi Decrease diastolic
Sex Filling time

Penekanan n.laryngeus recuren

SYMTOM ok dilatasi atr.kiri, dilatasi
co↓, congesty AF rapid a.pulmonalis
DYSPNEA PALPITATION HOARSENESS (ORTNER SYNDROME)
Ruptur bronch.vein,
odem paru, infarc
HAEMOPTYSIS paru
EMBOLIC HEMOSIDEROSIS  repeated hemoptisis

CHEST PAIN RHF

??, emboli koroner
Perjalanan MS : NYHA IV Untreat  all death in 10 years
- Reccurent
- Chronic autoimune proses
- Super imposed calcified valve
 PHYSICAL EXAMINTATION

FASIES MITRALISlow co, sistemic vasoconstriction. AF, irreguler pulse

Pinkish-purple patches on cheeks. RV ENLARG  RV
lift, PR, TR

DIASTOLIC THRILL  apex, left PH --> palpable P2 (2nd left ICS), Loud P2, PR,
Jugular venous pressure
lateral recumbent RV lift (left parasternal), S2 narrow split, single S2
Prominen v wave

OS : sudden tension ot c.tendinea MID DIASTOLIC MURMUR  setelah OS

S1 ↑↓ : and stenotic leaflet, sudenly stop, Turbulent flow across the stenotic valve
Wide closing ot leaflet,pressure↑ apexdiafragma stetoskop Pre systolic accentuation, bell stetoskop, apex,
Normal tidk terpisah lebar? S2-OS intervalseverity; makin  axilla
imobile  ↓. cepatLA press↑ Durationseverity
Bedakan dengan P2 GRAHAM STEELL MURMUR PR (PH) : decresendo
P2 ↑, S2 narow split Diastolic murmur LSB.
single S2 ↑ (PH) PAN SISTOL MURMUR TR (dialtasi RV, PH): ICS IV LSB
S3 RV,

- LAE : posisi PA
CXR : - RVH : retrosternal filling
- Kongesti : Upperlobe vascularity ↑, Kerley B lines
- Hemosiderin deposition
- Pulmonal ,menonjol
- LV normal
Severitas MS : PH, interval P2-OS, durasi murmur -

ECG AF; LAE : p mitral, bifasik di V1; RV Hypertrophy : r/s>1 V1 , s persisten, RAD

ECHO : - thickened leaflet

- Fussion Commisure
- LAE
- MVA : mild >2, mod 1,1-1,5, sev<1
- Trombus
- Velocity
- Wilkin score
- Aortic valve ?
 Sampai usia 40 thn
10 tahun stlh onset terakhir
Seumur hidup : high risk,
(prostetic valave?), severity
high risk pat prostetic valave, high risk
VHD, exposure
prosedure, prev endocarditis, CHD

Table 77–4 Medical Treatment of Mitral Stenosis

Antibiotic prophylaxis 
Aritmia (AF) : B blocker, Diltiazem verapamil,
  Recurrent rheumatic fever
DIGOXIN, cardioversi hanya bila hemodinamik tidak
  Infective endocarditis
stabil
Restrict activities (moderate/severe mitral stenosis)  ANTIKOAGULAN : Warfarin. (NOC : no eviden
  Severe exercise base) ms + af / ms + LAE/ms+trombus
  Competitive sports KONGESTI : diuretic
Arrhythmias  CHF : ACE-I
  Prevent or control PH : Venodilator , long acting nitrat.
  Atrial fibrillation/flutter Komorbit : RHD, IE
    Control ventricular rate
    Anticoagulation: start with IV heparin and warfarin; when INR is 2 to 3 discontinue heparin
    Restore sinus rhythm
Cardiac medications 
Pada MS + AF, MS dgn SR bila pada
  Warfarin anticoagulation: INR at 2 to 3
echo : trombus, SEC, LAE (D>50mm)
    Atrial fibrillation/supraventricular arrhythmias
    Systemic emboli
    LA thrombus
    Pulmonary emboli
    LV Systolic dysfunction
  Elevated pulmonary venous pressure: diureticsa
 
  "Heart failure"
    Pulmonary congestion: diureticsa
    Pulmonary edema: diuretics,a venodilators if necessarya 
    LV systolic dysfunction: digitalis, ACE inhibitors
    Elevated systemic venous pressure and fluid retention: digitalis, diuretics, ACE inhibitors;
 B blockers (second generation) after patients are stabilized and there is LV systolic
dysfunction.
ACE, angiotensin-converting enzyme; INR, international normalized ratio; LA, left atrial; LV, left ventricular.
a
Use judiciously; patients with severe mitral stenosis need an elevated LA pressure to maintain adequate LV filling and
cardiac output.
 MITRAL REGURGITATION

ETIOLOGI
Rheumatic Disease : pemendekan korda,
fussion ot commissures, retractile fibrosis
of leflets and chordae

Degenerative Mitral Regurgitation

- Calcification  eldery, accelerated by
HT, aortic stenosis, DM
- Connective tissue  Marfan
- Myxomatous degeneration  MVP

Infective Endocarditis
Interposition between leaflets , Ruptur Chordae
5 %  surgery

Ischemic and functional mitral regurgitation

LV dysfunction and dilatation, asymmetrical, transient
dysfunction ot papillary muscles. Respon to vasodilator

Weight-loss drug (FENFLURAMIN, PHENTERMIN ) Thickened cardiac valve  MR

MR lebih baik : SVR ↓ , PVR (LAP) ↑, sedkt takikardi

PATHOPHYSIOLOGY
Severity of MR
Direct consequences of MR 1. Mitral orifice during regurgitation
1. LA pressure ↑ 2. LV, LA Systolic press gradient
2. LA volume ↑ 3. SVR, PVR
3. Forward CO ↓ 4. LA complience, LV dilatation ?
4. LV volume related stress → regurgitant volume 5. Duration of regurgitation (systole)
 MRV = mitral regurgitant volume, MROA = mitral regurgitant orifice area, C =
constant, TS = time or duration of systole, LVP = LV mean systolic pressure,
and LAP = left atrial mean systolic pressure.

Preload ↑ → frankstarling → EF ↑
Afterload ↓ → a portion lv output direct to low pressure LA

Acute (tall v wave)→ odem paru, afterload ↓, EF ↑, shortening ↑

Kronis → LA dilatasi, LV dilatasi (eccentric hypertrophy) , low output
syndrome, AF, afterload N → End systolic volume, afterload, preload ↑

Volume overload →Frankstarling mechanism → EF↑ → SV↑ (nonfailling

heart) → Forward CO near normal level.
→ →→ LV dysfunction → HF.

Low normal EF → impaired myocardial function

Moderately reduce EF (40-50%) → severe, irreversible impairement
contractility → poorly after surgery
EF < 35% → advanced myocardial dysfunction

Inotropic, diuretic, vasodilator  reduce LV size  reduce regurgitant

orifice size → v wave ↓ → intensity and duration of systolic murmur.

LV afterload ↓ → shortening ↑ than tension developement

Coronary flow rate ↑,
Low incidence of myocardial ischemia
Determinan MVO2 :
- LV wall tension
- HR
- Contractility
Pada MR hanya shortening yang ↑↑ →
tidak mempengaruhi MVO2

END SYSTOLIC PRESSURE-VOLUME

→Evaluation LV function , useful index
→ pre operatif evaluation
→ > 40 mm → impaired LV systolic
function after surgery.

Neurohormonal : NE ↑, TNF a ↑(LV

remodeling), B receptor density ↓ →
terapi dengan B blocker.
CLINICAL MANIFESTATIONS (MR)

SYMPTOMS
Preserved EF → Symptom (+)
ACUTE : Odem paru PH
CHRONIC : Low output syndrome : Fatique, weakness
CHF : DOE, PND, OP
Severe chronic : RHF : edema perifer AF, hemoptisis
Pulmonal Hypertension

Carotid pulse is sharp, brisk

S2 wide split → Shortening LV
Diminished S1 ejection time PH : P2 > A2

Early diastolic
murmur→increase mitral
flow

S3 : Increase volume retuning to LV.

HOLOSYSTOLIC MURMUR (Pansystolic Murmur)
Not HF → left lateral decubitus
→ apeks menjalar ke axila
→spesifik untuk rematik (Anterior leaflet).
Cardiac palpation : Lateral displaced, Hyperdinamic
→ Sudden standing : diminished the murmur, squatting : Apical THRILL
augments it.
→ Valsava manuver →↓↓
→ tidak dipengaruhi inspirasi (beda dgn murmur TR → mengeras Predominan MR : S3, Rapid LV filling wave,
dengan inspirasi) LV impulse, Soft S1
→Pada ISKEMIK (POSTERIOR) regurgitasi bisa ke anterior katup,
posterior aorta, → at the base ot heart, murmur bisa terdengar Predominn MS : S1↑, OS, Short soft
seperti murmur AS (left sternal border). Bedanya : murmur AS systolic murmur, Short A2-OS interval
bisa berubah2 tiap beat, tergantung durasi sistol, murmur MR
bertambah keras dengan clench the fist (SVR ↑).

LV Enlarg, LAE, giant LA is rare

ECG Principle : LAE,

LVH : 1/3 psn dgn severe MR, RVH : 15%
AF
CXR
Acute / CHF  interstitial edema
(Kerley B lines)
Calcification ot anulus  posterior
third ot cardiac silhouette
Predominan MR : Kardiomegali, paru relatif normal
Predominan MS : mild kardiomegali, paru kongesti.

1.Hemodinamik ( large V wave)

CARDIAC 2.Severity MR ( MR regurgitant volume, regurgitant fraction) → FICK methode
3.LV Function
CATH 4. Coronary anatomy (angiography ) → age 40-50
MANAGEMENT

TH : ↑ CO, ↓ Regurgitan, ↓ pulmonary congestion

Pharmacologic Therapy → uncertain → Vasodilators, diuretic, inotropic (digoxin), spironolakton
Acute MR → Vasodilator (nifedipin, nitroprusside,ACEI)
In Chronic MR Vasodilator are less useful → only for HT or LV systolic dysfunction who not candidat for
surgery
AF → Digoxin/B blocker, Oral anticoagulan
ACEI in MR → conflicting result, blockade RAAS fail to improve LVEF and remodeling in canine model
(fibrosis (-))
B Blocker improved LV function in dog → need for large clinical trial
Prevention of IE (no longer recomended), prophylaxis rheumatic fever.

ACUTE MR PERCUTANEUS INTERVENTION

ALO + Shock pd pasn MCI ok ruptur m. Papillaris EVEREST I & II (Endovascular Valve Edge-to-
IE , Trauma edge repair study) → The prosedure reduce MR
→ hyperdinamic function + HF less efective than MVr
→ IABP, inotropic, vasodilators

MVr better than MVR :

FUNCTIONAL MR
- Loss of annular chordal papillary muscle
→ Aggressive medical management for LV systolic dysfunction
continue
→ Severe MR not usually improved by revascularization alone
- Risk of thromboembolism
→ persistence residual MR → mortality risk ↑
- Risk of hemorrhage
→ Severe MR → corrected at bypass
- IE
→ isolated severe MR surgery → ?
MVR : survival was not clearly better then the
natural history ot disease
 AORTIC STENOSIS

Etiology
1. Kongenital (bicuspid valve) ,
superimposed calcification
→ severe obstruction →
turbulen flow→injury ot
leaflet → inflamasi, fibrosis,
kalsifikasi.
2. Calcific Aortic valve disease →
SENILE (degenerative) AS
(normal or bicuspid)
- Common cause AS in adult
- Faktor resiko = FR
atherosclerosis
(lipid, DM, HT, smoker)
- Inflamasi katup (katup aorta :
wear and tear → shear stress),
stress oksidatif
- SEAS , ASTRONOMER →
statin tdk mempengaruhi
mortalitas
3. Rheumatic Aortic Stenosis.
- Adhesion and fusion ot
commissure,
inflamation, fibrosis
- Regurgitant and
stenotic
- Melibatkan katup
mitral (95%)

AS : chronic course → asymtomatik

AS →ASAFTERLOAD ↑↑
Afterload
↓ : wall stress → usaha untuk membuka katup
aorta=
Afterload ↑↑
↓P x r / 2h
→ isovolumetric contraction →→→LV dysfunction
Kompensasi : LV hypertrophy
→↓ kompensasi dengan LV hypertrophy (meningkatkan
↓ h)
Wall stress N CHF
↓ ↓
LV complience ↓↓ systolic dysfunction
Afterload mismatch →
↓ inadequate wall thickening
LV stiff → diastolic dysfunction → LVEDP ↑
↓
LAE → S4 → PCWP ↑ → kongesti paru→CHF
↓
AF
 g

Kontraksi atrium → sangat dibutuhkan untuk mengisi

ventrikel yang kaku (25%) → bila terjadi AF → mortalitas ↑
Afterload ↑↑→usaha lebih
meningkatkan pressure dari
volume Normal AVA : 3-4cm2

Pressure gradien

Gender difference : + concentric, ↑ eccentric

SVR → Contribute total LV afterload, Hypertension
increase total LV load.

AVA increase with exercise (±0,2 cm2)

→→Severe AS : FIXED CO→abnormal blood pressure
respon to exercise.
LVH → systolic pressure ↑→Prolongation of ejection →
MVO2 ↑
PH mild (+)
PA, RV, RA press ↑ → edema, water retention.
 CLINICAL MANIFESTATIONS
AS : slow progressive
Trias : 20 year 20% mild→severe
Age 50-70
1. ANGINA AS + Symptom : lethal
2. SYNCOPE
3. CHF ( DOE, OP, PND, Odema)

SYNCOPE
ANGINA : Cerebral blood flow ↓
- Fixed CO on exertion
1.1.1. O2 demand ↑ → LV mass↑, LV wall stress ↑, LV - Peripheral vasodilatation
systolic pressure ↑, Prolongation ejection Other :
2. O2 supplay ↓ → Diastolic pressure↑, AF, PH , sudden death
compression of intra-myocardial Coronary arteries GI bleeding → angiodysplasia (right colon), shear stress
induced platelet aggregation→von willebrand factor ↓→
Heyde Syndrome
Table 75–2 Physical Examination of Patients with Varying Severity of Aortic Valve Stenosis
  Mild Moderate Severe + Normal LV Severe + LV Severe + Heart
Function Dysfunction Failurea 
Arterial pulse Normal Slowly rising Parvus et tardus  Parvus et tardus  Small volume
Jugular venous Normal Normal Normal Normal ±
pulse
Carotid thrill ± ± ± ± ±
Cardiac impulse Normal Heaving Heaving, sustained Heaving Heaving or reduced
palpable a wave 
Precordial thrill ± ± Usually ++ ± –
Auscultation          
S4   – ± + + –
S3   – – – ± +
ESS/ EC + ± – – –
Peak of ESM Early Midsystole Late systole Late to midsystole, Midsystole, soft or
systole soft absent
S2 Normal Normal or Single or paradoxical Single Single
  single
ESM, ejection systolic murmur; ESS, ejection systolic sound; LV, left ventricular; S 2, second heart sound; S3, third heart
sound (diastolic gallop); S4, fourth heart sound (presystolic gallop). aThere may be signs of mitral and tricuspid
regurgitation and of pulmonary hypertension.

PARVUS AND TARDUS : rise slowly, longer time to reach peak,

Carotid palpation peak is reduce

Physical examination S2 splitting Single EJECTION SYSTOLIC

Severe AS : prolongation ejection,(ULSB
Systolic murmur
Systolic thrill : URSB, carotid
S2 (A2 inaudible), A2MURMUR
tumpang (ESM)
tindih P2
- Lokasi : Base of the heart & URSB)
LBBB,LV dysf → paradoxical spliting
- Radiated : carotids and apex (gallavardin phenomenon) →
=murmur MR
- Late peaking, grade 2-4/6, CHF : mid systole
- High pitch decresendo diastolic murmur + → murmur AR
- Varies from beat to beat
- Augmented by squatting, valsava manufer ↓↓
Table 75–4 Aortic Valve Disease: Indications for Coronary Arteriography
Patients 35 years
Patients <35 years
  Left ventricular dysfunction
  Symptoms or signs suggesting CAD
  Two or more risk factors for premature CAD (excluding gender)
MANAGEMENT

Table 75–13 Medical Treatment of Patients with Aortic Valve Stenosis

I. Antibiotic prophylaxis
  A. Infective endocarditis (See Chap. 85)
  B. Recurrent rheumatic carditis (See Chap. 74)
II. Restriction of activities
  A. Severe exercise Aortic Stenosis. Frontal radiograph demonstrates isolated
enlargement of the ascending aorta (white arrow)→post
  B. Competitive sports
stenosis dilatation. The left ventricle is enlarged (yellow
III. Arrhythmias arrow) and the heart is mildly enlarged overall. The
  A. Prevent and/or control descending aorta is not enlarged (green arrow).
  B. Restore sinus rhythm, if possible
IV. Cardiac medications (only if essential) No therapy can improve outcome
  A. Avoid negative inotropic and proarrhythmic agents if possible
Mild to mod AS: do not need any spesific therapy
mild→normal life, mod → avoid mod to severe act
  B. Diuretics—use cautiously
AF → reverted rapidly → urgency→Cardioversion
  C. Arteriolar and venodilators—use cautiously Severe+symptom → Surgery (AVR or TAVI)
V. Followup of asymptomatic patients PELLIKA study
  A. Mild aortic stenosis: every 2–5 years Surgery : AVR, TAVI, CBV (catheter balloon valvuloplasty)
  B. Moderate aortic stenosis: every 6–12 months
  C. Develop symptoms: immediate STATIN : under investigation
Table 75–14 Severe Aortic Valve Stenosis: Indications for Surgery
I. All symptomatic patients
  A. LV function normal: as soon as possible
Diuretics → accumulation ot fluid→hati2
  B. LV dysfunction: urgent hipovolumia
  C. Heart failure: emergent ACEI → symptomatic LV dysfunction not candidat
II. Asymptomatic patients for surgery →caution(hypotension)
  A. Patients undergoing surgery for CAD, aorta, other valves Bblocker → depressed myocardial function → K.I
  B. Associated significantly obstructed CAD Treat Hypertention
HF symptom : digoxin, diuretics, ACEI or ARB
  C. LV dysfunction
→no suit / waiting for surgery
  D. Progressive decline of LVEF →urgent for surgery
Maintenence Sinus rythm
Avoid Hypotension
  E. Marked or excessive LVH:
    1. 11–12 mm in smaller people, e.g., women
    2. 13-14 mm in larger people, e.g., men
  F. Patients aged 60–65 years Asymptomatic severe patn → controversy
  G. "Very" severe AS 0.7 cm2; 0.4 cm2/m2  →no data to support early AVR
  H. Others: →requires weighing benefit against the risk
    1. Abnormal response to exercise Balloon Valvuloplasty → important role in
       a. Hypotension/no or minimal increase of blood pressure pediatric. Adult → limited role : bridging to AVR
       b. Ischemia or TAVI
       c. LV dysfunction
       d. Arrhythmias PARTNER TRIAL (TAVI)
- TAVI non inferior for all-cause mortality at
    2. Arrhythmias
1year
       a. Ventricular/atrial tachyarrhythmias - ↑Cerecrovascular event, vascular complication
       b. A-V block >1° AVB - ↓ Bleeding and AF
Table 75–18 Suggested Indications for Catheter Balloon Valvuloplasty (CBV)
TAVI in
→Patients
for high with Severe Calcific Aortic
risk AVR
Valve Stenosisa
I. "Bridge" procedure to eventual AVR
  A. Cardiogenic shock
  B. Moderate to severe heart failure
  C. Emergent/urgent need for noncardiac therapeutic procedures (e.g., operation)
II. Patient with limited life span
  A. Noncardiac reasons (e.g., carcinoma)
  B. Cardiac reason(s) other than aortic stenosis
III. Others
  A. Patient at extremely high risk for AVR
  B. AVR not desirable for noncardiac reasons or cardiac causes other than aortic stenosis
  C. Patient refuses surgery
IV. Rare
  A. "Therapeutic test": patients with small stroke volume and small valve gradient, with valve stenosis suspected to be
severe but severity in doubt even after provocative diagnostic tests
 AORTIC REGURGITATION

ETIOLOGY

PATHOPHYSIOLOGY

AR → regurgitant volume → LV dilatasi → FRANK-STARLING MECHANISM

AR (seperti MR) → Acute vs Kronis. Acute : LV normal size and complience → LV diastolic
pressure↑→LAP & pulmonary press ↑ → pulmonary edema.

Kronis : LV compensatory → eccentric hypertrophy → LV complience ↑

→ volume ↑, LV diastolic pressure N → LA press N
→ regurgitan volume ↑ ↑
→ frank starling → stroke volume ↑↑,
→ diastolic press↓ (widened pulse pressure)
Compensatory → High Complience pump → large SV (25l/m)
→ asymtomatic
Remodelling LV , afterload mismatch→ Systolic dysfunction → CO↓ →CHF

Diatolic press ↓ → O2 supplay ↓ → increase LV size →

Angina
MR→against low press RA → kompensasi via frankstarling
AR→against SVR, →Afterload pada AR lbh ↑→kompensasi via
frank starling + hipertropi (dilatasi+hipertropi)

AS afterload↑ ok Press ↑, AR afterload ↑ ok volume( r) ↑ →

pada AR hipertropi + dilatasi.

AR : - LV dilatasi, - LV hipertrofi, Systolic hypertension

Preload mismatch → preload reserve has been reach

(pe↑ preload tdk me↑ SV ok afterload juga ikut meningkat)
Exercise : Afterload mismatch → hipertrofi tidak mampu menurunkan
- SVR ↑ → diastolic press↑ → regurgitant volume↓ afterload ok dilatasi ↑↑
- HR ↑ → diastolic time ↓ → regurgitant volume ↓ ↓
Dysfungsi LV→ CHF

Severity AR → duration of murmur → diastolic duration

→ SVR juga berpengaruh
CLINICAL MANIFESTATIONS

Symptoms : DOE, fatique, Uncomfortable sensation of a forceful heartbeat → lying down

Angina, Nocturnal Angina → ok saat tidur HR ↓ → waktu diastolik ↑ → regurgitan volume ↑ → SV↓
→ perfusi koroner ↓ → angina, diaphoresis.
Head pounding → emosional stress, exertion, takikardi

Stigmata

Compressed proximal→systolic,
compressed distal → diastolic
Diastolic press↓↓, korotkoff sounds persist to 0mmHg
(diastolic press rerely < 30 mmHg)
CHF → SVR ↑ → Diastolic pressure ↑ → widened pulse
pressure ↓

Pressing a glass slide on the lip, light trough fingertips

Early diastolic mrmur (decresendo) ICS

Diastolic thrill (3rd left ICS)
Blowing systolic murmur
→ SV↑
3 a 4 → ↑sittng forward
Precordium hyperdinamic
Apical impulse → displace
lateraly

Austin Flint Murmur →OK arus

regurgitant mendorong mitral anterior
TO and FRO murmur → turbulen (DD: MS→OS(+)

S1 soft → mitral leflt close to each other

Prematur mitral closure → prolong PR

S3 gallop → LV
dysfungtion
→ indikasi op
 S2 single,ok P2 tertutupi murmur
S2 narrow, paradox, absen

  Mild Moderate Severe Severe + Left Severe + Heart Failure +

Ventricular Systolic Left Ventricular Systolic
Dysfunction Dysfunction
Arterial pulse Normal Corrigan + to ++ Corrigan +++ Corrigan ++ Corrigan +
  Systolic Normal Increased + to ++ Increased +++ Increased ++ Normal/+
  Diastolic Normal Decreased + to ++ Decreased +++ to ++++ Decreased ++ to +++ Decreased +
  Pulse Often normal Increased + to ++ Increased +++ to ++++ Increased ++ to +++ Increased +
pressure
Cardiac Often normal Hyperdynamic Very hyperdynamic Hyperdynamic May be hypodynamic
impulse visible ± chest may rock
thrill

  Systolic – ± ± ± –
  Diastolic – – ± ± –
  S4  – – – – –
  S1  Normal Often soft Soft Soft Soft
  S2  Normal Normal or sing Often single Often single Often single
  S3  – + ++ to +++ +++ +++
  ESM ± + + to ++ + to ++ +
  AoDM + ++ +++ to ++++ ++ to +++ + to ++
Austin Flint – – ± – –
murmur

CXR → Cardiomegali (LV enlargement), enlarge of entire aorta

LV enlarge in inferior and leftward

Syphilitic Aortitis → linear cakcification ascensing aorta
Aneurysma and dilatation of aortic root → aortic root disease

ECG :
-LAD
-LV diastolic Volume overload (Q → AVL, V3-V6, Small wave V1)
-LV Strain (ST-T change)
-T tall precordial → early stage

TREATMENT

NO SPHESIFIC THERAPY

ASYMTOMATIC : - Mild to mod → Follow echo 12-24 months Echo : LV function, size.
- Severe, normal EF → 6 month (Long acting nifedipin ? )
- Treat Hypertension → increase regurgitant → Vasodilator (nifedipin) , ACEI
- Prefent Bradiaritmia and AF (B-blocker hati-hati) → treat vigorously
- Do not need AB prophylaxis for IE (see guidelines)
SYMTOMATIC → SURGERY

Vasodilator → Regurgitant volume ↓

PADUA TRIAL → Nifedipin in asymtomatic severe AR (vs digoxin)
→ Benefit
BARCELONA TRIAL → Not benefit
→ Subject not severe AR
ACE I : no benefit

Table 75–28 Medical Treatment of Patients with Aortic Regurgitation

I. Antibiotic prophylaxis
  A. Infective endocarditis
  B. Recurrent rheumatic carditis
II. Restriction of activities (moderate/severe AR)
  A. Severe exercise
  B. Competitive sports
III. Arrhythmias
  A. Prevent and/or control
  B. Restore sinus rhythm, if possible
IV. Cardiac medications
  A. Asymptomatic, normal LV function
    1. Mild AR: None
    2. Moderate AR: ? Nifedipine long-acting if no KI (?)
    3. Severe AR: Nifedipine long-acting
  B. Severe AR symptomatic (while waiting for surgery)
    1. Normal LV function: Nifedipine long-acting
    2. LV dysfunction: Digitalis
      ACE inhibitors
      Hydralazine ± nitrates, if needed
      Diuretics, if needed
      Dobutamine, if needed
  C. Severe AR + heart failure:
    Digitalis, diuretics, ACE inhibitors
    Hydralazine + nitrates
    IV nitroprusside, if IV therapy needed
    Dobutamine, if needed
V. Followup of asymptomatic patient
  A. Mild AR: Every 2–5 years
  B. Moderate AR: Every 1–2 years
  C. Severe AR: Every 6–12 months
  D. Develop symptoms: Early or immediate