KARAGANDA STATE MEDICAL

UNIVERCITY

STUDENT INDIVIDUAL WORK

SUBMITTED BY – GODARA MOTI LAL

GROUP NO. 3003

SUBJECT- Propaedeutics

Topic – Aortic Insufficiency

49 WM sent for “transplant” evaluation from local cardiologistHPI – DOE x 6mos-1year, insidious onset, also

with L sided Chest tightness when tired/stressed and occasionally awakens him at night, last 1-2hrs and relieved with anxiolytics. Occasional lightheadedness after taking Coreg. Denies PND, Orthopnea, cough, pre/syncope. Former maintenance worker, now on medical leave. Pt states trying to remain active (walking/ swimming) but limited by dyspnea

PMHx: • Chronic LBP• Obesity• OSA/ CPAP• Depression/Anxiety• Basal Cell CarcinomaSocial:• no alcohol, cocaine, tobacco or drugs; married with 1

teenage son Meds (at presentation)• Carvedilol 50 bid, Celebrex, Lasix, ASA, anxiolytic,

hydrocodone, Combivent MDI

PE: HR 65 BP 170/67

HNT: jvp est 10cm,

CV: nl S1/2, + S3, no S4; PMI displaced

laterally to ant ax; 3/6 diastolic

decrescendo m USB

Resp: basilar rales

Abd: obese, no ascites/masses

Ext: tr edema, distal pulses brisk

Lab: • Chem 142 \ 110 / 14 H/H 16.6/ 46

4.4 / 27 \ 1.4

TSH, LFT, FLP, WBC/PPC, Coags nl

ECG: NSR, PRWP, nl axis, no ischemia

Etiology

Physical Examination

Assessing Severity

Natural History

Prognosis

Timing of Surgery

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Any conditions resulting in incompetent aortic leafletsCongenital• Bicuspid valve

Aortopathy• Cystic medial necrosis

• Collagen disorders (e.g. Marfan’s)

• Ehler-Danlos

• Osteogenesis imperfecta

• Pseudoxanthoma elasticum

Acquired• Rheumatic heart disease

• Dilated aorta (e.g. hypertension..)

• Degenerative

• Connective tissue disorders

E.g. ankylosing spondylitis, rheumatoid arthritis, Reiter’s syndrome, Giant-cell arteritis )

• Syphilis (chronic aortitis)

Acute AI: aortic dissection, infective endocarditis, trauma

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Dyspnea, orthopnea, PND

Chest pain.

• Nocturnal angina >> exertional angina

• ( diastolic aortic pressure and increased LVEDP thus

coronary artery diastolic flow)

With extreme reductions in diastolic pressures

(e.g. < 40) may see angina

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Quincke’s sign: capillary

pulsation

Corrigan’s sign: water

hammer pulse

Bisferiens pulse (AS/AR >

AR)

De Musset’s sign: systolic

head bobbing

Mueller’s sign: systolic

pulsation of uvula

Durosier’s sign: femoral

retrograde bruits

Traube’s sign: pistol shot

femorals

Hill’s sign:BP Lower

extremity >BP Upper

extremity by

• > 20 mm Hg - mild AR

• > 40 mm Hg – mod AR

• > 60 mm Hg – severe AR

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Widened pulse pressure

• Systolic – diastolic =

pulse pressure

High pitched, blowing,

decrescendo diastolic

murmur at LSB

Best heard at end-

expiration & leaning

forward

Hands & Knee position

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S1 S2 S1

Apex:

• Enlarged

• Displaced

• Hyper-dynamic

• Palpable S3

• Austin-Flint murmur

Aortic diastolic

murmur• length correlates with

severity (chronic AR)

• in acute AR murmur

shortens as

Aortic DP=LVEDP

• in acute AR - mitral pre-

closure

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Assess severity by impact on peripheral signs and LV• peripheral signs = severity

• LV = severity

• S3

• Austin -Flint

• LVH

• radiological cardiomegaly

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Asymptomatic %/YNormal LV function (~good prognosis)• Progression to symptoms or LV dysfunction <

6• Progression to asymptomatic LV dysfunction <

3.5• 75% 5-year survival• Sudden death < 0.2

Abnormal LV function• Progression to cardiac symptoms 25

Symptomatic (Poor prognosis)• Mortality > 10

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…...bridging the care gap Bonow RO, et al, JACC. 1998;32:1486.

TX: Medical Surgery BEFORE LV dysfunction

ACC/AHA Class I• Symptomatic patients with preserved LVF (LVEF

>50%)

• Asymptomatic patients with mild to moderate LV dysfunction (EF 25-49%)

• Patients undergoing CABG, aortic or other valvular surgery

ACC/AHA Class II a• Asymptomatic patients with preserved LVEF but

severe LV dilatation (EDD>75 mm or ESD > 55mm)

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ACC/AHA Class II b• Patients with severe LV dysfunction (EF < 25%)

• Asymptomatic patients with normal systolic func-tion at rest (EF >0.50) and progressi ve LV dilata-tion when the degree of dilatation is moderatelysevere (EDD 70 to 75 mm, ESD 50 to 55 mm).

ACC/AHA Class III • Asymptomatic patients with normal systolicf unction at

rest (EF >0.50) and LV dilatation when the degree of dilatation is not severe (EDD <70 mm, ESD <50 mm).

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Etiology

Pathophysiology

History / Physical Findings

Natural History

Diagnosis

Management

Aortic Root• Age related dilatation

• Medial degeneration/ Marfans

• Dissection

• HTN

• Other ( osteogenesis imperfecta, Reiters, syphilitic aortitis, Bechet, psoriatic arthritis, relapsing polychondritis, UC arthritis, AS, giant cell arteritis

Aortic Valve• Rheumatic

• Calcific degeneration

• Congenital (Bicuspid, VSD)

• Myxomatous degeneration

• Endocarditis

• Structural degeneration of Bioprosthetic valve

• Other (SLE, AS, Takayasu, Whipple, Crohns)

increased LV EDVaddition of new sarcomeres in series/ elongation of myocytes and myocardial fibers (Eccentric Hypertrophy)enlarged chamber/ increased wall stress is stimulus for concentric hypertrophydilatation and hypertrophy with resultant recruitment of preload reserve allow compensation and maintenance of LV systolic functionmay be asymptomatic for decades until decompensated state develops, wall thickening unable to keep pace with hemodynamic load, increased interstitial fibrosis and decreased compliance symptoms of CHF ensue

Braunwald 6th ed

CO at rest may approach 25 L/min in severe AI with little increase in EDPvery large EDV (Cor Bovinum)

Braunwauld 6th ed

Braunwauld 6th ed

DOE, Orthopnea, PND• usually after 4th / 5th decade and significant

cardiomegaly and LV dysfxnAngina pectoris• develops later, nocturnal sxs prominent; often with

diaphoresis due to HR slowing with arterial DBP falling to low levels

Palpitations / Head pounding• especially in supine position, pounding of heart

against chest wall• tachycardia from stress/exertion may precipitate and

cause extreme discomfort for pt

From Braunwauld. Cardiovascular Dz, 6th ed.

de Musset sign – head bobbing with heartbeat

Corrigan pulse – “water hammer” pulse

Bisferiens pulse – brach/ fem arteries

Hill sign – popliteal > brachial by 60mmHg

Traube sign – “pistol shot sounds” over fem artery

Duroziez sign – sys m when femoral artery compressed proximally

and diastolic m when compressed distally

Quincke sign – capillary pulsations

Apical impulse - diffuse, hyperdynamic and displaced inf/lat

systolic thrill – base/suprasternal notch / carotid arteries

Diastolic murmur• high frequency, sitting up, leaning forward• duration > intensity correlates with severity • mild AR – early diastole, hi pitched blowing• severe AR – holodiastolic, rough• musical (“cooing dove”) – eversion/perforation of Ao cusp• Primary valve dz – heard best LSB 3-4 intercostal• Ao Root dz – heard best RSB

Austin Flint murmur• mid-late diastolic apical rumble – severe AR

Wide Pulse PressureSystolic flow murmur (/thrill)

Mortality rate for severe AI+CHF sxs > 20-50%/yr2

Bonow, et al. JACC Nov 1988 2Aronow , et a. Am J Cardiol 1994; 74: 286. l

2D/ M-Mode• AV/ Ao Root anatomic abnormalities• LV dimension / sphericity• AMVL – fluttering, reverse doming• increased EPSSDoppler• Color Flow Mapping• Continuous Wave• Flow reversal in desc Ao (100% sens 97% spec for

severe AI)Limitations – What is severe AI?

AMVL fluttering

Color Flow – top mild, bottom moderate

Vasodilators• goal is to reduce SBP, improve forward SV, reduce regurgitant

volumeUses• severe AR + sxs/ LV dysfxn• short term hemodynamic improvement in pt with symptomatic AR

before AVR• prolong compensated phase of asymptomatic patients• No indication for asymptomatic pt with mild AI and normal LV fxn

Studied in AI• Nifedipine, Hydralizine, ACEI, Nipride, Prazosin• Children/ severe AR – ACEI reversed LV dilatation/wall stress• avoid (-) inotrope in LV dysfxn

Rx CHF – diuretics, aldactone, dig

avoid vigorous exertion if symptomatic AI

control diastolic BP (increases regurg)

avoid BB - prolong diastole, increase AR

Goal is to intervene before irreversible LV

systolic dysfxn ensues• initially reversible, mainly due to afterload excess

– full recovery in LV size/fxn possible

• with progressive chamber dilatation, decreased

myocardial contractility >> afterload excess as

cause of LV dysfxn.

• associated with worse recovery of LV fxn and

increased mortality

Indications for AVR (Severe AR)1

• Sxs (NYHA III-IV) regardless of LV fxn

• Sxs (NYHA II) with evidence of progressing LV dysfxn ( LV ESD ~ 55, LV EF <50-55%)

• Angina (CHA Class II or higher) w or w/o CAD

• mild-mod LV dysfxn (EF 25-49%) regardless of sxs

• mod-sev AR and undergoing CABG or other valvular surgery

Predictors of Postoperative Prognosis• LV systolic function

• LV End Systolic Size ( LV ESD)

1 Bonow, et al. Circulation 1998;98:1949-84

Asymptomatic, nl LV size/fxn

Asymptomatic, ESD >55 EF < 50-55%• serial exam/ measurements q 2-4 mos

Symptomatic, mild-mod LV dysfxn

Symptomatic, severe LV dysfxn• Hi surgical risk, but worse with med Rx (mortality

20-50%)

• individualize

Preload kept high immediate postop

period to fill dilated LV

temporary IABP use may be necessary

until LV fxn improves early post op

Ao Root disease• annuloplasty or other valve sparing surgery

possible if pure Ao Root dz

Primary AV disease• valve replacement

Figure 46-42 Repair of the aortic valve in patient with severe AR. Conduit tailoring in the

supravalvular position. The conduit is cut to replace three (left), two (middle), or one (right)

individual sinuses. The aortic aneurysm is replaced and the valve is spared.

(From David TE, Feindel CM, Bos J: Repair of the aortic valve in patients with aortic

insufficiency and aortic root aneurysm. J Thorac Cardiovasc Surg 109:345, 1995.)

Braunwauld 6th ed

Figure 29-15 A. Björk-Shiley Monostrut

mechanical prosthesis. B. Sorin Allcarbon

monoleaflet mechanical prosthesis.

C. Medtronic-Hall mechanical prosthesis.

D. Omnicarbon mechanical prosthesis.

Edmunds. Cardiac Surgery in the Adult. Ch 29

Figure 29-16 A. Carpentier-Edwards Supra-

annular porcine bioprosthesis. B. Hancock II

porcine bioprosthesis. C. Hancock modified

orifice porcine bioprosthesis. D. St. Jude

Medical Bioimplant porcine bioprosthesis.