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AORTIC STENOSIS AND AORTIC REGURGITATION

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AORTIC STENOSIS AND AORTIC REGURGITATION PRESENTED BY: DR. Neeraj & DR. Bikash MODERATER: DR. Maya www.anaesthesia.co.in anaesthesia.co.in_at_gmail.com – PowerPoint PPT presentation

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Title: AORTIC STENOSIS AND AORTIC REGURGITATION


1
AORTIC STENOSIS
AND AORTIC REGURGITATION
  • PRESENTED BY
  • DR. Neeraj DR. Bikash
  • MODERATER DR. Maya

www.anaesthesia.co.in anaesthesia.co.in_at_gmail.co
m
2
AORTIC STENOSIS
3
Aortic valve
  • Normally - 3 cusps
  • - May be bicuspid or unicuspid
  • Normal AV diameter 1.9 to 2.3 cm
  • Normal AV area 2 - 4 cm2
  • (2.6 to 3.5 cm2 )
  • Cusps are named according to their relation to
    coronary ostia -
  • left ,right and non-coronary
  • Normal diameter of LVOT 2.2 0.2 cm

4
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5
Incidence
  • ΒΌ of all with patient chronic VHD
  • Malegt female
  • (80 of adult pt with symptomatic valvular
    AS are male )
  • It is the most common form of VHD in US

6
Classification
  • SUPRAVALVULAR
  • VALVULAR
  • SUBVALVULAR- Discrete
  • Tunnel
  • VALVULAR
  • Congenital (lt 30 yr)
  • Bicuspid (40-60 yr )
  • Secondary to inflammation
  • (40-60 yr )
  • Degenerative (gt70 yr )

7
Etiology
  • Congenital- Stenotic since birth
  • Bicuspid 1-2 of population
  • - Male gt female (3 1 )
  • - 6 have coartation of aorta
  • - Mechanical shear stress
  • produce injury stenosis

8
Cont.
9
Cont.
  • Secondary to inflammation-
  • -Mainly rheumatic
  • -MC cause of AS in India and world
  • -Isolate rheumatic AS- rare
  • (Rheumatic AS always associated with
    mitral valve
  • involvement and AR )
  • -Post inflammation -gt commissural
  • fusion

10
Cont.
  • Degenerative-
  • -MC cause of AS in US and EUROPE
  • -gt30 people of gt65yr have AV
  • sclerosis
  • -Stenosis is due to sclerosis and
  • calcification
  • -Progress from the base of the cusp
  • to the leaf-lets

11
Risk factors of AS
  • Bicuspid aortic valve
  • Risk factors for atherosclerosis
  • - age
  • - male sex
  • - smoking
  • - DM, HTN
  • - ? LDL , ? HDL , ? CRP
  • Rheumatic fever
  • Conditions with ?SV and altered calcium
    metabolism

12
Pathophysiology
  • Aortic stenosis
  • ?
  • Obstruction to LV ejection
  • ?
  • Pressure overload
  • ?
  • ?LV mass (?wall thickness)
  • ?
  • ? ? ? ?
    ? ?
  • ?
    ?
  • Compensated
    Decompensated
  • ?LV compliance
    Fibrosis? contractility
  • Normal contractility
  • ?
    ?
  • LV filling ?early
    LV dilatation
  • ?late
  • ?
    ?
  • SV normal
    SV decreased

13
Cont.
  • The LVH is due to increase wall tension,in
    accordance with Laplaces law
  • Wall tension PR/2H
  • p -
    intraventricular pressure
  • r inner radius
  • h wall
    thickness

14
Cont.
  • Pressure overload
  • ?
  • ?Peak systolic pressure
  • ?
  • ?Wall tension
  • ?
  • Parallel replication of
    sacromeres (-)
  • ?
  • Increase wall thickness
  • ?
  • Concentric hypertrophy
  • Concentric hypertrophy normalizes wall stress and
    thus preserve myocardial contractility

15
Cont.
  • Consequence of LVH
  • - Alternation in diastolic compliance
  • - Imbalance in myocardial
  • supply/demand relationship
  • - Possible deterioration of intrinsic
  • contractile performance of
  • myocardium

16
Cont.
  • Pressure volume loop in AS

17
Cont.
  • Increased chamber stiffness impedes early left
    ventricular filling
  • Hence atrial systole is critical in maintaining
    ventricular filling and SV
  • In AS atrial systole accounts for 40 of LVEDV.
    (Normally it contribute 15-20 of LVEDV )

18
Cont.
  • Although contractility is preserved,
    hypertrophied ventricle is sensitive to ischemia
    and LVF

19
Natural history
  • Prolonged latent period
  • Once moderate stenosis present rate of
    progression is
  • -0.3m/s jet velocity/yr
  • -Mean pressure gradient
  • 7 mm-hg/yr
  • -?in valve area 0.1cm2 /yr

20
Clinical presentation
  • Asymptomatic with ES murmur
  • Classical triad
  • (angina, dyspnea, syncope )
  • Sudden death
  • (without symptoms it is lt1 )

21
Cont.
  • Symptoms/signs
  • - Angina
  • -Syncope
  • -CHF
  • Life expectancy
  • 5 yr
  • 2-3 yr
  • 1-2 yr

22
Cont.
23
Physical findings
  • Delayed sustain peak of arterial pulse
  • (pulsus
    parvus et tardus )
  • Bifid apical LV impulse
  • Systolic thrill
  • Late peaking SE murmur
  • (2nd right
    intercostsl space )
  • Paradoxical S2
  • S4 (with LVH ) S3 (with LVF )
  • (Thrill and intensity of murmur does not
    correlate with severity )

24
Investigation
  • CXR and ECG
  • - LVH
  • - Dilatation of ascending aorta
  • - Aortic calcification

25
Echocardiography
  • 2D/Doppler TTE- test of choice
  • Provide information about-
  • - Etiology, location
  • - Valve gradient and area
  • - Systolic/diastolic LV function
  • - Concomitant RWMA
  • - Coartation associated with
  • bicuspid valve

26
Cardiac Catheterization
  • Provide information about
  • - Pressure gradient
  • - AVA
  • - Cardiac output

27
Severity of AS
Severity Mean gradient (mm Hg) AV area (cm2)
Mild lt25 gt1.5
Moderate 25-50 1-1.5
Severe gt50 lt1.0
Critical gt80 lt0.7
28
Cont.
  • Gradient across valve normal until orifice area
    reaches less than half of normal
  • Onset of symptoms
  • 0.9 cm2 with CAD
  • 0.7 cm2 without CAD

29
Anesthetic consideration of AS in non-cardiac
surgery
30
Risk assessment
  • Increased peri and postoperative risk depend on
    both patient-related and procedure related
    factor.
  • AS is MC VHD in elderly
  • -2 to 9 of adult who are gt65 yr are affected
    by AS
  • Stewart et al and Lindoos et al
  • patients with severe AS face a17.3 risk of
    cardiac complication and 13 mortality rate
    during non-cardiac surgery.
  • ( j.am coll
    cardiology)

31
Cont.
Study/yr AS/ all pt Study type RR Perioperative cardiac events/death in pt with AS vs. pt without AS
Goldman et al (1977 ) 23/ 1001 Prospective 3.2 13 vs. 1.6
O keefe et al (1989 ) 48/NA Retrospective NA 14 only in pt with AS
Torsher et al (1998 ) 19/ NA Retrospective NA 11 only in pt with AS
Rohde et al (2001 ) 67/570 Prospective 6.8 8/ NA for all pt
Kertai et al (2004) 108/324 Retrospective case/control 5.2 14 vs. 2 for all event
32
Cont.
  • Adverse perioperative risk in patient with AS
    depends-
  • - Severity of AS
  • - Presence of concomitant CAD
  • -Severity of surgical procedure
  • -50 of patient with AS and angina have CAD ,
  • - Patient lt40 yr with AS , with no chest
    pain and no
  • coronary risk factor ,prevalence of CAD
    is 3-5
  • ( Bonow et al,J Heart
    Valve Dis,19987 )

33
How to deal with healthy patient with AS facing
noncardiac surgery
  • Medical history and physical examination
    cornerstone of preoperative evaluation
  • According to Michael et al
  • (Chest
    2005128,2944-2953 )

34
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35
Cont.
  • Non cardiac surgery can be safely performed 3
    months after CABG with an cardiac risk reduction
    from 3.3 to 1.7
  • (Anesth Analg
    200294,)
  • But paucity of data for timing of valve
    replacement prior to elective noncardiac surgery

36
Role of echo and cardiac catheterization
  • Current recommendation-
  • TTE should be performed in every patient
    with suspected AS
  • Cardiac catheterization? no extra role and is
    replaced by TTE.
  • It is now performed-
  • -When coronary angiography is required
  • - There is any doubt in echo.
  • (mochizuki et al., curr opin cardiol
    2003/18)

37
Management of anesthesia in AS
  • Anesthetic goal avoidance of event that may
    further decrease CO
  • - Maintain normal sinus rhythm
  • - Avoid Brady and tachycardia
  • - Avoid sudden ? or ? in SVR
  • - Fluid management to maintain
  • venous return and LV filling

38
Cont.
  • Premedication
  • - Adequate premedication to decrease
  • undue preoperative excitement and
  • tachycardia
  • - Supplemental oxygen
  • - Antibiotic prophylaxis

39
Monitoring
  • Routine monitoring
  • Standard 5 lead ECG
  • v4 and v5 for ischemia
  • lead II for arrhythmia
  • Use of intraoperative TEE is desirable -value is
    currently undetermined

40
Cont.
  • Invasive hemodynamic monitoring is -
    Controversial
  • - Intra-arterial BP monitoring is
    desirable
  • - CVP poor estimate of LV filling
    when
  • compliance is reduced
  • - Risk with PAC is arrhythmia
    induced
  • hypotension or ischemia
  • - But PAC also allow for measurement
    of CO, SVO2
  • and possible trans-venous pacing
    when needed

41
Cont.
  • Induction
  • - Few studies
  • - But in severe AS narcotic based
  • induction should be preferred
  • - Preferred non-narcotic induction is
  • by etomidate
  • LMA should be preferred over ETT whenever possible

42
Cont.
  • Maintenance
  • -In severe AS many prefer pure narcotic
  • technique
  • -In mild- moderate AS inhalational
    agents
  • can be safely used
  • disadvantage -negative inotrophy
  • -risk of
    arrhythmia
  • -Although N2O has potential of ?SVR
    discussion regarding this is less critical

43
Cont.
  • Intra-op hypertension and tachycardia-
  • - ? conc. Inhalational agent
  • - If B blocker- esmolol is preferred
  • - Temptation to control intra-op
    hypertension with
  • vasodilators should be resisted
    (Kaplan's )
  • Intra-op hypotension-
  • - Regardless of cause treat with
    alpha-agonist
  • - Then address underline etiology

  • (Kaplan's)

44
Regional anesthesia and AS
  • Regional anesthesia decreases SVR ,hence not
    preferred over GA.
  • Epidural is preferred over spinal
  • Mild-moderate AS can tolerate spinal
  • and epidural
  • Severe AS spinal and epidural are
  • contraindicated
  • (stoelting coexisting diseases
    )

45
Cont.
  • Collard et al
  • - Continuous spinal (.25 bupivacain )
  • - 2 patients
  • - Sever AS
  • - Hip surgery
  • - Invasive monitoring
  • (Anesth.analg
    199585 )

46
  • THANK YOU

www.anaesthesia.co.in anaesthesia.co.in_at_gmail.co
m
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