Anes. and Valvular Disease.ppt anesthetic implications

this talks about various anesthetic implications in valvular heart disease

1. Valvular Heart Disease
&
Anesthetic Considerations
Wilford Hall Medical Center
Department of Anesthesiology
Presented By: Jerry A. Beyer, M.D.

2. LESIONS TO BE DISCUSSED
Mitral Stenosis (MS)
Mitral Regurgitation (MR)
Mitral Valve Prolapse (MVP)
Aortic Stenosis (AS)
Idiopathic Hypertrophic Subaortic Stenosis (IHSS)
Aortic Regurgitation (AR)
Mixed Lesions
Monitoring

3. SORTING IT ALL OUT
MS & AS Cause Pressure Overloads
MR & AR Cause Volume Overloads
Understand the pathophysiology of each lesion & choose
peri-operitive meds according to anticipated effect on:
RHYTHM
RATE
PRELOAD
CONTRACTILITY
AFTERLOAD
Exact control not always possible…pick a side for error &
manage accordingly

4. MITRAL STENOSIS
PATHOPYSIOLOGY

Mechanical obstruction to LVED filling
Increases LAV / LAP / PAP

Usually normal LV function

SV decreased during tachycardia

SV decreased when atrial contraction is lost A-Fib
Usually females / post rheumatic heart disease
DOE, Orthopnea, PND
Symptoms usually present at 50% obstruction of a normal
4-6 CM
2
valve area
Atrial enlargement often leads to A-Fib

5. MITRAL STENOSIS
INTRA-OP OBJECTIVES
RHYTHM – must maintain NSR
RATE – normal to low
PRELOAD – normal to low
CONTRACTILITY - optimize
AFTERLOAD – normal to slightly elevated
AVOID HYPOXEMIA / HYPERCARBIA (AS IN
ALL LESIONS THAT INCREASE PAP)

6. MITRAL REGURGITATION
PATHOPYSIOLOGY
Usually caused by rheumatic heart disease &
associated with multiple sclerosis
Isolated MR usually acute & occurs post AMI,
with ruptured cordae (endocarditis), or with
annular dilation from chronic HTN
LA volume overload & decreased forward flow

Beware of ECHO report stating normal EF in the
setting of even mild to moderate MR

7. MITRAL REGURGITATION
INTRA-OP OBJECTIVES
RHYTHM – NSR best, but not as important as in
MS
RATE – normal to elevated

PRELOAD – normal to elevated
CONTRACTILITY - optimize
AFTERLOAD – normal to decreased
FAST, FULL, FORWARD !!!

8. MITRAL VALVE PROLAPSE
PATHOPYSIOLOGY
Billowing of the posterior mitral leaflet into the LA
during systole
5%-10% of Americans, higher in young women

Usually benign but may cause cerebral embolic
events, endocarditis, MR, and sudden death
Often associated with A-FIB or SVT

9. MITRAL VALVE PROLAPSE
INTRA-OP OBJECTIVES
Prevent SBE

Mouth, Sinus, GI, or GU procedures

Is there associated MR?
IF no ECHO, you must assume there is MR
See SBE guidelines in pre-op syllabus for specific
recommended regimens

10. MITRAL VALVE PROLAPSE
INTRA-OP OBJECTIVES
Determine degree of MR if it is present and treat
as such
RHYTHM – NSR best

RATE – Normal to elevated
PRELOAD – Normal to elevated
CONTRACTILITY - Optimize
AFTERLOAD – normal to decreased

11. AORTIC STENOSIS
Congenital Bicuspid AoV 38%
Degenerative calcification 33%
Rheumatic/post-inflammatory 24%
Congenital unicuspid 2%
Hypoplastic 1%
Indeterminate 2%

12. AORTIC STENOSIS
Latency Period for AS
Bicuspid 48  6 years
Degenerative 66  12 years
Rheumatic 39  18 years
Risks

Sudden death (< 2%/yr)

Infective endocarditis(< 1%/yr)

13. AORTIC STENOSIS
Pathophysiology
Critical if AVA < 0.8 CM
2
or Gradient > 50 mmHG
?? Associated angina, dyspnea, syncope
Obstruction of aortic outflow tract causes
pressure overload in the LV, concentric LVH,
increased O
2 DEMAND, supply-demand
mismatch, IHD

14. AORTIC STENOSIS
Intra-op objectives
RHYTHM – must have NSR, LV is highly
dependent on normal LVEDV / LVEDP
RATE – Normal to slightly elevated, avoid
bradycardia (fixed SV like in a child)
PRELOAD – normal to increased to maintain LV
filling
CONTRACTILITY - Optimize
AFTERLOAD – normal to elevate (maintain CPP)

15. IDIOPATHIC HYPERTROPIC
SUBAORTIC STENOSIS (IHSS)
IHSS Synonyms
Hypertrophic obstructive cardiomyopathy
(HOCM)
Muscular subaortic stenosis
Different pathophysiology but similar intra-
op objectives to AS (with the addition of
limiting ionotropic state)

16. AORTIC REGURGITATION
Pathophysiology
Disease causing poor valve coaptation leading to
LV volume overload
Chronic AR can lead to LVH, supply-demand
mismatch, & IHD
Can be the result of rheumatic heart disease,
endocarditis, chronic HTN, thoracic aorta
dissection

17. AORTIC REGURGITATION
INTRA-OP OBJECTIVES
RHYTHM - NSR
RATE – normal to elevated to prevent increased LVEDV /
LEDP
PRELOAD – normal to elevated to improve forward flow
CONTRACTILITY - optimize
AFTERLOAD – normal to decreased to improve forward
flow and limit regurgitant fraction
AGAIN, REGURGITATION = FAST, FULL, FORWARD !!!

18. MIXED LESIONS
There is often more than one valvular
lesion which may occur in the same or
multiple valves
This can make choosing intra-op objectives
very challenging

19. MIXED LESIONS
Observe the patients vital signs in the clinic
records and pre-op…aim for what they are when
the patient is clinically optimized…this may give
you information about the predominant lesion
Error on the side of treating the most life
threatening lesion…usually this is AS
TEE can be extremely helpful in guiding your
treatment in the OR
Remember, the LV cardiac output can only be as
good as the RV cardiac output

20. MONITORING
Again … Always use NIBP, 5 lead
continuous EKG, PAO2
Also …Use IBP, CVP, PA, TEE as needed
depending on the complexity of the case