VALVULAR HEART DISEASE AND

ANAESTHESIA
MITRAL STENOSIS

MITRAL REGURGITATION

MITRAL VALVE
PROLAPSE
 Cardiac Output
+ +

Heart Rate Stroke Volume

- + + +
Increase Increase Increase
Parasympathetic Sympathetic End-diastolic
Activity Activity Volume
(and epi)

+
+ Increase
Venous
Return
 Another way to look at cardiac function:
Pressure - Volume Loops

130 Ejection
RAPID
120 C A = Mitral Valve
C EJECTION
110
Closure
100
B B = Aortic Valve Opens
LV Pressure 90 B
(mm Hg) 80 C = Aortic Valve
70 Isovolumic Closure
60 Relaxation
ISOVOLUMETRIC SV Isovolumic
ISOVOLUMETRI
Contraction D = Mitral Valve Opens
50 RELAXATION C
40 CONTRACTION
30
20
D A
10
A
10 20
D
30 40 50 60 70 80
CO = SV x HR
ESV EDV LV Volume (ml)
EF = SV / EDV
Diastolic Filling
The effects of increased HR on diastolic filling:
Mitral Stenosis: Etiology
 Primarily a result of rheumatic fever
(~ 99% of MV’s @ surgery show rheumatic
damage )
 Scarring & fusion of valve apparatus
 Rarely congenital
 Pure or predominant MS occurs in
approximately 40% of all patients
with rheumatic heart disease
 Two-thirds of all patients with MS are
 Mitral Stenosis: Natural
History
 Progressive, lifelong disease,
 Usually slow & stable in the early
years.
 Progressive acceleration in the later
years
 20-40 year latency from rheumatic
fever to symptom onset.
 Additional 10 years before disabling
symptoms
 Mitral Valve
Area

Normal 4 to 6 cm2
Mild stenosis 1.6 to 2.0
cm2
Moderate 1.1 to 1.5 cm2
Severe ≤ 1.0 cm2
 Recognizing Mitral
Stenosis
Palpation:
 Small volume pulse Auscultation:
 Tapping apex-palpable  Loud S1- as loud as S2 in
S1 aortic area
 +/- palpable opening  A2 to OS interval
snap (OS) inversely proportional
 RV lift to severity
 Palpable S2
 Diastolic rumble:
length proportional to
ECG: severity
 LAE, AFIB, RVH, RAD  In severe MS with low
flow- S1, OS & rumble
may be inaudible
Mitral Stenosis: Physical
Exam

S1 S2 OS S1

 First heart sound (S1) is accentuated

and snapping
 Opening snap (OS) after aortic valve
closure
 Low pitch diastolic rumble at the apex
 Pre-systolic accentuation (esp. if in
 Mitral Stenosis:
Pathophysiology

 Normal valve area: 4-6 cm2

 Mild mitral stenosis:
 MVA 1.5-2.5 cm2
 Minimal symptoms
 Mod mitral stenosis
 MVA 1.0-1.5 cm2 usually does not produce
symptoms at rest
 Severe mitral stenosis
 MVA < 1.0 cm2
 Mitral Stenosis:
Pathophysiology
Right Heart Pulmonary HTN
Failure: Pulmonary
Hepatic Congestion
Congestion LA Enlargement
JVD Atrial Fib
Tricuspid LA Thrombi
Regurgitation ↑ LA Pressure
RA Enlargement
RV Pressure
Overload
RVH LV Filling
RV Failure
Mitral Stenosis
STRAIGHTENING
OF LEFT HEART
BORDER
CALCIFICATION
OF MITRAL
VALVE
ANNULUS
WIDENING OF
CARINA
INDENTATION OF
OESOPHAGUS
 2-D Echo Findings in
MS
1. Thickened (> 3 mm) and calcified
mitral leaflets and subvalvular
apparatus.
2. “Hockey-stick” appearance of the
anterior mitral leaflet
in diastole (long-axis view).
3. “Fish-mouth” orifice in short-axis
view.
4. Immobility of posterior leaflet.
5. Increased Left Atrial Size.
M-mode mitral
valve(normal)
Thickened Leaflets in Mitral Stenosis

Mild Moderate Severe

Mitral stenosis.
Wedge is 23 while LVedp
from PV loop is 5 mmHg.
This is an 18 mm end
diastolic mitral gradient.
Note small stroke
volume due to
inadequate LV filling.
 Mitral Stenosis:
Complications
 Atrial dysrrhythmias
 Systemic embolization (10-25%)
 Risk of embolization is related to, age,
presence of atrial fibrillation, previous embolic
events
 Congestive heart failure
 Pulmonary infarcts (result of severe CHF)
 Hemoptysis
 Massive: 20 to ruptured bronchial veins (pulm
HTN)
 Streaking/pink froth: pulmonary edema, or
infection
 Endocarditis

 Anaesthetic
Considerations
 PRE-OP VISIT
 Degree of dyspnoea
 h/o haemoptysis( pulm venous
hypertension)
 Hoarseness( Ortner’s Syndrome)
 Intensity of S1

 S2-OS interval

 MDM with Pre systolic accentuation

 Anaesthetic Implications
 Anti-coagulants due to AF
 Digoxin for AF

 Diuretic therapy—electrolyte balance

 Fluid therapy---careful titration(

maintain adequate preload)
 Avoid tachycardia

 Avoid hypercarbia---premed ??

 Antibiotic prophylaxis ??

 Maintain systemic vascular

resistance.
 Short acting beta blockers beneficial
 Regional techniques with caution.
 Avoid light anaesthesia !!!!
 Sympathomimetics may be needed
to maintain forward output.
MITRAL REGURGITATION
 Mitral Regurgitation:
Etiology
 Valvular-leaflets  Annulus
 Myxomatous MV  Calcification, IE
Disease (abcess)
 Rheumatic  Papillary Muscles
 Endocarditis  CAD (Ischemia,
 Congenital-clefts Infarction,
 Chordae Rupture)
 HCM
 Fused/inflammator
y  Infiltrative
disorders
 Torn/trauma
 Degenerative
 LV dilatation &
 IE functional
regurgitation
 MR Etiology:Surgical
series
 MVP(20-70%)
 Ischemia (13-40%)
 RHD (3-40%)
 Infectious endocarditis(10-12%)
 MR Pathophysiology
 Chronic LV volume overload -»
compensatory LVE initially
maintaining cardiac output
 Decompensation (increased LV wall
tension) -»CHF
 LVE – » annulus dilation – » increased
MR
 Backflow – » LAE, Afib, Pulmonary
HTN
 MR Symptoms
 Similar to MS
 Dyspnea, Orthopnea, PND
 Fatigue
 Pulmonary HTN, right sided failure
 Hemoptysis
 Systemic embolization in A Fib
 Recognizing Chronic
Mitral Regurgitation
 Pulse:  Murmur-Fixed MR:
 brisk, low volume  pansystolic
 Apex:  loudest apex to axilla
 hyperdynamic
 laterally displaced
 no post extra-systolic
 palpable S3 +/- thrill accentuation
 late parasternal lift 2° to  Murmur-Dynamic
LA filling
MR(MVP)
 S 1 soft or normal
 mid systolic
 S 2 wide split (early A2)
unless LBBB  +/- click
 ↑ upright
 S 3 / flow rumble if
severe
Wave Sound
 EJECTION
PHASE

EDV
 MR Stages
LV size and function defined by echo
 Stage 1-compensated:
 End-diastolic dimension less 63mm, ESD less
42mm
 EF more than 60
 Stage 2-transitional
 EDD 65-68mm, ESD 44-45mm, EF 53-57
 Stage 3-decompensated
 EDD more than 70mm, ESD more than 45mm,
EF less than 50
 Anaesthetic Goals
 Decrease regurgitant fraction
 Facilitate forward output

FASTER FULLER
VASODIALATED
80-90 Adequate Minimally
beats/min preload vasodilated
 MONITORING
 Routine

 TEE
Will depend on the type of
 PA catheter surgery and severity of
MR
 Regional techniques beneficial…..
avoid drastic falls in blood pressure,
adequately preload
 Avoid suxamethonium related
bradycardia
 Prompt replacement of blood loss
 Vasodilators most beneficial in
patients with ventricular dilation and
associated systolic dysfunction
MITRAL VALVE
PROLAPSE PARASTERNAL
VIEW
 An inherited connective tissue
disorder
 Thickening and redundancy of mitral
valve
 Affects 5 – 10% of population, young
women more affected.
 Associations: Marfan’s Syndrome,
Rheumatic
endocarditis,Thyrotoxicosis,SLE
 Majority patients are asymptomatic
 Mostly non specific symptoms of
fatiguability, palpitations, etc.
 Rule out Coronary disease if chest
pain….since the chest pain is atypical
for angina
 Late systolic click and
CLICK
or late systolic
murmur
S S
1 2

Murmur
 M-MODE
M-MODE ECHO
ECHO
M
V
P

MITRAL VALVE PROLAPSE

N
O
R
M
A
NORMAL MITRAL L
VALVE
Anaesthetic Implications
 Goal of preop assessment is to
distinguish patients with a purely
functional disease from those with
symptomatic MR.
 Goals of management same as with
MR.
 Patients may be on beta blockers for
control of palpitations which should
be continued
 Antibiotic prophylaxis not needed if