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 EJECTION
120 C A = Mitral Valve Closure
C
110
B = Aortic Valve Opens
100
B
LV Pressure 90 B C = Aortic Valve Closure
(mm Hg) 80
70 Isovolumic
D = Mitral Valve Opens
60 Relaxation
ISOVOLUMETRIC SV Isovolumic
ISOVOLUMETRIC
Contraction
50 RELAXATION CONTRACTION
40
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 female.
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 S1  Loud S1- as loud as S2 in aortic
 +/- palpable opening snap area
(OS)  A2 to OS interval inversely
 RV lift proportional to severity
 Palpable S2
 Diastolic rumble: length
proportional to severity
ECG:  In severe MS with low flow-
 LAE, AFIB, RVH, RAD 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 sinus rhythm)
 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 Failure: Pulmonary HTN
Hepatic Congestion Pulmonary
JVD Congestion
Tricuspid Regurgitation LA Enlargement
RA Enlargement Atrial Fib
LA Thrombi
 LA Pressure

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.
6. Small Left Ventricle.
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
 Pulmonary infections
 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 Disease  Calcification, IE (abcess)
 Rheumatic  Papillary Muscles
 Endocarditis  CAD (Ischemia,
 Congenital-clefts Infarction, Rupture)
 Chordae  HCM
 Fused/inflammatory  Infiltrative disorders
 Torn/trauma  LV dilatation &
 Degenerative functional regurgitation
 IE  Trauma
 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 LA  Murmur-Dynamic
filling
MR(MVP)
 S 1 soft or normal
 S 2 wide split (early A2) unless
 mid systolic
LBBB  +/- click
  upright
 S 3 / flow rumble if severe

Wave Sound
 EJECTION PHASE

EDV
 MR
MR Stages
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 beats/min Adequate preload Minimally vasodilated
 MONITORING
 Routine

 TEE
Will depend on the type of surgery
 PA catheter 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 or late
CLICK
systolic murmur

S1 S2

Murmur
 M-MODE ECHO
M-MODE ECHO

M
V
P

MITRAL VALVE PROLAPSE

N
O
R
M
A
NORMAL MITRAL VALVE L
 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 no
evidence of regurgitation.