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Dr Sandeep Kumar KarDr Sandeep Kumar Kar
RMO –CUM CLINICAL TUTORRMO –CUM CLINICAL TUTOR
{Cardiac Anesthesiology}{Cardiac Anesthesiology}
I.P.G.M.E&R KOLKATAI.P.G.M.E&R KOLKATA
PREGNANCY WITHPREGNANCY WITH
MITRAL STENOSISMITRAL STENOSIS
ANESTHETICANESTHETIC
CONSIDERATIONSCONSIDERATIONS
(LONG CASE FORMAT)(LONG CASE FORMAT)
PARTICULARS OF THEPARTICULARS OF THE
PATIENTPATIENT
 Name – Mrs. XName – Mrs. X
 Age- 25 years.Age- 25 years.
 Sex-Female.Sex-Female.
 Religion-Humanity.(above allReligion-Humanity.(above all
religions)religions)
 Social status-Poor.Social status-Poor.
 Occupation-Housewife.Occupation-Housewife.
CHIEF COMPLAINTSCHIEF COMPLAINTS
• Patient is admitted with activePatient is admitted with active
labour pain at full term forlabour pain at full term for
institutional deliveryinstitutional delivery
• Shortness of breath for last 6Shortness of breath for last 6
weeks.weeks.
HISTORY OF PRESENTHISTORY OF PRESENT
ILLNESSILLNESS
 The breathlessness graduallyThe breathlessness gradually
progressive, exertional, nonprogressive, exertional, non
seasonal, grade III in severity.seasonal, grade III in severity.
 Cough not associated with anyCough not associated with any
fever .fever .
 No H/O chest pain, swelling of leg,No H/O chest pain, swelling of leg,
syncope, squatting, pain in leg,syncope, squatting, pain in leg,
neurodeficit.neurodeficit.
 H/O acute respiratory distress inH/O acute respiratory distress in
HISTORY OF PRESENTHISTORY OF PRESENT
ILLNESSILLNESS
• It is her first pregnancy.It is her first pregnancy.
• She experienced only mildShe experienced only mild
exertional dyspnea during her nonexertional dyspnea during her non
pregnant state.pregnant state.
• She was a diagnosed case of mitralShe was a diagnosed case of mitral
stenosis since her early adult hoodstenosis since her early adult hood
(15 yrs. Of age).(15 yrs. Of age).
• She had definite history of fever withShe had definite history of fever with
joint pain in her childhood (5 yrs ofjoint pain in her childhood (5 yrs of
age).age).
Treament historyTreament history
 The patient was on Tab. DigoxinThe patient was on Tab. Digoxin
(0.25mg) 1 OD for 5 days/week(0.25mg) 1 OD for 5 days/week
 Tab. Lasix (40mg) 1 bdTab. Lasix (40mg) 1 bd
 Syrup Pot chlor 2 tsf tdsSyrup Pot chlor 2 tsf tds
 prophylactic Inj. Penidura every 21prophylactic Inj. Penidura every 21
days.days.
PHYSICAL EXAMINATIONPHYSICAL EXAMINATION
• GENERAL SURVEYGENERAL SURVEY
Pt. is alert, conscious and co-operative.Pt. is alert, conscious and co-operative.
Build-Build- average,average,
State of nutrition-State of nutrition- poor,poor,
Decubitus-Decubitus- of choiceof choice,(preferably left,(preferably left
lateral)lateral)
FaciesFacies-- normalnormal
Pallor-Pallor- mildmild
Icterus-Icterus- absentabsent
Cyanosis-Cyanosis- absentabsent
Clubbing-Clubbing- absent.absent.
GENERAL SURVEYGENERAL SURVEY
Pulse -Pulse -
Rate-74/min,Rate-74/min,
Rhythm-regular,Rhythm-regular,
Volume- low,Volume- low,
all peripheral pulses areall peripheral pulses are
palpable,palpable,
condition of arterial wall-condition of arterial wall-
normal.normal.
no radio radial or radio femoralno radio radial or radio femoral
delaydelay
Blood pressure -Blood pressure - 100/76 mm of Hg.100/76 mm of Hg.
CVSCVS
• InspectionInspection –– no deformityno deformity..
• Palpation –Palpation – Apex beat in the left 5Apex beat in the left 5thth
ICSICS
½ inch in side the left MCL. Tapping in½ inch in side the left MCL. Tapping in
character.character.
• Diastolic thrillDiastolic thrill is palpable in the mitralis palpable in the mitral
area which is best felt in left lateralarea which is best felt in left lateral
position at the end of expiration.position at the end of expiration.
• Auscaltation –Auscaltation – S1-- short, sharp,S1-- short, sharp,
accentuated.accentuated. S2 – audible.S2 – audible.
P2 – Loud inP2 – Loud in
pulmonary areapulmonary area
contd…contd…
 Opening snap heard just after S2.Opening snap heard just after S2.
 Low pitched mid diastolic rumblingLow pitched mid diastolic rumbling
murmur of intensity IV/VI withmurmur of intensity IV/VI with
presystolic accentuation in the mitralpresystolic accentuation in the mitral
area without any radiation.area without any radiation. BestBest
heard with the bellheard with the bell of theof the
stethoscope, instethoscope, in left lateral positionleft lateral position ,,
at theat the height of expirationheight of expiration and afterand after
doing mild exercise.doing mild exercise.
EXAMINATION OF RESPIRATORYEXAMINATION OF RESPIRATORY
SYSTEMSYSTEM
Bilateral vesicular breathBilateral vesicular breath
sound.sound.
No adventitious sound.No adventitious sound.
EXAMINATION OF GASTROINTESTINALEXAMINATION OF GASTROINTESTINAL
SYSTEMSYSTEM
Abdomen -soft, 36 weeks as fundalAbdomen -soft, 36 weeks as fundal
heightheight
-umbilicus central in-umbilicus central in
position.position.
-no other palpable-no other palpable
lump,lump,
-fluid shift-absent.-fluid shift-absent.
-peristaltic sound--peristaltic sound-
EXAMINATION OF NERVOUS SYSTEMEXAMINATION OF NERVOUS SYSTEM::
No tremor, muscle wasting.No tremor, muscle wasting.
Power + TonePower + Tone upper limb-right-normal.upper limb-right-normal.
-left--left-
normal.normal.
 lower limb-right-normal.lower limb-right-normal.
-left--left-
normal.normal.
Deep tendon reflexes-normal.Deep tendon reflexes-normal.
Examination of cranial nerves-normal.Examination of cranial nerves-normal.
Obstetrical examinationObstetrical examination
 Uterine size – 36 wks.Uterine size – 36 wks.
 Position – left occipito-anteriorPosition – left occipito-anterior
 FHS – 160/min.FHS – 160/min.
AIRWAY EXAMINATIONAIRWAY EXAMINATION::
• Mouth opening-3 fingers.Mouth opening-3 fingers.
• No loose tooth/artificial denture.No loose tooth/artificial denture.
• Mallampati- grade II.Mallampati- grade II.
• Thyromental distance-6 fingers.Thyromental distance-6 fingers.
• Neck movement-within normal limits.Neck movement-within normal limits.
PROVISIONAL DIAGNOSISPROVISIONAL DIAGNOSIS::
Mitral stenosis of rheumatic originMitral stenosis of rheumatic origin
without any evidence of congestivewithout any evidence of congestive
heart failure and in sinus rhythm inheart failure and in sinus rhythm in
a primi para term mother posted fora primi para term mother posted for
CS.CS.
Etiology of MSEtiology of MS
• Almost always rheumatic in ourAlmost always rheumatic in our
setting.setting.
• Rarely congenital, SLE, carcinoidRarely congenital, SLE, carcinoid
syndrome, endocarditis, CVD,syndrome, endocarditis, CVD,
mucopolysccharoidosis.mucopolysccharoidosis.
• Pure MS approximately in 40%Pure MS approximately in 40%
rheumatic heart disease.rheumatic heart disease.
• Two – third of the all MS pt. areTwo – third of the all MS pt. are
female.female.
• Time gap of development symptomsTime gap of development symptoms
from rheumatic fever – two decade infrom rheumatic fever – two decade in
developed country but 5 – 15 yrs indeveloped country but 5 – 15 yrs in
developing countrydeveloping country ..
PathologyPathology
• Valve leaflets are diffusely thickenedValve leaflets are diffusely thickened
• Mitral commisure and cordaeMitral commisure and cordae
tendineae fused and shorten, valvetendineae fused and shorten, valve
cusp become rigid –cusp become rigid – fish mouth valve.fish mouth valve.
• Initial insult is rheumatic but laterInitial insult is rheumatic but later
changes may be a process resultingchanges may be a process resulting
from trauma to the valve caused byfrom trauma to the valve caused by
altered flow pattern due to initialaltered flow pattern due to initial
deformity.deformity.
• Thrombus formation and arterialThrombus formation and arterial
embolisation can occur.embolisation can occur.
Mitral stenosisMitral stenosis
PathophysiologyPathophysiology
 Mitral valve area (MVA):Mitral valve area (MVA):
NormalNormal  4 -- 6 sq. cm4 -- 6 sq. cm
Mild MSMild MS  1.5 – 2.5 sq. cm1.5 – 2.5 sq. cm
Moderate MSModerate MS  1.1– 1.5 sq. cm1.1– 1.5 sq. cm
Severe MSSevere MS  <1 sq. cm<1 sq. cm
Critical MSCritical MS < 0.6 sq. cm< 0.6 sq. cm
Mitral stenosisMitral stenosis
PathophysiologyPathophysiology
 Diastolic trans-mitral pressureDiastolic trans-mitral pressure
gradient:gradient:
Mild MS -- <5 mm Hg.Mild MS -- <5 mm Hg.
Moderate MS – 5 –12 mm Hg.Moderate MS – 5 –12 mm Hg.
Severe MS -- > 12 mm Hg.Severe MS -- > 12 mm Hg.
PATHOPHYSIOLOGYPATHOPHYSIOLOGY
MITRAL STENOSIS
Obstruction to LA emptying ↓LV filling
↑LA pressure↑LA size
↑pulm venous
pressure
↑pulm artery pressure
↓COPulm HTN
↑pulm vas
resistance
RV overload
TR
Perivascular edema, Pulm.Pulm.
Arteriolar constriction,Arteriolar constriction,
organicorganic
obliterative changes in theobliterative changes in the
pulm vascular bedpulm vascular bed
Obstruction to pulm blood
flow
↓lung compliance
↑work of breathing
Mitral stenosisMitral stenosis
PathophysiologyPathophysiology
• MVA < 2 sq. cmMVA < 2 sq. cm  increased pressureincreased pressure
gradient between LA & LV in diastole.gradient between LA & LV in diastole.
• Increased pressure gradient acrossIncreased pressure gradient across
MV – with decreased MVA or withMV – with decreased MVA or with
increased flow across MV.increased flow across MV.
• Increased flow across MVIncreased flow across MV 
increasing pressure gradient in anincreasing pressure gradient in an
exponential mannerexponential manner ( as pressure( as pressure
gradient varies with the square of thegradient varies with the square of the
flow).flow).
• Therefore, exercise and pregnancyTherefore, exercise and pregnancy
(increased blood volume & thus(increased blood volume & thus
increased flow) can cause significantincreased flow) can cause significant
increase in LA pressureincrease in LA pressure ..
Mitral stenosisMitral stenosis
PathophysiologyPathophysiology
 Increased HR (sinus tachycardia,Increased HR (sinus tachycardia,
AF)AF)  shortened diastolic fillingshortened diastolic filling
periodperiod  diminished time for LAdiminished time for LA
emptyingemptying  increased pressureincreased pressure
gradient across MV and increasedgradient across MV and increased
LA pressure.LA pressure.
 AF – additionally causes loss ofAF – additionally causes loss of
‘atrial kick’(contributes 30% to LV‘atrial kick’(contributes 30% to LV
filling)filling)  further reduction of LVfurther reduction of LV
fillingfilling  reduced cardiac out put.reduced cardiac out put.
Mitral stenosisMitral stenosis
PathophysiologyPathophysiology
• Increased LA pressureIncreased LA pressure  increasedincreased
pulmonary venous, capillary, arterialpulmonary venous, capillary, arterial
pressurepressure  risk of pulmonary edema.risk of pulmonary edema.
• Persistently elevated pulmonary arterialPersistently elevated pulmonary arterial
pressure (pulmonary hypertension, PAH)pressure (pulmonary hypertension, PAH)
 increased RV after loadincreased RV after load  RVHRVH 
RVFRVF  right sided CHF.right sided CHF.
• LV function is normal in most patients ofLV function is normal in most patients of
MS but poor LV function may be seen inMS but poor LV function may be seen in
25% of patients25% of patients because of LV fibrosis inbecause of LV fibrosis in
longstanding MS.longstanding MS.
Is LV function normal in mitralIs LV function normal in mitral
stenosis (controversy)stenosis (controversy)
 According to Bolen etal.According to Bolen etal.
 Fibrosis of the myocardiumFibrosis of the myocardium
secondary to rheumatic fever in thesecondary to rheumatic fever in the
posterobasal region of the ventricleposterobasal region of the ventricle
may be responsible formay be responsible for SWMA andSWMA and
decreased systolic function.decreased systolic function.
Is LV function normal in mitralIs LV function normal in mitral
stenosis (controversy)stenosis (controversy)
 Gash etalGash etal “ Under loaded“ Under loaded
ventricle’s fixed stroke volumeventricle’s fixed stroke volume
activates a reflex sympatheticactivates a reflex sympathetic
response and increases the SVRresponse and increases the SVR
thereby decreasing the ejectionthereby decreasing the ejection
phase indices.”phase indices.”
 ““Inotropically normal myocardium isInotropically normal myocardium is
simultaneously under loaded( ms)simultaneously under loaded( ms)
and afterload stressed(high SVR)and afterload stressed(high SVR)
that is afterload mismatched.”that is afterload mismatched.”
Modified New York AssociationModified New York Association
Functional Classification of HeartFunctional Classification of Heart
DiseaseDisease..
Class I: Asymptomatic except duringClass I: Asymptomatic except during
severe exertion.severe exertion.
Class II: Symptomatic with moderateClass II: Symptomatic with moderate
activity.activity.
Class III: Symptomatic with minimalClass III: Symptomatic with minimal
activity.activity.
Class IV: Symptomatic at rest.Class IV: Symptomatic at rest.
Age - usually younger population < 12 yrs
Sex – F (66 %) > M (34 %)
Symptoms:
1. SOB – commonest (in mild MS, by sudden change in
HR, vol-status, or CO e.g. severe exertion, excitement,
fever, severe anemia, paroxysmal AF or other
Tachycardia, Preg, thyrotoxicosis. As MS progress,
lesser stress ppt. dyspnea & also orthopnea, PND)
2. Palpitations,
3. Cough,
4. Haemoptysis (from rupture of pulm. Bronchial venous
connections 2nd
ary to PVH/ never fatal ),
6. Attacks of ac. Resp. distress ( pulm. edema)
cont.
Atypical presentationsAtypical presentations
• Atypical anginaAtypical angina ,, Chest pain in 10–15%Chest pain in 10–15%
of pts, evenof pts, even in the absence ofin the absence of
atherosclerosis;atherosclerosis; etiology often remainsetiology often remains
unexplained but may be emboli in theunexplained but may be emboli in the
coronary circulation or ac. RV pr.coronary circulation or ac. RV pr.
overload.overload.
• Pts may developPts may develop hoarsenesshoarseness as aas a
result of compression of the lt.result of compression of the lt.
recurrent laryngeal nv. by the enlargedrecurrent laryngeal nv. by the enlarged
LALA (Oatner syndrome )(Oatner syndrome )
• LV function is normal in the majorityLV function is normal in the majority
with pure MS, butwith pure MS, but impaired LVimpaired LV
functionfunction may be encountered inmay be encountered in upup
to 25%to 25% of pts &of pts & presumablypresumably
represents residual damage fromrepresents residual damage from
rheumatic myocarditis or coexistentrheumatic myocarditis or coexistent
hypertensive or IHD.hypertensive or IHD.
• 9.9.Malar flushMalar flush in face (pinched &in face (pinched &
blue facies).rare in indiansblue facies).rare in indians
• 10.10.Repeated pulm. Infection.Repeated pulm. Infection.
Examination
General DECUBITUSDECUBITUS: may be orthopnoeic: may be orthopnoeic
CYANOSIS: Present in severe MS with ac. pulm.CYANOSIS: Present in severe MS with ac. pulm.
edemaedema
OEDEMAOEDEMA: Bilateral pedal edema, accentuated in: Bilateral pedal edema, accentuated in
CCFCCF
NECK VEIN: Engorged in CCFNECK VEIN: Engorged in CCF
Prominent ‘a’ wave in pulm. HTNProminent ‘a’ wave in pulm. HTN
1. Pulse - low volume. Rhythm- usually regular,Rhythm- usually regular,
irregular in AFirregular in AF
2. BP: usually low.BP: usually low. Cold extremities.
3.3. RESPIRATION: may be tachypnoeicRESPIRATION: may be tachypnoeic
3. Engorged pulsatile neck veins, pedal edema,
tender hepatomegaly (Signs of RV failure). In pt.
with sinus rhythm & severe PH or associated
TR, JVP reveals prominent ‘a’ wave due
vigorous rt. atrial contraction && a gradual pr.a gradual pr.
ddecline after MV openingecline after MV opening (Y-descent).(Y-descent).
SystemicSystemic CVS-CVS-
InspectionInspection-- no deformity of precordium,no deformity of precordium,
- no venous prominence seen,- no venous prominence seen,
- visible pulm. Art. pulsation in left- visible pulm. Art. pulsation in left
2nd ICS in2nd ICS in
pulm. HTN.pulm. HTN.
PALPATION:PALPATION: **Apex beat-Apex beat- Lt 4th ICS, outsideLt 4th ICS, outside
MCL, tapping in character.MCL, tapping in character.
*Thrill-*Thrill- Diastolic thrill over apical area, bestDiastolic thrill over apical area, best
palpable in left lateral position at the heightpalpable in left lateral position at the height
of exp.of exp.
**Left parasternal heave-Left parasternal heave- in pulmonaryin pulmonary
HTN.HTN.
*Left parasternal impulse (rt ventricular*Left parasternal impulse (rt ventricular
tap).tap).
*Palpable S2*Palpable S2
Auscultation-
S1- short, sharp, accentuated
Opening snap -- audible just after S2 (just medial to
apex)
Mitral area- low pitched mid-diastolic rumbling
murmur
with presystolic accentuation of
varying
intensity without any radiation and
best
heard in left lateral position at the
height
expiration with the bell of the
stethoscope.
Pulmonary area- Pulmonary ejection click with
Pulmonary changesPulmonary changes
 VC, TLC, Max breathing capacity &VC, TLC, Max breathing capacity &
O2 uptake /unit of ventilation – mayO2 uptake /unit of ventilation – may
reduced.reduced.
 Also the elevated pulm. Venous pr.Also the elevated pulm. Venous pr.
& PAWP: ↓ C& PAWP: ↓ CLL , contribute to, contribute to
exertional dyspnea.exertional dyspnea.
Clinical assessment of severityClinical assessment of severity
• Assessing the AAssessing the A22 - OS gap.- OS gap.
• Assessing the severity of PAH.Assessing the severity of PAH.
• duration of the diastolic murmur.duration of the diastolic murmur.
ECGECG
 LA enlargement – wide and notchedLA enlargement – wide and notched
P wave (P mitrale) – mostP wave (P mitrale) – most
prominent in lead IIprominent in lead II
 RVHRVH
 Right axis deviationRight axis deviation
 f wave replacing P wave if atrialf wave replacing P wave if atrial
fibrillation developsfibrillation develops
ECGECG
CXRCXR
• Slight increase in the transverse diam. ofSlight increase in the transverse diam. of
heartheart
• Straightening of the left border of heartStraightening of the left border of heart
• Double contour of the right border of heartDouble contour of the right border of heart
• Evidence of PAH- dilated pulmonary arteryEvidence of PAH- dilated pulmonary artery
at hilum with peripheral prunningat hilum with peripheral prunning
• Dilatation of upper lobe pulmonary veinDilatation of upper lobe pulmonary vein
• Kerly’s B lineKerly’s B line
• Mitral valve calcificationMitral valve calcification
• Elevation of left upper lobe bronchusElevation of left upper lobe bronchus
• Multiple opacities due to hemosiderosisMultiple opacities due to hemosiderosis
Lt. Border - AuricularLt. Border - Auricular
appendage of LA.appendage of LA.
But mainly by LV.But mainly by LV.
Rt. Border – RARt. Border – RA
In MS: hypoplastic aortic knuckle
enlarged pulmonary bay
LA enlargement
Reduced LV size
Cephalization
Straightening
of left heart
Convexity from
enlarged left
atrial appendage
Echocardiogram
•Transvalvular peak & mean gradient
•Mitral orifice size
•Presence and severity of MR
•Extent of restriction of valve leaflets
•Degree of distortion of subvalvular apparatus
•Anatomic suitability of percutaneous mitral balloon
valvotomy (PMBV).
•Asses the ventricular chamber, LV function, PAP
[TEE is superior & use when TTE is inadequate. TEE is
especially indicated to exclude atrial thrombi before
PMBV].
Modified Duckett JonesModified Duckett Jones
criteria for diagnosingcriteria for diagnosing
Rheumatic heart diseaseRheumatic heart disease
Major criteria
• Carditis
• Arthritis
• Subcutaneous nodules
• Chorea
• Erythema Marginatum
Minor Criteria
• Clinical-
Fever
Arthralgia
• Laboratory - Acute phase reactants
Prolonged PR interval in ECG
Essential criteria
Evidence for recent streptococcal infection as
indicated by
•Increased ASO titer (> 250 todd units in west
bengal)
•Positive throat culture
•Recent scarlet fever
Diagnosis consists of :
Essential criteria + 2 major/ 1 major + 2 minor
criteria
Why does pregnancy aggravateWhy does pregnancy aggravate
the symptoms of mitral stenosis?the symptoms of mitral stenosis?
 Decrease inDecrease in SVRSVR
 Increase in HR 10-20 beats/min –Increase in HR 10-20 beats/min –
reduced diastolic filling time of LVreduced diastolic filling time of LV
 Increase in CO by 30-50%Increase in CO by 30-50% --
increase in transvalvular gradient –increase in transvalvular gradient –
rise in LA pressurerise in LA pressure
 Increase in blood volume by 30-Increase in blood volume by 30-
50%50% -increase in capillary-increase in capillary
hydrostatic pressure – pulmonaryhydrostatic pressure – pulmonary
Why does pregnancy aggravateWhy does pregnancy aggravate
the symptoms of mitral stenosis?the symptoms of mitral stenosis?
 During labour and deliveryDuring labour and delivery
sympathetic stimulation –sympathetic stimulation – rise in HRrise in HR
and COand CO
 Sudden rise in venous returnSudden rise in venous return due todue to
auto transfusion and IVCauto transfusion and IVC
compression –decompensationcompression –decompensation
Why does pregnancy aggravateWhy does pregnancy aggravate
the symptoms of mitral stenosis?the symptoms of mitral stenosis?
 Atrial enlargement in pregnancy –Atrial enlargement in pregnancy –
atrial fibrilationatrial fibrilation
 Hypercoagulability –Hypercoagulability –
thromboembolic riskthromboembolic risk
 During pregnancy pts symptomaticDuring pregnancy pts symptomatic
status increases by 1 or 2 NYHAstatus increases by 1 or 2 NYHA
class.class.
Just thinkJust think
Why tachycardia is
detrimental to the
patient?
• According to Gorlin formula:According to Gorlin formula: Pr. gradientPr. gradient
across valve is proportional to theacross valve is proportional to the
square of blood flowsquare of blood flow
• Flow = CO / diastolic filling timeFlow = CO / diastolic filling time
• Tachycardia (↓ diastolic filling time)Tachycardia (↓ diastolic filling time)
increasesincreases the pressure gradient by thethe pressure gradient by the
square of the original value.square of the original value.
• Acute elevation of LAP is rapidlyAcute elevation of LAP is rapidly
transmitted back to the pulm. capillaries.transmitted back to the pulm. capillaries.
• If pulm. capillary pr. rises above 25 mmIf pulm. capillary pr. rises above 25 mm
Hg,Hg, transudation of capillary fluid resultstransudation of capillary fluid results
in pulm. edema.in pulm. edema.
In shortIn short
↑↑HR→ ↓diastolicHR→ ↓diastolic
filling time→ ↑flow →filling time→ ↑flow →
↑pr. gradient across↑pr. gradient across
mitral valve → ↑LAPmitral valve → ↑LAP
→ pulm. edema.→ pulm. edema.
Therapeutic ApproachTherapeutic Approach
 Therapeutic approach is to reduceTherapeutic approach is to reduce
the heart rate and decrease leftthe heart rate and decrease left
atrial pressureatrial pressure
– Restrict physical activityRestrict physical activity
– Restrict salt intakeRestrict salt intake
– diureticsdiuretics
– Beta blockersBeta blockers
– Digoxin (if patient isDigoxin (if patient is in a. fib)in a. fib)
 During pregnancy clinical andDuring pregnancy clinical and
echocardiographic follow up toechocardiographic follow up to
be donebe done at 3 and 5 months andat 3 and 5 months and
every months thereafterevery months thereafter
 In pt unresponsive to medicalIn pt unresponsive to medical
therapytherapy PMC/BMVPMC/BMV to beto be
consideredconsidered after 20after 20thth
weekweek ofof
gestationgestation
 CMC during pregnancy stillCMC during pregnancy still
practised in developing worldpractised in developing world
 CPB during pregnancy risk isCPB during pregnancy risk is
same to mother as nonsame to mother as non
pregnant statepregnant state but fetalbut fetal
mortality is high.mortality is high.
Anti coagulationAnti coagulation
 Indications for anticoagulationIndications for anticoagulation
Patient with AF(> 48 hrs)Patient with AF(> 48 hrs)
Prior embolic eventPrior embolic event
Severe MS with left atrial dimension 55Severe MS with left atrial dimension 55
mm on ECHOmm on ECHO
 Heparin for first trimesterHeparin for first trimester
 Warfarin 12-36 weeksWarfarin 12-36 weeks
 After 36 weeks changed to heparinAfter 36 weeks changed to heparin
titrated to APTT leveltitrated to APTT level
Anaesthesia management –Anaesthesia management –
PrinciplesPrinciples
• Maintain sinus rhythmMaintain sinus rhythm and prevent rapidand prevent rapid
ventricular rates.ventricular rates.
• Atrial fibrillationAtrial fibrillation and tachycardia can alsoand tachycardia can also
precipitate worsening cardiac function.precipitate worsening cardiac function.
Aggressively treat new onset atrialAggressively treat new onset atrial
fibrillation pharmacologically or withfibrillation pharmacologically or with directdirect
cardioversion especially in thecardioversion especially in the
hemodynamically compromised patient .hemodynamically compromised patient .
• Avoid large, rapid falls in SVR.Avoid large, rapid falls in SVR. This isThis is
compensated for by increasing HR, whichcompensated for by increasing HR, which
can worsen cardiac function.can worsen cardiac function.
 Prevent increases in central bloodPrevent increases in central blood
volumevolume. Careful fluid management. Careful fluid management
and diuresis may be necessary.and diuresis may be necessary.
 Avoid factors that may increaseAvoid factors that may increase
pulmonary artery pressure (PAP).pulmonary artery pressure (PAP).
Prostaglandins,Prostaglandins, which may be usefulwhich may be useful
in treating uterine atony,in treating uterine atony, cancan
precipitate increases in pulmonaryprecipitate increases in pulmonary
vascular pressure.vascular pressure.
 LA filling to be kept high, butLA filling to be kept high, but
pulmonary edema to be avoided.pulmonary edema to be avoided. PAPA
pressure monitoring desirable.pressure monitoring desirable.
Effects of alteredEffects of altered
hemodynamicshemodynamicsAdverse
effects
Result Mechanism
Bradycardia CO Low cardiac
output
Tachycardia CO filling time
AF CO LV
filling/no atrial
kick
Preload CO LV filling
SVR CO stroke
volume
SVR CO SV (due to
tachycardia
related 
filling time)
Anesthetic optionAnesthetic option
• Evidence-based data on the idealEvidence-based data on the ideal
anesthetic and analgesic for the parturientanesthetic and analgesic for the parturient
with MS is lacking.with MS is lacking. Management must beManagement must be
individualized to optimize patient outcome.individualized to optimize patient outcome.
• The degree of monitoring should be basedThe degree of monitoring should be based
on theon the severity of the disease and theseverity of the disease and the
parturient”:s condition.parturient”:s condition.
• The concomitant use of invasiveThe concomitant use of invasive
hemodynamic monitorshemodynamic monitors is recommended inis recommended in
symptomatic parturients with criticalsymptomatic parturients with critical
stenosisstenosis ..
AnalgesiaAnalgesia
• It is important toIt is important to minimize painminimize pain andand
catecholamine release during labor.catecholamine release during labor.
• A carefully titratedA carefully titrated EpiduralEpidural for laborfor labor
and delivery addresses all theand delivery addresses all the
desired hemodynamic goals.desired hemodynamic goals.
Hemodynamic advantages ofHemodynamic advantages of
epidural anesthesiaepidural anesthesia
• Epidural analgesiaEpidural analgesia during the first stageduring the first stage
of labor canof labor can
• reduce PVR and SVR,reduce PVR and SVR,
• lower PAP, andlower PAP, and
• decrease CO to baseline levels.decrease CO to baseline levels.
• Rapid prehydration should be avoidedRapid prehydration should be avoided ..
• slow titration of local anesthetic solutionslow titration of local anesthetic solution
is recommended to minimiseis recommended to minimise
hemodynamic changes.hemodynamic changes.
Phenylephrine or ephedrine?Phenylephrine or ephedrine?
Unresolved controversyUnresolved controversy
 When treating hypotensionWhen treating hypotension ,,
phenylephrine is preferred overphenylephrine is preferred over
ephedrine as ephedrine may increaseephedrine as ephedrine may increase
the HR.the HR.
 Epinephrine-containing localEpinephrine-containing local
anesthetic solutions are best avoidedanesthetic solutions are best avoided
due to concerns about potentialdue to concerns about potential
tachycardia.tachycardia.
Evidences and logicEvidences and logic
 Ephedrine and dopamine act on the CVEphedrine and dopamine act on the CV
system in a manner almost exactlysystem in a manner almost exactly
reciprocal to the effects ofreciprocal to the effects of
sympathectomy associated with highsympathectomy associated with high
spinal or epidural anesthesiaspinal or epidural anesthesia (Butterworth JFT,(Butterworth JFT,
Austin JC, Johnson MD, et al. Effect of total spinal anesthesia on arterial andAustin JC, Johnson MD, et al. Effect of total spinal anesthesia on arterial and
venous responses to dopamine and dobuta-venous responses to dopamine and dobuta-
mine. Anesth Analg 1987;66(3):209–214.)mine. Anesth Analg 1987;66(3):209–214.)
 Phenylephrine also increases peripheralPhenylephrine also increases peripheral
vascular resistance and decreasesvascular resistance and decreases
venous capacitance, butvenous capacitance, but unlikeunlike
ephedrine or dopamine, it has minimalephedrine or dopamine, it has minimal
effects on myocardial contractility andeffects on myocardial contractility and
Evidences contd…Evidences contd…
 Placental vessels are usuallyPlacental vessels are usually
maximally dilated so placentalmaximally dilated so placental
perfusion is highly dependent onperfusion is highly dependent on
maternal BP.maternal BP.
 Phenylephrine inducedPhenylephrine induced
vasoconstriction of placental vesselvasoconstriction of placental vessel
is not clinically significant becauseis not clinically significant because
ofof large vascular reserve in alarge vascular reserve in a
normal placenta.normal placenta.
 Moran DH, Perillo M, La Porta RF, et al. Phenylephrine in theMoran DH, Perillo M, La Porta RF, et al. Phenylephrine in the
prevention of hypotension following spinal anesthesia for cesareanprevention of hypotension following spinal anesthesia for cesarean
deliery. J Clin Anesth 1991;3(4):301–305deliery. J Clin Anesth 1991;3(4):301–305 ..
The best strategy:The best strategy:
 Combined spinal–epidural (CSE)Combined spinal–epidural (CSE)
with an intrathecal opioid combinedwith an intrathecal opioid combined
with a dilute epidural infusionwith a dilute epidural infusion
minimizes sympathetic block andminimizes sympathetic block and
concomitant hypotension may be aconcomitant hypotension may be a
good option.good option.
Considerations in GAConsiderations in GA
• If GA is required, avoid drugs thatIf GA is required, avoid drugs that
produce tachycardia such asproduce tachycardia such as
atropine, pancuronium, ketamine,atropine, pancuronium, ketamine,
and meperidine.and meperidine.
• Vasodilating induction agentsVasodilating induction agents andand
volatile agents to be used with greatvolatile agents to be used with great
caution, as these tend tocaution, as these tend to reducereduce
SVR greatly.SVR greatly.
• Nitrous oxide to be avoided inNitrous oxide to be avoided in
established PAH.established PAH.
Best GA StrategyBest GA Strategy
• High dose narcotic (fentanyl 25 -30High dose narcotic (fentanyl 25 -30
mcg/kg)+ muscle relaxant (avoidmcg/kg)+ muscle relaxant (avoid
pancuronium) + ventilation with air-pancuronium) + ventilation with air-
oxygen mixture is a preferred option.oxygen mixture is a preferred option.
• Remifentanil may be the preferredRemifentanil may be the preferred
opioid in the peripartum setting due toopioid in the peripartum setting due to
its short context-sensitive half-lifeits short context-sensitive half-life
• Neonatal resuscitation should be readyNeonatal resuscitation should be ready
in hand.in hand.
Post- operative carePost- operative care
• TheThe intrapartum and immediateintrapartum and immediate
postpartumpostpartum periods are high risk as theperiods are high risk as the
PCWP increases in the presence ofPCWP increases in the presence of
severe MS (functional class III and IV).severe MS (functional class III and IV).
• Postoperative ventilation and intensivePostoperative ventilation and intensive
care may be necessary.care may be necessary.
• TheThe lowest possible dose of uterotoniclowest possible dose of uterotonic
agentagent is recommended as it mayis recommended as it may
produce significant adverseproduce significant adverse
cardiovascular effects.cardiovascular effects.
• Patients may need inotropic supportPatients may need inotropic support
as well as a pulmonary vasodilatoras well as a pulmonary vasodilator
such as nitroglycerin or sodiumsuch as nitroglycerin or sodium
nitroprusside .(Milrinone can be anitroprusside .(Milrinone can be a
good option).good option).
• In the appropriate patient, C/S mayIn the appropriate patient, C/S may
be followed by immediate correctivebe followed by immediate corrective
surgery, for example closed mitralsurgery, for example closed mitral
valvotomy..valvotomy..
Are prophylactic antibioticsAre prophylactic antibiotics
needed?needed?
 The use of prophylactic antibiotics is notThe use of prophylactic antibiotics is not
recommended for an uncomplicated electiverecommended for an uncomplicated elective
cesarean delivery in a woman who is not incesarean delivery in a woman who is not in
labor and has intact membranes.labor and has intact membranes.
 Indicated for procedures that causeIndicated for procedures that cause
bacteremia when the patients are atbacteremia when the patients are at increasedincreased
risk of I.E due to surgically constructedrisk of I.E due to surgically constructed
systemic – pulmonary shunts prostheticsystemic – pulmonary shunts prosthetic
valves RHD or previous I.Evalves RHD or previous I.E
ASRA guidelineASRA guideline
THANK YOUTHANK YOU
THANK YOU FOR
YOUR PATIENCE

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Long case pregnancy with mitral stenosis sandeep kumar kar

  • 1. Dr Sandeep Kumar KarDr Sandeep Kumar Kar RMO –CUM CLINICAL TUTORRMO –CUM CLINICAL TUTOR {Cardiac Anesthesiology}{Cardiac Anesthesiology} I.P.G.M.E&R KOLKATAI.P.G.M.E&R KOLKATA PREGNANCY WITHPREGNANCY WITH MITRAL STENOSISMITRAL STENOSIS ANESTHETICANESTHETIC CONSIDERATIONSCONSIDERATIONS (LONG CASE FORMAT)(LONG CASE FORMAT)
  • 2. PARTICULARS OF THEPARTICULARS OF THE PATIENTPATIENT  Name – Mrs. XName – Mrs. X  Age- 25 years.Age- 25 years.  Sex-Female.Sex-Female.  Religion-Humanity.(above allReligion-Humanity.(above all religions)religions)  Social status-Poor.Social status-Poor.  Occupation-Housewife.Occupation-Housewife.
  • 3. CHIEF COMPLAINTSCHIEF COMPLAINTS • Patient is admitted with activePatient is admitted with active labour pain at full term forlabour pain at full term for institutional deliveryinstitutional delivery • Shortness of breath for last 6Shortness of breath for last 6 weeks.weeks.
  • 4. HISTORY OF PRESENTHISTORY OF PRESENT ILLNESSILLNESS  The breathlessness graduallyThe breathlessness gradually progressive, exertional, nonprogressive, exertional, non seasonal, grade III in severity.seasonal, grade III in severity.  Cough not associated with anyCough not associated with any fever .fever .  No H/O chest pain, swelling of leg,No H/O chest pain, swelling of leg, syncope, squatting, pain in leg,syncope, squatting, pain in leg, neurodeficit.neurodeficit.  H/O acute respiratory distress inH/O acute respiratory distress in
  • 5. HISTORY OF PRESENTHISTORY OF PRESENT ILLNESSILLNESS • It is her first pregnancy.It is her first pregnancy. • She experienced only mildShe experienced only mild exertional dyspnea during her nonexertional dyspnea during her non pregnant state.pregnant state. • She was a diagnosed case of mitralShe was a diagnosed case of mitral stenosis since her early adult hoodstenosis since her early adult hood (15 yrs. Of age).(15 yrs. Of age). • She had definite history of fever withShe had definite history of fever with joint pain in her childhood (5 yrs ofjoint pain in her childhood (5 yrs of age).age).
  • 6. Treament historyTreament history  The patient was on Tab. DigoxinThe patient was on Tab. Digoxin (0.25mg) 1 OD for 5 days/week(0.25mg) 1 OD for 5 days/week  Tab. Lasix (40mg) 1 bdTab. Lasix (40mg) 1 bd  Syrup Pot chlor 2 tsf tdsSyrup Pot chlor 2 tsf tds  prophylactic Inj. Penidura every 21prophylactic Inj. Penidura every 21 days.days.
  • 7. PHYSICAL EXAMINATIONPHYSICAL EXAMINATION • GENERAL SURVEYGENERAL SURVEY Pt. is alert, conscious and co-operative.Pt. is alert, conscious and co-operative. Build-Build- average,average, State of nutrition-State of nutrition- poor,poor, Decubitus-Decubitus- of choiceof choice,(preferably left,(preferably left lateral)lateral) FaciesFacies-- normalnormal Pallor-Pallor- mildmild Icterus-Icterus- absentabsent Cyanosis-Cyanosis- absentabsent Clubbing-Clubbing- absent.absent.
  • 8. GENERAL SURVEYGENERAL SURVEY Pulse -Pulse - Rate-74/min,Rate-74/min, Rhythm-regular,Rhythm-regular, Volume- low,Volume- low, all peripheral pulses areall peripheral pulses are palpable,palpable, condition of arterial wall-condition of arterial wall- normal.normal. no radio radial or radio femoralno radio radial or radio femoral delaydelay Blood pressure -Blood pressure - 100/76 mm of Hg.100/76 mm of Hg.
  • 9. CVSCVS • InspectionInspection –– no deformityno deformity.. • Palpation –Palpation – Apex beat in the left 5Apex beat in the left 5thth ICSICS ½ inch in side the left MCL. Tapping in½ inch in side the left MCL. Tapping in character.character. • Diastolic thrillDiastolic thrill is palpable in the mitralis palpable in the mitral area which is best felt in left lateralarea which is best felt in left lateral position at the end of expiration.position at the end of expiration. • Auscaltation –Auscaltation – S1-- short, sharp,S1-- short, sharp, accentuated.accentuated. S2 – audible.S2 – audible. P2 – Loud inP2 – Loud in pulmonary areapulmonary area contd…contd…
  • 10.  Opening snap heard just after S2.Opening snap heard just after S2.  Low pitched mid diastolic rumblingLow pitched mid diastolic rumbling murmur of intensity IV/VI withmurmur of intensity IV/VI with presystolic accentuation in the mitralpresystolic accentuation in the mitral area without any radiation.area without any radiation. BestBest heard with the bellheard with the bell of theof the stethoscope, instethoscope, in left lateral positionleft lateral position ,, at theat the height of expirationheight of expiration and afterand after doing mild exercise.doing mild exercise.
  • 11. EXAMINATION OF RESPIRATORYEXAMINATION OF RESPIRATORY SYSTEMSYSTEM Bilateral vesicular breathBilateral vesicular breath sound.sound. No adventitious sound.No adventitious sound.
  • 12. EXAMINATION OF GASTROINTESTINALEXAMINATION OF GASTROINTESTINAL SYSTEMSYSTEM Abdomen -soft, 36 weeks as fundalAbdomen -soft, 36 weeks as fundal heightheight -umbilicus central in-umbilicus central in position.position. -no other palpable-no other palpable lump,lump, -fluid shift-absent.-fluid shift-absent. -peristaltic sound--peristaltic sound-
  • 13. EXAMINATION OF NERVOUS SYSTEMEXAMINATION OF NERVOUS SYSTEM:: No tremor, muscle wasting.No tremor, muscle wasting. Power + TonePower + Tone upper limb-right-normal.upper limb-right-normal. -left--left- normal.normal.  lower limb-right-normal.lower limb-right-normal. -left--left- normal.normal. Deep tendon reflexes-normal.Deep tendon reflexes-normal. Examination of cranial nerves-normal.Examination of cranial nerves-normal.
  • 14. Obstetrical examinationObstetrical examination  Uterine size – 36 wks.Uterine size – 36 wks.  Position – left occipito-anteriorPosition – left occipito-anterior  FHS – 160/min.FHS – 160/min.
  • 15. AIRWAY EXAMINATIONAIRWAY EXAMINATION:: • Mouth opening-3 fingers.Mouth opening-3 fingers. • No loose tooth/artificial denture.No loose tooth/artificial denture. • Mallampati- grade II.Mallampati- grade II. • Thyromental distance-6 fingers.Thyromental distance-6 fingers. • Neck movement-within normal limits.Neck movement-within normal limits.
  • 16. PROVISIONAL DIAGNOSISPROVISIONAL DIAGNOSIS:: Mitral stenosis of rheumatic originMitral stenosis of rheumatic origin without any evidence of congestivewithout any evidence of congestive heart failure and in sinus rhythm inheart failure and in sinus rhythm in a primi para term mother posted fora primi para term mother posted for CS.CS.
  • 17. Etiology of MSEtiology of MS • Almost always rheumatic in ourAlmost always rheumatic in our setting.setting. • Rarely congenital, SLE, carcinoidRarely congenital, SLE, carcinoid syndrome, endocarditis, CVD,syndrome, endocarditis, CVD, mucopolysccharoidosis.mucopolysccharoidosis. • Pure MS approximately in 40%Pure MS approximately in 40% rheumatic heart disease.rheumatic heart disease. • Two – third of the all MS pt. areTwo – third of the all MS pt. are female.female. • Time gap of development symptomsTime gap of development symptoms from rheumatic fever – two decade infrom rheumatic fever – two decade in developed country but 5 – 15 yrs indeveloped country but 5 – 15 yrs in developing countrydeveloping country ..
  • 18. PathologyPathology • Valve leaflets are diffusely thickenedValve leaflets are diffusely thickened • Mitral commisure and cordaeMitral commisure and cordae tendineae fused and shorten, valvetendineae fused and shorten, valve cusp become rigid –cusp become rigid – fish mouth valve.fish mouth valve. • Initial insult is rheumatic but laterInitial insult is rheumatic but later changes may be a process resultingchanges may be a process resulting from trauma to the valve caused byfrom trauma to the valve caused by altered flow pattern due to initialaltered flow pattern due to initial deformity.deformity. • Thrombus formation and arterialThrombus formation and arterial embolisation can occur.embolisation can occur.
  • 19. Mitral stenosisMitral stenosis PathophysiologyPathophysiology  Mitral valve area (MVA):Mitral valve area (MVA): NormalNormal  4 -- 6 sq. cm4 -- 6 sq. cm Mild MSMild MS  1.5 – 2.5 sq. cm1.5 – 2.5 sq. cm Moderate MSModerate MS  1.1– 1.5 sq. cm1.1– 1.5 sq. cm Severe MSSevere MS  <1 sq. cm<1 sq. cm Critical MSCritical MS < 0.6 sq. cm< 0.6 sq. cm
  • 20. Mitral stenosisMitral stenosis PathophysiologyPathophysiology  Diastolic trans-mitral pressureDiastolic trans-mitral pressure gradient:gradient: Mild MS -- <5 mm Hg.Mild MS -- <5 mm Hg. Moderate MS – 5 –12 mm Hg.Moderate MS – 5 –12 mm Hg. Severe MS -- > 12 mm Hg.Severe MS -- > 12 mm Hg.
  • 21. PATHOPHYSIOLOGYPATHOPHYSIOLOGY MITRAL STENOSIS Obstruction to LA emptying ↓LV filling ↑LA pressure↑LA size ↑pulm venous pressure ↑pulm artery pressure ↓COPulm HTN ↑pulm vas resistance RV overload TR Perivascular edema, Pulm.Pulm. Arteriolar constriction,Arteriolar constriction, organicorganic obliterative changes in theobliterative changes in the pulm vascular bedpulm vascular bed Obstruction to pulm blood flow ↓lung compliance ↑work of breathing
  • 22.
  • 23. Mitral stenosisMitral stenosis PathophysiologyPathophysiology • MVA < 2 sq. cmMVA < 2 sq. cm  increased pressureincreased pressure gradient between LA & LV in diastole.gradient between LA & LV in diastole. • Increased pressure gradient acrossIncreased pressure gradient across MV – with decreased MVA or withMV – with decreased MVA or with increased flow across MV.increased flow across MV. • Increased flow across MVIncreased flow across MV  increasing pressure gradient in anincreasing pressure gradient in an exponential mannerexponential manner ( as pressure( as pressure gradient varies with the square of thegradient varies with the square of the flow).flow). • Therefore, exercise and pregnancyTherefore, exercise and pregnancy (increased blood volume & thus(increased blood volume & thus increased flow) can cause significantincreased flow) can cause significant increase in LA pressureincrease in LA pressure ..
  • 24. Mitral stenosisMitral stenosis PathophysiologyPathophysiology  Increased HR (sinus tachycardia,Increased HR (sinus tachycardia, AF)AF)  shortened diastolic fillingshortened diastolic filling periodperiod  diminished time for LAdiminished time for LA emptyingemptying  increased pressureincreased pressure gradient across MV and increasedgradient across MV and increased LA pressure.LA pressure.  AF – additionally causes loss ofAF – additionally causes loss of ‘atrial kick’(contributes 30% to LV‘atrial kick’(contributes 30% to LV filling)filling)  further reduction of LVfurther reduction of LV fillingfilling  reduced cardiac out put.reduced cardiac out put.
  • 25. Mitral stenosisMitral stenosis PathophysiologyPathophysiology • Increased LA pressureIncreased LA pressure  increasedincreased pulmonary venous, capillary, arterialpulmonary venous, capillary, arterial pressurepressure  risk of pulmonary edema.risk of pulmonary edema. • Persistently elevated pulmonary arterialPersistently elevated pulmonary arterial pressure (pulmonary hypertension, PAH)pressure (pulmonary hypertension, PAH)  increased RV after loadincreased RV after load  RVHRVH  RVFRVF  right sided CHF.right sided CHF. • LV function is normal in most patients ofLV function is normal in most patients of MS but poor LV function may be seen inMS but poor LV function may be seen in 25% of patients25% of patients because of LV fibrosis inbecause of LV fibrosis in longstanding MS.longstanding MS.
  • 26. Is LV function normal in mitralIs LV function normal in mitral stenosis (controversy)stenosis (controversy)  According to Bolen etal.According to Bolen etal.  Fibrosis of the myocardiumFibrosis of the myocardium secondary to rheumatic fever in thesecondary to rheumatic fever in the posterobasal region of the ventricleposterobasal region of the ventricle may be responsible formay be responsible for SWMA andSWMA and decreased systolic function.decreased systolic function.
  • 27. Is LV function normal in mitralIs LV function normal in mitral stenosis (controversy)stenosis (controversy)  Gash etalGash etal “ Under loaded“ Under loaded ventricle’s fixed stroke volumeventricle’s fixed stroke volume activates a reflex sympatheticactivates a reflex sympathetic response and increases the SVRresponse and increases the SVR thereby decreasing the ejectionthereby decreasing the ejection phase indices.”phase indices.”  ““Inotropically normal myocardium isInotropically normal myocardium is simultaneously under loaded( ms)simultaneously under loaded( ms) and afterload stressed(high SVR)and afterload stressed(high SVR) that is afterload mismatched.”that is afterload mismatched.”
  • 28.
  • 29.
  • 30. Modified New York AssociationModified New York Association Functional Classification of HeartFunctional Classification of Heart DiseaseDisease.. Class I: Asymptomatic except duringClass I: Asymptomatic except during severe exertion.severe exertion. Class II: Symptomatic with moderateClass II: Symptomatic with moderate activity.activity. Class III: Symptomatic with minimalClass III: Symptomatic with minimal activity.activity. Class IV: Symptomatic at rest.Class IV: Symptomatic at rest.
  • 31. Age - usually younger population < 12 yrs Sex – F (66 %) > M (34 %) Symptoms: 1. SOB – commonest (in mild MS, by sudden change in HR, vol-status, or CO e.g. severe exertion, excitement, fever, severe anemia, paroxysmal AF or other Tachycardia, Preg, thyrotoxicosis. As MS progress, lesser stress ppt. dyspnea & also orthopnea, PND) 2. Palpitations, 3. Cough, 4. Haemoptysis (from rupture of pulm. Bronchial venous connections 2nd ary to PVH/ never fatal ), 6. Attacks of ac. Resp. distress ( pulm. edema) cont.
  • 32. Atypical presentationsAtypical presentations • Atypical anginaAtypical angina ,, Chest pain in 10–15%Chest pain in 10–15% of pts, evenof pts, even in the absence ofin the absence of atherosclerosis;atherosclerosis; etiology often remainsetiology often remains unexplained but may be emboli in theunexplained but may be emboli in the coronary circulation or ac. RV pr.coronary circulation or ac. RV pr. overload.overload. • Pts may developPts may develop hoarsenesshoarseness as aas a result of compression of the lt.result of compression of the lt. recurrent laryngeal nv. by the enlargedrecurrent laryngeal nv. by the enlarged LALA (Oatner syndrome )(Oatner syndrome )
  • 33. • LV function is normal in the majorityLV function is normal in the majority with pure MS, butwith pure MS, but impaired LVimpaired LV functionfunction may be encountered inmay be encountered in upup to 25%to 25% of pts &of pts & presumablypresumably represents residual damage fromrepresents residual damage from rheumatic myocarditis or coexistentrheumatic myocarditis or coexistent hypertensive or IHD.hypertensive or IHD. • 9.9.Malar flushMalar flush in face (pinched &in face (pinched & blue facies).rare in indiansblue facies).rare in indians • 10.10.Repeated pulm. Infection.Repeated pulm. Infection.
  • 34. Examination General DECUBITUSDECUBITUS: may be orthopnoeic: may be orthopnoeic CYANOSIS: Present in severe MS with ac. pulm.CYANOSIS: Present in severe MS with ac. pulm. edemaedema OEDEMAOEDEMA: Bilateral pedal edema, accentuated in: Bilateral pedal edema, accentuated in CCFCCF NECK VEIN: Engorged in CCFNECK VEIN: Engorged in CCF Prominent ‘a’ wave in pulm. HTNProminent ‘a’ wave in pulm. HTN 1. Pulse - low volume. Rhythm- usually regular,Rhythm- usually regular, irregular in AFirregular in AF 2. BP: usually low.BP: usually low. Cold extremities. 3.3. RESPIRATION: may be tachypnoeicRESPIRATION: may be tachypnoeic 3. Engorged pulsatile neck veins, pedal edema, tender hepatomegaly (Signs of RV failure). In pt. with sinus rhythm & severe PH or associated TR, JVP reveals prominent ‘a’ wave due vigorous rt. atrial contraction && a gradual pr.a gradual pr. ddecline after MV openingecline after MV opening (Y-descent).(Y-descent).
  • 35. SystemicSystemic CVS-CVS- InspectionInspection-- no deformity of precordium,no deformity of precordium, - no venous prominence seen,- no venous prominence seen, - visible pulm. Art. pulsation in left- visible pulm. Art. pulsation in left 2nd ICS in2nd ICS in pulm. HTN.pulm. HTN. PALPATION:PALPATION: **Apex beat-Apex beat- Lt 4th ICS, outsideLt 4th ICS, outside MCL, tapping in character.MCL, tapping in character. *Thrill-*Thrill- Diastolic thrill over apical area, bestDiastolic thrill over apical area, best palpable in left lateral position at the heightpalpable in left lateral position at the height of exp.of exp. **Left parasternal heave-Left parasternal heave- in pulmonaryin pulmonary HTN.HTN. *Left parasternal impulse (rt ventricular*Left parasternal impulse (rt ventricular tap).tap). *Palpable S2*Palpable S2
  • 36. Auscultation- S1- short, sharp, accentuated Opening snap -- audible just after S2 (just medial to apex) Mitral area- low pitched mid-diastolic rumbling murmur with presystolic accentuation of varying intensity without any radiation and best heard in left lateral position at the height expiration with the bell of the stethoscope. Pulmonary area- Pulmonary ejection click with
  • 37. Pulmonary changesPulmonary changes  VC, TLC, Max breathing capacity &VC, TLC, Max breathing capacity & O2 uptake /unit of ventilation – mayO2 uptake /unit of ventilation – may reduced.reduced.  Also the elevated pulm. Venous pr.Also the elevated pulm. Venous pr. & PAWP: ↓ C& PAWP: ↓ CLL , contribute to, contribute to exertional dyspnea.exertional dyspnea.
  • 38. Clinical assessment of severityClinical assessment of severity • Assessing the AAssessing the A22 - OS gap.- OS gap. • Assessing the severity of PAH.Assessing the severity of PAH. • duration of the diastolic murmur.duration of the diastolic murmur.
  • 39. ECGECG  LA enlargement – wide and notchedLA enlargement – wide and notched P wave (P mitrale) – mostP wave (P mitrale) – most prominent in lead IIprominent in lead II  RVHRVH  Right axis deviationRight axis deviation  f wave replacing P wave if atrialf wave replacing P wave if atrial fibrillation developsfibrillation develops
  • 41. CXRCXR • Slight increase in the transverse diam. ofSlight increase in the transverse diam. of heartheart • Straightening of the left border of heartStraightening of the left border of heart • Double contour of the right border of heartDouble contour of the right border of heart • Evidence of PAH- dilated pulmonary arteryEvidence of PAH- dilated pulmonary artery at hilum with peripheral prunningat hilum with peripheral prunning • Dilatation of upper lobe pulmonary veinDilatation of upper lobe pulmonary vein • Kerly’s B lineKerly’s B line • Mitral valve calcificationMitral valve calcification • Elevation of left upper lobe bronchusElevation of left upper lobe bronchus • Multiple opacities due to hemosiderosisMultiple opacities due to hemosiderosis
  • 42. Lt. Border - AuricularLt. Border - Auricular appendage of LA.appendage of LA. But mainly by LV.But mainly by LV. Rt. Border – RARt. Border – RA In MS: hypoplastic aortic knuckle enlarged pulmonary bay LA enlargement Reduced LV size
  • 45. Echocardiogram •Transvalvular peak & mean gradient •Mitral orifice size •Presence and severity of MR •Extent of restriction of valve leaflets •Degree of distortion of subvalvular apparatus •Anatomic suitability of percutaneous mitral balloon valvotomy (PMBV). •Asses the ventricular chamber, LV function, PAP [TEE is superior & use when TTE is inadequate. TEE is especially indicated to exclude atrial thrombi before PMBV].
  • 46.
  • 47.
  • 48.
  • 49. Modified Duckett JonesModified Duckett Jones criteria for diagnosingcriteria for diagnosing Rheumatic heart diseaseRheumatic heart disease
  • 50. Major criteria • Carditis • Arthritis • Subcutaneous nodules • Chorea • Erythema Marginatum Minor Criteria • Clinical- Fever Arthralgia • Laboratory - Acute phase reactants Prolonged PR interval in ECG
  • 51. Essential criteria Evidence for recent streptococcal infection as indicated by •Increased ASO titer (> 250 todd units in west bengal) •Positive throat culture •Recent scarlet fever Diagnosis consists of : Essential criteria + 2 major/ 1 major + 2 minor criteria
  • 52. Why does pregnancy aggravateWhy does pregnancy aggravate the symptoms of mitral stenosis?the symptoms of mitral stenosis?  Decrease inDecrease in SVRSVR  Increase in HR 10-20 beats/min –Increase in HR 10-20 beats/min – reduced diastolic filling time of LVreduced diastolic filling time of LV  Increase in CO by 30-50%Increase in CO by 30-50% -- increase in transvalvular gradient –increase in transvalvular gradient – rise in LA pressurerise in LA pressure  Increase in blood volume by 30-Increase in blood volume by 30- 50%50% -increase in capillary-increase in capillary hydrostatic pressure – pulmonaryhydrostatic pressure – pulmonary
  • 53. Why does pregnancy aggravateWhy does pregnancy aggravate the symptoms of mitral stenosis?the symptoms of mitral stenosis?  During labour and deliveryDuring labour and delivery sympathetic stimulation –sympathetic stimulation – rise in HRrise in HR and COand CO  Sudden rise in venous returnSudden rise in venous return due todue to auto transfusion and IVCauto transfusion and IVC compression –decompensationcompression –decompensation
  • 54. Why does pregnancy aggravateWhy does pregnancy aggravate the symptoms of mitral stenosis?the symptoms of mitral stenosis?  Atrial enlargement in pregnancy –Atrial enlargement in pregnancy – atrial fibrilationatrial fibrilation  Hypercoagulability –Hypercoagulability – thromboembolic riskthromboembolic risk  During pregnancy pts symptomaticDuring pregnancy pts symptomatic status increases by 1 or 2 NYHAstatus increases by 1 or 2 NYHA class.class.
  • 55.
  • 56. Just thinkJust think Why tachycardia is detrimental to the patient?
  • 57. • According to Gorlin formula:According to Gorlin formula: Pr. gradientPr. gradient across valve is proportional to theacross valve is proportional to the square of blood flowsquare of blood flow • Flow = CO / diastolic filling timeFlow = CO / diastolic filling time • Tachycardia (↓ diastolic filling time)Tachycardia (↓ diastolic filling time) increasesincreases the pressure gradient by thethe pressure gradient by the square of the original value.square of the original value. • Acute elevation of LAP is rapidlyAcute elevation of LAP is rapidly transmitted back to the pulm. capillaries.transmitted back to the pulm. capillaries. • If pulm. capillary pr. rises above 25 mmIf pulm. capillary pr. rises above 25 mm Hg,Hg, transudation of capillary fluid resultstransudation of capillary fluid results in pulm. edema.in pulm. edema.
  • 58. In shortIn short ↑↑HR→ ↓diastolicHR→ ↓diastolic filling time→ ↑flow →filling time→ ↑flow → ↑pr. gradient across↑pr. gradient across mitral valve → ↑LAPmitral valve → ↑LAP → pulm. edema.→ pulm. edema.
  • 59. Therapeutic ApproachTherapeutic Approach  Therapeutic approach is to reduceTherapeutic approach is to reduce the heart rate and decrease leftthe heart rate and decrease left atrial pressureatrial pressure – Restrict physical activityRestrict physical activity – Restrict salt intakeRestrict salt intake – diureticsdiuretics – Beta blockersBeta blockers – Digoxin (if patient isDigoxin (if patient is in a. fib)in a. fib)
  • 60.  During pregnancy clinical andDuring pregnancy clinical and echocardiographic follow up toechocardiographic follow up to be donebe done at 3 and 5 months andat 3 and 5 months and every months thereafterevery months thereafter  In pt unresponsive to medicalIn pt unresponsive to medical therapytherapy PMC/BMVPMC/BMV to beto be consideredconsidered after 20after 20thth weekweek ofof gestationgestation
  • 61.  CMC during pregnancy stillCMC during pregnancy still practised in developing worldpractised in developing world  CPB during pregnancy risk isCPB during pregnancy risk is same to mother as nonsame to mother as non pregnant statepregnant state but fetalbut fetal mortality is high.mortality is high.
  • 62. Anti coagulationAnti coagulation  Indications for anticoagulationIndications for anticoagulation Patient with AF(> 48 hrs)Patient with AF(> 48 hrs) Prior embolic eventPrior embolic event Severe MS with left atrial dimension 55Severe MS with left atrial dimension 55 mm on ECHOmm on ECHO  Heparin for first trimesterHeparin for first trimester  Warfarin 12-36 weeksWarfarin 12-36 weeks  After 36 weeks changed to heparinAfter 36 weeks changed to heparin titrated to APTT leveltitrated to APTT level
  • 63. Anaesthesia management –Anaesthesia management – PrinciplesPrinciples • Maintain sinus rhythmMaintain sinus rhythm and prevent rapidand prevent rapid ventricular rates.ventricular rates. • Atrial fibrillationAtrial fibrillation and tachycardia can alsoand tachycardia can also precipitate worsening cardiac function.precipitate worsening cardiac function. Aggressively treat new onset atrialAggressively treat new onset atrial fibrillation pharmacologically or withfibrillation pharmacologically or with directdirect cardioversion especially in thecardioversion especially in the hemodynamically compromised patient .hemodynamically compromised patient . • Avoid large, rapid falls in SVR.Avoid large, rapid falls in SVR. This isThis is compensated for by increasing HR, whichcompensated for by increasing HR, which can worsen cardiac function.can worsen cardiac function.
  • 64.  Prevent increases in central bloodPrevent increases in central blood volumevolume. Careful fluid management. Careful fluid management and diuresis may be necessary.and diuresis may be necessary.  Avoid factors that may increaseAvoid factors that may increase pulmonary artery pressure (PAP).pulmonary artery pressure (PAP). Prostaglandins,Prostaglandins, which may be usefulwhich may be useful in treating uterine atony,in treating uterine atony, cancan precipitate increases in pulmonaryprecipitate increases in pulmonary vascular pressure.vascular pressure.  LA filling to be kept high, butLA filling to be kept high, but pulmonary edema to be avoided.pulmonary edema to be avoided. PAPA pressure monitoring desirable.pressure monitoring desirable.
  • 65.
  • 66. Effects of alteredEffects of altered hemodynamicshemodynamicsAdverse effects Result Mechanism Bradycardia CO Low cardiac output Tachycardia CO filling time AF CO LV filling/no atrial kick Preload CO LV filling SVR CO stroke volume SVR CO SV (due to tachycardia related  filling time)
  • 67. Anesthetic optionAnesthetic option • Evidence-based data on the idealEvidence-based data on the ideal anesthetic and analgesic for the parturientanesthetic and analgesic for the parturient with MS is lacking.with MS is lacking. Management must beManagement must be individualized to optimize patient outcome.individualized to optimize patient outcome. • The degree of monitoring should be basedThe degree of monitoring should be based on theon the severity of the disease and theseverity of the disease and the parturient”:s condition.parturient”:s condition. • The concomitant use of invasiveThe concomitant use of invasive hemodynamic monitorshemodynamic monitors is recommended inis recommended in symptomatic parturients with criticalsymptomatic parturients with critical stenosisstenosis ..
  • 68. AnalgesiaAnalgesia • It is important toIt is important to minimize painminimize pain andand catecholamine release during labor.catecholamine release during labor. • A carefully titratedA carefully titrated EpiduralEpidural for laborfor labor and delivery addresses all theand delivery addresses all the desired hemodynamic goals.desired hemodynamic goals.
  • 69. Hemodynamic advantages ofHemodynamic advantages of epidural anesthesiaepidural anesthesia • Epidural analgesiaEpidural analgesia during the first stageduring the first stage of labor canof labor can • reduce PVR and SVR,reduce PVR and SVR, • lower PAP, andlower PAP, and • decrease CO to baseline levels.decrease CO to baseline levels. • Rapid prehydration should be avoidedRapid prehydration should be avoided .. • slow titration of local anesthetic solutionslow titration of local anesthetic solution is recommended to minimiseis recommended to minimise hemodynamic changes.hemodynamic changes.
  • 70. Phenylephrine or ephedrine?Phenylephrine or ephedrine? Unresolved controversyUnresolved controversy  When treating hypotensionWhen treating hypotension ,, phenylephrine is preferred overphenylephrine is preferred over ephedrine as ephedrine may increaseephedrine as ephedrine may increase the HR.the HR.  Epinephrine-containing localEpinephrine-containing local anesthetic solutions are best avoidedanesthetic solutions are best avoided due to concerns about potentialdue to concerns about potential tachycardia.tachycardia.
  • 71. Evidences and logicEvidences and logic  Ephedrine and dopamine act on the CVEphedrine and dopamine act on the CV system in a manner almost exactlysystem in a manner almost exactly reciprocal to the effects ofreciprocal to the effects of sympathectomy associated with highsympathectomy associated with high spinal or epidural anesthesiaspinal or epidural anesthesia (Butterworth JFT,(Butterworth JFT, Austin JC, Johnson MD, et al. Effect of total spinal anesthesia on arterial andAustin JC, Johnson MD, et al. Effect of total spinal anesthesia on arterial and venous responses to dopamine and dobuta-venous responses to dopamine and dobuta- mine. Anesth Analg 1987;66(3):209–214.)mine. Anesth Analg 1987;66(3):209–214.)  Phenylephrine also increases peripheralPhenylephrine also increases peripheral vascular resistance and decreasesvascular resistance and decreases venous capacitance, butvenous capacitance, but unlikeunlike ephedrine or dopamine, it has minimalephedrine or dopamine, it has minimal effects on myocardial contractility andeffects on myocardial contractility and
  • 72. Evidences contd…Evidences contd…  Placental vessels are usuallyPlacental vessels are usually maximally dilated so placentalmaximally dilated so placental perfusion is highly dependent onperfusion is highly dependent on maternal BP.maternal BP.  Phenylephrine inducedPhenylephrine induced vasoconstriction of placental vesselvasoconstriction of placental vessel is not clinically significant becauseis not clinically significant because ofof large vascular reserve in alarge vascular reserve in a normal placenta.normal placenta.  Moran DH, Perillo M, La Porta RF, et al. Phenylephrine in theMoran DH, Perillo M, La Porta RF, et al. Phenylephrine in the prevention of hypotension following spinal anesthesia for cesareanprevention of hypotension following spinal anesthesia for cesarean deliery. J Clin Anesth 1991;3(4):301–305deliery. J Clin Anesth 1991;3(4):301–305 ..
  • 73. The best strategy:The best strategy:  Combined spinal–epidural (CSE)Combined spinal–epidural (CSE) with an intrathecal opioid combinedwith an intrathecal opioid combined with a dilute epidural infusionwith a dilute epidural infusion minimizes sympathetic block andminimizes sympathetic block and concomitant hypotension may be aconcomitant hypotension may be a good option.good option.
  • 74. Considerations in GAConsiderations in GA • If GA is required, avoid drugs thatIf GA is required, avoid drugs that produce tachycardia such asproduce tachycardia such as atropine, pancuronium, ketamine,atropine, pancuronium, ketamine, and meperidine.and meperidine. • Vasodilating induction agentsVasodilating induction agents andand volatile agents to be used with greatvolatile agents to be used with great caution, as these tend tocaution, as these tend to reducereduce SVR greatly.SVR greatly. • Nitrous oxide to be avoided inNitrous oxide to be avoided in established PAH.established PAH.
  • 75. Best GA StrategyBest GA Strategy • High dose narcotic (fentanyl 25 -30High dose narcotic (fentanyl 25 -30 mcg/kg)+ muscle relaxant (avoidmcg/kg)+ muscle relaxant (avoid pancuronium) + ventilation with air-pancuronium) + ventilation with air- oxygen mixture is a preferred option.oxygen mixture is a preferred option. • Remifentanil may be the preferredRemifentanil may be the preferred opioid in the peripartum setting due toopioid in the peripartum setting due to its short context-sensitive half-lifeits short context-sensitive half-life • Neonatal resuscitation should be readyNeonatal resuscitation should be ready in hand.in hand.
  • 76. Post- operative carePost- operative care • TheThe intrapartum and immediateintrapartum and immediate postpartumpostpartum periods are high risk as theperiods are high risk as the PCWP increases in the presence ofPCWP increases in the presence of severe MS (functional class III and IV).severe MS (functional class III and IV). • Postoperative ventilation and intensivePostoperative ventilation and intensive care may be necessary.care may be necessary. • TheThe lowest possible dose of uterotoniclowest possible dose of uterotonic agentagent is recommended as it mayis recommended as it may produce significant adverseproduce significant adverse cardiovascular effects.cardiovascular effects.
  • 77. • Patients may need inotropic supportPatients may need inotropic support as well as a pulmonary vasodilatoras well as a pulmonary vasodilator such as nitroglycerin or sodiumsuch as nitroglycerin or sodium nitroprusside .(Milrinone can be anitroprusside .(Milrinone can be a good option).good option). • In the appropriate patient, C/S mayIn the appropriate patient, C/S may be followed by immediate correctivebe followed by immediate corrective surgery, for example closed mitralsurgery, for example closed mitral valvotomy..valvotomy..
  • 78. Are prophylactic antibioticsAre prophylactic antibiotics needed?needed?  The use of prophylactic antibiotics is notThe use of prophylactic antibiotics is not recommended for an uncomplicated electiverecommended for an uncomplicated elective cesarean delivery in a woman who is not incesarean delivery in a woman who is not in labor and has intact membranes.labor and has intact membranes.  Indicated for procedures that causeIndicated for procedures that cause bacteremia when the patients are atbacteremia when the patients are at increasedincreased risk of I.E due to surgically constructedrisk of I.E due to surgically constructed systemic – pulmonary shunts prostheticsystemic – pulmonary shunts prosthetic valves RHD or previous I.Evalves RHD or previous I.E
  • 80. THANK YOUTHANK YOU THANK YOU FOR YOUR PATIENCE