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PARTICULARS OF THE PATIENT : 1.Name – Mrs. Purnima Mondal 2.Age- 22 years. 3.Sex-Female. 4.Religion-Hindu. 5.Social status-Poor. 6.Occupation-Housewife. 7.Residence-Vill:Pukurkona,P.O:Mithipur,Dist:Murshidabad.


CHIEF COMPLAINTS : 1. Patient is admitted with active labour pain at full term for institutional delivery 2. S hortness of breath for last 6 weeks.


HISTORY OF PRESENT ILLNESS: The breathlessness gradually progressive, exertional , non seasonal, garde III in severity. Cough not associated with any fever . No H/O chest pain, swelling of leg, syncope, squatting, pain in leg, neurodeficit . H/O acute respiratory distress in night 1 week back.


It is her first pregnancy. She experienced only mild exertional dysponea during her non pregnant state. She was a diagnosed case of mitral stenosis since her early adulhood (15 yrs. Of age). She had definite history of rheumatic fever in her childhood (5 yrs of age). The patient was on Tab. Digoxin (0.25mg) 1 OD for 5 days/week, Tab. Lasix (40mg) 1 bd and Syrup Pot chlor 2 tsf tds with prophylactic Inj. Penidura every 21 days.


PHYSICAL EXAMINATION GENERAL SURVEY Pt. is alert, conscious and co-operative. Build- average, State of nutrition- poor, Decubitus - of choice, Facies - normal, Pallor- mild, Icterus - absent, Cyanosis- absent, Clubbing- absent.


GENERAL SURVEY….contd. Pulse- rate-74/min, rhythm-regular, volume-low, all peripheral pulses are palpable, condition of arterial wall-normal. no radio radial or radio femoral delay Blood pressure-100/76 mm of Hg.


CVS Inspection – no deformity. Palpation – Apex beat in the left 5 th ICS ½ inch in side the left MCL. Tapping in character. Diastolic thrill is palpable in the mitral area which is best felt in left lateral position at the end of expiration. A uscaltation – S1: short, sharp, accentuated. S2 – audible. P2 – Loud in pulmonary area


Opening snap heard just after S2. Low pitched mid diastolic rumbling murmur of intensity IV/VI with presystolic accentuation in the mitral area without any radiation. Best heard with the bell of the stethoscope, in left lateral position, at the height of expiration and after doing mild exercise.


EXAMINATION OF RESPIRATORY SYSTEM: Bilateral vesicular breath sound. No adventitious sound.


EXAMINATION OF NERVOUS SYSTEM : No tremor, muscle wasting. Power + Tone  upper limb-right-normal. -left-normal.  lower limb-right-normal. -left-normal. Deep tendon reflexes-normal. Examination of cranial nerves-normal.

Obstetrical examination:

Obstetrical examination Uterine size – 36 wks. Position – left oxiputo -anterior FHS – 160/min.


AIRWAY EXAMINATION : Mouth opening-3 fingers. No loose tooth/artificial denture. Mallampati- grade II. Thyromental distance-6 fingers. Neck movement-within normal limits.


PROVISIONAL DIAGNOSIS : M itral stenosis of rheumatic origin without any evidence of congestive heart failure and in sinus rhythm in a primi para term mother posted for CS.

Etiology of MS :

Etiology of MS Almost always rheumatic in our setting. Rarely congenital, SLE, carcinoid syndrome, endocarditis , CVD, mucopolysccharoidosis . Pure MS approximately in 40% rheumatic heart disease. Two – third of the all MS pt. are female. Time gap of development symptoms from rheumatic fever – two decade in developed country but 5 – 15 yrs in developing country.


Pathology Valve leaflet are diffusely thickened Mitral commisure and cordae tendineae fused and shorten, valve cusp become rigid – fish mouth valve. Initial insult is rheumatic but later changes may be a process resulting from trauma to the valve caused by altered flow pattern due to initial deformity. Thrombus formation and arterial embolisation occur.

Mitral stenosis Pathophysiology:

Mitral stenosis Pathophysiology Mitral valve area (MVA): Normal  4 -- 6 sq. cm Mild MS  1.4 – 2 sq. cm Moderate MS  1– 1.4 sq. cm Severe MS  <1 sq. cm

Mitral stenosis Pathophysiology:

Mitral stenosis Pathophysiology Diastolic trans-mitral pressure gradient: Mild MS -- <5 mm Hg. Moderate MS – 5 –12 mm Hg. Severe MS -- > 12 mm Hg.


PATHOPHYSIOLOGY MITRAL STENOSIS Obstruction to LA emptying ↓LV filling ↑LA pressure ↑LA size ↑pulm venous pressure ↑pulm artery pressure ↓CO Pulm HTN ↑pulm vas resistance RV overload TR Perivascular edema, Pulm. Arteriolar constriction, organic obliterative changes in the pulm vascular bed Obstruction to pulm blood flow ↓lung compliance ↑work of breathing

Mitral stenosis Pathophysiology:

Mitral stenosis Pathophysiology MVA < 2 sq. cm  increased pressure gradient between LA & LV in diastole. Increased pressure gradient across MV – with decreased MVA or with increased flow across MV. Increased flow across MV  increasing pressure gradient in an exponential manner ( as pressure gradient varies with the square of the flow). Therefore, exercise and pregnancy (increased blood volume & thus increased flow) can cause significant increase in LA pressure.

Mitral stenosis Pathophysiology:

Mitral stenosis Pathophysiology Increased HR (sinus tachycardia, AF)  shortened diastolic filling period  diminished time for LA emptying  increased pressure gradient across MV and increased LA pressure. AF – additionally causes loss of ‘atrial kick’  further reduction of LV filling  reduced cardiac out put.

Mitral stenosis Pathophysiology:

Mitral stenosis Pathophysiology Increased LA pressure  increased pulmonary venous, capillary, arterial pressure  risk of pulmonary edema. Persistently elevated pulmonary arterial pressure (pulmonary hypertension, PAH)  increased RV after load  RVH  RVF  right sided CHF. LV function is normal in most patients of MS but poor LV function may be seen in 25% of patients.

Modified New York Association Functional Classification of Heart Disease. :

Modified New York Association Functional Classification of Heart Disease . Class I: Asymptomatic except during severe exertion. Class II: Symptomatic with moderate activity. Class III: Symptomatic with minimal activity. Class IV: Symptomatic at rest.

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Age - usually younger population < 12 yrs Sex – F (66 %) > M (34 %) Symptoms: 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 ) Palpitations, 3. Cough, 4. Haemoptysis (from rupture of pulm . Bronchial venous connections 2 nd ary to PVH/ never fatal ), 6. Attacks of ac. Resp. distress ( pulm . edema ) cont.

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7 . Atypical angina , Chest pain in 10–15% of pts, even in the absence of atherosclerosis; etiology often remains unexplained but may be emboli in the coronary circulation or ac. RV pr. overload. Pts may develop hoarseness as a result of compression of the lt. recurrent laryngeal nv . by the enlarged LA LV function is normal in the majority with pure MS, but impaired LV function may be encountered in up to 25% of pts & presumably represents residual damage from rheumatic myocarditis or coexistent hypertensive or IHD. 8. Malar flush in face (pinched & blue facies ). 9. Repeated pulm . Infection.

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Examination General : DECUBITUS: may be orthopnoeic CYANOSIS: Present in severe MS with ac. pulm . edema OEDEMA: Bilateral pedal edema, accentuated in CCF NECK VEIN: Engorged in CCF Prominent ‘a’ wave in pulm . HTN 1. Pulse - low volume. Rhythm- usually regular, irregular in AF 2. BP: usually low. Cold extremities. 3. RESPIRATION: 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. a trial contraction & a gradual pr. d ecline after M V opening (Y-descent ).

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Systemic CVS- Inspection - no deformity of precordium , - no venous prominence seen, - visible pulm . Art. pulsation in left 2nd ICS in pulm . HTN. PALPATION: * Apex beat- Lt 4th ICS, outside MCL, tapping in character. * Thrill - Diastolic thrill over apical area, best palpable in left lateral position at the height of exp . * Left parasternal heave- in pulmonary HTN. *Left parasternal impulse ( rt ventricular tap). *Palpable S2

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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 of expiration with the bell of the stethoscope. Pulmonary area- Pulmonary ejection click with ejection systolic murmur in pulmonary HTN (due to relative obstruction). P 2 accentuated Closely split S 2 Systolic murmur - due to TR following RV dilatation

Pulmonary changes:

Pulmonary changes VC, TLC, Max breathing capacity & O2 uptake /unit of ventilation – may reduced. Also the elevated pulm . Venous pr. & PAWP: ↓ C L , contribute to exertional dyspnea .

Clinical assessment of severity:

Clinical assessment of severity Assessing the A 2 - OS gap. Assessing the severity of PAH. Intensity or duration of the diastolic murmur .


ECG LA enlargement – wide and notched P wave (P mitrale ) – most prominent in lead II RVH Right axis deviation F wave replacing P wave if atrial fibrillation develops


CXR Slight increase in the transverse diam. of heart Straightening of the left border of heart Double contour of the right border of heart Evidence of PAH- dilated pulmonary artery at hilum with peripheral prunning Dilatation of upper lobe pulmonary vein Kerly’s B line Mitral valve calcification Elevation of left upper lobe bronchus Multiple opacities due to hemosiderosis

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Lt. Border - Auricular appendage of LA. But mainly by LV. Rt. Border – RA In MS: hypoplastic aortic knuckle enlarged pulmonary bay LA enlargement Reduced LV size

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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 Jones criteria for diagnosing Rheumatic heart disease

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Major criteria Carditis Arthritis Subcutaneous nodules Chorea Erythema Marginatum Minor Criteria Clinical- Fever Arthralgia Laboratory - Acute phase reactants Prolonged PR interval in ECG

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Essential criteria Evidence for recent streptococcal infection as indicated by Increased ASO titer Positive throat culture Recent scarlet fever Diagnosis consists of : Essential criteria + 2 major/ 1 major + 2 minor criteria

Why does pregnancy aggravate the symptoms of mitral stenosis?:

Why does pregnancy aggravate the symptoms of mitral stenosis ? Increase in blood volume by 30-50% -increase in capillary hydrostatic pressure – pulmonary edema. Decrease in SVR Increase in HR 10-20 beats/min – reduced diastolic filling time of LV Increase in CO by 30-50% - increase in transvalvular gradient – rise in LA pressure


During labour and delivary sympathetic stimulation – rise in HR and CO Sudden rise in venous return due to autotransfution and IVC compression – decompensation Atrial enlargement in pregnancy – atrial fibrilation Hypercoagulability – thromboembolic risk During pregnancy pts symtomatic status increases by 1 or 2 NYHA class.

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Why tachycardia is detrimental?

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According to Gorlin formula: Pr. gradient across valve is proportional to the square of blood flow Flow = CO / diastolic filling time So, tachycardia ( ↓ diastolic filling time) ↑ s the pr. gradient by the square of the original value. Acute elevation of LA P is rapidly transmitted back to the pulm . capillaries. If pulm . capillary pr. rises above 25 mm Hg, transudation of capillary fluid results in pulm . edema. ►↑HR→ ↓ diastolic filling time → ↑flow → ↑p r. gradient across mitral valve → ↑ LA P → pulm . edema.

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Therapeutic approach is to reduce the heart rate and decrease left atrial pressure Restrict physical activity Restrict salt intake diuretics Beta blockers Digoxin (if patient is in a. fib)


During pregnancy clinical and echocardiographic follow up to be done at 3 and 5 months and every months thereafter In pt unresponsive to medical therapy PMC/BMV to be considered after 20 th week of gestation CMC during pregnancy still practised in developing world CPB during pregnancy risk is same to mother as non pregnant state but fetal mortality is high.

Anti coagulation:

Anti coagulation Indications for anticoagulation Patient with AF Prior embolic event Severe MS with left atrial dimension 55 mm on ECHO Heparin for first trimester Warfarin 12-36 weeks After 36 weeks changed to heparin titrated to APTT level

Anaesthetic management – Principles :

Anaesthetic management – Principles Maintain sinus rhythm and prevent rapid ventricular rates. Atrial fibrillation and tachycardia can also precipitate worsening cardiac function. Aggressively treat new onset atrial fibrillation pharmacologically or with direct cardioversion especially in the hemodynamically compromised patient . Avoid large, rapid falls in SVR. This is compensated for by increasing HR, which can worsen cardiac function.


Prevent increases in central blood volume. Careful fluid management and diuresis may be necessary. Avoid factors that may increase pulmonary artery pressure (PAP). Prostaglandins, which may be useful in treating uterine atony , can precipitate increases in pulmonary vascular pressure. LA filling to be kept high, but pulmonary edema to be avoided. PA pressure monitoring desirable.

Effects of altered hemodynamics:

Effects of altered hemodynamics

Anesthetic option:

Anesthetic option Evidence-based data on the ideal anesthetic and analgesic for the parturient with MS is lacking. Management must be individualized to optimize patient outcome. The degree of monitoring should be based on the severity of the disease and the woman’s condition. The concomitant use of invasive hemodynamic monitors is recommended in symptomatic parturients with critical stenosis .


It is important to minimize pain and catecholamine release during labor. A carefully titrated epidural for labor and delivery addresses all the desired hemodynamic goals. Epidural analgesia during the first stage of labor can reduce PVR and SVR, lower PAP, and decrease CO to baseline levels. Rapid prehydration should be avoided, and slow titration of local anesthetic solution is recommended to minimise hemodynamic changes.


When treating hypotension, phenylephrine is preferred over ephedrine, which may increase the HR. Epinephrine-containing local anesthetic solutions are best avoided due to concerns about potential tachycardia. Combined spinal–epidural (CSE) with an intrathecal opioid combined with a dilute epidural infusion minimizes sympathetic block and concomitant hypotension may be a good option.


If GA is required, avoid drugs that produce tachycardia such as atropine, pancuronium , ketamine , and meperidine . Vasodilating induction agents and volatile agents to be used with great caution, as these tend to reduce SVR greatly. Nitrous oxide to be avoided in established PAH. High dose narcotic ( fentanyl 25 -30 mcg/kg)+ muscle relaxant (avoid pancuronium ) + ventilation with air-oxygen mixture is a preferred option. Remifentanil may be the preferred opioid in the peripartum setting due to its short context-sensitive half-life Neonatal resuscitation should be ready in hand.


The lowest possible dose of uterotonic agent is recommended as it may produce significant adverse cardiovascular effects. The intrapartum and immediate postpartum periods are high risk as the PCWP increases in the presence of severe MS (functional class III and IV). Postoperative ventilation and intensive care may be necessary. Patients may need inotropic support as well as a pulmonary vasodilator such as nitroglycerin or sodium nitroprusside In the appropriate patient, C/S may be followed by immediate corrective surgery, for example closed mitral valvotomy ..

ASRA guideline:

ASRA guideline

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