Mitral stenosis is a narrowing of the mitral valve that causes obstruction of blood flow from the left atrium to the left ventricle. Rheumatic fever is the most common cause. Symptoms range from none in mild cases, to shortness of breath with exertion in moderate cases, to shortness of breath at rest in severe cases. Diagnosis is made through echocardiogram which can assess the severity based on metrics like mitral valve area and pressure gradients. Treatment depends on symptoms and severity, ranging from medications and lifestyle changes in mild cases, to balloon valvuloplasty or surgical commissurotomy in moderate to severe cases. Anesthetic management aims to avoid tachycardia and

1. PRESENTED BY: Dr. ANKUR KHANDELWAL,
Anaesthesiology & Critical care

2. INDEX
 INTRODUCTION
 ETIOLOGY
 PATHOPHYSIOLOGY
 SYMPTOMS AND SIGNS
 DIAGNOSIS
 ANESTHETIC MANAGEMENT

3.  INTRODUCTION
Mitral stenosis is the narrowing of mitral orifice as a result of
diffuse thickening of valve leaflets by fibrous tissue and calcific
deposits.
 ETIOLOGY
 Most common cause of mitral stenosis is rheumatic heart
disease.
 Females are affected more than males.
 Less common – carcinoid syndrome, left atrial myxoma, cor
triatriatum, rheumatoid arthritis, systemic lupus erythematosus
congenital.
 Pure MS approximately in 40% rheumatic heart disease.
 Time gap of development symptoms from rheumatic fever –
two decade in developed country but 5 – 15 yrs in developing
country

4. PATHOLOGY
 Thickening of valve leaflets and cusps become rigid.
 Fusion of mitral commissures.
 Shortening and fusion of chordae tendinae.
 All the changes leads to funnel shaped (fish mouth) valve.
 Calcification immobilize the leaflets and narrows the orifice
further.
 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.

5. PATHOPHYSIOLOGY
 Cardiac changes-
 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
 Symptoms at rest
 Mean gradient:
 >10 mmHg  Severe
 5-10 mmHg  Moderate
 <5 mmHg  Mild

6. Right Heart Failure:
Hepatic Congestion
↑JVP
Tricuspid Regurgitation
RA Enlargement
 Pulmonary HTN
Pulmonary Congestion
Atrial Fib
LA Thrombi
LA Enlargement
 LA Pressure
RV Pressure Overload
RVH
RV Failure
Obstruction of diastolic inflow
Prolonged early diastolic
mitral inflow &delayed filling
Pressure volume loops shifted
to left so LVEDP and LVEDV
are↓
PATHOPHYSIOLOGY

7. PULMONARY CHANGES
Pulmonary arterial hypertension results as-
 Increased left atrial pressure.
 Pulmonary arterial constriction.
 Interstitial edema in the wall of the small pulmonary vessels.
 Organic obliterative changes in the pulmonary vascular bed.
 At last if there is severe pulmonary arterial
hypertension→Tricuspid
regurgitation
 Pulmonary incompetence
 Reduced lung compliance and increased work of breathing.
 Right heart failure.

8. HEMODYNAMIC CHANGES THAT OCCURS AT VARIOUS
STAGES OF SEVERITY OF MITRAL STENOSIS
SEVERITY→ MILD
(1.5-2.5 cm2)
MODERATE
(1.1-1.5 cm2)
SEVERE
( < 1cm2 )
Left atrial
pressure N ↑ ↑↑
Pulmonary
arterial pressure N ↑ ↑↑ or ↑↑↑↑
Cardiac output
N N ↓ or ↓↓↓
Left atrial
pressure ↑ ↑↑
Pulmonary
arterial pressure ↑ ↑↑
Cardiac output
↑ ↑
AT
R
E
S
T
E
X
E
R
C
I
S
E

10. NATURAL HISTORY OF
MS
 Continuous progressive, life-long disease
 Slow, stable early course, latent period of 20-40
yrs from RF to onset of symptoms
 Onset of symptoms to disability- 10 yrs
 Atrial fibrillation- 30-40%
 Causes of death
 CHF
 Systemic embolism
 Pulmonary embolism
 Infection

11. HISTORY & CLINICAL EXAMINATION
 History of Rheumatic fever.
 SYMTOMS
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 due to pulmonary venous hypertension.)
2. Palpitations
3. Cough
4. Haemoptysis (from rupture of pulm. Bronchial venous connections 2ndary to PVH/
never fatal)
5. Easy fatiguability and syncope( due to reduced cardiac output)
6. Attacks of ac. Resp. distress ( pulm. edema)
7. Aytypical 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 acute RV pressure overload
8. Hoarseness due to compression of left recurrent laryngeal nerve by enlareged left
atrium (Ortner‟s Syndrome)
9. Oedema, ascites
10. Mitral facies or malar flush
11. Recurrent pulmonary infections
12. Symptoms of thromboembolic complications (e.g. stroke, ischaemic limb)

12. NYHA FUNCTIONAL CLASSIFICATION OF
PATIENT WITH HEART DISEASE
 CLASS Ι - Asymptomatic
 CLASS ΙΙ –Symptoms with ordinary activity but comfortable
at rest.
 CLASS ΙΙΙ –Symptoms with minimal activity but comfortable
at rest.
 CLASS ΙV – Symptoms at rest

13. EXAMINATIO
N
 General Examination
 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
 Pulse - low volume. Rhythm- usually regular, irregular in AF
 BP: usually low. Cold extremities.
 RESPIRATION: may be tachypnoeic
 Tender Hepatomegaly.

14. SYSTEMIC EXAMINATION
INSPECTION -- no deformity of precordium,
-- no venous prominence seen,
-- visible pulm. Art. pulsation in left 2nd ICS in
pulm. HTN
Palpation:
 Small volume pulse
 Tapping apex-palpable S1
 Palpable S2
 Thrill- Diastolic thrill over apical
area, best palpable in left lateral
position at the height of exp
 Left parasternal heave
Auscultation:
 Loud S1
 P2 component accentuated.
 A2-P2 Split.
 S2 to OS interval inversely proportional
to severity
 Diastolic rumble: length proportional to
severity
 In severe MS with low flow- S1, OS &
rumble may be inaudible
 Diastolic murmur (Graham-Steel)- high
pitched murmur heard at the cardiac
base secondary to pulmonary
regurgitation.

15. Clinical assessment of
severity
• Assessing the A2 - OS gap- Inversely proportional
to severity
• Duration of the diastolic murmur- directly
proportional to the length of the murmur
• Assessing the severity of PAH

17. INVESTIGATIO
NS
 Complete Haemogram
 Blood sugar
 Serum Electrolytes
 Liver function tests
 Renal Function tests
 Chest X- Ray
 ECG
 Echocardiography
 CT brain (in special cases)

18.  Chest X-Ray
 Slight increase in the transverse
diam. of heart
 Straightening of left border of cardiac
silhouette.
 Double contour of the right border of
heart
 Enlarged pulmonary conus
 Small Aortic knob.
 Dilatation of the upper lobe
pulmonary veins- Moustache or antler
sign.
 Backward displacement of the
esophagus by enlarged left atria.

23.  ELECTROCARDIOGRAPHY
 LA enlargement
 Manifest as a P wave lasting> 0.12 msec with prominent
negative deflection of its terminal component (duration: > 0.04
msec; amplitude: >0.10 mV) in V1;
 Broad, notched P waves in lead II, III and aVF.
Atrial fibrillation
F wave replacing P wave if atrial fibrillation develops
Right Ventricular hypertrophy
 Right axis QRS deviation, and tall R waves in V1 suggest RV
hypertrophy

26. ECHOCARDIOGRAPHY
 Diagnosis of Mitral Stenosis
 Assessment of hemodynamic severity
mean gradient, mitral valve area, Left atrial pressure, pulmonary artery pressure
 Extent of restriction of valve leaflets
 Assessment of size and function of the Ventricles.
 Reevaluation of patients with known MS with changing symptoms or signs.
 F/U of asymptomatic patients with mod-severe MS
 Anatomic suitability of percutaneous mitral balloon valvotomy (PMBV).

27.  Cormier‟s Grading of Mitral Valve Anatomy
Based on ECHO
ECHO group Mitral Valve Anatomy
GROUP 1 Pliable non-calcified anterior mitral leaflet and mild subvalvular
disease( thin chordae >/=10 mm long
GROUP 2 Pliable non-calcified anterior mitral leaflet and severe
subvalvular disease(thickened chordae>10mm)
GROUP 3 Calcification of mitral valve of any extent, as assessed by
fluroscopy, whatever the state of subvalvular apparatus

28. Treatment Modalities of Mitral
Stenosis Asymtomatic/ Mildly symptomatic Mitral stenosis
 Diuretics for congestive symptoms and restriction of salt intake.
 Drugs for rate control
 Prophylaxis against infective endocarditis
 Warfarin to patients with history of AF or thromboembolism
 Symtomatic Mitral Stenosis- unless there is a contraindication, mitral
valvotomy is performed in symptomatic patients with moderate or severe isolated
MS. Mitral valvotomy can be carried out by two techniques-
1. PMBV
2. Surgical( Open) Valvotomy using Cardiopulmonary Bypass.
Succesful valvotomy is defined by a 50% reduction in the mean mitral valve
gradient and a doubling of the mitral valve area.
Severe Mitral Stenosis/ Valve morphology not favourable for
PMBV/ MS with MR- Surgical Commissurotomy or MVR should be
carried out.

29. Predictors of poor outcome after surgical
procedure
 Age>65 yrs
 Presence of CAD
 LV dysfunction
 Severe pulmonary hypertension
 RV dysfunction
 Associated Co-Morbidities.

30.  PREOPERATIVE MEDICATIONS
 Antianxiety drugs decrease tachycardia associated with anxiety.
 Drugs used for heart rate control should be continued until the time of
surgery.
 If diuretics are used treat hypovolemia and hypokalemia if associated.
 Antibiotics for surgical and infective endocarditis prophylaxis.
 Anticoagulant therapy- based on following rationales:-
 1. Acceptable INR for surgery- An INR <1.5 is generally acceptable
 2. Risk of bleeding-
a) Discontinuation of warfarin is essential for the procedures associated
with a high risk of bleeding
b) Discontinuation of warfarin is usually not necessary for the
procedures associated with a low risk of bleeding

31.  3. Risk of thrombosis
 Management steps
Low risk of thrombosis High risk of thrombosis
AF without additional risk factors AF + either h/o stroke/TIA or >risk factors such as recent
CHF,HTN,Age>70 yrs, diabetes
DVT/PE occuring more than 3 months ago DVT/PE occuring in past 3 months.
Hypercoagulable state without recent
thrombotic episode
Hypercoagulable state with recent thrombotic episode
Newer model mechanical aortic prosthesis
and any tissue valves
Mechanical mitral prosthesis and old model aortic prosthesis
Low risk of thrombosis High risk of thrombosis
Discontinue warfarin 5 days prior to surgery Discontinue warfarin 5 days prior to surgery
Check INR the day before surgery, ensure
target INR<1.5
Start prophylactic or therapeutic LMWH
Restart warfarin at pre-op dose as soon as
hemostasis is assured and only after epidural
catheters are removed
Last dose of LMWH is not given any later than 24 hrs before the
procedure.
Recheck INR within one week after starting
warfarin and then at regular intervals.
Check INR the day before surgery, ensure target INR<1.5
Restart LMWH/ warfarin at pre-op dose as soon as hemostasis is assured
MANAGEMENT

32.  4. Timing of procedure
 If urgent or emergent procedures are to be undertaken in < 4-5
days and warfarin reversal is required, it may be satisfactory to
give 1-2 mg of Vitamin K orally in order to reverse the effect of
warfarin. When reversal of anticoagulation is required within 6
hours, intravenous Vitamin K and Octaplex® is required(Virally
Inactivated Plasma-Derived Concentrate). FFP can be given if
Octaplex is not available.
 5. Type of anaesthesia.
a) Local and general anesthesia can be safely administered to
a patient on warfarin.
b) Neuraxial blocks (e.g., epidural analgesia, spinal anesthesia
and retrobulbar blocks) should not be performed on patients
on warfarin

33. ASRA guideline

34. Anesthetic management
 The main objectives are-
 To avoid tachycardia.
 To maintain sinus rhythm. 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.
 To avoid hypovolemia and fluid overload.
 Avoid factors that may increase pulmonary artery pressure (PAP)

35. Effects of altered
hemodynamics
Adverse
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)

37. Why tachycardia is
detrimental?
 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.

38. MONITORING
 Noninvasive monitoring like HR, BP
, ECG, RR, SpO2.
 Invasive monitoring depends upon-
 1. Complexity of the operative procedure.
2.Magnitude of physiological impairment.
 The concomitant use of invasive hemodynamic
monitors is recommended in symptomatic
patients with critical stenosis.

39. ANAESTHESIA
TECHNIQUE REGIONAL ANAESTHESIA
 Patients may be very sensitive to the vasodilating effect of spinal and
epidural anesthesia.
 Epidural is preferable over spinal anesthesia because of the more gradual
onset.
 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---can be considered as a good option.
 Surgery under Peripheral Nerve Blocks can be the best anesthetic
technique wherever possible
 Hypothermia to be avoided as it increases PVR.

40. GENERAL ANAESTHESIA
 PREANAESTHETIC MEDICATIONS
 Avoid premedication with anticholinergics to avoid tachycardia.
 Opioids like fentanyl are used to give analgesia. Use generous
amounts of opioids to abolish hemodynamic response to
intubation. It will also decrease the requirement of induction
agents.
 Antianxiety drugs decrease tachycardia associated with
anxiety
 Epidural analgesia with opioids can be considered safely as a
supplement to GA whenever needed.
 PREOXYGENATION
Adequate preoxygenation to avoid any degree of hypoxia.

41.  INDUCTION
 General Anaesthetics with/without Muscle Relaxation
 There is no single “correct” agent. Any drug can be used
as long as hemodynamic goals are met.
 Patients with moderate to severe MS generally have slow
circulation that prolongs arm-brain circulation time.
 Induction agents should be double diluted and given
slowly in titrated doses.
 Etomidate is the best agent for hemodynamic stability, but
thiopentone can be used instead.
 Propofol should be avoided as it can lead to precipitous
hypotension.
 Ketamine to be avoided as it causes tachycardia.
 Induction with volatile anaesthetics to be avoided- causes
decreased SVR and cardiac output , hypotension.

42.  MUSCLE RELAXATION
 For muscle relaxation agents that do not release histamine are
preferred as histamine causes tachycardia and hypotension.
 Steroidal group of muscle relaxants does not cause histamine
release. Example are- VECURONIUM, ROCURONIUM except
PANCURONIUM.
 Benzylisoquinolinium group causes histamine release.
Example are –ATRACURIUM, CISATRACURIUM,
MIVACURIUM.
 Succinylcholine also causes slight release in histamine

43.  MAINTAINENCE
 Oxygen + Air + High dose narcotic or volatile
anaesthetics such as isoflurane, desflurane or
sevoflurane at low vol%
 Halothane is best avoided due to its arryhthmogenic
potential and high incidence of junctional rhythm
which can be disastrous in a patient with mitral
stenosis.
 In patients with PAH, nitrous oxide is best avoided
due to its effect on pulmonary resistance.
 Deep plane of anaesthesia should be maintained.
 Ensure appropriate ventilation and proper fluid
therapy.

44.  If there is intra-op tachycardia
1. Deepen the plane and ensure adequate analgesia
2. Use beta blockers like esmolol/propranolol or calcium
channel blockers like diltiazem.
 If atrial fibrillation occurs ventricular rate can be controlled with
esmolol, propranolol, diltiazem , digoxin or amidarone.
 For sudden supraventricular tachycardia –cardioversion.
DRUG LOADING DOSE MAINTENANCE
AMIODARONE 15mg/min for 10 min 0.5-1mg/ min for 6hrs
DIGOXIN 0.25mg 2hry until 1mg 0.125-0.25mg/day
DILTIAZEM 0.25mg/kg over 3-5 mins 5-15 mg/hr
ESMOLOL 500microg/kg over 1min 50ug/kg/min
METOPROLOL 5mg over 3-5 mins x 3
doses
1.25-5mg 6hrly
VERAPAMIL 5-10mg over 3-5 mins 2.5-10 mg/hr

45. Reversal of anesthesia.
 Nondepolarising muscle relaxants is achieved
slowly with neostigmine and glycopyrrolate to
reduce drug induced tachycardia caused by
glycopyrrolate.
Post operative management
 Proper pain management to avoid tachycardia.
 Risk of pulmonary edema and right heart failure
continue so cardiovascular monitoring should be
continued.
 Oxygen supplementation until adequate
oxygenation is established.
 Management of post op hypothermia and
shivering.

46. 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 delivery sympathetic stimulation – rise in HR
and CO
 Sudden rise in venous return due to autotransfusion and IVC
compression –decompensation
 Atrial enlargement in pregnancy – atrial fibrillation
 Hypercoagulability – thromboembolic risk
 During pregnancy pts symtomatic status increases by 1 or 2
NYHA class.

48. 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

49. Thank
You……….