The document presents a clinical case of a 22-year-old female student diagnosed with mitral stenosis, characterized by symptoms such as breathlessness, palpitations, and a productive cough. The patient's history includes rheumatic fever in childhood, and examinations reveal acute signs of mitral stenosis along with relevant diagnostic measures including ECG and echocardiogram. Treatment options span from medical management for milder cases to surgical interventions for severe mitral stenosis, including considerations for anesthetic management during surgery.

1. WELCOME TO CLINICAL
PRESENTATION
MITRAL STENOSIS
Prepared By: Dr Md Masum Hossain Arif
DA Student, SSMCMH

2. Particulars of the patient
Name: Miss Romana
Age: 22 years
Sex: Female
Religion: Islam
Occupation: Student
Marital status: Unmarried
Address: Sirajdikhan, Munshigonj.
Date of examination: 05/03/2018

3. Chief complains
Breathlessness for 2 months
Palpitation for 1 month
Cough for 1 month
Weakness for 1 month

4. History of present illness
According to the statement of the patient she was reasonably well 2
months back. Then she developed breathlessness which occur
occasionally. Initially ,the patient felt breathlessness during moderate
to severe exercise, but for the last 1 week, it is increasing gradually.
Now she feels breathlessness even on mild exertion. Occasionally she
experience nocturnal breathlessness usually at late night for which she
has to getup from sleep, walk & take a deep breath to be comfortable.

5. There is no history of breathlessness on lying flat(Orthopnea).
The patient also complaints of occasional palpitation with mild
exertion, even while going to toilet or dressing for last 1 month. She
complaints of cough with sputum which is mucoid in nature for last one
month, but not blood stained.
For the last 1 month she feels weak & fatigue. There is no history of
chest pain, swelling of legs, syncope, loss of consciousness, hoarseness
of voice or difficulty of swallowing.

6. History of past illness
The patient suffered from rheumatic fever in her childhood (arthritis
involving the big joints which were fleeting in nature), but there was no
abnormal limb movements.
Family history
Both of her parents are in good health. Her two brothers and two
sisters are also in good health. There is no such illness in her family.

7. Personal history
She is a student, nonsmoker, nonalcoholic.
Socioeconomic history
She is from a middle class family, living in a small house with good
sanitation and water supply facilities.

8. Drugs & allergic history
She was taking inj. Benzyl penicillin for few years. There is no history of
any allergic manifestation including drug medication ,vaccination or
any foods.
Immunization history
EPI schedule completed.
Menstrual history
Her menstrual cycle is regular.

9. General examination
Appearance : Ill looking & anxious
Build : Average
Nutrition : Average
Decubitus : On choice
Cooperation : Cooperative
Anemia : Mild
Jaundice : Nil
Cyanosis : Nil
Clubbing : Nil
Koilonychia : Nil
Leukonychia : Nil
Edema : Absent
Dehydration : Absent

10. Bony tenderness : Absent
pigmentation : Absent
Lymph node : Not palpable
Thyroid gland : Not enlarged
Body hair : Normal in distribution
pulse : 84 beats/min
Blood pressure : 110/70mmHg
Temperature : 98.4degree F
Respiration : 16 breaths /min
Neck vein : Not engorged
Skin condition : No scar mark or rash in the body

11. Systemic examination
Cardiovascular system
• Pulse:84 beats/min, which is low volume and regular in nature,
normal in character, no radio-femoral, radio radial delay. condition of
the vessels wall are normal.
• Neck vein: not engorged
• Blood pressure: 110/70mmHg.

12. Precordium
Inspection:
• Visible cardiac impulse in mitral area.
• No deformity or scar-mark
Palpation:
Apex beat : In left 5th intercostal space 9 cm from
midline, tapping in nature
Thrill : There is apical thrill, diastolic in nature
Palpable P2 : Absent
Left parasternal lift : Absent
Epigastric pulsation : Absent

13. Auscultation:
• First heart sound: Louder in all the areas, more prominent in mitral
area
• Second heart sound: Normal in all the areas.
• Murmur: There is a mid diastolic murmur in mitral area, which is low
pitched, localized, rough, rumbling (LLRR), best heard with the bell of
stethoscope, in left lateral position with breathing hold after
expiration, with presystolic accentuation.
• There is also opening snap, just medial to the mitral area.

14. Airway examination
(Look)
Normal mouth opening and neck movement.
(Evaluate)
• Thyro mental distance-7.5cm
• Sterno mandibular distance- 13cm
• Mouth opening > 3 fingers of patient
• Cervical Spine-Flexion and extension of the head and neck movement -
Normal.
• Neck circumference-37cm
• Mallampati class-1
• Auscultation- Vesicular breath sound, no added sound.
Examination of other systems reveals no abnormality.

15. Salient features
Miss Romana, 22 years old, a college student normotensive,
nondiabetic, non smoker, presented with breathlessness for 2 months,
palpitation, cough & weakness for 1 month. initially she felt
breathlessness during moderate to severe exercise, but last 1 week it is
gradually increasing. Now she feels breathlessness even on mild
exertion. Occasionally, she experience paroxysmal nocturnal dyspnea
but no history of orthopnea.
She also complain of occasional palpitation with mild exertion, even
while doing mild house hold activities. Cough is productive, with
mucoid sputum, but not associated with hemoptysis. For the last 1
month she feels weak & fatigue. There is no history of chest pain,
swelling of legs, syncope, loss of consciousness.

16. There is history of rheumatic fever in her childhood. All the family
members are healthy. She was taking inj. Benzyl penicillin for few years.
On general examination she is ill looking & anxious, and mildly anemic,
pulse rate is 84 beats/min which is low volume ,regular in rhythm,
normal in character, no radio -femoral and radio- radial delay, condition
of the vessels wall are normal.
blood pressure 110/70mmHg, temperature 98.4 degree and respiration
16 breaths/min, neck vein not engorged & lymph node &thyroid gland
not enlarged. There is no signs of dehydration, jaundice, cyanosis,
edema, koilonychia, leukonychia, pigmentation.

17. Provisional diagnosis
Chronic Rheumatic heart disease with mitral stenosis.
Differential diagnosis
• Tricuspid stenosis.
• Left atrial myxoma.

18. Investigations
X-ray chest P/A view.
ECG: “P” is bifid (P-mitrale. May be RVH, RAH, AF, etc).
To confirm, echocardiogram (2D or preferably color doppler).
Routine Investigations: CBC, Electrolyte, Urea, Creatinine, RBS, PT,
INR, APTT, Viral Markers, Liver Function Tests.

19. Case Discussion
Mitral stenosis is characterized by mechanical obstruction to left ventricular
filling due to a progressive decrease in the size of the mitral valve orifice.
The normal mitral valve orifice area is 4–6 cm²
Symptoms start < 2.5 cm²
Mild MS: 1.5-2.5 cm²
(Minimal symptoms, Dyspnea on severe exertion)
Moderate MS: 1.0-1.5
(Does not produce symptoms at rest, Pulmonary oedema)
Severe MS: < 1.0
( Symptoms at rest, Orthopnea )

20. Etiology
The most common cause is rheumatic heart disease
Primarily affects women.
Much less common causes
Carcinoid syndrome,
Left atrial myxoma,
Severe mitral annular
calcification,
Endocarditis,
Rheumatoid arthritis,
Systemic lupus erythematosus,
Congenital mitral stenosis,
Iatrogenic mitral stenosis after
mitral valve repair.

21. Symptoms
Dyspnoea
Orthopnoea
Paroxysmal Nocturnal Dyspnoea
Palpitation
Fatiguability
Haemoptysis
Recurrent Bronchitis
Cough
Chest pain
Right hypochondriac pain (Hepatomegaly)

22. Pathophysiology
Diffuse thickening of the mitral leaflets and subvalvular apparatus
Commissural fusion
Calcification of the annulus and leaflets are typically present
Contracture of Chordae and papillary heads
Valvular obstruction produces an increase in left atrial volume and
pressure.
With mild mitral stenosis, left ventricular filling and stroke volume are
maintained at rest by an increase in left atrial pressure.
Stroke volume will decrease during stress-induced tachycardia or when
effective left atrial contraction is lost, as with atrial fibrillation.

23. Pulmonary venous pressure is increased in association with the
increase in left atrial pressure
Transudation of fluid into the pulmonary interstitial space, decreased
pulmonary compliance, and increased work of breathing, which leads
to progressive dyspnea on exertion.
Changes in the pulmonary vasculature result in pulmonary
hypertension, and eventually right-sided heart failure may occur.
Episodes of pulmonary edema typically occur with atrial fibrillation,
sepsis, pain, and pregnancy.

24. Complication
Acute left heart failure and acute pulmonary edema
Pulmonary hypertension
Right ventricular failure
Atrial fibrillation
Atrial flutter
Ventricular or atrial premature beats
Embolic manifestation
Infective endocarditis
Recurrent bronchopulmonary infection
Ortener’s syndrome (Hoarseness of voice due to compression to left recurrent
laryngeal nerve due to enlarged left atrium)
Jaundice, cardiac cirrhosis.

25. Diagnosis
Chest Xray
• Straightening of the left heart border
• Elevation of the left mainstem
bronchus.
• The “double density” of an enlarged
left atrium
• Mitral calcification, and evidence of
pulmonary edema or pulmonary
vascular congestion.
• Upper lobar veins are dilated.
• Left bronchus is horizontal

26. ECG
• Broad notched P waves on the
ECG suggest left atrial
enlargement.
• Atrial fibrillation is present in
about one-third of patients with
severe mitral stenosis.
• Right ventricular enlargement.

27. Echocardiography
• Degree of leaflet thickening, calcification, changes in mobility, and
extent of involvement of the sub-valvular apparatus.
• Calculation of mitral valve area and measurement of the transvalvular
pressure gradient.
• Evaluation of cardiac chamber dimensions, pulmonary hypertension,
left and right ventricular function and other valvular disease, and
examination of the left atrial appendage for the presence or absence
of thrombus.
• Pulmonary hypertension is likely if the left atrial pressure is above 25
mm Hg
• Mitral transvalvular pressure gradient is higher than 10 mm Hg
(normal, <5 mm Hg), it is likely that mitral stenosis is severe.

29. CMRI can also help determine the severity of the mitral stenosis.
Clinically, mitral stenosis is recognized by the characteristic opening
snap that occurs early in diastole and by a rumbling diastolic heart
murmur best heard at the apex or in the left axilla
Stasis of blood in the distended left atrium predisposes patients to a
high risk of arterial thromboembolism.
Venous thrombosis is also more likely because of the decreased
physical activity of these patients.

30. Treatment
Medical management
Asymptomatic/Mild MS
Diuretics can decrease the left atrial pressure and relieve symptoms.
Restriction of salt intake.
Drugs for rate control: Beta blocker, digoxin.
Restriction of physical activity.
Antibiotics to prevent secondary infection.
Control of the heart rate is critical because tachycardia impairs left
ventricular filling and increases left atrial pressure.

31. If atrial fibrillation occurs
Heart rate control may be achieved with β-blockers, calcium channel
blockers, digoxin, or a combination of these medications.
Anticoagulation is required because the risk of embolic stroke in such
patients is about 7%–15% per year
Warfarin is administered to a target international normalized ratio
(INR) of 2.5–3.0.
Prophylaxis against recurrence of Rheumatic fever.

32. Symptomatic MS
Surgical correction of mitral stenosis is indicated when symptoms
worsen and pulmonary hypertension develops.
 Percutaneous balloon valvotomy.
Severe MS
If heavy valvular calcification or valve deformity is present
Surgical commissurotomy,
Valve reconstruction,
Valve replacement.

33. Anesthetic management
Management of anesthesia for noncardiac surgery in patients with
mitral stenosis includes
prevention and treatment of events that can decrease cardiac output
or produce pulmonary edema
Intraoperative Events That Have a Significant Impact on Mitral Stenosis
Sinus tachycardia or a rapid ventricular response during atrial fibrillation
Marked increase in central blood volume, as associated with overtransfusion or
head-down positioning
Drug-induced decrease in systemic vascular resistance
Hypoxemia and hypercarbia that may exacerbate pulmonary hypertension and
evoke right ventricular failure

34. Goals of Anaesthesia
Prevent AF with cardioversion or IV administration of amiodarone, β-
blockers, or calcium channel blockers.
Systemic blood pressure and systemic vascular resistance can be
maintained with vasoconstrictor drugs such as phenylephrine
Use of vasopressin may also be considered, since it has minimal
effect on pulmonary artery pressure.
Right ventricular failure may require support with inotropic and
pulmonary vasodilating drugs.

35. Preanaesthetic assessment
In patients with MS planned for any type of surgery preoperative evaluation and preparation are
evaluation and preparation are especially important for a successful outcome of the surgery
outcome of the surgery
Take detailed history and examination both general and
systemic
Assess the severity of the cardiac disease
The degree of impaired myocardial contractility
The presence of associated major organ system disease.
Recognition of compensatory mechanisms for
maintaining cardiac output
Evaluate patients hemodynamic state.
The presence of a prosthetic heart valve introduces
special considerations in the preoperative evaluation.
New York Heart Association Functional
Classification of Patients With Heart Disease
Class Description
I
II
III
IV
Asymptomatic
Symptoms with ordinary activity but
comfortable at rest
Symptoms with minimal activity but
comfortable at rest
Symptoms at rest

36. Preoperative medication
Antianxiety drugs decrease tachycardia associated with anxiety.
Drugs used for heart rate control should be continued until the time
of surgery
Diuretic-induced hypokalemia can be detected and treated
preoperatively.
Continue anticoagulant therapy for minor surgery,
Major surgery associated with significant blood loss requires
discontinuation of anticoagulation.

37. Anticoagulant Therapy

38. Oral anticoagulation should be discontinued atleast three days before
any major surgery
Subcutaneous conventional heparin or low-molecular-weight heparin
in prophylactic doses is substituted preoperatively.
A dose of heparin should be given 3–6 h preoperatively in patients
and heparin should be restarted as soon as possible post operatively
(preferably within 12 h).
Warfarin is restarted 24 hours postoperatively or when patients can
start oral intake.
In emergency surgery, the affect of warfarin needs to be neutralized
by FFP. In addition to this, vitamin K may also be given.

39. Anaesthetic techniques
Regional anaesthesia
Neuraxial anesthesia is an acceptable technique in the absence of
anticoagulation.
Peripheral nerve blocks may also be used safely.
Use of neuraxial anesthesia requires measures to avoid hypotension,
maintain adequate preload, and avoid tachycardia.
Combined spinal epidural anesthesia may allow better control of the level
of sympathectomy and reduction in blood pressure.
Rapid prehydration should be avoided.
Slow titration of local anesthetic is recommended.
Phenylephrine is preferred over Ephedrine.
Epinephrine containing local anesthetic should be avoided.
Hypothermia should be avoided as it increases PVR.
In severe MS regional anaesthesia is contraindicated.

40. General Anaesthesia
Induction
There is no single correct agent
Moderate to sever MS generally have slow circulation that prolongs arm-
brain circulation time.
Etomidate is the best agent for hemodynamic stability. Thiopentone can
also be used.
Avoid Propofol as it can causes hypotension.
Avoid Ketamine as it causes tachycardia.
Use volatile anesthetic with caution, causes decreased SVR and cardiac
output and hypotension.
Short-acting β-blockers such as Esmolol may be necessary to treat episodes
of tachycardia during induction.

41. Muscle Relaxation
Tracheal intubation and muscle relaxation should be accomplished by
neuromuscular blockers that do not induce either tachycardia or
hypotension from histamine release
Steroidal Group does not cause histamine release. Eg. Vecuronium,
Rocuronium except Pancuronium
Avoid Benzylisoquinolinium group as they cause histamine release.
Eg. Atracurium, Cicatracurium, Mivacurium.
Succinylcholine also causes slight release in histamine.

42. Maintenance
Maintenance of anesthesia is best accomplished using drugs with minimal
effects on heart rate, myocardial contractility, and systemic and pulmonary
vascular resistance.
nitrous/narcotic anesthetic or a balanced anesthetic that includes a low
concentration of a volatile anesthetic can achieve this goal.
Nitrous oxide can evoke pulmonary vasoconstriction and increase
pulmonary vascular resistance if pulmonary hypertension is present.
Halothane is best avoided due to its arrythmogenic potential. Low volume
Isoflurane, Desflurane or Sevoflurane can be used.
Deep plane of anaesthesia should be maintained.
Ensure proper fluid therapy. Avoid hyper/hypovolemia.

43. Reversal of anaesthesia
Should be achieved slowly with neostigmine and glycopyrolate to
reduce drug-induced tachycardia.
Monitoring
Monitoring of asymptomatic patients is no different from monitoring
of patients without valvular heart disease.
TEE can be useful in patients with symptomatic mitral stenosis.
Monitoring of intraarterial pressure, pulmonary artery pressure, and
left atrial pressure (pulmonary artery occlusion pressure) should be
considered.

44. Post Operative Management
Risk of pulmonary edema and right heart failure continues into the
postoperative period, so cardiovascular monitoring should continue.
Pain and hypoventilation with subsequent respiratory acidosis and
hypoxemia may be responsible for increasing heart rate and
pulmonary vascular resistance.
A period of mechanical ventilation, particularly after major thoracic
or abdominal surgery may be needed.
Relief of postoperative pain with neuraxial opioids can be very useful.
Anticoagulation should be restarted as soon as the risk of
perioperative bleeding has diminished.

45. Anesthetic management of a patient with prosthetic heart valve for
non-cardiac surgery
Patients with prosthetic heart valves are a challenge to any
anesthesiologist due to the risk of infective endocarditis, bleeding and
thrombosis.
Follow anticoagulant guideline.
Other anaesthetic goals remain same.
Patients with new generation prosthetic mechanical mitral valves should
receive warfarin to a target INR of 2.5–3.5 and for older types of valves the
target INR should be 3.5–4.5
warfarin should be changed to unfractionated heparin atleast 4–5 days
prior to surgery.
INR should be less than 1.5 for proceeding with surgery.
Infective endocarditis prophylaxis should be administered to all patients
with prosthetic heart valves.

46. Pregnancy and MS
What to consider?
In pregnancy There is
Increase in blood volume by 30-50%.
Increase in capillary pressure.
Decrease in SVR.
Increase in HR by 10-20b/min and CO by 30-50%.
During labour and delivery Sympathetic stimulation cause increase in
HR and CO.
Sudden rise in venous return due to autotransfusion and IVC
compression.
Hypercoagulability so thromboembolic risk.

47. Special measure should be taken
Use Heparin for 1st trimester, warfarin for 12-36 weeks
After 36 weeks switch to heparin titrated to APTT level.
Large boluses of oxytocin should be avoided as they cause profound
hypotension.
Ergometrine better avoided. PGF2 Alpha and Misoprostol are used
cautiously.
If planned for LUCS then anaesthetic choice should be directed to
keep the patient hemodynamically stable.
Pt should be kept in HDU for upto 72 hrs after delivery.
Plan and advise cardiac surgery in the second trimester for the
interest of the well being of mother if symptomatic.

48. A thorough understanding of the pathophysiology of valvular heart
disease is essential while planning anaesthesia and perioperative
care for such patients. Meticulous use of optimal fluids, close
monitoring of the changing haemodynamics and avoidance of
situations that can cause major reduction of cardiac output and fluid
shifts are mandatory to achieve good clinical outcome.

49. Reference
STOELTING’S ANESTHESIA AND CO-EXISTING DISEASE.
MORGAN AND MIKHAIL’S CLINICAL ANESTHESIOLOGY.
DAVIDSON’S PRINCIPAL AND PRACTICE OF MEDICINE.
MILLER’S ANESTHESIA.
YAO AND ARTUSIO’S ANESTHESIOLOGY.
www.ncbi.nlm.nih.gov
www.asra.com

50. THANK YOU