Mitralstenosis 130908040300-

1. Anaesthetic
Management
of
valvular
heart
disease

5. Case
Chief Complain
Palpitations since 6 weeks
Breathlessness since 4 weeks
Fatigue since 2 weeks

6. Case………………contd. History of Presenting Illness
Palpitatio
n
Breathlessness Fatigue
Intermittent
Associated with
exertion
Relieved on rest
6 weeks duration
Gradual in onset
Progressive in
nature (NYHA II)
Aggravated on
lying down
Relieved on
sitting up
4 weeks duration
Feeling of
weakness
2 weeks duration
There was no history of haemoptysis or recurrent respiratory
infections.

7. Case………………contd. Past History
No history of similar complaints
History of Rheumatic Heart Disease since 12 years of
age. Took treatment in the form of Penicillin injections
every 21 days for 8 years till age 20 and then
discontinued.
No history of cyanotic spells.
No history of hypertension, Diabetes Mellitus, Bronchial
Asthma

8. Case………………contd.
No history of similar complaints in the family was noted.
Personal History
Diet: Vegetarian
Appetite: reduced.
Bowel & Bladder: Normal.
Sleep: disturbed.
Habits: None
Family History

9. Case………………contd.
A young female patient, moderately built and nourished
No pallor, icterus, cyanosis, oedema, clubbing
Pulse rate – 90/min; Weight – 58 Kgs
Blood pressure – 110/70 mm of Hg; Height – 155 cms
Respiratory rate – 16/min;
Respiratory System:
Normal Vesicular Breath Sounds heard, No added sounds.
Central Nervous System: Normal. No neurological deficits.
General Physical Examination

10. Case………………contd.
Per abdominal examination: no abdominal distention. No free
fluid. No dilated veins.
Cardiovascular System:
Inspection: No deformity, Engorged superficial veins,
Scars or sinuses. No visible pulsations
Palpation: Apex beat felt in 5th intercostal space medial to left
midclavicular line, absence of left parasternal heave
Auscultation:
S1 S2 Heard.
Low pitched mid-diastolic murmur at apex. (no radiation)

11. Case………………contd.
Mitral Stenosis of Rheumatic Origin without evidence of
congestive cardiac failure.
Impression

12. Case………………contd.
Hb: 12.0 gm%
Differential count: Neutrophils – 71
Lymphocytes – 24
Monocytes – 02
Eosinophils – 03
Total count – 9, 800
Platelets: 273
PT INR: 1.0
BT: 3’ 00”
CT: 4’ 00”
Investigations

13. Case………………contd.
RBS: 99 mg/dl
Urea: 30 mg/dl
Creatinine: 1.1 mg/dl
Na+: 135mEq/l
K+: 4.8mEq/l
Cl-: 104mEq/l
HIV 1 & 2: Not detected
HBsAg: Not detected
Investigations

14. Case………………contd.
ECG: Sinus rhythm. Within normal limits. Heart rate: 80/min. Right
axis deviation.
2D ECHOCARDIOGRAPHY: Normal Left Ventricular systolic
function
No Regional Wall Motion
abnormalities
Ejection fraction: 56 %
Mitral Valve Area – 2.0 cms2
Transvalvular Pressure – 8 mm of
Hg.
Chest X – Ray: Cardiomegaly. Prominent bronchovascular
Investigations

15. Discussion
Causes: -
Palpitation
s
Tachyarrhythmias, Atrial fibrillation, Atrial
kick
Endocrine–Pheochromocytoma, Thyrotoxicosis,
Hypogylcemia
High Output states – Anemia, Pyrexia, Aortic
Regurgitation,
Patent Ductus Arteriosus.
Drugs – Atropine, Adrenaline, Aminophylline,
Thyroxine,
Caffeine, Tannin, Alcohol
Psychogenic – Prolonged anxiety
Idiopathic
Atrial kick -
Palpitations

16. Discussion
Cardiac
causes
Atrial kick -
Palpitations
Respiratory
causes
Hematological
Left heart failure
Congenital heart
disease
Acquired valvular
disease
Bronchial
Asthma
Severe Anaemia
Acquired valvular
disease -
Dyspnea
Coronary heart
disease
Breathlessness
hypertensive
heart disease
Cardiomyopath
y
Chronic
obstructive lung
disease
Chronic restrictive
lung disease
Pneumonia
Pulmonary
neoplasm/
embolism
Laryngeal/
Tracheal
obstruction

17. Discussion
Past History
Atrial kick -
Palpitations
Family History Personal
History
Rheumatic
Heart Disease
(RHD)
RHD – Most
common cause
40%
More common in
females, typically
detected in
childhood.
Family history of
Rheumatic Heart
Disease,
Congenital
Valvular defects
may be relevant
Disturbed sleep
in Paroxysmal
Nocturnal
Dyspnoea
Acquired valvular
disease -
Dyspnea
Recurrent
respiratory tract
infection
indicates
pulmonary
congestion
RHD,
Female
patient,
Childhood
history,
disturbed
sleep

18. Discussion
Oedema
Atrial kick -
Palpitations
Hepatomegaly Mitral Facies
Severe Mitral
stenosis
ultimately
leads to right
heart failure.
Seen in right
ventricular
failure and
pulmonary
hypertension.
Low Cardiac
Output in Mitral
Stenosis causes
peripheral
vasoconstriction
producing
pinkish purple
patches on
cheeks.
Mitral Flush due
to vasodilatation
(vascular stasis)
is seen
Seen in fair
Acquired valvular
disease -
Dyspnea
RHD,
Female
patient,
Childhood
history,
disturbed
sleep
General Physical Examination
Absent
here
Absent
here
Edema &
Hepatomegaly
absent – mild
disease

19. Discussion
Inspection
Atrial kick -
Palpitations
No deformity of precordium. –
Precordial bulge indicates early onset
and
longer duration of cardiac disease.
Acquired valvular
disease -
Dyspnea
RHD,
Female
patient,
Childhood
history,
disturbed
sleep
Cardiovascular Examination
Scar marks reveal previous surgeries
Engorged Neck Veins indicate high right heart
pressures
Edema &
Hepatomegaly
absent – mild
disease

20. Discussion
Palpation
Atrial kick -
Palpitations
Tapping character of the apex beat (palpable S1) is
typical.
Acquired valvular
disease -
Dyspnea
RHD,
Female
patient,
Childhood
history,
disturbed
sleep
Cardiovascular Examination
Palpable diastolic thrill in mitral area best felt in left
lateral position in full expiration.
Parasternal heave. (absent here)
If one finds engorged superficial veins look for
direction of flow.
Absent
Parasternal
heave – mild
disease
Edema &
Hepatomegaly
absent – mild
disease

21. Discussio
n
Auscultation
Atrial kick -
Palpitations
S1 is sharp, short, accentuated
Acquired valvular
disease -
Dyspnea
RHD,
Female
patient,
Childhood
history,
disturbed
sleep
Cardiovascular Examination
Opening Snap after S2
Low pitched mid-diastolic rumbling murmur with
presystolic accentuation of Grade IV
intensity in mitral area without any
radiation
Murmur best heard at cardiac apex with bell of
stethoscope in left lateral position at height of
expiration
Absent
Parasternal
heave – mild
disease
Edema &
Hepatomegaly
absent – mild
disease
Absence of click, split, rub or murmur over other areas
Opening snap
+murmur at
apex

22. Substantiation Atrial kick -
Palpitations
Acquired valvular
disease -
Dyspnea
RHD,
Female
patient,
Childhood
history,
disturbed
sleep
Absent
Parasternal
heave – mild
disease
Edema &
Hepatomegaly
absent – mild
disease
Opening snap
+murmur at
apex
Childhood
history
Female
Patient
Rheumatic
Heart
Disease Edema &
hepatomegaly
absent
Palpitation
s
Dyspnea
Absent parasternal
heave – mild disease
Opening Snap + low
pitched mid diastolic
murmur
2D – Echo – Mitral Valve 2.0
cms2,, Transvalvular pressure 8
mm of Hg
Mitral Stenosis of Rheumatic Origin without evidence
of congestive cardiac failure.

23. Anatom
y

24. Anatomy
Normal Orifice: 4 – 6
Cms2
4-6 cms2
< 2.5 cms2
1.5- 2.5 cms2
1.0 – 1.5 cms2
< 1.0 cms2
Mild MS – 1.5 – 2.5 Cms2
(Dyspnea on severe
exertion)
Moderate MS – 1.0 – 1.5
Cms2 (PND ± pulmonary
oedema)
Severe/ Critical- < 1.0
Cms2 (Orthopnea – Class
IV)
Symptoms start < 2.5
Cms2

25. Anatom
yMitral Valve area is calculated using Gorlin’s
Equation:
Area = Cardiac Output/ (DFP or SEP) (HR)
44.3 C √ΔP
DFP = Diastolic Filling
Pressure
C = Empirical Constant
SEP = Systolic Ejection
Period
ΔP = Pressure Gradient

26. Pathophysiolog
yDecreased LV
filling
Increased left atrial
pressure and
volume
Pulmonary vein
pressure
Transudation of fluid into
pulmonary interstitial
space
Pulmonary
compliance
Work of breathing
Progressive
Dyspnea
Adaptatio
n
Atrial Kick
Adaptatio
n
thickening of basement
membrane of pulmonary viens
Pulmonary
hypertension
Palpitation
s
Breathlessne
ss
Haemoptysi
s

27. Pathophysiology
Almost all chambers
are shown here ,
except…
Left Ventricle
So, are we to assume
that Left Ventricle
remains unaffected..?

28. Aetiology
1. Rheumatic Heart Disease
2. Congenital – Parachute Mitral Valve
3. Hunter’s Syndrome
4. Hurler’s Syndrome
5. Drugs – Methylsergide
6. Carcinoid syndrome
7. Amyloidosis
8. Mitral annular Calcification
9. Rheumatoid Arthritis
10.Systemic Lupus Erythematosis
11.Infective endocarditis with large vegetations.
12.Lutembacher’s Syndrome: Atrial Septal Defect (ASD) +
Mitral Stenosis (MS) rheumatic origin

29. Common symptoms
1. Dyspnoea
2. Orthopnea
3. Paroxysmal Nocturnal Dyspnea
4. Palpitation
5. Fatiguability
6. Haemoptysis
7. Recurrent Bronchitis
8. Cough
9. Chest pain
10.Right hypochondrial Pain
(hepatomegaly)

30. Complications
1. Acute left heart failure and acute pulmonary edema
2. Pulmonary hypertension
3. Right Ventricular failure
4. Atrial Fibrillation
5. Atrial Flutter
6. Ventricular or atrial premature beats
7. Embolic manifestations
8. Haemoptysis
9. Infective Endocarditis
10. Recurrent Broncho-pulmonary infections
11. Complications arising from enlarged left atrium:
Hoarseness of voice – left recurrent laryngeal nerve due to
enlarged left atrium (Ortner’s Syndrome)
Dysphagia – Oesophageal compression
12. Jaundice, Cardiac cirrhosis.

31. Treatment
1. Mild Mitral stenosis – Diuretics
Restriction of physical activity
Salt-restricted diet
2. When in Atrial Fibrillation – Digoxin (0.25 mg tablet)
β- Blockers
Calcium Channel Blockers
Control of heart rate is paramount, because tachycardia impairs left
ventricular filling and further increases left atrial pressure.
3. Anticoagulation – Warfarin to normalise INR

32. Treatment
4. Surgery if Pulmonary hypertension develops
Percutaneous balloon
valvotomy
Surgical commisurotomy
Valve reconstruction
5. Valve replacement
Starr-Edwards ball valve
Bjork-Shiley disc valve
Porcine bio-prosthesis
6. Prophylaxis against recurrence of rheumatic
fever

33. ANAESTHETIC MANAGEMENT

34. Mortality: 0 point-5%,1 point-27%,>1 point-75%
CARPREG Score

35. Anaesthetic Management
Principle
involved: Cardiac
Output
Decrease in cardiac
output
Hypotension
Tachycardia
Reduced
ventricular filling
Increased
ventricular filling
Trendelenbu
rg's position
Precipitation
of CHF
1
2
3

36. Anaesthetic Management
Principle involved:
1. Prevent decrease in cardiac output, as hypotension because of this
causes reflex tachycardia, which in turn reduces ventricular filling further
compromising cardiac output.
2. Avoid hypotension for the same reason listed above. If hypotension
ensues, treat with Ephedrine or Phenylephrine.
3. Avoid precipitating Congestive Heart Failure due to factors such as
Trendelenburg’s position
4. Avoid precipitation of Right Ventricular Failure
Hypercarbia
Hypoxemia
Lung Hyperinflation
Increase in lung water
If Right Ventricular Failure exists, treat with inotropes and pulmonary
vasodilators.

37. Anaesthetic Management
Preoperative Medication
1. Decrease anxiety (decreases tachycardia)
2. Drugs used to control heart rate to be continued till day of surgery
3. Hypokalemia if present secondary to diuretic therapy to be addressed
4. If intended surgery is a minor surgery, continue anticoagulant therapy
5. If intended surgery is a major surgery, discontinue anticoagulant therapy.
Induction of Anaesthesia
1. Avoid Ketamine – Increases heart rate, blood pressure
2. Avoid Atracurium – Increased histamine release causes hypotension
which
manifests as tachycardia.

38. Anaesthetic Management
Maintenance of Anaesthesia
1. Drugs should have minimal effects on hemodynamic pattern
2. Balanced anaesthesia with N2O/ Narcotic/ Volatile anaesthetic
3. N2O causes insignificant pulmonary vasoconstriction. It is significant
only if pulmonary hypertension exists. So, one needs to treat pulmonary
hypertension preoperatively.
4. Cardiac stable muscle relaxants are to be used. (preferably avoid
Pancuronium)
5. Avoid lighter planes of anaesthesia (To avoid tachycardia)
6. Fluid Management:
Avoid Hypervolemia - -> Worsens pulmonary edema
Avoid Hypovolemia - -> Sacrifices already decreased left ventricular
filling, which further decreases Cardiac output.
Hypovolemia secondary to blood loss and vasodilatory effects of

39. Anaesthetic Management
Monitoring
1. Transesophageal Echocardiography
2. Intra-arterial pressure
3. Pulmonary artery pressure to be monitored
4. Left atrial pressure
Principle:
1. Ensure adequacy of cardiac function
intravascular fluid volume
ventilation
oxygenation
A word of caution regarding Pulmonary artery pressure monitoring: -
When measured too frequently, the risk of pulmonary artery rupture is far too
high.

40. Anaesthetic Management
Post Operative
1. Assess postoperative risk of pulmonary oedema and right heart failure
and manage accordingly.
2. Avoid pain as pain begets hypoventilation which leads to respiratory
acidosis, hypoxemia which manifests as raised heart rate and
pulmonary vascular resistance.
3. After Major thoracic or abdominal surgery, the decreased pulmonary
compliance and increased work of breathing requires mechanical
ventilation.

41. Anaesthetic Management
General anesthesia has the advantages of speed of induction, control of
the airway, and superior hemodynamics.
Anaesthetic Goals:
1. Maintain the heart rate around 80-100 b/min .
2. Maintain Left Atrial Pressure high enough to take advantage of the
increased preload reserve.
3. Avoid pulmonary artery hypertension by treating hypercarbia,
hypoxemia, and acidemia.
4. Aggressively treat pulmonary artery hypertension with vasodilator
therapy to avoid RV failure. If RV failure does occur, inotropic support of
the RV and pulmonary vasodilation may be necessary. The presence of
PAH is the major factor that increase the mortality.

42. Anaesthetic Management
5. Avoid factors which depress the myocardium:(inhalation agents and
drugs)
6. Maintain awareness of potential for LV rupture.
7. Aggressive treatment of arrhythmias if they occur
8. Avoid profound changes in SVR
9. Attenuate pressor response(intubation, extubation, light plane of
anesthesia)
10. Adequate analgesia and adequate muscle relaxation guided by Neuro
muscular monitoring
11. Aspiration prophylaxis
12. Blood loss assessment and prompt replacement

43. Anaesthetic Management
Other advantages for general anaesthesia
1. Rapidly established are
2. Better hemodynamic stability
3. Prevention of aspiration as the airway is isolated
4. High FiO2 -which will reduce PVR
5. Ventilation controlled to avoid hypercarbia-which will increase PVR
6. FRC is increased by controlled ventilation
7. Ventilation of atelectatic areas –better V/Q
8. Sinus rhythm can be maintained. In case of SVT and Ventricular
arrhythmias promptly reverted by cardioversion

44. Anaesthetic Management
9. Peak airway pressure can be kept <20 cms H2O
10. Effective management of Pulmonary oedema - IPPV with PEEP, liberal
use of high dose morphine

45. AORTIC STENOSIS

46. CC: CHEST PAIN
HPI:
64 yo male admitted for chest pain that
started about 2 years ago; became
progressively worse, initially appeared
with walking aprox 1 mile and progress
to less then 1 block.
CP described as pressure in his mid-
chest, always with exertion, non
radiating, rated as 6-7/10, attenuated by
rest, accompanied by dyspnea on
exertion.
Denies palpitations or syncopal episodes.

47. PMHX
CAD (coronary artery disease)
Hypertension
Hyperlipidemia
Diabetes mellitus type II
Depression with anxiety attacks
Obesity

48. SOCIAL HISTORY
Married, 2 kids
Farmer
Never a smoker
Alcohol: 2 beers/ night

49. Mixtard insulin
lorazepam 0.5 mg PO tablet
CHOLECALCIFEROL, VITAMIN D3, PO
amlodipine10mg PO
aspirin 81 mg PO
Clopidogrel 300 mg PO
Esomeprazole 20 mg PO
losartan-hydrochlorothiazide 50-12.5 mg PO BI
bisoprolol 5mg PO Tab
atorvastatin 40 mg PO.
HOME MEDICATION

50. VITAL SIGNS
BP 146/58
Pulse 82
Temp (37 °C) (
Resp 20
Ht (1.88 m)
Wt (129.547 kg)
BMI 36.67 kg/m2
SpO2 97%

51. PHYSICAL EXAMINATION
Constitutional: NAD
:noy pqle ,jaundice or cyanosed
Neck: Normal ROM, No JVD, carotid upstrokes are preserved
without audible bruits.
Cardiovascular: RRR, S1&S2 normal. 2/6 Systolic
crescendo-decrescendo murmur present in right 2nd ic
area, no galops or rub.
Lungs: CTA, bilateral crackles in the bases
GI: Soft, NT, BS normal, No pulsatile masses.
Extremities: Intact distal pulses, No edema
Neurologic: AO x 3, Normal motor and sensory function, No
focal deficits.
Skin: Warm, Dry, No erythema, No rash.
Psychiatric: Normal affect and mood

52. LABS
WBC 9.6
RBC 4.68; Hb 15.5; Ht 43.4, MCV
93.2
Platelets 294
BNP 278
Na 135; K 3.8; Cl 99; CO2 22;
BUN 17, Cr 1.32; GFR 55
Chol 141, HDL 63, LDL 58, TG 98
Glucose 308
TSH 1.42

53. CXR
 Stable cardiomegaly.
 Mediastinal contours unremarkable.
 No pulmonary infiltrate or pleural effusion.
 Pulmonary vessels within normal limits.
IMPRESSION:
No acute disease

54. ECHO
 LV: The cavity size was normal.
 There was mild concentric hypertrophy.
 Systolic function was normal.
 The estimated EF: 50% to 55%.
 Severe hypokinesis of the mid-
distalanteroseptal myocardium.
 Mild hypokinesis of the lateral myocardium.
 abnormal LV (grade 1 DD).

55.  Aortic valve:
Moderate focal thickening and calcification.
Cusp separation was markedly reduced.
There was severe stenosis.
Mean gradient: 32mm Hg (S).
Peak gradient: 68mm Hg (S).
Valve area: 0.88cm^2(VTI).
Valve area: 0.83cm^2(Vmax).
Aorta: Aortic root dimension: 50mm (ED, M-mode).
The aortic root was dilated.
 LA: The atrium was moderately dilated

56. NORMAL AORTIC VALVES
EFFECTIVE AREA OF VALVE
OPENING = CROSS-SECTIONAL
AREA OF LV TRACT
(3.0 TO 4.0 CM2 )
Normal Bicuspid valve Geriatric
valve

57. AORTIC STENOSIS
Characterized by:
Obstruction to LV outflow
Intraventricular systolic pressure and wall tension
increase
Concentric hypertrophy
Decreased LV compliance
Reliance on atrial contribution

58. HEMODYNAMIC GOALS FOR THE
PATIENT WITH AS
Preload
- full, adequate intravascular volume to fill
noncompliantventricle and to maintain BP
Afterload
- already elevated but relatively fixed, coronary perfusion
pressure must be maintained
Contractility
- usually not a problem, inotropes may be helpful
preinduction in end-stage AS with hypotension
Watch out for vasodilation
Treat hypotension with phenylephrine

59. HEMODYNAMIC GOALS FOR THE PATIENT WITH
AS
Rate –
not too slow (decrease CO), not too fast (ischemia)
Rhythm -
Sinus!! Cardioversion if hemodynamic instability from SV
dysrhythmias
MVO2 (myocardial oxygen consumption)
- Ischemia is an ever present risk, Avoid tachycardia and
hypotension
Mild to moderate may tolerate spinal and epidural (epidual
preferred)
spinal and epidural contraindicated in severe AS
High risk of myocardial ischaemia

60. CHOICE OF DRUGS IN AS
Pt with mild to moderate AS can tolerate
neuroaxial blocks.
Techniques should be done cautiously.
Epidural preferable because of slower onset of
hypotension.
In severe AS is contra indicated.

61. GA
GA can produce both vasodilation and
hypotension.
Volatile agents should be controlled to prevent