1. ANESTHESIA FOR A PATIENT OF
MITRAL STENOSIS
Dr.RAJU.D
II-year PG
Anaesthesiology&Critical care
Moderator:Prof.Dr.R.PRATAP
MD,DA,DGO,Dip.Diab
HOD
Dept. of Anaesthesiology&Critical care
GSL Medical College&General Hospital
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.
ETIOLOGYAND PATHOLOGY-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.
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.
4. 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
7. VALVULAR FUNCTION TERMINOLOGY
Stenosis
Reduced movement of the valve;incomplete opening
and
closing.
Regurgitation
Valve leaflets are incompetent; do not prevent blood
from going backward.
Prolapse
During systole, the valve “bulges”/”billows” backward.
8. 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
9. Pulmonary changes
Pulmonary arterial hypertension results as-
1)Increased left atrial pressure.
2)Pulmonary arterial constriction.
3)Interstitial edema in the wall of the small pulmonary vessels.
4)Organic obliterative changes in the pulmonary vascular bed.
At last if there is severe pulmonary arterial hypertension→Tricuspid
regurgitation
Pulmonary in competence
Rt sided heart failure
10. 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
12. Symptoms
o Breathlessness
Fatigue
Oedema, ascites
Palpitation
Haemoptysis
Cough
Chest pain
Hoarseness
Mitral facies or malar flush
Symptoms of thromboembolic complications (e.g. stroke, ischaemic limb)
Are worsened by conditions that demand increase in cardiac output.
◦ Exertion,fever, anemia, pregnancy, thyrotoxicosis
13. 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
14. Signs
Palpation:
Small volume pulse
Tapping apex-palpable S1
Palpable S2
Atrial fibrillation
Signs of raised pulmonary capillary
pressure
Crepitations, pulmonary
oedema, effusions
Signs of pulmonary hypertension
RV heave, loud P2
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
15.
16. Lab examination
Chest x-ray
Straightening of left border of cardiac
silhouette.
Prominent main pulmonary arteries.
Dilation of the upper lob pulmonary
veins.
Backward displacement of the
esophagus by enlarged left atria.
17.
18.
19.
20.
21. ELECTROCARDIOGRAPHY
The ECG may show 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) inV1;
Broad, notched P waves in lead II; or both.
Low voltage inV1,
Right axis QRS deviation, and tall R waves inV1 suggest RV
hypertrophy
22.
23.
24. Echocardiography
Diagnosis of Mitral Stenosis
Assessment of hemodynamic severity
◦ mean gradient, mitral valve area, pulmonary artery
pressure
Assessment of right ventricular size and function.
Diagnosis and assessment of concomitant valvular lesions
Reevaluation of patients with known MS with changing
symptoms or signs.
F/U of asymptomatic patients with mod-severe MS
25. GOALS OF ANAESTHETIC MANAGEMENT IN COMMON
VALVULAR DISEASES
Disease Preload After
load
Rate
/min
Rhythm Contract
ility
A.S. N to
High
N to
High
Maintai
nbaselin
e(70-80)
Sinus Normal
(N)
A.R. Normal 90-100 Sinus N to
High
M.S. Normal Normal 65-80 Usually
A.F.
N to
High
M.R. Normal 90-100 Sinus N to H
26. Anesthetic management
The main objectives are- To maintain sinus rhythm
To avoid tachycardia
To avoid large increase in cardiac output
To avoid hypovolemia and fluid overload.
A thorough history and examination to be done.
Investigation- Hemogram
Blood sugar ,blood urea ,s.creatinine
x-ray chest
Electrocardiogram
Echocardiography
27. 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.
For minor procedures continue the anticoagulant therapy.
For major surgery discontinue.
For regional anesthesia anticoagulant tests should be performed.
ANESTHESIATECHNIQUE-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.
28. General Anesthesia
Premedication -Avoid premedication with anticholinergics to
avoid tachycardia. opioiods like fentanyl are used to give
analgesia.
Induction –Induction can be achieved with any available iv
induction agent except KETAMINE as it increases heart rate and
blood pressure.
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,
Benzylisoquinolinium group causes histamine release. Example
are –ATRACURIUM, CISATRACURIUM, MIVACURIUM.
Succinylcholine also causes slight release in histamine.
29. Maintenance
Accomplished by use of drugs with minimal effects on heart rate, contractility,
systemic and pulmonary vascular resistance.
Achieved by –nitrous oxide & opioid. low conc.Of volatile anesthetic
For muscle relaxation vecuronium is preferred.
Avoid light anesthesia.
Intra-op fluid administration should be carefully titrated because these patients
are very susceptible to volume overload and the development of pulmonary
edema.
Monitoring
Noninvasive monitoring like HR, BP , ECG, RR, SpO2.
Invasive monitoring depends upon-Complexity of the operative procedure.
-Magnitude of physiological impairment.
Transesophageal echocardiography could be useful in patients with symptomatic
mitral stenosis undergoing major surgery.
30. *In symptomatic patients and major surgery continuous monitoring
of IBP , pulmonary artery pressure and left atrial pressure should be
considered.
*If there is intra-op tachycardia –deepen the plane
β-blocker eg. Esmolol and propranolol.
*If hypotension occurs phenylephrine is preferred over ephedrine
because it lacks the β adrenergic activity.
*If atrial fibrillation occurs ventricular rate is controlled with
diltiazem and digoxin.
*For sudden supraventricular tachycardia –cardioversion.
31. Reversal of anesthesia.
Reversal 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.
33. Major criteria
Polyarthritis: A temporary migrating inflammation of the large
joints, usually starting in the legs and migrating upwards.
Carditis: Inflammation of the heart muscle (myocarditis) which can
manifest as congestive heart failure with shortness of
breath, pericarditis with a rub, or a new heart murmur.
Subcutaneous nodules: Painless, firm collections of collagen fibers
over bones or tendons.They commonly appear on the back of the
wrist, the outside elbow, and the front of the knees.
Erythema marginatum: A long-lasting reddish rash that begins on
the trunk or arms as macules, which spread outward and clear in the
middle to form rings, which continue to spread and coalesce with
other rings, ultimately taking on a snake-like appearance.This rash
typically spares the face and is made worse with heat.
Sydenham's chorea (St.Vitus' dance): A characteristic series of rapid
movements without purpose of the face and arms.This can occur
very late in the disease for at least three months from onset of
infection.
34. Minor criteria
Fever of 38.2–38.9 °C (101–102 °F)
Arthralgia: Joint pain without swelling (Cannot be included if
polyarthritis is present as a major symptom)
Raised erythrocyte sedimentation rate or C reactive protein
Leukocytosis
ECG showing features of heart block, such as a prolonged PR
interval[8] (Cannot be included if carditis is present as a major
symptom)
First Degree AV-Block [9]
Previous episode of rheumatic fever or inactive heart disease
Other signs and symptoms
Abdominal pain
Nose bleeds
Preceding streptococcal infection: recent scarlet fever, raised
antistreptolysinO or other streptococcal antibody titre, or
positive throat culture.[9]