Transcript ANESTHESIA FOR A PATIENT OF MITRAL STENOSIS

DR.SANDEEP SAINI
LLRM COLLEGE MEERUT
U.P. INDIA
INDEX
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INTRODUCTION
ETIOLOGY & PATHOLOGY
PATHOPHYSIOLOGY
SYMPTOMS AND SIGNS
DIAGNOSIS
ANESTHETIC MANAGEMENT
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INTRODUCTION- Mitral stenosis is the narrowing of mitral orifice as a result
of diffuse thickening of valve leaflets by fibrous tissue and calcific deposits.
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ETIOLOGY AND 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.
PATHOPHYSIOLOGY
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Cardiac changes-
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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
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Mean gradient:
 >10 mmHg  Severe
 5-10 mmHg  Moderate
 <5 mmHg  Mild
Pathophysiology
Right Heart Failure:
Hepatic Congestion
↑JVP
Tricuspid Regurgitation
RA Enlargement
RV Pressure Overload
RVH
RV Failure
 Pulmonary HTN
Pulmonary Congestion
Atrial Fib
LA Thrombi
LA Enlargement
 LA Pressure
Obstruction of diastolic inflow
Prolonged early diastolic
mitral inflow &delayed filling
Pressure volume loops shifted
to left so LVEDP and LVEDV
are↓
Pulmonary changes
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Pulmonary arterial hypertension results as1)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
HEMODYNAMIC CHANGES THAT OCCURS AT VARIOUS STAGES OF
SEVERITY OF MITRAL STENOSIS
SEVERITY→
AT
R
E
S
T
MILD
(1.5-2.5 cm2)
MODERATE
(1.1-1.5 cm2)
SEVERE
( < 1cm2 )
Left atrial
pressure
N
↑
Pulmonary
arterial pressure
N
↑
↑↑ or ↑↑↑↑
N
N
↓ or ↓↓↓
Left atrial
pressure
↑
↑↑
Pulmonary
arterial pressure
↑
↑↑
↑
↑
↑↑
Cardiac output
E
X
E
R
C
I
S
E
Cardiac output
Symptoms
Breathlessness
 Fatigue
 Oedema, ascites
 Palpitation
 Haemoptysis
 Cough
 Chest pain
 Hoarseness
 Mitral facies or malar flush
 Symptoms of thromboembolic complications (e.g. stroke, ischaemic
limb)
o
Are worsened by conditions that demand increase in cardiac output.
◦ Exertion,fever, anemia, pregnancy, thyrotoxicosis
NYHA FUNCTIONAL CLASSIFICATION OF PATIENT
WITH HEART DISEASE
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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
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
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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
Lab examination
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Chest x-ray
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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.
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ELECTROCARDIOGRAPHY
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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) in V1;
Broad, notched P waves in lead II; or both.
Low voltage in V1,
Right axis QRS deviation, and tall R waves in V1 suggest RV
hypertrophy
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Echocardiography
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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
Diagnosis
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History
Symptoms
Signs on physical examination
X-ray chest
Electrocardiogram
Echocardiography
Anesthetic management
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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
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PREOPERATIVE MEDICATIONS
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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.
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ANESTHESIA TECHNIQUE-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.
General Anesthesia
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Premedication -Avoid premedication with anticholinergics to avoid tachycardia.
opioiods like fentanyl are used to give analgesia.
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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, PANCURONIUM.
Benzylisoquinolinium group causes histamine release. Example are –
ATRACURIUM, CISATRACURIUM, MIVACURIUM.
Succinylcholine also causes slight release in histamine.
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Maintenance
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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.
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Monitoring
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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
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mitral stenosis undergoing major surgery.
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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.
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Reversal of anesthesia.
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Reversal nondepolarising muscle relaxants is achieved slowly with neostigmine and
glycopyrrolate to reduce drug induced tachycardia caused by glycopyrrolate.
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Post operative management .
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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.
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Thank
You……….