DR.SANDEEP SAINI LLRM COLLEGE MEERUT U.P. INDIA

INDEX

      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-

Normal valve area: 4-6 cm 2 Mild mitral stenosis :  MVA 1.5-2.5 cm 2      Minimal symptoms Mod mitral stenosis MVA 1.0-1.5 cm 2 usually does not produce symptoms at rest Severe mitral stenosis MVA < 1.0 cm2  Symptoms at rest 

Mean gradient

:    >10 mmHg  5-10 mmHg  Severe Moderate <5 mmHg  Mild

Pathophysiology

Right Heart Failure: Hepatic Congestion ↑JVP Tricuspid Regurgitation RA Enlargement RV Pressure Overload RVH RV Failure

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Pulmonary HTN Pulmonary Congestion Atrial Fib LA Thrombi LA Enlargement

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LA Pressure

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Obstruction of diastolic inflow

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Prolonged early diastolic mitral inflow &delayed filling

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Pressure volume loops shifted to left so LVEDP and LVEDV are↓

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

E X E R C I S E 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 ) AT R E S T

Left atrial pressure Pulmonary arterial pressure Cardiac output N N ↑ ↑ ↑↑ ↑↑ or ↑↑↑↑ N N ↓ or ↓↓↓ Left atrial pressure Pulmonary arterial pressure Cardiac output ↑ ↑ ↑↑ ↑↑ ↑ ↑

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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) Are worsened by conditions that demand increase in cardiac output.

◦ Exertion,fever, anemia, pregnancy, thyrotoxicosis

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

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 P 2 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

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

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 V 1 ; Broad, notched P waves in lead II; or both. Low voltage in V 1 , Right axis QRS deviation, and tall R waves in V 1 hypertrophy suggest RV

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

Diagnosis

      History Symptoms Signs on physical examination X-ray chest Electrocardiogram Echocardiography

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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

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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.

 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.

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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, PANCURONIUM.

Benzylisoquinolinium group causes histamine release. Example are – ATRACURIUM, CISATRACURIUM, MIVACURIUM. Succinylcholine also causes slight release in histamine.

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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.

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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 .

     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.

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 .

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.

Thank You……….