ANESTHESIA FOR A PATIENT OF MITRAL STENOSIS FOR NON CARDIAC SURGERY

PRESENTED BY: Dr. ANKUR KHANDELWAL, Anaesthesiology & Critical care

INDEX

INTRODUCTION ETIOLOGY PATHOPHYSIOLOGY SYMPTOMS AND SIGNS DIAGNOSIS ANESTHETIC MANAGEMENT

INTRODUCTION

Mitral stenosis is the narrowing of mitral orifice as a result of diffuse thickening of valve leaflets by fibrous tissue and calcific deposits.

ETIOLOGY 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.

Pure MS approximately in 40% rheumatic heart disease. Time gap of development symptoms from rheumatic fever – two

decade in developed country but 5 – 15 yrs in developing country

PATHOLOGY

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.

Initial insult is rheumatic but later changes may be a process resulting from trauma to the valve caused by altered flow pattern due to initial deformity.

Thrombus formation and arterial embolisation occur.

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

Right Heart Failure:Hepatic Congestion

↑JVPTricuspid Regurgitation

RA Enlargement

Pulmonary HTNPulmonary Congestion

Atrial FibLA Thrombi

LA Enlargement LA Pressure

RV Pressure Overload RVH RV Failure

Obstruction of diastolic inflowProlonged early diastolic mitral inflow &delayed fillingPressure volume loops shifted to left so LVEDP and LVEDV are↓

PATHOPHYSIOLOGY

PULMONARY CHANGES Pulmonary arterial hypertension results as-

Increased left atrial pressure. Pulmonary arterial constriction. Interstitial edema in the wall of the small pulmonary vessels. Organic obliterative changes in the pulmonary vascular bed. At last if there is severe pulmonary arterial

hypertension→Tricuspid

regurgitation Pulmonary incompetence Reduced lung compliance and increased work of breathing. Right heart failure.

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

NATURAL HISTORY OF MS

Continuous progressive, life-long disease Slow, stable early course, latent period of 20-40

yrs from RF to onset of symptoms Onset of symptoms to disability- 10 yrs Atrial fibrillation- 30-40% Causes of death CHF Systemic embolism Pulmonary embolism Infection

HISTORY & CLINICAL EXAMINATION History of Rheumatic fever. SYMTOMS

1. SOB – commonest (in mild MS, by sudden change in HR, vol-status, or CO e.g. severe exertion, excitement, fever, severe anemia, paroxysmal AF or other Tachycardia, Preg, thyrotoxicosis. As MS progress, lesser stress ppt. dyspnea & also orthopnea, PND due to pulmonary venous hypertension.)

2. Palpitations

3. Cough

4. Haemoptysis (from rupture of pulm. Bronchial venous connections 2ndary to PVH/ never fatal)

5. Easy fatiguability and syncope( due to reduced cardiac output)

6. Attacks of ac. Resp. distress ( pulm. edema)7. Aytypical angina- Chest pain in 10–15% of pts, even in the absence of

atherosclerosis; etiology often remains unexplained but may be emboli in the coronary circulation or acute RV pressure overload

8. Hoarseness due to compression of left recurrent laryngeal nerve by enlareged left atrium (Ortner’s Syndrome)

9. Oedema, ascites10. Mitral facies or malar flush11. Recurrent pulmonary infections12. Symptoms of thromboembolic complications (e.g. stroke, ischaemic limb)

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

EXAMINATION

General Examination

Decubitus: may be orthopnoeic Cyanosis : Present in severe MS with ac. pulm. edema Oedema : Bilateral pedal edema, accentuated in CCF Neck vein: Engorged in CCF

Prominent ‘a’ wave in pulm. HTN Pulse - low volume. Rhythm- usually regular, irregular in AF BP: usually low. Cold extremities. RESPIRATION: may be tachypnoeic Tender Hepatomegaly.

SYSTEMIC EXAMINATION INSPECTION -- no deformity of precordium, -- no venous prominence seen, -- visible pulm. Art. pulsation in left 2nd ICS in pulm. HTN

Palpation: Small volume pulse Tapping apex-palpable S1 Palpable S2 Thrill- Diastolic thrill over apical

area, best palpable in left lateral

position at the height of exp Left parasternal heave

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 Diastolic murmur (Graham-Steel)- high

pitched murmur heard at the cardiac base secondary to pulmonary regurgitation.

Clinical assessment of severity

• Assessing the A2 - OS gap- Inversely proportional to severity

• Duration of the diastolic murmur- directly proportional to the length of the murmur

• Assessing the severity of PAH

INVESTIGATIONS Complete Haemogram Blood sugar Serum Electrolytes Liver function tests Renal Function tests Chest X- Ray ECG Echocardiography CT brain (in special cases)

Chest X-Ray Slight increase in the transverse

diam. of heart Straightening of left border of cardiac

silhouette. Double contour of the right border of

heart Enlarged pulmonary conus Small Aortic knob. Dilatation of the upper lobe

pulmonary veins- Moustache or antler sign.

Backward displacement of the esophagus by enlarged left atria.

ELECTROCARDIOGRAPHY 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, III and aVF.

Atrial fibrillation

F wave replacing P wave if atrial fibrillation develops

Right Ventricular hypertrophy Right axis QRS deviation, and tall R waves in V1 suggest RV

hypertrophy

ECHOCARDIOGRAPHY Diagnosis of Mitral Stenosis

Assessment of hemodynamic severity mean gradient, mitral valve area, Left atrial pressure, pulmonary artery pressure

Extent of restriction of valve leaflets

Assessment of size and function of the Ventricles.

Reevaluation of patients with known MS with changing symptoms or signs.

F/U of asymptomatic patients with mod-severe MS

Anatomic suitability of percutaneous mitral balloon valvotomy (PMBV).

Cormier’s Grading of Mitral Valve Anatomy Based on ECHO

ECHO group Mitral Valve Anatomy

GROUP 1 Pliable non-calcified anterior mitral leaflet and mild subvalvular disease( thin chordae >/=10 mm long

GROUP 2 Pliable non-calcified anterior mitral leaflet and severe subvalvular disease(thickened chordae>10mm)

GROUP 3 Calcification of mitral valve of any extent, as assessed by fluroscopy, whatever the state of subvalvular apparatus

Treatment Modalities of Mitral Stenosis Asymtomatic/ Mildly symptomatic Mitral stenosis Diuretics for congestive symptoms and restriction of salt intake. Drugs for rate control Prophylaxis against infective endocarditis Warfarin to patients with history of AF or thromboembolism

Symtomatic Mitral Stenosis- unless there is a contraindication, mitral valvotomy is performed in symptomatic patients with moderate or severe isolated MS. Mitral valvotomy can be carried out by two techniques-

1. PMBV

2. Surgical( Open) Valvotomy using Cardiopulmonary Bypass.

Succesful valvotomy is defined by a 50% reduction in the mean mitral valve gradient and a doubling of the mitral valve area.

Severe Mitral Stenosis/ Valve morphology not favourable for PMBV/ MS with MR- Surgical Commissurotomy or MVR should be carried out.

Predictors of poor outcome after surgical procedure Age>65 yrs Presence of CAD LV dysfunction Severe pulmonary hypertension RV dysfunction Associated Co-Morbidities.

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. Antibiotics for surgical and infective endocarditis prophylaxis. Anticoagulant therapy- based on following rationales:- 1. Acceptable INR for surgery- An INR <1.5 is generally acceptable 2. Risk of bleeding-

a) Discontinuation of warfarin is essential for the procedures associated

with a high risk of bleeding

b) Discontinuation of warfarin is usually not necessary for the

procedures associated with a low risk of bleeding

3. Risk of thrombosis

Management steps

Low risk of thrombosis High risk of thrombosis

AF without additional risk factors AF + either h/o stroke/TIA or >risk factors such as recent CHF,HTN,Age>70 yrs, diabetes

DVT/PE occuring more than 3 months ago DVT/PE occuring in past 3 months.

Hypercoagulable state without recent thrombotic episode

Hypercoagulable state with recent thrombotic episode

Newer model mechanical aortic prosthesis and any tissue valves

Mechanical mitral prosthesis and old model aortic prosthesis

Low risk of thrombosis High risk of thrombosis

Discontinue warfarin 5 days prior to surgery Discontinue warfarin 5 days prior to surgery

Check INR the day before surgery, ensure target INR<1.5

Start prophylactic or therapeutic LMWH

Restart warfarin at pre-op dose as soon as hemostasis is assured and only after epidural catheters are removed

Last dose of LMWH is not given any later than 24 hrs before the procedure.

Recheck INR within one week after starting warfarin and then at regular intervals.

Check INR the day before surgery, ensure target INR<1.5

Restart LMWH/ warfarin at pre-op dose as soon as hemostasis is assured

MANAGEMENT

4. Timing of procedure

If urgent or emergent procedures are to be undertaken in < 4-5 days and warfarin reversal is required, it may be satisfactory to give 1-2 mg of Vitamin K orally in order to reverse the effect of warfarin. When reversal of anticoagulation is required within 6 hours, intravenous Vitamin K and Octaplex® is required(Virally Inactivated Plasma-Derived Concentrate). FFP can be given if Octaplex is not available.

5. Type of anaesthesia.

a) Local and general anesthesia can be safely administered to

a patient on warfarin.

b) Neuraxial blocks (e.g., epidural analgesia, spinal anesthesia

and retrobulbar blocks) should not be performed on patients

on warfarin

ASRA guideline

Anesthetic management The main objectives are-

To avoid tachycardia.

To maintain sinus rhythm. Aggressively treat new onset atrial fibrillation pharmacologically or with direct cardioversion especially in the hemodynamically compromised patient .

Avoid large, rapid falls in SVR. This is compensated for by increasing HR, which can worsen cardiac function.

To avoid hypovolemia and fluid overload.

Avoid factors that may increase pulmonary artery pressure (PAP)

Effects of altered hemodynamics

Adverse effects

Result Mechanism

Bradycardia CO Low cardiac output

Tachycardia CO filling time AF CO LV

filling/no atrial kick

Preload CO LV filling SVR CO stroke

volume SVR CO SV (due to

tachycardia related filling time)

Why tachycardia is detrimental? Increased HR (sinus tachycardia, AF)

shortened diastolic filling period diminished time for LA emptying increased pressure gradient across MV and increased LA pressure.

AF – additionally causes loss of ‘atrial kick’ further reduction of LV filling reduced cardiac out put.

MONITORING Noninvasive monitoring like HR, BP , ECG,

RR, SpO2. Invasive monitoring depends upon- 1. Complexity of the operative procedure.

2.Magnitude of physiological impairment. The concomitant use of invasive hemodynamic

monitors is recommended in symptomatic patients with critical stenosis.

ANAESTHESIA TECHNIQUE REGIONAL ANAESTHESIA 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. Rapid prehydration should be avoided, and slow titration of local anesthetic

solution is recommended to minimise hemodynamic changes. When treating hypotension, phenylephrine is preferred over ephedrine,

which may increase the HR. Epinephrine-containing local anesthetic solutions are best avoided due to

concerns about potential tachycardia. Combined spinal–epidural (CSE) with an intrathecal opioid combined with a

dilute epidural infusion minimizes sympathetic block and concomitant hypotension---can be considered as a good option.

Surgery under Peripheral Nerve Blocks can be the best anesthetic technique wherever possible

Hypothermia to be avoided as it increases PVR.

GENERAL ANAESTHESIA PREANAESTHETIC MEDICATIONS Avoid premedication with anticholinergics to avoid tachycardia. Opioids like fentanyl are used to give analgesia. Use generous

amounts of opioids to abolish hemodynamic response to intubation. It will also decrease the requirement of induction agents.

Antianxiety drugs decrease tachycardia associated with anxiety Epidural analgesia with opioids can be considered safely as a

supplement to GA whenever needed. PREOXYGENATION

Adequate preoxygenation to avoid any degree of hypoxia.

INDUCTION General Anaesthetics with/without Muscle Relaxation

There is no single “correct” agent. Any drug can be used as long as hemodynamic goals are met.

Patients with moderate to severe MS generally have slow circulation that prolongs arm-brain circulation time.

Induction agents should be double diluted and given slowly in titrated doses.

Etomidate is the best agent for hemodynamic stability, but thiopentone can be used instead.

Propofol should be avoided as it can lead to precipitous hypotension.

Ketamine to be avoided as it causes tachycardia. Induction with volatile anaesthetics to be avoided- causes

decreased SVR and cardiac output , hypotension.

MUSCLE RELAXATION

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 except PANCURONIUM.

Benzylisoquinolinium group causes histamine release. Example are –ATRACURIUM, CISATRACURIUM, MIVACURIUM.

Succinylcholine also causes slight release in histamine

MAINTAINENCE

Oxygen + Air + High dose narcotic or volatile anaesthetics such as isoflurane, desflurane or sevoflurane at low vol%

Halothane is best avoided due to its arryhthmogenic potential and high incidence of junctional rhythm which can be disastrous in a patient with mitral stenosis.

In patients with PAH, nitrous oxide is best avoided due to its effect on pulmonary resistance.

Deep plane of anaesthesia should be maintained. Ensure appropriate ventilation and proper fluid

therapy.

If there is intra-op tachycardia

1. Deepen the plane and ensure adequate analgesia

2. Use beta blockers like esmolol/propranolol or calcium

channel blockers like diltiazem. If atrial fibrillation occurs ventricular rate can be controlled with esmolol,

propranolol, diltiazem , digoxin or amidarone. For sudden supraventricular tachycardia –cardioversion.

DRUG LOADING DOSE MAINTENANCE

AMIODARONE 15mg/min for 10 min 0.5-1mg/ min for 6hrs

DIGOXIN 0.25mg 2hry until 1mg 0.125-0.25mg/day

DILTIAZEM 0.25mg/kg over 3-5 mins 5-15 mg/hr

ESMOLOL 500microg/kg over 1min 50ug/kg/min

METOPROLOL 5mg over 3-5 mins x 3 doses

1.25-5mg 6hrly

VERAPAMIL 5-10mg over 3-5 mins 2.5-10 mg/hr

Reversal of anesthesia. 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.

Why does pregnancy aggravate the symptoms of mitral stenosis? Increase in blood volume by 30-50% -increase in capillary

hydrostatic pressure – pulmonary edema. Decrease in SVR Increase in HR 10-20 beats/min – reduced diastolic filling time of LV Increase in CO by 30-50% - increase in transvalvular gradient –

rise in LA pressure During labour and delivery sympathetic stimulation – rise in HR and

CO Sudden rise in venous return due to autotransfusion and IVC

compression –decompensation Atrial enlargement in pregnancy – atrial fibrillation Hypercoagulability – thromboembolic risk During pregnancy pts symtomatic status increases by 1 or 2 NYHA

class.

Anti coagulation

Indications for anticoagulation Patient with AF Prior embolic event Severe MS with left atrial dimension 55 mm

on ECHO

Heparin for first trimester Warfarin 12-36 weeks After 36 weeks changed to heparin

titrated to APTT level

Thank

You……….