Mitral stenosis regurgitation pathophysiology anesthetic considerations for non cardiac surgery
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MITRAL STENOSIS & REGURGITATION Pathophysiology & Anesthetic considerations for non-cardiac surgery. Presenter: Dr Prashant Kumar. University College of Medical Sciences & GTB Hospital, Delhi. Mitral Stenosis. Mitral valve is present between LA & LV

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MITRAL STENOSIS & REGURGITATIONPathophysiology & Anesthetic considerations for non-cardiac surgery

Presenter: Dr Prashant Kumar

University College of Medical Sciences & GTB Hospital, Delhi


Mitral Stenosis

  • Mitral valve is present between LA & LV

  • Normal mitral valve orifice area (MVA): 4-6cm2

  • MVA <2.5cm2 leads to symptoms

  • Decrease in Mitral valve orifice area leading to chronic & fixed mechanical obstruction to LV filling is termed as MS.


Causes

  • Rheumatic Heart disease

  • SLE

  • Carcinoid syndrome

  • Active Infective Endocarditis

  • Left atrial myxoma

  • Congenital mitral stenosis

  • Massive Annular Calcification


Rheumatic mitral stenosis

  • More common in females (2/3rd of all pts)

  • Symptoms occur two decades after onset of Rheumatic fever

  • Age of presentation

    • Earlier in 20s-30s

    • Now in 40s-50s (slower progression)

  • Isolated MS in 40% cases of RHD

    • Remaining 60% cases associated with other valvular diseases- MR/AR


Patho-physiology

  • Immunological disorder initiated by Group A beta hemolytic streptococcus.

  • Antibodies produced against streptococcal cell wall proteins & sugars react with connective tissues & heart; result in rheumatic fever and symptoms like

    • Carditis

    • Arthritis

    • Subcutaneous nodules

    • Chorea

    • Erythema marginatum


  • Chronic cardiac & valvular inflammation leads to cardiac & valvular pathology

  • Valvular pathology

    Rheumatic fever involving mitral valves

    Valve leaflet thickening and fusion of commissures

    Increased rigidity of valve leaflets

    Thickening, fusion and contracture of chordae & papillary heads

    Leaflet calcification (long standing MS)

    Progressive reduction in mitral valve orifice area

    Mitral Stenosis


Mechanical obstruction to left ventricular diastolic filling

Adaptative ↑ in LAP to maintain LV filling

-------------------------------------------------------------------------

LA enlargement ↑ in pulmonary venous pressure → ↑ in pulmonary arterial pressure*

Atrial fibrillationTransudation of fluid into pulmonary interstitial space

Thrombus formation

Systemic thrombo-embolism ↓ed pulmonary compliance ↑Work of breathing

Progressive dyspnoea on exertion/rest

Acute conditions like AF, Pregnancy, Pain, sepsis

(↑ HR/CO)

Acute ↑ in LAP

Pulmonary edema

↑ in pulmonary arterial pressure*--------→ Pulmonary arterial hypertrophy (Pulmonary HTN)

RV hypertrophy and dilatation

RV failure


Pressure gradient between LA & LV

Effect of MS on left ventricle


Effect of heart rate

  • Gorlin formula

    Valve area = Transvalvular flow rate (ml/s)

    K x PG1/2

    (PG: Transvalvular pressure gradient, mmHg)

    (K is a hydraulic-pressure constant =38)

  • Tachycardia shortens diastole more proportionately than systole

  • Decreases the overall time for transmitral flow,

  • In order to maintain CO, the flow rate per unit time must increase

  • Pressure gradient increase proportionate to square of flow rate

  • ↑LAP → Pulmonary venous congestion and symptoms.

  • So, patients with MS do not tolerate tachycardia.


Effect of Atrial fibrillation in MS

  • Increased chances of thrombus formation & systemic thrombo-embolism

  • Normally effective atrial contraction is important in LV diastolic filling

    • In presence of AF

      • Loss of effective atrial contraction

      • ↑ed ventricular rate (↓ed diastolic filling time)

        Impaired LV filling (↓ed LV preload)

        decreased cardiac output


Diagnosis

  • Clinical presentation

    • Dyspnea, fatigue, orthopnea, PND, cough, hemoptysis,.

    • 10% patients have anginal type chest pain not attributable to CAD

    • Systemic thromboembolism (first symptom in 20% cases).

  • Physical examination

    • Low volume pulse

    • Sign & Symptoms of right sided heart failure - engorged neck veins, enlarged tender liver


  • Mitral facies

    ‘Pink purple patches on the cheeks, cyanotic skin changes from low cardiac output’

  • Cardiac auscultation

    • Opening snap

    • Rumbling diastolic murmur best heard at apex radiating to the axilla

    • Loud S2: pulmonary hypertension


  • ECG

    Broad notched P wave (left atrial enlargement)

    Atrial fibrillation


    Chest X-ray

    Normal to ↑ed cardiac shadow

    Straightening of the left heart of border and elevation of left main bronchus (left atrial enlargement)

    mitral calcification

    Evidence of pulmonary edema/ HTN

    LAA: Left atrial appendages, MPA: Main pulmonary artery, LPA: left pulmonary artery, RPA: Right pulmonary artery, Ao- Aortic knuckle (Ao)


    • Echocardiography

      • Anatomy/size of mitral valve & its appendages

      • severity of MS (area of orifice)

      • Size & function of ventricles

      • Estimation of pulmonary artery pressure

    • Cardiac catheterization and invasive measurement

      • Are almost never necessary

      • Reserved for situations ECHO sub-optimal/conflict with clinical presentation


    Severity of MS


    Guidelines

    “Symptomatic MS (progressive dyspnoea on exertion, exertional pre-syncope, heart failure) is an active cardiac condition & pt should undergo evaluation & treatment before non cardiac surgery”

    • Emergency surgery

      Mild / Moderate MS

      • High risk

      • Continue medication

      • Proceed with surgery

    • Severe MS

      • Very high risk consent

      • Post- op ventilatory consent


    • Pre-operative Optimization of patient

      • Atrial fibrillation

        Sinus rhythm/control of ventricular rate

        1.Digoxin (emergent IV digitalization:- loading dose 0.25mg iv over 15 minutes followed by 0.1mg every hour till response occur or total dose of 0.5-1.0mg. Monitor ECG, BP, CVP; HR <60bpm- Stop)

        2. CCB (verapamil/diltiazem: 0.075-0.15mg/kg IV)

        3. β-blocker (esmolol: 1mg IV)

        4. Amiodarone (loading: 100mg IV, infusion: 1mg/min IV for 6 hrs. 0.5mg/min for next 18 hrs)

        5. Cardioversion in hemodynamic unstable patients


    • Pulmonary HTN/Edema/RVF

      1. Oxygen

      2. Diuretic

      Loop diuretics

      High dose deleterious

      Combine with vasodilator

      3. Digitalis

      4. Morphine (0.1mg/kg)


    (Pre-operative Optimization of patient> Pulmonary HTN/Edema/RVF continued…)

    5. Vasodilators (NTG)

    Pulmonary vasodilation (↓PAP)

    Start from small dose (0.5–10 μg/kg/min)

    S/E: systemic hypotension

    6. Nesiritide

    Recombinant BNP (Brain natriuretic peptide)

    Arterial & venous dilatation

    Controls dyspnoea in Acute heart failure

    7. Myofilament calcium sensitizer (Levosimendan)

    Inodilators (↑es myocardial contractile strength, dilatation of systemic, pulmonary & coronary artery)


    (Pre-operative Optimization of patient> Pulmonary HTN/Edema/RVF continued…)

    8. Inotropic agents

    Norepinephrine

    Dopamine

    Dobutamine

    9. Inodilators

    Amrinone

    Milrinone


    • Elective surgery

      • Mild/ moderate MS

        • Proceed with surgery after evaluation

        • Continue medications

      • Severe MS

        • Cardiology referral/surgical correction

        • Patients taken in optimized condition


    Management of Anesthesia Anesthetic goals


    Pre medication

    • To decrease anxiety & any associated likelihood of adverse circulatory responses produced by tachycardia

    • Drug to control heart rate

    • Antibiotics (prophylaxis for infective endocarditis is no longer recommended) (Ref: Miller’s Anesthesia, 7th edition)


    Asymptomatic

    Standard non-invasive

    ECG,

    HR

    NIBP

    Pulse-oxymetry

    Capnograph

    Temperature

    Symptomatic pts or major surgery

    Standard non-invasive

    Serial ABG

    Invasive monitoring

    IBP

    CVP/PAC

    Echocardiography (TTE/TEE)

    Cardiac catheterization

    Monitoring


    Intra-operative management


    Non-opioid induction agents


    Muscle Relaxants


    Management

    Monitoring

    Oxygen

    Pain relief: multimodal including neuroaxial opioids

    Intravenous fluids

    Anticoagulants

    Complication

    Pulmonary congestion/edema

    Thrombo-embolism

    Heart failure

    Post-operative


    New York Heart Association functional classification of patients with heart disease


    Congestive Heart Failure

    • Diuretics: loop diuretics (furosemide 20-40mg IV); S/E: Hypokalemia

    • Digoxin:

    Therapeutic plasma concentration level: 0.5-2.0ng/ml


    Clinical manifestation of digitalis toxicity

    • Plasma level > 3ng/ml

    • Extra Cardiac: Anorexia, nausea, vomiting & abdominal pain (CTZ stimulation)

    • Cardiac: any type of atrial or ventricular arrhythmia, delayed conduction through AV Junction.

      • Atrial tachycardia with AV block is most common arrhythmia

      • Ventricular fibrillation is most frequently cause of death.

        Treatment of digitalis toxicity

    • Stop further dose

    • Correction of hypokalemia, hypomagnesemia, arterial hypoxemia

    • Drugs

      • Phenytoin (0.5-1.5mg/kg IV over 5min), lidocaine (1-2mg/kg IV), atropine (35-70µg/kg IV) for cardiac dysarrhythmia

      • Digiband (digoxin specific antibodies, Fab portion, IV preparation 40mg vial)

    • Insertion of a temporary artificial transvenous cardiac pacemaker


    Anticoagulant therapy

    • Management of Patients on warfarin

      • Emergency surgery

        • Discontinue warfarin

        • Give vitamin K 0.5 – 2.0 mg IV

        • FFP 15 ml/kg repeat if necessary

        • Accept for surgery if INR <1.5

    • Elective surgery

      • Stop 3 days preoperatively

      • monitor INR daily

      • Give heparin when INR <1.5


    • Stop heparin 6 hours prior to surgery

    • Check INR

    • Accept for surgery if INR <1.5

    • Restart heparin post-operatively as soon as possible

    • Both to be given for 2 – 3 days, stop heparin if INR 1.5 – 2.0.


    • Management of Patients on Heparin

      • Emergency surgery

        • Consider reversal with IV protamine 1 mg for every 100 IU of heparin

      • Elective Surgery

        • Stop heparin 6 hours prior to surgery

        • Check INR, accept for surgery if INR <1.5

        • Restart heparin in post-op as soon as possible

          If patient is on LMWH, we rarely need to stop it.


    Summary of MS

    • Is a low & fixed cardiac output condition

    • Stress condition like pregnancy, labour & sepsis, condition become worst- CHF, pulmonary edema, AF

    • Patients may be on diuretics, digitalis & anticoagulant therapy

    • Peri-operatively these patients have to be managed as per medications & guidelines

    • Tachycardia has to be avoided at any cost

    • Pulmonary vasculature resistance has to be reduced

    • Preload & afterload both should be maintained

    • NYHA I & II :- Epidural block or GA

    • NYHA III & IV :- GA preferred over epidural block


    Mitral Regurgitation


    • Retrograde flow of blood from LV to LA through incompetent mitral valve during systolic phase

      Causes

      • MR is almost always (90%) associated with MS in RHD

      • Degenerative processes of leaflets and chordal structures

      • Infective endocarditis

      • Mitral annular calcification


    • Functional

      Structurally normal leaflets and chordae tendineae

      • Ischemic heart disease (Ischemic MR)

      • Idiopathic dilated cardiomyopathy

      • Mitral annular dilatation


    Pathophysiology of MR

    Mitral regurgitation

    Systolic (Retrograde) ejection into LA

    Acute Chronic

    Volume overload in LA & LV ↓ed LV afterload (into LA)

    ↑ed LA, LV Pressure↑ed LA/LV size/ compliance

    Pulmonary edema ↓ed Cardiac outputLA dilatation↓ed contractility

    AF ↓ CO

    Pulmonary congestion


    Acute MR

    Sudden onset MR

    Sudden increase in LV preload

    Enhanced LV contractility ↑ed LAP (acute)

    (LV size: N) (LA size: N)

    Ejection into LA & ↑ed Pulm vascul pressure

    systemic circulation

    ↓ cardiac outputPulmonary congestion/edema


    Chronic compensated MR

    • Slow development of MR

      Chronic LV overloading

      Eccentric LV hypertrophy LA dilatation

      ↑LV radius, ↑ed wall tensionMaintenance of LAP

      Maintenance of LV systolic function Change in LV compliance

      (LVEDP maintained)

      After load/CO: maintained

      Gradual decline in LV systolic function

      Decompensated phase


    Decompensated phase

    Progressive LV dilatation

    Mitral annular dilatation↑ed wall stress/afterload

    Increased regurgitationdeteoration in LV syslolic

    & diastolic function

    ↑ed LAP

    Atrial enlargement Pulmonary congestion/edema/HTN

    Atrial FibrillationRV dysfunction/failure


    Pathophysiology of MS with MR

    MSMR

    Obstruction of blood flow systolic (retrograde) ejection into LA

    from LA to LV during diastole

    Volume overload in LA Volume overload in LV

    ↓ed LV filling↑ LAP LV dysfunction

    ↓ed CO

    ↓ed COLA dilatation

    ↑PVP/PAP

    (LV size/function: N)

    RV dysfunction


    MRMS


    Diagnosis

    • Clinical presentation

      • Fatigue, dyspnoea, orthopnoea/Systemic thrombo-embolism

    • Physical examination

      • Arterial pressure: N/↓

      • Pulse (Water Hammer pulse- ↓DBP, ↑ SBP)

      • Signs of RVF like ↑ JVP

      • Systolic thrill at apex (hyperdynamic circulation)

    • Cardiac auscultation

      • Holosystolic murmur

      • S1 is absent, soft or buried in the systolic murmur


    ECG

    Non-specific findings

    Atrial fibrillation

    LA enlargement/LV hypertrophy

    Chest X-ray

    Left heart chamber enlargement

    Pulmonary congestion


    • Echocardiography

      • Diagnosis/mechanism/severity of MR/MS

      • Impact on cardiac chamber size, pressure & function

      • Pulmonary artery pressure

      • Presence of thrombus

    • Cardiac catheterization with left ventriculography

      • invasive

      • Reserved for pts in whom ECHO is sub-optimal


    Severity of MR


    Management of Anesthesia

    Problems to be anticipated:

    • Pulmonary congestion/ edema

    • Atrial fibrillation/ thrombo-embolism

    • LV dysfunction: ↓ CO

    • Acute  in afterload following ET intubation & surgical stimulation  acute decompensation of LV

    • Bradycardia -  time for retrograde blood flow

    • Drug induced myocardial depression


    Anesthetic goals in MR Primary goals- Maintain forward systemic flow- Decrease the regurgitant fraction- Optimize RV function


    Anesthetic Goals in MS and MR


    Technique of anesthesia In MR

    Regional vs General Anesthesia in MR

    • Peripheral nerve blocks

      • Safe

      • Avoid intravascular drug injections (ultrasound/nerve stimulator guided blocks)

    • Central neuraxial blocks

      • Preload: ↓HR: ↔/ ↑/ ↓, Contractility: ↔

        Afterload: ↓Pulmonary vasculature: ↔

      • Mild/ Moderate MR (NYHA class I & II): SAB and epidural are well tolerated (avoid bradycardia)

      • Severe MR (NYHA class III & IV): Prefer GA over SAB and epidural


    Asymptomatic

    Standard non-invasive

    ECG,

    HR

    NIBP

    Pulse-oxymeter

    Capnograph

    Temperature

    Symptomatic pts or major surgery

    Standard non-invasive

    Serial ABG

    Invasive monitoring

    IBP

    CVP/PAC

    Echocardiography (TTE/TEE)

    Cardiac catheterization

    Monitoring


    Management of GA


    Non-opioid induction agents


    Muscle Relaxants


    Maintenance

    Narcotic oxygen relaxant technique

    Use of N2O – declined


    Summary of MR

    • 90% of Rheumatic MR are associated with MS

    • LV has to deal with large volume- only a fraction goes to systemic circulation

    • Patient may present with CHF, pulmonary edema & LV dysfunction

    • Patients may be on diuretics, digitalis & anticoagulants- to be managed as per patients condition and guidelines.

    • Bradycardia has to be avoided at any cost

    • Systemic vascular resistance (afterload) should be kept slightly low

    • Preload should me maintained

    • NYHA I & II :- neuraxial block or GA

    • NYHA III & IV :- GA preferred over neuraxial block


    Summary

    • Valvular heart disease poses challenge during anesthesia

    • We should know pathophysiology of each valvular heart diseases

    • Most of the time, valvular heart diseases occur in combination

    • Our aim is to maintain normal cardiac output & tissue perfusion by regulating heart rate/rhythm, preload, afterload, myocardial contractility.

    • Use of regional anesthesia is not contraindicated in theses patients, but proper patients selection & precaution are must.


    References

    • Kaplan’s Cardiac Anesthesia; 5th edition

    • Miller’s Anesthesia; 7th edition

    • Clinical Anesthesia; Barash, Cullen, Stoelting, 5th edition

    • Stoelting’s Anesthesia & Co-existing Disease; 5th edition

    • Harrison’s Internal Medicine; 17th edition

    • Wylie & Churchill- Davidson’s A Practice of Anesthesia; 7th edition

    • Clinical Anesthesia; Morgan 4th edition


    Thank you


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