Valvular Heart Disease v6

8/8/2019 Valvular Heart Disease v6

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Moderated by

Dr. Chitra

Presented by

Mukesh kumar sah

Anaesthesia for Valvular Heart Disease


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Contents

DefinitionDefinition

Types of VHDTypes of VHD

General Evaluation ofGeneral Evaluation of

PatientsPatients

History TakingHistory Taking

New York AssociationNew York Association

Functional ClassificationFunctional Classification

of Heart Diseaseof Heart Disease

Physical ExaminationPhysical Examination

Common ComplicationsCommon Complications

Laboratory EvaluationLaboratory Evaluation

Special StudiesSpecial Studies

PrePre--medicationmedication

Anti Coagulation ManagementAnti Coagulation Management

Special Valvular DisordersSpecial Valvular Disorders

Mitral Stenosis (MS)Mitral Stenosis (MS)

Mitral Regurgitation (MR)Mitral Regurgitation (MR)

Mitral Valve ProlapseMitral Valve Prolapse


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Definition Valvular Heart Disease (VHD)

An acquired or congenital

disorder of a cardiac valve

characterized either by

Stenosis (obstruction) or

Regurgitation (backward

flow of blood)


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Common Types of Valvular Heart Diseases

Mitral Stenosis

Mitral Regurgitation

Tricuspid Stenosis

and Regurgitation

Pulmonary Stenosis

and Regurgitation

Mitral Valve Prolapse

Aortic Stenosis

Idiopathic Hypertrophic

Subaortic AS

Aortic Regurgitation

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General Evaluation of Patients

Key Considerations

Severity of Lesion

Its Hemodynamic significance

Residual ventricular function

Presence of secondary effects on Pulmonary,Renal and Hepatic functions

Concomitant Coronary Artery Disease (CAD)


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History Taking

Key Considerations

Age

History of rheumatic fever, i/v drug abuse

Symptoms related to ventricular function

Exercise Tolerance

Fatigueability

Pedal edema

Shortness of breath (dyspnoea), when lying flat (orthopnoea), or at

night (paroxysmal nocturnal dyspnoea)

Chest pains and neurological symptoms as some valvular lesions

a/s with thromboembolic phenomenon


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History Taking

Prior procedures such as valvotomy or valve replacement and

their effects

Review of medications to evaluate efficacy and exclude

serious side effects. Commonly used agents

Digoxin

Diuretics

Vasodilators

ACE inhibitors

Anti-arrhythmics

Anticoagulants


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New York Heart Association - Functional

Classification of Heart Disease

Useful for grading clinical severity of heart failure and

estimating prognosis

Description Grade

Asymptomatic except during severe exertion 1

Symptomatic with moderate activity 2

Symptomatic with minimal activity 3

Symptomatic at rest 4


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Physical Examination

Abnormal Pulse with possible type of disorder

Pulse Abnormality Possible Disorder

Low Volumic Pulse Mitral Stenosis (MS)

Water Hammer PulseMitral Regurgitation (MR),

Aortic Regurgitation (AR)

Slow Rising Pulse Aortic Stenosis (AS)

Irregular Rate and Rhythm Atrial Fibrillation (AF)


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Search for signs of congestive heart failure

Right sided

Jugular Venous Distension

Hepatospleenomegaly

Pedal Edema

Left sided

S3 gallop

Pulmonary rales

Cardiomegaly

Neurologial deficits secondary to embolic phenomenon to be seen


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Auscultatory findings confirm the valvular dysfunction

S1

Closure of mitral and

tricuspid valves

S2

Closure of aortic and

pulmonic valves

S1 S2

Diastole

Systole

Diastole

S1

Closure of mitral and

tricuspid valves

S2

Closure of aortic and

pulmonic valves

S1 S2

Diastole

Systole

Diastole


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Common Complications

Acute and Chronic Heart Failure

Spontaneous Bacterial Endocarditis

Arrhythmias - AF

Thromboembolism-stroke, TIA

Abnormal heart structure


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Laboratory evaluation

Hemogram Anemia

Blood Glucose Exclude DM

Lipid Profile Risk factor for IHD

S.electrolytes Low K+ f/o diuretics

Urine R/M, s.creatinine BUN Renal Function Tests

S.bilirubin, SGOT, SGPT LFT( Right Heart Failure)

Arterial Blood Gases In Patients with Pulmonary Symptoms

PT and aPTT Reversal of Anti Coagulants

Chest X Ray Cardiac sizePulmonary Vascular Congestion

ECG

Rhythm and Conduction Abnormalities

RVH/LVHST-Segment ChangesSigns of digoxin toxicity (prolonged PRinterval and arrhythmias)


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Special Studies

For Diagnosis and Prognosis

Echocardiography

Radionucleotide ongiography

Cardial catheterization

Following things should be analyzed

Which valvular abnormality is most important hemodynamically?

What is the severity of that lesion?

Degree of ventricular impairment?

Hemodynamic significance of other identified abnormalities

Any evidence of CAD


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Pre-medication

Patients with Normal Ventricular Functions

Standard doses of any of used agents

Patients with Poor Ventricular Functions

Doses to be reduced in proportion to severity of ventricular

impairment

Supplemental O2

Pulmonary Hypertension


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Pre-medication

Antibiotic Prophylaxis

The risk of infective endocarditis in patients with Valvular Heart Disease following

bacteremic events including dental, oropharyngeal or nasopharyngeal, gastrointestinal or

genitourinary surgery any I & D is well established

Prophylaxis should follow general guidelines recommended by the American heart

association For Dental, Oral Respiratory Tract or Esophageal Procedures

Standard General Prophylaxis

Amoxicillin - Dosage: Adults - 2 gms, Children 50 mg/kg; Mode: Orally 1 hr before

Procedure

Inability to take Oral Medication

Ampicillin Dosage: Adults - 2 gms, Children 50 mg/kg; Mode: i/m or i/v 30 mins

before procedure

For Genitourinary or Gastrointestinal Procedures

For High Risk Patients

Ampicillin + Gentamycin ( Dosage: 1. 5 mg/kg, Mode i/m or i/v 30 mins before

procedure), six hours later Ampicillin (Dosage: Adults 1 gm children 25 mg/kg, Mode:

i/m or i/v ) or Amoxicillin (Dosage: Adults 1 gm, Children 25 mg/kg, Mode: Orally)

For High Risk Patients Allergic to Ampicillin

Vancomycin (Dosage: Adults 1 gm, Children 20 mg/kg) + Gentamycin ( adults &

children 1.5 mg/kg, Mode: i/m or i/v, within 30 mins before starting procedure)


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Pre-medication

Anticoagulation Management

Patients receiving anticoagulants can have their drug regimen interrupted 1-3 days

preoperatively

Warfarin stopped 3 days prior to Surgery and restart 2-3 days post operation

If thromboembolic risk deemed high, stopped the day before surgery and reversed

with vit K or fresh frozen plasma, i/v heparin therapy then initiated 12-24 hrs post-op

once surgery hemostasis is adequate

Incidence of thromboembolic complications increases with

Prior history of embolism and the presence of thrombus

Atrial fibrillation

Prosthetic mechanical valve

Caged ball mechanical prosthesis (starr edwards) highest (mitral or

tricuspid)

Tilting disc valves ( ST Judes) Intermediate

Bioprosthesis ( porcine or bovine tissue valves) lowest


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Special Valvular Disorders Mitral Stenosis

Etiology

Delayed complication of Rheumatic fever

66% of patients are females

Stenotic process begins after minimum period

of 2 years following acute disease and results

from progressive fusion and calcification of

value leaflets

Symptoms develop after 20 30 years when

orifice reduced to less than 2 cm2

Usually have symptoms when

areas reduced by 50%

Particulars Dimensions

Normal Aperture 4 6 cm2

Mildly Stenotic 1.5 2.5 cm2

Moderately Stenotic 1.1 1.5 cm2

Severe Stenotic < 1 cm2

Less than 50% patients Isolated MS

Remaining - Also have MR

Upto 25% rheumatic involvement of AV (AS or AR)


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Pathophysiology

Valve leaflets thicken, calcify

and become funnel shaped

(Fish Mouth Valve)

Restriction of blood flow

through the Mitral value results

in a transvalvular pressure

gradient That depends on CO,

HR (diastolic time) and

presence of normal Atrial kick


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Pathophysiology

Increase in either HR or CO

Supraventricular

Tacchycardias (AF)

Higher flow across Valve

Higher Transvascular

Pressure GradientLA Dilates

Blood Flow Statis

Formation of

Thrombi

Elevation in Left Atrial

Pressure

Transmitted to

Pulmonary Capillaries

If PCP > 25 mmHg

Transudation of Capillary

Fluid

Chronic PulmonaryVascular Changes

Irreversible Increase in

Pul. Vascular Resistance

Pulmonary Hypertension

Reduced Lung

Compliance

Ch. Dyspnoea

Rt. Ventricular Failure

Dilatation of RVTR or PR

Pulmonary Edema


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Diagnosis

Clinical manifestations

Chronic dyspnoea

Embolic events common in patients with MS and AF.

Dislodgement of clots from left atrium results in systemic

emboli most commonly cerebral, pulmonary emboli,

pulmonary infarction, hemoptysis and recurrent bronchitis

Chest pain occurs in 10-15% of patients - emboli in coronary

circulation or acute right ventricular pressure overload

Hoarseness due to compression of left recurrent laryngeal

nerve by enlarged left atrium


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Diagnosis

Physical findings

On palpation

Low volume pulse

Tapping apex

On auscultation

Opening Snap heard in expiration medial to cardiac apex,

follows S2 by 0.05 to 0.12 sec

OS followed by low pitched, rumbling, diastolic murmur heard

best at apex with pt. in left lateral recumbent position

S1 S2

Opening snap


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Diagnosis

Laboratory Evaluation

Chest X Ray

Straightening of left border of heart

Prominence of main pulmonary artery

Dilatation of upper lobe pulmonary veins

Backward displacement of esophagus by enlarged lt.

atrium

Kerly B lines in lower and mid lung fields

ECG

Right axis deviation and RVH

Tall and peaked P wave

Echo - most sensitive and specific


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Treatment

Medical management is primarily supportive

Limitation of physical activity

Anticoagulation ( with history of emboli, AF, old age)

Na+ restriction

Diuretics

Digoxin only in patients with AF and a rapid ventricular response

Beta blockers to control Heart Rate

Valve replacement

Valvuloplasty or Percutaneous transeptal ballon valvuloplasty Valve replacement surgery recurrent MS following valvuloplasty


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Anaesthetic Management

Objectives Heart Rate - Keep slow to allow for diastolic filling. Avoid sinus

tacchycardia

Rhythm Sinus rhythm

Preload maintain or slightly increase to help with ventricular

filling

Afterload SVR should be maintained, avoid decreases in SVR,

avoid increase in PVR

Contractility maintain to provide adequate CO

Monitoring

Direct intraarterial pressure

ECG-notched p wave

Pulmonary artery Pressure-prominent a wave and decreased y

decent


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Anaesthetic Management

Choice of agents

Regional Anaesthesia

Epidural is preferred over spinal due to gradual onset of

sympathetic block with epidural

General anaesthesia

Ketamine poor induction agent for GA because of sympathetic

stimulation

Pancuronium induced tachycardia to be avoided

Volatile agents produce undesirable vasodilatation or precipitatejunctional rhythm with loss of an effective Atrial kick

Halothane most suitable because it reduces Heart Rate and is least

vasodilating

NO2 avoided as causes increase in PVR


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Anaesthetic management

Intra-op tacchycardia

Deepening anaesthesia with opioid or b-blockers

(esmolol, proponalol)

In case of AF

control rate with diltiazem or digoxin

Sudden supraventricular tachycardia - cardioversion

As vasopressor - phenylephrine preferred over ephedrine

as former lacks b-agonist activity

Acute hypertension or afterload reduction done under

hemodynamic monitoring


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Mitral Regurgitation

A portion of LV volume is ejected back into

LA during systole because of an incompetent

valve

Etiology

Acute

Myocardial ischemia / infarction

( papillary muscle dysfunction or

rupture of a chorda tendenae)

Infective endocarditis

Chest trauma

Chronic Rheumatic fever

Congenital or developmental

abnormality of valve

Dilatation, destruction or calcification

of mitral annulus


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Pathophysiology

Reduction in forward SV due to backward flow of blood into left

atrium during systole ( can be as much as 50% of SV)

Left ventricle compensates by dilating and increasing end diastolic

volume

Regurgitation reduces left ventricular afterload but which may

enhance contractility

End systolic volume remains normal but eventually increases as

disease progresses

With time, patients with Chronic MR develop eccentric left ventricular

hypertrophy and progressive impairment in contractility


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Volume overload of LA

Volume overload of LV

Mitral regurgitation

LA dilationNormal LA

pressuresLV filling Fiber size

Stroke volume

Cardiac output and BP

maintained

Contractility

BP and CO

Reflexive arteriolar

constriction

SVR

Regurgitation

LA pressure Pulmonary

congestion

Early Late


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Pathophysiology

The regurgitant volume passing

through the mitral valve is

dependant on the

Size of the mitral valve orifice

Heart rate (systolic time)

Lt. ventricular lt. atrial

pressure gradient during

systole

Systemic vascular

resistance

Lt. atrial compliance


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Diagnosis

Clinical manifestations

Depend on degree of atrial compliance

Normal or reduced compliance (acute MR) pulmonary venous congestion and edema,

signs of right sided heart failure

Increased compliance (chronic MR) signs of

decreased cardiac output

Most patients exhibit features of both


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Diagnosis

Physical Findings

Hyperdynamic Apex

On auscultation

Wide splitting of S2 ( pre mature closure of

aortic valve)

Blowing pan systolic murmur best heard at theapex and often radiating to left axilla

S1S2


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Diagnosis


Chest X Ray

Left Atrial Enlargement

Pulmonary Venous Congestion

Kerly B Lines

ECG

Left Atrial Enlargement may be present

ECHO

To know the cause and degree of left ventricular function


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Treatment

Medical Treatment

Digoxin, Diuretic and Vasodilators

Surgical Valvuoplasty

Usually reserved for those with symptomatic MR

moderate(Regurgitant Volume 30 to 60% S V)

severe (Regurgitant Volume more than 60% S V)


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Anaesthetic Management Objectives

Heart Rate avoid slow heart rate (ideally 80 to 100 beats per

minute), faster rate decreases regurgitant volume

Rhythm maintain sinus rhythm

Preload - Excess fluid will dilate the left ventricle and worsen

regurgitation. Need adequate volume to maintain forward stroke

volume. Pre load reduce with Vasodilators and diuretics

Afterload Decreases are beneficial

Contractility minimize drug induced myocardial depression

Monitoring

Pulmonary Artery Pressure

Intraarterial pressure

ECG

Color flow Doppler TEE


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Mitral Valve Prolapse (MVP)

Also known as Systolic Click Murmur Syndrome, Barlows

Syndrome, Sloppy Valve Syndrome or Billowing Mitral Leaflet

Syndrome

Relatively common abnormality - present in 5% of general

population ( 15% of women)

Etiology

Sporadic

Familial

Connective tissue disorder

Marsan Syndrome

Esler Danlos Syndrome

Osteogenesis Imperfecta


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Mitral Valve Prolapse (MVP)

Pathology

myxomatous degeneration of valve leaflets. Mitral annulus may

be dilated.

Posterior mitral leaflet most commonly affected MVP causes stress on papilary muscles Dysfunction and

Ischemia of papilary Muscles More stress on diseased mitral

valve

Often associated with MR

Prolapse accentuated by maneuvers that decrease ventricularvolume (preload) like standing ,Valsalva

Prolapse diminished by maneuvers that increase ventricular

volume (preload) like squatting and isometric exercises


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Mitral Valve Prolapse - Diagnosis

Clinical Manifestations - Majority of patients areasymptomatic. In small percentage progressive myxomatosis

degeneration

Arrthymias (psVT, VT) Palpitation, Light Headedness,

Syncope

Chest pain

Embolic events (TIA)

Infective endocorditis

Florid MR

Sudden death


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Mitral Valve Prolapse - Diagnosis

Physical Findings

On Auscultation

Mid or late systolic click 0.14 seconds after S1 with or without a

late apical systolic murmur


Chest X Ray

ECG usually normal or inverted or biphasic T waves or ST segment

changes inferiorly

Paroxymal supra ventricular tachycardia common

Echo systolic prolapse of mitral valve leaflets in to left atrium.


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Anaesthetic Treatment

based on their clinical course

Most patients are asymptomatic and need only a/b prophylaxis

Patients with systolic murmur at risk for infective

endocarditis

Ventricular arrthymia may occur in intra-op / respond to

lidocaine or beta blockers

Relatively deep anaesthesia with a volatile agent usually

decreases incidence of intraop arrthymia

Hypovolemia and factors that increase ventricular emptying

increased sympathetic tone or decreased afterload should

be avoided

Phenylephrine preferred over ephedrine if there is need of

vasopressors


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Thank You!

Valvular Heart Disease v6

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