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Anaesthesia for Acyanotic Congenital Heart Disease

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Anaesthesia for Acyanotic Congenital Heart Disease Moderator: Prof. Chandralekha Presenters: Dr. Shalini Dr. Divya www.anaesthesia.co.in anaesthesia.co.in_at_gmail.com – PowerPoint PPT presentation

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Title: Anaesthesia for Acyanotic Congenital Heart Disease


1
Anaesthesia for Acyanotic Congenital Heart Disease
  • Moderator Prof. Chandralekha
  • Presenters Dr. Shalini
  • Dr. Divya
  • www.anaesthesia.co.in anaesthesia.co.in_at_gmail.c
    om

2
Epidemiology
  • Incidence of Congenital heart disease 8 per 1000
    live births
  • Acyanotic congenital heart disease
  • VSD 28
  • ASD (Secondum) 10
  • (Primum) 3
  • PDA 10
  • TAPVC 1
  • 85 of these children survive to adulthood.
  • 15 year survival rate 80 -- complex CHD
  • 95 -- simple
    CHD
  • 50 of patients with complex physiology are gt25
    years old
  • Moreover this population is growing at a rate of
    5 each year.
  • A diagnosis of congenital heart disease adds
    significant incremental risk of mortality in
    children
  • requiring inpatient noncardiovascular surgery.
    This outcome difference is present for both minor
    and major
  • surgical procedures, and regardless of whether
    mortality is measured at 1, 3, or 30 days. The
    incremental risk is greatest in neonates and
    infants where the presence of congenital heart
    disease is associated with a 2-fold increase in
    mortality from noncardiac surgery.
  • (Pediatrics 2000105332335)

3
Syndromes associated with ACHD
  • Extracardiac malformation in 20-45
  • Known chromosomal anomaly in 5 - 10
  • ASD -- Trisomy 21,18,13,XXXY,Del
    4p,5p,CHARGE,Fetal Hydantoin Syndrome,Fetal
    alcohol syndrome,Holt Oram ,Treacher
    collins,Noonans
  • VSD -- Trisomy 21,18,13,XXXY,Del
    4p,5p,CHARGE,Fetal Hydantoin Syndrome,Fetal
    alcohol syndrome, Del 10q, 13q, 18q, Fetal
    valproate syndrome, Elis van creveld syndrome,
    Apert

4
Cardiac Embryology
  • Embryogenesis from days 21 to 28. A, The cardiac
    loop is
  • formed. The heart tube is folded into an S-shaped
    dextroventral
  • convexity. B, The atria are partitioned. The
    septum primum
  • (in brown) grows from the inferior part of the
    atria to the
  • top, leaving a foramen called the ostium primum.
    The septum
  • secundum (in orange) comes from the top. The
    ostium primum
  • will be closed at the end of the fifth week by an
    expansion of
  • tissue coming from the endocardial cushions (in
    yellow). C, The
  • conus and the truncus are partitioned. The
    dextrodorsal and
  • sinistroventral conus ridges, which are isolated
    in the first picture,
  • partition the conus by a helical outgrowth into 2
    cavities
  • the subpulmonary and the subaortic coni. The
    truncus is partitioned
  • from the bottom upward from aorticopulmonary
    swellings,
  • leading to the formation of the aorta and
    pulmonary
  • arteries.
  • 1
  • Images in Cardiovascular Medicine
  • Downloaded from circ.ahajournals.org by on
    September 30, 2007

5
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6
ATRIAL SEPTAL DEFECT
  • Opening in the interatrial septum
  • i 1 in 500 live births
  • 6- 10 of CHD. 30 of CHD in adults
  • Females gtmales
  • Types
  • Ostium secondum(75)
  • Ostium primum(15)
  • Sinus venosis(10)
  • Patent foramen ovale(5)
  • Coronary sinus(rare)

7
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8
  • Pathophysiology
  • L?R shunt is dependant on
  • Size of defect
  • Relative compliance of rt. lt. ventricle
  • It induces dilatation of the RA, RV hypertrophy,?
    size of PA.
  • The L?R flow is typical biphasic one peak flow
    occurs during late systole early diastole (v
    wave), other during late diastole (a wave)
  • There may be R?L shunt component during
  • sudden intrathoracic pressure drops as in
    spontaneous ventilation,relaxing phase of
    valsalva maneuver
  • with ? in RV afterload (IPPV, PEEPgt15cm H2O)

9
  • Natural History
  • Small ASDs lt3mm nearly 100 close
    spontaneously
  • Medium 3 8 mm --80 close
    spontaneously
  • Large gt8mm -- probably will not
    close
  • Isolated ASDs usu asymptomatic in infancy
    childhood
  • gt40years mortality of non operated patients
    ? by 6 /year
  • gt60 years almost all symptomatic
  • Failure to thrive
  • CHF in 2nd or 3rd decade of life,Pul HTN in upto
    13 of unoperated children lt 10 years
  • Recurrent respiratory tract infections
  • Atrial arrhythmias
  • Atrial Fibrillation more common gt40years
  • Qp/Qs 2 ? 11
  • 3 ? 38
  • Eisenmangers syndrome
  • Paradoxical emboli

10
  • Residual defects foll repair
  • Residual ASD
  • RV dilatation/dysfunction not in those
    repairedlt5 years of age
  • LV dysfunction in those corrected in adulthood
  • Supravntricular arrhythmias

11
  • Clinical features
  • Hyperdynamic precordium
  • Wide fixed split S2
  • Functional ejection systolic murmur in left
    sternal border
  • ECG
  • Feartures of RA enlargement ,RVH, RAD
  • Incomplete RBBB
  • CXR
  • RAE, RVH, Pulmonary Artery dilated, pulmonary
    plethora
  • Echo
  • Qp/Qs ratio
  • Cardiac cath
  • ? in saturation of atleast 10 between vena cava
    PA.

12
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13
VSD
  • Most common CHD(20)
  • i 2.6 5.7 per 1000 live births
  • 10 of adult CHD
  • Types
  • Subpulmonary (5 7 ) , ass. With aortic valve
    insufficiency
  • Perimembranous (80 ) , ass with tricuspid valve
    abnormality
  • AV canal (5 8 )
  • Muscular (5 20)
  • Restrictive, Non restrictive
  • Small, medium, large

14
Anatomy
15
  • Pathophysiology
  • L?R shunt predominantly during systole. The
    septal defect is anatomically close to the RVOT
    such that the shunted blood bypasseshe RV cavity.
    Hence RV hypertrophies sec to pul. HTN only.
  • Adaptive mechanisms include ?Stroke
    volume,contractility,Heart rate myocardial mass

16
Features of VSD based on size
17
  • Natural History
  • Spontaneous closure of defects lt5mm before 5
    years of age
  • Natural course depends on
  • Size of defect
  • changes in PVR
  • Changes in the above with age
  • Large defects CHF in infancy(2- 6 weeks of life),
    when PVR falls
  • Failure to thrive
  • Recurrent Resp tract infection
  • Eisenmangers syndrome

18
  • Abnormalities in repaired adult patient
  • lt2 years of life residual defect unlikely
  • Late closure, or non restrictive , or moderately
    restrictive VSD closure are necessariy
    accompanied by varying degrees of pre op PAH
    PVOD
  • Residual VSD
  • LV dysfunction ?LVEDV, ?LV wall mass ? LVEF,
    abnormal response to exercise
  • Arrhythmias inc BBB or complete AV block, may
    have a PPI

19
  • Clinical features
  • Cardiomegaly
  • Restrictive VSD Pansystolic murmur Left sternal
    border radiating across the sternum
  • Non restrictive VSDDecrescendo murmur or absent
    murmur
  • ECG LVH
  • Echo LV enlarged , PA dilated
  • RVH proportionate to degree of PHT

20
VSD with PHT
21
Preop evaluation of CHD patient
  • Review underlying anatomy physiology of cardiac
    lesion
  • Previous cardiac surgeries palliative vs.
    reparative
  • Evaluate existing residua or sequelae
  • Assess other pre existing or congenital anomalies
  • Review information from last cardiological
    examination
  • Recent cardiac cath, echo
  • Functional status
  • Assess risk factors
  • Pulmonary HTN
  • Cyanosis
  • Reoperation
  • Arrhythmias
  • Vent dysfunction
  • Review changes since last cardiac examination
  • History physical examination
  • Lab data
  • Current medication

22
  • 6. Review proposed surgical procedure
  • Elective vs. emergent
  • Expected length invasiveness
  • 7. Plan treatment of potential complications
  • Dysrhythmias
  • Pulmonary hypertension
  • Ventricular dysfunction
  • 8. Plan post op care
  • Monitoring
  • Pain management
  • Cardiology follow up
  • 9. Discuss anaesthetic plan risk with
    patient/parent

23
  • Is the patients cardiac disease
  • The primary condition in his perioperative care?
  • One of several considerations?
  • A relatively minor consideration?

24
  • History
  • 1. Congestive heart failure
  • Infants
  • Cyanosis
  • Respiratory difficulty
  • Seizures
  • Failure to thrive
  • Children
  • Chronic cough
  • Cyanosis
  • ? activity during exercise
  • Excessive perspiration
  • Failure to thrive
  • Fatigue
  • Poor feeding
  • Syncope

25
  • 2. Cyanotic spells
  • 3. Recent illness esp., Resp tract infection
  • 4. Coexisting illness GERD, Reactive airway
    disease, seizure disorder

26
  • Examination
  • Airway
  • Cardiac
  • Respiratory
  • Investigation
  • Hemogram,Electrolytes
  • ECG, CXR,
  • Echo

27
  • Fasting Guidelines
  • Avoid dehydration/hypovolemia
  • Premedication
  • Benefits
  • Anxiolysis
  • ?cooperation
  • ?separation anxiety
  • ?cardiovascular liability
  • Detrimental effects
  • Hypoventilation
  • Hypotension
  • Pain on administration

28
Infective Endocarditis
  • Congenital heart disease (CHD)
  • Unrepaired cyanotic CHD, including palliative
    shunts and conduits
  • Completely repaired congenital heart defect with
    prosthetic material or device, whether placed by
    surgery or by catheter intervention, during the
    first 6 months after the procedure
  • Repaired CHD with residual defects at the site or
    adjacent to the site of a prosthetic patch or
    prosthetic device (which inhibit
    endothelialization)

29
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30
  • OT Preparation
  • Equipment
  • Anaesthesia machine check
  • Prepare for invasive monitoring
  • Set alarm limits appropriate for age patient
  • Emergency drugs
  • Infusions infusion pump
  • Monitoring
  • Pulse Oximetry
  • NIBP
  • ECG
  • Capnography
  • Urine Output, Temperature
  • CVP
  • IBP
  • TEE

31
  • Anaesthetic Goals
  • Bubble avoidance
  • Optimizing O2 delivery ventilatory function
  • Avoid hypovolemia
  • ? L?R shunt

32
  • Paradoxical Emboli
  • PFO
  • incidence 5 in 2D Echo
  • 27 Direct intraop visualization
  • Paradoxical emboli i 1-2per year/patient
  • Preferential shearing of IVC blood towards
    secondum ASD
  • Paradoxical emboli can occur during
  • Valsalva
  • PEEP,IPPV
  • Deep sea diving
  • Lap procedures
  • Sudden R?L shunt
  • sudden intrathoracic pressure drops as in
    spontaneous ventilation, ,relaxing phase of
    valsalva maneuver.

33
  • Bubble Avoidance
  • Remove all bubbles from iv tubing
  • Connect iv tubing to the venous cannula while
    there is free flow of iv fluid and blood
  • Eject small amount of solution from syringe to
    clear air from needle to hub before injection
  • Aspirate injection port of 3 way before injection
    to clear air
  • Hold the syringe upright to keep bubbles at the
    plunger end
  • Do not inject the last ml from the syringe
  • Do not leave a central line open to air

34
  • Induction
  • In L?R shunts with ? pulmonary blood flow, speed
    of inhalation induction is unchanged.
  • We found more episodes of severe hypotension an
    increased incidence of bradycardia and emergent
    drug use in the patients that received halothane
    than in patients who received sevoflurane
  • (Anesth Analg 20019211528)
  • Intravenous
  • Time to appear in systemic circulation is
    unchanged though peak plasma conc. Are lower
    effect is prolonged
  • Thiopentone? SVR, well tolerated in
    normovolemic, stable CHD
  • Propofol Significant ? in SVR MAP
  • Ketamine ? SVR, ? L?R shunt
  • Etomidate minimal cardiovascula effect

35
Hemodynamic Goals
  • Reduction of L?R shunt
  • Slight increase in preload as hypovolemia is
    poorly tolerated

36
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37
  • Hypovolemia is poorly tolerated in these
    patients.
  • The low resistance pulmonary circulation tends to
    steal volume from the high resistance systemic
    circulation. This is further increased by the
    systemic arterial vasoconstriction of hypovolemia

38
Pathophysiologic classification of shunts
39
Cardiac Grid - ASD
40
Cardiac Grid - VSD
41
  • ? PVR
  • PEEP
  • High airway pressures
  • Atelectasis
  • Hypoxia
  • Hypercarbia
  • Acidosis
  • ? HCT
  • Drugs
  • ? SVR
  • Anaes agents
  • Vasodilators

42
  • Controlled ventilation is optimal as
  • Many patients with CHD cannot tolerate the high
    conc. Of inhalation agents required during SV
  • Appropriate ventilation helps prevent atelectasis
    hypercarbia
  • Ventilation is a compromise between active
    hyperventilation preservation of mean
    intrathoracic pressure
  • Ideal tidal volume corresponds to FRC to obtain
    PaCO2 lowest mean intrathoracic pressure

43
  • At low Tidal volume hypercarbia atelectasis ?
    PVR
  • At high tidal volume large extra alveolar vesels
    are much compressed ? PVR

44
Central Neuraxial Blockade
  • Merit
  • ? SVR
  • Demerits
  • Incremental IPPV represents a weak ? compared
    with already elevated pulmonary pressure RV
    well adapted to ? afterload
  • IPPV allows hypervent ? PVR
  • Vasodil due to sudden profound fall in SVR can
    reverse shunt

45
Pregnancy L?R shunts
  • Modest L?R shunts are well tolerated during
    pregnancy
  • Anaesthetic management should pay attention to
  • Care to avoid bubble infusion
  • LOR to saline rather than air during epidural
    catheterization
  • Early administration of labor analgesia as pain ?
    SVR catecholamine release worsening L?R shunt
  • Slow onset of epidural anaesthesia is preferred
  • Monitoring of SpO2 provision of supplementary
    O2

46
  • Thank You

www.anaesthesia.co.in anaesthesia.co.in_at_gmail.c
om
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