ACYANOTIC HEART DISEASE

PRESENTER :- BIKASH RAY

MODERATOR :- DR.VIMI REWARI

www.anaesthesia.co.in

anaesthesia.co.in@gmail.com
 No h/o
 Swelling of body & face.
 ↓ urine output.
 Yellowish discolouration.
 Abd. distension.

 No h/o decreased /absent movement of

extremities.
 H/o past illness
 Patient had h/o recurrent RTI in past
frequency gradually decreasing

 No history of any other significant medical or

surgical illness

 No h/o failure to thrive

Family history
not significant

Birth & developmental history

 Antenatal – no maternal illness

no drug/alcohol intake

 Natal – Full Term, vaginal delivery

neonatal period uneventful

 Development – normal motor and personal

social development
 Immunization history
Adequately immunised for age

 Feeding & dietary history

Vegetarian
Normal solid and liquid intake

 Treatment history
Patient not taking any medication
 General examination
 Wt = 20 kg
 Ht = 96 cm
 A febrile
 Conscious, active, cooperative

 No pallor ,cyanosis,jaundice,edema, clubbing

 No lymphadenopathy

 Neck veins- not engorged

 Pulse – 98/min, regular ,good volume, no
radio-radial or radio-femoral delay

 All peripheral pulse palpable

 BP = 100/58 mmHg
( lt arm, supine position )

 Peripheral venous access = adequate

 Systemic examination
 Cardiovascular system :-

 Inspection –
Precordium normal on inspection
No visible apical impulse
No visible pulsation
No scar mark visible
 Cont.
 Palpation :-
Apex
 Palpable at (L) 5th ICS, at mid-clavicular line
 No thrill palpable
 Parasternal heave not palpable

 Auscultation :-
S1 & S2 audible
Pan-systolic murmur at apex & LLSB
 Cont.
Respiratory system : -
 No chest wall deformity on inspection

 Respiratory rate 20/min, regular,

accessory muscles not working

 Auscultation:
 B/L air entry equal
 No added sounds
 Cont.
Central nervous system
 Higher functions – normal

 Cranial nerves, cerebellum, motor and sensory

examination – within normal limits

 Abdomen :-
 no distension or venous engorgement
 swelling in Lt groin, soft, non-tender,
cough impulse positive
 no organomegaly
 Cont.
Airway assessment
 Mouth opening > 4 cm

 Neck movement adequate

 MMP class I

 No facial deformity noted

 Teeth –intact

Spine examination
 No abnormality detected
 Provisional diagnosis

 Acyanotic congenital heart disease with

L-R shunt, probably ventricular septal defect,
not in failure, with Lt inguinal hernia
 Differential diagnosis
 ASD – age (older)
PAH ( absent)
murmur (ejection systolic)

 PDA – murmur (cont. machinary)

 Investigations
 Hb – 10.3  CXR-
normal heart size
 Tlc- 7300  ECG –
WNL
 Plt – 3.56  ECHO –
- small 3 mm VSD
 Bu -24 - L-R shunt
- no ASD,PDA,COA
 Na / k = 133 / 4.3 - normal ventricular
function
 Diagnosis

 Small asymptomatic VSD for herniotomy (Lt )

not in failure
 PAC orders
 Adequate NPO

 Inform written consent of parents

 Ampicilin 50 mg / kg ,iv ,30 minutes before

surgery
 Anesthetic plan
 General anesthesia with neuraxial block
 Induction :-
pre o2 -- propofol + fentanyl
laryngeal mask airway
 Maintenance :
O2+ N2O+ ISOFLURANE
Controlled ventilation
 Post induction :- Lt lateral position
caudal epidural with PAP
 INTRA-OPERATIVE CONCERNS
 Air embolism

 Shunt reversal

 Pulmonary hypertension

 Volume overload - LVF

 BUBBLE AVOIDANCE
 Remove all bubbles from IV tubing.
 Connect IV tubing to venous cannula while there is free flow
of IVF and blood.
 Eject small amount of solution from syringe to clear air from
hub to needle before injection.
 Aspirate injection port of 3-way before injection

 Hold syringe upright - bubbles at plunger end.

 Do not inject last ml from the syringe.

 Do not leave central line open to air.

 To prevent worsening of shunt
 SVR to be kept below normal
 PVR to be kept normal or above

- Minimal FiO2
- Adequate tidal volume
- Low RR, PEEP
- PaCO2 40-50 mmHg
- Temperature
- Epidural
 FACTORS AFFECTING PVR
 ↑ PVR  ↓PVR
 Sympathetic  Anesthesia
stimulation– pain ,
light anesthesia  ↑ pH , ↓PaCO2, ↑
PaO2
 ↓pH, ↑PaCO2 ,
↓ PaO2  ↓intrathoracic
pressure--- SV,
 Hypothermia normal lung volumes
 ↑ intrathoracic  Drugs
pressure--  PDE inhibitors
Controlled vent,  Isoproterenol
PEEP ,atelectasis  PGE1,PGI2,NO
Indications of IE prophylaxis
 Post-op

 Sedation

 Analgesia

 Decongestive treatment

 monitoring
 Prevalence
Congenital
Incidence of CHD :8 / 1000 live birth
 Cyanotic: 22%

 Acyanotic: 68%
 VSD 25%
 ASD 6%
 PDA 6%
 PS 5%
 AS 5%
 VSD
 Most common CHD
 10 % of adult CHD
 TYPES :-
1. Subpulmonary (5-7 % )- with AV insufficiency
2. Perimembranous (80 %)-with tricuspid valve
abnormality
3. A-V canal (5-8%)
4. Muscular (5 -20 % )- multiple defect

 Restrictive , non- restrictive

 Small, medium, large (in relation to aortic root )
ANATOMY
Severity of VSD :–

- loud P2, parasternal lift/heave

- duration of murmur

- diastolic murmur at mitral area

- features of CCF
 Syndrome associated with VSD
 Extra cardiac malformation in 20-45 %

- Trisomy 21,18,13
- CHARGE syndrome
- Fetal hydantion syndrome
- Fetal alcohol syndrome
- Fetal valproate syndrome
- Apert syndrome
 Features of VSD based on size

Shunt Gradient ↑ PVR RVP RVH LVH Murmur

Small L–R High -- N No Yes PSM

Medium L-R 20mm Hg ± Mild ↑ Mild Yes PSM

Large L-R None + ↑ Yes Yes Decreased

R-L

Large R-L None + Yes No None

with
PVR
 NATURAL HISTORY
 Spontaneous closure of defects less than 5mm before
5 yrs of age (40-50%).
 Natural course depends on – size, change in PVR, age
 Large defects – CHF in infancy (2-6 wks), when PVR
falls
 Tachypnea, Distress, Sweating while feeding, Failure to
thrive
 CHF- apathetic, no movement, weak cry, diaphoretic,
hepatomegaly
 Indications for surgical closure- >6.5 mm, Qp:Qs ratio
>2
 LARGE L- R SHUNT

↑ PVR ↑ PA FLOW
↑PA PRESSURE
↑ LA SIZE
↑LA PRESSURE ENLARGEMENT OF VESSELS
BRONCHIAL HYPERTROPHY
INTERSTITIAL AND
ALVEOLAR EDEMA AIRWAY OBSTRUCTION

↑ AIRWAY RESISTANCE
↓ PULMONARY COMPLIANCE

INCREASED WORK OF BREATHING

GAS TRAPPING, ATELECTASIS, INFECTION
VSD IN PREGNANCY
 Sobha

 23 yr , female, primigravida

 D.o.A - 25.2.08

 Haryna
 Presented with

 36 week of pregnancy with h/o cardiac

disease for elective LSCS

 Past history
 h/o "heart disease " diagnosed at birth but not on any
follow- up

 H/o recurrent LRTI during childhood

 h/0 progressive exertional dyspnea since the first trimester

of her pregnancy.

 Evaluated in 2nd trimester for dyspnea- diagnosed as a case

of VSD

 No h/O any other significant medical or surgical illness

 Treatment history
Patient not on any medication

 General examination
wt = 68 kg ,ht = 154 cm

Afebrile

Consious, oriented

No pallor ,cyanosis,jaundice,edema, clubbing

No lymphadenopathy

Neck veins- not engorged

 Pulse – 9o/min, regular ,good volume, no
radio-radial or radio-femoral delay

 All peripheral pulse palpable

 BP = 130/88 mmHg ( lt arm, supine position )

 Peripheral venous access = adequate

 Systemic examination
 Cardiovascular system :-
 Inspection –
Precordium normal on inspection
No visible apical impulse
No visible pulsation
No scar mark visible
 Palpation :-
Apex
 Palpable at (L) 5th ICS, at mid-clavicular line
 No thrill palpable
 Parasternal heave not palpable

 Auscultation
:- S1 & S2 audible
Pan-systolic murmur at apex & LLSB
Respiratory system : -
 RR = 14/min

 Auscultation:
 B/L air entry equal
 No added sounds
Central nervous system
 Higher functions – normal

 Cranial nerves, motor and sensory examination –

within normal limits

Abdomen :-
 WNL for 34 week pregnancy
 Investigations

 Hb :- 14.4 g/dl
 Plt - 1.54 lakh
 Tlc – 6400
 Bu -28
 Sr. creatinine – 1
 Na / K = 148/ 4.5
 T. bil = 0.7
 CXR –
 ECG – LVH
 ECHO - small VSD (5mm )
 Anesthetic concern
1. Avoid accidental iv infusion of air bubble
2. Use loss of resistance to saline that air to
identify epidural space
3. Early administration of epidural anesthesia is
desirable.
4. Slow onset of epidural anesthesia is preferred
5. Patient should receive supplemental o2 &
oxygen saturation should be monitored
EISENMENGE
R SYNDROME

Pathophysiology
of the
Eisenmenger
syndrome.
Natural History: Course and Prognosis

 8% of patients with CHD & 11% of those with L-R

intracardiac shunting develop the Eisenmenger

 syndrome [CHD that may result in the Eisenmenger

syndrome include VSD,AV defect, PDA, ASD, D-TGA, and
surgically created aortopulmonary connections

 VSD :- 3% of patients who have a small or moderate-sized

defect ( 1.5 cm) and about 50% who have a large defect (>1.5
cm ) develop the Eisenmenger

 80% survival rate at 10 yr, 77% at 15 yr, and 42% at 25 yr

 Wood's Units unit of measure for PVR. One
Wood's Unit = PVR of an average healthy
person. That is:
MPAP = 13 mmHg
LAP = 8 mmHg
CO = 5 liters per minute
so average healthy PVR = (13 minus 8) divided
by 5, which equals one Wood's Unit
 Harneet
 8m male child
 Resident of Ludhiana
 Informant : mother
 Chief complaints

 Difficulty in feeding × 7 m
 Increased respiratory rate × 7m
 HOPI :
 H /O sweating while feeding , frequent
interruption while feeding
 H/O fast breathing with chest retractions
 H/O visible cardiac pulsation
 H/O poor weight gain
 No H/O bluish discolouration while crying
 No H/O abdominal distention
 ↓urine output
 swelling of face and feet
 No H/O fever with spots over body
 Past history :

 No history of any other illness in past

 Family history : first child , no similar
complaints
 Antenatal history :
 Regular follow up
 No intake of drugs , no H/O fever with rash
 USG normal
 Birth history : full term vaginal delivery at
hospital
 Cried immediately after birth
 Developmental history :
 Can sit without support and hold head
 Immunization history :
 Adequately immunized for age
 Treatment history :
 Furosemide + spironolactone and digoxin
 General physical examination :

 Conscious lying on bed

 Pallor – absent
 No cyanosis ,ikterus , clubbing or edema
 VITALS:
 PR :120 /min regular rhythm ,normal
volume ,no delay
 BP: 86/ 50 mm hg right arm supine
 RR : 48/min subcostal retractions present
 Temp : afebrile to touch
 Height : 64 cm
 Weight : 6.2kg
 Anterior fontanalle : not depressed
 Venous access : adequate
 No other visible malformations
Systemic Examination :-
 Cardiovascular system :
 Inspection :- precordial bulge - present
visible pulsation +
no scar mark
abnormality of skeletal
structure.
 Palpation :- Apex beat – left 5th ICS in MCL

palpable thrill.
parasternal lift.

58
 Auscultation :- S1 & S2 audible
S2 accentuated & split over
pulmonary area.
Pan-systolic murmur at
apex & LLSB.

59
 Respiratory system :
 Inspection : no visible chest wall deformity
 No visible pulsation seen
 Auscultation: B/L vesicular air sounds +, no
added sounds Central
nervous system :-
 conscious, apathetic
 no sensory or motor deficit
 reflexes normal.
 Provisional diagnosis :-
Acyanotic congenital heart disease with left to
right shunt without CHF or infective endocarditis

61
 Investigations:
 Hb – 11.2
 TLC – 9600
 Na /K – 146/ 4.6
 CXR - cardiomegaly , ↑ pulmonary vascularity
 Echo : LA + LV enlarged , RA/ RV normal , 8
mm mid muscular VSD , mild MR
 Features of VSD based on size

Shunt Gradient ↑ PVR RVP RVH LVH Murmur

Small L–R High -- N No Yes PSM

Medium L-R 20mm Hg ± Mild ↑ Mild Yes PSM

Large L-R None + ↑ Yes Yes Decreased

R-L

Large R-L None + Yes No None

with
PVR
 Cardiac Grid
Preload HR Contractility PVR SVR

VSD (L→R) ↑ N N ↑ ↓
unrepaired

VSD (L→R) ↑ N N N N
repaired

VSD (R→L) ↑ N N ↓ ↑
 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.
ATRIAL SEPTAL DEFECT
Opening in the interatrial septum
i: 1 in 500 live births
6- 10% of CHD. 30% of CHD in adults
Females >males
Types:
1. Ostium secondum(75%)
2. Ostium primum(15%)
3. Sinus venosis(10%)
4. Patent foramen ovale(5%)
5. Coronary sinus(rare)
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, PEEP>15cm H2O)
Natural History:
Small ASD’s <3mm – nearly 100% close spontaneously
Medium 3 – 8 mm --80% close spontaneously
Large >8mm -- probably will not close

 Isolated ASD’s usu asymptomatic in infancy & childhood

>40years mortality of non operated patients ↑ by 6% /year
>60 years almost all symptomatic
 Failure to thrive
 CHF in 2nd or 3rd decade of life,Pul HTN in upto 13% of unoperated
children < 10 years
 Recurrent respiratory tract infections
 Atrial arrhythmias
 Atrial Fibrillation – more common >40years
Qp/Qs ≤2 → 11%
≥3 → 38%
 Eisenmanger’s syndrome
 Paradoxical emboli
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.
VSD
Most common CHD(20%)
i: 2.6 – 5.7 per 1000 live births
10% of adult CHD
Types:
I. Subpulmonary (5 – 7 %) , ass. With aortic valve
insufficiency
II. Perimembranous (80% ) , ass with tricuspid valve
abnormality
III. AV canal (5 – 8 %)
IV. Muscular (5 – 20%)
Restrictive, Non restrictive
Small, medium, large
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
Preop evaluation of CHD patient
1. Review underlying anatomy & physiology of cardiac lesion
A. Previous cardiac surgeries – palliative vs. reparative
B. Evaluate existing residua or sequelae
2. Assess other pre existing or congenital anomalies
3. Review information from last cardiological examination
A. Recent cardiac cath, echo
B. Functional status
4. Assess risk factors
i. Pulmonary HTN
ii. Cyanosis
iii. Reoperation
iv. Arrhythmias
v. Vent dysfunction
5. Review changes since last cardiac examination
A. History & physical examination
B. Lab data
C. Current medication
6. Review proposed surgical procedure
A. Elective vs. emergent
B. Expected length& invasiveness
7. Plan treatment of potential complications
C. Dysrhythmias
D. Pulmonary hypertension
E. Ventricular dysfunction
8. Plan post op care
F. Monitoring
G. Pain management
H. Cardiology follow up
9. Discuss anaesthetic plan & risk with patient/parent
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
2. Cyanotic spells
3. Recent illness esp., Resp tract infection
4. Coexisting illness: GERD, Reactive airway disease,
seizure disorder…
Fasting Guidelines:
Avoid dehydration/hypovolemia

Premedication:
Benefits:
Anxiolysis
↑cooperation
↓separation anxiety
↓cardiovascular liability
Detrimental effects:
Hypoventilation
Hypotension
Pain on administration
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
Anaesthetic Goals:
1. Bubble avoidance
2. Optimizing O2 delivery & ventilatory function
3. Avoid hypovolemia
4. ↓ L→R shunt
Paradoxical Emboli
PFO
incidence: 5% in 2D Echo
27% Direct intraop visualization
Paradoxical emboli i: 1-2%per 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.
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 2001;92:1152–8)

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
 Hemodynamic Goals
1. Reduction of L→R shunt
2. Slight increase in preload as hypovolemia is
poorly tolerated
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
 Pathophysiologic classification of shunts

Type of shunt Features Degree of shunt Examples

Dependent Large & Variable,depends Large

unretsricted;pre on PVR& SVR ASD,VSD
ssures approx
equal
Restrictive Small,restricted Relatively ,SmallASD
fixed,low to VSD
moderate
volume,ind of PVR
& SVR
↑ PVR ↓ SVR
PEEP Anaes agents
High airway pressures Vasodilators
Atelectasis
Hypoxia
Hypercarbia
Acidosis
↑ HCT
Drugs
Controlled ventilation is optimal as:
i. Many patients with CHD cannot tolerate the
high conc. Of inhalation agents required
during SV
ii. 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
 PVR & Ventilation

PVR

Pul. Vol
Series1

 At low Tidal volume: hypercarbia & atelectasis ↑ PVR

 At high tidal volume: large extra alveolar vesels are
much compressed& ↑ PVR
 Central Neuraxial Blockade

Merit:
↓ SVR
Demerits:
1) Vasodil due to sudden profound fall in SVR
can reverse shunt