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ANESTHETIC
CONSIDERATIONS IN
TRICUSPID ATRESIA
& TRANSPOSITION
OF GREAT VESSELSDr.Verdah Sabih
PGT Anesthesia
Holy family Hosp.Rwp
INTRODUCTION:
Tricuspid atresia :
 complete agenesis of
tricuspid valve without
any direct communication
b/w RA & RV
 3% of CHD
 3rd most common cause
of cyanotic CHD
 An ASD or VSD is always
present
 Extra cardiac anomalies
present in 20%
ETIOLOGY:
Almost always congenital  Characterized by:
 Small RV
 Large LV
 Small VSD &PDA
 Diminished pulmonary
circulation
 cyanosis
PATHOPYSIOLOGY:
 Due to tricuspid agenesis, the blood cannot flow
from the RA to the RV.Blood ultimately cannot enter
the lungs.
 Instead, the blood passes through ASD between
the RA &LA. In the LA, it mixes with oxygenated
blood returning from the lungs. This mix of
oxygenated and de-oxygenated blood is then
pumped out into the body. This causes oxygen level
in the blood to be lower than normal.
 The lungs receive blood either through a VSD
between the right and left ventricles, or through
ductus arteriosus that connects the pulmonary
artery to the aorta.
MANAGEMENT:
 Primarily surgical
 Either an operation to increase pulmonary blood
flow (shunt)
 Or to decrease pulmonary blood flow (pulmonary
artery band)
 Fontan’s procedure
ANESTHETIC GOALS:
 Anesthetic management is very challenging
 Profound cyanosis may impair non invasive
monitoring of oxygen saturation
 Nitrous oxide or sevoflorane used for inhalational
induction followed by a change to narcotics based
anesthetic once intravenous access established
 MAP must be kept up to maintain shunt patency
 Careful rehydration necessary despite fluid deficit
preoperatively
 Maintain the hemostasis of PVR to SVR ratio &
ventricular performance
LV
PRELOA
D
HR RHYTHM CONTRA
CTILITY
SVR PVR
Maintain
or higher
rate
Maintain
orhigher
rate
Maintain
sinus
rhythm
Maintain
or
increase
maintain
or
 Early tracheal extubation & spontaneous ventilation
are desirable
 Positive inotropic drugs (dopamine) with or without
vasodilators (nitroprusside)are often required to
optimize cardiac output & maintain low PVR
 Monitoring the CVP to assess the intravascular fluid
volume & to detect sudden impairment of LV
function & increased PVR
 Peak & mean airway pressure must be maintained.
TRANSPOSITION OF GREAT ARTERIES:
 5% of CHD
 10% of all neonatal cyanotic CHD
 Failure of truncus arteriosus to go spiral so that
aorta arises from the anterior portion of RV & the
pulmonary artery from LV
PATHOPHYSIOLOGY:
 Due to complete seperation of pulmonary &
systemic circulation , systemic venous blood
traverses RA,RV, aorta & systemic circulation
 Pulmonary venous blood traverses LA,LV,
pulmonary arteries & lungs
 Circulation is parallel instead of normal in series
circulation
 Survival is posible only if there is communication
between the 2 circulations in the form of a
VSD,ASD or PDA
SIGNS & SYMPTOMS:
 Cyanosis (in the 1st week of life)
 Tachypnea
 Respiratory distress
 Non specific systolic ejection murmur
 Congestive heart failure (tachypnea, tachycardia,
sweating & poor feeding)
 Right axis deviation &RV hypertrophy on ECG
 Cardiac shadow “egg shaped with a narrow stalk”
on CXR
TREATMENT:
 Immediate management involves creating
intracardiac mixing or increasing the degree of
mixing
 Infusions of PG E1 to maintain patency of DA
 Ballon atrial septostomy
 Oxygen administration to decrease PVR & increase
pulmonary blood flow
 Diuretics & digoxin for CHF
 Mustard’s/ senning’soperation(venous switch)
 Arterial switch procedure
ANESTHETIC MANAGEMENT:
 Doses & rates of IV administered drugs have to
decreases(distribution of drugs with minimal dilution
to heart & brain)
 Onset of inhaled anesthesia delayed(small amount
reaches systemic circ.)
 Induction & maintenance are accomplished with
ketamine combined with muscle relaxants to
facilitate tracheal intubation
 Ketamine can be supplemented with opiods or
benzodiazepines for maintenance
 Nitrous oxide-limited application
 Potential cardio depressant effects of volatile
anesthetics– not used
 Selection of muscle relaxant to avoid histamine-
induced changes in systemic BP----- Pancuronium
used(inc. HR & systemic BP)
 Dehydration must be avoided during perioperative
period(inc. hematocrit--- inc incidence of cerebral
venous thrombosis)
 Prophylaxis for thrombosis & dysarhythmias
Tricuspid atresia & transposition of great arteries

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Tricuspid atresia & transposition of great arteries

  • 1. ANESTHETIC CONSIDERATIONS IN TRICUSPID ATRESIA & TRANSPOSITION OF GREAT VESSELSDr.Verdah Sabih PGT Anesthesia Holy family Hosp.Rwp
  • 2. INTRODUCTION: Tricuspid atresia :  complete agenesis of tricuspid valve without any direct communication b/w RA & RV  3% of CHD  3rd most common cause of cyanotic CHD  An ASD or VSD is always present  Extra cardiac anomalies present in 20%
  • 3. ETIOLOGY: Almost always congenital  Characterized by:  Small RV  Large LV  Small VSD &PDA  Diminished pulmonary circulation  cyanosis
  • 4. PATHOPYSIOLOGY:  Due to tricuspid agenesis, the blood cannot flow from the RA to the RV.Blood ultimately cannot enter the lungs.  Instead, the blood passes through ASD between the RA &LA. In the LA, it mixes with oxygenated blood returning from the lungs. This mix of oxygenated and de-oxygenated blood is then pumped out into the body. This causes oxygen level in the blood to be lower than normal.  The lungs receive blood either through a VSD between the right and left ventricles, or through ductus arteriosus that connects the pulmonary artery to the aorta.
  • 5.
  • 6. MANAGEMENT:  Primarily surgical  Either an operation to increase pulmonary blood flow (shunt)  Or to decrease pulmonary blood flow (pulmonary artery band)  Fontan’s procedure
  • 7. ANESTHETIC GOALS:  Anesthetic management is very challenging  Profound cyanosis may impair non invasive monitoring of oxygen saturation  Nitrous oxide or sevoflorane used for inhalational induction followed by a change to narcotics based anesthetic once intravenous access established  MAP must be kept up to maintain shunt patency  Careful rehydration necessary despite fluid deficit preoperatively  Maintain the hemostasis of PVR to SVR ratio & ventricular performance
  • 8. LV PRELOA D HR RHYTHM CONTRA CTILITY SVR PVR Maintain or higher rate Maintain orhigher rate Maintain sinus rhythm Maintain or increase maintain or
  • 9.  Early tracheal extubation & spontaneous ventilation are desirable  Positive inotropic drugs (dopamine) with or without vasodilators (nitroprusside)are often required to optimize cardiac output & maintain low PVR  Monitoring the CVP to assess the intravascular fluid volume & to detect sudden impairment of LV function & increased PVR  Peak & mean airway pressure must be maintained.
  • 10. TRANSPOSITION OF GREAT ARTERIES:  5% of CHD  10% of all neonatal cyanotic CHD  Failure of truncus arteriosus to go spiral so that aorta arises from the anterior portion of RV & the pulmonary artery from LV
  • 11.
  • 12. PATHOPHYSIOLOGY:  Due to complete seperation of pulmonary & systemic circulation , systemic venous blood traverses RA,RV, aorta & systemic circulation  Pulmonary venous blood traverses LA,LV, pulmonary arteries & lungs  Circulation is parallel instead of normal in series circulation  Survival is posible only if there is communication between the 2 circulations in the form of a VSD,ASD or PDA
  • 13. SIGNS & SYMPTOMS:  Cyanosis (in the 1st week of life)  Tachypnea  Respiratory distress  Non specific systolic ejection murmur  Congestive heart failure (tachypnea, tachycardia, sweating & poor feeding)  Right axis deviation &RV hypertrophy on ECG  Cardiac shadow “egg shaped with a narrow stalk” on CXR
  • 14. TREATMENT:  Immediate management involves creating intracardiac mixing or increasing the degree of mixing  Infusions of PG E1 to maintain patency of DA  Ballon atrial septostomy  Oxygen administration to decrease PVR & increase pulmonary blood flow  Diuretics & digoxin for CHF  Mustard’s/ senning’soperation(venous switch)  Arterial switch procedure
  • 15. ANESTHETIC MANAGEMENT:  Doses & rates of IV administered drugs have to decreases(distribution of drugs with minimal dilution to heart & brain)  Onset of inhaled anesthesia delayed(small amount reaches systemic circ.)  Induction & maintenance are accomplished with ketamine combined with muscle relaxants to facilitate tracheal intubation  Ketamine can be supplemented with opiods or benzodiazepines for maintenance  Nitrous oxide-limited application
  • 16.  Potential cardio depressant effects of volatile anesthetics– not used  Selection of muscle relaxant to avoid histamine- induced changes in systemic BP----- Pancuronium used(inc. HR & systemic BP)  Dehydration must be avoided during perioperative period(inc. hematocrit--- inc incidence of cerebral venous thrombosis)  Prophylaxis for thrombosis & dysarhythmias