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Pediatric
Cardiopulmonary Bypass
Dr K P Gourav
Senior Resident
PGIMER
Cardiopulmonary Bypass
• Cardiopulmonary bypass (CPB) isolates the cardiopulmonary system to
facilitate surgical repair, oxygenates blood, and removes carbon dioxide
without causing permanent damage to the blood, cardiopulmonary system
or end organs
• CPB must perform the functions of the intact system for a finite period of time, providing
gaseous exchange and adequate perfusion to all organs without doing any permanent
damage.
• Pediatric perfusion plan requires an array of equipment matched to the patient size,
expected pump flow rates and diagnosis specific factors.
CPB for infants vs adults
• Immature organ systems
• Smaller circulation blood volumes
• Higher oxygen consumption rate
• Reactive pulmonary vascular bed
• Presence of intracardiac and extracardiac shunting
• Impaired temperature control
• Poor tolerance to microemboli
Physiological differences between Immature and Mature Myocardium
• Energy Substrate
 Adult myocardium under aerobic condition derives 95% ATP, from oxidation of long chain fatty
acids
 Neonatal heart derives ATP from oxidation of Glucose in aerobic (36 ATP) as well as anaerobic
conditions(2 ATP) indicates its greater tolerance to ischemia.
 Substrate change from glucose to free fatty acids is due to in 5’AMP activated protein kinase, in
this period uptake of glucose reduces leading to increase in insulin and more glycogen storage
subsequently less ischemia tolerance
CALCIUM METABOLISM
• More sensitive and dependent on extracellular calcium,
• Less developed sarcoplasmic reticulum
• ReducedSarcoplasmic reticularCa+ ATPaseactivity that
active transport of calcium in the luminal side of SR
• Decrease calcium storage reduced RYANODINE
RECEPTOR ACTIVATION
ENZYME SYSTEM
ANTIOXIDANT
• Superoxide dismutase, catalase, glutathione
reductase
• Scavenges oxygen free radicals( superoxides,
hydrogen peroxide, lipid peroxide, hydroxyl
radical) that cause peroxidation of
phospholipids in cell membrane resulting in
cell damage.
• Reduced in immature myocardium,esp TOF
5’NUCLEOTIDASE
• Catalyzes the conversion of adenosine
monophosphate to adenosine which passes
easily into extracellular space depleting the
adenosine nucleotide pool which helps in
postischmeic recovery.
• Reduced in immature myocardium more
tolerant to ischemia
Catecholamine sensitivity
• Decreased sensitivity
• Uncertain
Ischemic Preconditioning
• Adaptive mechanism induced by brief
period of reversible ischemia
increasing the hearts resistance to a
subsequent longer period of ischemia
• Protective for mature myocardium
• Chronic hypoxia reduced tolerance to
myocardial ischemia
Normal vs Stressed myocardium
• Normal neonatal myocardium is more tolerant to ischemia but not the stressed
myocardium
• Stressors like severe hypoxemia , chronic cyanosis, ventricular hypertrophy are
present in neonates and infants causing depletion of high energy phosphates,
glycogen and Krebs cycle intermediates.
• Volume and pressure loading increases myocardial oxygen demand and
ventricular hypertrophy leading to hypoperfusion of the subendocardium.
• Collaterals in Cyanotic lesions increased left heart return, rewarming and washing
of cardioplegia.
Ischemic tolerance of the immature heart
• Immature heart has a greater tolerance to hypoxia and
• ischemia than the adult
• : greater glycogen stores
• : improved anaerobic metabolism
• : better maintenance of ischemic calcium exchange
• : higher levels of adenosine triphosphate
• : increased amino acid substrate utilization
Myocardial protection
Hypothermia
• Hypothermia reduces myocardial
oxygen consumption
• MVO2:
working stage 6.7ml (adults 8ml),
empty beating heart 3.2ml
(adults5.6ml),
 K arrested @37˚C 1.3ml (adults
1.1ml)
 15˚C hypothermia 0.37ml
 15˚C K arrested heart 0.32ml
Cardioplegia arrest
• Diastolic arrest
• Preserves myocardial function during
the arrest period and limits reperfusion
injury
• Blood cardioplegia: carry O2, buffer,
similar osmotic comp., free radical
scavenging
• Del nido: 30ml/kg, 4:1ratio, reduces
energy consumption, blocks calcium into
intracellular space, lower troponin T
release.
Smaller circulating blood volume
• Circuit capacity cannot be reduced proportionate to patient size
• Significant hemodilution
• → ↓ clotting factors, plasma proteins → dilutional coagulopathy
• → ↓ colloid osmotic pressure → interstitial edema
• → electrolyte imbalance
• → ↑release of stress hormones
• → activation of complement, WBC, platelets
• In neonate : as much as 200~300% of patient's blood volume
• In adults : about 25~33% of patient's blood volume
Prime and Hemodilution
D. Whiting et 246 al. / Best Practice & Research Clinical Anaesthesiology 29 (2015) ;
BOSTON
significant decline was observed in mean
platelet count during the first hour of perfusion
and 3 h
At 24 h - comparable in albumin and control
circuits
Advantage of Albumin in Prime?
Journal of Cardiothoracic and Vascular Anesthesia, Vol 18, No 4 (August), 2004: pp 429-437
Advantage of FFP in Prime?
The authors reported significantly
less chest tube drainage
and shorter lengths of mechanical ventilation and intensive
care unit (ICU) stay in the FWB arm
Advantage of Fresh Whole Blood in Prime?
J Thorac Cardiovasc Surg 2008;136:1442-9
authors found patients managed with FWB had increased
ICU length of stay and more
fluid overload compared to the group receiving RWB in the
CPB prime
Pump Flow rate
• Extrapolated from adult data
• Less than 1.6L/m2/min - increase in lactate.
• At 2-2.4L/m2/min – no increase in lactate
In the absence of shunts
Serum lactate is measured during CPB to ensure
adequate systemic blood flow.
How to Assess flow in CPB in CHD adequate?
• Pediatrics with CHD
• anatomic heterogeneity of patients
• differences in age-based and weight-based flows.
• Mixed venous oxygen saturation –
• indicator of adequate systemic blood flow,
• but it does not directly measure the adequacy of cellular oxygenation
• Serum lactate –
• indicates the presence of anaerobic metabolism,
• better reflect the adequacy of cellular oxygenation.
• should routinely measured 10 min after the initiation of CPB and then every 30 min.
• urine output on CPB –
• Renal function is assessed by
How to minimize the need for transfusion in
pediatric congenital heart surgery
• Many methods
• use of near-infrared spectroscopy (NIRS) - allowed clinicians to tailor
blood transfusion intraoperatively based on real-time data during the
various stages of an operation.
Wiley-Blackwell; 2015.
Accepting Low hematocrit?
J Thorac Cardiovasc Surg 2008;135:347-54
Very low prime volume feasible?
Retrograde autologous priming feasible in children?
Still, the use of RAP in pediatrics, particularly
neonates and infants, appears to have limited practical
use and the technique has not been universally adopted.
Modification in priming?
British Journal of Anaesthesia, 118 (5): 788–96 (2017
Ultrafiltration
• Excess volume in the cardiotomy venous reservoir –
• crystalloid component of cardioplegia,
• crystalloid valve testing solutions
• Conventional UF is utilized in nearly all pediatric bypass cases.
• MUF allows the ultrafiltration of CPB circuit volume as well as the patient's
blood volume after weaning from CPB.
• The major advantage of MUF over CUF is that it allows hemoconcentration
to continue once CPB has been terminated allow greater degree of
hemoconcentration than CUF alone.
MUF better than CUF?
J. Clin. Med. 2018, 7, 498
Alfa stat vs PH stat
Bypass considerations in
congenital heart surgeries
Aortic regurgitation/insufficiency
• Single venous cannulation
• Dual Venous cannulation – If associated with other lesion
• Flow 3.5L/m2/min (higher than normal)
• Cardioplegia –
• 1.5–2 times the normal dose (to account for volume lost
to regurgitation)
• direct administration if the initial root dose is not
effective.
• LV vent
• AI increases the blood from the aortic cannula will flow retrograde to the LV
• Decompress LV distension due to AR
• amount of LV vent return - rough surrogate for degree AR.
• Go on bypass slowly to prevent LV distention secondary to
• the AI andor
• VF due to a cool prime directly perfusing the coronaries.
• If the patient fibrillates before an LV vent is placed,
• immediately decrease the pump flow to prevent LV distention
• Increased risk of systemic hypoperfusion
• if a significant amount of forward flow is lost retrograde across the aortic
valve to a left ventricular vent.
• pressure may increase suddenly and significantly
• Once the aortic cross clamp is on (and loss to the ventricle is prevented),
• BP fluctuations can occur
• Surgical work at aortic sinus to transverse arch - may stimulates the aortic
baroreceptors - may produce acute changes in BP on bypass.
• cautious in treating such fluctuations - quite temporary.
• higher than normal blood pressure during rewarming and myocardial
reperfusion
• to aid in coronary blood flow & to prevent VF if the ventricle is hypertrophied.
• BP low - When allowing for ejection
• aorta has been opened surgically
Aortic Stenosis
• bypass pump should be primed and kept ready
• CPR difficult
• Flow – 2.5- 3l/min/m2
• Cardioplegia
• higher cardioplegia delivery pressures/flows if significant ventricular
hypertrophy exists - ensure proper myocardial distribution of cardioplegia.
• more than the standard cardioplegia dose (ventricular hypertrophy)
• Keep Blood pressure low
• While coming off bypass/post op (aorta suture lines)
• But maintain perfusion pressure to avoid VF in hypertrophy.
Aortopulmonary collaterals
• MAPCA ligation before CPB – should be tried
• Otherwise Systemic flow compromised
• Flow increased – 3.5-5L/min/m2
• Anticipate oxygenator/cannula
• Flow will be increased 1st to increase BP
• NIRS
• Ventricular distension
• Dec EF (low temp, dec Ca+ due to hemodialation)
• LV vent+
CONT…..
• Temp decrease
• Compromise systemic and cerebral circulation
• Hct 30-35 during CPB
• compromised cerebral blood flow
• PH stat (increase CO2)
• Cerebral vasodilation
• Pulmonary vasoconstriction
• Blood products – kept in hand
• Due to increase in blood flow, reservoir can become empty
• ALFA AGONIST - debate
• Increase BP
• Systemic vasoconstriction lead to decrease systemic circulation, increase
pulmonary circulation
bidirectional Glenn shunt
• SVC cannula will be placed in the innominate vein or high in the SVC
• lower cannula may be placed in the atrium instead of the IVC if no additional intracardiac
work is needed.
• Cardioplegia is not normally required
• LV vent normally is not needed.
• Be aware of the status of the BTS or Sano
• Control immediately on bypass
• If not
• increased pump flows to compensate for pulmonary runoff.
• displayed CVP value - unusable
• if an applied SVC clamp includes the catheter
Fontan procedure
• High Hct
• may not need blood in the prime
• may receive FFP - correction of factor deficiencies
• Cardioplegia - required for lateral tunnel technique
• Bicaval cannulation
• SVC cannulation - higher than normal/innominate vein)
• IVC cannulation lower than normal to facilitate creating
the intra-atrial baffle or extracardiac conduit.
• displayed CVP value - unusable if an applied SVC clamp
includes the catheter.
PDA
Normally closed without CPB
CPB – Complicated PDA, associated with other defects
Closed before CPB
If NOT
• Flow increased – 3.5-5L/min/m2
• Flow to be increased 1st to increase BP
• NIRS
• Ventricular distension
• LV vent+
• Rectal Temperature – not recommended (Runoff/ associated COA)
• ALFA AGONIST - Better avoid
• BP -unacceptably high once the duct is ligated.
Coarctation of the aorta
• left heart bypass
• LA to the descending aorta/femoral artery for
isolated coarctation repair
• Flow to DTA to be titrated depending upon
upper body circulation
• If complete bypass
• Flow to be decreased when DTA was clamped
to avoid overflow to the cerebral circulation
Interrupted aortic arch
• Two arterial cannula –
• ascending aorta and PDA are needed for true
interrupted arches
• Cardioplegia required
• circulatory arrest for correction
• Regional perfusion techniques -
• pump flows of 20–60 cc/kg/min through the
arterial cannula with flow directed to the cerebral
• Cerebral and somatic NIRS monitoring is commonly
used
LSVC
• If bridging vein is present or if the LSVC flow is
minimal
• pump sucker IN RV
• low flow sucker can be placed in the LSVC
• LSVC may be ligated below the bridging vein
• bridging vein absent/small
• third venous cannula may be needed.
TAPVC/PAPVC
• sucker in the left atrium/ LV vent
• LA/LV may be undersized
• large variations in filling pressures with minimal change in volume status
during weaning
• careful not to overfill during separation from bypass.
• Scimitar syndrome
• form of PAPVC
• The right lung is commonly hypoplastic and its blood supply is via MAPCAs.
Truncus arteriosus
• Truncal valve regurgitation
• require direct coronary delivery of cardioplegia.
• 1.5–2 doses of cardioplegia
• LV vent – to decompress LV
• flow - 3.5 L/min/m2
• Systemic blood pressure can be low (before cross clamp)
• Increase by increasing the flow
• After cross clmap – increase in blood pressure
• Flow to be adjusted
• Pulmonary arteries - controlled before or soon after commencing
bypass (runoff to the pulmonary circulation can compromise systemic perfusion)
• Aortic pressure - kept in low normal while coming Off bypass and
Post CPB - as aorta was open
Aortopulmonary window
• Single venous cannulation (dual stage if available)
• flow - 3.5 L/min/m2
• to compensate for pulmonary runoff until the window is
controlled.
• branch pulmonary arteries Controlled - before or soon after
commencing bypass
• since runoff to the pulmonary circulation can compromise
systemic perfusion (like a PDA, BTS, or MAPCAs)
• LV vent
• Terminate CPB with low BP – aorta is open
Anomalous left coronary artery from the
pulmonary artery
• Flow rate - 3.0 L/min/m2
• cardioplegia
• flow to the aortic and pulmonary roots in order to adequately
arrest and protect the heart.
• LV vent
• Cardioplegia is frequently given
• left and right pulmonary arteries controlled before cross
clamping
• to ensure cardioplegia delivery into the pulmonary root reaches
the anomalous coronary artery
• Increased hematocrit before coming off bypass
• sick myocardium.
THANK YOU
Children with CHD – huge anatomic heterogeneity of heart
differences in age-based and weight-based flows.
Check
For adequacy of flows

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Pediatric cardiopulmonary bypass

  • 1. Pediatric Cardiopulmonary Bypass Dr K P Gourav Senior Resident PGIMER
  • 2. Cardiopulmonary Bypass • Cardiopulmonary bypass (CPB) isolates the cardiopulmonary system to facilitate surgical repair, oxygenates blood, and removes carbon dioxide without causing permanent damage to the blood, cardiopulmonary system or end organs • CPB must perform the functions of the intact system for a finite period of time, providing gaseous exchange and adequate perfusion to all organs without doing any permanent damage. • Pediatric perfusion plan requires an array of equipment matched to the patient size, expected pump flow rates and diagnosis specific factors.
  • 3. CPB for infants vs adults • Immature organ systems • Smaller circulation blood volumes • Higher oxygen consumption rate • Reactive pulmonary vascular bed • Presence of intracardiac and extracardiac shunting • Impaired temperature control • Poor tolerance to microemboli
  • 4.
  • 5. Physiological differences between Immature and Mature Myocardium • Energy Substrate  Adult myocardium under aerobic condition derives 95% ATP, from oxidation of long chain fatty acids  Neonatal heart derives ATP from oxidation of Glucose in aerobic (36 ATP) as well as anaerobic conditions(2 ATP) indicates its greater tolerance to ischemia.  Substrate change from glucose to free fatty acids is due to in 5’AMP activated protein kinase, in this period uptake of glucose reduces leading to increase in insulin and more glycogen storage subsequently less ischemia tolerance
  • 6. CALCIUM METABOLISM • More sensitive and dependent on extracellular calcium, • Less developed sarcoplasmic reticulum • ReducedSarcoplasmic reticularCa+ ATPaseactivity that active transport of calcium in the luminal side of SR • Decrease calcium storage reduced RYANODINE RECEPTOR ACTIVATION
  • 7. ENZYME SYSTEM ANTIOXIDANT • Superoxide dismutase, catalase, glutathione reductase • Scavenges oxygen free radicals( superoxides, hydrogen peroxide, lipid peroxide, hydroxyl radical) that cause peroxidation of phospholipids in cell membrane resulting in cell damage. • Reduced in immature myocardium,esp TOF 5’NUCLEOTIDASE • Catalyzes the conversion of adenosine monophosphate to adenosine which passes easily into extracellular space depleting the adenosine nucleotide pool which helps in postischmeic recovery. • Reduced in immature myocardium more tolerant to ischemia
  • 8. Catecholamine sensitivity • Decreased sensitivity • Uncertain Ischemic Preconditioning • Adaptive mechanism induced by brief period of reversible ischemia increasing the hearts resistance to a subsequent longer period of ischemia • Protective for mature myocardium • Chronic hypoxia reduced tolerance to myocardial ischemia
  • 9.
  • 10. Normal vs Stressed myocardium • Normal neonatal myocardium is more tolerant to ischemia but not the stressed myocardium • Stressors like severe hypoxemia , chronic cyanosis, ventricular hypertrophy are present in neonates and infants causing depletion of high energy phosphates, glycogen and Krebs cycle intermediates. • Volume and pressure loading increases myocardial oxygen demand and ventricular hypertrophy leading to hypoperfusion of the subendocardium. • Collaterals in Cyanotic lesions increased left heart return, rewarming and washing of cardioplegia.
  • 11. Ischemic tolerance of the immature heart • Immature heart has a greater tolerance to hypoxia and • ischemia than the adult • : greater glycogen stores • : improved anaerobic metabolism • : better maintenance of ischemic calcium exchange • : higher levels of adenosine triphosphate • : increased amino acid substrate utilization
  • 12. Myocardial protection Hypothermia • Hypothermia reduces myocardial oxygen consumption • MVO2: working stage 6.7ml (adults 8ml), empty beating heart 3.2ml (adults5.6ml),  K arrested @37˚C 1.3ml (adults 1.1ml)  15˚C hypothermia 0.37ml  15˚C K arrested heart 0.32ml Cardioplegia arrest • Diastolic arrest • Preserves myocardial function during the arrest period and limits reperfusion injury • Blood cardioplegia: carry O2, buffer, similar osmotic comp., free radical scavenging • Del nido: 30ml/kg, 4:1ratio, reduces energy consumption, blocks calcium into intracellular space, lower troponin T release.
  • 13. Smaller circulating blood volume • Circuit capacity cannot be reduced proportionate to patient size • Significant hemodilution • → ↓ clotting factors, plasma proteins → dilutional coagulopathy • → ↓ colloid osmotic pressure → interstitial edema • → electrolyte imbalance • → ↑release of stress hormones • → activation of complement, WBC, platelets • In neonate : as much as 200~300% of patient's blood volume • In adults : about 25~33% of patient's blood volume
  • 15. D. Whiting et 246 al. / Best Practice & Research Clinical Anaesthesiology 29 (2015) ; BOSTON
  • 16. significant decline was observed in mean platelet count during the first hour of perfusion and 3 h At 24 h - comparable in albumin and control circuits Advantage of Albumin in Prime?
  • 17. Journal of Cardiothoracic and Vascular Anesthesia, Vol 18, No 4 (August), 2004: pp 429-437
  • 18. Advantage of FFP in Prime?
  • 19. The authors reported significantly less chest tube drainage and shorter lengths of mechanical ventilation and intensive care unit (ICU) stay in the FWB arm Advantage of Fresh Whole Blood in Prime? J Thorac Cardiovasc Surg 2008;136:1442-9
  • 20. authors found patients managed with FWB had increased ICU length of stay and more fluid overload compared to the group receiving RWB in the CPB prime
  • 21. Pump Flow rate • Extrapolated from adult data • Less than 1.6L/m2/min - increase in lactate. • At 2-2.4L/m2/min – no increase in lactate In the absence of shunts Serum lactate is measured during CPB to ensure adequate systemic blood flow.
  • 22. How to Assess flow in CPB in CHD adequate? • Pediatrics with CHD • anatomic heterogeneity of patients • differences in age-based and weight-based flows. • Mixed venous oxygen saturation – • indicator of adequate systemic blood flow, • but it does not directly measure the adequacy of cellular oxygenation • Serum lactate – • indicates the presence of anaerobic metabolism, • better reflect the adequacy of cellular oxygenation. • should routinely measured 10 min after the initiation of CPB and then every 30 min. • urine output on CPB – • Renal function is assessed by
  • 23. How to minimize the need for transfusion in pediatric congenital heart surgery • Many methods • use of near-infrared spectroscopy (NIRS) - allowed clinicians to tailor blood transfusion intraoperatively based on real-time data during the various stages of an operation. Wiley-Blackwell; 2015.
  • 24. Accepting Low hematocrit? J Thorac Cardiovasc Surg 2008;135:347-54
  • 25. Very low prime volume feasible?
  • 26. Retrograde autologous priming feasible in children? Still, the use of RAP in pediatrics, particularly neonates and infants, appears to have limited practical use and the technique has not been universally adopted.
  • 28. British Journal of Anaesthesia, 118 (5): 788–96 (2017
  • 29. Ultrafiltration • Excess volume in the cardiotomy venous reservoir – • crystalloid component of cardioplegia, • crystalloid valve testing solutions • Conventional UF is utilized in nearly all pediatric bypass cases. • MUF allows the ultrafiltration of CPB circuit volume as well as the patient's blood volume after weaning from CPB. • The major advantage of MUF over CUF is that it allows hemoconcentration to continue once CPB has been terminated allow greater degree of hemoconcentration than CUF alone.
  • 31. J. Clin. Med. 2018, 7, 498
  • 32. Alfa stat vs PH stat
  • 33.
  • 34.
  • 35.
  • 37. Aortic regurgitation/insufficiency • Single venous cannulation • Dual Venous cannulation – If associated with other lesion • Flow 3.5L/m2/min (higher than normal) • Cardioplegia – • 1.5–2 times the normal dose (to account for volume lost to regurgitation) • direct administration if the initial root dose is not effective.
  • 38. • LV vent • AI increases the blood from the aortic cannula will flow retrograde to the LV • Decompress LV distension due to AR • amount of LV vent return - rough surrogate for degree AR. • Go on bypass slowly to prevent LV distention secondary to • the AI andor • VF due to a cool prime directly perfusing the coronaries. • If the patient fibrillates before an LV vent is placed, • immediately decrease the pump flow to prevent LV distention
  • 39. • Increased risk of systemic hypoperfusion • if a significant amount of forward flow is lost retrograde across the aortic valve to a left ventricular vent. • pressure may increase suddenly and significantly • Once the aortic cross clamp is on (and loss to the ventricle is prevented), • BP fluctuations can occur • Surgical work at aortic sinus to transverse arch - may stimulates the aortic baroreceptors - may produce acute changes in BP on bypass. • cautious in treating such fluctuations - quite temporary.
  • 40. • higher than normal blood pressure during rewarming and myocardial reperfusion • to aid in coronary blood flow & to prevent VF if the ventricle is hypertrophied. • BP low - When allowing for ejection • aorta has been opened surgically
  • 41. Aortic Stenosis • bypass pump should be primed and kept ready • CPR difficult • Flow – 2.5- 3l/min/m2 • Cardioplegia • higher cardioplegia delivery pressures/flows if significant ventricular hypertrophy exists - ensure proper myocardial distribution of cardioplegia. • more than the standard cardioplegia dose (ventricular hypertrophy) • Keep Blood pressure low • While coming off bypass/post op (aorta suture lines) • But maintain perfusion pressure to avoid VF in hypertrophy.
  • 42. Aortopulmonary collaterals • MAPCA ligation before CPB – should be tried • Otherwise Systemic flow compromised • Flow increased – 3.5-5L/min/m2 • Anticipate oxygenator/cannula • Flow will be increased 1st to increase BP • NIRS • Ventricular distension • Dec EF (low temp, dec Ca+ due to hemodialation) • LV vent+
  • 43. CONT….. • Temp decrease • Compromise systemic and cerebral circulation • Hct 30-35 during CPB • compromised cerebral blood flow • PH stat (increase CO2) • Cerebral vasodilation • Pulmonary vasoconstriction
  • 44. • Blood products – kept in hand • Due to increase in blood flow, reservoir can become empty • ALFA AGONIST - debate • Increase BP • Systemic vasoconstriction lead to decrease systemic circulation, increase pulmonary circulation
  • 45. bidirectional Glenn shunt • SVC cannula will be placed in the innominate vein or high in the SVC • lower cannula may be placed in the atrium instead of the IVC if no additional intracardiac work is needed. • Cardioplegia is not normally required • LV vent normally is not needed. • Be aware of the status of the BTS or Sano • Control immediately on bypass • If not • increased pump flows to compensate for pulmonary runoff. • displayed CVP value - unusable • if an applied SVC clamp includes the catheter
  • 46. Fontan procedure • High Hct • may not need blood in the prime • may receive FFP - correction of factor deficiencies • Cardioplegia - required for lateral tunnel technique • Bicaval cannulation • SVC cannulation - higher than normal/innominate vein) • IVC cannulation lower than normal to facilitate creating the intra-atrial baffle or extracardiac conduit. • displayed CVP value - unusable if an applied SVC clamp includes the catheter.
  • 47. PDA Normally closed without CPB CPB – Complicated PDA, associated with other defects Closed before CPB If NOT • Flow increased – 3.5-5L/min/m2 • Flow to be increased 1st to increase BP • NIRS • Ventricular distension • LV vent+ • Rectal Temperature – not recommended (Runoff/ associated COA) • ALFA AGONIST - Better avoid • BP -unacceptably high once the duct is ligated.
  • 48. Coarctation of the aorta • left heart bypass • LA to the descending aorta/femoral artery for isolated coarctation repair • Flow to DTA to be titrated depending upon upper body circulation • If complete bypass • Flow to be decreased when DTA was clamped to avoid overflow to the cerebral circulation
  • 49. Interrupted aortic arch • Two arterial cannula – • ascending aorta and PDA are needed for true interrupted arches • Cardioplegia required • circulatory arrest for correction • Regional perfusion techniques - • pump flows of 20–60 cc/kg/min through the arterial cannula with flow directed to the cerebral • Cerebral and somatic NIRS monitoring is commonly used
  • 50. LSVC • If bridging vein is present or if the LSVC flow is minimal • pump sucker IN RV • low flow sucker can be placed in the LSVC • LSVC may be ligated below the bridging vein • bridging vein absent/small • third venous cannula may be needed.
  • 51. TAPVC/PAPVC • sucker in the left atrium/ LV vent • LA/LV may be undersized • large variations in filling pressures with minimal change in volume status during weaning • careful not to overfill during separation from bypass. • Scimitar syndrome • form of PAPVC • The right lung is commonly hypoplastic and its blood supply is via MAPCAs.
  • 52. Truncus arteriosus • Truncal valve regurgitation • require direct coronary delivery of cardioplegia. • 1.5–2 doses of cardioplegia • LV vent – to decompress LV • flow - 3.5 L/min/m2 • Systemic blood pressure can be low (before cross clamp) • Increase by increasing the flow • After cross clmap – increase in blood pressure • Flow to be adjusted • Pulmonary arteries - controlled before or soon after commencing bypass (runoff to the pulmonary circulation can compromise systemic perfusion) • Aortic pressure - kept in low normal while coming Off bypass and Post CPB - as aorta was open
  • 53. Aortopulmonary window • Single venous cannulation (dual stage if available) • flow - 3.5 L/min/m2 • to compensate for pulmonary runoff until the window is controlled. • branch pulmonary arteries Controlled - before or soon after commencing bypass • since runoff to the pulmonary circulation can compromise systemic perfusion (like a PDA, BTS, or MAPCAs) • LV vent • Terminate CPB with low BP – aorta is open
  • 54. Anomalous left coronary artery from the pulmonary artery • Flow rate - 3.0 L/min/m2 • cardioplegia • flow to the aortic and pulmonary roots in order to adequately arrest and protect the heart. • LV vent • Cardioplegia is frequently given • left and right pulmonary arteries controlled before cross clamping • to ensure cardioplegia delivery into the pulmonary root reaches the anomalous coronary artery • Increased hematocrit before coming off bypass • sick myocardium.
  • 55. THANK YOU Children with CHD – huge anatomic heterogeneity of heart differences in age-based and weight-based flows. Check For adequacy of flows

Notas do Editor

  1. PLATELETS initially adhered to the artificial surfaces of the system, re-appeared in the circulating blood. lost much of their a-granula content, and circulate as nonfunctional platelet ghosts.
  2. Head and neck MAPCA – addressed 1st – otherwise cerebral compromise
  3. MONITOR LOOKS BE GOOD , BUT LACTATE AND BASE DEFICIT WILL INCREASE IN ALFA BLOCKERS.
  4. Head and neck MAPCA – addressed 1st – otherwise cerebral compromise
  5. Head and neck MAPCA – addressed 1st – otherwise cerebral compromise
  6. Head and neck MAPCA – addressed 1st – otherwise cerebral compromise
  7. Head and neck MAPCA – addressed 1st – otherwise cerebral compromise
  8. Head and neck MAPCA – addressed 1st – otherwise cerebral compromise