1. Deep Hypothermic Circulatory Arrest in Pediatric Cardiac Surgery 2009
Nabila Fahmy, MD
Professor of Anesthesiology
Ain Shams University

2. Cessation of the blood circulation for some time during surgery of the arch and repair of congenital heart defects is normally required to allow a bloodless operation field..
Hypothermia is the most important mechanism for end-organ protection, particularly the brain, during such operations.
Cardiopulmonary bypass is used for core cooling before deep hypothermic circulatory arrest (DHCA) is initiated .

3. WHAT IS DHCA?

4. DEEP HYPOTHERMIC CIRCULATORY ARREST (DHCA)
Mild hypothermia – 30 C to 34 C
Moderate hypothermia – 25 C to 30 C
Deep hypothermia – 15 C to 22 C
Circulatory arrest – no flow in the blood vessels
DHCA – no blood flow during deep hypothermia

5. HOW DO WE DO DHCA?

6. TECHNIQUE OF DHCA Usually planned
Most protocols involving DHCA involve the following :
Administration of barbiturates, usually thiopental for the reduction of cerebral metabolism.
Mannitol to help reduce potential increased intracranial pressure and to reduce free radicals.
Steroids to promote cell membrane integrity and reduce brain swelling.
Cooling is started before CPB by simply cooling the operating room and with ice packing to the head After systemic heparinization and cannulation are performed, CPB is started and cooling is begins for at least minutes. The patient's body temperature is monitored by means of esophageal, tympanic, and rectal routes. After adequate cooling is achieved, the circulation is arrested to allow the surgeon to perform the critical part of the reconstruction. The duration of DHCA is limited to the shortest time possible. After circulation is restarted, the rest of the repair is performed during the rewarming phase.
The anesthetic and surgical plan involves mutual goals of tissue and organ protection by decreasing cellular metabolism and substrate delivery during the absence of perfusion.

7. WHY DHCA?

8. ADVANTAGES OF DHCA Bloodless operating field with improved exposure
Decreased exposure to cardiopulmonary bypass with its sequelae (such as activation of white cells and endothelium, activation of cascades, consumption of coagulation factors and platelets, hemolysis, etc.)
Diminished risk of embolism (solids and gases)
No cannulas in the operating field
Less distortion of heart - cannulas are not in place
DHCA offers brain protection for a period of about minutes.
Reduced CMRO2 to be approximately 10%-15% of its normothermic base line.
Lower plasma activated complement (C3a), interleukin 8, interleukin 6 (when compared with low-flow CPB)
Bellinger DC, et al. N Engl J med. 1995;332:

9. The duration of DHCA is limited to the shortest time possible as (landmark boston circulatory arrest study, march 2007)
3-5 mins of cerebral ischemia can be tolerated at 37 c.
15 mins c.
41 mins c.

11. CEREBRAL PHYSIOLOGY DURING
CARDIAC SURGERY
CLINICAL STUDIES (Greeley, Kern, Ungerdeider)
HAVE BEEN UNDERTAKEN IN THE LATE 1980s
TRHOUGH MID 1990s TO UNDERSTAND
NEUROPHYSIOLOGY IN INFANTS AND CHILDREN
DURING CARDIAC SURGERY INVOLVING CPB
AND DHCA
CNS HAS A HIGH METABOLIC NOTE & LIMITED ENERGY STORES
CNS IS THE MOST SENSITIVE ORGAN TO ISCHEMIA
ATTENTION HAS BEEN CENTERED ON NEUROLOGIC OUTCOME WHEN PERFUSION IS REDUCED, LEADING TO NEUROLOGIC COMPLICATIONS IN THE POSTOPERATIVE PERIOD.

12. THE REPORTED INCIDENCE OF NEUROLOGICAL COMPLICATIONS
AFTER PEDIATRIC CARDIAC SURGERY
RANGES FROM 2% TO 25%
Austin EH III,Edmonds HI,Auden SM et al.
Benefit of neurophysiological monitoring for pediatric
Cardiac surgery.J Thorac Cardiovasc Surg 1997;114 :707-15
Menache CC,du Plessis AJ,Wessel DL et al.
Current incidence of acute neurologic complications
After open heart operation in children
Ann Thorac Surg 2002; 73:1752.8

13. Neurologic morbidity include
seizures
stroke
changed tone and mental status
motor disorders -
time to recovery of EEG activity .
Abnormal cognitive function
Post Pump choreoatherosis paraplegia
Areas most vulnerable to ischemic Injury :
Neocortex
Hippocompus
Striatum

14. mechanism of brain injury involves binding of glutamate to NMDA receptor , increasing the intracellular ca++ and subsequently activates proteases phospholipases and deoxyribonucleases , promotes the generation of free radicals cell injury , cell death .
Hypothermia the release of glutamate
During DHCA , microemboli can be detected .

15. THE ETIOLOGY OF NEUROLOGICAL
DYSFUNCTION IN CHILDREN IS FOR THE MOST
PART ISCHEMIA
PATHOPHYSIOLOGIC MECHANISMS ACCOUNTING
FOR NEUROLOGIC INJURY INCLUDE:
rate and extent of cooling and rewarming
management of CPB
prolonged DHCA
anemia
low cardiac output

16. 16

17. 17

18. UNDER DEEP HYPOTHERMIC CPB CBF IS REDUCED BUT THERE IS AN
EXPONENTIALLY GREATER REDUCTION
IN CMRO2.
A STATE OF LUXURY PERFUSION EXISTS
WITH AN EXCESS OF FLOW RELATIVE
TO OXYGEN CONSUMPTION; 1:75 (conferring cerebral protection)
IN PATIENTS UNDERGOING DHCA CBF AND
CMRO2 REMAIN DECREASED AFTER
REWARMING AND WEANING FROM CPB
Sara Lozano, MD , Emad Mossad, MD – Journal of Cardiothoracic and Vascular Anesthesia. Volume 18, Issue 5, Pages (October 2004)

20. IMPROVING NEUROLOGIC OUTCOMES20

21. Acid -- Base Management
BLOOD GAS MANAGEMENT (a-stat vs pH-stat)
DURING CPB SIGNIFICANTLY AFFECTS
CEREBRAL PHYSIOLOGY AN MAY HAVE
AN IMPACT ON NEUROLOGICAL OUTCOME
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22. pH-stat strategy – adding carbon dioxide - compensates for this shift.
Changes in cellular pH during hypothermia are mediated through pco2 homeostasis.
When blood is cooled during cardiopulmonary bypass, pH becomes more alkaline.
pH-stat strategy – adding carbon dioxide - compensates for this shift.
This situation causes pH to increase as temperature decreases and electrochemical neutrality to be maintained.
Carbon dioxide is a potent cerebral vasodilator.
α-stat strategy – electrochemical neutrality is maintained by keeping pH normal in temperature-uncorrected gases. 22

23. i.e,
α-stat strategy – arterial blood measured at 37 C with pH of 7.40 and arterial pCO2 of 40 mm Hg
(the hypothermic blood is alkalemic and hypocapneic)
pH-stat strategy – hypothermic arterial blood at pH of 7.40 and arterial pCO2 of 40 mm Hg
(blood at 37 C is acidemic and hypercapneic)

24. PaCO2 26 mmHg PaCO2 26 mmHg PaCO2 40 mmHg
Stat pH stat
pH pH 7.26
PaCO2 40 mmHg PaCO2 56 mmHg
lab 37oC
28 oC
pH pH CO pH 7.4
PaCO2 26 mmHg PaCO2 26 mmHg PaCO2 40 mmHg

25. ADVANTAGES/DISADVANTAGES
α-stat strategy: preserves autoregulation, optimizes cellular enzyme activity, but less metabolic suppression
pH-stat strategy: improves cerebral blood flow, cerebral oxygenation, and brain cooling efficiency during CPB, but greater risk of microembolism and free radical-mediated damage 25

26. Higher Hematocrit Improves Cerebral Outcome After Deep Hypothermic Circulatory Arrest
Extreme hemodilution (hematocrit < 10%) causes inadequate oxygen delivery during early cooling and higher hematocrit (30%) achieved with blood prime results in improved cerebral recovery after circulatory arrest.
Shin’oka T, Shum-Tim D, Jonas RA, Lidov HGW, Laussen PC, Miura T and du Plessis A
Children’s Hospital Boston/Harvard Medical School
J Thorac Cardiovasc Surg 1996;112: 26

27. Temperature Management
No difference between surface and core cooling. Provide adequate duration of cooling (> 20 min) before institution of DHCA. Avoid rapid cooling, avoid rapid rewarming and hyperthermia in postoperative period.
Sharma R, et al. Neurological evaluation and intelligence testing in the child
with operated congenital heart disease. Ann Thorac Surg 2000; 70: 575–581
Cottrell SM et al. Early postoperative body temperature and developmental
outcome after open heart surgery in infants. Ann Thorac Surg 2004; 77: 66–71

28. Neuroprotective drugs

29. Current recommendations and results of clinical trials
Drug
Basis
Current recommendations and results of clinical trials
Pre-operative use of
methyl prednisolone
Lesser inflammatory response
after CPB;
cerebral function recovers
earlier.
Intravenous methyl prednisolone
10 mg/kg administered 8 hours
and 2 hours prior to surgery in high
risk groups like neonates
Barbiturates
Suppresses EEG activity; can
cause reduction
in high-energy phosphates
which is
detrimental after circulatory
arrest.
Not recommended prophylactically
Aprotinin
Beneficial effect on recovery
of cerebral high
energy phosphates and
intracellular pH.
No clear evidence favoring use in pediatric CPB.

30. Allopurinol, NAC
May reduce injury due to
free radicals. NAC
may improve myocardial
function.
No clear data.
NMDA antagonists
(magnesium, selfotel)
Reduce excitotoxicity
No benefit in human trials.
Nimodipine (calcium channel antagonist)
Reduces cellular injury mediated
by calcium influx during reperfusion.
Negative results in human stroke trials.
Erythropoetin (EPO)
EPO switches off apoptosis
Limits excitotoxic cell death
Mediated by NMDA - R
Blocks the inflammatory cascade
EPO is a cerebral vasodilator
EPO 1000 units/kg IV for 3 doses –
12 hours pre-op / after CPB then 24
hours after.

31. Slowing of neuronal metabolism Slow apoptosis and block iCa++
Inhaled anesthetics
Isoflurane
Desflurane
Slowing of neuronal metabolism
Slow apoptosis and block iCa++
neuronal injury and death.
Be placed in the CPB sweep gas flow
Vasodilation
It would appear desirable to use this agents liberally on CPB.
Even seeking to achieve a target blood level while cooling. Especially if DHCA or other such techniques are to be used.
CPB: cardiopulmonary bypass; EEG: electroencephalograph; NAC: N-acetyl cysteine; NMDA: N-methyl D-aspartate
Langley SM, et al. Eur J Cardiothorac Surg 2000.
Clancy RR, et al. Pediatrics 2001.
Miller SP, et al. Ann thorac Surg 2004.
Bickler PE, Fahlman CS. Anesth Analg 2006, 103.

33. EEG
it is a rough guide to anesthetic depth
it is affected by temperature,CPB,anesthetics
not easy to use
BIS (BISPECTRAL INDEX)
it is currently used to guide the depth of anesthesia
easy to use - less reliable during hypothermia
SjVO2 (JUGULAR VENOUS BULB OXYMETRY)
it is considered the gold standard of global cerebral
oxygenation
it is invasive
Unilateral SjVO2 may not reflect contralateral events

34. TCD (TRANSCRANIAL DOPPLER ULTRASOUND)
it is a sensitive real-time monitor of CBF, can detect microemboli
it monitor the middle cerebral artery
Absent signal during DHCA.
S- 100B (Biochemical marker)
Detects preexisting neurologic deficit
Multiple sampling periods required
NIRS (NEAR-INFRARED SPECTROSCOPY)
it is a non-invasive optical technique
most devices utilize 2-4 wavelengths of infrared light
at nm, where oxygenated and deoxygenated
hemoglobin have distinct absorption spectra
two depth of light penetration are used to subtract
out data from the skin and skull resulting in brain
oxygenation value
Changes in cerebral vascular composition will affect rSO2 reading
Useful during DHCA.

37. Conclusion
Survival after neonatal and infant cardiac surgery has improved dramatically, but quality of life, including neurodevelopmental outcomes, still needs study and improvement. It is important to protect the brain using established strategies,and test new strategies with carefully designed follow-up studies. Potential exists for significant improvement in this area.

38. Thank you