Canadian Journal of Anaesthesia

, Volume 42, Issue 11, pp 964–971

Persistent low cerebral blood flow velocity following profound hypothermic circulatory arrest in infants

  • Brendan O’Hare
  • Bruno Bissonnette
  • Desmond Bohn
  • Peter Cox
  • William Williams
Reports of Investigation

Abstract

Acute neurological morbidity following repair of congenital heart disease (CHD) in infancy is well recognized, particularly with the modalities of hypothermic cardiopulmonary bypass (CPB) and profound hypothermic circulatory arrest (PHCA). Reduced O2 delivery (perfusion defect) during rewarming following PHCA has been shown in the operating room. This reduction in cerebral blood flow coincides with disordered cerebral metabolism and oxygen utilisation after PHCA. The objective of this study was to extend the period of investigation of cerebral blood flow velocity (CBFV) behaviour in infants following PHCA to determine if hypoperfusion persisted in the paediatric intensive care unit (PICU). Ten patients undergoing CHD surgery were divided, based on the pump modality employed, into either mild hypothermic CPB or profound hypothermic CPB with circulatory arrest. Following admission to the PICU, sequential recordings of the mean CBFV in the middle cerebral artery, anterior fontanelle pressure, haemodynamic variables, tympanic membrane temperature, haematocrit and PaCO2 were performed. The PHCA group had a consistently reduced CBFV compared with the control group (P < 0.05). The CBFV values at one, two and four hours were 60 ± 11, 51.8 ± 11.4 and 52.6 ± 11.9 respectively in the mild hypothermic CPB group. The CBFV values at one, two and four hours were 26.6 ± 6.8, 32.6 ± 10 and 34 ± 8 respectively in the PHCA group. There was no difference in cerebral perfusion pressure between both groups. Tympanic temperature, haematocrit and PaCO2 did not vary between groups at any interval. This study demonstrates a sustained reduction in the CBFV pattern following PHCA into the postoperative period despite adequate cerebral perfusion pressures. This abnormality correlates with electroencephalographic aberrations documented after PHCA. It supports the concept of a prolonged unreactive cerebrovascular bed which could potentially contribute to the acute neurological morbidity following PHCA in neonates.

Key words

anaesthesia: paediatric brain: blood flow measurement techniques: Doppler ultrasound, transcranial surgery: cardiac temperature: hypothermia 

Résumé

La morbidité neurologique infantile attribuable aux malformations cardiaques congénitales (MCG) opérées sous circulation extracorporelle (CEC) en hypothermie et sous arrêt circulatoire en hypothermie profonde (ACHP) est bien connue. En salle d’opération, on a déjà démontré une diminution de l’apport en oxygène (insuffisance de perfusion) au cours du réchauffement pendant l’ACHP. Cette réduction de la perfusion cérébrate coïncide avec un bouleversement du métabolisme cérébral et de l’utilisation de l’oxygène après l’ACHP. L’objectif de ce travail était d’étendre la durée de l’examen du comportement de la vélocite du débit sanguin cérébral (VDSC) après un ACHP chez les enfants pour déterminer si l’hypoperfusion persistait à l’unité des soins intensifs pédiatriques (UPSI). Après l’admission à l’UPSI, des enregistrements séquentiels de la VDSC moyenne de l’artère cérébrale moyenne, de la pression de la fontanelle antérieure, de l’hématocrite et de la PaCO2 ont été effectués. Le groupe ACHP avait une VDSC diminuée comparativement au groupe contrôle (P < 0,05). Les valeurs de la VDSC à la premiére, deuxième et quatrième heure étaient de 60 ± 11, 51,8 ± 11,4 et 52,6 ± 11,9 respectivement dans le groupe de la CEC légèrement hypothermique. On n’a pas trouvé de différence pour la pression cérébrate de perfusion entre les deux groupes. La température tympanique, l’hématocrite et la PaCO2 n’ont varié en aucun moment entre les groupes. Cette étude montre une réduction soutenue dans l’évolution de la VDSC aprés une ACHP pendant la période postopératoire malgré des pressions de perfusion adéquates. Cette anomalie concorde avec les changements électroencéphaliques trouvés aprèsc l’ACHP. Elle confirme le concept de non réactivité du lit cérébrovasculaire qui pourrait contribuer à la morbidité neurologique après l’ACHP chez le nouveau-né.

References

  1. 1.
    Ferry PC. Neurological sequelae of open-heart surgery in children. An ‘irritating question’. Am J Dis Child 1990; 144: 369–73.PubMedGoogle Scholar
  2. 2.
    Newburger JW, Jonas PA, Wernovsky G, et al. A comparison of the perioperative neurologic effects of hypothermic circulatory arrest versus low-flow cardiopulmonary bypass in infant cardiac surgery. N Engl J Med 1993; 329: 1057–64.PubMedCrossRefGoogle Scholar
  3. 3.
    Burrows FA, Hillier SC, McLeod ME, Iron KS, Taylor MJ. Anterior fontanel pressure and visual evoked potentials in neonates and infants undergoing profound hypothermic circulatory arrest. Anesthesiology 1990; 73: 632–6.PubMedCrossRefGoogle Scholar
  4. 4.
    Swain JA. Cardiac surgery and the brain (Editorial). N Engl J Med 1993; 329: 1119–20.PubMedCrossRefGoogle Scholar
  5. 5.
    Greeley WJ, Ungerleider RM. Assessing the effect of cardiopulmonary bypass on the brain. Ann Thorac Surg 1991; 52: 417–9.PubMedGoogle Scholar
  6. 6.
    Burrows FA, Bissonnette B. Cerebral blood flow velocity patterns during cardiac surgery utilizing profound hypothermia with low-flow cardiopulmonary bypass or circulatory arrest in neonates and infants. Can J Anaesth 1993; 40: 298–307.PubMedGoogle Scholar
  7. 7.
    Greeley WJ, Ungerleider RM, Smith LR, Reves JG. The effects of deep hypothermic cardiopulmonary bypass and total circulatory arrest on cerebral blood flow in infants and children. J Thorac Cardiovasc Surg 1989; 97: 737–45.PubMedGoogle Scholar
  8. 8.
    Greeley WJ, Kern FH, Ungerleider RM, et al. The effect of hypothermic cardiopulmonary bypass and total circulatory arrest on cerebral metabolism in neonates, infants and children. J Thorac Cardiovasc Surg 1991; 101: 783–94.PubMedGoogle Scholar
  9. 9.
    Mezrow CK, Sadeghi AM, Gandsas A, et al. Cerebral effects of low-flow cardiopulmonary bypass and hypothermic circulatory arrest. Ann Thorac Surg 1994; 57: 532–9.PubMedGoogle Scholar
  10. 10.
    Hillier SC, Burrows FA, Bissonnette B, Taylor RH. Cerebral hemodynamics in neonates and infants undergoing cardiopulmonary bypass and profound hypothermic circulatory arrest: assessment by transcranial Doppler sonography. Anesth Analg 1991; 72: 723–8.PubMedCrossRefGoogle Scholar
  11. 11.
    Mezrow CK, Midulla PS, Sadeghi AM, et al. Evaluation of cerebral metabolism and quantitative electroencephalography after hypothermic circulatory arrest and low-flow cardiopulmonary bypass at different temperatures. J Thorac Cardiovasc Surg 1994; 107: 1006–19.PubMedGoogle Scholar
  12. 12.
    an der Linden J, Astudillo R, Ekroth R, Scallan M, Lincoln C. Cerebral lactate release after circulatory arrest but not after low flow in pediatric heart operations. Ann Thorac Surg 1993; 56: 1485–9.PubMedGoogle Scholar
  13. 13.
    Bunegin L, Albin MS, Rauschhuber R, Martin AE. Intracranial pressure measurement from the anterior fontanelle utilizing a pneumoelectronic switch. Neurosurgery 1987; 20: 726–31.PubMedCrossRefGoogle Scholar
  14. 14.
    Gillard JH, Kirkham FJ, Levin SD, Neville BGR, Gosling RG. Anatomical validation of middle cerebral artery position as identified by transcranial pulsed Doppler ultrasound. J Neurol Neurosurg Psychiatry 1986; 49: 1025–9.PubMedCrossRefGoogle Scholar
  15. 15.
    Mezrow CK, Sadeghi AM, Gandsas A, et al. Cerebral blood flow and metabolism in hypothermic circulatory arrest. Ann Thorac Surg 1992; 54: 609–16.PubMedGoogle Scholar
  16. 16.
    Astudillo R, van de Linden J, Ekroth R, et al. Absent diastolic cerebral flow velocity after circulatory arrest but not after low flow in infants. Ann Thorac Surg 1993; 56: 515–9.PubMedCrossRefGoogle Scholar
  17. 17.
    Reimer H, Burrows FA, Bissonnette B. Cerebral metabolism during low-flow cardiopulmonary bypass and profound hypothermic circulatory arrest. Anesthesiology 1992; 77: A1135.CrossRefGoogle Scholar
  18. 18.
    Greeley WJ, Bracey VA, Ungerleider RM, et al. Recovery of cerebral metabolism and mitochondrial oxidation state is delayed after hypothermic circulatory arrest. Circulation 1991; 84: Suppl III: III-400–III-406.Google Scholar
  19. 19.
    Bode H. Pediatric Applications of Transcranial Doppler Sonography. Vienna: Springer-Verlag, 1988; 29–43.Google Scholar
  20. 20.
    Taylor RH, Burrows FA, Bissonnette B. Cerebral pressure-flow velocity relationship during hypothermic cardiopulmonary bypass in neonates and infants. Anesth Analg 1992; 74: 636–42.PubMedCrossRefGoogle Scholar
  21. 21.
    Buijs J, van Bel F, Nandorff A, Hardjowijono R, Stijnen T, Ottenkamp J. Cerebral blood flow pattern and autoregulation during open-heart surgery in infants and young children: a transcranial, Doppler ultrasound study. Crit Care Med 1992; 20: 771–7.PubMedCrossRefGoogle Scholar
  22. 22.
    Marsh ML, Shapiro HM, Smith RW, Marshall LF. Changes in neurologic status and intracranial pressure associated with sodium nitroprusside administration. Anesthesiology 1979; 51: 336–8.PubMedCrossRefGoogle Scholar
  23. 23.
    Rogers AT, Prough DS, Gravlee GP, et al. Sodium nitroprusside does not dilate cerebral resistance vessels during hypothermic cardiopulmonary bypass. Anesthesiology 1991; 74: 820–6.PubMedCrossRefGoogle Scholar
  24. 24.
    Bouma GJ, Muizelaar JP. Relationship between cardiac output and cerebral blood flow in patients with intact and with impaired autoregulation. J Neurosurg 1990; 73: 368–74.PubMedGoogle Scholar
  25. 25.
    Huber P, Handa J. Effect of contrast material, hypercapnia, hyperventilation, hypertonic glucose and papaverine on the diameter of the cerebral arteries. Angiographic determination in man. Invest Radiol 1967; 2: 17–32.PubMedCrossRefGoogle Scholar
  26. 26.
    Volpe JJ, Perlman JM, Hill A, McMenamin JB. Cerebral blood velocity in the newborn: the value of its determination. Pediatrics 1982; 70: 147–52.PubMedGoogle Scholar
  27. 27.
    Bishop CCR, Powell S, Rutt D, Browse NL. Transcranial Doppler measurement of middle cerebral artery blood flow velocity: a validation study. Stroke 1986; 17: 913–5.PubMedGoogle Scholar
  28. 28.
    Kontos HA. Validity of cerebral blood flow calculations from velocity measurements. Stroke 1989; 20: 1–3.PubMedGoogle Scholar
  29. 29.
    Aaslid R, Markwalder T-M, Nornes H. Noninvasive transcranial Doppler ultrasound recording of flow velocity in basal cerebral arteries. J Neurosurg 1982; 57: 769–74.PubMedCrossRefGoogle Scholar
  30. 30.
    Greeley WJ, Ungerleider RM, Kern FH, Brusino FG, Smith R, Reves JG. Effects of cardiopulmonary bypass on cerebral blood flow in neonates, infants, and children. Circulation 1989; 80: Suppl I: I-209–I-215.Google Scholar
  31. 31.
    Glauser TA, Rorke LB, Weinberg PM, Clancy RR. Acquired neuropathologic lesions associated with the hypoplastic left heart syndrome. Pediatrics 1990; 85: 991–1000.PubMedGoogle Scholar
  32. 32.
    Gottesman RD, Rosenblatt B, Gotman J, Tchervenkov CI. Continuous EEG monitoring following corrective congenital heart surgery in a pediatnc critical care unit. Clin Invest Med 1994; 17 (Suppl.): B21.Google Scholar
  33. 33.
    Greeley WJ. Con: deep hypothermic circulatory arrest must be used selectively and discreetly. J Cardiothor Vase Ahesth 1991; 5: 638–40.CrossRefGoogle Scholar

Copyright information

© Canadian Anesthesiologists 1995

Authors and Affiliations

  • Brendan O’Hare
    • 1
    • 2
  • Bruno Bissonnette
    • 1
  • Desmond Bohn
    • 2
  • Peter Cox
    • 2
  • William Williams
    • 3
  1. 1.Department of AnaesthesiaThe Hospital For Sick Children and the University of TorontoTorontoCanada
  2. 2.Department of Critical CareThe Hospital For Sick Children and the University of TorontoTorontoCanada
  3. 3.Division of Cardiovascular Surgery, Department of SurgeryThe Hospital For Sick Children and the University of TorontoTorontoCanada
  4. 4.Department of AnaesthesiaThe Hospital for Sick ChildrenToronto

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