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35 - Acidosis and alkalosis

from Section 4 - Specific conditions associated with fetal and neonatal brain injury

Published online by Cambridge University Press:  12 January 2010

By
Ronald S. Cohen
Edited by
David K. Stevenson ,
William E. Benitz ,
Philip Sunshine ,
Susan R. Hintz  and
Maurice L. Druzin
David K. Stevenson
Affiliation:
Stanford University School of Medicine, California
William E. Benitz
Affiliation:
Stanford University School of Medicine, California
Philip Sunshine
Affiliation:
Stanford University School of Medicine, California
Susan R. Hintz
Affiliation:
Stanford University School of Medicine, California
Maurice L. Druzin
Affiliation:
Stanford University School of Medicine, California
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Summary

Introduction

As part of normal homeostasis, the pH of arterial blood is fairly tightly controlled by normal physiologic processes. Healthy adults maintain a reasonably stable pH, ranging from 7.35 to 7.45, and the initial pH after birth can range from 7.11 to 7.36. Acidosis (low pH) and alkalosis (high pH) occur commonly when there are disturbances of the body's normal physiology. This can result from either a pathologic process or medical interventions. When they are due to, or associated with, a pathologic process, the abnormal pH may be blamed for any long-term consequences of that event. Similarly, when a medication or treatment results in an abnormal pH, any long-term consequences may be assigned to that intervention. In both situations, it is not clear whether the underlying physiologic disturbance is responsible for the adverse long-term outcome, or whether the abnormal pH played a role, and if so, how important that role may have been.

Acidosis

Acidosis is known to accompany ischemia, and has been used as a marker for tissue hypoxia and damage. However, it is unclear whether or not acidosis per se is a cause of injury. To examine this issue, we need to separate the two clinical subtypes of acidosis – respiratory and metabolic.

Respiratory acidosis

Respiratory acidosis occurs when carbon dioxide (CO2), produced by metabolism, builds up in the body and dissolves in the bloodstream.

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Fetal and Neonatal Brain Injury , pp. 402 - 408
Publisher: Cambridge University Press
Print publication year: 2009

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References

Hickling, KG, Henderson, SJ, Jackson, R. Low mortality associated with low volume pressure limited ventilation with permissive hypercapnia in severe adult respiratory distress syndrome. Intensive Care Med 1990; 16: 372–7.CrossRefGoogle ScholarPubMed
Mariani, G, Cifuentes, J, Carlo, WA. Randomized trial of permissive hypercapnia in preterm infants. Pediatrics 1999; 104: 1082–8.CrossRefGoogle ScholarPubMed
Ni Chonghaile, M, Higgins, B, Laffey, JG. Permissive hypercapnia: role in protective lung ventilatory strategies. Curr Opin Crit Care 2005; 11: 56–62.CrossRefGoogle ScholarPubMed
Carlo, WA. Permissive hypercapnia and permissive hypoxemia in neonates. J Perinatol 2007; 27: S64–70.CrossRefGoogle Scholar
Hernandez, MJ, Brennan, RW, Vannucci, RC, et al. Cerebral blood flow and oxygen consumption in the newborn dog. Am J Physiol 1978; 234: R209–15.Google ScholarPubMed
Reivich, M, Brann, AW, Shapiro, H. Reactivity of cerebral vessels to CO2 in the newborn rhesus monkey. Eur Neurol 1971; 6: 132–6.CrossRefGoogle Scholar
Rosenberg, AA, Jones, MD, Traystman, RJ, et al. Response of cerebral blood flow to changes in pCO2 in fetal, newborn, and adult sheep. Am J Physiol 1982; 242: H862–6.Google ScholarPubMed
Griesen, G. Cerebral blood flow and energy metabolism in the newborn. Clin Perinatol 1997; 24: 531–46.CrossRefGoogle Scholar
Dietz, V, Wolf, M, Keel, M, et al. CO2 reactivity of the cerebral hemoglobin concentration in healthy term newborns measured by near infrared spectrophotometry. Biol Neonate 1999; 75: 85–90.CrossRefGoogle ScholarPubMed
Jayasinghe, D, Gill, AB, Levene, MI. CBF reactivity in hypotensive and normotensive preterm infants. Pediatr Res 2003; 54: 848–53.CrossRefGoogle ScholarPubMed
Kaiser, JR, Gauss, CH, Williams, DK. The effects of hypercapnia on cerebral autoregulation in ventilated very low birth weight infants. Pediatr Res 2005; 58: 931–5.CrossRefGoogle ScholarPubMed
Kenny, JD, Garcia-Prats, JA, Hilliard, JL, et al. Hypercarbia at birth: a possible role in the pathogenesis of intraventricular hemorrhage. Pediatrics 1978; 62: 465–7.Google ScholarPubMed
Levene, MI, Fawer, CL, Lamont, RF. Risk factors in the development of intraventricular haemorrhage in the preterm neonate. Arch Dis Child 1982; 57: 410–17.CrossRefGoogle ScholarPubMed
Kaiser, JR, Gauss, CH, Pont, MJ, et al. Hypercapnia during the first 3 days of life is associated with severe intraventricular hemorrhage in very low birth weight infants. J Perinatol 2006; 26: 279–85.CrossRefGoogle ScholarPubMed
Kaiser, JR, Gauss, CH, Williams, DK. Surfactant administration acutely affects cerebral and systemic hemodynamics and gas exchange in very low birth weight infants. J Pediatr 2004; 144: 809–14.Google ScholarPubMed
Gleason, CA, Short, BL, Jones, MD. Cerebral blood flow and metabolism during and after prolonged hypocapnia in newborn lambs. J Pediatr 1989; 115: 309–14.CrossRefGoogle ScholarPubMed
Fabres, J, Carlo, WA, Phillips, V, et al. Both extremes of arterial carbon dioxide pressure and the magnitude of fluctuations in arterial carbon dioxide pressure are associated with severe intraventricular hemorrhage in preterm infants. J Pediatr 2007; 119: 299–305.CrossRefGoogle ScholarPubMed
Vannucci, RC, Towfighi, J, Heitjan, DF, et al. Carbon dioxide protects the perinatal rat brain from hypoxic–ischemic damage. Pediatrics 1995; 95: 868–74.Google ScholarPubMed
Vannucci, RC, Towfighi, J, Brucklacher, RM, et al. Effect of extreme hypercapnia on hypoxic–ischemic brain damage in the immature rat. Pediatr Res 2001; 49: 799–803.CrossRefGoogle ScholarPubMed
Komori, M, Takada, K, Tomizawa, Y, et al. Permissive range of hypercapnia for improved peripheral microcirculation and cardiac output in rabbits. Crit Care Med 2007; 35: 2171–5.CrossRefGoogle ScholarPubMed
Xu, L, Glassford, AJM, Giaccia, AJ, et al. Acidosis reduces neuronal apoptosis. NeuroReport 1998; 9: 875–9.CrossRefGoogle ScholarPubMed
Laffey, JG, Tanaka, M, Engelberts, D, et al. Therapeutic hypercapnia reduces pulmonary and systemic injury following in vivo lung reperfusion. Am J Respir Crit Care Med 2000; 162: 2287–94.CrossRefGoogle ScholarPubMed
Laffey, JG, Engelberts, D, Kavanagh, BP. Buffering hypercapnic acidosis worsens acute lung injury. Am J Respir Crit Care Med 2000; 161: 141–6.CrossRefGoogle ScholarPubMed
Fujita, M, Asanuma, H, Hirata, A, et al. Prolonged transient acidosis during early reperfusion contributes to the cardioprotective effects of postconditioning. Am J Physiol Heart Circ Physiol 2007; 292: H2004–8.CrossRefGoogle ScholarPubMed
Carlo, WA, Stark, AR, Wright, LL, et al. Minimal ventilation to prevent bronchopulmonary dysplasia in extremely-low-birth-weight infants. J Pediatr 2002; 141: 370–5.CrossRefGoogle ScholarPubMed
Thome, UH, Carroll, W, Wu, T-J, et al. Outcome of extremely preterm infants randomized at birth to different PaCO2 targets during the first seven days of life. Biol Neonate 2006; 90: 218–25.CrossRefGoogle ScholarPubMed
Miller, JD, Carlo, WA. Safety and effectiveness of permissive hypercapnia in the preterm infant. Curr Opin Pediatr 2007; 19: 142–4.CrossRefGoogle ScholarPubMed
,American College of Obstetricians and Gynecologists. Committee on Obstetric Practice. Umbilical cord blood gas and acid–base analysis. Obstet Gynecol 2006; 108: 1319–22.
Evans, OB. Lactic acidosis in childhood: Part I. Pediatr Neurol 1985; 1: 325–8.CrossRefGoogle ScholarPubMed
Bar, A, Riskin, A, Iancu, T, et al. A newborn infant with protracted diarrhea and metabolic acidosis. J Pediatr 2007; 150: 198–201.CrossRefGoogle ScholarPubMed
Debray, FG, Lamber, M, Chevalier, I, et al. Long-term outcome and clinical spectrum of 73 pediatric patients with mitochondrial diseases. Pediatrics 2007; 119: 722–33.CrossRefGoogle ScholarPubMed
Bhati, RS, Sheridan, BC, Mill, MR, et al. Heart transplantation for progressive cardiomyopathy as a manifestation of MELAS syndrome. J Heart Lung Transplant 2005; 24: 2286–9.CrossRefGoogle ScholarPubMed
Schurr, A. Lactate: the ultimate cerebral oxidative energy substrate? J Cerebral Blood Flow Metabol 2006; 26: 142–52.CrossRefGoogle ScholarPubMed
Bergersen, LH. Is lactate food for neurons? Comparison of monocarboxylate transporter subtypes in brain and muscle. Neuroscience 2007; 145: 11–19.CrossRefGoogle ScholarPubMed
Pirchl, M, Marksteiner, J, Humpel, C. Effects of acidosis on brain capillary endothelial cells and cholinergic neurons: relevance to vascular dementia and Alzheimer's disease. Neurol Res 2006; 28: 657–64.CrossRefGoogle ScholarPubMed
Gilbert, E, Tang, JM, Ludvig, N, et al. Elevated lactate suppresses neuronal firing in vivo and inhibits glucose metabolism in hippocampal slice cultures. Brain Res 2006; 1117: 213–23.CrossRefGoogle ScholarPubMed
Ammari, AN, Schulze, KF. Uses and abuses of sodium bicarbonate in the neonatal intensive care unit. Curr Opin Pediatr 2002; 14: 151–6.CrossRefGoogle ScholarPubMed
Murki, S, Kumar, P, Lingappa, L, et al. Effect of a single dose of sodium bicarbonate given during neonatal resuscitation at birth on the acid–base status on first day of life. J Perinatol 2004; 24: 696–9.CrossRefGoogle ScholarPubMed
Lokesh, L, Kumar, P, Murki, S, et al. A randomized controlled trial of sodium bicarbonate in neonatal resuscitation: effect on immediate outcome. Resuscitation 2000; 60: 219–23.CrossRefGoogle Scholar
Beveridge, CJE, Wilkinson, AR. Sodium bicarbonate infusion during resuscitation of infants at birth. Cochrane Database Syst Rev 2006; (1): CD004864.Google ScholarPubMed
Laffey, JG, Kavanagh, BP. Hypocapnia. N Engl J Med 2002; 347: 43–53.CrossRefGoogle ScholarPubMed
Cassin, S, Dawes, GS, Mott, JC, et al. The vascular resistance of the foetal and newly ventilated lung of the lamb. J Physiol 1964; 171: 61–79.CrossRefGoogle ScholarPubMed
Rudolph, AM, Yuan, S. Response of the pulmonary vasculature to hypoxia and H+ ion concentration changes. J Clin Invest 1966; 45: 399–411.CrossRefGoogle ScholarPubMed
Peckham, GJ, Fox, WW. Physiologic factors affecting pulmonary artery pressure in infants with persistent pulmonary hypertension. J Pediatr 1978; 93: 1005–10.CrossRefGoogle ScholarPubMed
Fox, WW, Duara, S. Persistent pulmonary hypertension in the neonate: diagnosis and management. J Pediatr 1983; 103: 505–14.CrossRefGoogle ScholarPubMed
Marron, MJ, Crisafi, MA, Driscoll, JM, et al. Hearing and neurodevelopmental outcome in survivors of persistent pulmonary hypertension of the newborn. Pediatrics 1992; 90: 392–6.Google ScholarPubMed
Brett, C, Dekle, M, Leonard, CH, et al. Developmental follow-up of hyperventilated neonates: preliminary observations. Pediatrics 1981; 68: 588–91.Google ScholarPubMed
Ferrara, B, Johnson, , Chang, PN, et al. Efficacy and neurologic outcome of profound hypocapneic alkalosis for the treatment of persistent pulmonary hypertension in infancy. J Pediatr 1984; 105: 457–61.CrossRefGoogle ScholarPubMed
Bernbaum, JC, Russell, P, Sheridan, PH, et al. Long-term follow-up of newborns with persistent pulmonary hypertension. Crit Care Med 1984; 12: 579–83.CrossRefGoogle ScholarPubMed
Ballard, RA, Leonard, CH. Developmental follow-up of infants with persistent pulmonary hypertension of the newborn. Clin Perinatol 1984; 11: 737–44.CrossRefGoogle ScholarPubMed
Leavitt, AM, Watchko, JF, Bennett, FC, et al. Neurodevelopmental outcome following persistent pulmonary hypertension of the neonate. J Perinatol 1987; 7: 288–91.Google ScholarPubMed
Bifano, EM, Pfannenstsiel, A. Duration of hyperventilation and outcome in infants with persistent pulmonary hypertension. Pediatrics 1988; 81: 657–61.Google ScholarPubMed
Cohen, RS, Stevenson, D, Malachowski, N, et al. Late morbidity among survivors on respiratory failure treated with tolazoline. J Pediatr 1980; 97: 644–7.CrossRefGoogle ScholarPubMed
Graziani, LJ, Baumgart, S, Desai, S, et al. Clinical antecedents of neurologic and audiologic abnormalities in survivors of extracorporeal membrane oxygenation. J Child Neurol 1997; 12: 415–22.CrossRefGoogle ScholarPubMed
Lyrene, Rk, Welch, KA, Godoy, G, et al. Alkalosis attenuates hypoxic pulmonary vasoconstriction in neonatal lambs. Pediatr Res 1985; 19: 1268–71.CrossRefGoogle ScholarPubMed
Schreiber, MD, Heymann, MA, Soifer, SJ. Increased arterial pH, not decreased PaCO2, attenuates hypoxia-induced pulmonary vasoconstriction in newborn lambs. Pediatr Res 1986; 20: 113–17.CrossRefGoogle Scholar
Chang, AC, Zucker, HA, Hickey, PR, et al. Pulmonary vascular resistance in infants after cardiac surgery: role of carbon dioxide and hydrogen ion. Crit Care Med 1995; 23: 568–74.CrossRefGoogle ScholarPubMed
Lee, KJ, Hernandez, G, Gordon, JB. Hypercapnic acidosis and compensated hypercapnia in control and pulmonary hypertensive piglets. Pediatr Pulmonol 2003; 36: 94–101.CrossRefGoogle ScholarPubMed
Walsh-Sukys, MC, Tyson, JE, Wright, LL, et al. Persistent pulmonary hypertension of the newborn in the era before nitric oxide: practice variation and outcomes. Pediatrics 2000; 105: 14–20.CrossRefGoogle ScholarPubMed
Hansen, NB, Nowicki, PT, Miller, RR, et al. Alterations in cerebral blood flow and oxygen consumption during prolonged hypocarbia. Pediatr Res 1986; 20: 147–50.CrossRefGoogle ScholarPubMed
Kusada, S, Shisida, N, Miyagi, N, et al. Cerebral blood flow during treatment for pulmonary hypertension. Arch Dis Child Fetal Neonatal Ed 1999; 80: F30–3.CrossRefGoogle Scholar
Menke, J, Michel, E, Rabe, H, et al. Simultaneous influence of blood pressure, PCO2, and PO2 on cerebral blood flow velocity in preterm infants of less than 33 weeks' gestation. Pediatr Res 1993; 24: 173–7.CrossRefGoogle Scholar
Kaiser, JR, Gauss, CH, Williams, DK. The effects of hypercapnia on cerebral autoregulation in ventilated very low birth weight infants. Pediatr Res 2005; 58: 931–5.CrossRefGoogle ScholarPubMed
Soul, JS, Hammer, PE, Tsuji, P, et al. Fluctuating pressure-passivity is common in the cerebral circulation of sick premature infants. Pediatr Res 2007; 61: 467–73.CrossRefGoogle ScholarPubMed
Kennedy, C, Sakurada, O, Shinohara, M, et al. Local cerebral glucose utilization in the newborn macaque monkey. Ann Neurol 1982; 12: 333–40.CrossRefGoogle ScholarPubMed
Vannucci, RC, Vannucci, SJ. Perinatal brain metabolism. In Polin, RA, Fox, WW, Abman, SH, eds., Fetal and Neonatal Physiology, 3rd edn. Philadelphia, PA: Saunders, 2004: 1713–25.CrossRefGoogle Scholar
Graham, EM, Apostolou, M, Mishra, OP, et al. Modification of the N-methyl-d-aspartate (NMDA) receptor in the brain of newborn piglets following hyperventilation induced ischemia. Neurosci Lett 1996; 218: 29–32.Google ScholarPubMed
Fritz, KI, Zubrow, AB, Ashraf, QM, et al. The effect of moderate hypocapnic ventilation on nuclear Ca2+-ATPase activity, nuclear Ca2+ flux, and Ca2+/calmodulin kinase IV activity in the cerebral cortex of newborn piglets. Neurochem Res 2004; 29: 791–6.CrossRefGoogle Scholar
Naulty, CM, Weiss, IP, Herer, GR. Progressive sensorineural hearing loss in survivors of persistent fetal circulation. Ear Hear 1986; 7: 74–7.CrossRefGoogle ScholarPubMed
Hendricks-Munoz, KD, Walton, JP. Hearing loss in infants with persistent fetal circulation. Pediatrics 1988; 81: 650–6.Google ScholarPubMed
Calvert, SA, Hoskins, EM, Fong, KW, et al. Etiological factors associated with the development of periventricular leukomalacia. Acta Paediatr Scand 1987; 76: 254–9.CrossRefGoogle ScholarPubMed
Graziani, LJ, Spitzer, AR, Mitchell, DG, et al. Mechanical ventilation in preterm infants: neurosonographic and developmental studies. Pediatrics 1992; 90: 515–22.Google ScholarPubMed
Wiswell, TE, Graziani, LJ, Kornhauser, MS, et al. Effects of hypocarbia on the development of cystic periventricular leukomalacia in premature infants treated with high-frequency jet ventilation. Pediatrics 1996; 98: 918–24.Google ScholarPubMed
Shankaran, S, Langer, JC, Kazzi, SN, et al. Cumulative index of exposure to hypocarbia and hyperoxia as risk factors for periventricular leukomalacia in low birth weight infants. Pediatrics 2006; 118: 1654–9.CrossRefGoogle ScholarPubMed
,HiFO Study Group. Randomized study of high-frequency oscillatory ventilation in infants with severe respiratory distress syndrome. J Pediatr 1993; 122: 609–19.
Wiswell, TE, Graziani, LJ, Kornhauser, MS, et al. High-frequency jet ventilation in the early management of respiratory distress syndrome is associated with a greater risk for adverse outcomes. Pediatrics 1996; 98: 1035–43.Google ScholarPubMed
Keszler, M, Modanlou, HD, Brudno, DS, et al. Multicenter controlled clinical trial of high-frequency jet ventilation in preterm infants with uncomplicated respiratory distress syndrome. Pediatrics 1997; 100: 593–9.CrossRefGoogle ScholarPubMed
Klinger, G, Beyene, J, Shah, P, et al. Do hyperoxaemia and hypocapnia add to the risk of brain injury after intrapartum asphyxia? Arch Dis Child Fetal Neonatal Ed 2005; 90: F49–52.CrossRefGoogle ScholarPubMed
Vento, M, Asensi, M, Sastre, J, et al. Oxidative stress in asphyxiated term infants resuscitated with 100% oxygen. J Pediatr 2003; 142: 240–6.CrossRefGoogle ScholarPubMed
Laski, ME, Sabatini, S. Metabolic alkalosis, bedside and bench. Semin Nephrol 2006; 26: 404–21.CrossRefGoogle ScholarPubMed
Shaer, AJ. Inherited primary renal tubular hypokalemic alkalosis: a review of Gitelman and Bartter syndromes. Am J Med Sci 2001; 322: 316–32.CrossRefGoogle ScholarPubMed
Naesens, M, Steels, P, Verberckmoes, R, et al. Bartter's and Gitelman's syndromes: from gene to clinic. Nephron Physiol 2004; 96: 65–78.CrossRefGoogle Scholar
Kagalwalla, AF. Congenital chloride diarrhea: a study in Arab children. J Clin Gastroenterol 1994; 19: 36–40.CrossRefGoogle ScholarPubMed
Hihnala, S, Höglund, P, Lammi, L, et al. Long-term clinical outcome in patients with congenital chloride diarrhea. J Pediatr Gastroenterol Nutr 2006; 42: 369–75.CrossRefGoogle ScholarPubMed
Sasse, S, Kribs, A, Vierzig, A, et al. A staged protocol for the treatment of persistent pulmonary hypertension of the newborn. Klin Padiatr 1997; 209: 301–7.CrossRefGoogle ScholarPubMed

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