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Cardiovascular transition at birth: a physiological sequence.
Hooper, Stuart B; Te Pas, Arjan B; Lang, Justin; van Vonderen, Jeroen J; Roehr, Charles Christoph; Kluckow, Martin; Gill, Andrew W; Wallace, Euan M; Polglase, Graeme R.
Afiliação
  • Hooper SB; 1] The Ritchie Centre, MIMR-PHI Institute of Medical Research, Monash University, Clayton, Victoria, Australia [2] Department of Obstetrics and Gynecology, Monash University, Clayton, Victoria, Australia.
  • Te Pas AB; Department of Pediatrics, Leiden University Medical Centre, Leiden, The Netherlands.
  • Lang J; The Ritchie Centre, MIMR-PHI Institute of Medical Research, Monash University, Clayton, Victoria, Australia.
  • van Vonderen JJ; Department of Pediatrics, Leiden University Medical Centre, Leiden, The Netherlands.
  • Roehr CC; 1] The Ritchie Centre, MIMR-PHI Institute of Medical Research, Monash University, Clayton, Victoria, Australia [2] Monash Newborn, Monash Medical Centre, Clayton, Victoria, Australia.
  • Kluckow M; Department of Neonatalogy, Royal North Shore Hospital and University of Sydney, Sydney, New South Wales, Australia.
  • Gill AW; Centre for Neonatal Research and Education, The University of Western Australia, Perth, Western Australia, Australia.
  • Wallace EM; 1] The Ritchie Centre, MIMR-PHI Institute of Medical Research, Monash University, Clayton, Victoria, Australia [2] Department of Obstetrics and Gynecology, Monash University, Clayton, Victoria, Australia.
  • Polglase GR; 1] The Ritchie Centre, MIMR-PHI Institute of Medical Research, Monash University, Clayton, Victoria, Australia [2] Department of Obstetrics and Gynecology, Monash University, Clayton, Victoria, Australia.
Pediatr Res ; 77(5): 608-14, 2015 May.
Article em En | MEDLINE | ID: mdl-25671807
The transition to newborn life at birth involves major cardiovascular changes that are triggered by lung aeration. These include a large increase in pulmonary blood flow (PBF), which is required for pulmonary gas exchange and to replace umbilical venous return as the source of preload for the left heart. Clamping the umbilical cord before PBF increases reduces venous return and preload for the left heart and thereby reduces cardiac output. Thus, if ventilation onset is delayed following cord clamping, the infant is at risk of superimposing an ischemic insult, due to low cardiac output, on top of an asphyxic insult. Much debate has centered on the timing of cord clamping at birth, focusing mainly on the potential for a time-dependent placental to infant blood transfusion. This has prompted recommendations for delayed cord clamping for a set time after birth in infants not requiring resuscitation. However, recent evidence indicates that ventilation onset before cord clamping mitigates the adverse cardiovascular consequences caused by immediate cord clamping. This indicates that the timing of cord clamping should be based on the infant's physiology rather than an arbitrary period of time and that delayed cord clamping may be of greatest benefit to apneic infants.
Assuntos

Texto completo: 1 Base de dados: MEDLINE Assunto principal: Sistema Cardiovascular / Fenômenos Fisiológicos Cardiovasculares / Parto Limite: Female / Humans / Newborn / Pregnancy Idioma: En Revista: Pediatr Res Ano de publicação: 2015 Tipo de documento: Article País de afiliação: Austrália

Texto completo: 1 Base de dados: MEDLINE Assunto principal: Sistema Cardiovascular / Fenômenos Fisiológicos Cardiovasculares / Parto Limite: Female / Humans / Newborn / Pregnancy Idioma: En Revista: Pediatr Res Ano de publicação: 2015 Tipo de documento: Article País de afiliação: Austrália