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Effect of prenatal cocaine on respiration, heart rate, and sudden infant death syndrome
Author(s) -
Silvestri Jean M.,
Long Joyal M.,
WeeseMayer Debra E.,
Barkov Gary A.
Publication year - 1991
Publication title -
pediatric pulmonology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.866
H-Index - 106
eISSN - 1099-0496
pISSN - 8755-6863
DOI - 10.1002/ppul.1950110409
Subject(s) - medicine , sudden infant death syndrome , apnea , bradycardia , periodic breathing , heart rate , asphyxia , cardiorespiratory fitness , anesthesia , prenatal cocaine exposure , respiration , respiratory rate , respiratory system , sudden death , pediatrics , pregnancy , gestation , blood pressure , prenatal exposure , anatomy , biology , genetics
We studied 114 neonates by pneumocardiogram recordings in order to examine the effects of cocaine with and without opiate exposure on neonatal respiration, heart rate, apparent life threatening events (ALTE), and sudden infant death syndrome (SIDS). In full‐term infants exposed to cocaine without opiates we found increased longest apnea duration and more episodes of bradycardia, but decreased periodic breathing and average heart rate than in control full‐term infants. Term infants prenatally exposed to cocaine with opiates also had less periodic breathing. Preterm infants exposed to cocaine with and without opiates had decreased apnea density and periodic breathing compared with preterm controls. Discriminant analysis to determine whether perinatal asphyxia or exposure to other drugs could predict cardiorespiratory abnormalities showed no consistent relationship. In 72 of 114 infants available for follow‐up, no ALTE occurred but two were lost to SIDS. Our data support the hypothesis that prenatal cocaine exposure may perturb, albeit subtly, the maturation of respiratory control, resulting in disruption of postnatal respiration.