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Intrauterine Tobacco Smoke Exposure and Congenital Heart Defects Sharron Forest, DNP, RN, NNP-BC; Sandra Priest, MSN, RN, NNP-BC

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Intrauterine Tobacco Smoke Exposure and Congenital Heart Defects Sharron Forest, DNP, RN, NNP-BC; Sandra Priest, MSN, RN, NNP-BC DOI: 10.1097/JPN.0000000000000153 Continuing Education r r J Perinat Neonat Nurs Volume 30 Number 1, 54–63 Copyright C 2016 Wolters Kluwer Health, Inc. All rights reserved. Intrauterine Tobacco Smoke Exposure and Congenital Heart Defects Sharron Forest, DNP, RN, NNP-BC; Sandra Priest, MSN, RN, NNP-BC ABSTRACT Forty-six percent of deaths from congenital malforma- Tobacco use and second-hand smoke exposure during tions and 3% of all infant deaths are attributed to CHDs.3 pregnancy are linked to a host of deleterious effects Clinical research clearly shows an association between on the pregnancy, fetus, and infant. Health outcomes fetal cigarette smoke exposure and CHDs. This article improve when women quit smoking at any time during the presents an overview of recent studies demonstrating pregnancy. However, the developing heart is vulnerable to the association as well as clinical implications for prac- noxious stimuli in the early weeks of fetal development, a tice for perinatal and neonatal nurses. time when many women are not aware of being pregnant. Congenital heart defects are the most common birth PREVALENCE AND EFFECTS OF SMOKING defects. Research shows an association between maternal DURING PREGNANCY tobacco exposure, both active and passive, and congenital The pregnancy risk assessment monitoring system heart defects. This article presents recent evidence (PRAMS) administered by the Centers for Disease supporting the association between intrauterine cigarette Control and Prevention in collaboration with state smoke exposure in the periconceptional period and health departments, is a state- and population-based congenital heart defects and discusses clinical implications surveillance system that monitors selected self-reported for practice for perinatal and neonatal nurses. behaviors occurring during the 3 months before, during, Key Words: congenital heart defect etiology, intrauterine and the 3 months after pregnancy. According to PRAMS tobacco smoke exposure, maternal smoking in pregnancy, data, the prevalence of maternal smoking before and second-hand smoke in pregnancy during pregnancy is 24.7% and 12.3%, respectively.4 Infants of women who smoke are nearly twice as likely to be preterm and are at higher risk of being small- moking during pregnancy is likely the most for-gestation and low birth weight.5,6 Other fetal and modifiable behavior associated with detrimen- neonatal complications associated with smoking during Stal pregnancy and childhood health outcomes. pregnancy include intrauterine demise, neonatal death, Fetal exposure to second-hand smoke (SHS) is also and respiratory disease.5 Musculoskeletal defects, limb harmful to the fetus. Among the deleterious effects of reduction defects, missing or extra digit defects, intrauterine tobacco smoke exposure is the develop- clubfoot, craniosynostosis, facial defects, eye defects, ment of congenital heart defects (CHDs). The incidence gastrointestinal defects, oral clefts and many other 1 of CHDs is 6 to 8 per 1000 births, and worldwide, birth defects are associated with maternal smoking 2 1.35 million newborns are born with a CHD each year. in pregnancy.7 Problems, including type I diabetes mellitus and visual problems, may develop after the Author Affiliation: University of Texas Medical Branch, Galveston. neonatal period.8,9 Pregnant nonsmokers exposed to Disclosure: The authors have disclosed that they have no significant SHS during the pregnancy may be affected. Adverse relationships with, or financial interest in, any commercial companies pregnancy and fetal and neonatal outcomes associated pertaining to this article. with maternal exposure to SHS include stillbirth, Corresponding Author: Sharron Forest, DNP, RN, NNP-BC, University of Texas Medical Branch, 301 University Blvd, Galveston, TX 77555 preterm birth, low birth weight, reduced gross motor ([email protected]). function, and congenital malformations including 10–14 Submitted for publication: August 5, 2015; accepted for publication: CHDs. Fetal and neonatal health outcomes improve November 29, 2015 when mothers quit smoking at any time during the 54 www.jpnnjournal.com January/March 2016 Copyright © 2016 Wolters Kluwer Health, Inc. Unauthorized reproduction of this article is prohibited. pregnancy; unfortunately, the developing fetal heart Cardiac anomalies make up the largest category of is susceptible to the harmful effects of intrauterine birth defects. The exact mechanism by which smok- cigarette smoke exposure early in pregnancy. ing is related to CHD is not fully understood. Alter- ations and variations in genes contribute to the ori- gin of CHDs.19 More than 85% of CHDs are thought VULNERABILITY OF THE DEVELOPING HEART to be the result of a complex interaction between ma- The fetal heart begins to work toward full develop- ternal exposures to environmental toxins and genetic ment by 16 days postconception. The earliest indica- susceptibilities.20 An estimated 2% of CHDs are related tion of heart development is the development of the to environmental toxins,15 andasmuchas1.4%ofCHDs cardiogenic cords. Cords of mesenchymal cells become may be attributed to maternal smoking in pregnancy.14 canalized early to form 2 thin-walled endothelial tubes Active and passive exposure to cigarette smoke called “endocardial heart tubes.” The tubes fuse to form during pregnancy exposes the fetus to more than 4000 a single heart tube. A series of constrictions and dila- chemicals, many of which are carcinogenic, mutagenic, tions develop distinct regions of the heart such as the or toxic.21,22 Carbon monoxide (CO), cadmium, and sinus venosus, the primitive atrium, the primitive ven- nicotine are environmental toxins found in cigarettes tricle, the bulbus cordis, and the truncus arteriosus. The and cigarette smoke that have adverse effects on the primitive heart tube grows rapidly and bends upon it- placenta and developing fetus.23–25 Carbon monoxide self to form a U-shaped bulboventricular loop. As the inhibits the blood’s ability to deliver oxygen to body development continues, the U-shaped heart loops into tissues and vital organs by binding to hemoglobin and an S-shaped heart. By the fifth week of gestation, the forming carboxyhemoglobin. Hemoglobin is subse- cardiac separation is complete and the heart is divided quently unavailable for transporting oxygen, resulting into a 4-chambered heart. Partitioning of the bulbus in a hypoxic environment for the fetus. Atrial septal cordis and the truncus arteriosus results in the devel- defects (ASDs), and conotruncal defects, particularly opment of the truncal ridges and bulbar ridges. The tetralogy of Fallot, are associated with CO exposure in fused mesenchymal ridges form the aorticopulmonary utero.23,26 Atrial septal defects occur between weeks septum that divides the truncus arteriosus and the bul- 4 and 5 of gestation.15 Conotruncal heart defects are bus cordis into the ascending aorta and the pulmonary also known as outflow tract defects. Common types trunk.15,16 Since most CHDs occur between the second of conotruncal heart defects are truncus arteriosus, and ninth week of gestation, the fetal heart is suscep- transposition of the great arteries, double outlet of tible to malformations due to teratogens, including to- the right ventricle, and tetralogy of Fallot. Conotruncal bacco smoke, before many women even suspect that heart defects occur between the 35th and 45th day they are pregnant.17 Table 1 describes CHDs associated of gestation.3,15 Cadmium accumulates in the placenta with fetal exposure to cigarette smoke. and inhibits the metabolism of cortisol, which results in Table 1. Congenital heart defects associated with intrauterine tobacco smoke exposure15,18 Congenital heart Gestational defect Description of defect Embryology timing Atrial septal Abnormal opening in the septal wall Ostium secundum defect—excessive 4-5 wk defect between the right and left atria cell death and resorption of the septum primum or inadequate development of the septum secundum Truncus The pulmonary artery and the aorta are Lack of truncal separation into the Approximately arteriosus a single vessel in the heart pulmonary artery and the aorta day 35 Transposition of The 2 main arteries carrying blood out Lack of rotation of the great vessels Approximately the great of the heart are switched in position after separation day 45 arteries Tetralogy of Fallot Combination of 4 defects, ventricular Incomplete rotation of the great Approximately septal defect, pulmonary stenosis, arteries, resulting in malalignment of day 45 right ventricular hypertrophy, and vessels with rightward deviation and overriding aorta a narrow right ventricular outflow tract Atrioventricular Deficiency of the atrioventricular Abnormal development of the Days 26-35 septal defect septum endocardial cushions The Journal of Perinatal & Neonatal Nursing www.jpnnjournal.com 55 Copyright © 2016 Wolters Kluwer Health, Inc. Unauthorized reproduction of this article is prohibited. fetal growth restriction.25 Fetal growth restriction may mothers. There were several limitations of this study, be an indication of poor perfusion and fetal hypoxia. which include the following: the researchers were un- Nicotine also contributes to hypoxia. Blood flow to the able to confirm CHD diagnoses in the medical record, placenta is restricted secondary to the vasoconstrictive and using International Classification of Diseases, Ninth effects of catecholamines released from the adrenals Revision, discharge codes may not have been reliable and
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