Myocardial injury and performance in hypoxaemic neonates: Effects of oxygen and carbon dioxide during reoxygenation : An experimental study in newborn pigs
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AbstractDefinition of asphyxia Asphyxia is a Greek term and means loss of pulse (1). There is no clear definition of the term, though perinatal asphyxia or birth asphyxia often is defined as impaired placental- or pulmonary oxygen delivery to the neonate. As a consequence the neonate is going through a period of hypoxaemia and hypercapnia with a subsequent respiratory and metabolic acidosis (1). In clinical work, the diagnosis of perinatal asphyxia predominantly is based on its consequences, and there is a general agreement that a combination of perinatal stress (i.e. fetal bradycardia, acidosis, low Apgar scores), multiple organ affection and neurological symptoms (i.e. hypoxic ischemic encephalopathy) are required for the diagnosis (2).
Cardiac abnormalities in perinatal asphyxia. Myocardial performance may vary subsequent to asphyxia. The cardiac dysfunction is often underdiagnosed and requires a high index of suspicion to detect (3;4). The clinical picture varies from brady- or tachycardia to cardiogenic shock (1;5).
Myocardial failure subsequent to asphyxia was first reported in 1961 (6). The authors described a group of asphyxiated neonates with left ventricular (LV) heart failure within the first 24 hours of life. A decade later three term infants were reported with a syndrome of acute LV failure accompanied by cyanosis and pulmonary and systemic venous congestion (7). Rowe et al. (8) classified the cardiac abnormalities following asphyxia in 1978, broadly as:
1) Transient myocardial ischaemia of the newborn
2) Transient mitral regurgitation of the newborn
3) Transient tricuspid regurgitation of the newborn
4) Persistent pulmonary hypertension of the newborn
Increased pulmonary artery pressure (PAP) and tricuspid regurgitation is the most common, and although the cardiac abnormalities were described as separate clinical entities, it is important to understand that the distinction may not be clear, and there is much overlap in the pathogenesis. In severely asphyxiated neonates post-mortem autopsies have showed ischemic papillary muscle necrosis and diffuse subendocardial left ventricular (LV) necrosis secondary to perinatal asphyxia (9;10).
The aetiology of asphyxia in the newborn is multifactorial, including abruption or infarction of the placenta, excessive uterine contraction, fetal or maternal bleeding, and compression of the umbilical cord. Infection is contributing to its severity, and the clinical picture in severe asphyxia may present similar to what is seen in severe congenital heart disease, thus it is mandatory to evaluate these neonates by echocardiography to exclude congenital heart disease.
Publications included in the thesis
I. Børke W.B., Munkeby B.H., Mørkrid L., Thaulow E., Saugstad O.D., Resuscitation with 100% O2 does not protect the myocardium in hypoxic newborn piglets. Archives Dis Child 2004; 89(2)F156-F160 Abstract
II: Fugelseth D., Børke W.B., Lenes K., Matthews I., Saugstad O.D., Thaulow E., Restoration of cardio-pulmonary functions with 21% vs. 100% O2 after hypoxaemia in newborn pigs. Arch Dis Child Fetal Neonatal Ed. 2005 May;90(3):F229-f234 Abstract
III. Børke W.B., Munkeby B.H., Halvorsen B., Bjørnland K., Tunheim S.H., Borge G.I.A, Thaulow E., Saugstad O.D., Increased myocardial matrix metalloproteinases in hypoxemic newborn pigs during resuscitation. Effects of oxygen and carbon dioxide. Eur J Clin Invest 2004; 34(7):459-466 Abstract
IV: Børke W.B., Edvardsen T., Fugelseth D., Lenes K., Ihlen H., Saugstad O.D., Thaulow E., Reduced left ventricular function in hypoxemic newborn pigs. A strain Doppler echocardiographic study. Submitted