Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0020672 (hypothermia)
 17,327 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In pediatric cardiology tcPO2 is useful in monitoring cyanotic children given high-risk therapy such as balloon septostomy or drugs with controversial effects such as tolazoline in persistent fetal circulation. tcPO2 during administration of 100% oxygen enables a rapid, noninvasive differentiation between cyanosis due to intracardiac right-to-left shunt and that due to low cardiac output or pulmonary ventilation or diffusion difficulty. The size of the right-to-left shunt can be roughly estimated from the highest value of tcPO2, this estimation being influenced by anemia, hypothermia, and acidosis, among other factors. A trend of the tcPO2 rise is evident 90 seconds after the beginning of oxygen breathing. If tcPO2 does not rise at least 40 mm Hg over the initial value, a significant right-to-left shunt must be suspected. Interpretation of tcPO2 rise is difficult in dynamic right-to-left shunt, changing with oxygen breathing.
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PMID:tcPO2 in pediatric cardiology: application during balloon septostomy, tolazoline administration, and in children with right-to-left shunt. 53 16

Compared with whole body cooling (WBC), selective head cooling (SHC) of asphyxiated newborns presumably allows effective brain cooling with less systemic hypothermia and potentially fewer systemic adverse effects. It is not known if pulmonary dysfunction, one of the potential adverse systemic effects of therapeutic hypothermic neuroprotection, differs with the method of cooling. We sought to investigate if pulmonary mechanics and gas exchange during therapeutic hypothermia differ between WBC and SHC. The severity of pulmonary dysfunction was determined in 59 asphyxiated newborns receiving therapeutic hypothermic neuroprotection by either SHC ( N = 31) or WBC ( N = 28). Ventilatory parameters and simultaneous alveolar-arterial oxygen gradient (A-a DO (2)) and partial pressure of carbon dioxide, arterial (PaCO (2)) were measured before the start of cooling (baseline), and at 4, 8, 12, 24, 48, and 72 hours of cooling. The diagnosis of persistent pulmonary hypertension of the newborn (PPHN) was established by echocardiography. Clinical monitoring and treatment during cooling, whether SHC or WBC, were similar. All (96%) but two infants (from the SHC group) required mechanical ventilation of varying duration during cooling, and nine infants (15%) developed PPHN. The baseline ventilator pressures requirement, and A-a DO (2) were similar among the 48 ventilated infants without PPHN (WBC 23, SHC 25) at the start of cooling. Ventilatory requirements remained modest and did not differ with the method of cooling. Similar numbers of infants without PPHN were able to be extubated after improvement in respiratory status while being cooled (WBC 42.8% versus SHC 37.9%, P = 0.79, odds ratio [OR] 1.2, 95% confidence interval [CI] 0.4 to 3.5). Nine infants (WBC 5, SHC 4) developed PPHN. Six of the nine (WBC 4, SHC 2) required inhaled nitric oxide therapy, and one infant from the WBC group subsequently required extracorporeal membrane oxygenation. The incidence of PPHN was similar in both the WBC and SHC groups (17.8% versus 12.9%, P = 0.72, OR 1.5, 95% CI 0.3 to 6.1). Pulmonary dysfunction is common but not severe in asphyxiated infants during therapeutic hypothermia. Pulmonary mechanics and gas exchange do not differ with the method of achieving hypothermia.
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PMID:Pulmonary dysfunction and therapeutic hypothermia in asphyxiated newborns: whole body versus selective head cooling. 1902 Oct 92