71 research outputs found
Como minimizar a lesão pulmonar no prematuro extremo: propostas
OBJETIVO: Apresentar uma revisão das principais causas da nova displasia broncopulmonar e as estratégias utilizadas para diminuir sua incidência nos prematuros extremos. FONTES DOS DADOS: Para essa revisão, pesquisas foram feitas na MEDLINE (1996 a outubro de 2004), no Cochrane Database, em resumos da Society for Pediatric Research e recentes conferências sobre o tema. SÍNTESE DOS DADOS: A tecnologia e os novos conhecimentos científicos têm aumentado significantemente a sobrevida de prematuros extremos. Esse aumento da sobrevida resultou em aumento da incidência de displasia broncopulmonar. Atualmente, a displasia broncopulmonar é mais freqüentemente observada em recém-nascidos < 1.200 g. As características da displasia broncopulmonar nesses prematuros extremos, atualmente chamada de "nova" displasia broncopulmonar, são bastante diferentes da clássica descrita por Northway. A nova displasia broncopulmonar tem etiologia multifatorial, como volutrauma, atelectrauma, toxicidade ao oxigênio e reação inflamatória. Terapias como corticosteróide pré-natal, surfactante exógeno, pressão aérea positiva contínua nasal, novos tipos de ventilação mecânica e uma ventilação mais gentil têm sido usadas para tentar diminuir a gravidade da lesão pulmonar. CONCLUSÕES: Para prevenir a lesão pulmonar em prematuros extremos, é necessário minimizar os vários fatores que desencadeiam a displasia broncopulmonar e utilizar estratégias terapêuticas menos agressivas. O melhor conhecimento desses fatores de risco da displasia broncopulmonar poderá gerar novas terapêuticas, que, conjuntamente com o tratamento utilizado atualmente para minimizar a lesão pulmonar, serão fundamentais para uma melhor evolução clínica desses prematuros extremos
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Role of Glycine on the Depressed Ventilatory Response to Hypoxia in Hypothermic Newborn Piglets ♦ 1781
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Hybrid algorithm for automatic regulation of mechanical ventilation in premature infants based on expert rules and proportional differential control
Mechanically ventilated premature infants present with fluctuations in ventilation that cannot be addressed by conventional mechanical ventilation with fixed positive pressure and constant frequency. A hybrid algorithm for automatic targeting of minute ventilation and tidal volume by individual or combined closed loop control of the ventilator frequency and peak inspiratory pressure was developed. The objective of this system is to minimize the mechanical support and adapt to changes in ventilatory need. Under the most challenging conditions, the combined controller is more efficient than individual control
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Effects of Intermittent Nebulization of NONOate, DPTA/NO, on Group B Streptococcus-Induced Pulmonary Hypertension in Newborn Piglets
Background: A single dose of NONOate attenuates pulmonary hypertension (PH) induced by group B Streptococcus (GBS) infusion and this is accompanied by a decrease in systemic vascular resistance (SVR). Objective: The objective of the study was to determine whether two doses of the NONOate sustain the attenuation in GBS-induced PH without further systemic compromise. Methods: 15 anesthetized newborn piglets were randomized to receive placebo (n = 8) or two doses of nebulized DPTA/NO (n = 7) at 15 and 75 min after GBS-induced PH. Pulmonary artery (Ppa) and systemic (Psa) pressures, cardiac output (CO) and arterial blood gases were obtained at baseline and every 15 min until 180 min during GBS infusion. Results: Ppa and pulmonary vascular resistance (PVR) decreased significantly after the first dose of nebulized DPTA/NO and this effect was maintained after the second dose. Psa and SVR decreased after the first dose of DPTA/NO to values close to baseline and no further changes in systemic circulation were observed with repeated treatment. PVR/SVR increased with GBS infusion, but decreased after the first dose of DPTA/NO and remained significantly lower for 180 min. CO was significantly higher in the DPTA/NO group. Changes in Ppa, PVR, Psa, SVR, and CO with GBS infusion were not modified by placebo infusion. PaCO2, base deficit, and pH did not differ between groups. PaO2 was significantly lower in the DPTA/NO group after the second dose. Conclusion: These data demonstrated that GBS-induced PH is attenuated with two doses of DPTA/NO without significant systemic effect. The vasodilatory effect is more pronounced in the pulmonary than in the systemic vasculature, as suggested by lower PVR/SVR in the DPTA/NO group. We speculate that NONOates may have a clinical application in the management of PH in neonates
Changes in Ventilation and Oxygen Consumption during Acute Hypoxia in Sedated Newborn Piglets
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Decreased ventilatory response to hypoxia in sedated newborn piglets prenatally exposed to cocaine
OBJECTIVE: Infants exposed to cocaine in utero have been reported to have a higher incidence of apnea and altered ventilatory response to carbon dioxide and hypoxia. We investigated whether in utero cocaine exposure results in greater ventilatory depression during hypoxia in piglets.
METHODS: Cocaine hydrochloride, 1.0 or 2.0 mg/kg given intramuscularly, or saline solution was administered daily to pair-fed pregnant sows during the last month of gestation. Thirteen cocaine-exposed piglets (mean ± SD: age, 4.4 ± 1.3 days; weight, 2.10 ± 0.10 kg) and 15 saline solution-exposed piglets (age, 4.6 ± 1.1 days; weight, 2.32 ± 0.42 kg) were studied under chloral hydrate sedation. Minute ventilation (v̇
E), arterial blood pressure (BP), heart rate (HR), oxygen consumption (v̇
O
2), and arterial blood gases were measured in room air. During hypoxia (fraction of inspired oxygen = 0.10), the values for v̇
E, BP, and HR were obtained at 1, 5, and 10 minutes, v̇
O
2 was calculated during the last 5 minutes, and arterial blood gas samples taken after 10 minutes.
RESULTS: Basal v̇
E did not differ between saline solution- and cocaine-exposed animals. The increase in v̇
E at 1 minute of hypoxia was also similar. However, at 5 and 10 minutes of hypoxia, v̇
E was significantly lower in the cocaine group than in the saline group (6% ± 9% and 4% ± 10% vs 15% ± 13% and 21% ± 14%;
p <0.02). Mean baseline BP and the initial increase in BP during hypoxia were not different between groups. However, BP remained increased throughout hypoxia only in the saline solution-exposed animals (
p
<0.05). Changes in HR, v̇
O
2, arterial oxygen tension, and base excess during hypoxia were similar between groups.
CONCLUSIONS: These results show a decrease in the ventilatory response to hypoxia in newborn piglets prenatally exposed to cocaine. This change is most likely to be centrally mediated because the initial hypoxic hyperventilation was not modified by the intrauterine cocaine exposure. This decrease in ventilation cannot be explained by changes in metabolic rate or in cardiovascular or acid-base status. (J P
EDIATR 1996;128:389-95
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