ABSTRACT:We investigated return of spontaneous circulation and of cerebral oxygenation after asphyxia-induced cardiac arrest, using ventilation with air, throughout, or with 100% oxygen for a shorter or longer period. Arterial pressure, heart rate, regional cerebral oxygen saturation (CrS O2 ), and brain tissue oxygen tension (Pbt O2 ) were measured in 1-d-old piglets that were hypoventilated with air and left in apnea until cardiac arrest. They were randomly assigned to be resuscitated with air (n ϭ 13), or with oxygen for 3 (n ϭ 12) or 30 min (n ϭ 13) and then with air. Nine, 10, and 10 animals, respectively, needed closed chest cardiac massage. One, none, and one, respectively, died. Median (quartile range) times from start of ventilation until heart rate reached 150 bpm were 67 (60 -76), 88 (76 -126), and 68 (56 -81) s. They were not significantly different, nor were the arterial pressure responses, times until CrS O2 reached 30%, or times until Pbt O2 had increased by 0.1 kPa from its nadir. Peak Pbt O2 values during resuscitation T he optimal fraction of inspired O 2 (FiO 2 ) for resuscitation of asphyxiated neonates is still not settled, although clinical and experimental evidences indicate that 21% is superior to 100% (1-4). In most of these studies, the time of exposure to pure oxygen exceeded 5 min, and it is unknown whether a very brief exposure to high FiO 2 at the start of resuscitation might improve myocardial oxygenation and hasten the return of adequate heart function without causing an organ damage.In three studies of experimental asphyxia (5-7), arterial pressure was restored as quickly by air ventilation as with 100% oxygen. However, few of the animals in these studies needed closed chest cardiac massage (CCCM), and the possibility remains that subjects with asphyxia, so severe that CCCM is needed, might be easier to resuscitate with a high FiO 2 . We tested this in 1-d-old piglets in cardiac arrest caused by severe asphyxia and hypothesized that ventilation with 100% oxygen would restore heart rate (HR) and arterial pressure faster than would ventilation with air. In addition, return of cerebral oxygenation was analyzed, by measuring regional oxygen saturation (CrS O2 ) and brain tissue oxygen tension (Pbt O2 ). The asphyxia was induced by hypoventilation followed by apnea to achieve the high blood PCO 2 levels that are characteristic of severe clinical perinatal asphyxia (8).Because the Pbt O2 is relevant to the question whether a high FiO 2 after asphyxia might cause brain damage, we extended the recording of brain oxygenation beyond the immediate resuscitation phase. Ventilation with 100% oxygen was limited to 3 min in some animals to see whether this could avoid cerebral hyperoxia. METHODSThis study was approved by the Animal Ethics Research Committee of Lund University. The animals were cared for and handled in accordance with European Guidelines for Use of Experimental Animals.Animal preparation. Thirty-eight domestic piglets (12-to 36-h old) were premedicated with intramuscular ketamin...

ABSTRACT:The optimal inhaled oxygen fraction for newborn resuscitation is still not settled. We hypothesized that short-lasting oxygen ventilation after intrauterine asphyxia would not cause arterial or cerebral hyperoxia, and therefore be innocuous. The umbilical cord of fetal sheep was clamped and 10 min later, after delivery, ventilation with air (n ϭ 7) or with 100% oxygen for 3 (n ϭ 6) or 30 min (n ϭ 5), followed by air, was started. Among the 11 lambs given 100% oxygen, oxygen tension (P O2 ) was 10.7 (1.8 -56) kPa [median (range)] in arterial samples taken after 2.5 min of ventilation. In those ventilated with 100% oxygen for 30 min, brain tissue P O2 (Pbt O2 ) increased from less than 0.1 kPa in each lamb to individual maxima of 56 (30 -61) kPa, whereas in those given oxygen for just 3 min, Pbt O2 peaked at 4.2 (2.9 -46) kPa. The maximal Pbt O2 in airventilated lambs was 2.9 (0.8 -5.4) kPa. Heart rate and blood pressure increased equally fast in the three groups. Thus, prolonged ventilation with 100% oxygen caused an increase in Pbt O2 of a magnitude previously only reported under hyperbaric conditions. Reducing the time of 100% oxygen ventilation to 3 min did not consistently avert systemic hyperoxia. (Pediatr Res 65: 57-61, 2009) C urrent guidelines from the International Liaison Committee on Resuscitation breathe considerable uncertainty as to how much supplementary oxygen should be given during resuscitation of newborn asphyxiated infants (1). Previous recommendations were to be generous with oxygen, but recent guidelines from a number of countries, e.g. Australia, Canada, Finland, the Netherlands, Sweden, and the United Kingdom recommend initial ventilation with air, because of the results from several experimental (2-5) and clinical (6 -13) studies indicating that resuscitation with 100% oxygen is harmful. In the clinical studies, the time of exposure to 100% oxygen was typically 5-7 min (8,13), whereas only one animal study (5) has investigated an exposure time to oxygen less than 15 min.We speculated that very short times of exposure might not allow systemic hyperoxia to develop and so be harmless to the newborn infant, except for a possible negative effect on the lungs. In fact, the pulse oximetric saturation at 3 min after birth is usually below 80% (14,15) in the normal air-breathing infant, suggesting the presence of cardiac or pulmonary rightto-left shunts. One might expect that such shunts would delay the appearance of arterial hyperoxemia in the infant breathing pure oxygen. However, this has been studied neither in normal nor in asphyxiated subjects.We used a sheep model of term intrauterine asphyxia with postnatal resuscitation, and hypothesized that hyperoxia of arterial blood and of brain tissue could be prevented by limiting the period of ventilation with 100% oxygen to 3 min. We also investigated whether the speed of circulatory recovery, as reflected by the heart rate (HR) and mean arterial blood pressure (MAP) responses, and the speed of recovery of brain oxygenation, as reflected ...

Radical pericardiectomy provided superior 10-year survival and clinical functional improvement in patients with chronic constrictive pericarditis compared to sub-total pericaridectomy.

Background Nasal continuous positive airway pressure support (nCPAP) is the standard of care for prematurely born infants at risk of neonatal respiratory distress syndrome (nRDS). However, nasal intermittent positive pressure ventilation (NIPPV) may be an alternative to nCPAP in babies requiring surfactant, and in conjunction with surfactant nebulization, it could theoretically reduce the need for invasive mechanical ventilation. We compared lung deposition of nebulized poractant in newborn piglets supported by nCPAP or NIPPV. Methods Twenty‐five sedated newborn piglets (1.2‐2.2 kg) received either nCPAP (3 cmH2O, n = 12) or NIPPV (3 cmH2O positive end expiratory pressure+3 cmH2O inspiratory pressure, n = 13) via custom‐made nasal prongs (FiO2 0.4, Servo‐i ventilator). Piglets received 200 mg kg−1 of technetium‐99m‐surfactant mixture continuously nebulized with a customized eFlow‐Neos investigational vibrating‐membrane nebulizer system. Blood gases were taken immediately before, during, and after nebulization. The deposition was estimated by gamma scintigraphy. Results Mean surfactant deposition in the lungs was 15.9 ± 11.9% [8.3, 23.5] (mean ± SD [95% CI]) in the nCPAP group and 21.6 ± 10% [15.6, 27.6] in the NIPPV group (P = .20). Respiratory rates were similar in both groups. Minute volume was 489 ± 203 [360, 617] in the nCPAP group and 780 ± 239 [636, 924] mL kg−1 min−1 in the NIPPV group (P = .009). Blood gases were comparable in both groups. Conclusion Irrespective of the noninvasive ventilatory support mode used, relatively high lung deposition rates of surfactant were achieved with nebulization. The amounts of deposited surfactant might suffice to elicit a pulmonary function improvement in the context of nRDS.