Prophylactic surfactant supplementation does not fully protect against the harmful effect of large lung inflations during a short sensitive period immediately after birth.
Lung recruitment at birth does not improve the response to surfactant in immature lambs, but may instead have an adverse effect on lung function and morphology.
In surfactant-treated premature lambs the pressures at LIP and UIPexp are not related, showing that LIP does not indicate the pressure at which airways collapse.
The mechanical behavior of the lung and chest wall has not been determined in preschool children. We therefore obtained static expiratory pressure-volume (P-V) curves of the respiratory system, partitioned into lung and chest wall components using esophageal (Pes) and airway pressure (Paw) registration in 17 anesthetized children (0.2 to 15.5 yr) in the supine and lateral position. From the P-V curves the inspiratory capacity (IC), the chest wall elastance (Ecw), and the maximal compliance of the respiratory system (Crs) and lungs (C(lung)) were calculated and related to growth. At IC (Paw = 30 cm H(2)O), Pes was the same in the two positions: 11 +/- 3 cm H(2)O. In contrast, at end-expiration (Paw = 0), Pes was close to zero in the lateral position, but markedly positive in the supine position (7 +/- 2 cm H(2)O). C(lung) was similar in both positions and increased with growth. Thus, C(lung) in the lateral position (ml/cm H(2)O) = 0.0017 x length(2.26) (cm), r(2) = 0.90. Crs and IC were approximately 20% greater (p = 0.001) in the supine position than in the lateral, and correlated strongly (r(2) >/= 0.93) with power functions of length in both positions. Ecw expressed as a fraction of total respiratory system elastance (Ecw/Ers) was 33 +/- 12% in the lateral position and 12 +/- 16% supine (p < 0.001). We conclude that the respiratory mechanics in children correlated closely with body size and showed important differences between the supine and lateral positions.
Recent studies indicate a severely reduced coronary flow reserve (CFR) in neonates with congenital heart disease. The significance of these studies remains debatable, as the ability of the anatomically normal neonatal heart to increase coronary flow is currently unknown. This study was designed to establish normal values for CFR in newborns after administration of adenosine [pharmacologic CFR (pCFR)] and as induced by acute hypoxemia (reactive CFR). Thirteen mechanically ventilated newborn lambs were studied. Coronary flow velocities were measured in the proximal left anterior descending coronary artery before and after adenosine injection (140 and 280 g/kg i.v.) using an intracoronary 0.014-in Doppler flow-wire. Measurements were made at normal oxygen saturation (SaO 2 ) and during progressive hypoxemia induced by lowering the fraction of inspired oxygen. CFR was defined as the ratio of hyperemic to basal average peak flow velocity. In a hemodynamically stable situation with normal SaO 2 , pCFR was 3.0 Ϯ 0.5. pCFR decreased with increasing hypoxemia. Regression analysis showed a linear relation between SaO 2 and pCFR (R ϭ 0.86, p Ͻ 0.0001). Reactive CFR obtained at severe hypoxemia (SaO 2 Ͻ30%) was 4.2 Ϯ 0.8, and no significant further increase in coronary flow velocity occurred by administration of adenosine. Newborn lambs have a similar capacity to increase coronary flow in response to both pharmacologic and reactive stimuli as older subjects. Administration of adenosine does not reveal the full capacity of the newborn coronary circulation to increase flow, however, as the flow increase caused by severe hypoxemia is significantly more pronounced. Hemodynamic problems in the neonatal period, often related to congenital heart defects, may affect coronary blood flow (1-3). The coronary physiology in newborns has become of greater importance as cardiac surgery for congenital heart defects is increasingly performed in the neonatal period. Coronary flow reserve (CFR) has been found to be useful in evaluating the effects of cardiac disease and pathologic hemodynamic conditions on coronary flow dynamics in adults (4 -6). CFR is defined as the ratio of maximal coronary blood flow, as induced by reactive hyperemia or administration of vasodilators, divided by resting flow (4).Recent studies performed with positron emission tomography (PET) have shown low CFR in neonates and infants with congenital heart disease (1, 7). The significance of these studies remains debatable, as the ability of the anatomically normal neonatal heart to increase coronary flow is currently unknown (1, 7). The objective of this study was to provide normal values for CFR in the normal neonatal heart by administration of adenosine [pharmacologic CFR (pCFR)
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