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Computerised determination of spontaneous inspiratory and expiratory times during intermittent positive pressure ventilation
231
Tbe mechanical stability of newly forming septa during postnatal morphologic transformation from saccular to alveolar lung. D.G. TalberV’, D.G. Faganb, D.P. SouthallC,
aRoyal Postgraduate Medical School Institute of Obstetrics and Gynaecology, Queen Charlottes and Chelsea Hospital, Goldhawk Road, London W6 OXG, bDepartment of Histopathology, Queens Medical Centre, University Hospital, Nottingham NG7 2HU and ‘Academic Department of Paediatrics, University of Keele, North Staffordshire Hospital Centre, Stoke-on-Trent ST4 6QG, UK Burri and Weibel describe the postnatal transformation from saccular to alveolar lung as the forming of capillary loops over a central fibrous connective tissue core rising from the saccule walls [l]. Unlike mature alveolar walls, these primitive secondary septa are triple layer structures in which the crest fibrous support is only developing. They have been observed (post mortem) to have collapsed anisotropically against the sac walls [2], (alveolar septal collapse or ASC), masking capillaries and producing potential intra-pulmonary vascular shunt paths. While the dimensions of the structural elements can be studied by electron microscopy it is not feasible to study the micro-mechanics controlling this behaviour in vivo. Observational data from many sources has been linked in a computer model with graphical output to provide a substitute ‘test bed’ for experimentation. The relative strengths of the collapsing forces due to surface tension, and the support from elastin tibres developing within the septal crests, and pressures (pulmonary capillary and interstitial within the septal wall) were varied while observing the behaviour of the image produced. Under certain combinations of conditions collapse similar to that seen post mortem also occurred in the model. The model suggests ASC may increase lung recoil, but involves no immediate change in lung volume. ASC would be radiographically undetectable. Predisposing factors would be damage to the surfactant system and lack of sufficient tibril development to provide adequate support against existing surface tension. Acute precipitating factors would be expiration or pulmonary arteriolar vasoconstriction. 1 2
Burri, P.H. and Weibel, E.R. (1977): Lung ultrastructure and Lung, pp. 215-268. Editors: W.A. Hodson. Marcel Dekker, Fagan, D and Emery, J.L. (1970): Pulmonary inflation: a pearance and abnormal pressure-volume curves. Arch. Dis.
morphometry In: Development of the NY. correlation between histological apChild., 45, 145-146.
Computerised determination of spontaneous inspiratory and expiratory times during intermittent positive pressure ventilation. J.S. Ahluwalia, J.N.A. Mockridge and C.J.
Morley, University of Cambridge, Department of Paediatrics, Addenbrookes Hospital, CB2 2QQ, UK. Most unparalysed, preterm infants, ventilated for RDS, make spontaneous respiratory effort. A computerised system has been developed for on-line determination of spontaneous inspiratory (Ti) and expiratory (Te) times. A Graseby capsule, applied to the sub-xiphisternum, provides a signal of spontaneous respiratory effort, with little influence from the ventilator [ 11.Purpose-written
232
software analyses this waveform, to determine Ti and Te. Algorithms reject artefacts. The software has previously been validated using a pneumotach [2]. Twenty neonates (median birthweight 1477 g, median gestation 30 weeks), with RDS were studied during IPPV, for up to 30 min. Ventilator times and measured spontaneous Ti and Te (in seconds) are shown below. Time
Median
Ventilator Spontaneous
0.33 (0.30-0.45) 0.30 (0.26-0.33)
Ti (range)
Median
Te (range)
0.43 (0.3-1.2) 0.47 (0.33-0.65)
A method of determining respiratory timings has been developed for use during IPPV. Initial results show that infants breathe with a range of timings, that may be different from ventilator settings. This system will be a useful tool in further studies of infant and ventilator interactions, and has therapeutic potential. I 2
South, M. and Morley, C.J. (1986): Arch. Dis. Child, 61, 291-294 Mockridge, J.N.A. and Morley, C.J. (1991): Proceedings Fourth International and Neonatal Physiological Measurements, 261-264.
Conference
on Foetal
Metabolic Cost of Fever in the Newborn Rabbit. J. McIntyre, J. Vinter and D. Hull,
Department of Child Health, University Hospital, Nottingham, NG7 2UH, UK. Background: Metabolic rate often increases during a fever and contributes to a negative energy balance [ 11. It is usually considered to be due to an increase in biochemical reaction rates as a consequence of the higher temperature, the so called QlO effect. However, it may also be explained as a thermogenic response to a changed thermoregulatory set point. Methods: Fever was induced in newborn rabbits by injecting endotoxin. Oxygen consumption (VOz) and colonic temperature (Tc) were recorded prior to injection of endotoxin at a thermoneutral temperature (37°C). After injection of endotoxin, Tc and V02 were recorded for a further 270 min. In group one (n = 8) the environmental temperature was unchanged. In group two (n = 8) the environmental temperature raised to 39°C. Results: Prior to injection of endotoxin the mean Tc and VOz in each group was similar. In group one the mean increase in Tc was 1.O”C(P = 0.0009). In group two, the mean rise in Tc (2.2”C, P = 0.0001) was significantly greater (P = 0.006). Group one had a biphasic increase in VOz with a peak mean rise of 12.8 ml kg-‘min-’ (P = 0.0001). The V02 in group two did not change significantly. Conclusion: If left in the initial thermoneutral environment, newborn rabbits during a fever increase Tc and metabolic rate. If placed in a thermoneutral environment for a fever, they have a significantly higher Tc but do not increase metabolic rate. We find no evidence to support the concept of fever increasing metabolic rate due to a QlO effect. Providing an appropriate thermoneutral environment for a febrile infant may reduce the metabolic cost of their illness. 1
Baracos,
Y.E., Whitmore,
W.T. and Gale, R. (1987): Can. J. Physiol.
Pharmacol.,
65, 1248-1254.
Tbe mechanical stability of newly forming septa during postnatal morphologic transformation from saccular to alveolar lung. D.G. TalberV’, D.G. Faganb, D.P. SouthallC,
aRoyal Postgraduate Medical School Institute of Obstetrics and Gynaecology, Queen Charlottes and Chelsea Hospital, Goldhawk Road, London W6 OXG, bDepartment of Histopathology, Queens Medical Centre, University Hospital, Nottingham NG7 2HU and ‘Academic Department of Paediatrics, University of Keele, North Staffordshire Hospital Centre, Stoke-on-Trent ST4 6QG, UK Burri and Weibel describe the postnatal transformation from saccular to alveolar lung as the forming of capillary loops over a central fibrous connective tissue core rising from the saccule walls [l]. Unlike mature alveolar walls, these primitive secondary septa are triple layer structures in which the crest fibrous support is only developing. They have been observed (post mortem) to have collapsed anisotropically against the sac walls [2], (alveolar septal collapse or ASC), masking capillaries and producing potential intra-pulmonary vascular shunt paths. While the dimensions of the structural elements can be studied by electron microscopy it is not feasible to study the micro-mechanics controlling this behaviour in vivo. Observational data from many sources has been linked in a computer model with graphical output to provide a substitute ‘test bed’ for experimentation. The relative strengths of the collapsing forces due to surface tension, and the support from elastin tibres developing within the septal crests, and pressures (pulmonary capillary and interstitial within the septal wall) were varied while observing the behaviour of the image produced. Under certain combinations of conditions collapse similar to that seen post mortem also occurred in the model. The model suggests ASC may increase lung recoil, but involves no immediate change in lung volume. ASC would be radiographically undetectable. Predisposing factors would be damage to the surfactant system and lack of sufficient tibril development to provide adequate support against existing surface tension. Acute precipitating factors would be expiration or pulmonary arteriolar vasoconstriction. 1 2
Burri, P.H. and Weibel, E.R. (1977): Lung ultrastructure and Lung, pp. 215-268. Editors: W.A. Hodson. Marcel Dekker, Fagan, D and Emery, J.L. (1970): Pulmonary inflation: a pearance and abnormal pressure-volume curves. Arch. Dis.
morphometry In: Development of the NY. correlation between histological apChild., 45, 145-146.
Computerised determination of spontaneous inspiratory and expiratory times during intermittent positive pressure ventilation. J.S. Ahluwalia, J.N.A. Mockridge and C.J.
Morley, University of Cambridge, Department of Paediatrics, Addenbrookes Hospital, CB2 2QQ, UK. Most unparalysed, preterm infants, ventilated for RDS, make spontaneous respiratory effort. A computerised system has been developed for on-line determination of spontaneous inspiratory (Ti) and expiratory (Te) times. A Graseby capsule, applied to the sub-xiphisternum, provides a signal of spontaneous respiratory effort, with little influence from the ventilator [ 11.Purpose-written
232
software analyses this waveform, to determine Ti and Te. Algorithms reject artefacts. The software has previously been validated using a pneumotach [2]. Twenty neonates (median birthweight 1477 g, median gestation 30 weeks), with RDS were studied during IPPV, for up to 30 min. Ventilator times and measured spontaneous Ti and Te (in seconds) are shown below. Time
Median
Ventilator Spontaneous
0.33 (0.30-0.45) 0.30 (0.26-0.33)
Ti (range)
Median
Te (range)
0.43 (0.3-1.2) 0.47 (0.33-0.65)
A method of determining respiratory timings has been developed for use during IPPV. Initial results show that infants breathe with a range of timings, that may be different from ventilator settings. This system will be a useful tool in further studies of infant and ventilator interactions, and has therapeutic potential. I 2
South, M. and Morley, C.J. (1986): Arch. Dis. Child, 61, 291-294 Mockridge, J.N.A. and Morley, C.J. (1991): Proceedings Fourth International and Neonatal Physiological Measurements, 261-264.
Conference
on Foetal
Metabolic Cost of Fever in the Newborn Rabbit. J. McIntyre, J. Vinter and D. Hull,
Department of Child Health, University Hospital, Nottingham, NG7 2UH, UK. Background: Metabolic rate often increases during a fever and contributes to a negative energy balance [ 11. It is usually considered to be due to an increase in biochemical reaction rates as a consequence of the higher temperature, the so called QlO effect. However, it may also be explained as a thermogenic response to a changed thermoregulatory set point. Methods: Fever was induced in newborn rabbits by injecting endotoxin. Oxygen consumption (VOz) and colonic temperature (Tc) were recorded prior to injection of endotoxin at a thermoneutral temperature (37°C). After injection of endotoxin, Tc and V02 were recorded for a further 270 min. In group one (n = 8) the environmental temperature was unchanged. In group two (n = 8) the environmental temperature raised to 39°C. Results: Prior to injection of endotoxin the mean Tc and VOz in each group was similar. In group one the mean increase in Tc was 1.O”C(P = 0.0009). In group two, the mean rise in Tc (2.2”C, P = 0.0001) was significantly greater (P = 0.006). Group one had a biphasic increase in VOz with a peak mean rise of 12.8 ml kg-‘min-’ (P = 0.0001). The V02 in group two did not change significantly. Conclusion: If left in the initial thermoneutral environment, newborn rabbits during a fever increase Tc and metabolic rate. If placed in a thermoneutral environment for a fever, they have a significantly higher Tc but do not increase metabolic rate. We find no evidence to support the concept of fever increasing metabolic rate due to a QlO effect. Providing an appropriate thermoneutral environment for a febrile infant may reduce the metabolic cost of their illness. 1
Baracos,
Y.E., Whitmore,
W.T. and Gale, R. (1987): Can. J. Physiol.
Pharmacol.,
65, 1248-1254.