mal pulmonary function at the time of brain death may have declines in functioning, and only 15% to 20% of these patients' lungs are subsequently suitable for transplantation. 1-3 This may result from the pulmonary damage associated with brain injury 4 or the iatrogenic effects of mechanical ventilation. 5,6 There is evidence in various settings demonstrating that a lung protective strategy is beneficial. In patients with acute lung injury, ventilation See also pp 2592 and 2643 and Patient Page.
The case series consisted of ten children, ranged in age from one to three years (median 1.8 yrs), and in body weight from 10.2 to 13.5 kg (median 11.7 kg), in ASA class 1 or 2, all without lung disease. Having undergone general anaesthesia for cranial or abdominal CT scans, the patients were studied for pulmonary morphology. The first pulmonary CT scan was taken five min after induction of general inhalational anaesthesia; preoxygenation was avoided and an intraoperative FiO2=0.4 was used. Densities in dependent regions of both lungs were observed in all children. After ventilation with PEEP of 5 cmH2O, all the observed densities disappeared without impairment of heart rate, blood pressure, haemoglobin saturation and endtidal CO2 (PECO2). We conclude that the appearance in children of atelectasis cannot be explained by a reabsorption of O2 mechanism and by denitrogenation. However, a PEEP of 5 cmH2O is able both to recruit all the available alveolar units, and to induce the disappearance of atelectasis in dependent lung regions.
The case series consisted of ten children, ranged in age from one to three years (median 1.8 yrs), and in body weight from 10.2 to 13.5 kg (median 11.7 kg), in ASA class 1 or 2, all without lung disease. Having undergone general anaesthesia for cranial or abdominal CT scans, the patients were studied for pulmonary morphology. The first pulmonary CT scan was taken five min after induction of general inhalational anaesthesia; preoxygenation was avoided and an intraoperative FiO2=0.4 was used. Densities in dependent regions of both lungs were observed in all children. After ventilation with PEEP of 5 cmH2O, all the observed densities disappeared without impairment of heart rate, blood pressure, haemoglobin saturation and endtidal CO2 (PECO2). We conclude that the appearance in children of atelectasis cannot be explained by a reabsorption of O2 mechanism and by denitrogenation. However, a PEEP of 5 cmH2O is able both to recruit all the available alveolar units, and to induce the disappearance of atelectasis in dependent lung regions.
Peribronchial edema has been proposed as a mechanism enhancing airway responses to constrictor stimuli. Acute exposure to altitude in nonacclimatized lowlanders leads to subclinical interstitial pulmonary edema that lasts for several days after ascent, as suggested by changes in lung mechanics. We, therefore, investigated whether changes in lung mechanics consistent with fluid accumulation at high altitude within the lungs are associated with changes in airway responses to methacholine or exercise. Fourteen healthy subjects were studied at 4,559 and at 120 m above sea level. At high altitude, both static and dynamic lung compliances and respiratory reactance at 5 Hz significantly decreased, suggestive of interstitial pulmonary edema. Resting minute ventilation significantly increased by approximately 30%. Compared with sea level, inhalation of methacholine at high altitude caused a similar reduction of partial forced expiratory flow but less reduction of maximal forced expiratory flow, less increments of pulmonary resistance and respiratory resistance at 5 Hz, and similar effects of deep breath on pulmonary and respiratory resistance. During maximal incremental exercise at high altitude, partial forced expiratory flow gradually increased with the increase in minute ventilation similarly to sea level but both achieved higher values at peak exercise. In conclusion, airway responsiveness to methacholine at high altitude is well preserved despite the occurrence of interstitial pulmonary edema. We suggest that this may be the result of the increase in resting minute ventilation opposing the effects and/or the development of airway smooth muscle force, reduced gas density, and well preserved airway-to-parenchyma interdependence.
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