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Air trapping and alveolar hyperinflation may occur during mechanical ventilation in the presence of severe airway obstruction, during fast ventilator rates, and when expiratory time is compromised. Inadvertent positive end-expiratory pressure may occur with air trapping and increased mean airway pressure. The pulmonary artery pressure response to air trapping, produced during volume-regulated time-cycled ventilation, was studied in neonatal lamb lungs, isolated in situ, and perfused at a constant flow rate (50–75 ml.kg-1min-1), both before and after Ca2+-channel blockade with verapamil (5 mg). The hub of the endotracheal tube was narrowed to a 1.5-mm orifice to produce fixed proximal airway obstruction. Air trapping was then produced by lengthening inspiratory time from 25 to 80, at zero end-expiratory pressure. The magnitude of inadvertent positive end-expiratory pressure due to air trapping was estimated by end-expiratory occlusion pressure. End-expiratory occlusion pressure was 0.20 ≤ 0.03 kPa (1.7 ≤ 0.2 mm Hg) and 1.60 ≤ 0.01 kPa (11.8 ≤ 1.0 mm Hg), at 25 and 80 inspiratory times, respectively. On lengthening inspiratory time, mean pulmonary artery pressure (mPpa) increased briskly within 30 s followed by a gradual increase over the next 4 min. Verapamil blunted both the brisk and the gradual increase in mPpa on lengthening inspiratory time. Lengthening inspiratory time increased the mPpa by 2.0 ≤ 0.1 kPa (14.7 ≤ 0.8 mm Hg) from baseline, and verapamil reduced this increase to 1.3 ≤ 0.1 kPa (10.1 ≤ 0.6 mm Hg; p < 0.05 by analysis of variance). Verapamil did not affect changes in mean airway and peak inspiratory airway pressures and the magnitude of inadvertent positive end-expiratory pressure caused by lengthening inspiratory time. In the neonatal lamb, the Ca2+-channel-dependent portion of the mPpa response to air trapping amplifies the Ca2+-channel-independent portion, which represents the compressive effects of airway pressure on the pulmonary circulation.

Twenty-four children, aged 4 months to 16 years (nine patients 2 years old or younger), underwent balloon dilation angioplasty of hypoplastic or stenotic branch pulmonary arteries between July, 1981, and April, 1984. Most children had tetralogy of Fallot, with or without pulmonary atresia, or isolated peripheral pulmonary artery stenosis. Fifty-two dilations were attempted, 44 in the catheterization laboratory and eight in the operating room. Of these, 26 (50%) were judged successful; the average vessel diameter on angiogram increased from 4.1 ± 0.3 to 7.2 ± 0.3 mm (76%), the gradient across the narrowed segment fell from 60 ± 10 to 36 ± 5 mm (40%), pressure in the main pulmonary artery or right ventricle proximal to the obstruction decreased from 83 ± 10 to 66 ± 6 mm Hg (20%), and the radionuclide-determined fraction of cardiac output directed to the lung ipsilateral to the dilated pulmonary artery increased from 40 ± 4 to 51 ± 4 (28%). All changes were significant at the p < 0.005 level. Reasons for failure included inadequate technique (balloon too small, inability to position balloon or wire) in 14 and the refractory nature of the lesion itself in 11. Technical failures were age independent. Nondilatable lesions were more common in children more than 2 years old (10/25 versus 1/10) or with isolated peripheral pulmonary artery stenosis (5/7). Five of seven stenoses near previous shunts were nondilatable. One child exsanguinated when the pulmonary artery ruptured during dilation, but other complications were few. Eight dilations, followed up for an average of 6 months after dilation, showed angiographic persistence of improvement; two of four lesions were successfully redilated to a larger size. Balloon dilation angioplasty appears beneficial, both short and long term, for some patients with hypoplastic or stenotic branch pulmonary arteries, especially if performed early in life.

At the Children’s Hospital of Pittsburgh the extracorporeal membrane oxygenation program was started in 1980. The results of our experience from 1980 to 1985 were previously reported. In the past 2 years 39 additional newborn infants have been treated with this modality, with an overall survival rate of 79% (31/39). This survival rate is much better than that obtained in 33 neonates who had been treated in the previous 5 years (54%; p <0.05). A new aspect of our extracorporeal membrane oxygenation program is the use of total apneic lung rest for persisting pulmonary interstitial emphysema during support with the oxygenator. Six neonates were treated with this technique because of worsening pulmonary interstitial emphysema during extracorporeal circulation. Five of them survived. Another indication for extracorporeal membrane oxygenation in our pediatric population has been left ventricular or biventricular failure after cardiopulmonary bypass. Four of our seven patients treated for this indication are long-term survivors. At present, because of the impossibility of using other forms of left ventricular assist devices in the pediatric population, it seems that extracorporeal membrane oxygenation is the most effective treatment for left ventricular failure after cardiopulmonary bypass. From our experience, even in the absence of long-term follow-up of patients supported with extracorporeal membrane oxygenation, it appears that the benefits of this therapeutic modality far exceed the risks in the high-risk population for which it is being used.

We have shown that AAD reduces visceral blood flow(BF).cardiac index(CI), and urine output(UO) in the dog. To see if BF and UO could be restored by dopamine (D) and/or volume expansion (V), 7 chloralose anesthetized dogs had their abdomens distended with N2gas to 20 mmHg. Each experiment had five 30 minute steps––two distention control(C) periods and three intervention periods (D at 10μg/kg/min; V(D5LR) at 40 ml/kg/30'; or V+D). Left ventricular, pulmonary artery, aortic(Aop), inferior vena cava(IVC), and abdominal pressures were measured. Animals were sacrificed and renal cortical(ren), small bowel(sbo), and liver(lvr) samples obtained. BF was measured by radioactive microspheres. Results (X±SEM, *p<0.05 vs C; †p<0.01 vs C)In the presence of AAD, both V and D enhance abdominal visceral BF apparently in excess of their effects on driving pressure (Aop-IVC). UO and CI were significantly increased by V but unaltered by D. Thus, in the setting of AAD, V appears superior to D in restoring UO and systemic perfusion.

In children AAD often follows major trauma, surgery, or infection. We have shown that AAD reduced cardiac output 36% in the dog. This decrease in CO was attributed to either a decrease in contractility or actual fall in ventricular preload. To elucidate the mechanism of this change we studied the central hemodynamic effects of dopamine (D) and volume expansion (V) in dogs with AAD. 7 dogs were anesthetized, paralyzed, ventilated, and their abdomens distended by N2to mmHg. Animals were instrumented to measure right atrial, pulmonary artery wedge, left ventricle, aortic (Aop), and abdominal pressures and heart rate (HR). Each experiment had five 30 minute steps––two control distension (C) periods, three intervention periods (D at 10 μg/kg/min; V (D5LR) at 40 ml/kg/30'; or V+D). CO was measured and Systemic vascular resistance and stroke volume (SVR,SV) calculated. (Results X±SEM, *p<0.05 vs C; †p<0.01 vs C).V increased CO, SV, and decreased HR and SVR. D had little effect. These results suggest that the central hemodynamic effects of AAD are primarily due to reduced ventricular preload rather than diminished left ventricular contractility.