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Objective. Volume guarantee (synchronized intermittent mandatory ventilation [SIMV]+VG) is a novel mode of SIMV for automatic adjustment of the peak inspiratory pressure to ensure a minimum set mechanical tidal volume ([V.sub.T mech]), The objective of this study was to compare the effects of SIMV+VG with conventional SIMV on ventilation and gas exchange in a group of very low birth weight infants recovering from acute respiratory failure. Methods. Nine infants were initially studied during 2 consecutive 60-minute ventilatory modalities of conventional SIMV (ventilator settings by clinical team) and SIMV+VG 4.5 ([V.sub.T mech] set at 4.5 mL/kg) in random order. Eight additional infants were studied during the same ventilatory modalities plus 1 additional epoch consisting of SIMV+VG 3.0 ([V.sub.T mech] set at 3.0 mL/kg). Results. Peak inspiratory pressure was significantly lower during SIMV+VG 3.0. Mean airway pressure, [V.sub.T mech], number of large [V.sub.T mech] (>7 mL/kg), and mechanical minute ventilation ([V'.sub.E]) were reduced during SIMV+VG 4.5 compared with SIMV and were further reduced during SIMV+VG 3.0. Spontaneous [V'.sub.E] increased during SIMV+VG 4.5 and was even higher during SIMV+VG 3.0. The resulting total [ V'.sub.E] was higher during both SIMV+VG modes compared with SIMV. Arterial oxygen saturation by pulse oximetry, transcutaneous carbon dioxide tension, and fraction of inspired oxygen did not differ significantly, although transcutaneous carbon dioxide tension increased slightly during SIMV+VG 3.0. Conclusions. The short-term use of SIMV+VG resulted in automatic weaning of the mechanical support and enhancement of the spontaneous respiratory effort while maintaining gas exchange relatively unchanged in comparison to conventional SIMV. Pediatrics 2002;110: 529-533; mechanical ventilation, patient triggered ventilation, weaning., ABBREVIATIONS. VLBW, very low birth weight; SIMV, synchronized intermittent mandatory ventilation; PIP, peak inspiratory pressure; VG, volume guarantee ventilation; [V.sub.T mech], mechanical tidal volume; PEEP, positive end-expiratory pressure; FI[O.sub.2], fraction [...]

ABSTRACT. The effect of aminophylline on lung function was studied in 14 premature infants with apnea (gestational age, 30.2 weeks; birth weight, 1,052 gm). The infants showed compromised pulmonary function with a large difference in alveolar-arterial PO[sub 2] gradient (83.9 mm Hg), a low normal lung compliance of 1.1 ml/cm H[sub 2]O x kg, and a normal inspiratory resistance of 45.3 cm H[sub 2]O/liter/sec. Aminophylline therapy did not change these functions significantly, but it decreased the incidence of apneic episodes from 29.7 to 4.4 per day. The effectiveness of aminophylline in treating apnea in premature infants must be related to its central stimulating effect and not to an improvement in lung function and oxygenation. [ABSTRACT FROM AUTHOR]

Abstract. Anemia may increase the risk of tissue hypoxia in preterm infants. This could lead to respiratory center depression and an increased risk for apnea. Heart rate and breathing pattern were recorded in 30 preterm infants (gestational age 30.0 +/- 2.3 weeks, postnatal age 46.6 +/- 20.8 days, and weight 1,438 +/- 266 g) before and after a transfusion of 10 mL/kg of packed RBCs. All infants were stable clinically, breathing room air, and free of prolonged apneic episodes. After transfusion, hematocrit levels increased from 27.0% +/- 2.5% to 35.8% +/4.7%. Heart rate decreased from 157.2 +/- 13.6 beats per minute to 148.4 +/- 13.9 beats per minute. There was no change in respiratory rate or BP. The duration of periodic breathing decreased significantly, as did the duration of the longest periodic breathing episode (P < .01). The number of respiratory pauses lasting 5 to 10 seconds and the number of pauses lasting 11 to 20 seconds also decreased significantly (P < .05). The total duration of respiratory pauses, excluding pauses during periodic breathing, were significantly lower after transfusion (P < .05), as was the number of episodes of bradycardia. These results indicate that preterm infants have a more irregular breathing pattern while anemic than after correction of the anemia. The irregular breathing pattern is probably caused by mild hypoxic respiratory center depression. [ABSTRACT FROM AUTHOR]

Abstract, It has been suggested that apnea of prematurity may be caused by "immaturity" of central control of breathing. To test the validity of this hypothesis tidal volume (V[sub T]), alveolar ventilation (V[sub A]), alveolar PCO[sub 2] (P[sub A]CO[sub 2]), esophageal pressure change, and the slope of the CO[sub 2] response curve (change AV[sub E] [minute ventilation]/change P[sub A]CO[sub 2]) were determined in 18 infants with apnea (mean of 32 episodes of more than 20 seconds duration per day) and in 18 healthy newborns used as control subjects. The infants were matched for birth weight (1,068 g v 1,065 g), gestational age (30.2 weeks v 30.2 weeks), and postnatal age (8.6 days v 8.3 days). The results were as follows: V[sub T] (4.4 +/- 1.0 mL/kg v 5.3 +/- 1.6 mL/kg), V[sub A] (96 +/- 21 mL/ kg/min v 129 +/- 33 mL/kg/min), P[sub A]CO[sub 2] (45.4 +/- 8.5 mm Hg v 35.6 +/- 4.7 mm Hg), esophageal pressure change (4.5 +/- 0.9 cm H[sub 2]O v 6.0 +/- 1.8 cm H[sub 2]O), change V[sub E]/change P[sub A]CO[sub 2](20.2 +/10.6 mL/min/kg/mm Hg CO[sub 2] v 40.7 +/-19.9 mL/min/kg/ mm Hg CO[sub 2]). There was a significant difference between infants with and without apnea for all measurements. The results indicate a decreased respiratory center output and a depressed ventilatoty response to CO[sub 2] in infants with apnea. As there was no difference between the two groups in pulmonary mechanics or oxygenation, the findings support the hypothesis that a central disturbance in regulation of breathing is the cause of apnea in these infants. [ABSTRACT FROM AUTHOR]

Abstract. Airway obstruction is a cause of apnea in preterm infants. The activity of protective respiratory reflexes was determined in 18 preterm infants with apnea (mean of 32 episodes of more than 20 seconds duration per day) and in 18 neonates without apnea used as control subjects. This was done in order to elucidate the role of respiratory reflexes in apnea of prematurity. The infants were matched for birth weight (1,068 g v 1,065 g), gestational age (30.2 weeks v 30.2 weeks), and postnatal age (8.6 days v 8.3 days). The airway occlusion technique was used to determine the inspiratory prolongation of the occluded breath and the effective elastance of the respiratory system. Inspiratory prolongation is a measure for the reflex influence on inspiratory duration, and effective elastance reflects load compensating ability. Inspiratory prolongation was 7.3% +/- 33.5% in infants with apnea and 30.6% +/- 22.7% in the control group (P < .025). Effective elastance was 1.1 +/- 0.5 cm H[sub 2]O/mL in the apneic group and 1.5 +/- 0.5 cm H[sub 2]O/mL in the infants without apnea (P < .025). The results indicate that during exposure to respiratory loads, the infants with apnea maintained inspiratory effort poorly and had a decreased ability for load compensation. Their respiratory reflexes were significantly more immature than the reflex activity of the infants without apnea. This functional immaturity of respiratory reflexes may be a contributing factor in the etiology of apnea of prematurity. [ABSTRACT FROM AUTHOR]

ABSTRACT. The effects of aminophylline on the respiratory center output were studied in 14 premature infants with idiopathic apnea. The mean birth weight was 1,052 gm, and the mean gestational age was 30.2 weeks. These infants had a normal expired volume per minute (VE) [291 ml/(min x kg)] and a normal esophageal pressure change per breath (4.5 cm H[sub 2]O); however, their alveolar ventilation per minute (VA) was decreased [89 ml/(min x kg)], resulting in an elevated end-tidal PCO[sub 2] (P[sub A]CO[sub 2]) [47.8 mm Hg]. The reasons for the elevated P[sub A]CO[sub 2] were the relatively large anatomical dead spaces (VD) found in these infants (3.4 ml/kg), and a decreased slope of the CO[sub 2] response curve [22.2 ml/ (min x kg x mm Hg P[sub A]CO[sub 2])], with a shift of the curve to the right. Oxygen consumption was normal [7.0 ml/(min x kg)]. Forty-eight hours after initiating treatment with aminophylline (2 mg/kg of body weight every six hours), the incidence of apneic episodes decreased from 29.7 to 4.4 per 24 hours, VA and P[sub A]CO[sub 2] became normal secondary to a 33% increase in esophageal pressure change per breath, and the position of the CO[sub 2] response curve showed a significant shift to the left without change in slope. Oxygen consumption increased 20% from basal value. These findings support the hypothesis that apnea in premature infants is related to an immature respiratory center characterized by a decreased output. Aminophylline probably increases respiratory center output by lowering the threshold of the central chemorecepter to CO[sub 2]. [ABSTRACT FROM AUTHOR]