Prolonged Apnea in the Preterm Infant is Not A Random Event

Abstract

We tested the hypothesis that in preterm infants, prolonged apneas (apneas > or = 20 sec) are not random events but are preceded by frequent and progressively longer respiratory pauses associated with changes in ventilatory variables. We studied 36 preterm infants with apnea [birth weight 1190 +/- 60 g (mean +/- SEM), study weight 1300 +/- 60 g, gestational age 28 +/- 1 weeks, and postnatal age 23 +/- 2 days]. A nosepiece with a flow-through system was used to measure ventilation and alveolar gases. Throughout the monitoring period for each infant we established 10-min moving "window of observation" followed by a 1-min interval examined for the detection of a prolonged apnea. Within the 10-min window, three variables were defined: the number of apneic episodes, the maximum length of a single apneic episode, and the total duration of apneic time. During the following minute (eleventh) the presence or absence of a prolonged apnea was determined. Chi-square test for a linear-trend in the rate of prolonged apnea and multiple logistic regression analysis showed that the relative risk of a prolonged apnea increases significantly from preceding periods without apnea to preceding periods containing the potential predictors of prolonged apnea. The strongest predictor was total duration of apneic time in the previous 10 min. When the 1 min before prolonged apnea was compared with the 1 min of similar sleep state not having prolonged apnea, minute ventilation decreased, primarily due to a decrease in respiratory frequency. Oxygen saturation decreased and alveolar PCO2 did not change. These findings suggest that prolonged apnea is not a random event but is preceded by a disturbance of the respiratory control system characterized by (1) frequent apneas of progressive duration, (2) decrease in respiratory minute volume and frequency, and (3) decreased O2 saturation.

Isocitrate supplementation promotes breathing generation, gasping, and autoresuscitation in neonatal mice

“…The original design of the protocol is supported by clinical observations that repeated exposure to hypoxia occur frequently during episodes of sleep apnea (Lavie et al, ; Charboneau et al, 1994; Cala et al, ; Monserrat et al, 1996) and that autoresuscitation can fail following repeated apneic episodes in infants that suffer from SIDS (Stevens, ; Poets et al, , Sridhar et al, ). We slightly modified the protocol by progressively increasing the duration of the hypoxic challenges based on the observation that repeated periods of hypoxia, often of increasing duration, are observed in preterm infants (Daily et al, ; Steinschneider, ; Rigatto and Brady, ,b; Al‐Saedi et al, ).…”

The impact of preterm adversity on cardiorespiratory function

“…Apnoeas in preterm infants can be profound due to their low respiratory reserve capacity coupled with their high metabolic demands, apnoeas induce temporary bradycardia and loss of reflex neural drive from the lung (Fyfe, Yiallourou, Wong, & Horne, ; Gerhardt & Bancalari, ). Apnoeas are commonly preceded by periods of hypoventilation (Adams, Zabaleta, & Sackner, ; Al‐Saedi et al., ; Poets & Southall, ). Although the carotid body is likely to be anatomically mature at birth (Hervonen & Korkala, ), it takes time for the preterm to establish hypoxic and CO 2 thresholds after birth, which usually occurs over a period of hours to days of life (Darnall, ; Williams et al., ), but this may be delayed in infants with recurrent apnoea (Katz‐Salamon, ).…”

A Primer on Apnea of Prematurity

“…24 Prolonged apnea episodes are not random events; they often follow periods of disturbed respiratory control and are characterized by significant drops in oxygen saturation, decreased minute ventilation and respiratory rate, and increased frequency of shorter apnea episodes. 25 Infants with prolonged apneas also have increased periodic breathing. 25 Pure central apnea results from depressed bulbopontine respiratory center output, as evidenced by the complete lack of respiratory muscle activity.…”

“…25 Infants with prolonged apneas also have increased periodic breathing. 25 Pure central apnea results from depressed bulbopontine respiratory center output, as evidenced by the complete lack of respiratory muscle activity. 4 Central apnea can be induced by the preterm infant's "normal" physiological responses to hypoxia, hypercapnia, or acidosis.…”