Cardiovascular and Neurophysiologic Changes during Graded Duration of Apnea in Piglets

Abstract

ABSTRACT. To examine the interrelationship between the duration of apnea and changes in oxygen saturation, blood pressure, electroencephalogram (EEG), and heart rate, reflex apnea of 10, 20, 40, and 60 s duration was induced by stimulating the superior laryngeal nerves. Piglets (n = 11, age 5-14 days) were chronically instrumented for continuous monitoring of SaOz and blood pressure and for sampling arterial blood. Ventilation was recorded using whole body plethysmography and EEG and electrocardiogram were measured by acutely placed subcutaneous electrodes. Central apnea produced an immediate rise in blood pressure and a decrease in SaOz by 20 s. By 30 s into the apnea, EEG amplitude had already decreased. Major cardiac slowing did not occur until 80 s after the start of apnea. Hyperoxia delayed the start of desaturation, hypertension, and EEG attenuation. These data suggest that during superior laryngeal nerve-induced apnea in young piglets: 1) desaturation can reach profound levels rapidly, 2) EEG amplitude decreases substantially and becomes nearly isoelectric within 1 min, and 3) bradycardia is a late manifestation when compared to changes in oxygen saturation, blood pressure, and EEG. Apnea is a common problem in neonatal intensive care units with an incidence of 80-90% in infants weighing less than 1000 g (1,2). The importance of this phenomenon stems from the fact that apnea has been associated with cyanosis, bradycardia, altered neurologic state (3-7), and recently, with decreased cereL-21 blood flow (8).Despite the importance of apnea as a potentially detrimental phenomenon (9), the time of onset and the sequence of physiologic changes associated with apnea are unclear. Some infants require intervention at 10-15 s into an apnea, whereas some observations suggest that hypotonia and other indications of cerebral dysfunction do not occur until 45 s (3, 10). Similarly, the latency of bradycardia and its relationship to oxygen satura- Received May 19, 1987; accepted December 11, 1987 4(tion is variable. Bradycardia may occur early into an apnea, at a time before significant desaturation (3, 1 1, 12), but also can occur late in 40% of protracted apneas (1 3) or after the onset of EEG supression (14).The purpose herein was to examine the sequence of neurologic and cardiovascular consequences of graded periods of apnea. Prolonged neonatal apnea can be of variable etiology such as central nervous system immaturity, infection, metabolic disturbances, IVH, airway obstruction, and vagal reflex. For our studies, we used laryngeal stimulation to induce a central apnea secondary to reflex effect. In this way, apnea duration could be controlled by the duration of stimulus presentation and the cause for central apnea was consistent among experimental animals. Experiments were conducted in piglets because they have a similar time course of brain development and cardiovascular control systems as infants. Inasmuch as unterminated respiratory pauses up to 80 s duration were examined, similar studies on human infants could ...

EEG Suppression Associated with Apneic Episodes in a Neonate

“…This is similar to the effects described in animal studies when hypoxia has been used to induce severe EEG suppression [11]. In piglets, EEG amplitude has been shown to decrease markedly after approximately 30 seconds of apnea induced by stimulation of the superior laryngeal nerves [11].…”

Changes in apnea and autoresuscitation in piglets after intravenous and intrathecal interleukin-1β injection

“…The rationale for using piglets in research involving apnea, hypoxemia and purine metabolism is that much experience has been obtained on piglet/ apnea research [23,24,26,31], and that canthine oxidase is present in the lungs of rat, dog, cat and sheep, but probably not to any extent in man and pig [1]. When xanthine oxidase is present in the lungs, hypoxanthine is cleared from the circulation even during severe hypoxemia [33].…”

“…The Hx and X levels in plasma, CSF, vitreous humor and urine were analyzed using a HPLC method [38,43] with modifications as previously described [30,31].…”

Prolonged Dynamic Changes in Autonomic Heart Rate Modulation Induced by Acid Laryngeal Stimulation in Non-Sedated Lambs

“…In addition, some studies suggest that the cardiovascular responses are induced to some extent by apnea and arterial chemoreflex with a primary hypertensive and bradycardic reflex response to SLN input, a baroreflex bradycardia secondary to the reflex increase in BP, and a chemoreflex bradycardia secondary to reflex apnea. Termination of the bradycardia secondary to apnea would depend on resumption of breathing movements or, more specifically, to lung inflation [1,6,8,12,13,33] . As indicated previously, we did not observe the full range of responses frequently described as part of the LCR, such as apnea and arousal.…”

“…Cardiovascular adaptation to chemical stimulation of the larynx has been scantily described with studies mainly focused on the initial response or the response associated with an ongoing prolonged stimulation [1,6,8,[12][13][14] . Consequently, bradycardia has generally been considered as a consequence of apnea rather than a direct response to laryngeal stimulation.…”