Impact of bradycardia on cerebral oxygenation and cerebral blood volume during apnoea in preterm infants

Pichler, Gerhard; Urlesberger, Berndt; Müller, Wilhelm

doi:10.1088/0967-3334/24/3/304

Cited by 47 publications

(30 citation statements)

References 26 publications

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“…Although some groups have studied the influence of apnea of prematurity on cerebral oxygenation [14,15,16,17,18,19,20,21,22,24,25], only two of them have focused on different types of events [18,22] and neither of the two reported cerebral StO 2 , but instead reported hemoglobin concentrations as a measure of cerebral blood volume. …”

Section: Discussionmentioning

confidence: 99%

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Cerebral Oxygenation during Intermittent Hypoxemia and Bradycardia in Preterm Infants

et al. 2014

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Background: Episodes of hypoxemia and bradycardia frequently occur with apnea of prematurity in preterm infants. Little is known about the impact of different event types on the brain. Objectives: To describe the influence of hypoxemia and bradycardia, either isolated or in combination, on cerebral oxygenation. Methods: In 16 preterm infants with intermittent hypoxemia and/or bradycardia, cerebral tissue oxygen saturation (StO₂, as measured by near-infrared spectroscopy), heart rate and pulse oximetric saturation (SpO₂) were recorded simultaneously for 16 h. Events were classified as isolated bradycardia (type 1), isolated hypoxemia (type 2) or combined (simultaneous, type 3; bradycardia first, type 4; hypoxemia first, type 5). Primary outcome was a score representing the area below baseline for cerebral StO₂ desaturation during an event. Secondary outcomes were duration and depth of cerebral desaturation. Results: Patients had a median (range) gestational age of 25.9 (22.6-30.4) weeks and a postnatal age of 32.5 (7-58) days. The median (quartiles) number of events was 49 (34-58). Isolated hypoxemias were the most frequent events (24; 9-36) and isolated bradycardias the least common (0; 0-1). Cerebral StO₂ baseline was not different between event types. Cerebral desaturation score, duration of event and depth of cerebral desaturation were smallest for isolated bradycardias and largest for combined events, especially for those starting with hypoxemia followed by bradycardia. Regardless of event type, 12/16 infants maintained cerebral StO₂ >60% despite severe SpO₂ desaturations. Conclusions: Isolated bradycardias had the lowest impact on cerebral desaturation, and combined events had the highest. Most infants preserved cerebral oxygenation >60% during events.

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Section: Discussionmentioning

confidence: 99%

“…However, little is known about the impact of different event types on cerebral StO 2 . Published studies focused on one type only or did not differentiate between event types [14,15,16,17,18,19,20,21,22]. …”

Section: Introductionmentioning

confidence: 99%

Cerebral Oxygenation during Intermittent Hypoxemia and Bradycardia in Preterm Infants

et al. 2014

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“…Because of the perceived risk and potential adverse outcomes of asystolic events [21] , 1 of our infants was paced with an epicardial single-chamber demand pacemaker. In this infant, follow-up reveals no neurological or developmental abnormalities.…”

Section: Discussionmentioning

confidence: 99%

Asystole and Severe Bradycardia in Preterm Infants

Dorostkar¹,

Arko²,

Baird³

et al. 2005

Neonatology

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Transient episodes of apnea and bradycardia are common in preterm infants. Pronounced asystole or sinus arrest, however, is relatively rare and the clinical significance of such events is unknown. Objective: The purpose of our study was to: (1) evaluate the prevalence of severe bradycardic and asystolic events in infants studied with polygraphic cardiorespiratory monitoring, (2) characterize these events, and (3) correlate the events with other clinical findings. Methods: A total of 583 studies were performed in 454 preterm infants at a post-conceptional age 37.4 ± 2.5 (range 34–42 weeks). Asystolic pauses were defined as no QRS complex for ≧3 s consistent with a heart rate <20 beats per minute (bpm). Severe bradycardia was defined as no QRS for ≧2 s consistent with a heart rate of 21–30 bpm. Results: Eight infants (29.5 ± 3.9 weeks’ gestational age, birth weight 1,283 ± 445 g) met the criteria of having had at least 1 asystolic event (heart rate ≤20 bpm). These infants had a total of 32 episodes of bradycardia ≤30 bpm, of which 22 episodes were classified as asystole. During the asystolic episodes, the P-R interval remained unchanged in 21 of 22 episodes and prolonged in 1. One patient had non-sustained ventricular tachycardia before resumption of normal sinus rhythm. All asystolic events were associated with apnea (mean duration of 17.7 ± 9.4 s) and O₂ saturations fell by 10 ± 6%. A pH probe study was available in 9 of 22 asystolic events and 6 of 10 severe bradycardic events. Gastroesophageal reflux was temporally related to only one asystolic and two bradycardic events. Clinical follow-up of these infants at a mean age of 14 months (range 1–46) reveals no symptomatic sequelae; although 1 infant died from multisystem failure associated with multiple congenital anomalies. Conclusions: Asystolic pauses occur in 1.8% of a selected population of preterm infants who have been experiencing cardiorespiratory events, are related to respiratory pauses, and appear to have a benign long-term outcome, although future study should incorporate long-term neurodevelopmental outcome.

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“…51 Slowing of the heart rate to Ͻ80 beats per minute decreases blood flow velocity in the anterior cerebral arteries, which supply circulation to the brain. 52 During prolonged apnea with bradycardia, cerebral hypoperfusion could contribute to hypoxic-ischemic injury to the brain of the immature infant. 4 Following a prolonged apnea/bradycardia episode, transient compensatory cerebral hyperperfusion could potentially contribute to an insult to the preterm brain caused by hypoperfusion and subsequent reperfusion.…”

Section: Short-term Effectsmentioning

confidence: 99%

A Primer on Apnea of Prematurity

Stokowski

2005

Advances in Neonatal Care

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Apnea, the cessation of respiratory airflow, can begin in many preterm infants in the first week of life and can last until the day of discharge or beyond. This article provides an overview of the complex anatomic, physiological, and developmental mechanisms related to immaturity of both the central nervous system and musculature of the pulmonary system, that contribute to apnea of prematurity. Apnea of prematurity is a diagnosis of exclusion; an array of other conditions and stimuli can also cause apnea, including infections, pulmonary disease, and intracranial pathology. The standard clinical management of apnea, including cutaneous stimulation, methylxanthine therapy, and continuous positive airway pressure or ventilatory support, are discussed as well as newer investigational therapies, such as olfactory stimulation. Emerging evidence on the long-term neurodevelopmental impact of apnea is reviewed. Nursing measures to prevent and manage apnea are reviewed with an emphasis on parent education and preparation for discharge. Apnea resolves in most preterm infants as they approach term corrected gestational age; however, if it does not, options include continued hospitalization or, for infants with stable apnea, discharge with a home apnea monitor.

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Impact of bradycardia on cerebral oxygenation and cerebral blood volume during apnoea in preterm infants

Cited by 47 publications

References 26 publications

Cerebral Oxygenation during Intermittent Hypoxemia and Bradycardia in Preterm Infants

Cerebral Oxygenation during Intermittent Hypoxemia and Bradycardia in Preterm Infants

Asystole and Severe Bradycardia in Preterm Infants

A Primer on Apnea of Prematurity

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