Incidence and mechanism of bradycardia during apnoea in preterm infants.

Henderson‐Smart, David J; Butcher-Puech, M C; Edwards, Deborah A

doi:10.1136/adc.61.3.227

Cited by 87 publications

(43 citation statements)

References 16 publications

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“…[31][32][33] The heart must not slow excessively, however, otherwise dangerous circulatory depression could ensue. For this reason, vagal potentiation is considered a likely lethal predisposing factor in sudden infant death syndrome.…”

Section: Discussionmentioning

confidence: 99%

Long-Term Reprogramming of Cardiovascular Function in Infants of Active Smokers

et al. 2010

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Abstract-Newborn infants of smokers show symptoms of cardiovascular stress hyperreactivity. Persistent hyperreactivity could increase the risk of short-and/or long-term complications, such as hypertension. Here we determined whether incipient dysfunction in a smoker's infant persists or worsens with age, by comparing cardiovascular reflex function of control and tobacco-exposed infants longitudinally from birth to 1 year. We compared infants born at term to nonsmoking couples (controls; nϭ19) and mothers who smoked moderately (average consumptionϭ15 cigarettes per day; nϭ17). All were tested at 1 to 3 weeks, 3 months, and 1 year during sleep. We recorded blood pressure and heart rate noninvasively during passive repositioning (60°head-up tilt). Tilting control infants raised blood pressure slightly above baseline at 1 week (ϩ2%) and much more at 1 year (ϩ10%). This trend was reversed in the tobacco-exposed cohort (ϩ10% at 1 week but only ϩ4% at 1 year). At 3 months and 1 year, the heart rate response of tobacco-exposed infants to tilt was also abnormal (highly exaggerated). Our study reveals that maternal smoking leads to long-lasting "reprogramming" of infant blood pressure control mechanisms. The underlying dysfunction in a smoker's infant could plausibly be a precursor or early marker of long-term susceptibility to complications, such as raised blood pressure. (Hypertension. 2010;55:722-728.)

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Section: Discussionmentioning

confidence: 99%

Long-Term Reprogramming of Cardiovascular Function in Infants of Active Smokers

et al. 2010

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“…Mechanism of development of bradycardia has been subject of debate among various investigators. [56][57][58] Carbone et al 59 reported that apnea and drop in heart rate began simultaneously in 14% of medium and 25% of short apneas. Simultaneous development of apnea and bradycardia can be attributed to enhanced inhibitory responses to airway afferent stimulation.…”

Section: Relationship To Bradycardiamentioning

confidence: 99%

Apnea of prematurity: pathogenesis and management strategies

Mathew

2010

J Perinatol

105

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Apnea of prematurity (AOP) is a significant clinical problem manifested by an unstable respiratory rhythm reflecting the immaturity of respiratory control systems. This review will address the pathogenesis of and treatment strategies for AOP. Although the neuronal mechanisms leading to apnea are still not well understood, recent decades have provided better insight into the generation of the respiratory rhythm and its modulation in the neonate. Ventilatory responses to hypoxia and hypercarbia are impaired and inhibitory reflexes are exaggerated in the neonate. These unique vulnerabilities predispose the neonate to the development of apnea. Treatment strategies attempt to stabilize the respiratory rhythm. Caffeine remains the primary pharmacological treatment modality and is presumed to work through blockade of adenosine receptors A 1 and A 2 . Recent evidences suggest that A 2A receptors may have a greater role than previously thought. AOP typically resolves with maturation suggesting increased myelination of the brainstem.

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“…These studies did not measure oxygenation continuously, so both hypotheses remained essentially speculative. In 1986, HendersonSmart et al (8) recorded Sao2 during episodes of apnea and bradycardia in five preterm infants, using an ear oximeter with an electronic response time of 0.1 s. They reported that the interval between the onset of apnea and the onset of the fall in Sao2 was shorter than that between the onset of apnea and the onset of bradycardia and concluded that the bradycardias occurred as a response to a fall in Sao2. This conclusion, however, was recently challenged by Upton et al (9), who warned, appropriately, against infemng a cause-and-effect relationship from observations on the temporal relationship between hypoxemia and bradycardia.…”

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confidence: 99%

The Relationship between Bradycardia, Apnea, and Hypoxemia in Preterm Infants

et al. 1993

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ABSTRACT. The pathogenesis of bradycardias in preterm infants is poorly understood. Because their pathogenesis may involve both apnea and hypoxemia, we set out to analyze the proportion of bradycardias that were associated with an apneic pause and/or a fall in arterial oxygen saturation (Sao2), and the temporal sequence of the three phenomena, in overnight tape recordings of Saol (Nellcor NlOO in beat-to-beat mode), breathing movements, nasal airflow, and ECG in 80 preterm infants at the time of discharge from hospital. A bradycardia was defined as a fall in heart rate of 233% from baseline for 2 4 s, an apneic pause as a cessation of breathing movements and/or airflow for 2 4 s, and a desaturation as a fall in Sao2 to 580%. A total of 193 bradycardias were found in 46 (58%) of the recordings (median, three per recording; range 1-18). There was a close relationship between bradycardias, apneic pauses, and desaturations: 83% of bradycardias were associated with apneic pauses and 86% with desaturations. Where all three phenomena occurred in combination, the time from the onset of apnea to the onset of the fall in Sao2 was shorter (median interval, 0.8 s; range -4.9-+11.5 s) than that from the onset of apnea to the onset of bradycardia (median, 4.8 s; range -4.0-+14.0 s). Hence, most bradycardias (86%) commenced after the onset of the fall in Sao2. We conclude that bradycardia, apnea, and hypoxemia are closely linked phenomena in preterm infants. (Pediatr Res 34: 144-147, 1993)

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Incidence and mechanism of bradycardia during apnoea in preterm infants.

Cited by 87 publications

References 16 publications

Long-Term Reprogramming of Cardiovascular Function in Infants of Active Smokers

Long-Term Reprogramming of Cardiovascular Function in Infants of Active Smokers

Apnea of prematurity: pathogenesis and management strategies

The Relationship between Bradycardia, Apnea, and Hypoxemia in Preterm Infants

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