Upper airway patency in the human infant: influence of airway pressure and posture

Wilson, Stephen; Thach, Bradley T.; Brouillette, Robert T.; Abu-Osba, Yousef K.

doi:10.1152/jappl.1980.48.3.500

Cited by 135 publications

(67 citation statements)

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“…46,47 In the absence of muscle activity, pharyngeal airway in the neonate (with the head in the neutral position) becomes occluded at transmural pressures seen during tidal breathing. 48 This finding is consistent with the observation made by Safar et al 49 several decades ago. These investigators noted that the pharyngeal airway can become obstructed during induction of anesthesia when pharyngeal muscle activity is depressed.…”

Section: Neonatal Apnea Definition and Classificationsupporting

confidence: 92%

Apnea of prematurity: pathogenesis and management strategies

Mathew

2010

J Perinatol

109

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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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Section: Neonatal Apnea Definition and Classificationsupporting

confidence: 92%

Apnea of prematurity: pathogenesis and management strategies

Mathew

2010

J Perinatol

109

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“…Varying head position between flexion and extension can cause significant variations in size of the retroglossal space and hyoid position on lateral cephalometry [23]. Neck flexion makes the upper airway more susceptible to collapse, whilst neck extension makes the upper airway more resistant to collapse [54], irrespective of changes in general body posture. Mouth opening can cause increased upper airway resistance, since this results in dorsal movement of the ventral attachments of upper airway dilator muscles, with resultant shortening in muscle length and reduction in efficiency [55].…”

Section: Head Positionmentioning

confidence: 99%

“…Progressive hypercapnia, hypoxia, asphyxia and negative pressure application all produce an augmenting drive to upper airway dilator muscles [107][108][109][110][111][112]. Defects in such upper airway muscle responses, or inco-ordination of upper airway and diaphragm activity, have each been proposed as factors predisposing to OSA [54,107,108,110,113,114]. The complexity of the upper airway makes it unlikely that dysfunction of a single muscle group is responsible for OSA [104], and thus assessment of activity of any single muscle may not be a reliable index of upper airway obstruction [84].…”

Section: Upper Airway Dilator Muscle Activitymentioning

confidence: 99%

Pathophysiology of obstructive sleep apnoea

Deegan¹,

McNicholas²

1995

Eur Respir J

264

183

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Arousal plays an important role in the termination of each apnoea, but may also contribute to the development of further apnoea, because of a reduction in respiratory drive related to the hypocapnia which results from postapnoeic hyperventilation. A cyclical pattern of repetitive obstructive apnoeas may result.A better understanding of the integrated pathophysiology of OSA should help in the development of new therapeutic techniques.

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“…Neck extension increases the rigidity of the upper airway, making it more resistant to collapse from negative transmural pressure. 16 The infant -with a relatively larger tongue than the adult -is especially vulnerable to both genioglossal depression and head position. It is possible that some degree of neck flexion contributed to early upper airway obstruction in our two infants.…”

Section: Discussionmentioning

confidence: 99%

Negative pressure pulmonary oedema: a potential hazard of muscle relaxants in awake infants

et al. 1990

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We report t3vo cases of health3," infants who were given an IV intubating bolus of a nondepolarizing muscle reletrant (0.1 rag. kg -t vecuronium) We recently reported an infant who developed negative pressure pulmonary oedema (NPPE) upon emergence from general anaesthesia as a result of an obstructed tracheal tube. I Subsequently, we have observed two infants who have experienced NPPE secondary to airway obstruction occurring early in the course of an inhalational induction of anaesthesia. Both had received vecuronium while awake (crying, moving all extremities) to facilitate early control of the airway. Case reportsA fullterm four-week-old male infant was scheduled for cystoscopy and possible pyeloplasty. He entered the operating room with an IV infusion in place. Precordial stethoscope, ECG and pulse oximetry sensor were positioned and the alarm set at 90 per cent oxygen saturation. As the administration of 0.25 per cent halothane and 50 per cent N20 by mask was commenced, 0.1 mg.kg-I vecuronium was given IV. Within 30 sec, the oximeter alarm sounded, and the infant was observed making two maximal inspiratory efforts, with sternal collapse evident with both inspiratory attempts. The baby was cyanotic. Immediately, an oral airway was inserted and positive pressure ventilation was accomplished with 100 per cent 02. However, 02 saturation remained below 85 per cent and bloody foam was observed under mask. A tracheal tube was quickly inserted in spite of poor visualization of the glottis due to copious amounts of frothy fluid. Surgery was cancelled. In the recovery room, the infant's lungs were mechanically ventilated with the addition of 5 cm H20 PEEP, and he was given 1 mg" kg-1 furosemide for diuresis and 2 I-tg" kg-m fentanyi for sedation. The chest x-ray, which showed fluffy exudates soon after the event, CAN J ANAESTH 1990/ 37:5 /pp580-3

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Upper airway patency in the human infant: influence of airway pressure and posture

Cited by 135 publications

References 0 publications

Apnea of prematurity: pathogenesis and management strategies

Apnea of prematurity: pathogenesis and management strategies

Pathophysiology of obstructive sleep apnoea

Negative pressure pulmonary oedema: a potential hazard of muscle relaxants in awake infants

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