Category Archives: Severe Laryngotracheobronchitis

The Measurement of Thoraco-abdominal Asynchrony in Infants With Severe Laryngotracheobronchitis: Conclusion

There is normally a compensatory response to a decrease in Ve by an increase in either respiratory frequency or an increase in abdominal volume displacement, as measured by the Iabd. An increase in respiratory rate did occur during mild and moderate distortion when the tcPco2 was less than 45 mm Hg. With severe CWD and a tcPco2 greater than 50 mm Hg, however, there was a decrease in respiratory frequency. Previous work has suggested that, as an adaptive response to severe inspiratory flow limitation (markedly decreased Vt/Ti), there will be a compensatory increase in inspiratory time (Ti), and thus decrease in frequency as an alternate strategy to achieve gas exchange. Concomitant with the fall in frequency, there was a small increase in the Iabd that partially compensated for the fall in Irc and the decrease in respiratory frequency. These mechanisms failed to adequately defend alveolar ventilation and the increase in tcPco2 occurred. With recovery, as the Ve increased, there was a concomitant increase in Irc.
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The Measurement of Thoraco-abdominal Asynchrony in Infants With Severe Laryngotracheobronchitis: Discussion

The Measurement of Thoraco-abdominal Asynchrony in Infants With Severe Laryngotracheobronchitis: DiscussionThis study has shown that a predictable change in CWD occurs during the recovery from ventilatory failure in infants with severe LTB. The pattern of CWD consisted of asynchronous displacement of the chest wall and abdominal compartments during inspiration, resulting in a decrease in the Ve, and a decrease in Vt, principally through the loss of the chest wall excursion during inspiration. The chest wall motion, measured as Irc, was paradoxic to the abdomen in the most severe state, but with resolution of the clinical illness, the motion became temporally displaced rather than paradoxic. In this study, the progression of the CWD was quantitatively associated with an increasing phase angle, thus indicating that both the increase in asyn-chrony of chest wall motion (phase angle) and the decrease in chest wall displacement (Irc) contributed to alveolar hypoventilation. This is in agreement with previous observations and clinical scores where deterioration in the clinical condition was associated with more obvious inward movement of the lower part of the chest wall. The loss of the chest wall contribution led to a fall in Vt, a fall in Ve, and thus alveolar hypoventilation with elevated tcPco2.
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The Measurement of Thoraco-abdominal Asynchrony in Infants With Severe Laryngotracheobronchitis: Mutilation

The ventilatory volumes obtained for the six infants with LTB were normalized for body weight. The Ve increased from a minimum of 0.28 ± 0.06 L*min ~ ukg at a tcPco2 of 64 mm Hg to 0.63 ±0.09 L’min’Hcg at a tcPco2 of 28 mm Hg. The relationship of tcPco2 to Ve is shown in Figure 2 (lowest panel), and included in Table 1.
Further, the increase in Ve resulted principally through improvement in Vt which increased from 5.6 ± 0.6 mbkg with the most severe airflow obstruction (tcPco2 of 64 mm Hg) to 15.7 ±0.4 mbkg with clinical resolution when the tcPco2 was 28 mm Hg (Fig 2, center panel). Simultaneous with the increase in Vt, there was an initial increase in respiratory frequency from 50 breaths-min” at a tcPco2 of 64 mm Hg to a maximum of 69 breaths’min at 42 mm Hg, and then subsequently decreasing to 50 breaths*min“ at 28 mm Hg (Fig 2).
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The Measurement of Thoraco-abdominal Asynchrony in Infants With Severe Laryngotracheobronchitis: Results

The Measurement of Thoraco-abdominal Asynchrony in Infants With Severe Laryngotracheobronchitis: ResultsThe mean age of the 6 infants was 10 months (7 to 13 months) and mean weight was 7.1 kg (5.5 to 9.1 kg). Because of the selection of the infants, there was ventilatory failure present for the first recording of each subject. The magnitude of the CWD varied directly with the clinical severity of the disease, as illustrated in Figure 2, although there were three general patterns of chest wall motion in all subjects corresponding to different stages of illness. Firstly, the mildest abnormality, delayed expansion of the chest wall at the beginning of inspiration, was usually seen late in the recovery phase (Fig 1, left panel). This minimal distortion of the normal synchrony of movement of the two compartments was associated with the clinical resolution of the illness. The anticlockwise pattern of the Lissajous loop, and a phase angle (0m) of <30°, suggested that the ribcage did expand during inspiration, but was temporally delayed behind the excursion of the abdomen.
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The Measurement of Thoraco-abdominal Asynchrony in Infants With Severe Laryngotracheobronchitis: Analysis

When the infant was clinically stable, usually within 2 h of ICU admission, prospective respiratory monitoring was commenced during quiet sleep and continued throughout the illness until complete clinical resolution of both the illness and CWD. Throughout the progression of the illness, the tcPos was maintained greater than 55 mm Hg by judicious manipulation of the Flo, necessitating at times up to an Flo of 0.65. Racemic epinephrine was routinely administered to these infants, but all recordings were performed at least 1 h after a treatment with this inhaled medication.
The displacement of the chest wall and abdomen was monitored using a respiratory inductance plethysmograph (RIP) (Respitrace, Ambulatory Monitoring, Ardesley, NY) with the ventilatory move ments measured each 8 h until resolution of the illness. The inductance bands for the RIP (Respibands) were fixed on the chest at the nipple line and midabdomen as previously described for infants by Duffty et al,u with the position of the inductance bands not altered between measurements. Volume calibration for the RIP was not performed but the signals are recorded as an inductance (volts). The volume of each breath (Vt) was obtained from airflow (V), sensed at the mouth by a mask and pneumotachograph (Hewlett-Packard 21609B) and the V was subsequently integrated to Vt (Hewlett-Packard 8815A). All volume measurements were performed during quiet (non-REM) sleep as determined by direct observation and by electro-oculogram, recorded by a high-gain biologic signal amplifier (Hewlett-Packard 8816A). These epochs of quiet sleep constituted less than 15 percent of total time monitored, and were frequently of short duration, often lasting only 10 to 15 min. Simultaneously the transcutaneous oxygen and carbon dioxide (tcPoa and tcPcoJ tensions were measured (Kontron Scientific Ltd, Mississauga, Ontario), and heart rate was recorded.
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The Measurement of Thoraco-abdominal Asynchrony in Infants With Severe Laryngotracheobronchitis

The Measurement of Thoraco-abdominal Asynchrony in Infants With Severe LaryngotracheobronchitisThe assessment of the severity of respiratory disease in infants relies on clinical observation because of the difficulties in measuring ventilation in the infant. There are at least two clinical methods of assessing the severity, both of which include an assessment of chest wall distortion (CWD) during inspiration as an element of the severity score. Because this is a nonspecific respiratory system abnormality, CWD is thus interpreted as reflecting increased pleural pressure swings because of a change in the resistance to airflow within the respiratory system.
Chest wall distortion occurs during inspiration as the abnormal paradoxic inward movement of the lower chest wall, demarcated by the insertion of the diaphragm into the ribcage, representing a collapse of the lower chest wall at a time when the thoracic cavity is increasing in volume (ie, “out of phase” or paradoxic). This uncoupling of the ribcage-abdominal motion may result in a decrease in tidal volume (Vt), a decrease in alveolar minute ventilation (Ve), and thus ventilatory failure.
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