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PubMed · 745612

Bronchial asthma.

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J C Hogg. 1978. Bronchial asthma.. https://pubmed.ncbi.nlm.nih.gov/745612/

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Respiratory oscillation mechanics in infants with bronchiolitis during mechanical ventilation.

The aim of the study was to describe the pattern of respiratory oscillation mechanics and responses to positive end-expiratory pressure (PEEP) in bronchiolitis. Six infants were studied during the course of mechanical ventilation. A 20 Hz sinusoidal pressure variation was applied at the endotracheal tube where flow was measured with a pneumotachograph. Resistance and reactance obtained from the complex pressure-flow ratio were separated during inspiration (R(rs,i); X(rs,i)) and expiration (R(rs,e); X(rs,e)), and the differences between R(rs,i) and R(rs,e) (deltaR(rs)) and X(rs,i) and X(rs,e) (deltaX(rs)) were calculated. The data were corrected for the mechanical characteristics of the endotracheal tube. The measurements were repeated while PEEP was varied between 0 and 8 hPa. Two infants were found to have normal R(rs) and near-zero X(rs) and both parameters exhibited little change within the respiratory cycle or with varying PEEP. Four infants had high R(rs) at zero PEEP. In two, R(rs,i) was markedly elevated (108.5 and 85.2 hPa.s/L, respectively), and X(rs,i) was markedly negative (-25.0 and -22.5 hPa.s/L, respectively) at zero PEEP, while deltaR(rs) and deltaX(rs) were small. R(rs,i) and the absolute value of X(rs,i) decreased with increasing PEEP. This pattern of oscillation mechanics was consistent with low lung volumes and atelectasis, being reversed by increasing PEEP. In the remaining two subjects, R(rs,i) was moderately elevated (57.8 and 53.6 hPa.s/L, respectively) and X(rs,i) moderately negative (-12.5 and -7.7 hPa.s/L, respectively) at zero PEEP. DeltaR(rs) (-59.8 and -56.5 hPa.s/L, respectively) and delta(rs) (28.1 and 48.7 hPa.s/L, respectively) were large, but were dramatically reduced by increasing PEEP. These patterns were consistent with expiratory airflow limitation. Measurements of respiratory impedance are, therefore, informative in regard to the pathophysiological mechanisms occurring in bronchiolitis during mechanical ventilation, and they may be helpful in setting the level and assessing the effect of PEEP.

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The aim of our study was to determine the effects of pulmonary vascular engorgement on airways and pulmonary tissues in juvenile animals before and after methacholine (Mch)-induced changes in lung function. Five anesthetized, paralyzed, and thoracotomized piglets were studied before and during pulmonary vascular engorgement, induced by inflating a left atrial balloon catheter and by calculating respiratory mechanics from measurements of airway opening (Pao) and alveolar pressures (PA), respiratory flow (V'), and volume (V) recorded during mechanical ventilation, using the multilinear regression technique. A maximal increase of 15 mmHg in pulmonary artery pressure (Ppa) resulted in a mean increase in total lung elastance (EL) of 28.6% and in total lung resistance (RL) of 14.9%. Mch increased EL by 21.7% and RL by 29.0%. Inflation of the left atrial balloon with an associated increase in Ppa by 15 mmHg in the presence of Mch resulted in an increase in EL by a further 12.4% (to 135.4% of baseline) and in RL by a further 9.0% (to 139.5% of baseline). The change in RL was associated with a qualitatively similar change in both tissue resistance (Vti) and airway resistance (Raw) before and after Mch-induced changes in lung function. We conclude that increasing pulmonary vascular pressures, by increasing left partial pressure, alters lung function in juvenile animals by altering the mechanical properties of both airways and lung tissues. The methods used in the present study allow a direct assessment of the site of action of vascular engorgement in the lungs and provide a useful model for studying this phenomenon further.

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