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PubMed1998

Effects of spontaneous and hypercapnic hyperventilation on inspiratory effort sensation in normal subjects.

In order to elucidate if the inspiratory effort sensation (IES) associated with carbon dioxide (CO2) is independent of the concomitant increase in the ventilation, we studied 23 normal resting volunteers (mean age 34 +/- 11 yr) during CO2 rebreathing. Our main goal was to compare the IES at the same ventilation level under hypercapnic and isocapnic conditions. The protocol included: (1) basal measurements (BASAL); (2) hypercapnic ventilation (HV); (3) screen copy of ventilatory pattern during hypercapnia (COPY); (4) screen copy at basal end-tidal (partial) carbon dioxide pressure (PETCO2) (ISO); and (5) recovery (REC). During HV, PETCO2 increased to 54.8 +/- 0.78 mm Hg (p < 0.001) and ventilation (VE) from 12.0 +/- 0.50 to 28.1 +/- 1.19 L/min (p < 0.001). Borg value increased from 0.11 +/- 0.06 to 3.4 +/- 0.23 (p < 0.001). These values were not different during HV and COPY. During ISO, PETCO2 was 40.2 +/- 0. 59 mm Hg (not significant [NS] from BASAL), while VE remained unchanged: 29.9 +/- 1.29 L/min (NS from HV and COPY). Interestingly, the Borg value during the ISO decreased to 1.86 +/- 0.28 (p < 0.001 compared with HV and COPY). The increased IES induced by hypercapnic ventilation was reduced at the same ventilation level during isocapnic conditions. We suggest that CO2 generates an IES independent of the concomitant increase in ventilation.

Adult↗
PubMed1990

Flexible bronchoscopic removal of radioccult polyurethane foam, with pneumonitis in a hyperventilated lobe.

An intellectually delayed adult ingested and aspirated a large quantity of polyurethane foam, developing acute respiratory failure in association with partial airway obstruction. The foam was identified by flexible bronchoscopy and successfully removed from the bronchus intermedius and left mainstem bronchus with a retrieval basket. This facilitated normalization of blood gases and eventual recovery. However, the unobstructed right upper lobe became infiltrated radiographically, presumably resulting from regional hyperinflation and/or occult focal aspiration.

Adult↗
PubMed1985

Intermittent positive-pressure hyperventilation with high inflation pressures produces pulmonary microvascular injury in rats.

The mechanisms by which intermittent positive-pressure ventilation with high inflation pressure (HIPPV) induces pulmonary edema remain uncertain. In this study we investigated the physiologic and anatomic changes related to HIPPV at 45 cmH2O peak inspiratory pressure in rats. Edema was quantified by the extravascular lung water obtained from postmortem weighing and by 22Na distribution space. Pulmonary microvascular permeability was assessed by dry lung weight and fractional albumin uptake. After only 5 min of HIPPV, there was a significant increase in Na space, dry lung weight, and fractional albumin uptake when compared with that in control rats mechanically ventilated at 7 cmH2O peak inspiratory pressure. These changes suggest that edema may be due at least in part to alterations in microvascular permeability. Moderate peribronchovascular edema was present. At the ultrastructural level, some endothelial cells were found detached from their basement membrane. This lesion has been previously described in other types of pulmonary microvascular injury. The above findings remained almost unchanged after 10 min of HIPPV. After 20 min of HIPPV, we observed the outpouring of a high protein content alveolar flooding accompanied by a further significant increase in fractional albumin uptake and dry lung weight. Additional anatomic damage appeared including epithelial lesions and hyaline membranes. Thus, HIPPV edema presents all the features of high permeability edema. These results may be of concern in the ventilatory management of patients with acute respiratory failure in order to avoid additional damages induced by local overinflation.

Animals↗