Lung collapse during low tidal volume ventilation in acute respiratory distress syndrome.
BACKGROUND
Current ventilator management for acute respiratory distress syndrome (ARDS) incorporates low tidal volume (V(T)) ventilation in order to limit ventilator-induced lung injury. Low V(T) ventilation in supine patients, without the use of intermittent hyperinflations, may cause small airway closure, progressive atelectasis, and secretion retention. Use of high positive end-expiratory pressure (PEEP) levels with low V(T) ventilation may not counter this effect, because regional differences in intra-abdominal hydrostatic pressure may diminish the volume-stabilizing effects of PEEP.


METHODS
A 35-year-old man with abdominal compartment syndrome (intra-abdominal pressure > 48 cm H2O developed ARDS and was treated with V(T) of 4.5 mL/kg and PEEP of 20 cm H2O. Despite aggressive fluid therapy, appropriate airway humidification and tracheal suctioning, the patient developed complete bronchial obstruction, involving the entire right lung and left upper lobe. After bronchoscopy the patient was placed on a higher V(T) (7.0 mL/kg). Intermittent PEEP was instituted at 30 cm H2O for 2 breaths every 3 minutes. This intermittently raised the end-inspiratory plateau pressure from 38 cm H2O to 50 cm H2O. With the same airway humidity and tracheal suctioning practices bronchial obstruction did not reoccur.


CONCLUSIONS
Low V(T) ventilation in ARDS may increase the risk of small airway closure and retained secretions. This adverse effect highlights the importance of pulmonary hygiene measures in ARDS during lung-protective ventilation.
Kallet
R H
RH
Respiratory Care Services, Department of Anesthesia, University of California-San Francisco, at San Francisco General Hospital, NH:GA2, 1001 Potrero Avenue, San Francisco CA 94110, USA. richkallet@earthlink.net
Siobal
M S
MS
Alonso
J A
JA
Warnecke
E L
EL
Katz
J A
JA
Marks
J D
JD
D000328:Adult; D006801:Humans; D008297:Male; D011175:Positive-Pressure Respiration; D001261:Pulmonary Atelectasis / Q000209:etiology*; D012121:Respiration, Artificial / Q000009:adverse effects* / Q000379:methods; D012128:Respiratory Distress Syndrome / Q000503:physiopathology / Q000628:therapy*; D012137:Respiratory System / Q000378:metabolism; D013990:Tidal Volume