Effect of inner cannula removal on the work of breathing imposed by tracheostomy tubes: a bench study.

BACKGROUND: Tracheotomy has been used to assist in weaning patients from mechanical ventilation. Some patients fail to be weaned from the ventilator despite tracheostomy. We hypothesized that removing the inner cannula from the tracheostomy tube would decrease the tube's imposed work of breathing (WOB(IMP)). METHODS: The hypothesis was tested using a lung model, by measuring the change in WOB(IMP) when the inner cannula was removed. A mechanical lung model was developed using a test lung to simulate a spontaneously breathing patient. WOB(IMP) was measured with a commercially available lung mechanics monitor. Shiley size 6, 8, and 10 nonfenestrated tracheostomy tubes were tested with the inner cannula in and out. Breathing conditions were simulated using tidal volumes (V(T)) of 300 and 500 mL matched with breathing frequencies of 12, 24, and 32 breaths per minute, by using a ventilator to simulate spontaneous breathing through one side of the test lung. RESULTS: Under all the tested breathing conditions, WOB(IMP) for each of the 3 tracheostomy tubes was significantly reduced (p < 0.05) when the inner cannula was removed. Also, as simulated spontaneous inspiratory flow demand increased (ie, as V(T) and/or frequency were increased), WOB(IMP) also increased, and vice versa. With the cannula removed, WOB(IMP) was not significantly different between the size 6 and 8 tubes nor between the size 8 and 10 tubes when V(T) was 300 mL and frequency was 12 breaths per minute. CONCLUSIONS: There was a significant decrease in WOB(IMP) with each tube when the inner cannula was removed. WOB(IMP) increased with an increase in inspiratory flow demand (ie, increase in V(T) and/or frequency), as well as when tube size decreased. In weaning a tracheostomized patient from mechanical ventilation, increasing the internal diameter of the tube by removing the inner cannula may be beneficial. Further study is needed to determine if these findings are clinically important.

Surfactant treatment impairs gas exchange in a canine model of acute lung injury.

UNLABELLED: The effectiveness of surfactant (SURF) treatment in acute lung injury in the adult is controversial. In this study, we tested the effectiveness of early surfactant treatment in a commonly used animal model of acute lung injury, phorbol-myristate acetate (PMA), to see if it would attenuate the progression of lung injury. We measured the effect on lung compliance and whether positive end-expiratory pressure (PEEP) (10 cm H2O) during SURF administration had a synergistic effect. METHODS: Four groups of anesthetized dogs were studied: a) normals; b) PMA injury only; c) PMA injury + SURF; and d) PMA + SURF + PEEP. Lung injury was induced with 25-30 microg/kg of PMA. Responses were measured over 7 hrs. Surfactant was administered in the form of Survanta, 4 x 25 mg/kg doses via tracheal instillation 2.5 hrs after PMA. For the group receiving PEEP, 10 cm H2O PEEP was begun 1.5 hrs after PMA, 1 hr before SURF. Postmortem, the left lung was excised and inflated three times to total lung capacity (volume at 30 cm H2O) and expiratory compliance was measured with 25-100 mL volume increments. The trachea was then clamped and trapped volume was determined by water displacement. RESULTS: PMA-induced lung injury significantly reduced expiratory compliance and total lung capacity (p < .05 from normal). Wet/dry lung weights did not differ between groups. SURF without PEEP further decreased lung compliance as compared with PMA only. CONCLUSIONS: SURF administration after PMA injury causes marked reductions in lung compliance when no PEEP is coadministered. However, the loss of static expiratory lung compliance appears partly ameliorated by application of PEEP + SURF. Given that tracheal instillation of SURF is known to acutely elevate lung impedance in the first few hours after administration, coadministration of PEEP appears to be critically important in counteracting these early effects of surfactant instillation on the lung.

High-dose furosemide alters gas exchange in a model of acute lung injury.

PURPOSE: Furosemide is often used to reduce edema in patients with acute respiratory distress syndrome (ARDS). It was hypothesized that furosemide would reduce lung water and improve gas exchange in a phorbol-myristate acetate (PMA) model of acute lung injury. METHODS: Two groups of mongrel dogs received PMA (25 to 30 micrograms/kg) and continuous saline at 10 mL/kg/h; one group received PMA plus two 1-mg/kg doses of furosemide at 1 and 2 hours after PMA. Arterial blood gases on F1O2 = 1.0 and double-dilution lung water were measured at intervals over 7 hours. RESULTS: In dogs receiving PMA+furosemide, AaDO2 and shunt fraction increased compared with dogs receiving PMA only (AaDO2, P = .014; shunt, P = .017). There were no significant differences between the groups in lung water (P = .34) during the experiment or in wet/dry weight postmortem. Urine flow was markedly reduced in both groups; the kidneys appeared unresponsive to the diuretic effects of furosemide. Significant elevations in hematocrit and pulmonary vascular resistance were seen in furosemide-treated compared with PMA-only dogs. CONCLUSIONS: In this model of ARDS, which results in the absence of effective kidney function and multiple organ failure, furosemide compromises alveolar-capillary gas exchange and fails to influence the time course of lung water accumulation. The results suggest that the nondiuretic affects of furosemide cannot explain its purported clinical utility in ARDS.