Adverse Effects of Large Tidal Volume and Low PEEP in Canine Acid Aspiration

Abstract

When normal lungs are ventilated with large tidal volumes (VT) and end-inspired pressures (Pei), surfactant is depleted and pulmonary edema develops. Both effects are diminished by positive end-expiratory pressure (PEEP). We reasoned that ventilatory with large VT-low PEEP would similarly increase edema following acute lung injury. To test this hypothesis, we ventilated dogs 1 h after hydrochloric acid (HCl) induced pulmonary edema with a large VT (30 ml/kg) and low PEEP (3 cm H2O) (large VT-low PEEP) and compared their results with dogs ventilated with a smaller VT (15 ml/kg) and 12 cm H2O PEEP (small VT-high PEEP). The small VT was the smallest that maintained eucapnia in our preparation; the large VT was chosen to match Pei and end-inspired lung volume. Pulmonary capillary wedge transmural pressure (Ppwtm) was kept at 8 mm Hg in both groups. Five hours after injury, the median lung wet weight to body weight ratio (WW/BW) was 25 g/kg higher in the large VT-low PEEP group than in the small VT-high PEEP group (p less than 0.05). Venous admixture (Qva/Qt) was similarly greater in the large VT-low PEEP group (49.8 versus 23.5%) (p less than 0.05). We conclude that small VT-high PEEP is a better mode of ventilating acute lung injury than large VT-low PEEP because edema accumulation is less and venous admixture is less. These advantages did not result from differences in Pei, end-inspiratory lung volume, or preload (Ppwtm).(ABSTRACT TRUNCATED AT 250 WORDS)

Pathophysiology of Acute Lung Injury and the Acute Respiratory Distress Syndrome

“…90 The consequences of high-volume ventilation include increased permeability pulmonary edema in the uninjured lung 91,92 and enhanced edema formation in the injured lung. 93,94 Initial theories to explain these deleterious effects focused on alveolar overdistension, with injury attributed predominantly to capillary stress failure with resultant endothelial and epithelial injury. New evidence suggests that high tidal volume ventilation can also cause lung injury by initiating a proinflammatory cascade.…”

New strategies in mechanical ventilation for acute lung injury

“…The mechanisms of this ventilatorinduced lung injury [5] are various: regional alveolar overdistension by high airway inflation pressures [6,7] as well as large volumes (tidal volumes, lung inflation volume) [8][9][10][11]; increased shear forces generated by local alveolar overdistension in inhomogeneous lungs, e.g. at junctions between mobile (aerated alveoli) and immobile (collapsed or consolidated alveoli) structures [5,12]; but also repeated opening of collapsed alveoli [13], as well as the lung injury itself (e.g.…”

Comparison of acid-induced inflammatory responses in the rat lung during high frequency oscillatory and conventional mechanical ventilation

“…In a canine model, ventilation using VT of 30 mL/kg caused greater pulmonary edema than VT of 15 mL/kg [5]. In contrast, ventilation using VT of 6 mL/kg attenuated IL-6 and vascular endothelial growth factor receptor expression in the lungs of mice following acid instillation into the airways compared with VT of 17 mL/kg [7].…”

“…However, conventional ventilation strategies are associated with further pulmonary damage and inflammation during the management of patients and experimental models with ARDS [1 -4]. In particular, the large tidal volume (VT) and high peak airway pressure contribute to ventilation-induced lung injury [5,6].…”

“…Acid aspiration is a major cause of ARDS and acute lung injury leading to direct lung damage and acute inflammation [17], and has been used as an experimental model of ARDS due to aspiration pneumonia [17,18]. It was reported that 15mL/kg VT of CMV had a protective effect for acid-induced lung injury compared with 30 ml/kg [5], but there is little information at the further lower VT of CMV on inflammatory responses to acid instillation.…”