To induce volutrauma in healthy animals requires a very high tidal volume (from 20 to 40 mL/kg). Experimental models, however, do allow us to recognize the basic lesions of volutrauma and atelectrauma. Therefore, the transpulmonary pressure required in humans to reach TLC is twice that needed in pigs and three times that in rats. Indeed, the specific lung elastance, i.e., the proportionality constant between stress and strain that helps quantify the tendency for the lungs to recoil and resist deformation, is ~ 12–13 cmH 2O in man, ~ 6 cmH 2O in pigs, and ~ 4 cmH 2O in rats. Results obtained in animal experiments, however, cannot be translated directly to humans due to important species differences regarding structural tolerance. Insights into the mechanical causation of VILI are revealed when high ventilating stresses induce injury in previous healthy lungs that initially are free of possible damaging cofactors. If three of the ten cords do not elongate (in analogy to atelectasis), the remaining seven will support ~ 1430 g each (an increase in stress) and will be proportionally more stretched (an increase in strain). Each supports 1000 g (stress) and undergoes similar elongation from its resting baseline (strain). Let us assume that a load of 10 kg is sustained by 10 parallel and interconnected elastic cords that suspend it. Apart from opening and closing, these too are relevant forms of ‘atelectrauma’.Īnother important but often neglected physical amplifier of stress and strain (‘drop-out’) is rather intuitive. ![]() One consequence of microatelectasis is the generation of these stress risers, which encourage shearing stresses and also amplify the consequences of applied power to the ‘baby lung’. ![]() For injured lungs, the stress multiplier (which varies with PL) may exceed 2.0. Stress and strain amplify at interfaces between regions with different elasticity these junctions act as “stress risers”.
0 Comments
Leave a Reply. |