Lung Mechanics

When positive-pressure mechanical ventilation first started, large tidal volumes were used (10-15ml/kg), which caused stress fractures at the alveolar-capillary interface due to both barotrauma and volutrauma.  Alveolar rupture can cause pulmonary interstitial emphysema, pneumomediastinum, pneumothorax, inflammatory lung injury, or multiorgan injury from release of inflammatory mediators into the bloodstream (biotrauma).


Thus, lung protective ventilation was born and the ARDS protocol was put into effect (see previous blog post).  However, utilizing low tidal volumes also has problems -- instead of barotrauma, we see airway collapse -- especially at end expiration.  PEEP - positive end-expiratory pressure -- acts as a stent to keep small airways open at end expiration.


In order to monitor lung mechanics, we must decipher proximal airway pressures.  The peak pressure at end inspiration (Ppk) is a function of inflation volume, flow resistance, and chest elastic recoil force.


Thus, Ppk = resistance + elastance


In order to figure out whether resistance or elastance is contributing to the peak inspiratory pressure, we must occlude the expiratory tubing at end inspiration which determines the end-inspiratory plateau pressure.


Thus, Pplateau = elastance  AND   Ppk - Pplateau = airway resistance


So what does this all mean?  Well, using peak inspiratory pressures and plateau pressues, we can better evaluate a patient with acute respiratory decompensation and treat them appropriately.


Peak inspiratory pressure

    Decreased - air leak, hyperventilation

    No change - pulmonary embolus, extrathoracic process

    Increased -- check plateau pressure


Plateau pressure

    No change - airway obstruction, so think aspiration, bronchospasm, secrections, tracheal tube, obstruction

    Increased - decreased compliance, so think abdominal distension, asynchronous breathing, atelectasis, auto-PEEP, pneumothorax, pulmonary edema

Thanks to Dr. Amina Merchant for this post.