The Anesthesia Record

Today was our first clinical conference.  You see, every Wednesday morning at the ungodly hour of 0645, we are required to attend a conference in which the Baptist hospital CRNAs and (often an anesthesiologist) discuss any particularly interesting cases or topics related to the field of anesthesia.  I didn't quite know what to expect, which is probably for the best considering that if I'd anticipated the number of questions us newbies would be asked after a mere 2 days of orientation, I would have gotten very little sleep last night.

Fortunately, Dr. Tobin, the Chair of the hospital's Anesthesia Department, lead the discussion and really excelled at explaining the concepts that were covered.  The case at hand involved a patient who suffered complications on the operating table following an apparent laryngospasm.  What I found most interesting was Dr. Tobin's description and explanation of flash pulmonary edema.  It caused me to realize that, though I'd cared for a number of patient's diagnosed with this affliction while an ICU nurse, I had never before grasped the mechanism of injury.

According to Dr. Tobin's lecture, flash pulmonary edema may occur after too much pressure has been exerted on the pulmonary artery by way of the alveoli.  How might this happen?  First, it's important to understand that during normal respiration, the vacuum created in the alveolar spaces (the intra-airway pressure) during inspiration ranges from -5 to -10 mmHg.  However, an obstruction or laryngospasm exacerbates these figures as an even greater inspiratory force is exerted in an attempt to overcome the airway constricture.  In such cases, the intra-airway pressure during inspiration may register at -60 to -100 mmHg.  This massive pressure swing causes the alveoli to become more porous and, because pulmonary artery pressure is only around 25/15 mmHg (systolic/diastolic), fluid from the PA intravascular space weeps into the surrounding pulmonary tissue. This flooding of alveolar spaces not only prevents oxygen exchange, but also inactivates tissue surfactant.  Although this substance is slowly replaced by the alveoli, patients often require mechanical ventilation with a corresponding ICU stay while their lungs regain function.

I don't know about you, but my brain feels bigger.

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