A "few" things in the spirit of learning:
-Wheezing can be from a number of different causes. "Cardiac Wheezing" is not bronchoconstriction aka uneven alveolar emptying per se, it is from atelactasis caused by fluid from the blood (cardiogenic pulmonary edema) which causes dilution and washout of the surfactant, which will result in alveolar collapse.
-Many of your interventions are based on L/S and BP. It would be prudent to confirm adventitious L/S with a second provider (you). Same for BP if it is out of the norm.
-The ETCO2 waveform (which I realize you don't have, only the quantitative version, the number) would tell you whether or not uneven alveolar emptying is occuring.
-If you apply CPAP to a pt with total loss of plateau per quantitative capnography, they have no way to eliminate the air that the CPAP is delivering.
-The O2 dissociation curve begins to steepen downward below 90%, gets even steeper as you go past 80%, then basically freefalls past that, so 100% to 90% should occur more slowly than 90% to 80%, but below 80% the pt will de-sat very quickly. So, if your pt has a sat of 80% or less initially, you need to be pharmocologically aggressive, as well as plan to bag and (hopefully not have to) drop a tube ealier rather than later.
-The pt's RR was 12 with an SpO2 of 80%, in tripod, on home NC. Impending respiratoy arrest, for sure. No wonder the pt stopped breathing. She was tired and probably altered as well. "I start up a neb treatment in the back" should have been "I start up a neb treatment in the house right away as I get the BVM ready." I noticed you did a BGL in the house, but a neb in the bus. I know you thought it was COPD, my point is that you started meds several minutes too late in favor of a BGL, which is likely not a respiratory pt's primary problem, and also removal to the bus. Most patients can have interventions deferred until you're in the ambulance. This pt needed to be worked in the house. The first time someone dies on you while on the stair chair going down the stairs (happend to me) you'll understand.
-As the pt becomes more alkalotic, the Hb will hold the O2 molecules, but be reluctant to give them up - think of someone with a panic attack getting dizzy, worsening panic breathing, then passing out, typically with a sat of 100% and complaint of dyspnea. Differential Dx could be a PE, but that's another conversation. As the pt becomes more acidotic, the Hb will have a tougher time binding with O2. This is one reason why the O2 dissociation curve starts out shallow than becomes steep quite quickly as you go south of 90%.
-The pt may have a Cardiogenic Pulmonary Edema episode secondary to an MI. If the 12-lead shows inferior changes, a V4R is warranted to help rule out a RVI (infarct), where the RV is heavily dependent on preload, so NTG can bottom out the pt's BP quickly. This is why a fluid bolus should be more beneficial in a RVI (Starling's law aids the sick RV), vs pressors for a LVI.
-The tripod position was a clue that the pt was in extremis and needs aggressive Tx. The pt pulling the mask off her face suggests a change in mental status presumably from worsening hypoxia. Prepare to assist ventilations if CPAP is out of protocol at this point. If we were thinking COPD instead of CHF, then bag in the neb Tx in-line with the BVM if available.
-Get a good Hx to narrow your differentials towards the CHF - you didn't tell us anything about the pt's HPI except dyspnea x 2 days. Cool skin leads more towards CHF/APE. The distressed heart should cause a catecholamine response to help with perfusion. The pt's BP was WNL, but was likely elevated earlier before you were called. It seems that you caught the pt on the way back down with respect to BP and effort in breathing -resp failure due to fatigue.
Not trying to beat up on you, just want to make you aware of a few critical thinking items
