Negative Pressure Pulmonary Edema

We would like to point that according to the reporting we believe that the true etiology is a combination of NPPE type I and II. It seems that this patient had already developed the pathophysiology of type II NPPE due to progressive, though not critical (as flexible laryngoscopy revealed) narrowing of the larynx due to the external compression from the growing goiter. So, the patient was on the edge on manifesting a type II NPPE (recent onset of exertional dyspnea) when something critical ensued an undetected infection that led to mucosal edema or the sudden onset of narrow complex tachycardia as the authors wisely detected and states. So, the presenting episode of NPPE is presumably of type II, following the pathophysiology that the authors elegantly explained.