Looking for a little insight here. I had a patient suffering from a prolonged pneumonia accompanied with CHF/pulmonary hypertension. Audible congestion noted, auscultated sounds of scattered rhonchi, rales, slight expiratory wheeze. Vitals assessed, initial spo2 reading of 89. high flow nrb=98%. ETc02-poor wave form, slight rep. alkalosis. rapid, shallow, respirations at 34. 12-lead revealed bifisicular block, LVH.
18g IV established.
Now I wanted to splint the airways open with CPAP. Got into an argument with my Partner. He wanted to keep the NRB on and TX. There was clear signs of distress there, but he opted to treat as such due to normal saturation levles. There is a differance between hypoxia and hypoxemia.
Has anyone ever seen such a patient? Was NRB better than CPAP? False readings in CHF Patient's?
18g IV established.
Now I wanted to splint the airways open with CPAP. Got into an argument with my Partner. He wanted to keep the NRB on and TX. There was clear signs of distress there, but he opted to treat as such due to normal saturation levles. There is a differance between hypoxia and hypoxemia.
Has anyone ever seen such a patient? Was NRB better than CPAP? False readings in CHF Patient's?