P.E.A. in a living patient (medical mystery)

[fiveofpeep]

My patient arrived to the unit with the report that she had bouts of SVT requiring cardioversion. On arrival she was in sinus tachycardia. Within minutes; however, she bounced right into afib with a rapid ventricular rate of 160-220.This was sustained for more than three hours.

I decided to check a pulse to see how my patient could possibly be compensating with such prolonged cardiac output and noticed that the tapping reverberating against the pads of my fingers felt more like the slow trudge of bradycardia than the panicked thrumming of tachycardia. Sure enough, auscultation of the apical pulse revealed that the actual contractile beats were 1/3 to 2/3rds that of the electrical rate. IE EKG hr is 150, apical pulse is 50!

The only way I can think of this is that you know how sometimes P waves happen and they are nonconducted? Well in this situation perfect QRSs are conducted but they arent all leading to a contraction. They are noncontracted QRSs! This was evident on the a-line waveform which showed coinciding waveforms with only some of the QRS complexes.

What was this? Do you have any idea?

[kristenallene40]

Did you get a 12-lead? If so, what did it say? Could be artifact...sounds weird I know but just had a guy have VT of 300 rate and after interrigating his ICD, it turns out he only had a small run of SVT. The only thing we can think of is that it was artifact from his IJ dialysis cath with CVVHD going.

[fiveofpeep]

Thanks for your input :)

the 12 lead said multifocal atrial tach but the cardio consult and a couple other RN's agreed upon afib

I asked an instructor and he said that w/ afib you have a pulse deficit because the stroke volume is so poor that although there is myocardial contraction the sv is so crappy that a real CO doesnt happen. He said this is typical for afib.

My concern is how was my patient compensating if her heart was contracting all those times.