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?