Quote from Kara RN BSN
That reminds me, I've heard from intensivists in the past that if adenosine fails to convert SVT it's not true SVT. Anyone heard this before?
SVT is a blanket diagnosis for all tachyarrhythmias (sinus tach, a fib, a flutter, etc.) The specific tachyarrhythmia can only be determined through a 12 lead EKG interpretation d/t rapid HR and indistinguishable P waves on a single lead. If a pt's tachyarrhythmia doesn't respond to cardioversion, the source of the tachyarrhythmia is most likely not electrical in nature, but instead d/t another cause such as sympathetic stimulation (dehydration, hyperthyroidism, etc.)
If the EKG revealed an atrial etiology, I would think the doc would be more concerned with the pt throwing a clot from her atrium d/t blood pooling, and less with an existing PE. IMO. Also, a HR in the 240's sounds atrial. While it sounds like the pt was symptomatic (i.e. chest pain), she doesn't sound hemodynamically unstable as she was still perfusing with the high BP.
I'm curious what the pt's labs looked like, namely thyroid studies. Also, was a d-dimer drawn? Although not completely specific, an elevated d-dimer could better help support the doc's concern that the pt's CP was d/t a PE and not just poor coronary perfusion d/t a decreased cardiac output.
Also, I'm curious why the doctor drew the line about cardioverting after only a single dose of adenosine for fear of the pt throwing a clot when the intended purpose of adenosine is to cardiovert chemically. I would think that maxing out on adenosine before determining the pt wasn't responding would make more sense, especially since only one dose was given, and who knows how long the pt's heart could've maintained at a rate in the 240's.