Quote:
Originally Posted by Trapper John
Given the history of cardiomyopathy and the drugs on board along with the expression of a sense of impending doom in this patient, I would want to take a closer look at the lungs for signs of pulmonary edema. Do we have a PO2 on this patient? Standing by with a dose of digoxin might not be a bad idea.
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One of the things I like about this case is that the scenario I've given is actually how it played out. I got to do an H&P then look at the EKG before @#$& hit the fan, and had to develop a quick starting differential based solely on the info I had. Certainly more things were ordered later but for the sake of the scenario, let's work on the differential we have. Later on we can talk about ordering more studies.
There were no signs of pulmonary edema on auscultation and no other signs of acute decompensated CHF.
However you mentioned the history of cardiomyopathy, so I'm going to throw that on the differential. This guy has a history of hypertrophic cardiomyopathy that has *in theory* been corrected, but no treatment is perfect and all of the various procedures used to correct hypertrophic cardiomyopathy are no exception. Hypertrophic cardiomyopathy kills in two primary ways: its an arrhythmogenic condition unto itself and obstruction can occur when a combination of septal hypertrophy and systolic anterior motion of the mitral valve, where the valve flips over and blocks aortic outflow tract.
This obstruction is an important differential to consider because we treat it substantially differently than a normal cardiac arrest: goals are to increase preload (fluids) AND increase systemic vascular resistance (phenylephrine) while sparing any inotropic agents (epi, norepi included) to the extent possible.
So while I had (and still have) a hard time gauging how likely this guy would really be to have obstructive HCM, one can't ignore a history of HCM in a guy with scary-sounding syncope and chest pain.
So the list stands at:
Long QT
Hypertrophic Cardiomyopathy
MVP>Arrhythmia