One way I look at it is like this:
If the Pt is pulseless, consider that it takes a systolic BP of 40 to produce a palpable carotid pulse. With that fact in mind, a patient that has no palpable carotid pulse cannot be perfusing the brain with the required oxygen. Doppler is a waste of time. The goal here is to deliver O2 to the brain, and while a systolic of 30 may be detectable with a doppler, who cares? The brain is still starving for oxygen.
If he's awake, he's perfusing his brain, maybe not adequately, but perfusing none the less.
A cardiac patient who is having an inferior MI will frequently present atypically- they will most often complain of nausea and vertigo. Such a patient who has a seizure is likely experiencing runs of VT or VF. In such a case, time is critical and preventing the patient from going over the edge is a challenge.
The seizure activity is most likely the pseudo-seizure activity seen with syncope. A patient with a heart rate of 30 would likely have a syncopal event.
You did not mention what rhythm was producing the HR of 30. Was this a wide complex brady? Possibly a ventricular escape rhythm? Or was it a high degree AV block? Since this was an inferior wall, did you perform a 12 lead containing a right sided lead, such as V4R? If there was right sided involvement, that further complicates things.
Should have been done.
Atropine given in such cases has been known to precipitate VF. Atropine increases myocardial oxygen demand, and if it fails to increase cardiac output in the process, you have just made the problem worse.
Atropine increases myocardial oxygen demand by increasing heart rate. The faster a heart beats, the more o2 it consumes. If the atropine fails to increase hr, it shouldn't increase MVO2. Depending on underlying rythm, atropine could prove useful.
A better choice in such a case could be dopamine at 2-10 mcg/kg/min, assuming that pacing is not possible. Remember that this is a cardiogenic shock you are dealing with here.