Question: When running an ALS arrest where the patient is showing a PEA on the monitor with an accompanying high ETCO2, could we assume that this patient is in fact perfusing to some degree and pulses are just not palpable for various reasons (obesity, severe hypotension, etc.)?

Secondly, if the above assumption is correct, would it be prudent to stop CPR provided the ETCO2 remains high and administer Dopamine in hopes of increasing BP until pulses are palpable and BP obtainable; or should the vasopressor effects of Epinephrine be sufficient to facilitate this so just continue with Epinephrine q5 min and CPR?