Cardiovascular Critical Care II
| (e) | Prehospital methylprednisolone in primarily shockable rhythms was studied in a phase II |
|---|
study and demonstrated significant reductions in inflammatory markers associated with
may be warranted to determine the clinical impact of these findings.
iii.
Antiarrhythmics:
| (a) | No evidence that, in cardiac arrest, any antiarrhythmics increase survival to discharge. |
|---|---|
| (b) | Conflicting evidence on benefit of amiodarone and lidocaine (Table 3) in the prehospital |
arrest situation:
| (1) | Amiodarone or lidocaine may be considered for VF/pVT that is unresponsive to |
|---|
defibrillation (Circulation 2019;140:e881-e894).
| (2) | Investigation has found that amiodarone (300 mg) increased rates of survival to hospital |
|---|
admission compared to placebo in shock-refractory VF/pVT in those who received at
least 3 shocks and epinephrine (N Engl J Med 1999;341:871-8). Additionally, 5 mg/
kg amiodarone improved survival to hospital admission compared with 1.5 mg/kg
lidocaine (N Engl J Med 2002;346:884-90). These 2 studies did not find evidence of
improved survival to hospital discharge. Additionally, a comparison in patients with
VF/pVT considered refractory after at least 1 shock, which found that ROSC was higher
in patients receiving lidocaine compared with those receiving placebo, but not for those
receiving amiodarone. Survival to hospital admission was higher with amiodarone or
lidocaine compared to placebo, but no difference in survival with good neurological
outcome or survival to hospital discharge in any group (N Engl J Med 2016;374:1711-
22). These drugs may be particularly useful for patients with witnessed arrest, for whom
time to drug administration may be shorter (Circulation 2019;140:e881-e894).
| (3) | Amiodarone should be administered as undiluted intravenous/intraosseous push if |
|---|
pulseless. Dosing should be 300 mg with repeat dosing of 150 mg (Table 3).
| (4) | If pulse is obtained, the suggested dose is 150 mg, which must be given as slow |
|---|
intravenous piggyback over at least 15 minutes and is typically followed by a continuous
intravenous infusion.
| (5) | Hemodynamic effects of bradycardia and hypotension may be partly related to |
|---|
| (c) | Magnesium sulfate (Table 3) is effective for cardiac arrest caused by torsades de pointes. |
|---|
(i.e., caused by early afterdepolarizations during phase 2 of the action potential).
| (1) | Not effective when VF/pVT is not associated with torsades de pointes. |
|---|---|
| (2) | May consider for emergency magnesium replacement in patients who sustain cardiac |
arrest and are hypomagnesemic.
| (3) | Optimal dosing has not been established. |
|---|---|
| (d) | In patients with non-shockable rhythms that become shockable in OHCA, investigation has |
shown some numeric benefit of antiarrhythmics, perhaps warranting further investigation
in this patient group (Circulation 2017;136:2119-31).