Do ACLS medications make any difference in cardiac arrest?
The American Heart Association rates drugs and interventions according to the following scheme:
Procedure/treatment or diagnostic test/assessment should be performed/administered.
It is reasonable to perform procedure/administer treatment or perform diagnostic test/ assessment.
Procedure/treatment or diagnostic test/assessment may be considered
Procedure/treatment or diagnostic test/assessment should not be performed/administered. It is not helpful and may be harmful.
• Research just getting started• Continuing area of research• No recommendations until further research (e.g. cannot recommend for or against).
According to the 2005 AHA Guidelines for managing cardiac arrest:
Magnesium is IIa for Torsades.
Epinephrine and Amiodarone are class IIb.
Vasopressin, Atropine and Lidocaine are class Indeterminate.
In other words, according to the AHA, we have no idea if vasopressin, atropine and Lidocaine work, epi and amiodarone might work, and magnesium likely works. Not the best endorsement.
Now a new study has come out that makes the best attempt yet to answer this crucial question of whether or not ACLS cardiac arrest drugs work, as well as another question: “If the drugs aren’t doing any good, is it the drugs’ fault or perhaps the fault of poor CPR?”
Here’s the study:
It appeared is the November 25, 2009 issue of the Journal of the American Medical Association.
This was a prospective, randomized trial that took place in Oslo, Norway between May 1, 2003 and April 28, 2008. It involved patients 18 and over who suffered out-of-hospital nontraumatic cardiac arrest.
When medics arrived on scene and they opened a sealed envelope that instructed them to either start IV access and proceed with ACLS drugs or do ACLS without drugs and IV access. If ROSC (return of spontaneous circulation) occurred in the non-IV group, they were instructed to wait five minutes before starting an IV and proceeding with post-arrest care.
Medics did 3 minutes of CPR before shocking v-fib and 3 minutes between unsuccessful shocks per European guidelines.
Endotracheal intubation was the prefered airway method.
418 patients received IV meds, 433 did not. The primary outcome was survival to hospital discharge, while secondary outcomes such as hospital admission were also studied.
Patients were excluded if they arrested in the presence of EMS crews.
Personnel carried LifePak 12s capable of recording the quality and quantity of CPR.
Both groups had “adequate CPR” with compression and ventilation rates within the AHA guidelines. All resuscitated patient received therapeutic hypothermia.
Survival to Hospital Discharge
In the IV group 10.5% survived to hospital discharge versus 9.2% in the non-IV group.
Survival with favorable neurologic outcome was 9.8% versus 8.1% in favor of the IV patients.
ROSC was 40% in the IV group, 25% in the non-IV group.
43% IV group to 29% non-IV group in hospital admission
In patients with VT/VF as the presenting rhythm there was no difference between the groups.
In nonVF/VT, ROSC was 3 times higher in the IV group, but there was no difference in the survival rate because patients without the IV did 3 times better in the ICU than those who received the IV and ACLS drugs.
Patients with VF/VT had 10 fold likelihood of survival.
Patients with witnessed arrest had a two fold increase in survival.
Long-terms survival odds decreased by 17% for every minute without CPR
While the IV group did slightly better than the non-IV group, statistically, it was deemed insignificant due to the sample size. The trial would have had to have included 1400 for such a difference to be considered significant.
ACLS drugs make no difference in long-term survival.
IV meds do not delay or affect the quality of CPR.
Patients in VFib/VT may do better without ACLS drugs.
While ACLS drugs can help return circulation to patients in PEA and asystole, they may ultimately be toxic to these patients.
Thought for the Future
Either cardiac arrests patients outside of VF/VT are gennerally not saveable or we need better ACLS drugs.
This study squares with my observations. I have gotten ROSC many times in nonVF/VT patients, and that ROSC almost always comes shortly after I have given them IV epi. (Thus the phrase “That’s the epi talking.” )
Many times (in the old days) when I started working a patient in the house and gave epi down the tube, I would get nothing, but then once removed to the ambulance for transport (as everyone was transported then), I would get a peripheral IV, and give epi and suddenly have ROSC.
Earlier this week I had my first cardiac arrest of the new year, 80-year old man collapses in front of his wife. First responders start CPR. Patient is apneic with no pulse on my arrival. But the monitor shows a sinus brady at 40. I intubate the patient with an initial ETCO2 of 20. With IV epi, the ETCO2 almost immediately goes up to 70 — an indication of ROSC. It then stabilizes in the 35-40 range. We get a bounding pulse with a BP of 110/60. We start the hypothermia protocol. 10 minutes later, I see the ETCO2 start to steadily drop — all the way down to 20. BP is 58/30. Start the dopamine, right away the ETCO2 goes back to 40.* Bounding pulses again. We arrive at the ED with a BP of 120/70. I’m feeling that this could be a save.
An hour later, they are doing CPR on the patient again. When I check back, they tell me he is up in the ICU. He is septic and they have been having a hard time maintaining his BP, giving him 5 liters of saline and using multiple pressors.
Two days later he is in the obits.
Another one bites the dust.
With the exception of patients suspected to be victims of respiratory arrest, all my asystole/PEA ROSC patients have died in the ED or ICU.
The few true cardiac arrest survivors (nonrespiratory induced) I have had in my career have almost all been patients in their 50s and 60s who collapsed in a public place and recieved early CPR, and who (finding them to be in VFIB) I shocked on arrival.
* For an explanation of ETC02 in cardiac arrest see: