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Vasopressors in prehospital traumatic arrest

Blueflightmedic trauma at emergencyunit.com
Thu Dec 2 10:33:40 GMT 2010


Traumatic cardiac arrest has three causes. Hypovolaemia, hypoxaemia and
massive brain damage. Item 1 is treatable, item 2 may be and item 3 is not.

Atropine has been discontinued in the latest ILCOR/RCUK guidelines so that
should not be given. 

Adrenaline/epinephrine is not a recognised treatment for any of the above
conditions, and of no use in spontaneous cardiac arrest either:

Resuscitation
Volume 30, Issue 3 , Pages 243-249, December 1995
High dose and standard dose adrenaline do not alter survival, compared with
placebo, in cardiac arrest S.P. Woodhouse, S. Cox, P. Boyd, C. Case, M.
Weber.

Abstract 

This trial compared blinded 10 mg aliquots of adrenaline with placebo in 194
cardiac arrest patients treated in hospital using American Heart Association
guidelines. In-hospital and out-of-hospital arrests were included. Of the
339 eligible patients a large proportion (145 (45%)) were not randomised and
received open 1 mg aliquots of adrenaline. This group is also analysed.
Supervising physicians gave significant preference for males, patients with
no previous cardiac history and without multiple organ disease to be given
open 1 mg adrenaline. Patients in asystole at the time of consideration for
entry were preferentially placed in the trial group (114 (69%) vs. 170
(88%)) and patients in ventricular fibrillation were preferentially given
open 1 mg adrenaline (31 (21%) vs. 24 (12%) P < 0.03). The most beneficial
rhythm changes which led to survival were sinus rhythm and ventricular
tachycardia. Analysis of rhythm changes resulting from the dosing showed a
significant (P = 0.01) change to a beneficial rhythm with 10 mg adrenaline
but not for 1 mg adrenaline or placebo. This was not reflected by an
improvement in immediate survival. No significant differences in immediate
survival (IS) or hospital discharge (HD) exists between open 1 mg adrenaline
(IS 14 (9.7%), HD 3 (2%)) or the 10 mg adrenaline (IS 9 (9.6%), HD 0) vs.
placebo (IS 7 (7%), HD 0) trial arms. Patients reaching the point of use of
adrenaline have a uniformly poor immediate survival (8.8%) and hospital
discharge rate (0.9%). Dosing with 10 mg or 1 mg adrenaline does not
influence outcome compared with placebo.

A Randomised Placebo Controlled Trial of Adrenaline in Cardiac Arrest - the
PACA Trial. Ian Jacobs; Judith Finn; George Jelinek; Harry Oxer; Peter
Thompson

Background: Adrenaline (Epinephrine) remains the primary pharmacological
agent in cardiac arrest. Despite a total absence of any experimental trials
to establish efficacy, adrenaline is considered standard of care in
resuscitation.

Methods: We undertook a double-blind randomised placebo controlled trial of
adrenaline in out-of-hospital cardiac arrest in Perth, Western Australia
between August 2006 and November 2009. Patients were randomly assigned to
receive either 1 ml aliquots of adrenaline 1:1000 or Sodium Chloride (0.9%)
by means of computerised random number generator. Primary outcome was
survival to hospital discharge and secondary outcomes included return of
spontaneous circulation (ROSC) and neurological outcome (Cerebral
Performance Category Score) at hospital discharge. Odds ratios (OR) and 95%
confidence intervals were derived for these outcomes and analysis was on an
intention to treat basis.

Results: During the study period paramedics attended 4107 cardiac arrests of
which resuscitation was commenced in 1586 (38.6%) patients. Of these 602
(37.9%) were enrolled into the study with a further 67 (11.1%) being
excluded after randomisation. Of the remaining 535 patients 262 (48.9%) and
273 (51.0%) received placebo or adrenaline respectively. The percentage male
(70.6% versus 74.8%); mean age (64.8 versus 65.4 years) and percentage of
patients who received bystander CPR (55.7% versus 53.1%) were similar for
the adrenaline and placebo groups respectively. ROSC was achieved in 83
(30.4%) patients receiving adrenaline and 29 (11.1%) receiving placebo - OR=
3.51 [95% CI 2.21 to 5.58]. Survival to hospital discharge occurred in 11
(4.1%) and 5 (1.9%) of the adrenaline and placebo patients respectively -
OR= 2.16 [95% CI: 0.74 to 6.30]

Conclusions: The use of adrenaline in cardiac arrest was associated with a
significant increase in the proportion of patients achieving ROSC however
this improvement did not extend to survival to hospital discharge. As our
results are unable to rule out a clinically meaningful benefit of adrenaline
in terms of survival to hospital discharge, further investigation into the
post resuscitation period for those achieving ROSC is required in order to
identify management strategies to improve survival.

Efficacy of Intravenous Adrenaline Administration in Patients with
Out-of-Hospital Cardiac Arrest
Yoshio Tahara; Noriyuki Suzuki; Yoshihiro Moriwaki; Takayuki Kosuge;
Nobuyuki Harunari; Yasushi Matsuzawa; Kenichirou Saka; Kazutoshi Minami;
Masayoshi Kiyokuni; Naoki Nakayama; Katsutaka Hashiba; Nobuhiko Maejima;
Kazuo Kimura; Satoshi Umemura; Seiji Takanashi


Background: Adrenaline has been routinely administered to patients who
receive cardiopulmonary resuscitation (CPR); however, its effects on
outcomes remain unclear. Since April 2006, emergency medical technicians
(EMTs) have been able to administer intravenous adrenaline to patients
before arrival at the hospital in Japan. At present, some EMTs are qualified
to administer intravenous adrenaline to patients, while the others are not.
It is therefore an optimal time to compare the outcomes of patients with
out-of-hospital cardiac arrest (OHCA) according to whether they had received
intravenous adrenaline before admission.

Methods: This was a multicenter retrospective study. Of 7202 patients who
were admitted to 12 hospitals in Yokohama because of OHCA from April 2006
through October 2008, we studied 723 patients in whom an EMT secured
peripheral venous pathways before hospital admission. Patients were divided
into two groups: those in whom adrenaline was given intravenously before
admission by an EMT qualified to administer intravenous adrenaline
(adrenaline group) and those in whom intravenous adrenaline was not given
because the EMT was unqualified (non-adrenaline group). The outcomes
(prehospital return rate of spontaneous circulation, hospital admission rate
of survivors, survival rate at 1 month, and rate of favorable neurologic
recovery) were compared between the groups.

Results: The return rate of spontaneous circulation before arrival at the
hospital (11% vs. 6%, p=0.01) and the hospital admission rate among the
survivors (36% vs. 25%, p<0.01) differed significantly between the
adrenaline group (N=351) and the non-adrenaline group (N=372). However, the
survival rate at 1 month (3% vs. 3%, p=0.80) and the rate of favorable
neurologic recovery did not differ significantly between the groups (1% vs.
2%, p=0.13).

Conclusion: Intravenous adrenaline administration before arrival at the
hospital can improve short-term outcomes in patients with OHCA, but did not
increase the frequency of neurological outcome.

-----Original Message-----
From: trauma-list-bounces at trauma.org [mailto:trauma-list-bounces at trauma.org]
On Behalf Of caesar ursic
Sent: 02 December 2010 04:19
To: Trauma-List [TRAUMA.ORG]
Subject: Re: Vasopressors in prehospital traumatic arrest

My own admittedly anecdotal observations over the years have been that
patients pretty much dead at the scene (either asystolic or with an terminal
'escape' rhythm on ECG strip) are temporarily 'revived' by medics with doses
of epinephrine and atropine (producing some sort of cardiac rhythm with no
real cardiac output) that gets them to the ER just in time for the assembled
team to be 'compelled' into 'doing something' because - "look, the heart's
beating!"  Unfortunately despite chest tubes, more epinephrine, the
occasional anterolateral thoracotomy, closed chest compressions, etc - the
cardiac rhythm deteriorates and no BP is ever obtained.  So I think that in
the vast majority of patients just have their death pronouncements delayed
and many get unnecessary procedures performed.  of course the occasional
'medical' arrest presumed to be traumatic might benefit from prehospital
ACL-like drugs, but that's a rare exception.
I have no data with which to back this opinion up.  Just observation.




On Wed, Dec 1, 2010 at 1:58 PM, Kmattox <kmattox at aol.com> wrote:

> Futility.   When God puts her or his hand take yours off.   Recognize
> death.  Dead people tend to remain dead.   Do not make the ultimate
> pronouncement more painful and expensive.
>
> k
>
> Sent from my iPhone
>
> On 2010-12-01, at 4:00 PM, caesar ursic <cmursic at gmail.com> wrote:
>
> > What, if any, is the role of epinephrine or atropine (the "typical" ACLS
> > cardiac arrest drugs) in prehospital traumatic arrest?
> > Do you approach the 35 year old who has had 15 mins of prehospital CPR
> after
> > falling off a third story balcony (because he was found "pulseless and
> > bradycardic" at the scene) once he arrives in your ER any differently if
> he
> > has / has not received multiple doses of epi and atropine (assuming that
> the
> > patient is still pulseless but has some sort of ECG rhythm on arrival)?
> > Just curious.
> >
> > CM Ursic, MD
> > Honolulu
> > --
> > trauma-list : TRAUMA.ORG
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