ADRENALINE AND CARDIAC RESUSCITATION
How much to use, when to use it and when not to use it.
The resuscitation guidelines were born in the black-and-white television era, at the end of the 1950’s. The use of 1 mg of adrenaline which initially came from canine models, was introduced at this time and has been a major part of all resuscitations since then.
The clinical significance of adrenaline is uncertain. It’s been shown to give no improvement and even to decrease survival to hospital discharge and decrease the rate of favourable neurological outcomes(1). Steil(2) in the multi-centre OPALS study demonstrated no improvement in neurologically intact survivors to hospital discharge when using advanced life-support. We know that high-dose adrenaline doesn’t improve outcomes(3).
Jacobs(4), further randomised 601 cardiac arrest patients and found a significantly improved likelihood of achieving return of spontaneous circulation(ROSC) in the adrenaline group. There was a trend to increased survival to discharge in this group, unfortunately the study was underpowered.
IS THERE A RIGHT DOSE OF ADRENALINE?
Giving 1mg of adrenaline to a heart that has just resumed beating, can have dire consequences. The effect of markedly increased afterload against which a weak heart must beat, can result in a rapid loss of circulation. The adrenaline dose must be titrated to achieve adequate coronary and cerebral perfusion.
Our aim should be to achieve a coronary perfusion pressure of above 15 – 20 mmHg. This equates to diastolic blood pressure of 25 – 35 mmHg (5), which has been shown to provide adequate cerebral perfusion pressure.
Monitoring with an arterial line is the only way to do this accurately. As I have discussed at several EMCORE conferences, the aim is to locate the femoral artery with ultrasound during the first rhythm check pause and to then pass the catheter during the second rhythm check. This requires practice and coordination of the team.
If you don’t have an arterial line, don’t trust the pulse check, or the electrical wave form. Use the cardiac ultrasound to verify whether the heart is beating or not.
In the FEEL study(6) it was found the 38% of patients with asystole on the ECG, had coordinated cardiac motion on echo. It was further found that 58% of those in PEA had coordinated cardiac motion seen when the heart was visualised. Hypothesize what might happen with the massive alpha effects of giving 1 mg of adrenaline to these hearts. Keep the dose small if the heart is beating.
WHEN SHOULD ADRENALINE NOT BE GIVEN?
1. If the heart is beating and the diastolic blood pressure is > 40mmHg, don’t give adrenaline. If the blood pressure is less than this, a small amount can be given ie., 30-50mcg, but not the full 1mg.
2. In Refractory VT/VF. This is due to a catecholamine surge. Adrenaline only serves to increase that surge. If you can’t get the patient out of these rhythms for a prolonged period, then stop the adrenaline.
A recent study demonstrated esmolol as being very effective for these catecholamine driven arrhythmias. This was a small retrospective study(7) where they used 500mcg/kg as a bolus dose and then an infusion to follow. This may have been a small study, but the use of beta blockers for ‘electrical storm’ is known to be effective in these situations.
3. Do not give adrenaline late in the resuscitation.
Dumas(8) describes the three phases of cardiac resuscitation:
- The Electrical Phase: This occurs in the first few minutes following cardiac arrest. There is no place for adrenaline at this point.
- The Circulatory Phase: This lasts for 10-15 minutes and it is the phase where patients benefit most form CPR and adrenaline.
- The Metabolic Phase: This phase occurs approximately 20 minutes after a cardiac arrest. In this phase adrenaline has been found to be detrimental.
Consider not giving adrenaline after the first 3 doses or after 20 minutes into the resuscitation.
Giving the right dose of adrenaline at the right time and knowing when not to give it, are essential for improved survival from cardiac arrest.
References
- Reardon P. et al. Epinephrine in out of hospital cardiac arrest: A critical review. World J of EM. Vol 4, No 2, 2013.
- Steil I G et al. Advanced cardiac life-support and out of hospital cardiac arrest. NEJM 2004:351:pp647 -656.
- Steil I G et al. High dose epinephrine in adult cardiac arrest. NEJM 1992; 327: 1045-1050
- Jacobs I G et al. Affect of adrenaline on survival in out of hospital cardiac arrest: A randomised double blind placebo controlled trial. Resuscitation, September 2011. Vol 82, Iss 9, pp1138-1143.
- Sutton R M et al. Hemodynamic directed CPR improves short-term survival from asphyxia – associated cardiac arrest. Resuscitation 2013, May; 84 (5): pp696-701.
- Breitkreutz R et al. Focused echocardiographic evaluation of life-support and peri-resuscitation of emergency patients: A prospect of trial. Resuscitation November 2010, vol 81, iss 11 , pp 1527-1533.
- Driver BE et al. Use of esmolol after failure of standard Cardiopulmonary Resuscitation to treat patients with the refectory ventricular fibrillation. Resuscitation 2014 Oct; 85 (50): pp1337-1341.
- Dumas F et al. Is epinephrine during cardiac arrest associated with worst outcomes in resuscitated patients? JACC. Vol 64. No 22 Dec 9, 2014. pp2360-2367.
Dr Peter Kas
Dear A/Prof Dr Kas
Thank you for thin enlightening summary about Adrenaline role in resuscitation. This highlights the facts that Adrenaline is really a double sided sword and the current practice is to use its sharp edge, early, aggressively and for prolonged period of time. I hope some of the facts you have shared on your Blog could be incorporated into the currently available resuscitation guidelines.
[…] there a better way to dose epinephrine in cardiac arrest? Resus Australia has some epinephrine dosing recommendations […]
” after the first 3 doses or after 20 minutes into the resuscitation”
it seems the first 3 doses should occur far before 20 mins in almost all resus attempts, no?
It’s probably true in many cases. However in cases where there is witnessed arrest and CPR giving low flow and rapid response, we get them before that time. In situations where they have received 3 mg of adrenaline for example and they come in late, I don’t keep giving it.
All of your references are rather old without clear evidence. Refer to G. Perkin et al., NEJM, 2018: PARAMEDIC-2 trial (Pre-hospital Assessment of the Role of Adrenaline: Measuring the Effectiveness of Drug administration In Cardiac arrest). Significant increase of ROSC, only small increase of worse neurological outcome.
The point we all make and what we take away from these trials differ. My whole purpose is to try and get patients well and out. The Paramedic II trial gives me even greater hope. I’m interested in them getting to my ED. When that happens, when we treat them in the right way results in increased possibilities. That’s what I take from this. New trial, doesn’t change my practice much, not many other resuscitation guys approaches. Thanks for reading and for the comment. We debated this at the EMCORE.
Peter
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