In Part 2 of this episode on ACLS Guidelines – Atropine, Adenosine & Therapeutic Hypothermia, Dr. Steven Brooks and Dr. Michael Feldman discuss the removal of Atropine from the PEA/Asystole algorithm, the indications and dangers of Adenosine in wide-complex tachycardias, pressors as a bridge to transvenous pacing in unstable bradycardias, and the key elements of post cardiac arrest care including therapeutic hypothermia and PCI.

They answer questions such as: In which arrhythmias can Amiodarone cause more harm than good? Is there any role for transcutaneous pacing for asystole? When should Bicarb be given in the arrest situation? In what situations is Atropine contra-indicated or the dosage need to be adjusted? How has the widespread use of therapeutic hypothermia currently effected our ability to prognosticate post-arrest patients? What are the indications for PCI and thrombolysis in the cardiac arrest patient? Should we be using therapeutic hypothermia in the non-Vfib arrest patient? What is the best method for achieving the target temperature for the patient undergoing therapeutic hypothermia? and many more……

Written Summary and blog post written by Lucas Chartier, March 2011

Cite this podcast as: Brooks, S, Feldman, M, Helman, A. Part 2: ACLS Guidelines – Atropine, Adenosine & Therapeutic Hypothermia. Emergency Medicine Cases. March, 2011. Accessed [date].

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Pharmacology in ACLS Guidelines & Cardiac Arrhythmias

  • Atropine for Asystolenot recommended in asystole and PEA anymore, not due to negative studies, but rather to the realization that the evidence was always weak and therefore shouldn’t be considered positive
  • Atropine for Bradycardia: may increase ischemia in the setting of an MI, doesn’t work in transplant patients and is unlikely to work in patients with 2nd degree type II and 3rd degree block
  • Adenosine for Wide-complex Tachycardias: on top of stable narrow‐complex regular tachycardia, the 2010 guidelines recommend using it in stable wide‐complex regular (i.e. monomorphic) tachycardia as well as a diagnostic approach, given that it might unmask SVT with aberrancy but won’t do much for VT
    • Beware of the irregular (i.e. polymorphic) wide‐complex tachycardia, which may mask an alternative pathway such as Wolff‐Parkinson‐White’s, in which case adenosine may precipitate VF
    • Reduce the dose of adenosine (to 3mg) in post–cardiac transplant patients, those taking dipyridamole or carbamazepine, and when administered via a central vein access
  • Amiodarone or procainamide for Stable Vtach: the former has been shown in small studies to terminate dysrhythmias in only about 30% of cases, and latter, as much as 80%; patients receiving either should be monitored for QT prolongation and hypotension, and should never receive both medications due to the risk of refractory bradycardia and/or hypotension
  • NaHCO(sodium bicarbonate) in cardiac arrest: should not be used routinely because of resultant paradoxical intracellular acidosis, but may be considered in known or suspected hyperkalemia (eg, dialysis patient) TCA overdose, or documented pre‐existing metabolic acidosis as a cause for cardiac arrest
  • Inotropes for Bradycardia: dopamine (10μg/kg/min) or epinephrine (2‐10μg/min) drips may now be given as an alternative to transthoracic pacing, as a bridge to transvenous pacing

Post-cardiac arrest care

“Getting the pulse back is just the beginning”

  • Avoid SpO2 of 100% because it leads to increased production of harmful free radicals and increases mortality – aim instead for 94%
  • Avoid hyperventilation, which leads to hypocarbia and resultant cerebral vasoconstriction, which will worsen brain injury due to the decreased cerebral blood flow; also avoid hypotension
  • Activate emergency PCI for post‐arrest STEMI, and strongly consider for suspected high‐risk NSTEMI; PCI and therapeutic hypothermia can and should be done together; thrombolysis should be considered on an individual basis when PCI is not available; there is a theoretical increased bleeding risk when thrombolysis is combined with therapeutic hypothermia

emcases-updateUpdate 2023: A multicenter, parallel-group, randomized controlled trial including 428 unconscious adults with ROSC after OHCA found that targeting an oxygen saturation of 90-94% compared to 98-100% until admission to ICU did not significantly improve survival to hospital discharge (38.3% survival vs 47.9% survival respectively, difference -9.6%, 95%CI -18.9% to -0.2%) (EXACT trial). Note – the trial was stopped early due to the COVID-19 pandemic. Abstract

emcases-updateUpdate 2023: A pragmatic, cluster-randomized and cluster-crossover trial with 2,541 patients receiving mechanical ventilation in the ED or ICU comparing lower oxygen saturation target (90%, goal range 88-92%), intermediate target (94%, goal range 92-96%), and higher target (98%, goal range 96-100%) found that the number of ventilator free days and in hospital death by 28 days were not significantly different between the three groups. Median number of ventilator free days was 20, 21, and 21 respectively, and in hospital death by 28 days was 34.8%, 34%, and 33.2% respectively (PILOT RCT). Abstract

Therapeutic Hypothermia in the ACLS Guidelines

Therapeutic hypothermia (TH) – a good resource:

Reduces or stops destructive pathways such as cerebral edema and free radicals formation, which are caused by reperfusion after ROSC; has been shown to increase survival to hospital discharge with good neurological outcome (NNT of 6!)

Although strong evidence (i.e. RCTs) is available only for VF/VT as presenting rhythms, the 2010 guidelines recommend TH in PEA and asystole based on positive observational studies

TH should not be done in cardiac arrests resulting from trauma because it will worsen coagulopathy in a hypovolemic and bleeding patient, as well as in vasopressor‐resistant severe cardiogenic shock (controversial) because the cold will make the myocardium less responsive to drugs

Cooling should be started as soon as possible in the ED (not in the ICU) with cooled IV saline boluses (30cc/kg or 2L) with pressure bags, and ice packs to the axillae, groin and neck, even if the patient will go to the cath lab; goal of 32‐34°C within 6‐8hrs

Patients need to be adequately sedated (midazolam, fentanyl), but paralysis should only be used to prevent shivering (which often stops below 33.5°C) because it may mask seizure activity, which is rendered more likely by ischemic brain injury

Consider the following initial ventilation settings: Tidal volume of 6‐8mL/kg with rate adjusted to obtain an end‐tidal CO2 of 35‐40mmHg and FiO2 adjusted to obtain arterial saturation of 94%; also prevent hyperventilation and hypocarbia

Prognostication cannot be accomplished until 72hrs after the cardiac arrest, which is later than what used to be done in the pre‐cooling era

  • *note that recent evidence suggests that cooling to to 33°C may not have benefit compared with 36°C as per the NEJM ‘Targeted Temperature Management (TTM) Trial in 2013 (full pdf here)

emcases-update Update 2021: CAPTAIN CHILL (single-center, double-blind) randomized clinical trial of 367 comatose survivors of out-of-hospital cardiac arrest. Targeting moderate hypothermia (31 °C) for 24 hours, as opposed to mild hypothermia (32-36 °C; current guideline recommendation), did not reduce rate of death or poor neurologic outcomes at 180 days.   Abstract

For more on ACLS guidelines on EM Cases:

Episode 12 Part 1: ACLS Guidelines – What’s New & Controversial
Episode 71 ACLS Guidelines 2015 – Cardiac Arrest Controversies Part 1
Episode 72 ACLS Guidelines 2015 Post Arrest Care
EM Quick Hits 27 on Evidence for Bicarb in Cardiac Arrest 2021

Key References