ACLS 2015

This has already been the subject of numerous social media posts since the guidelines were released in November.  Here I'll just comment on what I believe to be the most important changes since 2010.

The full text of the guideline issue of Circulation is here.

A new and different format for future updates.

Instead of continuing with a single update release every 5 years ACLS guidelines will now transition to a continuously updating web based format. The link to that web site is here.

Scientific advances influence ethical decision making.

The loftiest ethical principles are next to useless if not supported by appropriate scientific understanding. Put another way, many bad decisions are made not because of fundamentally bad ethics but because of a lack of understanding about what available technology will and won't do. Examples relevant to ACLS 2015 include therapeutic hypothermia and ECMO.

New upper limits of compression rate and depth.

This became necessary to deal with a manifestation of the law of unintended consequences. When word got out that we should fall on top of the chest and push hard and fast people at times got carried away. Accumulating evidence suggested that excessive rate and depth were associated with lower ROSC rates and more injury, respectively. Here's what the new guidelines have to say about it:

In adult victims of cardiac arrest, it is reasonable for rescuers to perform chest compressions at a rate of 100 to 120/min (Class IIa, LOE C-LD). The addition of an upper limit of compression rate is the result of 1 large registry study associating extremely rapid compression rates with inadequate compression depth.

During manual CPR, rescuers should perform chest compressions at a depth of at least 2 inches or 5 cm for an average adult, while avoiding excessive chest compression depths (greater than 2.4 inches [6 cm]) (Class I, LOE C-LD).

But how do you gauge your own compression depth down to tenths of an inch?

New recommendations for patients with respiratory arrest and suspected opioid abuse.

From the executive summary:

For patients with known or suspected opioid addiction who have a definite pulse but no normal breathing or only gasping (ie, a respiratory arrest), in addition to providing standard BLS care, it is reasonable for appropriately trained BLS providers to administer intramuscular or intranasal naloxone (Class IIa, LOE C-LD).

At long last the guidelines acknowledge the Arizona protocol for cardiocerebral resuscitation (CCR) but don't go far enough.

Again from the executive summary:

For witnessed OHCA with a shockable rhythm, it may be reasonable for emergency medical service (EMS) systems with priority-based, multi-tiered response to delay positive-pressure ventilation by using a strategy of up to 3 cycles of 200 continuous compressions with passive oxygen insufflation and airway adjuncts (Class IIb, LOE C-LD).

We do not recommend the routine use of passive ventilation techniques during conventional CPR for adults, because the usefulness/effectiveness of these techniques is unknown (Class IIb, LOE C-EO). However, in EMS systems that use bundles of care involving continuous chest compressions, the use of passive ventilation techniques may be considered as part of that bundle (Class IIb, LOE C-LD).

For some background on CCR read here. The first sentence of the second paragraph above is misleading. Although data in support of CCR might be considered low level by some EBM purists the evidence in the aggregate is convincing, as cited in the link above. Despite evidence of better neurologically intact survival attributable to CCR it only gets a IIb recommendation. In this particular area the guideline, in my opinion, is about a decade out of date.

Despite an emerging body of evidence for point of care ultrasound it is given only brief mention in the guidelines.

From part 7 of the guideline:

Bedside cardiac and noncardiac ultrasound are frequently used as diagnostic and prognostic tools for critically ill patients.44 Ultrasound may be applied to patients receiving CPR to help assess myocardial contractility and to help identify potentially treatable causes of cardiac arrest such as hypovolemia, pneumothorax, pulmonary thromboembolism, or pericardial tamponade.45 However, it is unclear whether important clinical outcomes are affected by the routine use of ultrasound among patients experiencing cardiac arrest.

Changes in the recommendations for vasopressin.

It has been removed from the routine algorithms but inserted in a new bundle that has a low level recommendation. Again from the executive summary:

Vasopressin was removed from the ACLS Cardiac Arrest Algorithm as a vasopressor therapy in recognition of equivalence of effect with other available interventions (eg, epinephrine). This modification valued the simplicity of approach toward cardiac arrest when 2 therapies were found to be equivalent.

BUT…

A IIb recommendation for vasopressin as part of a bundle was given for in hospital cardiac arrest. From the executive summary:

The use of steroids in cardiac arrest is controversial. In OHCA, administration of steroids did not improve survival to hospital discharge in 2 studies, and routine use is of uncertain benefit. The data regarding the use of steroids for IHCA were more vexing. In 2 randomized controlled trials led by the same investigators, a pharmacologic bundle that included methylprednisolone, vasopressin, and epinephrine administered during cardiac arrest followed by hydrocortisone given after ROSC improved survival. Whether the improved survival was a result of the bundle or of the steroid therapy alone could not be assessed. As a result of this study, in IHCA, the combination of intra-arrest vasopressin, epinephrine, and methylprednisolone and postarrest hydrocortisone as described by Mentzelopoulos et al16 may be considered; however, further studies are needed before the routine use of this therapeutic strategy can be recommended (Class IIb, LOE C-LD).

The study in question is linked here.

ECMO (ECPR) is given a IIb recommendation in limited situations when expertise is available.

From part 6:

There is insufficient evidence to recommend the routine use of ECPR for patients with cardiac arrest. In settings where it can be rapidly implemented, ECPR may be considered for select patients for whom the suspected etiology of the cardiac arrest is potentially reversible during a limited period of mechanical cardiorespiratory support (Class IIb, LOE C-LD). Published series have used rigorous inclusion and exclusion criteria to select patients for ECPR. Although these inclusion criteria are highly variable, most included only patients aged 18 to 75 years, with arrest of cardiac origin, after conventional CPR for more than 10 minutes without ROSC. Such inclusion criteria should be considered in a provider’s selection of potential candidates for ECPR.

Lipid rescue (ILE) is given a IIb recommendation.

From part 10:

It may be reasonable to administer ILE, concomitant with standard resuscitative care, to patients with local anesthetic systemic toxicity and particularly to patients who have premonitory neurotoxicity or cardiac arrest due to bupivacaine toxicity (Class IIb, LOE C-EO). It may be reasonable to administer ILE to patients with other forms of drug toxicity who are failing standard resuscitative measures (Class IIb, LOE C-EO).

A multimodal approach to estimation of prognosis.

There are detailed updated recommendations for combining neuro exam findings, imaging findings, EEG findings and biomarkers in the guideline. Of interest, for intubated patients, failure to achieve an ETCO2 of greater than 10 is a negative indicator that can be combined with other findings in the estimation of prognosis.

Techniques to promote negative intrathoracic pressure and mechanical CPR devices were reviewed.

These were all either given a IIb recommendation or not recommend at all.

When PE is the cause of the arrest

From part 10:

In patients with confirmed PE as the precipitant of cardiac arrest, thrombolysis, surgical embolectomy, and mechanical embolectomy are reasonable emergency treatment options (Class IIa, LOE C-LD). Comparative data are not available to recommend one strategy over another. Patient location, local intervention options, and patient factors (including thrombolysis contraindications) are recognized elements to be considered. Thrombolysis can be beneficial even when chest compressions have been provided (Class IIa, LOE C-LD). Given the poor outcomes associated with fulminant PE in the absence of clot-directed therapy, standard contraindications to thrombolysis may be superseded by the need for potentially lifesaving intervention.

This, unfortunately, is not very helpful. In the peri-arrest situation the best opportunity for benefit with thrombolytic therapy usually comes when PE is only suspected, not confirmed. But for merely suspected PE the authors give no recommendation one way or the other, citing a lack of evidence.

Updated recommendations for post arrest evaluation and care.

An EEG is recommend for all comatose post arrest patients to diagnose possible seizure, whether or not motor activity is manifested. The guideline cites evidence that epileptiform activity, including non convulsive seizures, may have a prevalence as high as 22%. This is a class I recommendation. The recommendation for antiepileptic drugs is similar to that for status epilepticus in general.

A post arrest oxygen saturation target of 94% is recommended.

There being insufficient evidence, no blood glucose targets are recommended.

No special hemodynamic goals were recommended other than the avoidance of hypotension, meaning SBP below 90 or MAP below 65. This is a IIb recommendation.

Early cardiac catheterization is recommended for all patients in whom an acute coronary event is merely suspected, with or without ST elevation and regardless of neurologic status.

Therapeutic hypothermia is recommend for 24 hours for all post arrest patients not following commands, regardless of presenting rhythm or location of the arrest. No absolute contraindications were given. The new target is 32 to 36 C inclusive.

Defer estimation of neurologic prognosis until: 72 hours post ROSC in those not treated with hypothermia (add estimated time for sedatives and paralytics to wear off) and 72 hours post return to normothermia plus similarly added time in those treated with hypothermia. This often amounts to 4 or 5 days in hypothermia patients.