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2015 AHA BLS And Update 2015 AHA BLS and 40 l Nursing2016 l Volume 46, Number 2 www.Nursing2016.com Copyright © 2016 Wolters Kluwer Health, Inc. All rights reserved. ACLS guidelines By Karen Jean Craig-Brangan, BS, RN, EMT-P, and Mary Patricia Day, MSN, RN, CRNA ADVANCED CARDIOVASCULAR life support (ACLS) encompasses the entire spectrum of care from basic life support (BLS) to postcardiac arrest care. The 2015 American Heart Association (AHA) guidelines include recommendations on the use of I.V./intraosseous (I.O.) epinephrine, I.V./I.O. vasopressin during cardiac arrest, and end-tidal carbon dioxide (ETCO2) measurements to predict patient outcome.1 Let’s take a closer look at these changes and more. Managing cardiac arrest in an adult The Adult Cardiac Arrest Algorithm outlines a plan of care for the patient in cardiac arrest sec- ondary to pulseless ventricular tachycardia (pVT)/ ventricular fibrillation (VF). After determining unresponsiveness, apnea, and pulselessness, the clinician administers chest compressions and ventilations at a ratio of 30:2 respectively until an advanced airway is in place. Advanced air- ways include an endotracheal tube (ETT) or supraglottic airway (SGA) device such as a laryn- geal mask airway, laryngeal tube, or esophageal obturator airway. The new BLS guidelines recommend a com- pression rate of at least 100/minute and no great- er than 120/minute, and a compression depth of at least 2 in (5 cm) and no greater than 2.4 in (6 cm) for an average adult.2 Upper limits for both compression rate and depth have been provided TOCK in the updated guidelines based on preliminary /iS data suggesting that excessive compression MAGES I rates and depths can adversely affect patient out- comes. Push hard and fast, rotating the compres- USINESS B sor role every 2 minutes to prevent fatigue. Avoid ONKEY M excessive positive pressure ventilations, which www.Nursing2016.com February l Nursing2016 l 41 Copyright © 2016 Wolters Kluwer Health, Inc. All rights reserved. can increase intrathoracic pressure the cardiac arrest. The choice of an and reduce cardiac output, and advanced airway depends on the provide oxygen when available at skill level and training of the clini- maximum concentration by bag- cian placing it. No high-quality valve mask or advanced airway to evidence supports favoring endo- maximize the oxygen content of arte- tracheal intubation over bag-mask rial blood.2 ventilation or another advanced Attach the monitor/defibrillator as airway device in relation to overall soon as it’s available and analyze the survival or a good neurologic cardiac rhythm. Treat pVT/VF outcome.1 with defibrillation. Based on their Continuous waveform capnogra- greater success in dysrhythmia termi- phy for ETCO2 measurements nation, defibrillators using biphasic remains the most reliable method waveforms (biphasic truncated expo- of confirming and monitoring ETT nential or rectilinear biphasic) are placement when used in addition preferred to monophasic defibrilla- to clinical assessment. If continu- tors. The recommended energy dose ous waveform capnography isn’t for biphasic defibrillators is 120 to available, clinicians may use a 200 joules (J); if the manufacturer’s colorimetric and nonwaveform CO2 recommended energy dose is un- detector, an esophageal detector known, using the maximum energy device, or an ultrasound transducer dose available should be considered. Avoid excessive positive placed transversely on the anterior Subsequent defibrillation energy neck above the suprasternal notch doses should be equivalent or higher. pressure ventilations, to identify endotracheal or esopha- The shock energy dose for a mono- which can increase geal intubation.1 phasic defibrillator is 360 J. Perform intrathoracic pressure After an advanced airway is CPR for 2 minutes after defibrillation and reduce cardiac properly placed, the patient should and obtain I.V. or I.O. access if not be ventilated at a rate of 1 breath already established. output. every 6 seconds (10 breaths/ If VF/pVT persists with a rhythm minute) while continuous chest check during the compressor role dose epinephrine was no more ben- compressions are being performed. change at 2 minutes, defibrillate eficial than standard-dose epineph- This is a change from the previ- again. Biphasic doses can be equiv- rine in terms of survival to discharge ously recommended 1 breath every alent to the first shock administered with good neurologic recovery, sur- 6 to 8 seconds (8 to 10 breaths/ (120 to 200 J) or higher. Monopha- vival to discharge, or survival to minute), again to simplify the sic doses remain at 360 J. If the hospital admission. algorithm for learners. defibrillator unit is capable of esca- A single dose of I.V./I.O. vaso- Continuous waveform capnogra- lating energies, it’s reasonable to use pressin was an option to consider in phy can be used to evaluate the them for the second and third pVT/VF, pulseless electrical activity quality of CPR; for instance, an 1 shock. (PEA), and asystole to replace either ETCO2 less than 10 mm Hg or an After the second defibrillation the first or second dose of I.V./I.O. arterial relaxation diastolic pressure attempt, continue CPR for 2 min- epinephrine in the 2010 guidelines. less than 20 mm Hg indicates a utes and administer I.V./I.O. epi- However, one notable change in the need to improve CPR quality by nephrine 1 mg. This dose may be 2015 guidelines is the removal of optimizing chest compression repeated every 3 to 5 minutes. Epi- vasopressin from the adult cardiac parameters. For example, assess nephrine’s vasoconstrictor effects, arrest algorithm. Studies indicate compression rate, depth, and which increase coronary and cere- that vasopressin has no advantage chest recoil. bral perfusion pressure during CPR, over epinephrine and has been re- If pVT/VF persists, another shock are beneficial in cardiac arrest. How- moved to simplify the cardiac arrest is administered after 2 minutes of ever, current research doesn’t sup- algorithm.1 CPR. At this time, an anti arrhythmic port the routine use of high-dose The team leader may consider agent may be considered. Recom- I.V./I.O. epinephrine (range of 0.1 to placing an advanced airway and mendations include I.V./I.O. amio- 0.2 mg/kg). In clinical trials, high- using ETCO2 measurements during darone; I.V./I.O. lidocaine may be 42 l Nursing2016 l Volume 46, Number 2 www.Nursing2016.com Copyright © 2016 Wolters Kluwer Health, Inc. All rights reserved. considered as an alternative to amio- the need for targeted temperature darone for pVT/VF unresponsive to management (TTM) and interven- Reversible causes CPR, defibrillation, and vasopressor tions for ST-elevation myocardial of cardiac arrest therapy. infarction (STEMI). in an adult1 The patient should be evaluated Avoiding hypoxemia that can for an underlying reversible cause worsen organ injury is a top prior- Assess adults with persistent dysrhythmias for the following of the persistent dysrhythmia using ity. Administer the highest available potentially reversible “Hs and Ts” the “Hs and Ts” as recommended oxygen concentration until the and initiate appropriate 3 in the 2010 AHA guidelines. (See arterial oxyhemoglobin saturation interventions. Reversible causes of cardiac arrest in or the partial pressure of arterial • hypovolemia • an adult.) oxygen (PaO2) can be measured. hypoxia • Once return of spontaneous cir- At that point, decrease the FiO2 to hydrogen ion (acidosis) culation (ROSC) from cardiac arrest maintain a saturation of 94% to • hypo-/hyperkalemia due to pVT/VF is achieved, the 99%. Remember, peripheral • hypothermia 2015 guidelines state that evidence vasoconstriction may make using • tension pneumothorax • is inadequate to support routine pulse oximetry difficult immedi- tamponade, cardiac • use of lidocaine or beta-blockers. ately after ROSC. toxins • thrombosis, pulmonary In addition, no data support the Recommended ventilation goals • thrombosis, coronary. routine use of steroids alone for include the maintenance of normo- patients experiencing in-hospital carbia (ETCO2, 30 to 40 mm Hg or 1 cardiac arrest. PaCO2, 35 to 45 mm Hg). Modify least 24 hours. Outcome prediction these goals as needed based on such for patients not treated with TTM Asystole/PEA factors as acute lung injury, high air- should occur no earlier than 72 The adult cardiac arrest algorithm way pressures, or cerebral edema.4 hours after cardiac arrest. Patients also outlines a plan of care for the Keep in mind that if the patient’s treated with TTM are typically eval- patient presenting with asystole or temperature is below normal, PaCO2 uated at 4.5 to 5 days after ROSC. PEA. This involves high-quality CPR lab values may be higher than the The 2015 guidelines recom- as previously described. patient’s actual values. mend against the routine initiation After I.V./I.O. access is estab- Managing BP is particularly of induced cooling in the prehos- lished, epinephrine 1 mg is recom- important. Studies demonstrate a pital setting. After rewarming from mended every 3 to 5 minutes. The significant relationship between TTM to normothermia, fever, use of vasopressin as an alternative systolic BP and mean arterial pres- which is associated with worsen- to epinephrine has been removed sure (MAP) and patient outcomes. ing ischemic brain injury, should from the asystole/PEA algorithm in Immediately correct hypotension, be prevented. the 2015 guidelines.1 An advanced defined as a systolic pressure of less The 2015 postcardiac arrest airway (ETT or SGA device) with than 90 mm Hg or MAP less than guidelines also address seizure continuous waveform capnography 65 mm Hg.4 detection and treatment. Electroen- should be considered as the resusci- The 2010 guidelines encouraged cephalography (EEG) should be tative effort continues. The patient is consideration of induced hypother- promptly performed and interpret- reevaluated every 2 minutes for the mia (32 to 34° C [89.6 to 93.2° F] ed in comatose patients after ROSC presence of a shockable rhythm.
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