Vissia S. Pinili, MSN, RN, CPAN, CCRN, Nicole R. Keller, PharmD, BCNSP and Glenn N. Levine, MD, FACC, FAHA

1. Why was the A-B-C (airway, breathing, compression) sequence of cardiopulmonary resuscitation (CPR) changed to C-A-B (compression, airway, breathing)?

    According to American Heart Association (AHA) guidelines for CPR and emergency cardiovascular care (ECC), chest compression were often delayed while the rescuer opened the airway to give mouth-to-mouth breaths, retrieved a barrier device, or gathered and assembled ventilation equipment. Starting the resuscitation sequence with chest compressions is also hoped to encourage more persons to initiate CPR.

2. What factors constitute “high-quality CPR”?

    Components of high-quality CPR include:

3. What is your first step if you are alone and come across an unresponsive adult victim with no signs of breathing?

    Activate the emergency response system and get an automated external defibrillator (AED), if available in the area, then return to the victim. If you return with an AED, turn it on and follow the prompt. If no AED is available, check for a pulse and begin CPR until emergency medical services (EMS) arrives to take over.

    Figure 39-1 is an algorithm for adult basic life support (BLS) decisions and actions. A summary of key BLS components for treating adults, children, and infants is given in Table 39-1.

4. For patients with respiratory arrest (but with a perfusing heart rhythm), how often should breaths be delivered?

    For respiratory arrest with a perfusion cardiac rhythm, breaths should be delivered every 5 to 6 seconds (10-12 breaths/min).

5. What is the most common cause of airway obstruction in the unconscious adult patient?

    In adults the most common cause of airway obstruction in an unconscious patient is loss of tone in the throat muscles, leading to airway occlusion by the tongue. This may be treated by head tilt–chin lift, jaw thrust, or insertion of an oropharyngeal airway.

6. How many joules of energy are indicated for the treatment of ventricular fibrillation (VF) or pulseless ventricular tachycardia (VT) when using a biphasic defibrillator?

    Biphasic defibrillators are now used at many institutions, replacing the older monophasic defibrillators. The amount of energy will often be device specific, ranging from 120 to 200 J. If the appropriate setting is unknown, use 200 J. Additional shocks should be equivalent or higher energy. This contrasts to the older monophasic defibrillators, for which a setting of 360 J is recommended.

7. In order, what are the preferred routes of drug administration?

8. After the first unsuccessful shock of a patient with VF or pulseless VT, which two drugs should be considered?

9. After several unsuccessful shocks, and treatment with epinephrine or vasopressin, what other drugs (and their doses) should be considered?

    Amiodarone (or lidocaine if amiodarone is not available) should be considered. Soberingly, no antiarrhythmic has ever actually been shown to improve survival to hospital discharge, although amiodarone has been shown to increase rates of survival to hospital admission.

10. If the patient is in torsades de pointes, in addition to defibrillation, what medication can be considered?

    Magnesium can be given at a dose of 1 to 2 g IV or IO. It is recommended that it be diluted in 10 mL of 5% dextrose in water (D5W) and administered over 5 to 20 minutes.

11. After administering a drug via a peripheral IV, what steps should be taken to promote delivery of the drug to the central circulation?

    After administering a drug via a peripheral IV, a 20-mL bolus of IV fluid should be administered and the extremity should be elevated for 10 to 20 seconds.

12. Can one shock a hypothermic patient who is in VF or VT?

    Yes, but there is a caveat. For the hypothermic patient (temperature less than 30° C [86° F]) in VF or VT, a single defibrillation is deemed appropriate.

13. If a person who was in VF or VT is successfully defibrillated, and amiodarone is to be started to prevent further VF or VT, what is the dosing (assuming he or she has not already received any amiodarone)?

    The following regimen is what is given in the ACLS booklet and is the “classical” loading of amiodarone. An initial bolus of 150 mg IV is given over 10 minutes. This is followed by an infusion of 1 mg/min for 6 hours (total 360 mg), then an infusion of 0.5 mg/min over the next 18 hours (540 mg).

14. What are the treatable causes of pulseless electrical activity?

    Because pulseless electrical activity (PEA) has such a poor prognosis unless a reversible cause of the rhythm is quickly identified and addressed, it is important to commit to memory the treatable causes of PEA. The H’s and T’s of PEA are given in Table 39-2. Hypovolemia and hypoxemia are reported to be the two most common and easily reversible causes of PEA.

    An algorithm for ACLS of adult cardiac arrest (including patients exhibiting PEA) is given in Figure 39-2.

15. What drugs can be considered in a patient with PEA?

    Epinephrine and vasopressin can be used, as described earlier for the treatment of VF or VT, although no vasopressors has been shown to increase survival in PEA. Atropine is no longer recommended for asystole or PEA.

16. In bradycardic patients, such as those with hears block, what are the primary treatments if they are symptomatic and suffering from poor perfusion?

    The immediate use of transcutaneous pacing is now emphasized for patients with symptomatic bradycardia. While preparations are being made for transcutaneous pacing, the following pharmaceutical interventions should be considered:

17. Is transcutaneous pacing recommended for the treatment of a patient in asystole?

    As noted in the ACLS algorithm, several randomized controlled trials have failed to show benefit from attempted transcutaneous pacing in patients in asystole. Thus, it is not currently recommended in this situation.

18. In a symptomatic yet stable patient with a regular narrow complex tachyarrhythmia, what drug is recommended as a first-line agent?

    Adenosine has become the drug of choice for a symptomatic yet stable patient with a narrow complex tachyarrhythmia. The distinction between stable and unstable is subjective, but the symptomatic yet stable patient might be described as one who is slightly lightheaded (systolic blood pressure [SBP] of approximately 80 mm Hg) or having mild shortness of breath or chest discomfort. Patients experiencing more severe symptoms would be those with altered mentation because of low blood pressure, or with moderate to severe shortness or breath or chest discomfort. Note that although adenosine, which blocks AV conduction, may terminate some narrow complex tachycardias, such as AV nodal reentrant tachycardia (AVNRT) or AV reentrant tachycardia (AVRT), it will not terminate rhythms such as atrial flutter or atrial tachycardia (although it may lead to a transient decrease in conduction through the AV node and slower ventricular response rate, allowing identification of the rhythm). Adenosine would not be expected to terminate an irregular narrow complex tachycardia, because the genesis of these rhythms does not involve the AV node.

19. What is the dosing regimen for adenosine, and what are its primary side effects?

    The adenosine dosing regimen is a 6 mg rapid IV push, followed (if no rhythm conversion) by a 12 mg rapid IV push. The half-life of adenosine is only several seconds, so every effort must be made to administer it quickly and ensure its quick delivery to the central circulation (see Question 11). The effects of adenosine may be potentiated by dipyridamole or carbamazepine (consider a starting dose of 3 mg) and blocked by theophylline or caffeine. Adenosine may cause the patient to experience flushing, shortness of breath, or chest discomfort. Because it can cause bronchospasm, it should be avoided in patients with significant reactive airway disease. The practitioner should also be aware that because of its profound effects on AV nodal conduction, it may result in asystole for several seconds or more, an often disconcerting occurrence to the practitioner watching the telemetry monitor. Prolonged asystole has been reported in patients with transplanted hearts and following central venous administration; a lower dose of 3 mg should be considered in such situations.

20. After return of spontaneous circulation (ROSC), what intervention has been shown to improve neurologic recovery in comatose patients?

    Therapeutic hypothermia improves neurologic recovery in comatose patients. Patients are cooled to 32° to 34° C for 12 to 24 hours via surface cooling devices (ice bags and/or cooling blankets) and cold, non–dextrose containing, isotonic fluids (30 mL/kg). Decisions on percutaneous coronary intervention (PCI) are not affected by therapeutic hypothermia.

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