Page 269 - Hall et al (2015) Principles of Critical Care-McGraw-Hill

CHAPTER 25: Cardiopulmonary Resuscitation 173

treatment for this phase—but the need for new translational research in TABLE 25-4 Standard ACLS Medications and Doses
this area is vital. The tools of molecular biology, proteomics, and cellular
physiology are likely to provide important insights and to create new Medication ACLS Dosing
biosensors that can guide clinical therapies. It is not unrealistic to believe Amiodarone 300 mg IV bolus, second dose 150 mg IV bolus
that major improvements in survival rates will result as we change our Epinephrine 1 mg IV bolus every 3-5 minutes (10 mL of a 1:10,000 solution)
current practices in the near future. 57
Vasopressin 40 U IV bolus can replace first or second dose of epinephrine
AUTOMATIC EXTERNAL DEFIBRILLATORS Note: A more comprehensive list of ACLS medications and their dosing regimens can be found in the
ACLS manual published by the American Heart Association. It is important to stress that very little data
Given the assumption that early defibrillation remains the best treat- suggest that any of these medications actually improve survival to hospital discharge.
ment for VF/VT cardiac arrest, a number of devices have been devel-
oped to allow inexperienced users to defibrillate victims before the
arrival of medical personnel (reviewed in ref. 54). These devices, known an improvement in initial resuscitation but did not demonstrate an
44
as automatic external defibrillators (AEDs), have become ubiquitous in improved survival to hospital discharge. There are no definitive data to
airports and other public locations. These simple-to-use defibrillators demonstrate a survival benefit from atropine or lidocaine and as such,
contain waveform analysis software that determines whether a shock atropine was removed from the treatment algorithm for asystolic cardiac
is warranted when a layperson attaches sensing pads to the chest of arrest and is only indicated in bradycardic pulseless electrical activity.
a comatose individual. Appropriate shocks are then delivered. Audio Similarly, bicarbonate, while widely administered during cardiac arrest,
prompts guide the user through the process. has not been proven to aid resuscitation. In fact, ACLS guidelines only
The placement of AEDs in public places has been shown to affect recommend bicarbonate infusion in a small subset of cardiac arrest
15
survival from cardiac arrest, supporting the concept that earlier defibril- patients, namely, those known to be hyperkalemic. Doses of standard
lation correlates with improved outcomes. However, the majority of ACLS medications are given in Table 25-4.
57
cardiac arrests occur in the home, not in public. Data from Seattle sug- Thrombolytic therapy in cardiac arrest has received recent inter-
gest that as many as 70% of out-of-hospital cardiac arrests take place in est because a number of uncontrolled studies and cohort series have
residences, and only 21% occur in public locales. Whether AEDs should suggested a benefit from the use of urokinase or t-PA. 66-68 A small but
1
be available for home installation, much like fire extinguishers, remains well-executed controlled study recently demonstrated no improvement
an active question. As AEDs become smaller, smarter, and cheaper, this in return of spontaneous circulation or survival with t-PA in the treat-
69
debate may tip toward home availability. 58 ment of PEA arrest. A larger European study is currently ongoing and
Whether AEDs should be placed in hospital wards remains another may help resolve this controversy, and certain subsets of cardiac arrest
topic under current discussion. Although hospital resuscitation teams patients may be found to benefit from this treatment modality. At this
59
include ACLS-trained personnel, most “first responders” in the hospi- point, it is fair to say that thrombolytic therapy may be attempted if
tal setting are nurses or other health care staff who may not be ACLS there is strong evidence to suspect pulmonary embolism as the cause
proficient and therefore unlikely to perform defibrillation. It has been of arrest. 65,70,71
argued that the availability of AEDs in the hospital would allow for rapid
defibrillation attempts before the arrival of resuscitation teams, though LIMITATIONS ON CARDIAC ARREST EFFORTS
current data are mixed. However, the presence of AEDs would not be
sufficient—nurses and other health care workers would have to accept The idea of a chemical code, that is, performing resuscitation with
defibrillation as a possible primary responsibility. There are some data pharmacologic agents only and not with chest compressions or defi-
to suggest nurses would support such a role. 60 brillation, is not controversial insofar as there is no disagreement
among expert providers. Studies have demonstrated clearly that the
INDUCED HYPOTHERMIA IN CARDIAC ARREST concept lies much more in the realm of mythology or wishful thinking
than in science. The only controversy is that the concept has persisted
In the search for novel cardiac arrest therapies, induced hypothermia has in hospitals and among health care workers across the world to this
72
generated a great deal of recent interest, spurred by two well-conducted day. It is important to stress the following point because the chemical
studies showing improved survival when patients were cooled to 32°C to code is often presented to family members as an option for care of
34°C after resuscitation from cardiac arrest. 61,62 An international recom- their loved one: Cardiac arrest is not a medical problem treatable by
mendation has been issued based on this evidence that patients should medications only.
be cooled after out-of-hospital cardiac arrest; data on in-hospital cardiac In a similar vein, the slow code, in which efforts to resuscitate are
arrest are still under discussion but international guidelines recommend intentionally delayed or limited by rescuers, is ethically unacceptable.
73
63
consideration of induced hypothermia in these patients. Much work Patients who are full code should have every appropriate effort made to
remains to further define this treatment, regarding both depth and dura- resuscitate them; decisions regarding appropriateness of resuscitation
tion of hypothermia. Novel techniques for cooling patients are under efforts should be made by patients and their primary physicians, not by
development as well, including multiphase coolant fluids and cooling a resuscitation team at the time of arrest.
catheters. Chapter 26 of this book is devoted to this exciting field of
induced hypothermia. ETHICAL ISSUES
PHARMACOLOGIC THERAPY OF CARDIAC ARREST The ethical dimensions of cardiac arrest treatment are complex and
important for physicians to consider. 74,75 Decisions regarding termina-
CPR and electrical defibrillation are the central treatment modalities tion of efforts and even the decision not to initiate efforts in the first
for cardiac arrest in current practice. While medications such as epi- place should be calibrated carefully depending on the individual case
nephrine, vasopressin, and amiodarone have been incorporated into in question. The growing establishment of do-not-resuscitate (DNR)
treatment algorithms for cardiac arrest, to this day they do not have any protocols has allowed patients and their families to avoid the traumatic
proven survival benefit. A surge of interest in “high-dose” epinephrine and often futile efforts of resuscitation.
64
in recent years was quelled when a number of studies demonstrated It cannot be stressed enough that physicians should initiate frank and
no benefit from this approach. 43,65 Current interest in amiodarone truthful end-of-life discussions with patients early in their care, before
as a treatment for VF/VT is based largely on one study that showed hospitalization or cardiac arrest appear on the horizon. In this fashion,

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