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7C: A Guide to the International ACLS Algorithms
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Summary/Overview
The ILCOR algorithm presents the actions to take and decisions
to face for all people who appear to be in cardiac arrest—unconscious,
unresponsive, without signs of life. The victim is not breathing
normally, and no rescuer can feel a carotid pulse within 10 to 15
seconds. Since 1992 the resuscitation community has examined and
reconfirmed the wisdom of most recommendations formulated by
international groups through the 1990s. Sophisticated clinical trials
provided high-level evidence on which to base several new drugs and
interventions. Finally, we have learned that we should continue to
place a strong emphasis after 2000 on building a base of critically
appraised, international scientific evidence. Evidence-based review
opened many eyes; only a small proportion of resuscitation care rests
on a base of solid evidence.
Note: The numbers below, such as "1 (Figure 1
),"
match numbers in the algorithms.
Figure 1: ILCOR Universal/International ACLS Algorithm
Figure 1, the ILCOR
Universal/International ACLS Algorithm, and Figure 2, the
Comprehensive ECC Algorithm, are groundbreaking efforts to unify and
simplify the essential information of adult ACLS. They demonstrate the
integration of the steps of BLS, early defibrillation, and ACLS.
The ILCOR algorithm (Figure 1) shows how simply the overall
approach can be presented, with minimum elaboration of separate
steps. The Comprehensive ECC Algorithm (Figure 2) provides more
details, particularly to support the AHA teaching approach based on the
Primary and Secondary ABCD Surveys. Both algorithms depict many of the
concepts and interventions that are new since
1992.
Notes to the ILCOR Universal/International ACLS
Algorithm
1 (Figure 1)
BLS algorithm. The simple instruction
"BLS algorithm" directs the rescuers to start the 6 basic steps of
the international BLS algorithm:
- Check responsiveness
- Open the airway
- Check breathing
- Give 2 effective breaths
- Assess circulation
- Compress chest (no signs of circulation
detected)
Note that step 6 does not use the term
"pulse." In their 1998 BLS guidelines, the European Resuscitation
Council and several ILCOR councils dropped a specific reference in
their algorithms to "check the carotid pulse." They replaced the
pulse check with a direction to "check for signs of circulation,"
namely, "look for any movement, including swallowing or breathing
(more than an occasional gasp)." Their guidelines instruct rescuers
to "check for the carotid pulse" as one of the "signs of
circulation," but the pulse check does not receive the prominent
emphasis that comes from inclusion in the algorithm. By 2000 many
locations had confirmed the success of this European approach.
Additional evidence had accumulated that the pulse check was not a good
diagnostic test for the presence or absence of a beating
heart. After international panels of experts reviewed the evidence at
the Guidelines 2000 Conference, they also endorsed the approach of
omitting the pulse check for lay responders from the International
Guidelines 2000.
2 (Figure 1)
Attach defibrillator/monitor; assess
rhythm. Once the responders start the BLS algorithm, they are
directed to attach the defibrillator/monitor and assess the rhythm.
3 (Figure 1)
VF/pulseless VT. If they are using a
conventional defibrillator and the monitor displays VF, the rescuers
attempt defibrillation, up to 3 times as necessary. If using an AED,
the rescuers follow the signal and voice prompts of the device,
attempting defibrillation with up to 3 shocks. After 3 shocks they
should immediately resume CPR for at least 1 minute. At the end of the
minute, they should repeat rhythm assessment and shock when
appropriate.
4 (Figure 1)
Non-VF rhythm. If the conventional
defibrillator/monitor displays a non-VF tracing or the AED signals
"no shock indicated," the responders should immediately check the
pulse to determine whether the nonshockable rhythm is producing a
spontaneous circulation. If not, then start CPR; continue CPR for
approximately 3 minutes. With a non-VF rhythm the rescuer needs to
return and recheck the rhythm for recurrent VF or for spontaneous
return of an organized rhythm in a beating heart. At this point the
algorithm enters the central column of comments.
5 (Figure 1)
During CPR: tracheal tube placement; IV
access. In this period the rescuers have many tasks to accomplish.
The central column includes the major interventions of ACLS: placing
and confirming a tracheal tube, starting an IV, giving appropriate
medications for the rhythm, and searching for and correcting reversible
causes. Note that the ECC Comprehensive Algorithm (Figure 2)
conveys this same approach using the memory aid of the Secondary ABCD
Survey. In this survey A=advanced airway (tracheal tube
placement); B=confirmation of tube location,
oxygenation, and ventilation; and C=circulation access
via IV line and circulation medications.
6 (Figure 1)
VF/VT refractory to initial shocks:
epinephrine or vasopressin. The ILCOR Universal Algorithm
indicates that response personnel give all cardiac arrest patients a
strong vasopressor, either epinephrine IV or vasopressin. This
recommendation for vasopressin is one of the more interesting new
guidelines. The discussions on adding amiodarone are detailed
later in this section.
Consider buffers, antiarrhythmics, pacing,
atropine; search for and correct reversible causes. This short
phrase covers a multitude of interventions discussed and debated during
the Evidence Evaluation Conference and the international Guidelines
2000 Conference: multiple antiarrhythmics, neutralization of acidosis,
and transcutaneous pacing. The word "consider" has become an
informal code in the resuscitation community interpreted to mean that
we lack the evidence that establishes one intervention as superior to
another. Whether this means that two interventions are equally
effective or equally ineffective is a debate being waged constantly in
resuscitation research.
7 (Figure 1)
Consider causes that are potentially
reversible. This guideline applies primarily to non-VF/VT
patients. For this group there is often a specific cause of the loss of
an effective heartbeat. The International Guidelines 2000 take the
innovative step of listing the 10 most common reversible causes of
non-VF/VT arrest at the bottom of the algorithm. This is discussed in
detail in the section on pulseless electrical
activity. End of Algorithm
Notes
Figure 2: Comprehensive ECC Algorithm
Both the ILCOR Universal Algorithm and the Comprehensive ECC
Algorithm (Figure 2) convey the concept
that all cardiac arrest victims are in 1 of 2 "rhythms": VF/VT
rhythms and non-VF rhythms.
- Non-VF comprises asystole and PEA, which are treated alike.
- Therefore, there is no critical need to separate the subjects into VF,
pulseless VT, PEA, or asystole.
All cardiac arrest victims receive the same 4 treatments
- CPR
- Tracheal intubation
- Vasoconstrictors
- Antiarrhythmics
The only distinguishing treatment for arrest victims is that
rescuers treat VF/VT patients with defibrillatory shocks.
The algorithms in Figures 1 and 2 demonstrate a simple
concept. The ILCOR Universal Algorithm and the Comprehensive ECC
Algorithm are the only teaching/learning displays rescuers will need
because they treat everyone in cardiac arrest this way.
Notes to the Comprehensive ECC
Algorithm 1 (Figure 2)
Begin Primary ABCD Survey.
Unresponsive; not breathing. Boxes 1 and 2 cover the steps of the BLS
Algorithm and cover the Primary ABCD Survey. The survey is a
memory aid and conveys no therapeutic value as stated and displayed.
The Primary and Secondary ABCD Surveys are simple mnemonics that assist
initial learning. They also provide a useful mental "hook" for
later review and recall. Listing more details within the algorithm
provides easy review of the steps, especially when the learner has not
participated routinely in actual resuscitation attempts.
2 (Figure 2)
VF/VT: attempt defibrillation (up
to 3 shocks if VF persists). Rhythm assessment and continued CPR
are at the center of the Comprehensive ECC Algorithm. The metaphor of a
clock ticking away for a cardiac arrest victim in VF is overused but
accurate. With each minute of persistent VF, the probability of
survival declines. Two clocks are racing. One is the clock that
measures the therapeutic interval (from collapse to arrival
of the defibrillator). One is the clock that measures the
irreversible damage interval (from cessation of blood flow
to the brain to the start of permanent, irreversible brain death).
Here is an observation that will put the racing
clocks into perspective. Several experts have observed that great
amounts of time and money are spent on the development of new
defibrillation waveforms, novel antiarrhythmics, innovative
vasopressors, and fresh approaches to ventilation and
oxygenation. The total combined effect on survival of
these interventions is equivalent to nothing more than cutting the
interval from collapse to defibrillatory shock by 2
minutes.1C
3 (Figure 2)
Non-VF/VT. The ILCOR recommendation
is to consider the non-VF/VT rhythms as one rhythm when the patient is
in cardiac arrest. Consider non-VF/VT as either asystole or PEA. The
treatment in the algorithm is the same for both: epinephrine,
atropine, transcutaneous pacing. Electrical activity on the monitor
screen is a more positive rhythm than asystole. Later in this
discussion PEA and asystole are presented in much greater
detail.
Both rhythms have a "differential diagnosis" in
terms of what entities can produce a PEA and an asystolic
rhythm. Responders must aggressively evaluate PEA victims to discover a
potential reversible cause. There is a narrow diagnostic
interval of just a few minutes at the discovery of PEA. Asystole, on
the other hand, is rarely salvaged unless a reversible cause (eg,
severe hyperkalemia, overdose of phenothiazine) is
found. Only occasionally does asystole respond to epinephrine
in higher doses, atropine, or pacing, because the patient is simply
destined to die, given the nature of the original precipitating
event.
4 (Figure 2)
Secondary ABCD Survey. Use of a
vasopressor: epinephrine for non-VF/VT, vasopressin for
refractory VF. This section of the algorithm makes the same points
about persistent arrest from VF/VT and non-VF/VT as the ILCOR Universal
Algorithm. The ECC Comprehensive Algorithm, however, uses the memory
aid of the Secondary ABCD Survey, a device repeated in all the cardiac
arrest algorithms. The algorithm notes expand on these concepts.
5 (Figure 2)
Potentially reversible causes.
Sudden VF/VT arrests are straightforward in their management.
Management consists of early defibrillation, which can succeed
independently of other interventions and independently of discovery of
the cause of the arrhythmia. With non-VF/VT arrest, however,
successful restoration of a spontaneous pulse depends almost entirely
on recognizing and treating a potentially reversible cause. As an aide
mémoire, Figure 1 places the following list,
referred to as "the 5 H’s and 5 T’s," in the algorithm
layout: The "5 H’s"
- Hypovolemia
- Hypoxia
- Hydrogen ion (acidosis)
- Hyperkalemia/hypokalemia and
metabolic disorders
- Hypothermia/hyperthermia
The "5 T’s"
- Toxins/tablets (drug overdose, illicit
drugs)
- Tamponade, cardiac
- Tension pneumothorax
- Thrombosis, coronary
- Thrombosis, pulmonary
Figure 2, the Comprehensive
ECC Algorithm, expands the table of reversible causes by listing
possible therapeutic interventions next to each of the potential
causes.
Consider: Is one of the following conditions
playing a role?
Hypovolemia (volume infusion)
Hypoxia (oxygen, ventilation)
Hydrogen ion—acidosis (buffer,
ventilation)
Hyperkalemia (CaCl plus
others)
Hypothermia (see Hypothermia Algorithm in
Part 8)
"Tablets" (drug overdoses, accidents)
Tamponade, cardiac (pericardiocentesis)
Tension pneumothorax
(decompress—needle decompression)
Thrombosis, coronary
(fibrinolytics)
Thrombosis, pulmonary
(fibrinolytics, surgical evacuation)
End of Algorithm
Notes
Newly Recommended Agent: Vasopressin for VF/VT
People knowledgeable about the ACLS recommendations during the
1990s will immediately notice that the recommendations for the
requisite vasoconstrictor, epinephrine, have changed. The first
3 algorithms—the ILCOR Universal Algorithm, the Comprehensive ECC
Algorithm, and Ventricular Fibrillation—each contain the
same recommendation for vasopressin as an adrenergic agent equivalent
to epinephrine for VF/VT cardiac arrest.
This is one of the most important new recommendations in the
International Guidelines 2000. Vasopressin, the natural substance
antidiuretic hormone, becomes a powerful vasoconstrictor when
used at much higher doses than normally present in the body.
Vasopressin possesses positive effects that duplicate the positive
effects of epinephrine. Vasopressin does not duplicate the
adverse effects of epinephrine. (See "Pharmacology II:
Agents to Optimize Cardiac Output and Blood Pressure" for more
detailed material on vasopressin.)
Vasopressin received a Class IIb recommendation (acceptable, not
harmful, supported by fair evidence) from the panel of international
experts on adrenergics. Notice that vasopressin is recommended as a
single, 1-time dose in humans. Vasopressin requires less frequent
administration because the 10- to 20-minute half-life of vasopressin is
much greater than the 3- to 5-minute half-life of
epinephrine.
After the single dose of vasopressin, the algorithms allow a return to
epinephrine if there is no clinical response to vasopressin.
This return to epinephrine has no specific human evidence to
provide support, although at least 1 clinical trial in Europe is under
way. In an informal poll of the experts on the adrenergic panel, every
person accepted this recommendation to return to epinephrine
after 10 to 20 minutes. (The possibility of a second dose of
vasopressin in 10 to 20 minutes was discussed and seems rational.
However, this was listed as a Class Indeterminate recommendation
because we lack research in humans that addresses this question.)
The rather imprecise time range between the dose of vasopressin and the
administration of subsequent epinephrine allows flexibility in
the decisions about when to give subsequent adrenergics. The dilemma
is: give too soon and cause adverse effects from excessive vasopressin;
give too late and the chances of a positive outcome vanish.
Primary and Secondary ABCD Surveys
In some locations, particularly in courses for ACLS providers, the
learners are taught a memory aid called the Primary and Secondary ABCD
Surveys. These 8 steps apply to all
cardiovascular-cardiopulmonary emergencies.
Course directors crafted the ABCD surveys to help ACLS providers
remember the specific action steps. By memorizing the 2 surveys, ACLS
students learn specific actions in a specific sequence. The surveys use
the familiar mnemonic of the first 4 letters of the alphabet, and they
maintain the traditional actions associated with those 4 letters:
A=Airway
B=Breathing
C=Circulation
D=Defibrillation (or Differential Diagnosis in the Secondary ABCD
Survey)
Because repetition is a well-documented aid to learning, the elements
of the Primary and Secondary ABCD Surveys are repeated in several other
algorithms: VF/VT, PEA, and asystole.
Figure 3, VF/pulseless VT, conveys more
details about the Secondary ABCD Survey:
A=Airway control with endotracheal intubation
B=Breathing effectively: verify with primary and secondary
confirmation of proper tube placement
C=Circulation, which incorporates vital signs, ECG monitoring,
access to the circulation via IV lines, and then administration of
rhythm-appropriate medications
D=Differential Diagnosis
A directive to "consider the differential diagnoses" improves the
resuscitation protocols, because this is a recommendation to stop and
think: What caused this arrest? With the addition of this step,
resuscitation teams will identify more cardiac arrests with reversible
causes. Although we lack evidence that supports use of this memory aid,
its use has the strong appeal of common sense.
The Secondary ABCD Survey in Figure 2 states perhaps the most
important new recommendations for out-of-hospital care providers.
- We make stronger and more explicit recommendations to confirm
tracheal tube placement.
- We recommend that resuscitation personnel take specific actions to
prevent tube dislodgment after an initial correct placement.
During the years 1999 to 2000, publications about out-of-hospital
pediatric resuscitation documented high rates of tube
dislodgment. The researchers discovered that on arrival and
evaluation in the Emergency Department, 8% to 12% of tracheal tubes
were in the esophagus or hypopharynx. Given the study design,
researchers were unable to determine whether these possibly lethal
mishaps were due to incorrect initial tube placement or dislodgment
after placement. This information has heightened concerns that ACLS
providers may be committing undetected harm while performing our most
critical interventions.
Figure 3: VF/Pulseless VT
Figure 3 covers the treatment of VF/pulseless VT in more
depth than Figures 1 and 2. Figure 3 was created
as a teaching aid to convey specific details about the Primary and
Secondary ABCD Surveys. The treatments outlined in Figures 1, 2, and 3 are identical: CPR, defibrillation if VF/VT,
advanced airway control, intravenous access,
rhythm-appropriate medications.
Always Assume VF (Figures 1 Through
3)
Note that Figure 1, the ILCOR Universal ACLS
Algorithm, Figure 2, the ECC Comprehensive Algorithm, and Figure 3, the Ventricular Fibrillation/Pulseless VT
Algorithm, state this precept unequivocally: rescuers must assume that
all adult sudden cardiac arrests are caused by VF/pulseless
VT. All training efforts therefore place a strong emphasis on immediate
recognition and treatment of VF/pulseless VT. Proper treatment with
early defibrillatory shocks allows VF/pulseless VT to provide the
majority of adult cardiac arrest survivors. Several mature EMS systems,
such as Seattle/King County, Washington, USA, have collected data for
>25 years. Year after year VF/VT contributes 85% to 95% of the
survivors.
Energy Levels for Shock and Defibrillation
Waveforms
The appearance of biphasic waveform defibrillators has generated
great enthusiasm in the resuscitation community. Reaching EMS
organizations in 1996, the first biphasic defibrillator approved for
market shocked at only 1 energy level, approximately 170 J.
Competitive market forces stirred up considerable controversy over the
efficacy of biphasic waveform shocks in general and nonescalating
energy levels in particular. This unseemly chapter in the history of
medical device manufacturers has been reviewed in detail in a Medical
Scientific Statement from the Senior Science Editors and the chairs of
the ECC subcommittees.1C Biphasic waveform defibrillators
are conditionally acceptable—regardless of initial shock
energy level and regardless of the energy level of subsequent shocks
(nonescalating). The condition that must be met is clinical data that
confirms equivalent or superior effectiveness to monophasic
defibrillators when used in the same clinical context. For example, to
meet this condition manufacturers cannot compare rescue defibrillatory
shocks delivered to a fibrillating heart in the Electrophysiology
Stimulation Laboratory versus defibrillatory shocks delivered to
patients with 12-minute-old VF in the absence of CPR efforts from
bystanders. (See "Defibrillation" in Part 6 for more detail on
waveforms and energy levels.) The International Guidelines 2000 panel
experts, the ILCOR representatives, and other delegates
thought that the class of recommendation for biphasic shocks,
nonescalating energy levels, should be upgraded from Class IIb in 1998
to Class IIa in 2000.
CPR, VF, and Defibrillation
After 3 unsuccessful attempts to achieve defibrillation, the first
3 algorithms instruct rescuers to provide approximately 1 minute of
CPR. This produces some reoxygenation of the blood and
some circulation of this blood to the heart and brain. The precise
effect of this minute of CPR on refractory VF is unclear.
Stimulated by the 1999 publication of a retrospective analysis
of out-of-hospital cardiac arrest data from the Seattle, Washington,
EMS system, the Evidence Evaluation Conference (September 1999)
included this topic on its agenda. The EMS personnel initially used a
protocol in which arriving EMTs attached an AED and analyzed
and shocked any VF rhythms as quickly as possible. Later the protocol
directed the EMTs to perform 60 to 90 seconds of CPR before attaching
the AED and shocking VF. The survival rates to hospital discharge were
significantly higher during the period of prescribed preshock CPR.
Other experts argued that a fibrillating myocardium suffers
unrelenting deterioration as long as VF continues, CPR or no CPR. A
minute or so of preshock CPR does not prevent this deterioration. This
guideline recommendation was classed as Indeterminate because the
quality and amount of evidence, on both sides of the question, were at
lower levels: retrospective data (Level 5) and extrapolation of data
from other sources (Level 7), particularly animal studies (Level
6).
Diminishing Roles for Drugs in VF Arrest
The ILCOR Universal Algorithm, the Comprehensive ECC
Algorithm, and similar comments in Figure 3 relegate adrenergic
agents, antiarrhythmic agents, and buffer therapy to secondary roles
for both VF and non-VF patients. This secondary role applies to
time-honored agents such as epinephrine, lidocaine,
procainamide, and buffer agents and to newly available agents
such as amiodarone. Meticulous, systematic review reveals that
relevant, valid, and credible evidence to confirm a benefit due to
these agents simply does not exist. This does not mean that
resuscitation drugs were selected capriciously by the pioneers of
resuscitation decades ago. They applied common sense, rational
conjecture, and extrapolations from animal studies to arrive at the
antiarrhythmics used over the past decade. If an agent is shown in
animal models to raise the fibrillation threshold
and lower the defibrillation threshold, then a reasonable
assumption would be that the drug would facilitate defibrillation of
the human heart to a perfusing rhythm. This sort of rational conjecture
produced the rather eclectic groups of drugs that have stocked
resuscitation kits for more than a decade.
In addition, it was not until the 1990s that researchers discovered the
dismal truth that antiarrhythmic drugs were acting more like
proarrhythmic agents. Drugs given to prevent VF/VT arrest appear to
generate VF/VT arrest. With critical reappraisal these disturbing
discoveries undermined the validity and credibility of scores of
excellently designed and executed studies. Through the use of critical
appraisal, most researchers in this area realized that the only proper
evaluation of new resuscitation agents had to be prospective,
randomized clinical trials in which the only acceptable control group
had to be placebo.
Designs of studies of new drugs versus standard therapy were
unacceptable for the obvious reason—if both standard therapy and the
new drug made cardiac arrest victims worse, we could never obtain valid
results. The adverse effects would not be recognized unless one agent
was significantly worse than the other. Ironically, the researchers
would conclude that the less worse drug was actually a superior agent
of positive benefit to patients. See "Pharmacology I: Agents for
Arrhythmias" and "Pharmacology II: Agents to Optimize
Cardiac Output and Blood Pressure" for more detailed material
that supports these observations.
New Class of Recommendation for Epinephrine and
Lidocaine: Indeterminate
An immense amount of animal research and lower-level human
research exists on epinephrine in cardiac arrest. These
projects are remarkable in the homogeneity of results—the findings
are consistently and invariably positive. But almost
no valid, consistent, and relevant human evidence exists to
support epinephrine over placebo in human cardiac arrest.
Clinical researchers have not conducted prospective,
placebo-controlled, clinical trials in humans on this topic.
Consequently, the international, evidence-based guidelines had to
conclude that epinephrine was Class Indeterminate.
Similarly, no study has shown that lidocaine is effective as an
agent to use in human arrest from refractory, shock-resistant
VF. Our growing awareness of the proarrhythmic effects of
antiarrhythmics now requires that researchers evaluate
lidocaine and other antiarrhythmics against placebo, and not against
some other antiarrhythmics. No clinical differences will be observed if
2 antiarrhythmics are equally ineffective or even equally harmful. At
this time, therefore, lidocaine receives a Class Indeterminate
recommendation.
Notes to Figure 3: VF/Pulseless VT
Algorithm
Assume that VF/VT persists after each
intervention. 1 (Figure 3)
Defibrillatory shock waveforms
- Use monophasic shocks at listed energy
levels (300 J, 300 to 360 J, 360 J) or biphasic shocks at
energy levels documented to be clinically equivalent (or superior) to
the monophasic shocks. 2
(Figure 3)
2A Confirm tube placement with
- Primary physical examination criteria
plus
- Secondary confirmation device (end-tidal
CO2, end-diastolic diameter) (Class
IIa)
2B Secure tracheal tube
- To prevent dislodgment, especially in patients at
risk for movement, use purpose-made (commercially available) tracheal
tube holders, which are superior to tie-and-tape methods (Class
IIb)
- Consider cervical collar and backboard for transport
(Class Indeterminate)
- Consider continuous, quantitative end-tidal
CO2 monitor (Class IIa)
2C Confirm oxygenation and
ventilation with
- End-tidal CO2 monitor
and
- Oxygen saturation monitor
3 (Figure 3)
3A
Epinephrine (Class Indeterminate) 1 mg IV push every
3 to 5 minutes. If this fails, higher doses of epinephrine (up
to 0.2 mg/kg) are acceptable but not recommended (there is growing
evidence that it may be harmful).
3B Vasopressin is recommended only for
VF/VT; there is no evidence to support its use in asystole or PEA.
There is no evidence about the value of repeat vasopressin doses. There
is no evidence about the best approach if there is no response after a
single bolus of vasopressin. The following Class Indeterminate action
is acceptable, but only on the basis of rational conjecture. If there
is no response 5 to 10 minutes after a single IV dose of vasopressin,
it is acceptable to resume epinephrine 1 mg IV push
every 3 to 5 minutes. 4 (Figure 3)
4A Antiarrhythmics are
indeterminate or Class IIb: acceptable; only fair evidence supports
possible benefit of antiarrhythmics for shock-refractory
VF/VT.
- Amiodarone (Class IIb) 300 mg IV
push (cardiac arrest dose). If VF/pulseless VT recurs, consider
administration of a second dose of 150 mg IV. Maximum cumulative dose:
2.2 g over 24 hours.
- Lidocaine (Class Indeterminate) 1.0 to 1.5
mg/kg IV push. Consider repeat in 3 to 5 minutes to a maximum
cumulative dose of 3 mg/kg. A single dose of 1.5 mg/kg in cardiac
arrest is acceptable.
- Magnesium sulfate 1 to 2 g IV in
polymorphic VT (torsades de pointes) and suspected hypomagnesemic
state.
- Procainamide 30 mg/min in refractory
VF (maximum total dose: 17 mg/kg) is acceptable but not recommended
because prolonged administration time is unsuitable for cardiac
arrest.
4B Sodium bicarbonate 1
mEq/kg IV is indicated for several conditions known to provoke sudden
cardiac arrest. See Notes in the Asystole and PEA Algorithms for
details. 5 (Figure 3)
Resume defibrillation attempts: use 360-J (or
equivalent biphasic) shocks after each medication or after each minute
of CPR. Acceptable patterns: CPR-drug-shock (repeat) or
CPR-drug-shock-shock-shock
(repeat). End of Algorithm
Notes
Figure 4: Pulseless Electrical Activity
The absence of a detectable pulse and the presence of some
type of electrical activity other than VT or VF defines this group of
arrhythmias. When electrical activity is organized and no pulse
is detectable, clinicians traditionally have used the term
electromechanical dissociation (EMD). This term, however, is
too specific and narrow. Strictly speaking, EMD means that organized
electrical depolarization occurs throughout the myocardium,
but no synchronous shortening of the myocardial fiber occurs and
mechanical contractions are absent.
In the early 1990s the international resuscitation community began to
adopt the summary term pulseless electrical activity (PEA).
PEA would more accurately embrace a heterogeneous group of
rhythms that includes pseudo-EMD, idioventricular rhythms,
ventricular escape rhythms, postdefibrillation
idioventricular rhythms, and bradyasystolic
rhythms. Additional research with cardiac ultrasonography and
indwelling pressure catheters has confirmed that often a pulseless
patient with electrical activity also has associated mechanical
contractions. These contractions are too weak to produce a blood
pressure detectable by the usual methods of palpation or
sphygmomanometry. Of utmost importance, ACLS providers must know that
PEA is often associated with specific clinical states that can be
reversed when identified early and treated
appropriately.
Notes to Figure 4:
Pulseless Electrical Activity
Both VF/VT and PEA are "rhythms of survival."
People in VF/VT can be resuscitated by timely arrival of a
defibrillator, and people in PEA can be resuscitated if a reversible
cause of PEA is identified and treated appropriately. The PEA algorithm
puts great emphasis on searching for specific, reversible causes of
PEA. The algorithm features a table of the top 10 causes of PEA,
arranged as the "5 H’s and 5 T’s." If reversible causes are not
considered, rescuers will have little chance of recognition and
successful treatment. Sodium bicarbonate provides a good example of how
the cause of the PEA relates to the therapy. Sodium bicarbonate can
vary between being a Class I intervention and being a Class III
intervention, depending on the
cause. 1 (Figure 4)
Sodium bicarbonate 1 mEq/kg is used as
follows:
Class I (acceptable, supported by definitive
evidence)
- If patient has known, preexisting
hyperkalemia Class
IIa (acceptable, good evidence
supports)
- If known, preexisting bicarbonate-responsive
acidosis
- In tricyclic antidepressant overdose
- To alkalinize urine in aspirin or other drug
overdoses
Class IIb (acceptable, only fair evidence provides
support)
- In intubated and ventilated patients with long arrest
interval
- On return of circulation, after long arrest
interval May be harmful (Class
III) in hypercarbic acidosis
2 (Figure 4)
Epinephrine:
recommended dose is 1 mg IV push every 3 to 5 minutes (Class
Indeterminate).
- If this approach fails, higher doses of
epinephrine (up to 0.2 mg/kg) may be used but are not
recommended.
- (Although one dose of vasopressin is acceptable for
persistent or shock-refractory VF, we currently lack evidence to
support routine use of vasopressin in victims of PEA or asystole.)
3 (Figure 4)
Atropine: the shorter atropine dose interval
(every 3 to 5 minutes) is possibly helpful in cardiac
arrest.
- Atropine 1 mg IV if electrical activity is
slow (absolute bradycardia=rate <60 bpm) or
- Relatively slow (relative bradycardia=rate
less than expected, relative to underlying condition)
End of Algorithm
Notes
Other observed pulseless cardiac arrest
arrhythmias are those in which the electrical activity (QRS
complex) is wide versus narrow and fast versus slow. Most clinical
studies have observed poor survival rates from PEA that is wide-complex
and slow. These rhythms often indicate malfunction of the
myocardium or the cardiac conduction system, such as occurs
with massive AMI. These rhythms can represent the last
electrical activity of a dying myocardium, or they may
indicate specific critical rhythm disturbances. For example,
severe hyperkalemia, hypothermia, hypoxia,
preexisting acidosis, and a large variety of drug overdoses can be
wide-complex PEAs. Overdoses of tricyclic antidepressants,
ß-blockers, calcium channel blockers, and digitalis will produce a
slow, wide-complex PEA.
In contrast, a fast, narrow-complex PEA indicates a relatively normal
heart responding exactly as it should for severe hypovolemia,
infections, pulmonary emboli, or cardiac tamponade. These
conditions have specific interventions.
The major action to take for a cardiac arrest victim in PEA is to
search for possible causes. These rhythms are often a response to a
specific condition, and helpful clues can appear if one simply looks at
the electrical activity width and rate.
Hypovolemia is the most common cause of electrical activity without
measurable blood pressure. Through prompt recognition and appropriate
therapy, the many causes of hypovolemia can often be corrected,
including hypovolemia from hemorrhage or from
anaphylaxis-induced vasodilation. Other causes of PEA are cardiac
tamponade, tension pneumothorax, and massive pulmonary
embolism.
Nonspecific therapeutic interventions for PEA include
epinephrine and (if the rate is slow) atropine, administered as
presented in Figure 4. In addition, personnel should
provide proper airway management and aggressive hyperventilation
because hypoventilation and hypoxemia are frequent causes of PEA.
Clinicians can give a fluid challenge because the PEA may be due to
hypovolemia.
Immediate assessment of blood flow by Doppler ultrasound may reveal
an actively contracting heart and significant blood flow. The blood
pressure and flow, however, may fall below the threshold of detection
by simple arterial palpation. Any PEA patient with a
Doppler-detectable blood flow should be aggressively treated. These
patients need volume expansion, norepinephrine, dopamine,
or some combination of the three. They might benefit from early
transcutaneous pacing because a healthy myocardium exists
and only a temporarily disturbed cardiac conduction system stands
between survival and death. Although in general PEA has poor outcomes,
reversible causes should always be targeted and never missed when
present.
Figure 5: Asystole: The Silent Heart Algorithm
Patients in cardiac arrest discovered on the defibrillator’s
monitor screen to be in asystole have a dismal rate of
survival—usually as low as 1 or 2 people out of 100 cardiac arrests.
During a resuscitation attempt, brief periods of an organized complex
may appear on the monitor screen, but spontaneous circulation rarely
emerges. As with PEA, the only hope for resuscitation of a person in
asystole is to identify and treat a reversible cause.
Figure 5, the Asystole Algorithm,
outlines an approach much more in keeping with our current
understanding of the issues surrounding asystole. The Asystole
Algorithm focuses on "not starting" and "when to stop." With
prolonged, refractory asystole the patient is making the transition
from life to death. ACLS providers who try to make that
transition as sensitive and dignified as possible serve their patients
well.
Notes to Figure 5: Asystole
1 (Figure 5)
Scene Survey: DNAR
patient? If Yes: do not start/attempt
resuscitation. Any objective indicators of DNAR status?
Bracelet? Anklet? Written documentation? Family statements? If Yes: do
not start/attempt resuscitation.
- Any clinical indicators
that resuscitation attempts are not indicated, eg, signs of death? If
Yes: do not start/attempt
resuscitation. 2 (Figure 5) Confirm true asystole
- Check lead and cable connections
- Monitor power on?
- Monitor gain up?
- Verify asystole in another lead?
3 (Figure 5)
Sodium bicarbonate 1 mEq/kg
- Indications for use include the following: overdose of
tricyclic antidepressants; to alkalinize urine in overdoses; patients
with tracheal intubation plus long arrest intervals; on return of
spontaneous circulation if there is a long arrest
interval.
- Ineffective or harmful in hypercarbic acidosis.
4 (Figure 5)
Transcutaneous pacing
- To be effective, must be performed early, combined with
drug therapy. Evidence does not support routine use of transcutaneous
pacing for asystole. 5
(Figure 5)
Epinephrine
- Recommended dose is 1 mg IV push every 3 to 5 minutes.
If this approach fails, higher doses of epinephrine (up to 0.2
mg/kg) may be used but are not recommended.
- We currently lack evidence to support routine use of
vasopressin in treatment of asystole.
6 (Figure 5)
Atropine
- Use the shorter dosing interval (every 3 to 5 minutes)
in asystolic arrest.
7 (Figure 5) Review
the quality of the resuscitation attempt
- Was there an adequate trial of BLS? of ACLS? Has the
team done the following:
- Achieved tracheal intubation?
- Performed effective ventilation?
- Shocked VF if present?
- Obtained IV access?
- Given epinephrine IV? atropine
IV?
- Ruled out or corrected reversible causes?
- Continuously documented asystole >5 to 10 minutes after
all of the above have been accomplished?
8 (Figure 5)
Reviewed for atypical clinical features?
- Not a victim of drowning or hypothermia?
- No reversible therapeutic or illicit drug
overdose? —"Yes" to the
questions in Notes 7 and 8 means the resuscitation team complies with
recommended criteria to terminate resuscitative efforts where the
patient lies (Class
IIa) —If the
response team and patient meet the above criteria, then withhold urgent
field-to-hospital transport with continuing CPR=Class III (harmful; no
benefit) 9 (Figure 5) Withholding or stopping resuscitative efforts
out-of-hospital
If criteria in 7 and 8 are fulfilled:
- Field personnel, in jurisdictions where authorized,
should start protocols to cease resuscitative efforts or to pronounce
death outside the hospital (Class IIa).
- In most US settings, the medical control official must
give direct voice-to-voice or on-scene authorization.
- Advance planning for these protocols must occur. The
planning should include specific directions for —Leaving the
body at scene —Death certification —Transfer to
funeral service —On-scene family advocate —Religious
or nondenominational counseling
End of Algorithm
Notes
Asystole most often represents a
confirmation of death rather than a "rhythm" to be treated. Team
leaders can cease efforts to resuscitate the patient from confirmed and
persistent asystole when the resuscitation team has done the
following:
- Provided suitable basic CPR
- Eliminated VF
- Achieved successful tracheal intubation with primary and secondary
confirmation of tube placement
- Confirmed throughout the efforts that the tube was secure and had not
been dislodged
- Monitored oxygen saturation and end-tidal CO2 to
ensure that the best possible oxygenation and
ventilation were achieved
- Established successful IV access
- Maintained these interventions for
10 minutes, during which time the
confirmed rhythm was asystole
- Administered all rhythm-appropriate medications
- Updated waiting family members, spouses, or available friends about the
severity of the patient’s condition and lack of response to
interventions
- Discussed the concept of programs to support family presence during
resuscitative attempts and offered that option to appropriate family
members. Note that family presence at resuscitative efforts is not a
spur-of-the-moment offer, extended or not extended at the whim of
supervising physicians. Rather, family presence at resuscitative
efforts requires a formal program, with advance planning, assigned
roles, and even rehearsals.
When to Stop?
Is it possible to state a specific time interval beyond
which rescuers have never resuscitated patients? Does every
resuscitation attempt have to continue for that length of time to
guarantee that every salvageable person will be identified and saved?
As outlined in the algorithm notes, the resuscitation team must make a
conscientious and competent effort to give patients "a trial of CPR
and ACLS," provided that the person had not expressed a decision to
forego resuscitative efforts. The final decision to stop efforts can
never be as simple as an isolated time interval, but clinical judgment
and a respect for human dignity must enter the decision making. Many
people among the resuscitation community strongly believe that we have
erred greatly in the tendency to try prolonged, excessive resuscitative
efforts.
Emergency medical response systems should not require the field
personnel to transport every victim of cardiac arrest back to a
hospital or Emergency Department (ED). In European countries most
out-of-hospital ALS care is provided by medical doctors, so decisions
about stopping CPR, transportation back to the ED, and
pronouncing death are handled by an authorized medical doctor in the
field. Transportation with continuing CPR is justified if there are
interventions available in the ED that cannot be performed in the field
(such as central core rewarming equipment) or field interventions (such
as tracheal intubation) that were unsuccessful in the field.
In the United States, outdated concepts of EMS care can linger for
years. For example, many systems still dictate the practice of "scoop
and run" on all major medical patients, not just major trauma. For
nontraumatic cardiac arrest solid evidence confirms that ACLS care in
the ED offers no advantage over ACLS care in the field. Stated
succinctly—if ACLS care in the field cannot resuscitate the victim,
neither will ED care. Civil rules, administrative concerns, medical
insurance requirements, and even reimbursement enhancement have
frequently led to requirements to transport all cardiac arrest victims
back to a hospital or ED. If these are unselective requirements, they
are inappropriate, futile, and ethically unacceptable. There should be
no requirements for ambulance transport of all patients who
suffer an out-of-hospital cardiac arrest. This is especially true when
the patient is pulseless and CPR is continued during transport.
Researchers and EMS experts continue to publish observational studies
on this practice of transporting all field resuscitations back to an
ED, most often for pronouncement of death. To have the resuscitation
team succeed with one of these victims and then have the victim survive
to hospital discharge is extremely rare—usually <1%.
Likewise, it is inappropriate for clinicians to apply routine
"stopping rules" without thinking about the particular situation.
"Part 2: Ethical Aspects of ECC and CPR" provides a more detailed
discussion of these issues. Cessation of efforts in the prehospital
setting, following system-specific criteria and under direct medical
control, should be standard practice in all EMS
systems.
Figure 6: Bradycardia
Notes to Figure 6: Bradycardia
1 (Figure 6)
If the patient has serious signs or
symptoms, make sure they are related to the slow rate.
2 (Figure 6) Clinical manifestations include
- Symptoms (chest pain, shortness of breath, decreased
level of consciousness)
- Signs (low blood pressure, shock, pulmonary
congestion, congestive heart failure) 3
(Figure 6) If the patient is
symptomatic, do not delay transcutaneous pacing while
awaiting IV access or for atropine to take effect.
4 (Figure 6) Denervated transplanted hearts will not
respond to atropine. Go at once to pacing,
catecholamine infusion, or both.
5 (Figure 6) Atropine should be given in repeat
doses every 3 to 5 minutes up to a total of 0.03 to 0.04 mg/kg. Use the
shorter dosing interval (3 minutes) in severe clinical
conditions. 6 (Figure 6) Never treat the combination of third-degree
heart block and ventricular escape beats
with lidocaine (or any agent that suppresses
ventricular escape rhythms).
7 (Figure 6) Verify
patient tolerance and mechanical capture. Use analgesia and sedation as
needed.
End of Algorithm
Notes
Transcutaneous pacing is a Class I intervention
for all symptomatic bradycardias. If clinicians are
concerned about the use of atropine in higher-level blocks, they should
remember that transcutaneous pacing is always appropriate, although not
as readily available as atropine. If the bradycardia is severe and the
clinical condition is unstable, implement transcutaneous pacing
immediately.
There are several other cautions to remember about treatment of
symptomatic bradycardias. Lidocaine may be
lethal if the bradycardia is a ventricular
escape rhythm and unwary clinicians think they are treating
preventricular contractions or slow VT. In addition,
transcutaneous pacing can be painful and may fail to produce effective
mechanical contractions. Sometimes the patient’s "symptom" is not
due to the bradycardia. For example, hypotension, associated with
bradycardia, may be due to myocardial dysfunction or hypovolemia rather
than to conducting system or autonomic problems.
Figure 6 lists interventions in a
sequence based on the assumption of worsening clinical severity. Give
patients who are "precardiac arrest," or moving in that direction,
multiple interventions in rapid sequence. Begin preparations for
pacing, IV atropine, and administration of an
epinephrine infusion. If the patient displays only
mild problems due to the bradycardia, then atropine 0.5 to 1.0 mg
IV can be given in a repeat dose every 3 to 5 minutes, to a total
of 0.03 mg/kg. (For severe bradycardia or asystole, a maximum dose of
0.04 mg/kg is advisable.) Selection of the dosing interval (3 to 5
minutes) requires judgment about the severity of the patient’s
symptoms. The provider should repeat atropine at shorter intervals for
more distressed patients. Dopamine (at rates of 2to
5 µg/kg per minute) can be added and increased quickly to 5 to 20
µg/kg per minute if low blood pressure is associated with the
bradycardia. If the patient displays severe symptoms, clinicians can go
directly to an epinephrine infusion.
Transcutaneous pacing should be initiated quickly in patients who do
not respond to atropine or who are severely symptomatic,
especially when the block is at or below the His-Purkinje level. Newer
defibrillator/monitors have the capability to perform transcutaneous
pacing. This intervention, unlike insertion of transvenous pacemakers,
is available to and can be performed by almost all ECC providers. This
gives transcutaneous pacing enormous advantages over transvenous pacing
because transcutaneous pacing can be started quickly and conveniently
at the bedside.
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References
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1.
Cummins RO, Hazinski MF, Kerber RE,
Kudenchuk P, Becker L, Nichol G, Malanga B, Aufderheide TP, Stapleton
EM, Kern K, Ornato JP, Sanders A, Valenzuela T, Eisenberg M. Low-energy
biphasic waveform defibrillation: evidence-based review applied to
emergency cardiovascular care guidelines: a statement
for healthcare professionals from the American Heart Association
Committee on Emergency Cardiovascular Care and the
Subcommittees on Basic Life Support, Advanced Cardiac Life Support, and
Pediatric Resuscitation. Circulation. 1998;97:1654–1667.[Full Text]
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7D: The Tachycardia Algorithms
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Major New Concepts for the International Guidelines 2000
At the 1999 Evidence Evaluation Conference and the Guidelines 2000
Conference, experienced electrophysiologists, arrhythmia
experts, and clinical cardiologists led the evidence review and
discussions on the tachycardias (Figures 7, 8, and 9). They
brought their expertise, their experience using new antiarrhythmics,
and their knowledge of the incumbent tachycardia algorithm.
The evidence reviews and discussions contributed many insights,
revisions, and new medications. The tachycardia algorithm
from the early 1990s forced an immediate decision in regard to
"stable versus unstable." That same emphasis remains in 2000—the
most important clinical decision to make when a rapid heart rate is
noted is whether the patient is also experiencing signs and symptoms
due to the rapid heart rate. In such situations the universal
recommendation is immediate cardioversion rather than a trial of
antiarrhythmics (see Figure 10, Electrical Cardioversion
Algorithm).
For tachycardic patients not in need of immediate cardioversion, the
International Guidelines 2000 place much more emphasis on 2 themes not
previously highlighted:
- Making a specific rhythm diagnosis
- Recognizing those tachycardic patients who have significantly impaired
cardiac function (ejection fraction <40%; overt signs of heart
failure)
Emphasis on these themes has resulted in not just 1 complicated
algorithm for tachycardias but 3 new algorithms and 1
table. The Guidelines 2000 Conference experts, clinicians, and teachers
resisted any activity that would make ACLS training and learning more
complicated. On learning of the background rationale, however, clinical
leaders in resuscitation have accepted the need for more expansive
algorithms, in return for providing better and safer acute care.
Specific Rhythm Diagnosis
Adenosine, first approved for marketing shortly before the
publication of the 1992 guidelines, has been a highly successful agent
for supraventricular arrhythmias. Teaching has
emphasized its safety and its diagnostic capabilities. If a
patient’s monitor displayed a wide-complex tachycardia,
clinicians became almost cavalier about pushing in higher and higher
amounts of adenosine to see whether the rhythm converted out of
a presumed supraventricular tachycardia with
aberrancy. Most such patients are in VT with wide complexes. Faced with
persistent wide-complex tachycardia, after 3 or 4 boluses
of adenosine the clinician faced a dawning realization
that treatment with adenosine or multiple calcium channel
blockers for 30 to 45 minutes of persistent tachycardia was
not helpful. This approach also exposes the patient to unpleasant side
affects of adenosine, the possibility of worse rhythms, and a
destabilization of heart rate and blood pressure. Consequently the
International Guidelines 2000 attempt to avoid the simplistic approach
of overuse of adenosine for diagnostic purposes.
Instead, the clinicians are expected to devote more attention to making
explicit diagnoses, within the scope of their available resources.
Antiarrhythmics or Proarrhythmics?
The other new concept that dominates the 2000 approach to
tachycardias comes from continued evidence that
antiarrhythmics are just as likely to be proarrhythmic agents as they
are to be antiarrhythmic agents. Their tendency to induce
arrhythmias becomes particularly acute in damaged or impaired
hearts. In damaged hearts normal functional myocardium is
interlaced with scarred and damaged tissue. These areas become the
source of reentry arrhythmias, irritable foci, and blocked
conduction.
Regardless of their Vaughn-Williams classification, all antiarrhythmics
are capable of a proarrhythmic effect. When a second antiarrhythmic is
added to this milieu the negative consequences escalate exponentially.
Consequently—with rare exceptions—the International Guidelines 2000
recommend 1 and only 1 antiarrhythmic per patient. This should lead to
far fewer events in which >1 antiarrhythmic causes significant
worsening of the patient’s condition and a much lower threshold to
cardiovert patients nonurgently, before they become significantly more
symptomatic.
Figure 7: The Tachycardia Overview Algorithm
The classic "chicken or egg" dilemma occurs often in
symptomatic tachycardia events. Did the stress
and discomfort of acute, severe, substernal chest pain lead to a
cardiac response of tachycardia? or did the marginally
compromised heart develop ischemia and chest pain as the
sequelae of a paroxysmal tachycardia? The patients
diagnosed as "unstable" will immediately be treated with urgent,
electric, synchronized cardioversion. Note:
The numbers of notes, such as "Note 1," match numbers in the
algorithms.
Note to Figure 7: The Tachycardia Overview
Algorithm
Unstable condition must be related to the
tachycardia. Signs and symptoms may include chest pain,
shortness of breath, decreased level of consciousness,
low blood pressure, shock, pulmonary congestion, congestive
heart failure, and AMI.
End of Algorithm Note
The Tachycardia Overview Algorithm (Figure 7) divides tachycardias into
4 diagnostic categories. (In the algorithm the 4 columns
have a number at the top to better orient the reader):
- Atrial fibrillation/flutter
- Narrow-complex tachycardias
- Wide-complex tachycardias of unknown type
- Stable monomorphic and polymorphic
tachycardia
1. Atrial Fibrillation/Atrial Flutter (Column 1)
Figure 7 reminds the ACLS provider of the focus for
evaluation:
- Is the patient clinically unstable?
- Is cardiac function impaired?
- Is Wolff-Parkinson-White syndrome present?
- Was the onset of the atrial fibrillation or atrial flutter
clearly recognized by the patient? Has the atrial fibrillation/flutter
been present for more than or less than 48 hours?
The treatment focus for atrial fibrillation/flutter is on 4 areas as
well:
- Unstable versus stable? Treat urgently.
- Control rate with agents that reduce the rate of conduction
across the AV node.
- Convert the rhythm with either medications or cardioversion
when indications are present and urgent.
- Provide anticoagulation if indicated.
See "Section 5: Pharmacology I" and "Section 6: Pharmacology
II" for more detailed presentations on these
topics.
The table accompanying Figure 7 provides treatment details for
atrial fibrillation and flutter. The table displays the major
questions to ask and factors to consider when formulating a treatment
plan for atrial fibrillation/flutter:
- What is the cardiac status? normal? impaired?
- Does the person have Wolff-Parkinson-White syndrome?
- What is the duration of the atrial fibrillation? Can you date and time
the onset unequivocally? Is the duration less than or more than 48
hours? Is anticoagulation indicated? Electrical cardioversion?
- Would pharmacological conversion pose higher risk of emboli?
- Is the rate too high?
2. Tachycardia (Atrial Fibrillation and
Flutter)
See the table accompanying Figure 7.
Narrow-Complex Tachycardias
The ACLS provider needs to move from the end of column 2,
Narrow-Complex Tachycardias (Figure 7), to Figure 8: Narrow-Complex
Supraventricular Tachycardia.
Figure 7, under Narrow-Complex Tachycardias,
demonstrates the emphasis in 2000 on establishing a specific diagnosis
first by close ECG analysis, then by consulting
cardiology specialists if available. The
consultants may choose to use esophageal-lead ECGs or
echocardiograms as well as serial 12-lead ECGs. In narrow-complex,
stable supraventricular tachycardias, the
algorithm recommends diagnostic use of vagal maneuvers and
adenosine. These diagnostic efforts should yield a
diagnosis such as PSVT, ectopic atrial tachycardia, or
MAT.
The overview algorithm then directs the clinician to Figure 8, Narrow-Complex Supraventricular Tachycardia.
Here clinicians make the clinical assessment of cardiac function, with
ejection fractions <40% qualifying as
enough compromise to alter the therapeutic approach.
Figure 8: Narrow-Complex Supraventricular Tachycardia
In general, narrow-complex supraventricular
tachycardias can be treated with amiodarone,
ß-blockers, or calcium channel blockers if cardiac function is
preserved. (This list is in alphabetical order and does not imply that
1 of these 3 is better than another.) If cardiac function is
compro-mised, then the drug options narrow to only
amiodarone, the agent with the best balance between side
effects and effectiveness in heart failure patients. Note the
prohibition to DC cardioversion in all patients with impaired cardiac
function.
3. Stable Wide-Complex
Tachycardias: Unknown Type
Figure 7, Column 3, recommends the same
diagnostic/therapeutic approach as recommended for
narrow-complex tachycardias. After a series of
diagnostic efforts clinicians should be able to establish
into which of 3 arrhythmic categories the wide-complex
tachycardia belongs:
- Narrow-complex tachycardia with aberrancy obscuring
the narrow QRS (subsequently these patients are referred to Figure 8: Narrow-Complex Supraventricular
Tachycardia)
- Stable monomorphic or polymorphic VT (subsequently these
patients are referred to Figure 9: Stable
VT: Monomorphic or Polymorphic)
- Stable wide-complex tachycardia: if this is
the most likely rhythm diagnosis for you and your patient, proceed to
evaluate the cardiac functional status. Figure 7 shows that DC
cardioversion and amiodarone are recommended treatments for
those tachycardic patients who have clinical heart failure. Be careful
with adding anything else to the treatment for these patients. For the
patient with well-preserved cardiac function, choose either DC
cardioversion (Figure 10) or
procainamide or amiodarone. Most experts choose DC
cardioversion as their first treatment and treatment of choice for all
wide-complex tachycardias regardless of cardiac function.
That way they can easily add another antiarrhythmic if the
cardioversion fails; however, the converse (use cardioversion if
antiarrhythmic fails) does not always hold
true.
Figure 9: Stable Ventricular Tachycardia: Monomorphic or
Polymorphic?
4. Monomorphic and Polymorphic VT
Figure 7, Column 4, directs the clinician to Figure 9 for more details on the treatment of those stable VTs that
fall into 2 subsets: monomorphic VT and polymorphic VT. If the
polymorphic VT has a prolonged QT interval, it becomes a question
of whether the patient is suffering from torsades de pointes. With such
an exotic name it is only right that the rhythm of polymorphic VT
looks distinctive and unusual, with the entire rhythm tracing
resembling an up-and-down, thick-and-thin pattern characterized as a
"spindle and node" pattern.
Polymorphic VT merits special attention because it is a common
arrest rhythm suffered by drug overdose patients and toxin patients
from exposures to nonmedicinal drugs.
Figure 9 provides directions for the immediate treatment of
these arrhythmias, with the cardiac function status of primary
importance. Notice that amiodarone is becoming the only
antiarrhythmic agent acceptable for the elderly and those with
progressive decline in cardiac function.
See the callout notes for stable VTs for more details.
Notes to Figure 9: Stable VT: Monomorphic or
Polymorphic?
1 (Figure 9)
Monomorphic VF with normal cardiac
function
Use just 1 agent (to avoid proarrhythmic effects of
combination therapy).
This reduces adverse side effects. Choose 1 agent from
these lists:
Top agents
- Procainamide (IIa)
- Sotalol (IIa)
Others acceptable
- Amiodarone (IIb)
- Lidocaine (IIb)
2 (Figure 9)
Monomorphic or polymorphic VT with
impaired cardiac function
If clinical signs are suggestive of impaired
LV function (ejection fraction <40% or congestive heart failure) in
either long- or normal-QRS tachycardias, use
- Amiodarone (IIb)
- Lidocaine (IIb)
then use
- Synchronized cardioversion
3 (Figure 9)
Detailed dosing of amiodarone
(Class IIb) in patients with impaired cardiac function
- 150 mg IV bolus over 10 minutes (international dose:
5 mg/kg)
- Repeat 150 mg IV (over 10 minutes) every 10 to 15
minutes as needed
- Alternative infusion: 360 mg over 6 hours (1 mg/min over
6 hours), then 540 mg over the remaining 18 hours (0.5 mg/min)
- Maximum total dose: 2.2 g in 24 hours. This means
that all doses (including those used in resuscitation)
should be added together, so the total cumulative dose per 24 hours is
limited to 2.2 g
- See guidelines or ECC Handbook Drug Table
4 (Figure 9)
Detailed dosing of lidocaine (Class
Indeterminate) in patients with impaired cardiac function
- 0.5 to 0.75 mg/kg IV push
- Repeat every 5 to 10 minutes
- Then infuse 1 to 4 mg/min
- Maximum total dose: 3 mg/kg (over 1 hour)
5 (Figure 9)
If rhythm is suggestive of torsades
de pointes
- Stop/avoid treatments that prolong QT
- Identify and treat abnormal electrolytes
Medications (all Class
Indeterminate):
- Magnesium
- Overdrive pacing (with or without ß-blocker)
- Isoproterenol (as temporizing measure to overdrive
pacing)
- Phenytoin or lidocaine
End of Algorithm Notes
This article has been cited by other articles:
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M. A. Peberdy and J. P. Ornato
Progress in Resuscitation: An Evolution, Not a Revolution
JAMA,
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A. K. Jacobs, E. M. Antman, D. P. Faxon, T. Gregory, and P. Solis
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P. Moyer, J. P. Ornato, W. J. Brady Jr, L. L. Davis, C. A. Ghaemmaghami, W. B. Gibler, G. Mears, V. N. Mosesso Jr, and R. D. Zane
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Developed in Collaboration With the European Heart, D. P. Zipes, A. J. Camm, M. Borggrefe, A. E. Buxton, B. Chaitman, M. Fromer, G. Gregoratos, G. Klein, A. J. Moss, et al.
ACC/AHA/ESC 2006 Guidelines for Management of Patients With Ventricular Arrhythmias and the Prevention of Sudden Cardiac Death--Executive Summary: A Report of the American College of Cardiology/American Heart Association Task Force and the European Society of Cardiology Committee for Practice Guidelines (Writing Committee to Develop Guidelines for Management of Patients With Ventricular Arrhythmias and the Prevention of Sudden Cardiac Death)
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Developed in Collaboration With the European Heart, D. P. Zipes, A. J. Camm, M. Borggrefe, A. E. Buxton, B. Chaitman, M. Fromer, G. Gregoratos, G. Klein, A. J. Moss, et al.
ACC/AHA/ESC 2006 Guidelines for Management of Patients With Ventricular Arrhythmias and the Prevention of Sudden Cardiac Death: A Report of the American College of Cardiology/American Heart Association Task Force and the European Society of Cardiology Committee for Practice Guidelines (Writing Committee to Develop Guidelines for Management of Patients With Ventricular Arrhythmias and the Prevention of Sudden Cardiac Death)
J. Am. Coll. Cardiol.,
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D. P. Zipes, D. P. Zipes, A. J. Camm, M. Borggrefe, A. E. Buxton, B. Chaitman, M. Fromer, G. Gregoratos, G. Klein, A. J. Moss, et al.
ACC/AHA/ESC 2006 guidelines for management of patients with ventricular arrhythmias and the prevention of sudden cardiac death--executive summary: A report of the American College of Cardiology/American Heart Association Task Force and the European Society of Cardiology Committee for Practice Guidelines (Writing Committee to Develop Guidelines for Management of Patients with Ventricular Arrhythmias and the Prevention of Sudden Cardiac Death) Developed in collaboration with the European Heart Rhythm Association and the Heart Rhythm Society.
Eur. Heart J.,
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7A: Principles and Practice...
References
