Download Advanced life support guidelines

British Journal of Anaesthesia 1997; 79: 172–177
Advanced life support guidelines
C. E. ROBERTSON
In 1992, the European Resuscitation Council (ERC)
published guidelines for advanced life support
(ALS). These guidelines were produced by an
international group of experts and based on
consensus views of the available literature. This
European initiative brought together individuals
and organizations in a unique endeavour.
However, it was recognized that because of the
changing nature and incomplete knowledge in
the field of cardiopulmonary resuscitation (CPR),
that regular review and re-assessment would be
required.
In the past 5 yr considerable changes have
occurred. Some of the answers to previously
unknown and difficult problems, such as the
potential value of high-dose catecholamines and use
of alternative techniques to increase antegrade blood
flow during closed chest compression, are now
available. Important new advances have occurred in
the technology associated with resuscitation, in
particular defibrillation. Manual defibrillators
require a level of rhythm recognition and interpretation that many health care professionals find
difficult. Semi-automated and automated defibrillators are now widely available, particularly in the
pre-hospital environment. The 1992 guidelines were
not designed with these devices in mind.
For all of these reasons, a review of the guidelines
was both apposite and timely. The formation of the
International Liaison Committee on Resuscitation
(ILCOR) has facilitated this process by making
possible worldwide cooperation and discussion.
Representatives from North America, Europe,
Southern Africa and Australasia have collaborated to
produce the ILCOR advisory statements on resuscitation which were published in April 1997. This
article summarizes the ALS component of the
advisory statements with particular reference to their
use in the UK. The UK, under the aegis of the
Resuscitation Council (UK), has accepted the task
of assessing these new ALS guidelines on behalf of
the ERC under the title “The 1997 Guidelines for
use in the UK”.
(Br. J. Anaesth. 1997; 79: 172–177).
Key words
Complications, cardiac arrest. Heart, resuscitation. Heart,
defibrillators. Advanced life support.
General principles
One of the most difficult tasks of educators is to
maintain a consistent and logical approach within
the framework of an easily retained message. The
limitations of guideline production and use must be
acknowledged. Slavish adherence to rigid instructions is rarely practicable or indeed advisable. As
often happens in medicine, interpretation with
commonsense and an appreciation of intent is
necessary.
This is particularly the case in the field of
resuscitation where our knowledge is at best
incomplete. It is hoped that these guidelines, while
offering a clear approach, will also allow individuals
with specialist knowledge the opportunity to modify
them according to the level of their expertise and the
specific clinical situation or environment in which
they are used.
The commonest cause of adult sudden cardiac
arrest is ischaemic heart disease. The majority of
individuals who die from an acute coronary syndrome
do so before reaching hospital and emphasis on prevention of cardiac arrest is essential. In relation to this,
the correct and timely management of peri-arrest
arrhythmias may prevent the development of cardiac
arrest41 41a (see also page 198).
A small, but important, group of patients develop
cardiac arrest in special circumstances; examples
include trauma, hypothermia, immersion, drug
overdose, anaphylaxis, hypovolaemia, etc. While the
ALS guidelines are universally applicable, in these
situations specific modifications may be needed to
increase the chances of success.
Specific ALS interventions
TRANSTHORACIC DEFIBRILLATION
By far the commonest primary arrhythmia in adult
cardiac arrest is ventricular fibrillation (VF).2 51 In
some patients, this is preceded by a short period of
ventricular tachycardia (VT) which deteriorates in
waveform to VF. Early detection and treatment of
these rhythms is central to the chances of successful
outcome. The majority of eventual survivors of
cardiac arrest come from this group.21 59 The
more rapidly a patient can be defibrillated in these
COLIN E. ROBERTSON, MB, CHB, MRCP(UK), FRCP, FRCS, FFAEM,
Department of Accident and Emergency Medicine, and Surgery,
Royal Infirmary, Lauriston Place, Edinburgh EH3 9YW.
Advanced life support guidelines
circumstances, the greater the chance of obtaining a
perfusing cardiac rhythm and the higher the ultimate
success rate. It has been estimated that the chances
of successful defibrillation decline by approximately
2–7 % with each minute that a patient remains in
cardiac arrest.38 This decline reflects rapid depletion
of myocardial high energy phosphate stores,44 and is
mirrored in the deterioration of the amplitude and
characteristics of the VF waveform.42 Basic life
support (BLS) can slow the rate of decline but does
not reverse it. As a consequence, the priority is to
reduce the delay between the onset of cardiac arrest
and defibrillation.
One of the most interesting developments has
been the use of new techniques during defibrillation.
These include altering the waveform of the shock,
automatically adjusting the energy administered
according to transthoracic impedance or producing
sequentially overlapping shocks with rapidly shifting
electrical vectors.5 23 32 With most conventional
manual defibrillators, the defibrillation waveform
used has a damped monophasic sinusoidal pattern.
New machines delivering biphasic waveforms can,
with lower energies, produce shocks with similar
success rates. This technique has the advantage
that the inevitable myocardial injury produced by
defibrillation is reduced.
An alternative technique is available with some
automated defibrillators. These measure the
patient’s transthoracic impedance immediately
before administration of shock and then deliver a
shock based on current flow. Current-based defibrillation is particularly useful in patients who have
unusually high or low transthoracic impedance
values.
Irrespective of the type of machine used, the
correct defibrillation technique is important to
reduce transthoracic impedance and maximize the
chance of success. Only a small proportion of the
delivered electrical energy traverses the heart
during transthoracic defibrillation so that efforts to
maximize this are important. Common faults
include inadequate contact of the paddles or selfadhesive pads with the chest wall, failure or
inadequate use of couplants to aid current passage
between the paddles and chest wall, and faulty
paddle positioning or size.1 3 30 53 One paddle should
be placed to the right of the upper part of the
sternum below the clavicle, the other just outside the
position of the normal cardiac apex (V4–5 position).
Placement over the breast tissue in female patients
should be avoided to reduce transthoracic
impedance. Other positions, such as apex-posterior,
can be considered if the standard position is unsuccessful. Polarity of the electrodes appears to
influence success with internal implantable defibrillators, but during transthoracic defibrillation the
polarity of the paddles is unimportant.
On a practical note, it is important to realize that
after administration of a defibrillating shock there is
often a delay of a few seconds before an ECG trace
of diagnostic quality is obtained. Furthermore, even
when a electrical rhythm compatible with cardiac
output is obtained after a defibrillating shock,
temporary impairment of cardiac contractility is
173
often present and the first few cardiac cycles may be
associated with a weak, or difficult to palpate, central
pulse. It is important to recognize these phenomena
and allow for them rather than concluding that
electromechanical dissociation has developed.
CPR TECHNIQUES
Several new experimental techniques have been
investigated and evaluated over the past few years;
these include simultaneous compression and ventilation, high impulse external chest compression, interposed abdominal compression, vest CPR and active
compression/decompression CPR.15 Some of these
techniques have been shown experimentally to
improve the haemodynamic state associated with
CPR and in some cases to improve survival in animal
models. It is disappointing that at present there are
no clinical data showing unequivocal improvement
in outcome in large-scale human studies with any of
these techniques.50 56 Consequently, the new guidelines do not recommend any change in the technique
of closed chest compression.
AIRWAY MANAGEMENT AND VENTILATION
In 1996, an ERC working group published guidelines for the advanced management of the airway
and ventilation during CPR.6 These are incorporated into the advanced life support guidelines and
their detailed aspects are covered separately in this
issue of the journal.
After cardiac arrest and during CPR, normal
pulmonary physiological characteristics are altered.
There is an increase in deadspace and a reduction in
lung compliance because of the development of
pulmonary oedema. These changes may compromise gas exchange and serve to focus attention on
the delivery of oxygenation and ventilation of the
patient’s lungs. The aim should be to provide a
fractional inspired oxygen concentration ( FIO2 ) of
1.0. Fortuitously, carbon dioxide production and its
delivery to the pulmonary circulation is limited by
the relatively low cardiac output achieved during
CPR. As a consequence, high tidal volumes are
unnecessary to achieve adequate carbon dioxide
excretion and the prevention of hypercapnia. This
situation may, however, require some modification if
carbon dioxide producing buffers are administered
(see below) and relative increases in minute ventilation are required to prevent carbon dioxide build-up
and the development of hypercapnic acidosis.
DRUG DELIVERY DURING CPR
The optimal method of drug administration during
CPR is still the pervenous route.24 Central venous
cannulae can deliver drugs rapidly and efficiently to
the central circulation. In general, provided cardiac
arrest has not ensued as a consequence of hypovolaemia, the central veins are often full; nevertheless, central venous cannulation by whatever route
(e.g. internal jugular or subclavian) requires considerable technical proficiency. The risks associated
with the technique of central cannula insertion are
174
significant. Well recognized complications include
pneumothorax (with the possibility of the development of tension), arterial puncture, air embolus and
catheter malposition. Some of these can be life
threatening and early detection may be difficult.
Obviously, if a central venous cannula is already in
situ, it should be used. Otherwise, for an individual
patient, the decision to attempt central venous
cannulation depends on the skill of the operator,
available equipment, nature of the surrounding
events and time scale. If the decision is made to
perform central venous cannulation it must never
delay defibrillation attempts, performance of CPR or
security of the airway.
Where a peripheral venous route is used, a flush of
20–50 ml of 0.9% saline is given after drug administration to expedite entry to the central circulation.
Administration of drugs by the tracheal route is
theoretically attractive, particularly if there is no
immediate access to the systemic circulation. During
the management of cardiac arrest, tracheal intubation frequently precedes venous cannulation,
particularly in patients where venous access is
rendered difficult by obesity or previous drug use.
Unfortunately, the early promise shown by tracheal
drug administration has not been confirmed.
Impaired absorption and unpredictable pharmacodynamics means that drug administration by this
route remains a second line approach.
Drugs which can be given by this route are also
limited, currently to adrenaline, lignocaine and
atropine. It is recommended that doses of 2–3 times
the standard i.v. dose are given, diluted up to a total
volume of at least 10 ml in 0.9 % saline. After
administration, five ventilations are given in an
attempt to maximize absorption from the distal
bronchial tree. Theoretically, administration of the
agent by deep endobronchial application would be
advantageous. This would necessitate the use of a
catheter inserted via the tracheal tube. Surprisingly,
for lignocaine, no advantage was demonstrated from
deep endobronchial administration.
DRUG THERAPY DURING CPR
Over 100 yr ago, adrenaline was used to produce
peripheral vasoconstriction and re-start the hearts of
animals in asystole. For the past 40 yr adrenergic
agents have been advocated as the mainstay of
pharmacological therapy in cardiac arrest. There is
no doubt that experimentally adrenaline (and other
adrenergic agonists) can improve myocardial and
cerebral blood flow.45 In animal studies this can
result in improved resuscitation success rates. These
effects are dose-dependent and higher doses are
more effective than the “standard” dose of 1 mg.
Unfortunately, the human clinical experience is
much less clearcut. There is little evidence that
adrenaline unequivocally improves survival or
neurological recovery rates in humans after cardiac
arrest.26 62 Although slightly increased rates of
spontaneous circulation have been seen in some
clinical studies with high-dose adrenaline, there was
no overall improvement in survival rate.7 10 40 55
It is interesting to conjecture why there are these
British Journal of Anaesthesia
marked differences between experimental and
clinical results. They may in part reflect the differences in underlying pathology between the human
and animal heart, together with the relatively long
periods of cardiac arrest before ALS procedures
enable adrenaline to be given in the clinical setting.
Furthermore, it is possible that higher doses of
adrenaline could be counter-productive in the postresuscitation period by increasing myocardial oxygen
consumption, adversely affecting patterns of endocardial, epicardial and pulmonary blood flows, and
inducing the pattern of myocardial injury known as
contraction band necrosis.46 58
To date, there has been no randomized,
controlled study in humans comparing standard
dose adrenaline (1 mg every 3 min) with placebo of
sufficient power to provide an unequivocal result.
Pending this, it is recommended that the indication,
dose and time intervals between doses of adrenaline
remain unchanged.
The risks of routinely administering adrenaline
to patients in whom cardiac arrest is provoked by,
or associated with, solvent abuse, cocaine and
other sympathomimetic drugs should also be
remembered.37 39 52
The use of antiarrhythmic agents to prevent
arrhythmias is well established. Their use to facilitate
defibrillation is, however, much less clear. There is
no doubt that animal models have dramatically
improved our knowledge of the mechanisms of
arrhythmogenesis and antiarrhythmic drug actions.4
As with adrenaline, however, extrapolation from
the animal to the clinical model is fraught with
problems.
Of all the antiarrhythmic agents used in cardiac
arrest, we know more about lignocaine than any
other drug. Initial concerns that lignocaine increased
the ventricular defibrillation threshold are probably
more related to the experimental technique than an
effect of the drug.13 17 20 31 43 In humans, the energy
requirements for defibrillation were not increased
when lignocaine was given.36 Whether lignocaine
was more efficacious than other agents, such as
bretylium, is unknown. The CALIBRE study, a
multicentre study which is currently evaluating these
two agents in this situation, is now underway.
Pending this, it is recommended that no change
be made in relation to previous recommendations
on the use of lignocaine, bretylium or other
antiarrhythmic agents.
The use of atropine in the treatment of haemodynamically compromising bradyarrhythmias and
some forms of heart block is well established.41
Atropine has previously been advocated in the
management of asystole on the basis that an increase
in vagal tone could produce arrhythmias or reduce
the potential efficacy of other therapies in re-starting
an electrical rhythm.61 Evidence of efficacy of
atropine in asystole is limited to small series and case
reports.8 16 28 57 Nevertheless, the prognosis of
asystolic states is so poor and the likelihood of
significant adverse effects produced by atropine so
limited, that its use in this situation can be considered. In healthy human volunteers, a single dose
of 3 mg i.v. is sufficient to block vagal activity
Advanced life support guidelines
175
completely and this dose is recommended if atropine
is considered for asystole.12
Provided that effective basic life support is
performed, arterial blood-gas analysis shows neither
rapid nor severe development of acidosis during
cardiorespiratory arrest in previously healthy
individuals.25 54 Arterial blood-gas analysis is commonly performed to assess acid–base status, but
alone may be misleading. Even co-terminously
measuring arterial and mixed central venous bloodgas samples may be of little value in estimating
the internal milieu of myocardial and cerebral
intracellular acid–base status.11 29 34 60
In the past, administration of sodium bicarbonate
as a buffer was advised to reverse the potentially
deleterious effects of acidosis. Potential adverse
effects of sodium bicarbonate administration include
alkalaemia, hyperosmolarity and carbon dioxide production. Other agents, such as sodium carbonate,
Carbicarb (a mixture of sodium carbonate and
sodium bicarbonate), tromethamine (THAM) and
tribonate (a mixture of sodium bicarbonate, THAM,
phosphate and acetate) have been suggested to
minimize some of these effects.22 However, there is
no clinical evidence to suggest that carbon dioxide
consuming buffers, or indeed any buffer, are
effective in increasing survival rates after human
cardiac arrest.19 33 35 The best method of reversing
acidosis associated with cardiac arrest is to restore
spontaneous circulation. At present, in the UK,
sodium bicarbonate remains the buffer of choice. It
is suggested that its judicious use is limited to
patients with severe acidosis (arterial pH less than
7.1 and base deficit less than 910) and to cardiac
arrest occurring in special circumstances, such as
hyperkalaemia or tricyclic antidepressant overdose.
The universal ALS algorithm
Figure 1 Algorithm for advanced life support management.
BLS:Basic life support.
There is now a single algorithm for ALS
management; it is applicable for health care
providers using manual, semi-automatic or
automatic defibrillators (fig. 1). Each step of the
algorithm presupposes that the one before has been
unsuccessful.
The route of access to the ALS algorithm
depends primarily on the events surrounding the
cardiac arrest. In many situations, such as out-ofhospital cardiac arrest, basic life support will
already have been started. This must continue
while the monitor/defibrillator is being attached. In
patients who are already monitored, clinical and
electrocardiographic detection of cardiac arrest
should be nearly simultaneous. In these situations,
patients who have had a witnessed collapse can
have a single precordial thump administered pending attachment of the monitor/defibrillator or if
there is any delay in administration of the first
defibrillating shock.9 47
Analysis of the ECG rhythm must take place
within the clinical context. Movement artefact, lead
disconnection and electrical interference can all
mimic cardiac arrest rhythms. For the rescuer with a
manual defibrillator, the crucial decision is whether
or not the rhythm present is VF/VT. If VF/VT is
suspected, defibrillation must occur without delay.
The first shock is given with an energy level of 200 J
for a standard monophasic shock, or its equivalent if
a biphasic waveform in used. If the first defibrillating
shock is unsuccessful, a shock of the same energy
(200 J) is repeated. If still unsuccessful a third shock
is given, this time at 360 J.
A check of a major pulse is performed if, after a
defibrillating shock, an ECG rhythm compatible
with cardiac output is obtained. If, however, the
monitor/defibrillator indicates that VF persists, then
the additional shocks in the sequence of three can be
administered without a further pulse check.
With modern monitor/defibrillators it is possible,
if necessary, to administer the first three shocks
within a period of 60 s, and in the majority of
patients who are treated successfully, defibrillation
occurs after one of the first three shocks. If the first
sequence of three shocks is unsuccessful, the best
chance for restoring a perfusing rhythm is still
defibrillation but correction of reversible causes or
aggravating factors, and attempts to maintain
myocardial and cerebral perfusion and viability, are
indicated at this stage.
176
Potential causes or aggravating factors leading
to persistent VF/VT may include electrolyte
imbalance, hypothermia and drugs or toxic agents
for which specific therapy may be required (see fig.
1). These interventions, together with checking
defibrillating
paddle/electrode
positions
and
contacts, should occur during the 1-min period of
CPR.
During this time, attempts are made to secure
advanced airway management and ventilation and to
institute venous access. The first dose of adrenaline
is given.
It is unlikely that even with a highly trained team
all of these aspects will be completed within this first
CPR interval, but further opportunity will occur
with the next cycle.
The ECG rhythm is then re-assessed. If VF is still
present, the next sequence of defibrillating shocks is
started without delay. These shocks are all at 360 J
(or equivalent).
Provided that resuscitation was started appropriately, sequential loops of the left-hand side of the
algorithm are continued, allowing further sequences
of defibrillating shocks, CPR and the ability to
perform/secure advanced airway and ventilation
techniques and drug delivery. As long as resuscitation has been started appropriately, it should not
normally be abandoned while the ECG rhythm is
still recognizably VF/VT.
If at the time of initial rhythm analysis, VF/VT can
be positively excluded, clearly defibrillation is not
appropriate. In this situation, the right-hand side of
the algorithm is followed. These patients may have
asystole or electromechanical dissociation (EMD).
Any electrical rhythm associated with cardiac arrest
will, if untreated, deteriorate to asystole. The
prognosis for these rhythms is, in general, much less
favourable14 27 but nevertheless there are some
situations where they have been provoked by
remediable conditions which, if detected and treated
promptly, may lead to success. The common causes
are listed in figure 1 and may be recalled under the
headings of the 5 H’s and 4 T’s.
Cardiac pacing may be of value in patients with
extreme bradyarrhythmia. Its efficacy in true
asystole is unproved, except in cases of trifascicular
block where p waves are present. If pacing is
contemplated and delay occurs before its
institution, external cardiac percussion (fist pacing)
may be effective in producing cardiac output,
particularly in those situations where myocardial
contractility has not been critically compromised.18 48 49 While the search for, and correction
of, these potential causes of arrest are underway,
basic life support with advanced airway management and ventilation, venous access, etc, should
occur as before, and adrenaline is administered
every 3 min.
After 3 min of CPR, the ECG rhythm is
re-assessed. If VF/VT has developed, then the
left-hand side of the algorithm is followed. If a
non-VF/VT rhythm still persists, loops of the righthand side of the algorithm continue for as long as
is considered appropriate for resuscitation to
continue.
British Journal of Anaesthesia
References
1. Adgey AAJ, Dalzell GNW. Paddle/pad placement for
defibrillation in adults. British Journal of Intensive Care 1994;
(Suppl.): 14–16.
2. Adgey AAJ, Devlin JE, Webb SW, Mulholland H. Initiation
of ventricular fibrillation outside hospital in patients with
acute ischaemic heart disease. British Heart Journal 1982; 47:
55–61.
3. Alyward PE, Keiso R, Hite P, Charbonnier F, Kerber RE.
Defibrillator electrode-chest wall coupling agents: Influence
on transthoracic impedance and shock success. Journal of the
American College of Cardiology 1985; 6: 682–686.
4. Babbs CF, Yim GKW, Whistler SJ, Tacker WA, Geddes LA.
Elevation of ventricular defibrillation threshold in dogs by
antiarrhythmic drugs. American Heart Journal 1979; 98:
345–350.
5. Bardy GH, Gliner BE, Kudenchuk PJ. Truncated biphasic
pulses for transthoracic defibrillation. Circulation 1995; 91:
1768–1774.
6. Baskett PJF, Bossaert L, Carli P, Chamberlain D, Dick W,
Nolan JP, Parr MJA, Scheidegger D, Zideman D. Guidelines
for the advanced management of the airway and ventilation
during resuscitation. A statement by the Airway and
Ventilation Management Group of the ERC. Resuscitation
1996; 31: 201–230.
7. Brown CG, Martin DR, Pepe PE, Steuven H, Cummins RO,
Gonzakz E, Jastremski M. A comparison of standard-dose
and high-dose epinephrine in cardiac arrest outside the hospital. The Multicenter High-dose Epinephrine Study Group.
New England Journal of Medicine 1992; 327: 1051–1055.
8. Brown DC, Lewis AJ, Criley JM. Asystole and its treatment:
The possible role of the parasympathetic nervous system in
cardiac arrest. Journal of the American College of Emergency
Physicians 1979; 8: 448–452.
9. Caldwell G, Millar G, Quinn E, Vincent R, Chamberlain
DA. Simple mechanical methods for cardioversion: defence
of the precordial thump. British Medical Journal 1985; 291:
627–630.
10. Callaham ML, Modsen CD, Barton CW, Saunders CE,
Pointer J. A randomised clinical trial of high-dose
epinephrine and norepinephrine vs. standard dose
epinephrine in prehospital cardiac arrest. Journal of the
American Medical Association 1992; 268: 2667–2672.
11. Capparelli EV, Chow MSS, Kluger J, Fieldman A.
Difference in systemic and myocardial blood acid–base status
during cardiopulmonary resuscitation. Critical Care Medicine
1989; 17: 442–446.
12. Chamberlain DA, Turner P, Sneddon JM. Effects of atropine
on heart-rate in healthy man. Lancet 1967; ii: 12–15.
13. Chow MSS, Kluger J, Lawrence R, Fieldman A. The effect of
lidocaine and bretylium on the defibrillation threshold during
cardiac arrest and cardiopulmonary resuscitation. Proceedings
of the Society for Experimental Biological Medicine 1986; 182:
63–67.
14. Cobbe SM, Redmond MJ, Watson JM, Hollingsworth J,
Carrington DJ. “Heartstart Scotland”—initial experience of a
national scheme for out of hospital defibrillation. British
Medical Journal 1991; 302: 1517–1520.
15. Cohen TJ, Tucker KJ, Lurie KG, Redberg RF, Dutton JP,
Dwyer KA, Schwab TM, Chin MC, Gelb AM,
Scheinman MM, Schiller NB, Callaham ML. Active
compression–decompression. A new method of cardiopulmonary resuscitation. Journal of the American Medical
Association 1992; 267: 2916–2923.
16. Coon GC, Clinton JE, Ruiz E. Use of atropine for
bradyasystolic prehospital cardiac arrest. Annals of Emergency
Medicine 1981; 10: 462–467.
17. Dorian P, Fain ES, Davy JM, Winkle RA. Lidocaine causes a
reversible, concentration-dependent increase in defibrillation
energy requirements. Journal of the American College of
Cardiology 1986; 8: 327–332.
18. Dowdle JR. Ventricular standstill and cardiac percussion.
Resuscitation 1996; 32: 31–32.
19. Dybvik T, Strand T, Steen PA. Buffer therapy during out-ofhospital cardiopulmonary resuscitation. Resuscitation 1995;
29: 89–95.
Advanced life support guidelines
20. Echt DS, Black JN, Barbey JT, Coxe DR, Cato E. Evaluation
of antiarrhythmic drugs on defibrillation energy requirements
in dogs. Sodium channel block and action potential prolongation. Circulation 1989; 79: 1106–1117.
21. Ekstrom L, Herlitz J, Wnnerblom B, Axelsson A, Bang A,
Holmberg S. Survival after cardiac arrest outside hospital
over a 12-year period in Gothenburg. Resuscitation 1994; 27:
181–188.
22. Gazmuri RJ, von Planta M, Weil MH, Rackow EC. Cardiac
effects of carbon dioxide-consuming and carbon dioxidegenerating buffers during cardiopulmonary resuscitation.
Journal of the American College of Cardiology 1990; 15: 482–49.
23. Greene HL, Dimarco JP, Kudenchuk PJ. Comparison of
monoplasic and biplasic defibrillating pulse waveforms for
transthoracic cardioversion. American Journal of Cardiology
1995; 75: 1135–1139.
24. Hapnes S, Robertson C. CPR—drug delivery routes and
systems. Resuscitation 1992; 24: 137–142.
25. Henreman PL, Ember JE, Marx JA. Development of acidosis
in human beings during closed chest and open chest CPR.
Annals of Emergency Medicine 1988; 17: 672–675.
26. Herlitz J, Ekstrom L, Wennerblom B, Axelsson A, Bang A,
Holmberg S. Adrenaline in out of hospital ventricular fibrillation. Does it make any difference. Resuscitation 1995; 29:
195–201.
27. Herlitz J, Ekstrom L, Wennerblom B, Axelsson A, Bing A,
Holmberg S. Survival among patients with out-of-hospital
cardiac arrest found in electromechanical dissociation.
Resuscitation 1995; 29: 97–106.
28. Iseri LT, Humphrey SB, Sirer EJ. Prehospital bradyasystolic
cardiac arrest. Annals of Internal Medicine 1978; 88: 741–745.
29. Javateri S, Clendending A, Papadakos N, Brody JS. pH
changes in the surface of brain and in cisternal fluid in dogs in
cardiac arrest. Stroke 1984; 15: 553–558.
30. Kerber RE, Grayzel J, Kennedy J, Jensen SR. Elective
cardioversion: influence of paddle electrode location and size
on success rates and energy requirements. New England
Journal of Medicine 1981; 305: 658–662.
31. Kerber RE, Pandian NG, Jensen SR et al. Effect of lidocaine
and bretylium on energy requirements for transthoracic
defibrillation; Experimental studies. Journal of the American
College of Cardiology 1986; 7: 397–405.
32. Kerber RE, Spencer KT, Kallock M. Overlapping sequential
pulses: a new waveform for transthoracic defibrillation.
Circulation 1994; 89: 2369–2379.
33. Kette F, Weil MH, Gazmuri RJ. Buffer solutions may
compromise cardiac resuscitation by reducing coronary
perfusion pressure. Journal of the American Medical
Association 1991; 266: 2121–2126.
34. Kette F, Weil MH, Gazmuri RJ, Bisera J, Rackow EC.
Intramyocardial hypercarbic acidosis during cardiac arrest
and resuscitation. Critical Care Medicine 1993; 21: 901–906.
35. Koster RW. Correction of acidosis during cardio-pulmonary
resuscitation. Resuscitation 1995; 29: 87–88.
36. Lake CL, Kron IL, Mentzer RM, Crampton RS. Lidocaine
enhances intraoperative ventricular defibrillation. Anesthesia
and Analgesia 1986; 65: 337–340.
37. Lange RA, Cigarroa RG, Yancy CW, Flores ED. Cocaineinduced coronary artery vasoconstriction. New England
Journal of Medicine 1989; 321: 1557–1562.
38. Larsen MP, Eisenberg MS, Cummins RO, Hallstrom AP.
Predicting survival from out-of-hospital cardiac arrest: a
graphic model. Annals of Emergency Medicine 1993; 22:
1652–1658.
39. Lathers CM, Tyan LSY, Spino MM, Agarwal I. Cocaineinduced seizures, arrhythmias and sudden death. Journal of
Clinical Pharmacology 1988; 28: 584–593.
40. Lindner KH, Ahrieferd FW, Prengel AW. Comparison of
standard and high-dose adrenaline in the resuscitation of
asystole
and
electromechanical
dissociation.
Acta
Anaesthesiologica Scandinavica 1991; 35: 253–256.
41. Management of periarrest arrhythmias. A statement for the
Advanced Cardiac Life Support Committee of the European
Resuscitation Council 1994. Resuscitation 1994; 28: 151–159.
41a First update. Resuscitation 1996; 31: 281.
177
42. Mapin DR, Brown CG, Dzuonczyk R. Frequency analysis of
the human and swine electrocardiogram during ventricular
fibrillation. Resuscitation 1991; 22: 85–91.
43. Natale A, Jones DL, Kim Y-H, Klein GJ. Effects of lidocaine
on defibrillation threshold in the pig: evidence of anesthesia
related increase. PACE 1991; 14: 1239–1244.
44. Neumar RW, Brown CG, Robitaille PL, Altschuld RA.
Myocardial high energy phosphate metabolism during ventricular fibrillation with total circulatory arrest. Resuscitation
1990; 19: 199–226.
45. Redding JS, Pearson JW. Evaluation of drugs for cardiac
resuscitation. Anesthesiology 1963; 24: 203–207.
46. Rivers EP, Wortsman J, Rady MY. The effect of total cumulative epinephrine dose administered during human CPR on
haemodynamic, oxygen transport and utilisation variables in
the post-resuscitation period. Chest 1994; 5: 1315–1316.
47. Robertson C. The precordial thump and cough techniques in
advanced life support. Resuscitation 1992; 24: 133–135.
48. Sandoe E. Ventricular standstill and percussion. Resuscitation
1996; 32: 3–4.
49. Scherf D, Bornemann C. Thumping of the precordium in
ventricular standstill. American Journal of Cardiology 1960; 5:
30–40.
50. Schwab TM, Callaham ML, Madsen CD, Utecht TA. A
randomised
clinical
trial of active
compression–
decompression CPR vs. standard CPR in out of hospital
cardiac arrest in two cities. Journal of the American Medical
Association 1995; 273: 1261–1268.
51. Sedgewick ML, Dalziel K, Watson J, Carrington DJ, Cobbe
SM. The causative rhythm in out-of-hospital cardiac arrests
witnessed by the emergency medical services in the
Heartstart Scotland project. Resuscitation 1994; 27: 55–59.
52. Sheperd RT. Mechanism of sudden death associated with
volatile substance abuse. Human Toxicology 1989; 8:
287–292.
53. Sirna SJ, Ferguson DW, Charbonnier F, Kerber RE.
Electrical cardioversion in humans: factors affecting
transthoracic impedance. American Journal of Cardiology
1988; 62: 1048–1052.
54. Steedman DJ, Robertson CE. Acid base changes in arterial
and central venous blood during cardiopulmonary resuscitation. Archives of Emergency Medicine 1992; 9: 169–176.
55. Steill IG, Hebert PC, Weitzman BW, Wells GA, Raman S,
Stark RM, Higginson LAJ, Ahuja J, Dickenson GE. High
dose epinephrine in adult cardiac arrest. New England Journal
of Medicine 1992; 327: 1045–1050.
56. Steill IG, Hebert PC, Wells GA, Laupacis A, Vandem Leen
K, Dreyer JF, Eisenhauer MA, Gibson J, Higginson LAJ,
Kirby AS, Mahon JL, Maloney JP, Weitzman BN. The
Ontario trial of active compression–decompression cardiopulmonary resuscitation for in-hospital and prehospital cardiac arrest. Journal of the American Medical Association 1996;
275: 1417–1423.
57. Steuven HA, Tonsfeldt DJ, Thomson BM. Atropine in
asystole: Human studies. Annals of Emergency Medicine 1988;
13: 815–817.
58. Tang W, Weil MH, Sun S, Noc M, Yang L, Gasmuri
RJ. Epinephrine increases the severity of post-resuscitation myocardial dysfunction. Circulation 1995; 92:
3089–3093.
59. Tunstall-Pedoe H, Bailey L, Chamberlain D, Marsden A,
Ward M, Zideman D. Survey of 3765 cardiopulmonary
resuscitations in British hospitals (the BRESUS Study).
British Medical Journal 1992; 304: 1347–1351.
60. von Planta J, Weil MH, Gazmuri RJ, Bisera J, Rackow EC.
Myocardial acidosis associated with CO2 production during
cardiac arrest and resuscitation. Circulation 1989; 80:
684–692.
61. von Planta M, Chamberlain D. Drug treatment of
arrhythmias
during
cardiopulmonary
resuscitation.
Resuscitation 1992; 24: 227–232.
62. Woodhouse SP, Cox S, Boyd P, Case C, Weber M. High
dose and standard dose adrenaline do not alter survival
compared with placebo, in cardiac arrest. Resuscitation 1995;
30: 243–249.