Arab-Resuscitation Council guidelines for Adult
Cardiopulmonary Resuscitation
Professor
of Anesthesia
Consultant in-Charge, of Surgical Intensive Care
Unit.
Department of Anesthesia
College of Medicine
King
Saud University, King Khalid University
Hospital, Riyadh. P.O. Box 2925. 11461. Saudi Arabia
Mohamed A. Seraj, FFARCSI
Chairman, National CPR Committee
Professor and
Consultant Anesthetist
Department of Anesthesia
College of Medicine
King Saud University
P.O. Box 2925
Riyadh 11461, Saudi Arabia
Delivered
at the 6th pan-Arab Congress on Anesthesia, Intensive Care, Pain and
Emergency-disaster Medicine
Abu
Dhubi 2000
Jan 16th-20th
2000
Abstract
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. 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 Australia 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 Arabic countries, under the aegis of the Arab Resuscitation
Council (ARC), this body has accepted the task of assessing these new ALS
guidelines
Introduction
Weather you are
American medically trained or otherwise. It seems now that you should be aware
of the Arab Resuscitation Council (ARC) guidelines. Which is in accordance with
the current sound medical information. The formation of the International
Liaison Committee on Resuscitation (ILCOR) has facilitated this process by
making possible worldwide cooperation and discussion or resuscitation
procedures. Representatives from North America, Europe, Southern Africa and
Australia have collaborated to produce the ILCOR advisory statements on resuscitation,
which were published in April 1997. [1-9]
The importance of cardiopulmonary resuscitation (CPR) is evident, the American heart association started the effort of standardization, updating and educating in various level of CPR skills. In the Middle East Saudi Heart Association did the first effort of that kind. [1,2]
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. For all of these reasons, a
review of the guidelines was both apposite and timely. [2-10]
This article
summarizes, the ALS component of the advisory statements, with particular
reference to their use in the Arabic countries, under the aegis of the Arab
Resuscitation Council (ARC), This body has accepted the task of assessing these
new ALS guidelines
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 ischemic 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 arrhythmia may prevent the development of
cardiac arrest
A small, but
important, group of patients develop cardiac arrest in special circumstances;
examples include trauma, hypothermia, immersion, drug overdose, anaphylaxis,
hypo-volemia, 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). 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. The more rapidly a patient can be
defibrillated in these 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.
This decline reflects rapid depletion of myocardial high-energy phosphate
stores, and is mirrored in the deterioration of the amplitude and
characteristics of the VF waveform. 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. 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 self-adhesive 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. 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 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
Some of these techniques have been
shown experimentally to improve the hemodynamic 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. Consequently, the
new guidelines do not recommend any change in the technique of closed chest
compression.
AIRWAY
MANAGEMENT AND VENTILATION
After cardiac arrest
and during CPR, normal pulmonary physiological characteristics are altered.
There is an increase in dead space and a reduction in lung compliance because
of the development of pulmonary edema. 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, the
relatively low cardiac output achieved during CPR limits carbon dioxide
production and its delivery to the pulmonary circulation. 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 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. 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 hypovolemia, 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 significant. Well-recognized complications include pneumothorax
(with the possibility of the development of tension), arterial puncture, air
embolus, and catheter mal-position. 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 years ago,
adrenaline was used to produce peripheral vasoconstriction and re-start the
hearts of animals in asystole. For the past 40 years 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. 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 clear-cut.
There is little evidence that adrenaline unequivocally improves survival or
neurological recovery rates in humans after cardiac arrest. 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
It is interesting to
conjecture why there are these 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 post-resuscitation 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.
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.
The use of antiarrhythmic agents to prevent arrhythmia 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. 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.
In humans, the energy requirements for defibrillation were not increased when
lignocaine was given. Whether
lignocaine was more efficacious than other agents, such as bretylium, is unknown.
The CALIBRE study, a multicentre study that 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 hemodynamically compromising bradyarrhythmias and some forms
of heart block is well established. 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. Evidence of efficacy of atropine in asystole
is limited to small series and case reports.
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 completely and
this dose is recommended if atropine is considered for asystole.
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. Arterial blood-gas analysis is commonly performed to
assess acid-base status, but alone may be misleading. Even measuring arterial
and mixed central venous blood-gas samples may be of little value in estimating
the internal milieu of myocardial and cerebral intracellular acid-base status.
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 alkalemia, 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. 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. The best
method of reversing acidosis associated with cardiac arrest is to restore
spontaneous circulation. At present,
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 -10) and to cardiac arrest occurring in
special circumstances, such as hyperkalaemia or tricyclic antidepressant
overdose.
There is now a single
algorithm for ALS management; it is applicable for health care providers using
manual, semi-automatic or automatic defibrillators 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-of-hospital 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.
Analysis of the ECG
rhythm must take place within the clinical context. Movement artifact, 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.
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. 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 favorable but nevertheless there are some situations where they have been
provoked by remediable conditions, which, if detected and treated promptly, may
lead to success.
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. 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
right-hand side of the algorithm continue for as long as is considered
appropriate for resuscitation to continue.
References
1.
American Heart Association. Standard and guidelines for
CPR and emergency cardiac care. Dallas: American Heart Association, 1986
2.
Flint LS. Strengthening the chain of survival. Bull Saudi
Heart Assoc 1990;2(3):154-64.
3.
American Heart Association. Risk of infection during
CPR training and rescue supplemental guidelines. JAMA 1989;262(19): 2714-5.
4.
Willens J. Big changes in the wind. Nursing 1991:53-6.
5.
Channa AB. What's new in cardiopulmonary resuscitation and
emergency cardiac care. Bull Saudi Heart Assoc 1989; 1 (4):173-8.
6.
Cummins RO, Chamberlain DA, Abramson NS, et al. Recommended
guidelines for uniform reporting of data from out-of-hospital cardiac arrest:
the Utstein style. Ann Emerg Med 1991;20:861-74.
7. Seraj
M. A (editorial)
Future trends in emergency cardiac care and cardiopulmonary resuscitation; Journal of the Saudi Heart Association, Vol.
4, No. 3, 1992
8. TAKROURI M.S.M. (Editorial) CPR in Saudi Arabia and
Call for Arab Resuscitation Council M.E.J. Anesth. 1998(16)3.
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in Saudi Arabia -past, Present and future-: M.E.J.Anesth, 1990:10(5)
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