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Arab-Resuscitation Council     Guidelines


T he Arab Resucitation Council
Arab-Resuscitation council guidelines


Proposal of Pan-Arab-resuscitation council as guidelines for Adult Cardiopulmonary

M.S.M. Takrouri Professor of anesthesia King Khalid University Hospital, Riyadh.
11461. P.O.Box 2925. Saudi Arabia

Dear brothers,

    Whether you are American trained or otherwise. It seems you have now to build up the guidelines of ARC in a way acceptable to the Arab rescuer.
     This is one aspect we are going to put for discussion and debate. Recently Dr. El-Dawlatly asked about what he can do on sea side and how he can make training. We can not
discuss this issue without first agree about who should deliver the resuscitation and who he is
going to link. (See archive No 0) on the Arab-Resuscitation list. The formation of the International
Liaison Committee on Resuscitation (ILCOR) has facilitated the process of unification of
guidelines. which is 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 report summarizes the ALS component of the advisory statements with particular reference to their use in the Arabic world. The pan-Arab Resuscitation Council then could accept this guidlines. (See aechives 1,2,3  on the Arab-Resuscitation list).

General principles
    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 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 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. .

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, carbon dioxide production and its
delivery to the pulmonary circulation are 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 and relative increases in minute
ventilation are required to prevent carbon dioxide build-up and the development of hypercapnic

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 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. The Advances in universal ALS algorithm 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
favourable 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.

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.

1- ROBERTSON, C. E., Resuscitation Br. J. Anaesth.
1997; 79:172-177
2- TAKROURI, M.S.M., (Editorial) CPR in Saudia Arabia and call for Arab
Resuscitation Council M.E.J.Anesth. 1998 (16)3:

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