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Arab-Resuscitation Council guidelines for Adult Cardiopulmonary Resuscitation


M.S.M. Takrouri FFARCSI

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




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



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



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.




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.




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.




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.





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.

The 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 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.



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