1. The ABCs of the rescue alphabet for resuscitation were reconsidered from the view points of education and evaluation. It was strongly felt by some conference participants that the "A" of the ABCs of CPR which stands for "airway" should be changed to the "assessment" phase in order to determine unresponsiveness, breathlessness, pulselessness, and to emphasize the importance of evaluation before commencing the treatment.

However, the steering committee of the conference felt that since the ABCs of CPR have been an integral part of CPR education for 30 years, the ABCs of CPR should remain, at least for the time being, as "airway, breathing, and circulation."

2. From the viewpoints of safety, effectiveness, ease of teaching or training, and sequencing into other related maneuvers, one-man CPR teaching to the layman or public was unanimously agreed upon; however, medical professionals will continue to be taught two-rescuer CPR.

3. Concerning the opening of the airway, the public should be taught only head-tilt/chin-lift maneuver. The previous neck-lift/head-tilt maneuver, i.e., the extension at the Atlanto-occipital joint, has been totally withdrawn. However, the jaw-thrust, both in adults and children, for opening the airway is still one of the recommended methods. Trained personnel can open the airway by the triple-airway maneuver, i.e., head-tilt/ mouth-open, coupled with jaw-thrust.³

4. In mouth-to-mouth, mouth-to-nose, or mouth-to-mask ventilations, a new major change involves the rescuer to administer two initial ventilations with a slow respiratory flow rate of about 11/2s each, instead of the former four quick full breaths. These ventilations would no longer create a "staircase" effect which result in the esophageal opening pressure to exceed which can produce gastric distension, regurgitation, and aspiration.

5. Cricoid pressure (Sellick's maneuver) was suggested to be applied during ventilation to reduce the incidence of gastric insufflation and regurgitation. This technique is quite effective in children, and the present recommendation is to teach this method to all EMTs and other rescue personnel.

6. For the -single-rescuer CPR sequence, the external cardiac compression-ventilation ratio remains the same (15:2), but the number of chest compressions is increased from 60 to 80/min to 80 to 100/min.

7. In the two-rescuer sequence, the compression-ventilation ratio remains 5:1, but the frequency of compressions should be increased from 60/min to 80 to 100/min. There should be a pause of 1 to 11/2s for each ventilation in order to allow adequate oxygen delivery, i.e., 1 ventilation is alternated with 5 chest compressions, with a pause between the two acts and not interposed between the compressions. However, after tracheal intubation, the above mentioned synchronized maneuver can be abandoned, and ventilation can be interposed or superimposed during external cardiac massage. Endotracheal intubation is of a gold standard for adequate oxygenation and should be taught to EMTS.

8. Regarding foreign-body airway obstruction, two main changes were implemented. The Heimlich maneuver (subdiaphragmatic abdominal thrusts) was deemed as the preferred method to dislodge foreign bodies from the airway. Back blows have been completely eliminated in adults. Reservations were expressed, however, for the Heimlich maneuver in neonates and in infants of less than one year in age. The present recommendation is in favor of the previous practice of back blows and chest thrusts.

The number of Heimlich maneuvers in adults was increased from 6 to 10, instead of the previous 4 back blows and chest thrusts or abdominal thrusts. For infants, the number of back blows and chest thrusts remains four, and they can be alternated with each other till the foreign body is expelled or the infant becomes unconscious.

9. In obese victims or pregnant women, 6 to 10 chest thrusts or chest compressions, as previously attempted, will still hold place.

10. Finger sweep should only be used in unconscious victims with suspected airway obstruction, and not in conscious and spontaneously breathing persons.

11. For a child aged between I to 8 years, no changes were suggested except the rate of external cardiac compressions which increased from 80 to 100/min in adult CPR, and the compression-ventilation ratio in one-man or two-man CPR child) remains 5:1.

12. When applying closed cardiac compressions on infants, the breast bone should be compressed one finger breath below the originally suggested imaginary line which is between the two nipples.

13. Resuscitation in special situations like near drowning, electric shock, trauma, and hypothermia is, more or less, on the same guidelines which were recommended in the 1980s.

14. The role of the esophageal obturator airway (EOA) and its - modified version, the esophageal gastric tube airway, for ventilating patients whose endotracheal tube cannot be inserted is commendable. However, it can only be inserted blindly into the esophagus of relaxed, comatose, or apneic adult victims by experienced personnel. The EOA is contraindicated in conscious patients and children and is certainly, not in anyway, a replacement for the endotracheal tube. Fewer complications such as esophageal lacerations, gastric ruptures, anterior displacements of the airway, and tracheal intubations have been reported.

15. Although no transmission of viral infection during mouth-to-mouth resuscitation has been documented, it was suggested that all hospital and EMT personnel must be encouraged to use airway adjuncts for ventilation to avoid cross infection of dangerous infectious diseases.

Changes in ventilation, compression techniques, and electric therapy have been discussed; hereon, the discussion will cover the new recommendations in advanced cardiac life support (ACLS). The establishment and maintenance of an intravenous line and an early endotracheal intubation are essential since they are an integral part of ACLS for drug, fluid, and ventilation therapies. Where the intravenous route is not accessible, atropine, Xylocaine (lidocaine), naloxone, and adrenaline can be instilled through the endotracheal tube into the lungs for immediate pharmacological action.

Calcium chloride and isoprenaline are no longer recommended in the routine treatment of cardiac arrest. The use of bicarbonate during CPR also remains controversial. The new drugs included are nitroglycerine, verapamil, and amrinone. As far as neonatal resuscitation is concerned, the new guidelines discourage the use of calcium and atropine since neither has been shown to be effective in acute resuscitation. Sodium bicarbonate is only recommended if there is proven metabolic acidosis. It is therefore discouraged for treating brief cardiac arrests or episodes of bradycardia.

Bicarbonate: This drug does not enjoy the same popularity and priority as it used to. Since there are very few data documenting that the therapy of buffers improves outcome, the routine use of this drug is not recommended. On the contrary, there are laboratory and clinical data indicating that bicarbonate:

2. Shifts the oxygen dissociation curve to the left (alkalemia) and inhibits the oxygen release.

3. Induces undesirable hyperosmolarity and hypernatremia which, particularly in neonates and infants, may produce ventricular hemorrhage.^6,7

4. Produces paradoxical acidosis due to generation of carbon dioxide (260 to 280 mm Hg for each 50 mEq) which rapidly crosses the blood brain barrier and worsens the acid base state intracellularly and within the cerebrospinal fluid.⁸ This also necessitates extremely efficient ventilation without any compromise to rid of the carbon dioxide being generated. Thus, it is mandatory to institute an efficient and prompt ventilation with 100% oxygen via an endotracheal tube to combat the metabolic acidosis with respiratory alkalosis, rather than infuse bicarbonate immediately.

7. Interacts and inactivates the simultaneously administered catecholamines which are direly needed in the first few minutes of CPR.⁹

Thus, bicarbonate should be used, if at all, only after more effective interventions have been implemented such as defibrillation, cardiac compression, support of 100% oxygen ventilation after intubation of inotropic pharmacological support by sympathomimetic amines, and anti-dysrhythmic therapy.

Calcium: Although the normal physiological action of this cation plays an important and critical role in the myocardial contractile performance as an inotropic agent and in impulse formation (automacity), the retrospective and perspective studies have failed to demonstrate its benefits in the setting of cardiac arrest. On the contrary, there is sufficient data to support that high levels induced by iatrogenic administration of calcium may be detrimental. ^10-12

Moreover, the ischemic or anoxic injury triggers the release of calcium into cytoplasmic and mitochondrial milieu. Thus, to continue the use of calcium without convincing evidence of its effectiveness for resuscitation seems highly inappropriate and inadvisable at this juncture. It can cause coronary artery spasm and also increases the myocardial irritability.¹³ Moreover, excessive and unmonitored doses may stop the heart in systole, particularly in digitalized patients, and such a systolic arrest can be very difficult to revive. It is also dangerous to prescribe this drug in hypokalemia. However, calcium therapy can safely be employed in hyperkalemia, hypocalcemia (e.g., after massive and multiple blood transfusions) or in disease states when cardiac arrest has occurred due to calcium and vitamin D deficiency, secondary to malabsorption, hypoparathyroidism, neonatal tetany, adrenal failure with hyperphosphatemia, sodium fluoride toxicity, calcium channel-blocker toxicity, and weaning from cardiopulmonary bypass.

Isoprenaline: Isoprenaline is a synthetic sympathomimetic amine with a pure beta-receptor stimulant action (i.e., cardiac inotropic, chronotropic, and vasodilatory actions). As expected, the cardiac output and cardiac work will be increased, exacerbating ischemia which leads to infarction and dysrhythmias in the ischemic setting. Because of peripheral vasodilation (and fall in diastolic blood pressure), the drug does not generally increase the mean blood pressure and does not enhance the coronary and cerebral perfusion during CPR. The drug, therefore, does not by itself enhance restoration of spontaneous circulation.^14,15 isoprenaline has seemingly no place-during active CPR. The only indication for isoprenaline in ACLS is immediate temporary control of atropine resistant bradycardia or heart block which significantly can affect the hemodynamics. This is only a temporary measure to buy time until a pacemaker can be effectively placed to combat the two above- mentioned entities.

Atropine Sulphate: Atropine is a classic parasympatholytic drug that reduces vagal tone, enhances the rate of discharge of the sino-atrial node, and facilitates atrioventricular conduction. Instead of inducing tachycardia, the drug reduces the likelihood of ventricular fibrillation, triggered by myocardial hypoperfusion, which is associated with extreme bradycardia and heart blocks (but not in complete atrioventricular block where isoprenaline is definitely indicated and the former has no place). Atropine, therefore, has essentially no place during CPR except possibly in refractory asystole.¹⁶ When the spontaneous circulation has resumed and the heart rate has dropped to or below 50 beats/min or when there is bradycardia with premature ventricular complexes or hypotension, then atropine is indicated.^17-21 Atropine may also be beneficial in the presence of atrioventricular block at the nodal level.

We will now discuss the drugs that were unanimously agreed to be added to the armamentarium of ACLS. The list of suggested drugs to be included was in favor of vasodilators (nitroglycerine), calcium channel-blockers (verapamil), and inotropic agents (amrinone). Although all the above-mentioned drugs have little or no immediate place in the active phase of CPR, they do have a definite place in the immediate postresuscitation phase when spontaneous restoration of circulation has been established.

Nitroglycerine: Nitroglycerine is a classic direct vasodilator which is used for the relief of acute anginal pain (sublingually). Nitroglycerine relaxes the smooth muscles by binding them to specific vascular receptors to form disulfide bonds. The drug is now used for the reduction of the pre-load and after-load by peripheral venous (and to a lesser degree arterial) dilation and for pharmacological phlebotomy in protracted cardiac failure due to myocardial infarction. Nitroglycerine is also a good coronary vasodilator and is used as an alternative to nitroprusside. It is more preferred than nitroprusside because the latter may exacerbate ischemia. However, when the left ventricular pressure is reduced, the arterial vasodilator afforded by the nitroglycerine is lost, whereas the nitroprusside still retains the arterial vasodilator effects even when the filling pressures are reduced. Thus, nitroprusside is preferred for the treatment of hypertension in absence of congestive heart failure.²² In the ischemic setting, the initial dosage of nitroglycerine should be approximately 10 μg/min, and increments of 5 to 10 μglmin can be increased every 5 to 10 min until favorable response is achieved.

Amrinone: Amrinone is a bi-pyridine derivative with strong inotropic actions and is mainly a phosphodiesterase inhibitor. Therefore, it has vasodilator actions which result in a dramatic decrease in the after-load and pre-load. The drug is contraindicated in fluid-depleted or hypovolemic patients. The hemodynamic actions of amrinone are nearly the same as dobutamine.²³ Amrinone increases the force of contraction of atrial and ventricular muscles without effecting the spontaneous right atrial rate. The effects of the drug are not blocked by propranolol or reserpine pre-treatment and are least dependent on cyclic adenosine monophosphate, phosphodiesterase activity, or Na,K-ATPase activity in the cardiac muscles. Amrinone certainly has a place in the treatment of congestive heart failure and congestive cardiomyopathies. It may almost double the cardiac index and left ventricular stroke work without increasing oxygen consumption and affecting coronary artery blood flow. Amrinone is effective, both orally and intravenously, and has a low potential for serious side-effects. The role of this drug in pediatric and neonatal resuscitation is yet to be evaluated.

The initial dose should be in a range of 0.75μglkg, slowly followed by an infusion of 5 to 10 Microg/kg/min. In higher dosages, it may exacerbate myocardial ischemia and warrants hemodynamic monitoring. Amrinone should certainly be considered in those patients who suffer from severe congestive heart failure which has been refractory to diuretics, vasodilators, and conventional inotropic agents.

Calcium Channel-Blockers: These drugs are derivatives of papaverine and are effective for treating supraventricular tachycardia that will not require cardioversion. In cardiac arrest, calcium entry blockers may have two beneficial effects: (1) preservation of myocardium (protection by pretreatment) and (2) reduction of vulnerability to ventricular fibrillation.

Verapamil, a negative inotropic, causes reduction in myocardial oxygen consumption. The drug is also a coronary artery vasodilator. Verapamil slows the conduction and prolongs refractoriness in the atrioventricular node, terminating supraventricular tachycardia that uses the atrioventricular node as a re-entrant pathway. It also slows the ventricular response to atrial flutter and fibrillation, as well as atrioventricular nodal tachycardia. Since the drug blocks the slow response actions, it has a potential for treating the dysrhythmias which are associated with ischemia. Having mentioned all the beneficial pharmacological actions, verapamil is still in need of experimental studies to prove its efficacy in actual cardiac arrest situations for restoration of spontaneous circulation.

All calcium channel-blockers are also cerebral vasodilators; although the pharmacology of these drugs seems attractive, they have some deleterious effects such as dose- dependence, slowing of the atrioventricular conduction leading to electromechanical dissociation, and cardiac standstill.²⁴ Myocardial negative inotropic and vasodilator effects may produce hypotension and tachyarrhythmias with atrial fibrillation, sometimes leading to ventricular fibrillation. These effects may facilitate accessory conduction in patients with Wolff-Parkinson-White syndrome, leading to tachyarrhythmias and congestive heart failure. Hypotension, produced by calcium channel-blockers, is easily reversible with calcium chloride, adrenaline, noradrenaline, and dopamine.

In summary, the 1985 conference recommended new changes for CPR; it established new standards and guidelines for CPR (both in basic and advanced cardiac life support), reviewed emergency cardiac care, and stressed the role of bystander CPR. The penetration of professional people into the community with strong prevention messages (prudent heart living), at the delivery time of CPR training, will unprecedently have an enormous impact on cardiovascular morbidity and mortality.