Over the past decade many exciting and promising new approaches of delivering CPR have been studied. Considerable data have accumulated suggesting that forward flow during CPR is generated, at least in part, by the development of elevated intrathoracic pressure with an extrathoracic arteriovenous pressure difference. This mechanism, known as the "thoracic pump," has been documented during "cough-CPR" and has led to numerous attempts at optimizing the outcome by increasing intrathoracic pressure in CPR. Studies have demonstrated improved flows with simultaneous ventilation and sternal compression, with static or interposed abdominal compression, with longer duration compression, and with various combinations of these maneuvers. Other recent studies have suggested that the cardiac compression mechanism may indeed be operative, at least under certain circumstances, and that CPR may be optimized by increasing the force and rate of compression. Still others have advocated a simple change in the sequence of initiating ventilation and compression. Which, if any, of these newly advocated methods improve the outcome when applied to man remains to be established. If any of these techniques is shown to be more advantageous, its widespead use will depend on its applicability without adjuncts and its teachability to the lay public.

Current basic life support (BLS) protocols do not address the physiologic effects of accidental hypothermia in prehospital care. The extreme levels of bradycardia, bradypnea, and peripheral vasoconstriction that often accompany profound hypothermia may complicate the accurate diagnosis of cardiopulmonary arrest in the unmonitored patient. Although CPR is indicated in the truly pulseless, apneic victim of hypothermia, chest compressions may convert nonpalpable but adequately perfusing sinus bradycardia to ventricular fibrillation. This dilemma had led to disagreement among clinicians and researchers in hypothermia about prehospital care protocols for the severely hypothermic patient. This article reviews the controversy and recommends the application of a normal BLS protocol to hypothermic patients presenting in apparent cardiopulmonary arrest.

Special resuscitation situations are cardiopulmonary arrests requiring modification or extension of conventional life support techniques. Significant controversy exists with regard to several aspects of special resuscitation, including whether or not there is a need to clear the airway of a near-drowning victim with the Heimlich maneuver and whether CPR should be initiated in an unmonitored hypothermic patient showing no signs of life. The previous standards and guidelines almost entirely neglected the management of cardiac arrest due to traumatic injury. The conference panel on Special Situations recommended that: the Heimlich maneuver should only be performed on near-drowning victims when the rescuer suspects that foreign matter is obstructing the airway or the victim fails to respond appropriately to mouth-to-mouth ventilation, further investigation is needed to better define the need for, the risks of, and the timing of the Heimlich in the near-drowning victim, there should be an expanded section in the standards and guidelines describing the differences in the management of a victim whose cardiac arrest is due to traumatic injury, CPR is indicated and should be done on a pulseless, unmonitored hypothermic patient in the field, but that a longer time to check for a pulse (up to one minute) may be required, and guidelines that the panel proposed be used for management of the underwater submersion victim in cardiac arrest.

Cerebral neurons can tolerate at least 20 min of normothermic ischemic anoxia. Cerebral recovery from more than 5 min of cardiac arrest is hampered by complex secondary derangements of multiple organ systems after reperfusion. There is increasing support of our hypothesis that this "postresuscitation syndrome" includes the following: secondary cerebral perfusion failure, cerebral reoxygenation injury (cell-necrotizing cascades), and cerebral "intoxication" from derangements of extracerebral organs. To be optimal for the brain, CPR with optimal perfusion pressure must be started as promptly as possible. Significant though inconsistent mitigation of permanent brain damage after prolonged complete global brain ischemia has been achieved in animal outcome preparations with the use of the following treatments initiated at the start of reperfusion: brain-oriented extracerebral life support by protocol, intra-arterial hemodilution, hypertension, and artificial circulation, barbiturates, calcium-entry blockers, free-radical scavengers, and multifaceted treatments. We currently recommend treatment 1 for patient care and treatment 2 for clinical feasibility trials. Treatment 3, thiopental loading (starting 10 to 50 min after restoration of spontaneous circulation), was tested in a randomized clinical trial and was not shown to confer a statistically significant benefit. A calcium-entry blocker is under clinical investigation. Many other novel treatments appear promising but further animal studies are required. The complex multifactorial pathogenesis of postcardiac arrest encephalopathy requires systematic multicenter development of etiology-specific combination therapies.

The esophageal obturator airway (EOA) has been in use for over a decade and has been inserted over 3 million times. It has given rise to a body of literature, some of it controversial, concerning the role of the device. Data concerning the ventilatory efficiency, safety, complications, limitations, indications, and contraindications as well as mortality and morbidity associated with its use are presented and its present role in CPR is described. In line with the recommendations of the 1985 Standards Committee, the EOA is regarded as a useful device in CPR, which complements the endotracheal tube in the training of paramedics.

Available clinical data indicate that an initial shock energy of 200 J will defibrillate the majority of patients. There is no advantage in starting at a higher energy, and lower energy shocks may be safer. Measurements of transthoracic impedance may permit the use of even lower energy levels for initial shocks. If the initial shock fails to defibrillate it should be repeated immediately, at the same energy level, and then increased if defibrillation is still not achieved. If the initial shock defibrillates but refibrillation occurs later there is no reason to increase the energy; it should be repeated at 200 J. We suggest the following energy selection algorithm for defibrillation (VF = ventricular fibrillation): (Formula: see text).

This presentation summarizes advances in electrical therapy of cardiovascular emergencies. The urgency of delivering definitive therapy is emphasized, and the roles of automatic internal and external defibrillators, practical external pacing, and mechanical techniques for cardioversion and defibrillation are evaluated. Standard position of the electroplates is recommended except in patients who have permanently implanted pacemakers. In these patients, the defibrillation electrodes should be at least 5 inches from the pacemaker generator. The energy requirement for defibrillation of ventricular fibrillation is reviewed, with the conclusion that the initial defibrillatory shock should be 200 J. The determinants of the transthoracic impedance are important, especially if low-energy shocks are to be used, since a high transthoracic impedance results in a poor success rate for defibrillation with low-energy shocks. When high-energy (360 J) shocks are to be used, transthoracic impedance appears to be of less importance.

Three forms of treatment are available for patients with paroxysmal supraventricular tachycardia (PSVT): nonpharmacologic, pharmacologic, and electrical. Nonpharmacologic treatments increase vagal tone and include the traditional carotid sinus massage and Valsalva maneuver as well as head-down tilt, activation of the diving reflex, and use of the pneumatic antishock garment. The most effective currently available pharmacologic agent is verapamil. Hemodynamically stable patients whose PSVTs are refractory to verapamil may be treated with digitalis. Patients with antegrade accessory pathway conduction (such as those with Wolff-Parkinson-White syndrome) and a history of atrial fibrillation should be treated with intravenous procainamide if they are hemodynamically stable and with synchronized electrical countershock if they are hemodynamically unstable. Synchronized electrical countershock is the treatment of choice for hemodynamically unstable patients.

Blood flow during closed-chest CPR may result from variations in intrathoracic pressure rather than selective compression of the cardiac ventricles. During chest compression, the thoracic and abdominal cavities are subjected to positive pressure fluctuations. It has been suggested that compression of the abdomen may improve left heart outflow during CPR by limiting diaphragmatic movement or improving venous return. Abdominal compression has been performed experimentally with pneumatic abdominal binders and with the abdominal compartment of the conventional military antishock trouser (MAST) garment. The MAST garment might also improve cardiac output with CPR through an "autotransfusion" effect. In animal studies, MAST-augmented CPR has improved systolic pressures; it has not been shown to improve vital organ perfusion. In the only available clinical study, CPR with the MAST did not improve survival from prehospital cardiac arrest when compared with conventional CPR alone. If inflation of the MAST does produce blood displacement from the peripheral to the central venous circulation, such an effect may be detrimental in that the arteriovenous pressure gradients necessary for vital organ flow may be adversely affected. Inflation of the MAST during CPR may also adversely effect artificial ventilation. Selective abdominal binding also increases systolic pressures during CPR but does not improve subdiaphragmatic venous return. Although abdominal binding may increase common carotid flow, it has not been shown to improve cerebral or myocardial perfusion when compared with conventional CPR alone. These CPR adjunct techniques have not been shown to improve outcome from cardiac arrest and should remain experimental until further well-designed studies addressing regional vital organ flow and outcome of resuscitation are performed.

The use of bicarbonate during cardiopulmonary resuscitation remains controversial. The present standards, suggested in large part by the investigations of Bishop and Weisfeldt, and the acknowledged toxicity of treatment with bicarbonate led to aggressive use of hyperventilation, the frequent monitoring of pH, and a reduction in bicarbonate administration. However, to date no studies have indicated an improvement in outcome to support the importance of these changes. Instead, controversy continues concerning the most appropriate buffer and whether the pH gradient induced between venous and arterial beds during CPR is of importance. To date, a viable alternative regimen has not been proposed. Thus, at present there is little new data upon which to base a major change in strategy, although the logic of reducing further the use of bicarbonate seems compelling. The choice of antiarrhythmic therapy is equally difficult. Initially, experimental studies suggested a more potent antifibrillatory effect for bretylium than for lidocaine. Subsequent studies have challenged these initial experimental results and clinical data have failed to indicate the benefit of one drug over the other. There is little information to suggest that these agents are more effective than the aggressive use of defibrillation alone in patients with ventricular fibrillation. It therefore seems improbable that a definitive decision concerning the use of one or another of these agents can be made.

Cardiopulmonary resuscitation in children is not well studied; many of the current recommendations for advanced pediatric life support (APLS) are based on anecdotal experience rather than scientific study. The following are unique issues in APLS requiring a consensus decision: What are the best methods of vascular access and of drug delivery and dosages? What constitutes minimal paramedic training and equipment? There are also many shared controversies between APLS and ACLS, including the use of calcium, epinephrine vs isoproterenol, methoxamine, and bicarbonate. This article presents the scientific basis for these controversial issues and highlights areas where information is lacking. A discussion of these questions generated a consensus on some issues and hopefully will stimulate further study to answer the questions that were raised.

Atropine, calcium, calcium-channel blockers, beta-adrenergic-receptor blockers, oxygen, morphine, vasodilators, and potent diuretics are frequently used in advanced cardiac life support (ACLS). Since the last AHA conference on ACLS standards, little controversy has arisen regarding the use of oxygen, morphine, vasodilators, or potent diuretics. In 1979, a full vagolytic dose of atropine was recommended for use early in the course of asystolic or bradycardiac arrest. Since then reports suggest that this higher dose of atropine may be of some limited value in treating this highly resistant form of arrest. The routine use of calcium for asystole, bradycardiac arrest, and electromechanical dissociation has come under intense scrutiny. Studies have failed to demonstrate improved survival and have found potentially deleterious levels of serum calcium when calcium was administered according to AHA standards. It is also possible that postanoxic cerebral injury is exacerbated by the use of calcium. No controversy exists, however, concerning the use of calcium for the moribund patient with possible hypocalcemia or with an excess of calcium-channel blockers. The use of calcium-channel blockers has been advocated to prevent or retard the intracellular accumulation of calcium, which may cause irreversible postanoxic tissue damage. Calcium-channel blockers may also be useful in preventing or decreasing cerebral and coronary arteriospasm. These drugs have antianginal properties that may decrease ischemia. The antiarrhythmic effect of verapamil is particularly useful in the treatment of uncomplicated paroxysmal supraventricular tachycardia. Verapamil and diltiazem slow conduction through the atrioventricular node and may be used to slow the ventricular response in atrial fibrillation and flutter.(ABSTRACT TRUNCATED AT 250 WORDS)

The Cardiovascular Pharmacology II panel met during the AHA National Conference on Standards and Guidelines for CPR and emergency cardiac care to consider the use of catecholamines, pressor agents, digitalis, and corticosteroids during advanced cardiac life support. During cardiac arrest, catecholamines and pressor agents have been shown to improve the rate of success of resuscitation. The useful properties of these drugs are mediated by strong alpha-adrenergic stimulation resulting in improved coronary perfusion. beta-Adrenergic stimulation during cardiac arrest is unimportant for resuscitation and potentially harmful. Studies have not demonstrated a difference between mixed agonists and alpha-agonists with respect to overall outcome. Consequently, the panel recommended that epinephrine continue to be the primary vasopressor for use during cardiac arrest. For cardiovascular support in the hemodynamically unstable patient, the panel recommended that drugs be chosen for specific pharmacologic actions that will allow the needed physiologic manipulation guided by objective hemodynamic measurements. The panel found that digitalis preparations and corticosteroids have very limited use in emergency cardiac care.

The proper management of patients with acute myocardial infarction changes frequently as new data develop in this complex area. The present recommendations concerning the use of oxygen and morphine and the treatment of hypotension and congestive heart failure require little change save the addition of new agents. However, considerable new data have been derived in the area of limitation of myocardial infarct size. Several studies suggest that the early administration of beta-blockers or intravenous nitroglycerin may benefit patients with acute infarction. We must seriously consider whether the data supporting the use of these agents justify a recommendation that they be used routinely for patients with acute infarction. The role of thrombolytic agents, although widely used already, must also be addressed as data supporting its use build. Additionally, there are suggestive data that the aggressive treatment of hypertension is beneficial, and this approach may well merit advocacy. The prophylactic use of lidocaine and the ubiquitous use of nitrates necessitate reevaluation, although presently both agents are widely used. The aggressive use of electrical therapy for supraventricular arrhythmias and the lack of indication for the treatment of asymptomatic bradycardia with atropine in patients with acute infarction must be added to the previous National Conference standards.

Hemodynamic effects of intravenous administration of amrinone include increases in dP/dt, cardiac output, and stroke work with decreases in left ventricular filling pressure and systemic vascular resistance. Unlike other injectable positive inotropic agents, it does not increase myocardial oxygen consumption, a distinct advantage in patients with coexisting ischemic disease. Amrinone does not have deleterious effects on atrioventricular conduction and appears to have little arrhythmogenic potential. Side effects of intravenous administration are generally minor but include a reversible thrombocytopenia. Additional studies conducted in short-term low-output states are needed to define more completely its role in the treatment of this condition.

The positive inotropic/vasodilator agent MDL 17,043 was evaluated to determine its usefulness for both short-term support of the failing circulation and long-term treatment of patients with congestive heart failure. Both intravenous and oral administration of MDL 17,043 significantly increased cardiac output, stroke volume, stroke work index, and heart rate, and significantly decreased pulmonary arterial wedge, right atrial, and mean arterial pressures as well as systemic and pulmonary arteriolar resistance. Such hemodynamic responsiveness persisted in patients on long-term oral therapy with MDL 17,043. When compared with dobutamine, the peak hemodynamic effects of MDL 17,043 were similar except for somewhat greater increases in heart rate with dobutamine and somewhat greater decreases in mean pulmonary arterial and wedge pressures with MDL 17,043. Both intravenous and oral MDL 17,043 elevated plasma renin activity. Oral doses were rapidly absorbed, and the drug had an elimination half-life of about 20 hr. Although the majority of patients showed clinical improvement at 1 month, this effect tended to wane over time leading to either recurrent heart failure or death. Mortality rates at 1 year are about 46% in class III patients and 97% in class IV patients on long-term oral MDL 17,043. The results of these studies suggest that MDL 17,043 may be useful in the short-term management of the failing circulation; however, its value in the long-term management of patients with chronic heart failure remains unclear and requires further studies for resolution.