During the past decade our understanding of the complex interaction between cardiac muscle and coronary vascular growth has increased substantially. Some types of cardiac hypertrophy, for example, left ventricular hypertrophy secondary to hyperthyroidism, are associated with increased coronary vascular growth. However, in most animal preparations of hypertrophy and in several clinical types of hypertrophy of the left and/or right ventricles, pathologic cardiac enlargement impairs the ability of the coronary circulation to allow normal increases and perfusion in response to intense dilator stimuli. In general, clinical studies have demonstrated far more profound abnormalities than studies in experimental animals. These observations provide a plausible explanation of why patients with hypertrophied ventricles often exhibit signs and symptoms of myocardial ischemia in the absence of coronary obstructive disease. The recent observation that experimentally produced left ventricular hypertrophy secondary to renal hypertension augments infarct size and the incidence of sudden lethal arrhythmias has additional implications relevant to the interaction between cardiac hypertrophy and myocardial perfusion. Although coronary reserve is impaired in many types of pathologic hypertrophy, the anatomic or biochemical basis for these observations remains elusive.

A short and up-to-date review on the great advances made in the field of the atrial natriuretic factor (ANF) is presented. All the short active peptides (up to 33 AA) isolated after purification of atrial homogenates have the same core of 23 amino acids (Ser 103-ARG 125). The ANF liberated in the medium of cultures of rat atrial cardiocytes is the 26 amino acid Arg 101-Tyr 126. Cloning of the cDNA encoding for ANF and of the rat, mouse, and human ANF gene has been accomplished. ANF has a most potent and short-lasting diuretic and natriuretic effect that appears to be predominantly due to a significant increase in glomerular filtration rate. ANF inhibits the release of aldosterone both in vitro and in vivo. It produces a profound inhibition of vascular contraction induced by norepinephrine and angiotensin II. This vasorelaxation is followed by a prolonged refractory period. ANF administration corrects the hypertension in 2K-1C hypertensive rats and in spontaneously hypertensive rats. Specific high-density binding sites have been found in the brain, especially in the hypothalamus, subfornical organ, median eminence, area postrema, and nucleus tractus solitarius, all areas involved in the brain control of hypertension and in the regulation of salt and water. ANF has no effect on the known sodium transport mechanisms across cell membrane. It has a major effect on the stimulation of guanylate cyclase activity, especially in renal glomeruli. Specific radioimmunoassay procedures have been established and results of preliminary studies that establish clearly that ANF is a circulating hormone are presented.

The finding that blood flow during external chest compression may be due to increased intrathoracic pressure, and the subsequent reporting of increased carotid blood flow with simultaneous ventilation and chest compression or with abdominal binding during CPR ignited a flurry of investigations into alternative approaches to CPR. A number of alterations of the conventional CPR technique were proposed, many resulting in improved hemodynamics when compared with standard CPR techniques in the same subject. However, some of the proposed methods increased cerebral blood flow but decreased myocardial perfusion. Others improved systolic pressures but decreased vital organ blood flow. More importantly, most studies with survival as an end point failed to show a benefit when alternative approaches to CPR were used. Therefore, it is unlikely that there will be significant changes in the recommendations for the use of adjuncts during CPR. Not all studies support the conclusion that blood flow during closed-chest compression is secondary to increased intrathoracic pressure. It is probable that in man there is a spectrum. In some individuals the predominant mechanism of blood flow during CPR may be cardiac and/or vascular compression, and in others flow may be secondary to an increased intrathoracic pressure.

Calcium channel-blocking drugs have potent antiarrhythmic and antianginal effects and in addition may reduce the extent of cellular injury after anoxia/ischemia. Verapamil is the treatment of choice (90% effective) for uncomplicated episodes of paroxysmal supraventricular tachycardia. All three calcium-channel blockers available, diltiazem, nifedipine, and verapamil, can reduce the frequency of angina occurring both at rest and with exertion. Calcium may mediate several cytotoxic events during the reperfusion period after prolonged ischemia that lead to irreversible cell injury. There is experimental evidence that calcium-channel blockers may reduce the cellular influx of calcium after ischemia and reperfusion, and thereby attenuate cerebral and myocardial injury, although most studies have failed to show benefit of treatment unless the drug is administered before the onset of ischemia. Most trials using calcium-channel blockers in the setting of acute myocardial infarction have failed to show a benefit of treatment. The safety and efficacy of calcium-channel blockers have yet to be shown in controlled studies of human resuscitation, although the potential for such treatment, if it is effective in attenuating myocardial cerebral cellular injury, could be enormous.

Calcium chloride has been advocated since the 1920s for the resuscitation of asystole, electromechanical dissociation (EMD), and ventricular fibrillation. Reports of side effects and complications have been numerous. Studies of calcium assays following American Heart Association recommended dosages have shown dangerously elevated serum levels. Large retrospective clinical studies in Milwaukee and Tampa have found no evidence of improved survival with calcium chloride in asystole and EMD. A prospective randomized double-blind study comparing calcium chloride and saline controls in the Milwaukee Paramedic system for asystole and EMD using standard AHA protocols showed no statistically significant difference in resuscitation rates or long-term survival between the calcium and no-calcium groups for the rhythm of asystole. Although patients with EMD had statistically improved resuscitation rates when calcium chloride was given, only one of the patients survived to hospital discharge. Because of the low rates of resuscitation and long-term survival in patients presenting in asystole and EMD, proving that calcium chloride does not enhance survival would require large multicenter trials. However, since no controlled study has ever documented significant benefit, its routine use in asystole and EMD cannot be supported. Calcium has long been used in medical treatment of hypocalcemic and hyperkalemic states and should be administered in moribund patients who have the proper clinical history and clinical signs of hypocalcemia.

More than 30 million Americans are disabled. Wide experience has shown that these conditions do not prevent these individuals from becoming proficient in the knowledge and skills of CPR. Instructional materials and methods can be modified to help this special population learn CPR despite handicaps. The American Heart Association has supported these special efforts since 1978, but no comprehensive resource exists for CPR instructors interested in helping the "physically challenged" individual learn CPR. This article addresses general and specific suggestions for teaching selected handicapped populations. They are: hearing impaired, visually impaired, other physical impairment such as obesity, chronic obstructive pulmonary disease, arthritis, angina, and other medical conditions that may limit one's ability to learn the psychomotor skill of CPR.

The addition of interposed abdominal compressions (IACs) to otherwise standard CPR enhances artificial circulation both in anesthetized dogs with ventricular fibrillation and in electrical models of the circulation that demonstrate fundamental mechanisms generating flow. Manual abdominal compressions cause both central aortic and central venous pressure pulses but, because of differences in venous and arterial capacitance, the former are usually greater than the latter. Thus mean perfusion pressure is enhanced. Limited clinical studies confirm that IAC-CPR can improve perfusion pressures in humans, and reported complications of the technique are rare in animals and man. However, no study has demonstrated that IAC-CPR improves either short- or long-term survival after cardiac arrest in man. Accordingly, the method remains experimental and cannot be recommended for basic life support at the present time.

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.