Introduction: Although the hemodynamic superiority of open chest cardiopulmonary resuscitation has long been recognized, its advantages with respect to the brain have only recently been investigated. Yashon demonstrated the ability of open chest CPR to maintain EEG activity during prolonged resuscitation. Alifimoff showed improved cerebral reco-very in dogs after open chest CPR. Byrne has demonstrated that internal cardiac massage can provide nearly normal cerebral blood flow in dogs as opposed to the 30% of normal seen during standard CPR, which consists of 60 chest compressions per min with a ventilation interposed after every fifth compression and 50% compression duration.

Introduction: Standard closed-chest CPR (SCPR) produces only 6–30% of normal blood flow. It is unlikely that this can sustain the viability of the brain for more than a few minutes in most CPR attempts, although in occasional cases of human resuscitation external CPR for up to two hours has been followed by recovery of consciousness. Thus various methods have been employed to improve this low perfusion state. It has been shown that abdominal compression by hand or MAST-suit can augment carotid artery blood flow during CPR but causes complications. Openchest CPR (OCCPR) has also been proven to be hemodynamically superior to SCPR. Since neurologic recovery has been studied after prolonged periods of total circulatory arrest but not after prolonged periods of CPR, we compared the prolonged use of SCPR and OCCPR in terms of ability to sustain signs of cerebral function during CPR and permit cerebral recovery after CPR.

From many recent publications and also from a pathophysiologic standpoint, it has become abundantly clear that probably the most important factor determining the outcome of any attempt at resuscitation is the period of time elapsed between the onset of the calamity and the initiation of “CPR.” In most of the reports on the effects of time-related variables the initiation of effective cardiopulmonary resuscitation is usually not clearly defined.

What exactly is meant by “initiation of CPR?” Since 1966 CPR has been instructed according to the “A-B-C-schedule.”

The CPR committee of the Dutch Heart Association currently recommends for the management of sudden cardiac arrest, the initiation of external cardiac compressions before airway control and ventilation, which may be termed the “CAB” sequence. This differs from the ABC sequence, recommended by the American Heart Association, in which the patient is ventilated first. Supporters of the CAB sequence reason that, since most sudden cardiac deaths are due to ventricular fibrillation, the blood in the arterial system should be well oxygenated at the onset of such an episode. We conducted these studies to characterize the decline in arterial blood gases during 5 min of cardiac arrest, followed by external cardiac compressions alone, vs followed by external cardiac compressions with ventilation. In addition, we studied the decline in arterial blood gases and ventricular fibrillation without therapy.

We could obtain good results similar to other groups with a device for cardiac compression and automatic ventilation during CPR. The following paper will not discuss the experience with such a device, but the further development and improvement of a device already used and found to be useful.

The further development seemed to be necessary since we tried to utilize new hemodynamic results important for external cardiac compression and ventilation. Other reasons were problems occurring with its practical use.

The automatic implantable defibrillator is an electronic device designed to continuously monitor cardiac rhythm, identify ventricular fibrillation and deliver corrective defibrillatory discharges, when indicated. Physically similar to early pacemakers, it weights 250 grams and has a volume of 145 cc (Figure 1). All materials in contact with body tissue are biocompatible. The defibrillating electrodes are made from titanium and silicone rubber. One electrode, designed for placement in the superior vena cava near the right atrial junction, is located on the distal end of an intravascular catheter. The second electrode, in the form of a flexible rectangular patch, is placed extrapericardially over the apex of the heart. The outside surface of the apical electrode is insulated to achieve optimal current distribution.

The device is powered by lithium batteries having a projected monitoring life of approximately 3 years or a discharge capability of approximately 100 shocks. The sensing system detects ventricular fibrillation by monitoring a sampled probability density function of ventricular electrical activity.

The effect of positive inotropic agents on circulation and ventricular fibrillation threshold are not fully understood during the influence of metabolic acidosis during circulatory arrest. This is the same case with alkalosis, caused by the over-correction of sodium bicarbonate. Furthermore, the role of calcium during CPR is not clear.

Therefore, we investigated the influence of metabolic acidosis and alkalosis with and without the administration of the positive inotropic substances epinephrine and calcium upon contractility and ventricular fibrillation threshold.

Monitoring of the level of neurological response is an essential component of the diagnostic and therapeutic process in the management of craniocervical injury and neurological catastrophes. When Hippocrates reminded us that “No Head Injury is so mild that it can be neglected,” he cannot have been aware of the significance of the lethal factors of cerebral swelling and intracranial hematoma contributing to poor survival. Neither can he have known how these factors could be detected. Coma scales have evolved to indicate when deterioration is likely and intervention indicated.

Many hospitals use simple grades of responsiveness for their unconscious patients, but the widespread habit of recording the level of response in an abstract manner is as meaningless as measuring temperature in units of feverishness. There is a requirement for a device which can be expressed in numerical terms and, when necessary, related to an analogue or graphical mode.

Ischemic and traumatic brain insults may be followed by pulmonary failure, which is a frequent cause of death in cases of multi-trauma, cardiac arrest and stroke. Pulmonary edema (PE) can occur secondary to events in the central venous nervous system (CNS). This is generally termed neurogenic pulmonary edema (NPE). It is not known which of the following 4 factors of the modified Starling equation of pulmonary edema development are involved in the development of NPE: a) filtration coefficient, that is, increased membrane permeability; b) abnormal hydrostatic pressure gradient; c) abnormal oncotic pressure gradient; and d) blockage or overwhelming of lymphatic drainage (Fig. 1).

Resuscitation of the brain after ischemic-anoxic brain injury remains a controversial topic. There is, however, presently a certain therapeutic optimism in this field. Ours is partly based on the recognition of a post-resuscitation disease, that is, treatable pathologic processes in all organs after restoration of adequate perfusion pressure and arterial oxygenation. Also, Hossmann has shown that neurons can survive longer periods of anoxia than previously assumed.

There have been reports on experimental focal ischemia indicating beneficial effects of barbiturates and moderate hemodilution before and after initiation of focal ischemia. After complete temporary global brain ischemia (GBI), as in cardiac arrest, however, results so far have been conflicting and controversial.

Retrospective studies of the mechanisms of drowning are difficult to make for a number of reasons. First, the severity of the immersion incident is hard to classify; therefore, conclusions drawn from the outcome of a number of incidents grouped together may be erroneous. Second, confusion results from traditional attempts to separate victims into those who immerse in salt water from those who immerse in fresh. This is an analysis of 61 individual cases of immersion published in the last 20 years, but not previously subjected to group analysis such as those published by Modell, Conn and Simcock.

Results

In 61 cases reviewed, males outnumbered females by almost 4 to 1 (48/13), 17 died and 44 survived (Table 1). When placed in age groups, those most at risk fell into the 0–5 years old group, comprising 43% of the total; but this group also contained the greatest proportion of survivors (Figure 1).

There have been 81 patients brought to Treliske Hospital, Truro, UK in the last 6 years, having been rescued from near-drowning. Only 5 have been declared dead on arrival and not treated. We consider that hypothermia is a major factor in patients who have apparently drowned, particularly when it has been known that they were strong swimmers. In 1980, 45% of all drownings had rectal temperatures less than 35°C. The sea temperature around our shores varies between 5°C in January and 15.5°C in September. Hypothermia causes little problem until a central temperature of 35°C or less is reached. Between 35°C and approximately 32°C there is disorientation and incoordination, which may make swimming difficult to maintain efficiently. Below 32°C there is loss of consciousness; when this occurs, the victim's head drops below the water level and drowning occurs just as quickly as in a victim who is unconscious on entering the water.

Recent case reports have shown that persistent hypoxia after the resuscitation of nearly-drowned patients is a major problem. PEEP ventilation could be successfully applied in such a condition. After PEEP valves for manually operated resuscitators became available, the question arose of how beneficial the immediate application of positive end expiratory pressure of 5 cm H2O would be for lungs damaged by either seawater or fresh water. This question was examined by means of standardized animal experiments.

Material and Methods

In four test groups comprising 34 randomly selected young pigs, either 25 ml fresh water/kg body weight, or else 12.5 ml salt water/kg body weight, were instilled by way of an endotracheal tube. This was followed by a period of apnea lasting 4 min and subsequent ventilation with 100% oxygen for a 2 hour period. The 32 animals which survived the first part of the experiment were then subjected to either PEEP or ZEEP ventilation therapy without further medication.

Each year 4,000–9,000 people die in the USA from hyperthermia-related crises, such as heat stroke and febrile convulsions. In most of these cases, variable combinations of hot environment, physical exercise, dehydration, and infection can be identified. Heat stroke is a complex clinical picture with poorly understood pathophysiology and unexplored resuscitation potentials. Protection of vital organs against hyperthermia is also important for cancer therapy.

This study (1978–1980) was aimed exclusively at the effects of controlled hyperthermia. In pilot experiments on lightly anesthetized dogs and rhesus monkeys, brain temperature was raised to 42°C for 1/2–1 hour by immersion heating. This was followed by cooling to normothermia. Partial recovery with a lucid period of 1 hour or longer was followed by diffuse gastrointestinal bleeding and irreversible shock in spite of standard life support measures.

Accidental or intentional carbon monoxide poisoning is common throughout the year. In the Midwest, however, accidental exposures are more common during the winter months when the furnaces are overworked or malfunction. Consequently, enmasse exposures to the poisonous gas are frequently encountered during this season. Adding to the problem are the energy conservation efforts. Doors, windows and other ventilation avenues are tightly sealed, and solid fuel might be substituted to save other expensive conventional fuels. Other causes of carbon monoxide poisoning are blocked exhaust systems, automobiles with inadequate mufflers, fires and solvent (methylene chloride, etc.) usage in poorly ventilated areas, e.g., basements. The exact incidence of nonfatal subacute carbon monoxide poisoning is not available. National Clearinghouse Bulletin reported that in 1978, out of 376 reported exposures, there were eight fatalities. A figure which has been frequently quoted in the literature is that each year in the United States, approximately 3,500 deaths are caused by carbon monoxide poisoning.

The Maryland Institute for Emergency Medical Services Systems (MIEMSS) is the smoke and carbon monoxide (CO) inhalation referral center for Maryland, particularly Baltimore City and the five surrounding counties. The majority of our patients are from the Baltimore/Washington corridor.

The use of a short screening battery of psychometric tests is an important method for improving the clinical approach to the diagnosis of CO poisoning. Our own experience and a literature survey have shown how poorly the CO level correlates with clinical signs and symptoms. We have reported on six patients who were unconscious from CO poisoning but had a carboxyhemoglobin (HbCO) level of under 1%, and we have seen apparently well oriented patients with HbCO levels of 45%. From these experiences, we have concluded that the HbCO level is only an indicator of exposure to CO, not necessarily of the severity of poisoning. These large discrepancies have necessitated the development of a supplemental test, such as the psychometric battery, to determine generalized cerebral dysfunction.

Extensive experiments in animals and humans, as well as clinical experience in disaster areas, have shown that expensive devices and complicated inhalation narcotics are not suited for anesthesia under disaster conditions. Today, the most important drugs are intravenous and, in emergencies, also intramuscular preparations which do not cause any significant central respiratory depression:

1. Ketamine, suited for routine anesthesia under disaster conditions; and

2. Gamma-Hydroxy-Butyric-Acid (Somsanit), suited for poor risk patients with hypoxic injuries and/or shock.

The setting up of anesthesia units and any future planning in this field has to be considered in the context of the social and economic development of the country. The situation requires a different attitude towards the handling of anesthesia, where malnutrition, kwashiorkor and parasites are the dominant diseases. One sixth of the world's population is permanently undernourished, and the figure might even be higher in many “developing countries.” Problems of an esthesia in most areas in Africa include: (1) insufficient supply of drugs; (2) inadequate equipment; (3) lack of anesthetic manpower; and (4) underestimation of the importance of anesthesia.

In a considerable number of cases, many polytraumatized patients in a state of hemorrhagic shock, who require immediate surgical treatment, there is craniocerebral trauma. Ketamine is viewed, on one hand, as an appropriate induction anesthetic, due to its circulatory stimulating effect in treating shock victims, and, on the other hand, it is rejected for treating patients with craniocerebral injuries, because of the danger of possible increase in intracranial pressure (ICP). Therefore, we examined the effects of ketamine on ICP and calculated the cerebral perfusion pressure, using test animals in a state of hemorrhagic shock and a space occupying intracranial process.

Diazepam is a commonly used drug for suicidal attempts. The antagonistic effect of physostigmine in these patients is poorly understood.

We studied the interaction of large doses of diazepam and either physostigmine or galanthamine hydrobromide using dose-response curves in 21 cats. After establishing dose-response curves for diazepam, half of the animals received 0.02 mg/kg of physostigmine intravenously. Two minutes later 8, 10, 12, or 14 mg/kg of diazepam was administered intravenously. After 2, 5, and 10 min, animals were evaluated for their response to noise and pain stimuli. The other half of animals were given 0.2 mg/kg of galanthamine intravenously and evaluated for diazepam effect using the same criteria. Sufficient number of days were allowed for the animals to recover from diazepam.