Benign tumors of the pediatric spine: statistical notes

Consensus exists that a do-not-attempt-resuscitation order (DNAR) is appropriate if a resuscitation attempt is futile. Less agreement exists when this point is reached. We investigated the influence of three major considerations for in-hospital DNAR orders: expected survival probability after resuscitation, prospects of the patients' current condition without a cardiac arrest and the patients' autonomous decision not to want resuscitation. We calculated an expected survival probability according to two multi-morbidity prediction scores for each patient, assuming the event of cardiac arrest. The prospects of the current condition without a cardiac arrest was estimated by the patients' physician, in terms of life expectancy and quality of life (level of dependency after discharge and pain). The patients' preference was documented from the medical records. A total of 470 patients were included in the study. Fifty-eight patients (12%) had a DNAR-order, 11 of these patients (19%) wanted no resuscitation. The patients' prospects (life expectancy, dependency after discharge), and age proved to be independently associated with the presence of a DNAR order. The odds ratio (OR) for the presence of a DNAR order was 37 (CL 14-107) for an estimated life expectancy less than 3 months, 13 (CL 4-41) for a life in a nursing home and four (CL 2-12) for an age of 80 years and older. Expected survival probability after resuscitation and pain were not independently associated with a DNAR order. We conclude that resuscitation is considered futile on the basis of the patients' age and prospects without cardiac arrest and that the impact of expected survival probability on these decisions is small.     

Chronic treatments with 5-HT1A agonists attenuate posthypoxic myoclonus in rats

Following 10 min cardiac arrest and resuscitation, male Sprague-Dawley rats developed posthypoxic myoclonus. This phenomenon peaked at 14 days and disappeared by 60 days after cardiac arrest. From previous results, the 5-hydroxytryptamine (5-HT) system was implicated in the pathogenesis of the disease. In the present study, we investigated the involvement of 5-HT1A receptors in posthypoxic myoclonus in rats. Single injections of 5-HT1A agonists, buspirone (5 and 10 mg/kg body wt.) or 8-OH-DPAT (1, 2, and 4 mg/kg), had no effect on either the intensity or time course of the disease. In contrast, multiple injections (twice a day for 7 or more days) of buspirone (10 mg/kg) or 8-OH-DPAT (4 mg/kg) significantly attenuated the myoclonus scores of animals (p < 0.05). The results indicate that chronic stimulation of 5-HT1A receptors in the brain may accelerate endogenous compensatory mechanisms and shorten the time course of the disease.     

Diagnosis of death in comatose patients under resuscitation treatment: a critical review of the Harvard report

In this Article, which draws primarily on continental West European views on death and dying, the author contends that the Harvard criteria for irreversible coma (1968) are not reliable for diagnosing death in comatose patients under resuscitation treatment. The Article suggests that use of the Harvard Criteria to diagnose death leaves such patients legally unprotected against surgical assaults such as organ removal and biomedical experiments while they still may be living and capable of perception, possibly including the perception of pain and the spoken word. An alternative to the Harvard Criteria--angiography--is offered, and several additional issues related to the definition and diagnosis of death are discussed. Finally, the author suggests that even prior to death, termination of resuscitation treatment of irreversibly comatose patients, though followed by death, should be lawful.     

Serum neuron-specific enolase as early predictor of outcome after cardiac arrest

OBJECTIVE: To examine the prognostic value of serum neuron-specific enolase for early prediction of outcome in patients at risk for anoxic encephalopathy after cardiac arrest. DESIGN: Prospective study. SETTING: Coronary intensive care unit of the University of Heidelberg. PATIENTS: Forty-three patients (66.8 +/- 12.7 [SD] yrs, range 33 to 85) who had had either primary or secondary cardiac arrest, followed by cardiopulmonary resuscitation (CPR). INTERVENTIONS: Serial blood samples and clinical examinations. MEASUREMENTS AND MAIN RESULTS: Serum neuron-specific enolase concentrations were determined after CPR on 7 consecutive days. Twenty-five patients remained comatose and subsequently died; 18 patients survived the first 3 months and had no relevant functional deficit at 3-month follow-up. Neuron-specific enolase concentrations were correlated with neurologic outcome. Concentrations of >33 ng/mL predicted persistent coma with a high specificity (100%) and a positive predictive value of 100%. Overall sensitivity was 80%, with a negative predictive value of 78%. Serum concentrations of neuron-specific enolase exceeded this cutoff value no more than 3 days after cardiac arrest in 95% of patients in whom these concentrations had exceeded 33 ng/mL. CONCLUSIONS: In patients who have been resuscitated after cardiac arrest, serum neuron-specific enolase concentrations of >33 ng/mL predict persistent coma with a high specificity. Values below this cutoff level do not necessarily indicate complete recovery, because this method has a sensitivity of 80%.     

Cumulative epinephrine dose during cardiopulmonary resuscitation and neurologic outcome

BACKGROUND: Epinephrine is the drug of choice in advanced cardiac life support, but it can have deleterious side effects after restoration of spontaneous circulation. OBJECTIVE: To investigate the association between the cumulative epinephrine dose used in advanced cardiac life support and neurologic outcome after cardiac arrest. DESIGN: Retrospective cohort study. SETTING: University hospital. PATIENTS: Adults admitted to the emergency department with witnessed, nontraumatic, normothermic ventricular fibrillation cardiac arrest and unsuccessful initial defibrillation. MEASUREMENTS: Functional neurologic outcome was regularly assessed by cerebral performance category (CPC) within 6 months after cardiac arrest. A CPC of 1 or 2 was defined as favorable recovery. RESULTS: Among 178 enrolled patients, the median cumulative epinephrine dose administered was 4 mg (range, 0 to 50 mg). In 151 patients (84%), spontaneous circulation was restored; 63 of these 151 patients (42%) had favorable neurologic recovery. Patients with an unfavorable CPC received a significantly higher cumulative dose of epinephrine than did patients with a favorable CPC (4 mg compared with 1 mg; P < 0.001). This finding persisted after stratification by duration of resuscitation. After possible cofounders were controlled for, the cumulative epinephrine dose remained an independent predictor of unfavorable neurologic outcome. CONCLUSIONS: The results indicate that an increasing cumulative dose of epinephrine administered during resuscitation is independently associated with unfavorable neurologic outcome after ventricular fibrillation cardiac arrest.     

Cardiopulmonary cerebral resuscitation and acidosis

It is still controversial whether sodium bicarbonate is effective for the correction of acidemia during cardiopulmonary resuscitation (CPR). To resolve this issue, we must clarify the influence of acidosis accompanied by cardiac arrest on the cardiac and cerebral resuscitability. The influence of acidosis on cardiac resuscitability The factors which determine the cardiac resuscitability during asystole or ventricular fibrillation are the presser response to administered catecholamines and the threshold of defibrillation. However, there is still no evidence that acidosis inhibits these factors during CPR. Recent reports suggested that CO2 itself impaired cardiac resuscitability rather than acidosis. On the other hand, our study using isolated perfused rat hearts proposed that the effect of acidosis is not still eliminated. The influence of acidosis on the cerebral resuscitability There are two contrary opinions. One is that acidosis deteriorates the cerebral damage after resuscitation. The other is that acidosis is rather protective against the cerebral damage. In the studies which support the latter opinion, the evaluation of the effect of reperfusion is lacking. Accordingly, any factors which develop during the reperfusion phase may be enhanced by acidosis. These findings indicate that the influence of acidosis accompanied by cardiac arrest is complicated and that it includes many unresolved questions. Until we clarify these questions, we can not conclude that the correction of acidemia is necessary during CPR.     

Current concepts in cardiopulmonary resuscitation

The "chain of survival" is important in the resuscitation of a patient who has had a cardiac arrest. The provision of Basic Life Support (BLS) and Advanced Cardiac Life Support (ACLS) is essential in this "chain of survival." Both BLS and ACLS have undergone several revisions since their initial inception. This article reviews (1) the current established and investigational issues of cardiopulmonary resuscitation, (2) the incidence and outcomes of anesthesia-related cardiac arrest, (3) the use of cardiopulmonary bypass in resuscitation, and (4) cerebral protection during and after resuscitation.     

Concentration dependence of sodium permeation and sodium ion interactions in the cyclic AMP-gated channels of mammalian olfactory receptor neurons

We explored the hypothesis that brain damage after cardiac arrest caused by ventricular fibrillation (VF) needs different therapies than that after asphyxiation, which has been studied less thoroughly. In 67 healthy mongrel dogs of both sexes cardiac arrest (at normothermia) by ventricular fibrillation (no blood flow lasting 10 min) or asphyxiation (no blood flow lasting 7 min) was reversed by normothermic external cardiopulmonary resuscitation, followed by intermittent positive-pressure ventilation for 20 h, and intensive care to 96 h. To ameliorate ischemic brain damage, the calcium entry blocker lidoflazine or a solution of free radical scavengers (mannitol and L-methionine in dextran 40) plus magnesium sulphate, was given intravenously immediately upon restoration of spontaneous circulation. Outcome was evaluated as functional deficit, brain creatine kinase (CK) leakage into the cerebrospinal fluid (CSF) and brain morphologic changes. Lidoflazine seemed to improve cerebral outcome after VF but not after asphyxiation. Free radical scavengers plus magnesium sulphate seemed to improve cerebral outcome after asphyxiation, but not after VF. After VF, scattered ischemic neuronal changes in multiple brain regions dominated, and total brain histopathologic damage scores correlated with final neurologic deficit scores at 96 h (r = 0.66) and with peak CK levels in CSF (r = 0.81). After asphyxiation, in addition to the same ischemic neuronal changes, microinfarcts occurred, and there was no correlation between total brain histopathologic damage scores and neurologic deficit scores or CK levels in CSF. CONCLUSIONS: Different mechanisms of cardiac arrest, which cause different morphologic patterns of brain damage, may need different cerebral resuscitation treatments.     

Do advanced cardiac life support drugs increase resuscitation rates from in-hospital cardiac arrest? The OTAC Study Group

STUDY OBJECTIVE: The benefit of Advanced Cardiac Life Support (ACLS) medications during cardiac resuscitation is uncertain. The objective of this study was to determine whether the use of these medications increased resuscitation from in-hospital cardiac arrest. METHODS: A prospective cohort of patients undergoing cardiac arrest in 1 of 5 academic hospitals was studied. Patient and arrest factors related to resuscitation outcome were recorded. We determined the association of the administration of ACLS drugs (epinephrine, atropine, bicarbonate, calcium, lidocaine, and bretylium) with survival at 1 hour after resuscitation. RESULTS: Seven hundred seventy-three patients underwent cardiac resuscitation, with 269 (34. 8%) surviving for 1 hour. Use of epinephrine, atropine, bicarbonate, calcium, and lidocaine was associated with a decreased chance of successful resuscitation (P <.001 for all except lidocaine, P <.01). While controlling for significant patient factors (age, gender, and previous cardiac or respiratory disease) and arrest factors (initial cardiac rhythm, and cause of arrest), multivariate logistic regression demonstrated a significant association between unsuccessful resuscitation and the use of epinephrine (odds ratio . 08 [95% confidence interval .04-.14]), atropine (.24 [.17-.35]), bicarbonate (.31 [.21-.44]), calcium (.32 [.18-.55]), and lidocaine (.48 [.33-.71]). Drug effects did not improve when patients were grouped by their initial cardiac rhythm. Cox proportional hazards models that controlled for significant confounders demonstrated that survivors were significantly less likely to receive epinephrine (P <. 001) or atropine (P <.001) throughout the arrest. CONCLUSION: We found no association between standard ACLS medications and improved resuscitation from in-hospital cardiac arrest. Randomized clinical trials are needed to determine whether other therapies can improve resuscitation from cardiac arrest when compared with the presently used ACLS drugs.     

Properties of recombinant bacteriophage T4 tail sheath protein and its deletion fragments

We aimed to determine whether our results were any better or worse than other published reports and to examine the efficacy of the West Midlands Ambulance Service (WMAS) policy of applying cardiopulmonary resuscitation (CPR) and manual ventilation to all unwitnessed cardiac arrests in preference to immediate defibrillation. All cardiac arrests were studied from October 1994 to September 1996. In all unwitnessed arrests, crews undertook CPR and manually ventilated the lungs via a mask or an endotracheal tube with a bag and valve or a mechanical resuscitator using an FIO2 of 1 or 0.21 for at least 2 min before defibrillation was attempted. There were 3403 diagnosed cardiac arrests but, in these, the diagnosis was not certain. CPR and advanced life support (ALS) were applied in 3380 patients and return of spontaneous circulation (ROSC) was obtained in 554, giving a success rate of 16.4%. A total of 364 patients were accepted into hospital, 90 patients died in A&E but 274 patients were admitted to ICU/CCU. Seventy died within 24 h, 69 died after 24 h and 135 were discharged alive and well without cerebral damage. The final success to discharge rate was 49.27%. Of those discharged, 69 had a circulatory arrest period of more than 4 min but in only 10 was a bystander available to start CPR. The European Resuscitation Council Guidelines recommending immediate defibrillation for unwitnessed arrests are not supported by these results. The apparent lack of cerebral damage and the percentage success suggests that resuscitation considerations should be as brain orientated as they are heart orientated. The elapsed time periods reported challenge several shibboleths.     

Hypertonic saline dextran prime reduces increased intracranial pressure during cardiopulmonary bypass in pigs

Children and adults who develop neurologic deficits after cardiac surgery may experience cerebral ischemia during cardiopulmonary bypass. Increased intracranial pressure (ICP) may contribute to cerebral ischemia during bypass. Hypertonic saline dextran (HSD), a hyperosmotic, hyperoncotic resuscitation solution, decreases ICP in trauma resuscitation. We hypothesized that HSD would decrease ICP, reduce brain water, and reduce intravascular fluid requirements during bypass. Twelve swine were divided into two bypass groups: Group 1 (ISO = isotonic) received as prime 1 L of lactated Ringer's solution and 500 mL of 6% hydroxyethyl starch. Group 2 (HSD = hypertonic saline/dextran) received as prime 1 L of lactated Ringer's solution, 500 mL of 6% hydroxyethyl starch, and 1 mL/kg of 24% hypertonic saline/25% dextran. Normothermic bypass was instituted at 100 mL.kg-1.min-1. ICP increased significantly during bypass with ISO prime but not with HSD. Brain water in the cerebrum did not differ between groups but was reduced in the cerebellum to 75.9% +/- 1.4%. We conclude that HSD prevented any significant increase in ICP during normothermic bypass, and substantially improved fluid balance during bypass. In cardiac surgery patients in whom maintaining decreased ICP and reducing isotonic fluid administration is important, HSD may be a useful addition to the bypass prime solution.     

Optimizing resuscitation outcomes with pharmacologic therapy

Pharmacologic therapy plays a key role in the emergency resuscitation of patients with cardiac arrest. The Advanced Cardiac Life Support guidelines sanctioned by the American Heart Association provide flexible treatment protocols (algorithms) that serve as a valuable tool for clinicians. Vasoactive (vasopressive) therapy with epinephrine is of primary importance in all patients with nonperfusing rhythms (for example, ventricular fibrillation [VF], pulseless ventricular tachycardia [VT], electromechanical dissociation [EMD], and asystole) because it raises myocardial and cerebral perfusion pressures, thereby increasing the likelihood of successful resuscitation. Antiarrhythmic drugs play a secondary role to electrocardioversion in the treatment of VF and pulseless VT. Despite continued investigation and recent advances in our understanding of the role of drugs and other therapeutic interventions, the short-term and long-term prognoses of patients with cardiac arrest, especially out-of-hospital arrest, remain dismal. Clearly, much study into the prevention and treatment of sudden cardiac death is desperately needed.     

Normoxic ventilation after cardiac arrest reduces oxidation of brain lipids and improves neurological outcome

BACKGROUND AND PURPOSE: Increasing evidence that oxidative stress contributes to delayed neuronal death after global cerebral ischemia has led to reconsideration of the prolonged use of 100% ventilatory O2 following resuscitation from cardiac arrest. This study determined the temporal course of oxidation of brain fatty acyl groups in a clinically relevant canine model of cardiac arrest and resuscitation and tested the hypothesis that postischemic ventilation with 21% inspired O2, rather than 100% O2, results in reduced levels of oxidized brain lipids and decreased neurological impairment. METHODS: Neurological deficit scoring and high performance liquid chromatography measurement of fatty acyl lipid oxidation were used in an established canine model using 10 minutes of cardiac arrest followed by resuscitation with different ventilatory oxygenation protocols and restoration of spontaneous circulation for 30 minutes to 24 hours. RESULTS: Significant increases in frontal cortex lipid oxidation occurred after 10 minutes of cardiac arrest alone with no reperfusion and after reperfusion for 30 minutes, 2 hours, and 24 hours (relative total 235-nm absorbing peak areas=7.1+/-0.7 SE, 17.3+/-2.7, 14.2+/-3.2, 16.1+/-1.0, and 14.0+/-0.8, respectively; n=4, P<0.05). The predominant oxidized lipids were identified by gas chromatography/mass spectrometry as 13- and 9-hydroxyoctadecadienoic acids (13- and 9-HODE). Animals ventilated on 21% to 30% O2 versus 100% O2 for the first hour after resuscitation exhibited significantly lower levels of total and specific oxidized lipids in the frontal cortex (1.7+/-0.1 versus 3.12+/-0.78 microg 13-HODE/g wet wt cortex., n=4 to 6, P<0.05) and lower neurological deficit scores (45.1+/-3.6 versus 58.3+/-3.8, n=9, P<0.05). CONCLUSIONS: With a clinically relevant canine model of 10 minutes of cardiac arrest, resuscitation with 21% versus 100% inspired O2 resulted in lower levels of oxidized brain lipids and improved neurological outcome measured after 24 hours of reperfusion. This study casts further doubt on the appropriateness of present guidelines that recommend the indiscriminate use of 100% ventilatory O2 for undefined periods during and after resuscitation from cardiac arrest.     

AIDS dementia complex with generalized myoclonus

Focal and segmental, but not generalized, myoclonus have been described with human immunodeficiency virus (HIV) infection. We describe three patients with generalized myoclonus and acquired immunodeficiency syndrome (AIDS) dementia complex. In each, myoclonus persisted until death, invariably after a course of a few months. In two patients, myoclonus was elicited by sudden auditory stimuli and resembled a startle response. This form of myoclonus may be subcortical in origin. We suggest that the AIDS dementia complex be included among the causes of myoclonic dementia.     

Modulation of biochemical activity of hepatocytes in culture by matrix substratum

If critical care nurses and advanced practice nurses could identify patients with an increased risk of an unsuccessful outcome from cardiac arrest resuscitation in the hospital, such patients could be monitored with a heightened vigilance. This is the first nursing study to examine pre-existing variables and outcome of cardiac arrest resuscitation in hospitalized patients. The investigators found that heart rate and respiratory rate increased significantly 8 hours before the cardiac arrest in patients with an unsuccessful outcome of resuscitation.     

Assessment of acute myocardial necrosis after cardiopulmonary resuscitation and cardioversion by means of combined thallium-201/technetium-99m pyrophosphate tomography

Diagnosis of acute myocardial necrosis by means of conventional electrocardiographic criteria or the release of cardiac enzymes is often difficult or even impossible in patients with out-of-hospital cardiac arrest due to ventricular fibrillation with subsequent cardiopulmonary resuscitation including several DC countershocks. Simultaneous thallium-201/technetium-99m pyrophosphate (PYP) tomography was prospectively applied to 57 patients without typical clinical or electrocardiographic signs of acute myocardial infarction within 48 h after successful resuscitation from out-of-hospital cardiac arrest. Scintigraphic evidence of acute necrosis was present in 23/57 patients (40%). Increased 99mTc-PYP uptake in the pericardial tissue was found in 24 patients (42%). Maximal creatine kinase (CK) concentration was increased in 50/57 patients (88%). CK-MB activity averaged 68+/-52 U/l in patients with positive and 17+/-13 U/l in patients with negative tomograms (P<0.0005), demonstrating the validity of 201Tl/99mTc-PYP tomography. It may be concluded that simultaneous 201Tl/99mTc-PYP tomography is a valuable tool for evaluation of myocardial necrosis after cardiopulmonary resuscitation including DC countershock. Acute myocardial necrosis, as indicated by scintigraphy, represents a potential trigger for the occurrence of ventricular fibrillation. Therefore, 201Tl/99mTc-PYP tomography can be recommended in order to guide further diagnostic and therapeutic interventions in patients after cardiopulmonary resuscitation in whom the underlying cause of the occurrence of ventricular fibrillation is obscure.     

Arterial-venous carbon dioxide tension difference after hypothermic cardiopulmonary bypass

Arterial-venous carbon dioxide tension difference (Pv-aCO2) is known to become high after severe hemorrhage shock and resuscitation. We hypothesized that Pv-aCO2 might be high after cardiac surgery because of the oxygen debt occurred during hypothermic cardiopulmonary bypass (CPB). Blood pressure, cardiac index, hemoglobin, the arterial and mixed venous blood gases were repeatedly measured every 6 hours for 24 hours following cardiac surgery in 60 adult patients who underwent hypothermic CPB. Immediately after the surgery, Pv-aCO2 was extremely high, then gradually decreased to within normal ranges 12 hours later (8.0 +/- 2.9 mmHg vs 5.9 +/- 3.1 mmHg. p < 0.01). Factors which significantly correlated to Pv-aCO2 were cardiac index, oxygen delivery, minimum rectal temperature and duration of CPB. Oxygen debt during hypothermic CPB might cause significantly high Pv-aDO2. At least 12 hours were necessary to recover from anaerobic status to physiological condition.     

Marginal gap of crowns made with a phosphate-bonded investment and accelerated casting method

BACKGROUND: Most patients undergoing in-hospital cardiac resuscitation will not survive to hospital discharge. OBJECTIVE: To derive a decision rule permitting the discontinuation of futile resuscitation attempts by identifying patients with no chance of surviving to hospital discharge. PATIENTS AND METHODS: Patient, arrest, and outcome data for 1077 adult patients undergoing in-hospital cardiac resuscitation was retrieved from 2 randomized clinical trials involving 5 teaching hospitals at 2 university centers. Recursive partitioning was used to identify a decision rule using variables significantly associated with death in hospital. RESULTS: One hundred three patients (9.6%) survived to hospital discharge. Death in hospital was significantly more likely if patients were older than 75 years (P<.001), the arrest was unwitnessed (P = .003), the resuscitation lasted longer than 10 minutes (P<.001), and the initial cardiac rhythm was not ventricular tachycardia or fibrillation (P<.001). All patients died if there was no pulse 10 minutes after the start of cardiopulmonary resuscitation, the initial cardiac rhythm was not ventricular tachycardia or fibrillation, and the arrest was not witnessed. As a resuscitation rule, these parameters identified all patients who survived to hospital discharge (sensitivity, 100%; 95% confidence interval, 97.1%-100%). Resuscitation could have been discontinued for 119 (12.1%) of 974 patients who did not survive, thereby avoiding 47 days of postresuscitative care. CONCLUSIONS: A practical and highly sensitive decision rule has been derived that identifies patients with no chance of surviving in-hospital cardiac arrest. Prospective validation of the rule is necessary before it can be used clinically.     

Changes in serum dopamine beta hydroxylase activity related to coma

Dopamine Beta Hydroxylase (DBH) activity was determined in 24 deeply comatose patients enrolled in the Collaborative Study of Cerebral Survival. All patients had been without cerebral responsiveness or spontaneous respirations for at least 15 minutes. Patients were examined, EEGs performed and blood for DBH drawn within 24 hours of the cerebral insult. DBH activity was lower in the deeply comatose patients than in a group of 51 age matched normal individuals. It is postulated that destruction or inactivation of the central nervous system (CNS) and particularly of the cerebrum may result in lowered serum DBH activity through decreased activation of sympathetic nerve terminals.     

Endoscopic CO2 laser excision of large or recurrent laryngeal saccular cysts in adults

BACKGROUND: Most paediatric cardiac arrest studies have been conducted in the USA, where paramedics provide prehospital emergency care. We wanted to study the outcome of paediatric cardiac arrest patients in an emergency medical system which is based on physician staffed emergency care units. METHODS: We analysed retrospectively the files of 100 prehospital cardiac arrest patients from Southern Finland during a 10-year study period. The patients were less than 16 years of age. RESULTS: Fifty patients were declared dead on the scene (DOS) without attempted resuscitation, and cardiopulmonary resuscitation (CPR) was initiated in 50 patients. The sudden infant death syndrome was the most common cause of arrest in the DOS patients (68%) as well as in those receiving CPR (36%). Asystole was the initial cardiac rhythm in 70% of the patients in whom CPR was attempted. Resuscitation was successful in 13 patients, 8 of whom were ultimately discharged. Six of the patients survived with mild or no disability and 4 of them had near-drowning aetiology. In multivariate analysis, the short duration of CPR (< or = 15 min) was the only factor significantly associated with better survival. CONCLUSIONS: Although prehospital care was provided by physicians, the overall rate of survival was found to be equally poor as reported from systems with paramedics. The only major difference between physician- and paramedic-staffed emergency care units is the ability of physicians to refrain from resuscitation already on the scene when prognosis is poor.